The source of infection are patients with clinically expressed or latent forms of the disease. Adenovirus is excreted with upper respiratory tract secretions up to the 25th day of illness, with feces - up to 1.5 months.
The route of transmission is airborne, but the possibility of alimentary transmission of the infection cannot be ruled out.
The incidence is year-round with an increase in cold weather, but pharyngoconjunctival fever is more often diagnosed in the summer.
Children and middle-aged people are more likely to get sick. The incidence is especially high in newly formed groups during the first 2-3 months (for example, military personnel). Elderly people rarely get sick with adenovirus infection.
Immunity is type-specific, so repeated cases of the disease are possible.
The incubation period ranges from 4 to 14 days (usually 5-7 days).
Adenovirus infection is characterized by a combination of pharyngitis, rhinitis and lymphadenopathy.
Both acute and gradual onset of the disease is possible. Body temperature may be subfebrile or febrile, remains elevated for 1-2 weeks, may be prolonged and have two waves, but is tolerated relatively well. In adenovirus infection, occurring only with damage to the upper respiratory tract, the temperature persists for 2-3 days and usually does not exceed subfebrile numbers.
Febrile temperature and its prolonged persistence are more typical for children under 7 years of age; subfebrile temperature is more typical for children over 7 years of age.
Subjective manifestations of intoxication may include: chills, mild and intermittent headache, myalgia, arthralgia, weakness, lethargy, drowsiness, and loss of appetite.
From the first day of illness, nasal congestion is observed with scanty or abundant (especially in children) serous discharge, which quickly becomes serous-mucous, and may become mucopurulent.
Catarrhal bilateral conjunctivitis occurs in 1/3 of patients, but often begins as unilateral. Membranous conjunctivitis occurs mainly in preschool children. The disease begins acutely and is severe. Body temperature reaches 39-40°C and persists for 5-10 days.
Catarrhal, follicular, membranous conjunctivitis develops on the 2nd-4th day. Sometimes on the first day of the disease the lesion is unilateral, and after a few days both eyes are involved. Conjunctivitis is characterized by burning, stinging, a feeling of sand in the eyes, profuse lacrimation, swollen eyelids, hyperemic eyelid skin, narrowed eye slits.
Pharyngitis is characterized by moderate pain, a burning sensation, a scratchy feeling, or a sore throat.
Acute laryngotracheobronchitis is observed in young children and is characterized by hoarseness, the appearance of a rough "barking" cough, and the development of stenotic breathing. Often, a false croup syndrome occurs, in which (unlike diphtheria) there is no aphonia. Bronchitis rarely develops in adults.
Pneumonia develops mainly in young children.
With adenovirus infection, the skin may be pale or hyperemic, the face may become puffy, and sometimes there may be a papular rash.
The conjunctivae are brightly hyperemic, edematous, the discharge is scanty, pinpoint hemorrhages in the conjunctivae or sclera are possible. On the 2nd-3rd day, the conjunctivae become granular due to the bulging of the follicles.
With membranous conjunctivitis, the eyelids are sharply swollen, soft to palpation, on the 4th-6th day, grayish films appear on the cartilaginous parts of the eyelids and transitional folds, which do not spread to the eyeballs and are rejected without a defect in the mucous membrane.
A long course of conjunctivitis is typical, and hemorrhage into the sclera is possible.
Keratoconjunctivitis in children is rare. It is not accompanied by respiratory tract damage. After 6-7 days, keratitis occurs against the background of disappearing conjunctivitis. A sharp decrease in the sensitivity of the cornea, subepithelial infiltrates without a tendency to ulceration are noted. It is long-term, but benign. The foci of corneal opacity completely disappear after 3-6 months.
Pharyngitis is characterized by congestive hyperemia and swelling of the posterior pharyngeal wall, hyperplasia of submucosal lymphoid follicles (granularity may take on the appearance of a "cobblestone pavement"). The palatine tonsils may be enlarged, in some patients, loose white plaques in the form of dots and islands are visible, easily removed with a spatula (they can be unilateral or bilateral).
Lymph node enlargement is primarily manifested by enlargement of the submandibular and cervical lymph nodes. In systemic lymphadenopathy, enlargement of the axillary, inguinal, mediastinal mesenteric lymph nodes is possible (symptoms of peritoneal irritation may appear). The lymph nodes are not greatly enlarged, their consistency is soft elastic, they are usually painless, not fused with each other or with surrounding tissues, and do not suppurate.
Muffled heart sounds and a soft systolic murmur at the apex develop only in severe forms of the disease.
Dry wheezing may be heard in the lungs against the background of harsh breathing.
Enlargement of the liver (33%) and spleen (25%) is possible (they will disappear as the catarrhal syndrome subsides).
In 22% of patients with adenovirus infection (mainly in children under 3 years of age) diarrhea is present; pain in the epigastrium is also possible.
Otitis, sinusitis, pneumonia.
Early laboratory diagnosis of adenovirus infection is possible by detecting viral antigen in the epithelial cells of the nasopharyngeal mucosa using the immunofluorescence method.
Serological diagnostics is retrospective (the complement fixation reaction with the adenovirus antigen is used): an increase in the antibody titer in paired sera by 4 or more times is considered diagnostic.
In CBC usually there are no changes; sometimes moderate leukopenia and aneosinophilia are detected; ESR is normal or moderately elevated.
The concentration of C-reactive protein in 18% of patients with adenoviral tonsillitis does not exceed 15 mg/l, in 27% it is in the range of 15-30 mg/l, and in 37% it exceeds 60 mg/l.
During anterior rhinoscopy in the dry rhinitis phase, hyperemia and injection of the vessels of the mucous membrane, its dryness, and absence of discharge are noted.
Chest X-ray reveals widening of the lung roots and forced bronchovascular pattern, infiltrative changes. Adenoviral pneumonia can be focal or confluent.
Morphologically: cellular lesions caused by adenoviruses are characterized by a unique cytopathic effect, by which they are recognized. Cells infected with adenoviruses become rounded, lose their normal structure, form grape-like clusters, and eventually die.
Nowadays, in patients with adenovirus infection, such typical symptoms as tonsillitis, conjunctivitis, and hepatomegaly are recorded relatively rarely – in 16-29% of cases.
Adenovirus infection, mild
Amebiasis occurs in all countries of the world, but a particularly high incidence is observed in tropical and subtropical climates, where amebiasis accounts for 10-15% of all acute gastrointestinal diseases in humans.
Every year, the incidence of intestinal amebiasis in the world is about 50 million people.
All age groups of both sexes suffer from amebiasis.
The source of infection is human who releases cysts into the environment with feces. Epidemiologically, the most dangerous are carriers of amoebas. The release of cysts can continue for many years.
The infection mechanism is fecal-oral; transmission routes: food, water, contact. The factors of pathogen transmission are most often food products (especially vegetables and fruits) and water, less often - unwashed hands and household items. The spread of amoeba cysts is facilitated by flies and cockroaches.
Amebiasis is characterized by sporadic incidence. In endemic regions, the disease is registered year-round, but most cases (78%) occur in the summer-autumn period.
There are three main forms of manifest amebiasis: intestinal, extraintestinal and cutaneous. It is believed that in the vast majority of cases, when infected with amoeba, asymptomatic carriage develops.
Acute intestinal amebiasis is the most common manifest form of infection.
The incubation period lasts from 1-2 weeks to 3 months or longer.
Acute onset of the disease is observed in 78% of patients, gradual onset in 22% of patients.
In 65.3% of patients with intestinal amebiasis, subfebrile temperature is recorded, in 22.7% - fever from 38.2 to 39.4°C, in 12% of patients the body temperature remains normal.
All patients experience weakness; 52% complain of moderate headache, 62% of loss of appetite. Nausea is noted by 78% of patients, vomiting by 50.7%, flatulence by 29.3%. Most patients experience vomiting 1–3 times, 7.3% experience multiple vomiting.
Overall, the patients' condition remains satisfactory.
From the first days of the disease, all patients develop loose stools: at first, abundant feces, with a sharp odor; later, the frequency of defecation increases, the stool loses its fecal character, the amount of mucus and blood increases. The frequency of stool in 82.7% of patients does not exceed 10 times a day. Mucus is present in 94% of patients. Some patients note the appearance of blood in the stool even with formed stool. As the disease progresses, the stool may acquire the appearance of "raspberry jelly" (mucus soaked in blood).
All patients with intestinal amebiasis complain of abdominal pain: initially diffuse, then in 37.3% of patients it is localized in the right iliac region, and in 62.7% of patients it spreads along the entire large intestine.
Pain is constant in 46% of patients; 35.7% of patients complain of cramping, cutting pain before defecation. If the rectum is involved, painful tenesmus is possible. Abdominal discomfort is noted by 19.3% of patients, flatulence - by 29.3% of patients, rumbling along the intestines - by 20.7%.
The abdomen is soft or slightly distended, painful on palpation along the large intestine.
Symptoms of intestinal amebiasis usually persist for no more than 4-6 weeks. Subsequent remission can last from several weeks to several months, but then the clinical picture of chronic amebiasis may appear, which continues for many years, if not treated.
With chronic intestinal amebiasis asthenia, hypochromic anemia, hypoproteinemia, and hypovitaminosis gradually increase.
There is a recurrent and continuous course of chronic intestinal amebiasis.
In the recurrent form, periods of exacerbation alternate with periods of remission. In the continuous form, there are no periods of remission, the disease proceeds with periodic weakening or strengthening of symptoms.
During an exacerbation, the frequency of bowel movements can reach 20-30 times a day or more. Pain is weak or absent. Patients complain of an unpleasant taste in the mouth, a burning sensation, and soreness of the tongue. Appetite is decreased or absent.
Cardiovascular system: pulse lability, tachycardia, and muffled heart sounds are observed.
The abdomen is retracted, painful on palpation in the iliac regions.
In uncomplicated intestinal amebiasis, the liver is usually of normal size or slightly enlarged, painless. The spleen is not enlarged.
Extraintestinal amebiasis
Liver amebiasis is more common, and it can occur both with acute intestinal amebiasis and after several months or even years. Men get sick much more often than women.
Liver amebiasis occurs acutely, subacutely and chronically. It is observed in two clinical forms: as amebic hepatitis and liver abscess.
Acute amoebic hepatitis usually develops against the background of intestinal amebiasis.
Body temperature is often subfebrile, with periodic rises to febrile levels, but may remain normal.
Jaundice шы rare.
The liver enlarges (sometimes to a significant size), hardens, and sometimes becomes extremely painful.
Liver abscesses can be single or multiple, and are usually localized in the right lobe of the liver.
The temperature rises to 39 degrees and above. Temperature curves of remittent, hectic or constant type. Fever is accompanied by chills, profuse sweating when the temperature drops.
Pain in the right hypochondrium, radiating to the right shoulder, intensifying with breathing, changing position, and palpation of the liver is often noted.
On examination: sharpened facial features, sallow skin tone. Jaundice sometimes develops. In severe cases, swelling of the feet and shins appears.
Heart sounds are muffled, blood pressure is low, tachycardia.
The abdomen is usually swollen, weakly participates in the act of breathing, muscle tension is often determined in the right hypochondrium. The liver is enlarged.
In chronic amoebic liver abscess, the fever becomes irregular, weakness and exhaustion increase, and constant pain in the right hypochondrium persists. The liver is enlarged, painful, and if the abscess is localized on its anterior surface, it can be felt as a tumor formation.
Pulmonary amebiasis develops with hematogenous spread of amoebas to the lungs or with a liver abscess breaking through into the pleural cavity. Clinically, it occurs as a specific pleuropneumonia or lung abscess.
Pneumonia is characterized by chest pain, cough with phlegm, sometimes with an admixture of blood.
The temperature is normal or subfebrile.
Fine bubbling rales are heard in the lungs.
Amebic pneumonias are characterized by a sluggish course and without specific treatment can develop into lung abscesses.
Amebic lung abscesses usually take a chronic course. The temperature is subfebrile with periodic rises to high numbers. Sputum is abundant and bloody ("chocolate" sputum, "anchovy sauce").
The formation of amoebic abscesses in the brain is accompanied by the development of focal and general cerebral symptoms. Patients experience severe headaches, nausea, vomiting; the temperature is subfebrile or normal. Neurological symptoms depend on the localization of the abscesses and the degree of damage to the brain centers.
Amebiasis of the skin: erosions or extensive ulcers appear on the skin, mainly in the perianal area, perineum and buttocks, usually deep, slightly painful, with blackened edges, and an unpleasant odor.
Complications of intestinal amebiasis: pericolitis, perforation of the intestinal wall with subsequent peritonitis, gangrene of the mucous membrane, bleeding, intestinal strictures, rectal prolapse.
Liver abscesses are complicated by perihepatitis, purulent peritonitis, pleurisy, pericarditis. Mortality in amoebic liver abscesses without specific treatment reaches 25% and higher.
Lung abscesses sometimes lead to purulent pleurisy, empyema, pyopneumothorax, and hepatopulmonary fistulas.
The main method for detecting amoebas is microscopy of native preparations stained with Lugol's solution and iron hematoxylin according to Heidenhain. The study is carried out repeatedly: the diagnosis can be removed only after 4 negative stool tests.
Confirmation of the diagnosis is provided by the detection under a microscope of tissue forms in sputum, abscess contents, ulcer material, and detection of a large vegetative form of amoeba in feces. Detection of luminal forms and cysts of amoeba in feces is insufficient for a final diagnosis.
Freshly excreted feces are examined (no later than 10-15 minutes after defecation, sometimes multiple parasitological examination of feces is required). Provocation with laxatives is contraindicated.
It is also possible to cultivate amoebas on artificial nutrient media with bacteria (Robinson's medium).
Serological reactions: with intestinal amebiasis after the 7th day, serological tests are positive in 60-70% of patients, with amoebic abscess - in more than 95%. In IHR, antibodies in a titer of 1:128 and higher can be detected for 10 or more years after the infection.
During morphological examination of an abscess biopsy, trophozoites (vegetative forms) can be detected in the parietal space.
CBC: anemia is detected in 48.7% of patients, a decrease in the concentration of erythrocytes to 3.0 * 10 ^ 12 / l - in 34.6% of patients. In 14% of patients, the number of erythrocytes is reduced to 2.3 * 10 ^ 12 / l. Moderate leukocytosis up to 13.8 * 10 ^ 9 / l is observed in 38.7% of patients. Eosinophilia up to 12% is detected in 16% of patients. An increase in ESR to 35 mm / h is noted in 28% of patients.
Complete blood count in chronic amebiasis: hypochromic anemia, eosinophilia, monocytosis, lymphocytosis, increased ESR.
Complete blood count in amoebic hepatitis: moderate leukocytosis is detected.
CBC in amoebic abscess: neutrophilic leukocytosis (15-50*10^9/l), increased ESR. With prolonged course, hypochromic anemia develops.
Coprogram: leukocytes in feces are elevated in all patients: up to 30–40 in the field of vision in 54.7% of patients, more than 100 in the field of vision in 45.3% of patients. In 96% of patients, erythrocytes are elevated in feces: up to 50 erythrocytes in the field of vision in 38.9% of patients, more than 100 erythrocytes and up to closure of the fields of vision in 61.1% of patients.
Biopsy: The microscopic picture in amoebic colitis is characterized by the presence of amoebic trophozoites, deformation of the crypts and ulceration of the mucous membrane. The ulcers are surrounded by a narrow ridge of hyperemia and edema.
Endoscopic examination reveals inflammatory changes in the rectum and sigmoid colon in all patients, catarrhal-follicular proctosigmoiditis in 40.1% of patients (the mucous membrane is hyperemic, edematous, with pronounced follicles covered with a yellowish cheesy coating). In 45.2% of patients, against the background of hyperemic mucous membrane, there are multiple hemorrhages, erosions and small ulcers measuring 3-5 mm (rarely up to 1 cm), covered with fibrin.
Classic endoscopic picture of amoebiasis: ulcers are often located at the tops of folds, have undermined edges, the bottom can reach the submucosa, covered with pus and necrotic masses; the mucosa, free of ulcers, looks little changed, almost normal.
Currently, ulcerative colitis is detected in 5.6% of patients. The mucous membrane of the large intestine is clearly hyperemic, edematous, loose, bleeding (easily vulnerable), with a large number of erosions and ulcers. No unchanged areas of the mucous membrane are found. A large amount of mucopurulent mass with blood is determined in the lumen.
The endoscopic picture in chronic intestinal amebiasis is varied. Along with ulcers, cysts, polyps, and amoebomas can be detected, which are difficult to differentiate during examination.
Irrigoscopy in acute amoebiasis reveals uneven filling of the colon sections, the presence of spasm and rapid bowel movement. In chronic intestinal amoebiasis, the same changes are revealed, as well as the absence of haustration, sometimes - cicatricial changes with intestinal stenosis. Amoebomas give filling defects and simulate tumors during fluoroscopy.
Chest X-ray in case of amoebic abscess reveals a high position of the diaphragm with decreased mobility of the right dome; in case of subdiaphragmatic localization of the abscess, effusion in the right pleural sinus can be determined.
Radiologically, in amoebic pneumonia, infiltrative changes are detected, and in amoebic lung abscess, a cavity with a horizontal fluid level in the affected lung is determined.
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Acute intestinal amoebiasis of moderate severity
Ascariasis is widespread in humid zones of temperate, subtropical and tropical zones, is rarely recorded in dry steppes, and is absent in high mountains, deserts and permafrost zones.
Among patients with ascariasis, children predominate (59.2%); women are also slightly more likely to get sick (54.4%).
The source of infection is humans. The lifespan of female parasites is about 1.5 years, so in the absence of reinvasion, humans remain a source of infection for one and a half years.
Routes of transmission: water, food, contact.
Transmission factors: vegetables, fruits, berries, dirty hands, household items.
When collecting an epidemiological history, it turns out that 70.4% of patients (mostly children) eat unwashed vegetables, bite their nails, lick their hands, do not wash their hands after returning from the street and before eating, and in rare cases, eat soil.
Natural susceptibility to ascariasis is high.
Ascariasis is registered more often among rural residents than among urban residents. Most often, children, agricultural workers and gardeners get sick in places where there is no centralized sewage system, and the contents of cesspools are used as fertilizer.
City residents become infected due to poor personal hygiene and consumption of unwashed or poorly washed berries, vegetables, and herbs purchased from small private farms or grown in their own gardens and summer cottages.
Seasonality in the temperate climate zone - from April to October; in warm and humid climates, the incidence is year-round.
Immunity is not expressed. Immunity to superinvasion and reinvasion is formed in endemic regions: immune factors against ascaris larvae reduce the intensity of invasion.
The clinical course of ascariasis is divided into two phases: early (migration) and late (intestinal).
The early phase is often asymptomatic.
In the manifest course, malaise appears 2-3 days after infection. Body temperature is usually normal, less often subfebrile. Patients note general weakness, headaches, sweating, and myalgia.
As part of Loeffler's syndrome, a cough appears (dry or with a small amount of mucous, less often mucopurulent sputum, hemoptysis), shortness of breath, chest pain; dry or moist rales are heard in the lungs.
Some patients develop itchy skin, an itchy urticarial rash, or small vesicles on the hands and feet.
Sometimes it is possible to detect dullness of percussion sound over pulmonary infiltrates.
Hepatosplenomegaly is possible.
The late (intestinal) phase of ascariasis is manifested by dyspepsia (67.7%) and asthenia (32.8%). Dyspeptic syndrome prevails in all age groups.
Patients complain of changes in appetite (usually a decrease), weight loss, nausea, sometimes vomiting during painful attacks, a feeling of bitterness in the mouth, spastic (often paroxysmal) pain (82%) in the epigastrium, around the navel or in the right iliac region, diarrhea, alternating diarrhea with constipation.
Abdominal pain is short-lived and not intense, appears periodically, does not have a permanent localization, often (about 50%) occurs in the morning before breakfast or in the evening before bed.
19% of sick children report bloating and rumbling in the abdomen. It occurs both on an empty stomach and after eating; in some children, rumbling in the abdomen is observed at night.
Stool changes in 59% of sick children; some patients with diarrhea have admixture of mucus in their stool.
In children under 3 years of age, appetite disturbance can manifest itself as refusal to eat, restlessness while eating, cravings for sweets, a sharp increase in appetite, and lack of satiety.
The helminths may be expelled with feces or through vomit.
Fatigue, memory impairment, irritability, headache, dizziness, sleep disturbance are noted, hysterical seizures, epileptiform convulsions, meningism are possible. Sometimes - dilated pupils, anisocoria, photophobia, amblyopia.
Sleep disturbance is observed in 50% of preschool children: restless sleep with increased motor activity during sleep, disturbance in the depth of sleep with frequent awakenings at night, and sometimes nightmares.
Allergization occurs in 14.4% of children in the form of allergic dermatitis, urticarial or maculopapular rashes, and skin itching.
18% of children have a delay in physical development, insufficient weight gain or weight loss over the past year.
Paleness, dryness and flaking of the skin, extremities that are cold to the touch can be detected in 19% of patients, hyperhidrosis of the palms and feet - in 11% of children, depigmentation of nails - in 8% of children.
Enlargement of peripheral lymph nodes is observed in 9% of children (up to 1 cm, dense, painless).
Some patients experience hypotension.
Percussion and auscultation disturbances from the respiratory system are not detected during the intestinal phase of ascariasis.
Intestinal obstruction, obstructive jaundice, reactive pancreatitis, purulent cholangitis, liver abscesses, appendicitis, peritonitis, asphyxia (when adult worms are thrown from the stomach into the pharynx and then aspirated). In some cases, dry or effusion pleurisy occurs.
In the early (migratory) phase, roundworm larvae can sometimes be found in sputum.
In the intestinal phase, it is possible to detect helminth eggs in the feces. Due to the low sensitivity of microscopy, repeated examinations are recommended at intervals of 1-2 weeks.
Both roundworm eggs and the parasites themselves can be detected in the stool. The female has a length of 20-40 cm (thickness 3-6 cm), the male 15-25 cm (thickness 2-4 cm).
Serological tests have not received widespread practical use.
It is possible to examine stool for roundworm DNA using PCR.
In the CBC during the migration phase, the number of leukocytes is usually normal, less often - leukocytosis (14.3%). Eosinophilia is detected in 64.9% of patients, usually occurs simultaneously with infiltrates in the lungs and can reach 60-80%. ESR is elevated in 28.6% of patients (average 17 mm/h).
In the CBC during the intestinal phase: moderate hypochromic or normochromic anemia (35.7%); eosinophilia does not always occur.
In 35.7% of patients there is an increase in ALT (on average 47.2 IU/l), in 21.4% there is an increase in the thymol test. The concentration of bilirubin and cholesterol is within normal limits.
X-ray and computed tomography of the lungs during the migration phase reveal round (or irregularly shaped) infiltrates with unclear contours and a heterogeneous structure, which quickly change shape and location. The contours of the infiltrates become smooth when atelectasis appears.
Infiltrates can be single or multiple, found in one lobe or throughout all lung fields within 2-3 weeks. During the control MSCT (after 7-10 days), positive dynamics are recorded - some of the infiltrates disappear, others significantly decrease in size.
Ultrasound of the biliary tract reveals signs of biliary dyskinesia (42.8%), hepatomegaly (21.4%).
Contrast radiography of the abdominal organs makes it possible to detect the parasite against the background of the passage of barium suspension in the intestinal lumen.
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Ascariasis complicated by intestinal obstruction.
Balantidiasis is predominantly registered in tropical and subtropical regions, which is associated with the climatic and cultural features of these countries, as well as with the low level of sanitation. The greatest amount of cases of the disease are described in China, Iran, the Philippines, Brazil, Venezuela, Egypt, Zaire, Sudan, Papua New Guinea, Hawaii.
Balantidiasis is most often diagnosed in people aged 21-40. Men and women get sick equally often. The frequency of infection in people correlates with the level of education.
The source of infection is most often pigs, less often cattle and rats; humans are considered as a source of infection by some researchers.
Balantidiasis most often affects young animals. These are mainly weaned piglets; healthy carriers are more common in adult animals. The infection rate in free-ranging pigs is higher than in caged pigs.
The transmission mechanism is feco-oral - it is realized through contaminated water (including that used for melioration), vegetables, soil; infection is possible through contact and household contact when caring for animals.
Balantidiasis is registered as sporadic cases, mainly among rural residents engaged in pig farming, using water and vegetables contaminated with balantidia cysts (their infection rate is estimated at 4–5%).
In 1926, balantidiasis was frequently reported among tea plantation workers in Cachar, Assam..
The development of the disease is facilitated by: unsanitary conditions, close contact with pigs, immunosuppression (some authors believe that balantidiasis does not develop in immunocompetent individuals). It was noted that most of the sick farmers did not regularly treat their work clothes and did not decontaminate them before washing.
Balantidiasis can occur in subclinical, acute, chronic continuous and recurrent forms (it is believed that carriage of balantidia is predominant).
The incubation period is 5–30 days (usually 10–15).
With subclinical balantidiasis there are no intestinal disorders, the patients consider themselves healthy. However, during rectoscopy, you can find catarrhal-hemorrhagic and characteristic ulcerative lesions in the distal colon. Liver dysfunction, hypo- and avitaminosis C, and eosinophilia in the blood are revealed.
Acute balantidiasis occurs in most cases with the presence of intoxication and symptoms of colitis, according to the severity of which mild, moderate and severe forms of the disease are distinguished.
The disease begins acutely, the temperature rises to a high level (sometimes with chills) or subfebrile temperature is observed, headache, nausea, repeated vomiting, flatulence are disturbing, and weakness progresses.
Balantidiasis is characterized by anorexia and moderate abdominal pain. Cutting abdominal pain is also possible, and if the rectum is involved, tenesmus.
The stool is abundant, liquid, often with an admixture of mucus, blood (about 12% of patients) and pus, with a putrid odor. The frequency of bowel movements can vary from 3-5 in mild cases to 15-20 or more times in severe cases.
Dryness and coating of the tongue can often be seen.
Often, spasm and pain in the colon, enlargement and pain in the liver are determined. In severe cases, there may be signs of peritoneal irritation.
As balantidiasis progresses, the patient loses weight.
The duration of acute balantidiasis does not exceed 2 months. Without treatment, it becomes chronic.
The chronic relapsing form of balantidiasis lasts 5-10, and sometimes more years, with alternating periods of exacerbations and remissions. The duration of exacerbations is usually from 7-10 to 20-30 days, remissions - 3-6 months. During the remission period, clinical disorders are not detected.
Signs of general intoxication are less pronounced than in the acute form of the disease; intestinal symptoms predominate in the clinical picture.
Stool 2-3 times a day, with mucus (rarely with blood). The abdomen is swollen, painful along the ascending colon. Fibrocolonoscopy: ulcerative changes.
The chronic continuous form of balantidiasis is characterized by a monotonous course with moderate toxic and intestinal symptoms over a number of years. In the absence of etiotropic therapy, cachexia may develop.
Acute appendicitis, intestinal bleeding, perforation of colon ulcers with peritonitis.
Extraintestinal complications are possible: liver abscesses, damage to the urinary tract.
The diagnosis is confirmed by detecting Balantidia in feces or in the contents of intestinal ulcers (scraping is taken during endoscopy). The feces must be examined no later than 20 minutes after defecation.
CBC: moderate hypochromic anemia, MCV is moderately elevated, moderate leukocytosis, eosinophilia up to 5-12%, in severe cases leukocytosis increases to 20-25×10^9/l with neutrophilia and band shift, ESR increases to 30-40 mm/h. High neutrophilia is considered an unfavorable sign.
The level of total protein is decreased, the content of α-2 and γ-globulins is increased with a reduced level of albumin
The concentration of alkaline phosphatase and transaminases is increased.
Decreased concentration of sodium, chlorides and bicarbonate.
A stool test for occult blood is always positive.
Fibrocolonoscopy: in the acute period, 12.7% of patients have scanty small ulcers in the colon, in which balantidia can be detected.
Most often, ulcers occur along the folds of the mucous membrane and in places where the intestinal wall bends, have uneven, undermined thickened edges, and the bottom is covered with gelatinous necrotic bloody-purulent masses, often black in color.
Ulcers vary in size and time of formation, the area of some can reach several square centimeters. After the rejection of necrotic masses, a cavity remains, communicating with the lumen of the intestine.
During morphological examination: initially, areas of edema and hyperemia appear on the folds of the membrane, an infiltrate is formed consisting of lymphocytes, histiocytes and neutrophils. Increased proliferation of the intestinal crypt epithelium, its necrosis with the formation of erosions and ulcers are noted.
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Acute balantidiasis of moderate severity
In Germany and Austria, 5-20% (depending on age group and region of residence) of healthy donors are seropositive; in Switzerland - 20%.
In the USA, where B. burgdoferi sensu stricto is widespread, Lyme disease occurs predominantly with damage to the musculoskeletal system; in Europe, cutaneous manifestations predominate (lymphocytoma cutis, chronic atrophic acrodermatitis), which is associated with the distribution area of B. afzelii.
In the countries of Eurasia and North America, chronic tick-borne borreliosis is registered in 3.5–45.0% of patients even after a course of antibacterial treatment of the acute infectious process, and without antibacterial therapy – in 60.0% of patients.
The average age of patients in the group with the non-erythematous form of borreliosis was 42.5 years, which is significantly lower than in the group with erythema – 53 years.
The source of infection are wild animals (rodents, birds, deer, etc.); humans are not a source of infection. When hunting for them, ticks climb plants up to one and a half meters high.
The main transmission route is transmissive, since borrelia are unstable in the environment (they die when dried out; at a temperature of 50°C they die within 10 minutes; they die under the influence of ultraviolet radiation; they are well preserved at low temperatures).
The vector is ticks of the genus Ixodes (I. Ricinus, I. Persulcatus, I. dammini, I. scapularis). It is assumed that different genetic types of B. miyamotoi are associated with different species of vector ticks.
Infection occurs when a tick infests, when tick feces get on the skin, when a tick ruptures (if removed carelessly), and when material gets into a wound.
As a rule, ticks attack people outside the city, less often in city parks, cemeteries, etc.
The probability of infection from a bite from an infected tick is less than 5%.
The infection rate of ticks with Borrelia reaches 60% in foci, and coinfection of ticks with different types of Borrelia is possible.
The risk group includes persons engaged in agricultural, irrigation and drainage, construction, procurement, industrial, geological, exploration, expeditionary, deratization, disinfestation, landscaping, logging, forest management activities, as well as laboratory workers.
Transplacental transmission is possible.
The alimentary route of infection through consumption of goat's or cow's milk is discussed.
Seasonality is related to tick activity. The first patients with tick bites are usually registered in March-April, the last ones - in October-November (the peak of activity is in May-June).
There are acute (up to 3 months), subacute (3-6 months) and chronic borreliosis.
In acute and subacute borreliosis, an erythematous form and a non-erythematous form (with predominant damage to the nervous system, heart, and joints) are distinguished.
Chronic course (more than 6 months) can be continuous and recurrent with predominant damage to the nervous system, joints, skin, heart.
By severity: severe, moderate, mild Lyme disease.
The incubation period lasts 1-30 days (in 86.4% of patients 1-14 days). A longer incubation period is observed in the group of patients with the non-erythematous form of the disease (12±2 days).
The incubation period in 15% of cases can exceed 4 weeks (up to 2 months).
The onset is acute or subacute with the appearance of pain, itching, a feeling of constriction or impaired sensitivity at the site of tick infestation. In the erythematous form, the acute onset of the disease is recorded in 71.43% of patients.
The severity of intoxication is variable: body temperature may remain normal, but may also reach a febrile level. Subfebrile temperature (37.1-38.5°C) is observed in 68.57% of patients with the erythematous form, fever - in 19.5%. With the non-erythematous form, an increase in body temperature from 38.1 to 39.5°C is recorded in 80% of patients.
The febrile period lasts 2-7 days; after the body temperature drops, subfebrile temperature is sometimes observed for several days.
Patients complain of chills, fever, moderate headache (12.1-32.1%), dizziness, muscle aches (3.6-14.6%), bone pain, arthralgia (7.6%), weakness (21.9-68.6%), fatigue (31.4%), malaise, nausea. Often, against the background of intoxication, there is a sore throat and dry cough.
Typical migratory erythema appears in 65.8-70% of patients.
Initially, a red spot or papule appears at the site of the tick bite. As it grows, the peripheral part of the erythema remains bright and hot to the touch, and the central part becomes pale (ring-shaped erythema), although in some patients it has the appearance of a homogeneous spot.
The size of the erythema can be from 3 to 70 cm, but the severity of the disease is not related to their size. Several red rings may appear within the outer border, the central part of which fades over time.
Erythema can persist for months, although sometimes it disappears without treatment after 2-3 weeks or several days. With etiotropic therapy, it quickly regresses and completely disappears by the 7th-10th day. Hyperpigmentation and peeling of the skin persist for some time at the site of resolved erythema.
In the area of erythema, patients may feel itching (41%), pain (47.1%) or burning.
Erythema is considered a reliable sign of the disease if its diameter is more than 5 cm and the following three conditions are met: erythema occurs at the site of the tick bite, is capable of centrifugal growth, the time between the bite and the appearance of erythema corresponds to the incubation period.
The appearance of erythema earlier than 3 days from the moment of infestation is considered an allergic reaction to the bite.
In 10-40% of patients, erythema is absent, and then the clinical picture includes only fever and non-specific symptoms of intoxication.
Urticarial rash and conjunctivitis are possible.
One third of patients experience enlargement of the lymph nodes close to the entry point of infection.
Signs of damage to the musculoskeletal system are observed both in the acute and chronic periods of the disease. Lyme arthritis can occur within 4 days to 2 or more years after the appearance of erythema migrans.
The development of arthralgia, mono- and oligoarthritis with the involvement of large joints, more often knees, is typical, polyarthritis occurs less often. Less typical is the involvement of small joints of the hands and feet.
Symptoms of cardiovascular damage are usually short-lived, often recorded at the height of the fever. Cardiological symptoms may appear within 7 days to 7 months (median 21 days) from the appearance of erythema.
Most often, these are AV blocks with a favorable outcome in 90% of cases. Sinoatrial, atrial blocks, blocks at the level of the His bundle branches, and Purkinje fibers are also possible. The degree of blockade repeatedly changes from I to III and back during the day, often being asymptomatic.
There are known cases of complete transverse heart block that required the installation of artificial temporary pacemakers.
In 67% of cases, Lyme carditis is combined with skin manifestations of the disease, in 27% - with neuroborreliosis, but there are also cases in which Lyme carditis is the only manifestation of the disease.
The period of hematogenous spread of infection is characterized by the greatest clinical polymorphism.
Secondary erythemas often appear. They are smaller in size, lighter in color, their number can reach 100, and their localization is not related to the bite site.
In 1-6% of cases, benign lymphocytoma occurs - a thickening of the skin on the earlobe (more often in children) or in the area of the nipple of the mammary gland (more often in adults), less often - in other areas (face, chest, limbs).
Lymphocytoma is a single, very slowly growing, dense infiltrate or nodule, the color of which can vary from pink to bright red, red-brown or dark purple. Subjective sensations are absent or the patient notes mild itching. The nodule persists from several days to months and even years.
In 10-90% of patients, the nervous system is affected: neuritis, polyneuropathy (in 83% of patients), serous meningitis (2.6%), Bannawart syndrome (meningoradiculoneuropathy - a combination of damage to the meninges and peripheral nervous system), radiculoneuritis.
Neuritis of the cranial nerves occurs in more than half of patients. Most often, it is bilateral paralysis of the facial nerve (more than 36% of cases of neuroborreliosis in Europe; more often in children), often with paresis of the facial muscles, numbness and tingling of the affected half of the face, pain in the ear or lower jaw, without clear sensory disturbances.
Less frequently, the oculomotor, optic, auditory, and IX-X pairs of cranial nerves are affected.
Peripheral nerve damage is observed in 1% of patients. Radicular disorders of sensitivity occur in the cervical, thoracic, and lumbar spine. Patients complain of pain, numbness, tingling, crawling, burning, etc. Typically, there is a decrease in the motor functions of certain muscle groups, and a decrease in tendon reflexes. These disorders are asymmetrical.
Serous meningitis is accompanied by headaches of varying intensity, nausea, vomiting, photophobia, soreness of the eyeballs, stiffness of the occipital muscles, and, less commonly, other symptoms of irritation of the meninges.
Bannwarth syndrome includes serous meningitis and damage to the spinal nerve roots (mainly in the cervical-thoracic spine). It is characterized by a sluggish course, atypical radicular (at chest level) intractable pain (mainly at night, leading to insomnia). Without treatment, the pain can persist for months, and with antibiotic therapy it disappears within a few days.
In 1/3 of patients, symptoms of mild encephalitis are detected in the form of sleep disturbances, decreased attention, memory impairment, increased excitability, emotional disorders, etc.
Amyotrophic syndrome can develop as a result of limited segmental radiculoneuritis, isolated neuritis of the facial nerve, mononeuritis regional to the site of tick attachment, widespread polyradiculoneuritis (Bannwarth syndrome), and myelitis.
Neurological disorders usually disappear completely within 1 month, but can recur and become chronic.
Within a few weeks from the moment of infection, approximately 8% of patients develop signs of heart damage: atrioventricular blocks (usually first or second degree, less often complete), intraventricular conduction disturbances, and less often myocarditis and pericarditis.
The duration of cardiac symptoms ranges from several days to 6 weeks.
At this stage, transient pains in bones, muscles, tendons, periarticular bags without external signs of inflammation are possible. These symptoms are observed for several weeks, relapses are possible.
Chronic course of Lyme borreliosis in 45% of cases is accompanied by damage to the musculoskeletal system, which occurs on average 1.5 years after the tick bite.
Recurrent oligoarthritis of large joints, especially knees (often unilateral) is typical; in some cases, symmetrical polyarthritis develops; small joints may also be affected. Arthritis is accompanied by destruction of bones and cartilages.
Arthralgia affects 93.3-100% of patients with lesions of the joint system: pain at rest (25.4%) and during physical exertion (16.7%), morning stiffness of the joints (7.8-56.7%) are possible.
Periarticular changes are detected in 11.8% of patients (myalgia - in 8.8%, enthesopathies - pain at the sites of tendon attachment - in 2.9%).
Chronic atrophic acrodermatitis is possible with B. afzelii infection: cyanotic-red spots on the extensor surfaces of the extremities, which tend to grow peripherally, merge, and become periodically inflamed. Gradually, the skin at the site of the spots atrophies and takes on the appearance of tissue paper. The process develops over several months and years.
Symptoms of neuroborreliosis develop on average 1.8 years after the tick bite. In chronic neuroborreliosis, all parts of the nervous system (central, peripheral and autonomic) are involved in the pathological process.
Encephalomyelitis develops rarely. Emotional lability (63%), rapid mood swings, increased excitability, fatigue (67%), bursting headaches localized in the frontal-parietal regions (42-76.8%), forgetfulness (25-56.7%), slowness of thinking (36.7%), and impaired ability to use existing knowledge (26.7%) are observed.
Patients with neuroborreliosis show ataxia (66.7%): instability in the Romberg pose, impaired performance of the finger-nose and heel-knee tests. 40% of patients have impaired abdominal reflexes, 33.3% have impaired superficial sensitivity, and 6.7% have pathological Babinski and Rossolimo foot reflexes.
Polyneuropathy is accompanied by impaired sensitivity (42%), distal paresthesia (33%), radicular pain, etc.
Significant motor disorders are not registered. The decrease in muscle strength is limited to moderate weakness in the fingers. Muscle tone is preserved.
In 63.3% of patients, tachycardia, profuse sweating, bright dermographism and lability of blood pressure are observed.
Changes in the cardiovascular system develop on average 2.3 years after the tick bite and are detected in 10-30.4% of patients with chronic tick-borne borreliosis.
Patients complain of discomfort (7.8%) or pain in the heart area of a pressing or stabbing nature (41.2%), attacks of palpitations or interruptions (15.7%), shortness of breath during physical exertion (13.7%). Sinus bradycardia is noted in 23.5% of cases.
After antibiotic therapy, conduction disturbances, signs of left ventricular hypertrophy and decreased voltage of the waves persist, which may indicate cardiosclerosis that developed before treatment.
In all patients, organ system lesions are combined. The most common variants are: lesions of joints and the nervous system - 53.3%, joints, the nervous system and the heart - 33.3%.
Chronic Lyme disease occurs with alternating remissions and relapses, sometimes becoming continuously relapsing.
Complications are very rare.
Screening examination in patients without symptoms of borreliosis who have received antibiotic prophylaxis is not advisable: given its effectiveness (87-99%), detection of antibodies will not change the patient management tactics.
The bacteriological method of diagnosing Lyme disease is the most reliable, but is not used in practice due to its duration (4-10 weeks), the high cost of nutrient media and insufficient sensitivity.
The sensitivity of the culture depends on the material, stage of the disease, experience of the personnel, and genotype of the spirochetes. The sensitivity of skin biopsy from erythema migrans is estimated at 40-60%, and of peripheral blood plasma samples from untreated patients with early disseminated infection is about 40% (higher in patients with multiple erythema migrans).
Variations of the Barbour-Stoenner-Kelly medium and modified Kelly-Pettenkofer medium are used for culturing B. Burgdorferi.
Cultures are examined using darkfield microscopy or fluorescence microscopy after staining aliquots with acridine orange.
Cultures must be incubated for at least 8-12 weeks before they can be considered negative.
PCR allows to detect Borrelia DNA in biopsies, blood, urine, cerebrospinal fluid. Moreover, their concentration in cerebrospinal fluid is lower than in blood and urine. The sensitivity of PCR of skin biopsies is quite high, but due to the traumatic nature of this method, it is not used routinely.
The diagnosis of chronic borreliosis can be confirmed by examining biopsies of the altered epidermis using the PCR method (but after 6 weeks of illness, the sensitivity of PCR is only 10-30%).
In this case, a positive PCR result in a seronegative patient with a long history of the disease is most likely a false positive.
Serological diagnostics is complicated by the late appearance of antibodies to borrelia. IgM usually appear from the 3rd week of illness, and IgG - after the 6th week. Detection of intrathecal antibodies is possible from the 2nd week of illness, and after 6-8 weeks they are determined in 99% of patients (sometimes in the absence of antibodies in the blood). It is possible to detect antibodies in the intra-articular fluid.
A positive indirect immunofluorescence reaction (IIFR) with an antigen from Borrelia is considered to be a 2-fold increase in the antibody titer after 3 weeks from the onset of the disease. In the absence of an increase in the antibody titer over time, a titer of 1:40 is diagnostic.
ELISA allows for the differential detection of IgM and IgG.
In IIFR, during the first month of the disease, antibodies are detected in only 5-13% of patients, in ELISA - in 44%, in immunoblot - in 32-100%.
IgM disappears by the 3rd to 60th month of illness, while IgG persists for up to 23 years or more. Sometimes patients may remain seropositive (including IgM) for many years even after adequate antibiotic therapy.
Patients with Lyme arthritis almost always have serum IgG antibodies to B. burgdorferi; negative IgG serology excludes Lyme arthritis. The absence of antibodies in chronically ill immunocompetent patients usually excludes borreliosis.
However, seronegative variants of the disease are possible. False negative serology results may be associated with the use of test systems prepared on the basis of a selective spectrum of antigens without taking into account the genotype characteristics of borrelia common in the region.
With early initiation of antibiotic therapy, antibodies to Borrelia may also not be detected.
False positive results can occur, for example, in syphilis.
In children, compared to adults, false-positive IgM results are statistically significantly less common: 4.9% compared to 34.1%. The number of questionable or false-positive IgG ELISA results did not differ statistically significantly between children and adults.
Lyme disease may become a diagnosis of temptation, in which serologic diagnostic results are interpreted according to the clinician's intentions and personal perceptions.
ELISA results may be considered false positive based on the results of an immune blot (Western blot) that detects IgM (if the duration of the disease is less than 4 weeks) and IgG against B. burgdorferi.
However, false-positive detection of IgM against B. burgdorferi by Western blot may occur in more than 40% of parvovirus-infected patients, as well as in patients with granulocytic anaplasmosis, Epstein-Barr virus carriers, and in patients with autoimmune diseases.
In the CBC in the acute period - normocytosis or leukocytosis and an increase in ESR.
In the CBC in patients with Lyme arthritis, a moderate increase in ESR is noted, on average no higher than 20–30 mm/h.
CRP levels in patients with Lyme arthritis are either normal or moderately elevated, and creatine phosphokinase level is elevated.
Rheumatoid factor and antinuclear antibodies are usually negative, but may be positive at low titers.
In the cerebrospinal fluid in case of CNS damage - predominantly lymphocytic pleocytosis in the range of 6-1100 cells in 1 μl (on average 100-220), protein concentration is increased (3-8 g/l), glucose is normal or slightly decreased, lactate level is slightly increased or normal.
On the ECG of patients with the erythematous form, changes of a hypoxic nature are revealed (flattening and inversion of the T wave, prolongation of the Q-T interval).
During the period of dissemination, atrioventricular block of varying degrees and diffuse myocardial lesions are recorded on the ECG.
When examining the joints, osteoporosis, cartilage depletion, cortical and marginal erosions, and sometimes subarticular sclerosis and osteophytosis can be detected.
MRI (including MR angiography) is very important in the differential diagnosis of neuroborreliosis. In neuroborreliosis, MRI can detect cerebral ischemia and stenosis of intracranial vessels.
Morphological examination of lymphocytomas reveals pronounced lymphocytic infiltration of the dermis.
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Acute Lyme borreliosis, non-erythematous form, mild
The age group 21–40 years is predominantly affected (44.6%), with women predominating (67.7%).
Group outbreaks are recorded more often (84.6%), while sporadic cases are less common (15.4%).
The incidence is year-round; some increase in incidence is observed in autumn and winter.
Transmission factors are usually home-canned products: canned mushrooms, vegetable salads, fruit compotes (apricots, peaches, cherries), sea buckthorn jam, pickled cucumbers and tomatoes. Less often, transmission factors are smoked fish and smoked sausages.
The disease begins acutely: dizziness, severe weakness, malaise, and sometimes headache appear. Subfebrile temperature (37.1–37.5°C) is usually observed in patients with a short incubation period.
All patients complain of nausea. About half of the patients complain of acute cramping or moderate pain, mainly in the epigastric region, followed by vomiting and loose stools without pathological impurities less than 10 times a day (usually 3-5 times).
Often, already during the period of gastrointestinal symptoms, the passage of food through the esophagus is disrupted (a “lump in the throat” sensation appears).
By the end of the day or on the second day, the disease enters the paralytic stage: hypermotility of the gastrointestinal tract is replaced by persistent atony, body temperature normalizes, the main neurological signs of the disease appear (they appear in various combinations, sequences and severity).
In the absence of gastrointestinal symptoms, the disease may manifest with dizziness, weakness and ophthalmoplegia.
Patients complain of "fog in the eyes", "a grid before the eyes", poorly distinguish objects close by (acute farsightedness is corrected with plus lenses), cannot read. Double vision appears. Ptosis of varying severity develops.
Several hours after ophthalmoplegia, the functioning of the muscles of the tongue and pharynx is disrupted (phonoplegia and phagoplegia).
Phonoplegia goes through 4 stages: first, hoarseness of the voice or a decrease in its timbre appears; then - dysarthria due to a violation of the innervation of the tongue ("mush in the mouth"); then - an open nasal voice due to paralysis of the soft palate (the soft palate does not phonate); finally - complete aphonia due to paralysis of the vocal cords.
Phagoplegia: the pharyngeal reflex is absent, there is a sensation of a foreign body in the pharynx ("unswallowed tablet"), choking, difficulty swallowing first solid and then liquid food, water. Due to denervation of the soft palate, when trying to swallow water, it pours out through the nose. In severe cases, complete aphagia occurs. Aspiration is possible, while the cough reflex is reduced, which leads to attacks of suffocation when food, liquid or mucus enters the larynx with the subsequent development of aspiration pneumonia, purulent tracheobronchitis.
Denervation of the salivary glands leads to a disruption of salivation (dry mouth).
Muscle weakness progresses.
Denervation of the intercostal muscles causes shortness of breath, a feeling of lack of air, and slurred speech. With complete paralysis of the intercostal muscles, patients feel the chest being compressed "as if by a hoop."
Due to paresis or paralysis of the diaphragm muscles, expectoration of sputum, which accumulates in the subglottic space, is impaired. A thick, viscous mucous film in the supra- and subglottic space can lead to asphyxia.
Due to denervation of the gastrointestinal tract, persistent constipation develops.
Sometimes acute urinary retention or involuntary constant urination is present.
For differential diagnosis, the absence of sensory disturbances is important.
On physical examination:
Consciousness is clear, but the patients are adynamic.
Initially, muscle weakness is most pronounced in the occipital muscles, as a result of which such patients may have a drooping head and are forced to support it with their hands.
The face is mask-like. The nasolabial fold is smoothed out, the patient cannot bare his teeth.
During the height of the illness, the gait is unsteady (“drunk”).
The skin and oral mucosa are dry; as respiratory failure progresses, cyanosis of the lips appears.
The pupillary reflex is weak or absent, anisocoria is possible. Convergent strabismus, diplopia, vertical nystagmus, mydriasis (pupils are dilated, sluggish or do not react to light at all), ptosis (usually bilateral) are noted; in severe cases, the eyeballs may be immobile.
Ptosis and muscle weakness can be detected by physical exercise (open and close your eyes tightly several times, measure muscle strength repeatedly using a dynamometer).
Due to the weakness of the intercostal muscles, breathing becomes shallow and barely noticeable.
The tongue protrudes with difficulty, sometimes jerkily. The soft palate hangs down, the palatal reflex is decreased or absent.
The mucous membrane of the oropharynx is dry.
Changes in the cardiovascular system are detected mainly in moderate and severe cases of the disease. Bradycardia alternates with tachycardia, hypo- or hypertension is possible.
Breathing is shallow, rapid, and respiratory sounds are weakened.
The abdomen is moderately distended, peristaltic sounds are sharply weakened.
Handshake strength is reduced.
There are no meningeal symptoms.
More persistent neurological symptoms are observed when consuming liquid contaminated products (compotes, jam).
Severity:
Mild: only ophthalmoplegia is present.
Moderate: glossopharyngeal muscles are involved.
Severe: the appearance of respiratory failure and severe bulbar disorders, or the innervation of the intestine and urinary tract is impaired.
Specific: myositis (usually develops in the 2nd week of the disease).
Nonspecific: pneumonia, tracheobronchitis, pyelitis, pyelonephritis, sepsis.
Cultivation of C. botulinum from stool does not confirm botulism, since its spores can be found in the intestines of healthy people.
Serological tests are ineffective because even lethal concentrations of the toxin do not provoke antibody formation.
A biological test on mice allows us to confirm the presence of botulinum toxin in the blood and determine its type.
In CBC there are no particular deviations from the norm, with the exception of monocytosis, which is also not always present. Leukocytosis, neutrophilia, and increased ESR should alert you to possible bacterial complications of botulism.
An increase in CPK-MB and AST is noted.
In moderate and severe cases, troponin levels may be elevated.
Blood oxygen saturation may be decreased.
ECG: change in the terminal part of the ventricular complex; in severe cases - up to complete AV block and ventricular fibrillation.
Laryngoscopy: the glottis is gaping.
Minute respiratory volume can be decreased
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Botulism, severe, complicated by aspiration pneumonia.
The disease is common in countries with developed grazing cattle breeding (South America, North Africa, Australia, New Zealand).
More often, hydatid echinococcosis is detected in middle-aged people.
The main source of infection is domestic dogs, less often - wolves and jackals. The parasite's eggs are shed in the animals' feces, contaminating their fur and the environment.
The main routes of transmission: contact, food, water. Human infection occurs through contact with infected animals (through unwashed hands), when picking berries and herbs, and drinking water, contaminated with helminth eggs.
The possibility of transplacental transmission of helminthiasis has been proven.
Risk groups: slaughterhouse workers, shepherds, tanners.
There are primary and secondary echinococcosis.
In uncomplicated cases, the disease is asymptomatic for years and can be detected accidentally. The first symptoms appear several years or decades after infection.
Patients complain of headaches, weakness, sometimes shortness of breath and palpitations, loss of appetite, weight loss, pressure, discomfort, sometimes pain in the right hypochondrium, itchy skin, rashes. Nausea, vomiting, and stool disturbances are possible.
When the cyst is localized in the right lobe of the liver, the pain syndrome is similar to that of cholecystitis. When localized in the left lobe, heartburn, belching, and vomiting appear.
In some cases, low-grade fever, urticaria, subicteric sclera, or jaundice are observed.
If the cyst is located subdiaphragmatically, the percussion sound over the lower parts of the right lung may be dulled.
The liver is enlarged (with a long course of the disease, hepatomegaly can be significant), with a deep cyst it becomes dense and painful on palpation, with a superficial location the cyst can be palpated in the form of a soft-elastic dome-shaped protrusion.
Manifestations of pulmonary echinococcosis are determined by the location of the cyst. Even a small cyst located near the pleura manifests itself early as pain, and when localized near the bronchus, a cough appears.
The most common complication of echinococcosis is cyst suppuration. It is accompanied by increased pain, fever, and severe leukocytosis.
Cholangitis, opening of a cyst into the abdominal and pleural cavity with the development of peritonitis and pleurisy are possible.
Compression of the bile ducts can lead to obstructive jaundice and, less commonly, biliary cirrhosis and amyloidosis.
Pulmonary echinococcosis can be complicated by repeated pulmonary hemorrhages and acute cardiovascular failure.
Cyst rupture can be caused by a blow, heavy lifting, or rough palpation. In this case, severe pain and allergic reactions of varying severity appear, up to anaphylactic shock.
When an echinococcal cyst ruptures, the scolex and small daughter vesicles contained in it can seed neighboring cavities and organs.
Cases of spread of liver echinococcus through the diaphragm into the adjacent parts of the pleura and lung (formation of daughter cysts in the lung tissue) have been described.
Serological tests give a positive result in 90% of cases of liver echinococcosis and in 60% of cases of lung infection.
Microscopic investigation is possible when a cyst breaks through into hollow organs: detection of fragments of the parasite in stool and sputum.
In the CBC: eosinophilia, increased ESR.
Ultrasound of the abdominal cavity and lungs: you can see a multilayer capsule of echinococcus, internal septa, daughter cysts, the liquid nature of the cyst contents, the presence of an echogenic suspension, early signs of calcification. There may be initial signs of cyst erosion and the appearance of gas bubbles, and the presence of pleural effusion in the adjacent part of the lung.
X-ray of the lungs: the cyst is clearly demarcated from the lung tissue, has a visual fluid density, an oval or somewhat wavy outer shape. There may be air between the fibrous and cuticular membranes; Due to the different density of the cyst fluid and the air that has penetrated into it, a fluid level is observed in the cyst. There may be pleural effusion, small areas of calcification, shell-like calcification, or intense capsule calcification.
On radiographs with mediastinal echinococcus - expansion of the mediastinal shadow. When echinococcosis is localized in the mediastinum, pericardial echinococcosis is detected in 20% of cases.
CT scan of the lungs: a cyst with the presence of daughter cysts, a multilayered capsule, calcification of varying degrees, the presence of air (with bronchial erosion due to the growth of the parasite) and fluid level. Damage of the pleura is possible (the structure of pleural echinococcus is similar to pulmonary echinococcus).
When the membranes of the echinococcus are destroyed, the cyst is infected, or there is an abundance of waste products, the density of the cyst increases, which makes it impossible to distinguish the cyst from a soft tissue formation.
MRI: liquid nature of the contents inside the zone of changes, the presence of septate structures.
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Primary echinococcosis of the liver
Hymenolepiasis is widespread (more often registered in areas with dry and hot climates): it is widespread in Latin America, North America, Italy, Iran, Pakistan, Turkmenistan, Uzbekistan, and the Republic of Moldova.
The incidence rate among children aged 3-14 years is 3-3.5 times higher than the incidence rate among adults.
The source of infection is human. In the case of D. minuta, the final host and reservoir of infection can be rodents, and the intermediate hosts can be flea larvae, cockroaches, mealworms and other insects; humans become infected by accidentally swallowing infected insects.
The mechanism of transmission is fecal-oral (alimentary and contact routes).
Transmission factors can be household items, toys and food products contaminated with helminth eggs.
The parasite eggs are not very stable in the environment. They are sensitive to drying and high temperatures. When dried on glass slides at room temperature, they die in 60-70 hours. In river water at a temperature of 18-20 °C, they survive for about a month. On human hands, they remain viable for up to 2 hours.
The occurrence of secondary cases of invasion in organized groups (kindergartens, nurseries) indicates gross violations of sanitary and hygienic norms and rules.
The incidence of hymenolepiasis is recorded throughout the year with some increase in the summer-autumn months, which is associated with an increase in the proportion of vegetables and fruits in the diet.
Immunity is unstable; cases of reinfection are frequent.
In 30% of cases, hymenolepiasis is asymptomatic. In children, manifest hymenolepiasis is more severe.
The incubation period is about 2 weeks.
Patients complain of nausea, vomiting, heartburn, decreased or lack of appetite, salivation, and aching dull pain in the abdomen.
The pain is localized in the umbilical region, is paroxysmal, and is not associated with food intake. The pain may bother the patient daily or occur intermittently for several days.
Typically, loose stools mixed with mucus.
Skin itching, rash, conjunctivitis, vasomotor rhinitis, asthma attacks, and Quincke's angioedema are possible.
Some patients experience subfebrile temperature and short-term, more significant increases in temperature.
Over time, asthenoneurotic syndrome progresses (weakness, fatigue, memory impairment, decreased performance, headache, irritability, dizziness, fainting, headache, somnambulism).
Epileptiform syndrome (epileptiform seizures, muscle twitching) is possible.
With prolonged course, weight loss and symptoms of anemia develop.
On examination: pale skin, intermittent skin rashes, moderately distended abdomen, pain on palpation, most often in the umbilical region, sometimes hepatomegaly.
Hypotension and signs of myocardial dystrophy are possible.
More than half of children and about 85% of adults recover spontaneously within a year after infection, but cases of long-term infestations (up to 20 years or more) are not uncommon.
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Coproovoscopy: when examining fresh feces to detect helminth eggs, flotation enrichment methods of Kalantaryan, Fulleborn, Kato are used. Parasite eggs are excreted cyclically (feces are recommended to be examined three times at intervals of 15-20 days).
The effectiveness of microscopy is increased by provocation with phenasal: it is recommended to give the patient niclosamide in a reduced dose (0.5-1.0 g) together with 1 g of a laxative (purgen) the evening before the examination. Niclosamide destroys the tapeworm strobila, as a result of which a large number of eggs enter the intestinal lumen and are excreted with feces.
Serological diagnostics of hymenolepiasis has not been developed.
In CBC normo- and hypochromic anemia, leukocytosis, neutrophilia, moderate eosinophilia (20-30% of cases), and increased ESR are possible.
In some patients, there is a slight increase in aminotransferase activity, an increase in bilirubin level, and a decrease in albumin level.
Ultrasound of the abdominal cavity: enlargement of the mesenteric lymph nodes is possible.
ECG: reduction and deformation of the R wave in all leads is possible.
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Acute hymenolepiasis, moderate
The source of infection is a variety of rodents that carry the infection asymptomatically.
You can become infected through aerogenous, water, food, or contact. Several cases of blood-contact infection of laboratory staff and medical personnel serving patients with HFRS have been described.
The disease occurs more often in men (70-90% of patients), mainly of the most active age (from 16 to 70 years; average age 37.5±2.2 years). However, the results of serological screening of the population indicate underdiagnosis of HFRS in women.
The incidence of HFRS-Puumala gradually increases from April to October, then decreases until the end of November. Patients with HFRS-Kurkino apply between November and March, with the highest increase in incidence in December (47.6%) and January (44.9%). Thus, the incidence is year-round, and its rise is usually associated with the beginning of the summer season and the harvest period.
Both urban and rural residents are involved in the epidemic process. The risk group for HFRS-Dobrava consists of rural residents, who become infected mainly during agricultural work (most often when caring for livestock).
Among working patients with HFRS, the following are often registered: agricultural workers, laborers, plumbers, car mechanics, installers, security guards, surveyors.
Immunity is usually lifelong.
Asymptomatic variants of HFRS are rarely revealed.
The incubation period lasts from 4 to 49 days (most often from 14 to 21 days).
Sometimes there is a short prodrome: asthenia, slight myalgia, moderate general weakness and catarrhal symptoms, low-grade fever.
HFRS is characterized by a cyclical (staging) clinical picture.
The initial period lasts from 1 to 10 days (usually 4-5).
The onset is always acute: the temperature rises to febrile levels with chills and headache.
Patients complain of chills (95.8%), weakness (95.8-100%), headache (8-76% depending on severity), fatigue, photophobia, retro-orbital pain, pain in the eyeballs (disappear within 1-5 days).
Visual impairment is quite specific to HFRS: decreased visual acuity, a feeling of “fog”, “flies” or “mesh” before the eyes, blurred vision). Double vision is not typical! Ocular symptoms are regestered in 6.5% of patients with mild, 20.4-29% with moderate, and 41.3-100% with severe HFRS.
Patients are bothered by severe dry mouth.
On the 3-4th day of illness, lower back pain appears (about 50% of patients), a change in the color of urine is observed in 33.3% of patients.
Even in the initial stage of the disease, hemorrhagic symptoms may appear: bloody crusts in the nasal passages, moderate nosebleeds.
There may be complaints of nausea (13-74.4%), vomiting (51.1-53.7% for moderate, 81.6% for severe), abdominal pain (more often in the oligoanuric period), loose stools up to 2- 5 times a day (24.7% for moderate, 35.3-48.8% for severe). Interestingly, in six out of seven fatal cases, the onset of the disease was accompanied by gastrointestinal disorders that masked other symptoms of HFRS.
Cough in the absence of rhinitis is possible (25.0%).
On physical examination, a “hood” symptom is noted: hyperemia of the skin of the face, neck, upper chest (11% of mild patients, 16% of moderate patients, 43% of severe patients), pasty eyelids, puffiness of the face (33.3%).
Already from the 3-5th day of illness, single petechiae may appear in the supra- and subclavian areas, in the armpits, on the anterior surface of the chest (9.7-19%), hematomas at injection sites (in 64.5% of moderate and all severe patients). Hemorrhagic syndrome is detected in 9.5% of patients with moderate disease and in 14-30% with severe disease.
Injection of the sclera is detected in 66.7%. In 38.7% of moderate and most severe patients, hemorrhages in the sclera are present.
Hyperemia of the mucous membranes of the pharynx is detected in 76.2%. In most patients, on the 2-3rd day of illness, petechiae can be detected on the palate. The tongue is coated.
Relative bradycardia (14.3-65%) and muffled heart sounds are possible. The severity of these symptoms usually correlates with the severity of the disease.
In some patients, arterial hypotension is recorded on the 3rd-4th day of illness (28.6%).
The abdomen is tender in the hypochondrium due to hepatosplenomegaly. Hepatomegaly is detected in 38.1%, splenomegaly - in 19% of patients. Some patients (16.7%) may have a positive Pasternatsky sign already in the initial period.
Against the background of severe intoxication, in some patients meningeal symptoms may be revealed.
Oliguric period (from 2-4 to 8-11 days of illness).
Body temperature decreases in 80% of cases, but its decrease is accompanied by a worsening (not an improvement) in the condition: nausea, vomiting, hiccups (with severe uremia) appear or intensify, dry mouth (with moderate and severe cases - in 84% and 100% of patients respectively), insomnia or drowsiness, headache, hemorrhagic syndrome increases.
Vomiting up to 6-8 times a day (sometimes more) appears in most patients 1-2 days after the appearance of lower back pain. It is not related to the intake of food or drugs. In the same period, pain appears in the abdomen, flatulence is often noted.
Lower back pain of varying severity appears or increases, diuresis decreases.
In patients with mild, moderate and severe HFRS pain and heaviness in the lower back are noted in 20%, 76-90% and 96-100% of cases, respectively. In moderate and severe HFRS, abdominal pain present in 53% and 82% of cases, respectively, nausea and vomiting - in 35% and 72% of cases. Absence of pain syndrome or localization of pain only in the abdomen indicates an atypical course of the disease.
Hyperemia of the skin of the face and the upper half of the chest can persist or be replaced by pallor in patients with significant kidney injury. Skin is dry.
Hemorrhagic rash is found in 39% of moderate and 48% of severe cases. Even before the spontaneous appearance of a hemorrhagic rash, the positive symptoms of pinch and tourniquet become. Hemorrhagic impregnation of eyelids is possible. Purpura may appear, and in severe cases — ecchymoses.
There is no pronounced swelling, but ussually the pastiness of the eyelids and face remains.
The scleras are injected. Subictericity of the sclera is possible (7.3% for moderate cases, 9.7% for severe cases). Hemorrhage into the sclera (the “cherry brown” symptom) is observed in 2% of mild cases, 22% and 56% of moderate and severe cases, respectively.
Hyperemia of the mucous membranes of the pharynx persists. The tongue is dry, covered with a gray or brown coating. In 23.8%, petechial enanthema is detected on the soft palate.
Relative or absolute bradycardia is often recorded. In the prodromal and first half of the oliguric period, arterial hypotension is more often recorded, in the second half - arterial hypertension.
Dry wheezing is sometimes heard in the lungs; in severe cases, patients complain of shortness of breath.
Palpation of the abdomen reveals bloating, local or diffuse pain, sometimes with symptoms of peritoneal irritation. Sometimes moderate hepatomegaly and pain on palpation in the projection of the kidneys are detected. A positive Pasternatsky symptom is detected, most often on both sides. Oliguria in severe cases can reach anuria.
The polyuric period begins from the 9th to 13th day of the disease.
Vomiting stops, headache, lower back and abdominal pain gradually disappear; hemorrhagic syndrome regresses, sleep and appetite normalize, and the daily amount of urine increases (up to 3-5 l).
Heaviness and discomfort in the lower back, weakness, and dry mouth persist for a long time.
Diuresis increases (maximum daily diuresis is observed on the 15th–16th day of illness). Daily diuresis varies in mild patients from 2200 to 3000 ml, in moderate patients - from 3100 to 5000 ml, in severe patients - from 5000 to 7800 ml. Nocturia is common.
Some patients retain moderate arterial hypertension, bradycardia or tachycardia.
Toxic shock (the risk increases on the 4-6th day of illness), pulmonary edema, cerebral edema, disseminated intravascular coagulation syndrome, azotemic uremia, profuse bleeding, rupture of the kidney capsule (more often occurs in the oligoanuric period), eclampsia, pneumonia (due to addition of secondary bacterial flora).
Serological tests: enzyme-linked immunosorbent assay, indirect immunofluorescence reaction, hemagglutination reaction.
Indirect immunofluorescence reaction: an increase in antibody titer by 4 or more times (interval 5-7 days; first analysis - on days 4-7 of the disease).
ELISA: detection of IgM antibodies confirms the diagnosis.
IgM to the HFRS pathogen in the patient’s serum can be detected from the 6th to the 56th days of the disease. IgG appear from the 6th day, reaches a high level by the 11th day and remains at these values up to 5 months from the onset of the disease; IgG can be detected for the rest of patient’s life.
PCR of blood is more effective in the first days of the disease.
Unlike other bunyaviruses, hantaviruses are not pathogenic to laboratory animals and are difficult to culture on vertebrate cell lines.
CBC:
in the initial period, leukopenia, low ESR, thrombocytopenia are registered;
in the oligoanuric period, moderate neutrophilic (62.5%) leukocytosis (45.8%), an increase in ESR to 40 mm/h is recorded.
Thrombocytopenia is detected in 66.7% of patients. In severe cases, 99.3% of patients had thrombocytopenia below 150*10^9, in 12.3% - below 50*10^9.
Already in the initial period, the concentration of red blood cells and hemoglobin in the blood increases. Mild anemia is observed in 28.6%, increased hemoglobin and red blood cells - in 19% of patients.
ESR does not increase significantly, and in severe cases it even decreases to 5 mm/h and below. An increase in ESR is observed in 33.3% of cases. ESR in 90.5% of patients is in the range of 13-40 mm/h.
During the first days of the polyuric period, dehydration (increase in hematocrit) is possible.
In a urine analysis since the first day of oliguria, the following changes are observed:
proteinuria: protein concentration in mild patients usually does not exceed 0.6 g/l, in moderate patients it varies from 0.4 to 1.3 g/l, in severe patients – from 1.4 to 2.5 g/l (sometimes up to 33-60-85 g/l);
microhematuria (48%);
macrohematuria (32,5%);
cylindruria (hyaline and granular cylinders are found in the sediment, sometimes long, rough “fibrin” Dunaevsky cylinders appear);
leukocyturia is possible.
Detection of vacuolated renal epithelial cells in urine is considered to be pathognomonic for HFRS.
Urinalysis according to Zimnitsky: from the middle of the oligoanuric and in the polyuric period, all patients have hyposthenuria, 50% have hypoisosthenuria: the relative density of urine decreases to 1001-1003.
Azotemia becomes most pronounced by the 7-10th day of illness. The increase can be insignificant (or even absent) in mild forms and reach values of 60.0 mmol/l for urea and 2000.0 µmol/l for creatinine in severe forms of the disease. However, more often upon admission, urea is at the level of 11.2±9.1 mmol/l, creatinine - 183.5±149.8 µmol/l.
An increase in total bilirubin is detected in 1.9-9.6%, an increase in ALT (and to a lesser extent AST) - in the vast majority of patients. The increase in bilirubin is usually slight. Transaminases are elevated within 3 norms in 49.7% of patients, higher - in 9.2%.
Thymol test is higher than normal in 50% of cases.
Hyperkalemia, hyponatremia and hypochloremia are common.
CRP was elevated in all patients.
There are signs of hypocoagulation: a decrease in fibrinogen to 1-2 g/l, PTI to 30-60%; fibrinogen A in severe HFRS is increased (4-6 g/l - in 46.7%; more than 6 - in 6.6%); fibrinogen B is positive in 93.3%.
In severe cases, glucose is increased: 5.5-7.6 mmol/l in 20% of patients, 7.6-9.9 mmol/l in 6.6% of patients.
Circulating immune complexes in patients with moderate HFRS dynamically increase by 4 times, in patients with severe HFRS - by 2 times.
With moderate HFRS over time (on days 8–12 and 16–21 of illness), a significant increase in the absolute number of CD3+ cells by 27.8%, CD4+ by 35.4%, and CD8+ by 33.3% was observed. In severe HFRS, there is a decrease in the absolute number of CD3+ cells compared to healthy individuals by 32.2%, CD4+ by 46.7%; an amount of CD8+ cells is normal. In case of severe HFRS, the indicators of T-cell failure persisted over time (on days 8–12 and 16–21 of illness).
Ultrasound of the abdomen and kidneys reveals hepatosplenomegaly (45.8%), an increase in the size of the kidneys and the thickness of their parenchyma (29.1%), as well as diffuse changes in the liver (20.8%). In severe cases of HFRS, fluid can be detected in the abdominal cavity and/or pelvis in 33.9% of patients.
X-ray of the chest: in severe cases of HFRS, fluid in the pleural cavity can be detected in 16.45%.
Clinical manifested haemorrhagic syndrom and kidney failure are regestered less frequently nowadays
HFRS, moderate
The source of infection is a sick person from the last hours of incubation; the patient is the mots contagious in the first 3-5 days of the disease, less contagious until the 8th day of the disease; a small amount of the virus sometimes can be detected for up to 3 weeks.
The main rout of transmission is airborne, the additional one is contact. A sick person, when sneezing and coughing, spreads the virus by 1,5-2 meters.
Immunity is short-lived (less than 1 year).
Seasonality: usually in winter (approximately November to March). Influenza virus type C does not cause epidemic outbreaks, but circulates year-round.
The incubation period is from 12 to 48 hours.
The clinical picture consists of two main syndromes: intoxication and catarrh of the upper respiratory tract.
Body temperature rises sharply to high level, which is usually accompanied by chills, weakness, headache (more often in the forehead and brow ridges, there is often pain in the eyeballs and retro-orbital pain, increasing with eye movement); many patients complain of paresthesia.
Catarrh is “dry” on the first day, that is, the nose is stuffy, but there is no discharge, and attempts to blow the nose do not bring relief. The cough is also dry and quite painful.
On the 2nd day, nasal discharge and sputum usually appear (both transparent), over time, the catarrh becomes more and more productive, the cough becomes less painful, and blowing the nose brings short-term relief.
Severe scleritis, hyperemia or pastiness of the face are common.
The mucous membranes of the pharynx are hyperemic (often hyperemic with a cyanotic tint), and “viral granulation” can be seen on the soft palate.
Lymphadenitis is usually strictly regional and mild (small painless mobile angular lymph nodes).
The more severe the flu, the greater the chance of detecting relative bradycardia in the patient.
An atypical form of influenza can be diagnosed if there is no catarrhal syndrome (acarrhal form) or intoxication (afebrile form).
Hypertoxic form: pulmonary edema. In the first days of illness, the patient develops shortness of breath against the background of high fever. Pallor, cyanosis (usually acrocyanosis) are possible; bilateral dry, then moist rales may appear in the lungs, and then zones of “silent” lung in the lower sections (percussion sound can be dulled here). In case of hemorrhagic pulmonary edema, terminal patients may have reddish sputum.
Hypertoxic form: cerebral edema. In the first days of the disease, against the background of a high fever, the patient experiences an intensified headache (if initially it was localized in the forehead, it can become diffuse), photophobia appears, and then consciousness is impaired. The patient may be agitated, disoriented, hallucinations are possible, followed by lost of consciousness up to coma. In this case, meningeal symptoms (meningismus), sometimes focal symptoms, may appear. Blood pressure usually rises.
Hypertoxic form: toxic shock. In the first days of the disease, against the background of high fever, the patient’s blood pressure decreases dramatically and heart rate increases. An increase in the shock index is accompanied by clinical manifestations of hemodynamic disorders (acrocyanosis, dispnea, loss of consciousness, etc.).
Pneumonia usually occurs after the 5th day of the disease. It manifests with the second wave of fever, patient complains of shortness of breath; quite often, patients complain of pain in the chest on one side, which intensifies with deep breathing.
On auscultation, wheezing is much stronger on one side (usually on the right in the lower lobe); pleural friction noise, crepitation, moist rales, dullness of percussion sound over the lesion are possible. Crepitation can be heard with the patient lying on the affected side (Kuravitsky maneuver) or after short coughs. The sputum usually becomes purulent (yellow, green, gray).
In case of sinusitis, against the background of the second wave of fever, pain appears in the projection of the affected sinus, the discharge from the nose turns yellow or green, and sometimes streaks of blood appear. The pain intensifies with light tapping on the bone in the projection of the sinus. Many patients already have a history of sinusitis.
The easiest way to distinguish complications from the hypertoxic form is to take into account the day of illness: the hypertoxic form develops in the first 1-3 days of the illness, complications - usually after the 5th day. In addition, hypertoxic forms usually develop in unvaccinated people (usually young and middle-aged), and complications occur in the elderly and patients with immunosuppression of various origins.
During a declared epidemic, the diagnosis is made on the basis of clinical and anamnestic data.
The diagnosis can be confirmed by detection of viral RNA (using PCR) in scrapings from the nose and mucous membrane of the soft palate. PCR is more sensitive in the first days of the disease.
The fluorescent antibody method can be used as a rapid test: it also applies to early diagnosis.
It is possible to confirm influenza serologically, but if the paired serum method is implemented in noncomplicated cases, most patients will recover before taking the first blood sample.
In patients with uncomplicated influenza in CBC: leukopenia with relative lymphomonocytosis and normal ESR. The development of complications is usually accompanied by neutrophilic leukocytosis and increased ESR.
If the patient has not recovered by the 5th day of illness, an x-ray should be prescribed: of the lungs - if bronchitis or pneumonia is suspected, of the paranasal sinuses - if sinusitis is suspected.
Do remember, that both pneumonia and sinusitis are more often unilateral.
If you check x-ray of the chest in patient with severe influenza in the first days of illness, it is likely to find bilateral shadows, wich are the sign of interstitial pneumonia or pulmonary edema.
ECG: in severe cases, you can find a decrease in the voltage of the waves, and sometimes conduction disturbances.
In CSF: no pathological changes are detected in the cerebrospinal fluid.
Before the emergence of the swine flu virus, influenza deaths typically occurred in children and the elderly. With the advent of the H1N1 virus, mortality in the middle age group increased significantly, and in the clinical picture of the disease, hemorrhagic syndrome became more clearly visible.
Influenza, a typical form of moderate severity.
Influenza, a typical form of severe course, complicated by community-acquired right-sided lower lobe pneumonia of severe course.
Influenza, hypertoxic form: cerebral edema.
Dirofilariasis is not included in the list of parasitoses subject to mandatory registration, therefore statistical data on this disease should be assessed critically.
The development of larvae in the body of mosquitoes occurs at an ambient temperature above 14ºС. At an optimal temperature (23–28ºС), the larvae reach invasive maturity in 8–17 days. Therefore, the northern boundary of the habitat of dirofilaria is 53–57° N.
Dirofilariasis is characterized by focal distribution (Southern and Eastern Europe, Asia Minor, Central Asia and Sri Lanka).
Subcutaneous dirofilariasis (D. repens) is widespread among residents of Uzbekistan, Georgia, Armenia, Ukraine, Moldova, Belarus, Kazakhstan, and Russia.
Dirofilaria repens и Dirofilaria immitis вызывают разные формы заболевания: подкожный дирофиляриоз и висцеральный соответственно. На территории России и Беларуси встречается именно подкожный дирофиляриоз, а висцеральная форма характерна для таких стран, как Япония, США, Канада, Австралия, Южная Европа.
The maximum incidence occurs in the age group of 30-39 years, however, no significant differences in age-related incidence (except for the obvious minimum in the 1-9 year group) are observed.
Women get sick somewhat more often (according to data from different authors, from 64.6% to a prevalence of 2.6 times).
Typically, a person becomes infected while doing agricultural work, during outdoor recreation (fishing, hunting, tourism), and also in places where there are significant mosquito populations and infected animals.
According to statistics, patients most often seek treatment in May, June and December, and less often in March and August.
The incubation period depends on the reactivity of the organism and the growth rate of the parasite and is approximately 1 month, but can be longer, up to several years.
In Europe, the subcutaneous localization of the parasite is more common (67%) and under the conjunctiva of the eye (27% of cases). Cases of helminth localization in the lymphatic vessel of the parietal region of the head, in the lung, root of the tongue, testicle, and peritoneum of the small pelvis have been described.
Most often, diseases in humans are caused by D. repens (up to 10–17 cm in length), less often by D. immitis (up to 25–30 cm in length); the thickness of the helminths is 0.3–1.2 mm. In the vast majority of cases, single females (9.5–15 cm) are found, less often single males (6.5–8 cm). The lifespan of adult parasites ranges from four months to two years.
At first, a small lump the size of a millet grain appears at the site of the mosquito bite, sometimes accompanied by itching. Soon the itching and lump may disappear, but later the lump appears again and increases, reaching a diameter of 0.5-4.0 cm. Patients complain of itching (from moderate to very strong), pain on palpation and even at rest. The skin above the lump is usually slightly hyperemic, sometimes moderate swelling is noted. Interestingly, according to statistics, the right-sided localization of the helminth predominates.
Then the parasite begins to migrate, the movement of which causes discomfort to patients. The movement of the seal or the helminth itself under the skin can reach 15 cm per day, and no traces are left in the old place of its presence. The movement of the parasite from the skin of the right hypochondrium through the left supraclavicular region and the left part of the lower jaw to the conjunctiva of the left eyeball has been described. Increased migration occurs when the skin is exposed to UHF during physiotherapy, warmed up with compresses and even when antiseptics are applied.
Sometimes dirofilariasis can cause intoxication (weakness, headache, nausea, increased body temperature).
Dirofilariae can be localized in the eyelids, conjunctiva, anterior chamber of the eye, sclera, tissues of the eye socket. Such patients may experience a sensation of a foreign body in the eye, redness of the eyelid skin, ptosis, blepharospasm, a sensation of the parasite moving inside the subcutaneous (submucous) seal.
When the skin of the eyebrows and eyelids is affected, it is sharply edematous, pasty, immobile, blepharospasm, dense nodules, granulomas, swelling are formed under the skin. Patients complain of itching, lacrimation, pain at rest and during palpation, a sensation of a foreign body in the eye, movement. Conjunctivitis develops: the mucous conjunctiva is edematous, hyperemic for several days, through it the twisted body of the helminth is visible. Symptoms disappear after it migrates to the eye socket or is removed surgically.
Visceral dirofilariasis with lung damage is often asymptomatic and is detected accidentally during routine chest X-rays.
In many patients, the disease has a recurrent course with phases of remission and exacerbation.
After the helminth is removed, clinical signs usually disappear.
If the helminth is not removed in a timely manner, inflammation may develop in the soft tissues, as well as the formation of an abscess.
Morphological examination of the removed worm allows us to confirm the diagnosis.
CBC: there is no anemia, eosinophilia is not characteristic (sometimes it is present within 8-11%), ESR is within normal limits.
Uranalisis: without pathology.
Blood glucose is normal.
X-ray in visceral dirofilariasis with lung damage, a rounded (“coin-shaped”) shadow 1–2 cm in diameter is usually detected.
Example of MSCT: in the medial and middle parts of the left upper eyelid, a formation measuring 19.1 × 6.5 × 8.9 mm is determined, with clear uneven contours, delimited from the surrounding soft tissues, homogeneous, with a density of +38 HU. The left eyeball is of regular shape, unchanged in size, no structural changes were detected. The optic nerve, extraocular muscles, retrobulbar fatty tissue show no signs of pathological changes.
Ultrasound example: a formation measuring 19×6.2×9 mm, with clear even contours, clearly delimited from the surrounding soft tissues, with a thin echogenic capsule, reduced echogenicity, heterogeneous echostructure, in the projection of the formation a structure of irregular shape with echogenic walls and a hypoechoic lumen is clearly visualized. During scanning, movement of the above inclusion is noted, while with an increase in the time of exposure to ultrasound, the activity increased. In the color Doppler mode, the formation is avascular.
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Dirofilariasis of the skin
The spread of diphyllobothriasis is associated with large freshwater bodies. Its foci predominate in Northern Europe, the Eastern Mediterranean, the Great Lakes region of the United States, Canada and Alaska.
81-93% of patients are adults (usually around 35-50 years old).
Cases of diphyllobothriasis are registered in urban and rural areas, with a predominance of rural residents.
Source of infection - humans, cats, pigs, dogs, bears. However, the source does not pose a direct danger to others due to the complex life cycle of the parasite.
Route of transmission - food.
Transmission factors: improperly cooked red fish, river fish, fresh or insufficiently salted caviar, especially of home-made origin.
Rare cases of infection have been reported when using poorly washed cutting boards and utensils.
The parasite's lifespan in the human body can reach 25 years. During this time, diphyllobothriasis can be latent.
The incubation period in the case of manifest disease is usually from 20 to 60 days.
The disease begins gradually with dyspeptic symptoms: nausea (5-66%), vomiting (1-41%), rumbling (6-46%), bloating (1.5-58%), discomfort in the epigastrium (6-63.5%), cramping pain in the epigastrium or throughout the abdomen (5.5-86.5%), unstable or loose stools (8-86%), alternating constipation and diarrhea, decreased appetite (80%), increased appetite (1%).
Asthenia gradually increases: weakness (8-78%), weight loss (1.5-3%), headache, dizziness, drowsiness.
Allergic reactions are possible: skin itching (1-1.5%), swelling of the face (1%), hands (1%), dry mouth (1%).
In case of massive invasion, subfebrile temperature and even febrile temperature are possible.
Most often, patients seek medical attention due to the release of parasite parts during defecation (50-84%). The release of strobila fragments distinguishes diphyllobothriasis from invasion by bovine and pork tapeworms.
With prolonged invasion, signs of astheno-neurotic syndrome and B12-deficiency anemia increase.
Irritability and depression are possible; in severe cases, funicular myelosis develops with disturbance of superficial and deep sensitivity: paresthesia or numbness along the peripheral nerves, ataxia, and later - spasticity and hyperreflexia.
With anemia, dizziness, weakness, palpitations, paresthesia or pain in the tongue are observed, which intensify when taking medications, eating sour or salty foods. In severe cases, Hunter's glossitis is observed - the appearance of bright red painful spots on the tongue, cracks, then the papillae atrophy, the tongue becomes smooth, shiny ("varnished").
Sometimes red, painful spots or cracks appear on the mucous membranes of the mouth and esophagus.
Tachycardia, enlargement of the cardiac borders, soft systolic murmur at the apex, and hypotension are noted.
In rare cases, hepatomegaly and splenomegaly are detected.
In patients with a lot of helminths in the small intestine, obstructive intestinal obstruction may occur.
Approximately 2% of patients develop B12-deficiency anemia.
The diagnosis is confirmed by detecting helminth eggs or fragments of its body, consisting of several, but not separate segments, in the feces.
In CBC: progressive anemia, aniso- and poikilocytosis, variable eosinophilia (more common with recent invasion), increased ESR. Megaloblasts, Jolly bodies, Cabot rings, hyperchromic macrocytes, polychromatophilic erythrocytes and erythrocytes with basophilic granularity are detected in small quantities.
A decrease in reticulocytes, relative lymphocytosis and neutropenia, and thrombocytopenia are observed.
An increase in indirect bilirubin is possible.
Morphological examination of the mucous membrane of the colon reveals signs of chronic catarrhal-hemorrhagic colitis with pronounced activity of the pathological process and moderate atrophy of the intestinal glands.
In the inflammatory cellular infiltrate in post-diphyllobothriasis colitis, the content of fibroblasts is reduced. An increase in the height of the superficial epithelium is noted. In the epithelial layer of the intestinal glands, increased mitotic activity is preserved in the germinal zones.
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Diphyllobothriasis
According to some data, 97.5% of measles patients are aged 15-30, of which 55.6% are schoolchildren and students. According to other data, among adults who become ill, 65.0% are people aged 30 and older.
Men and women get sick with almost equal frequency.
Among those infected with measles, city dwellers predominate (81.3%).
The source of infection is a sick person who releases the virus from the last 2 days of the incubation period until 4 days from the appearance of the rash.
In complicated cases of measles, the period of virus shedding can be extended to 10 days from the moment the rash appears.
“Healthy” carriage is impossible.
Patients should be isolated for 7 days (in complicated cases - for 17 days, those who received prophylactic immunoglobulin - for 21 days). Children who were in contact with the patient are not subject to isolation for the first 7 days.
The transmission route is airborne. The risk of infection is directly proportional to the duration of contact with the patient: 24 hours - 40%, 48 hours - 60%, 72 hours - 80%.
In 50% of cases, intra-family contact or contact with colleagues at work is registered. As a nosocomial infection, measles is registered in 30.4% of patients.
If a pregnant woman becomes infected, vertical transmission is possible.
The contact route is not realized due to the low stability of the virus in the environment.
More than half of patients fall ill in the second quarter of the year. Measles is least common in the autumn.
Those who are not vaccinated (84.28%) or vaccinated only in childhood fall ill significantly more often. Ten years after vaccination, protective antibody titers are recorded in only 36% of those vaccinated.
Post-infectious immunity is usually lifelong: recurrent infections are extremely rare.
The incubation period lasts from 7 to 14 days. After prophylactic administration of immunoglobulin, it can be extended to 15-21 days. The average duration of the incubation period is 9 days. 34.8% of patients indicate contact with a patient with measles 10-12 days before the onset of the disease.
Most often, patients are admitted to hospital on the 3rd to 7th day of illness.
In adults, intoxication is usually more pronounced than in children, and catarrhal symptoms are less pronounced. The "maturation" of measles has led to an increase in the proportion of moderate and severe forms.
In the initial period, patients complain of weakness (95.6%), headache at the height of fever (84.3%), chills (56.8%), malaise, loss of appetite, fatigue, sleep disturbance. Arthralgia and myalgia are rare (2.5% of cases).
In 96.7% of patients, body temperature rises sharply and decreases by the 3rd-4th day of illness. In previously vaccinated patients, body temperature may remain normal throughout the illness. In 34.8% of patients, only subfebrile temperature is recorded.
In 79.3% of patients, a constant type of temperature curve (febris continua) is recorded, while in the rest, remitting fever (febris remittens) is recorded with daily fluctuations of 1–2 degrees.
Morning temperature is sometimes higher than evening temperature. Patients are lethargic or irritable.
Stimson's catarrhal triad is typical: conjunctivitis, rhinitis, laryngitis.
From the first days of the disease, rhinitis with abundant discharge appears: first serous, then serous-purulent. The presence of mucous discharge from the nose is noted by 31.5% of adults and 94.2% of children.
Dry or wet cough is noted by 60.9% of patients for 2-13 days. In children, the cough often becomes "barking" and is accompanied by hoarseness and stenotic breathing.
Conjunctivitis, according to various data, is recorded in 18.5-73.7% of patients (less common in adults, more common in children).
From the first days (usually by the 4th-5th day) there is photophobia, lacrimation, swelling of the eyelids, hyperemia of the conjunctiva, injection of the sclera (10.9% of adults and 40% of children). In the morning, the eyelids may stick together due to the presence of purulent discharge.
Scleroconjunctivitis persists until the 4th-5th day of the rash, and photophobia disappears as the rash fades.
Sore throat when swallowing (57.6% of adults and 34.3% of children) and a scratchy throat (14.1%) are also possible.
Catarrhal symptoms are often combined with dyspepsia: nausea and vomiting (16.8%), abdominal pain (7.5%), loose stools (short-term diarrhea in the catarrhal period, according to various sources, is recorded in 15.2-36.7% of adults and 8-62.9% of children). After the 5th day of illness, diarrhea is rare and can be regarded as a complication of measles.
Physical examination may reveal puffiness of the face (11.8%), eyelids (15%), swollen nose and lips.
Hyperemia of the facial skin is observed in 65% of patients.
The mucous membranes of the oropharynx are hyperemic and injected in 92.4% of sick adults and 77.1% of children. "Viral" granularity is possible.
The tongue is moist, coated with a white coating, and salivation is increased.
In 39.1% of patients, hyperemia and hypertrophy of the palatine tonsils are observed.
Measles enanthem may appear as small red spots located on the mucous membrane of the soft and hard palate, and/or Belsky-Filatov-Koplik spots, which are pathognomonic for measles.
According to some data, Belsky-Filatov-Koplik spots are registered in 80% of cases, according to others - only in 23.9% of adults and 37.1% of children admitted in the first 4 days of illness.
They are most often localized on the mucous membrane of the cheeks at the level of the premolars (less often on the mucous membrane of the lips and gums) and are small (1-2 mm in diameter) whitish spots, slightly raised above the level of the mucous membrane, surrounded by a narrow border of bright hyperemia. In appearance, they resemble semolina or bran.
In adults, Belsky spots are usually more numerous and more widespread than in children.
Sometimes Belsky spots merge and spread to all the mucous membranes of the mouth and conjunctiva. Cases of Belsky spots appearing in the anus and vulva have been described.
With the appearance of exanthema in children, Belsky-Koplik-Filatov spots often disappear, but in 36.7% of adults they can persist in the first 2-4 days of the rash period.
After the spots disappear, you can notice a “velvety” texture to the mucous membrane in their place.
Somewhat earlier than Belsky spots or simultaneously with them, 70.3% of patients develop irregularly shaped red spots the size of a pinhead on the mucous membrane of the soft (sometimes hard) palate. After 1-2 days, they disappear against the background of general hyperemia of the mucous membrane of the palate. In 14.4%, measles enanthem is detected on the conjunctiva.
Sometimes small itchy spots (“prodromal rash”) appear on the face, torso and limbs of patients on the 2nd or 3rd day of illness.
The catarrhal period usually lasts 3-5 days; in adults it can last up to 6-8 days.
At the end of the catarrhal period, the temperature drops, sometimes to normal (“temperature cut”).
In adults, exanthema usually appears on the 3rd-4th day of illness, in children - on the 4th-5th day of illness.
With the appearance of the rash, rhinitis and conjunctivitis decrease, intoxication increases, 55% of patients have a rise in temperature to 390C and higher; tracheobronchitis often persists, tachycardia and hypotension are detected. Body temperature normalizes on the 4-5th day of the rash (longer hyperthermia may indicate the presence of complications).
Measles exanthema is characterized by a staged rash: on the 1st day, elements of the rash appear on the face, neck (first at the border of hair growth); on the 2nd day - on the trunk, arms and thighs; on the 3rd day - on the shins and feet (while the rash on the face begins to fade).
At first, soft to the touch reddish papules with a diameter of about 2 mm appear, then irregularly shaped spots with a diameter of, as a rule, more than 10 mm "spread" around them. The elements are bright, their number increases.
The rash may be moderately itchy: 13.4% of patients with no history of allergies report itching.
In severe cases (about 10% of patients), a few petechiae appear. In 6.3% of cases, the rash is represented only by roseola.
The rash elements are most densely located on the face, neck and upper body. In 22.5-50% of patients, the spots tend to merge with the formation of continuous erythematous fields with scalloped edges. However, even with the densest rash, areas of completely normal skin can be found between the spots. The rash is more abundant in adults.
The duration of the exanthema period is on average 8 days (from 4 to 15). The elements of the rash fade, hyperpigmentation remains in their place, bran-like peeling is observed (especially on the face and body). Peeling lasts 5-7 days, hyperpigmentation - 1-2 weeks.
Peripheral lymph nodes (posterior cervical, occipital, axillary) are enlarged in most patients during the catarrhal period and during the period of rashes; sometimes they are sensitive or painful upon palpation. In adults, lymphadenitis is more pronounced (enlarged to 1.0-1.5 cm).
Enlarged lymph nodes are usually detected simultaneously with the appearance of a rash in patients.
In the first week of the disease, tachycardia (40.6-68.5%) and muffled tones (41.3%) without dilatation of the heart borders, moderate increase in blood pressure (7.6% with a history of hypertension) or arterial hypotension (1.9%) are observed. Then - bradycardia, dilatation of borders, systolic murmur may appear at the apex and at Botkin's point.
When auscultating the lungs, harsh breathing (48.7%), dry (25%) and wet (6.3%) wheezing are heard.
Some patients with measles develop hepatomegaly.
Mitigated measles develops in those who have been vaccinated, previously sick, or received immunoglobulin.
It proceeds easily: the catarrhal period is reduced to 1-2 days and proceeds at a normal or subfebrile temperature, the catarrh is mild; Belsky spots are often absent; the rash appears at one time (without characteristic stages) or can be ascending, the elements are smaller and paler, the rash is less abundant and not so prone to merging, the period of rashes is shortened. The incubation period is 21-26 days.
Pneumonia, bronchitis, bronchiolitis, false croup; keratoconjunctivitis; myocarditis, glomerulonephritis, hepatitis, meningoencephalitis, encephalitis.
Meningitis, meningoencephalitis and polyneuritis most often occur in adults (usually during the pigmentation period).
The immunofluorescence reaction of respiratory secretions allows the detection of viral antigens.
In serological diagnostics, a titer increase of 4 times or more is considered diagnostic.
The optimal time for collecting blood for serological studies is 4-5 days after the onset of the rash (1st serum) and no earlier than 10-14 days after collecting the first sample (2nd serum).
A sensitive method is ELISA: IgM can be detected as early as 2 days after the rash appears, IgG appear after 10 days from the onset of the rash and reach a maximum by the 18th-22nd day. ELISA is also recommended to be performed dynamically (the interval between studies is 10-14 days): an increase in the IgG titer by 4 or more times confirms the diagnosis of measles.
PCR: Viral RNA can be detected in blood and throat swabs before the rash appears.
In material from the nasopharynx and oropharynx, measles virus RNA can be detected even in the last 3-5 days of the incubation period.
The optimal time for performing PCR is the first 3-5 days of illness.
It is advisable for persons who have had contact with a patient with measles to take the first PCR sample 5-7 days after contact.
CBC: in case of uncomplicated measles, leukopenia (21.5-22.8%) or normocytosis, eosinopenia, monocytosis (16.9%) are detected, ESR may be within normal limits or slightly elevated (25.9-66.3%); thrombocytopenia is possible (39.1%); during the period of rashes, plasma cells may appear. Red blood is usually without pathology.
In adults, neutrophilia, lymphopenia, and aneosinophilia are more often detected.
Urine analysis: moderate proteinuria (45.7%), erythrocyturia and leukocyturia (28.3%).
In 40.2-87% of adults, measles is accompanied by an increase in transaminase activity (on average 67-100 U/l), although in 20% of cases this may be associated with concomitant viral hepatitis. An increase in transaminase activity is not accompanied by an increase in bilirubin levels or an increase in liver size.
Microscopic examination of throat smears may reveal giant multinucleated cells.
Microscopic examination of sputum, nasal mucus or urine in the initial period and in the first two days after the appearance of the rash can reveal multinucleated giant cells.
Microscopy of CSF: in measles encephalitis, lymphocytosis and increased protein are detected.
ECG: diffuse myocardial changes (30.6%).
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Typical measles, moderate, complicated by acute otitis media.
Leptospirosis is considered to be the most common zoonosis in the world. It is found on all continents except Antarctica, and is especially widespread in tropical countries. The disease is most common in East and Southeast Asia; intensive outbreaks were registered in Japan, India, and Vietnam. The most significant natural focus of leptospirosis in the world is in Indonesia, where the infection of rodents with leptospira reaches 10-50%.
There are 2 groups of sources of infection. First are rodents (voles, mice, rats) and insectivores (hedgehogs, shrews). Second group are domestic (pigs, cattle, sheep, goats, horses, dogs) and fur-bearing animals (foxes, arctic foxes, nutria). Rodents excrete Leptospira in urine for a long time, while others excrete Leptospira during acute disease. In adult animals, leptospirosis is often mild, while in young animals it is more manifested.
A human with leptospirosis is not a source of infection.
The transmission with water dominates, contact and alimentary transmission is less common. Epidemic outbreaks are often associated with swimming in lakes and rivers. Rather dangerous are drinking, washing, bathing or wading in lakes or low-flowing rivers, slaughtering infected animals, cutting meat, and consuming insufficiently heat-treated meat or milk. Wet soil and pasture grass also can be transmission factors.
Leptospires are very invasive, so contact with contaminated water on the skin or mucous membranes is enough to infect a person.
The disease is often of an occupational nature. Workers on farms, slaughterhouses, milkmaids, shepherds, veterinarians, as well as hunters, fishermen, and taxidermists often fall ill.
Leptospirosis is characterized by a pronounced summer-autumn seasonality with a maximum incidence in August.
Men are more often affected (94%), average age of patients is 42.7 years.
The incubation period lasts from 4 days to 1 month (usually 7-9 days).
Prodrome is not typical.
The initial period of the disease lasts about a week, but in severe cases it can be shorter.
The disease begins acutely: body temperature with chills reaches a maximum within 1-2 days. In 65.5% of patients, there is an increase in body temperature to febrile levels (38–39.9ºC); less often - pyretic fever (40–40.9ºC) – in 34.5% of cases. Body temperature remains at a high level for 5-10 days, then decreases with a short lysis, but at the same time intoxication increases, vomiting appears, aversion to food, and hemorrhagic syndrome intensifies.
In some patients, especially if antibiotics were not prescribed, after 3-12 days a second wave of fever is observed, which is usually shorter than the first one.
Patients complain of severe headache, insomnia, lack of appetite, and thirst.
Nausea and vomiting are observed in more than half of patients, abdominal pain and diarrhea - in 25% of cases.
A very typical symptom is severe muscle pain, especially in the calf (48.3% of patients). The muscles of the thigh and lumbar region also may be involved in the process; palpation is very painful. In some patients, myalgia is accompanied by pronounced skin hyperesthesia (severe burning pain). Muscle pain is so severe that patients have difficulty moving or cannot move at all (in severe forms).
Nosebleeds appear early, but may be absent by the time of admission to the hospital. The severity of nosebleeds can be assessed using the WHO scale. In 96% of cases of leptospirosis, grade 1 bleeding is noted. (a total of less than 1 hour in time, not requiring medical intervention and red blood cell transfusion). With heavy nosebleeds, bloody vomiting may occur.
On physical examination, one can detect hyperemia and pastiness of the face; the skin of the neck and upper chest is also hyperemic (“hood symptom”). Hyperemia of the face and neck is observed in 20% of patients.
From the 3-5th day of illness, exanthema appears in 20-50% of patients. The elements of the rash are polymorphic, located on the skin of the torso and limbs. The rash can be morbilliform, rubella-like, or less often scarlet-like. Urticarial elements may also occur. Macular rash tends to merge elementsж in these cases, erythematous fields are formed. Erythematous exanthema is the most common.
Hemorrhagic rash (usually petechiae) appears with more severe leptospirosis. Petechiae are usually localized on the lateral surfaces of the body, in the elbows and armpits; after an ECG - in places where chest electrodes are applied, equipped with rubber suction cups; under the tonometer cuff on the upper extremities; in axillary regions; on the neck; anterior abdominal wall; much less often - on the lower extremities and face. The incidence of petechiae directly correlates with the severity of thrombocytopenia and reaches 40.4%.
Post-injection hematomas (2nd grade of bleeding according to WHO) are recorded with equal frequency in the initial period and the height of leptospirosis. The appearance of extensive hematomas indicates the severity of the condition and is an unfavorable prognostic sign. In patients with severe leptospirosis, medium-sized hematomas appear - 7-8 cm in diameter.
In the group of patients with severe leptospirosis, clinical manifestations of hemorrhagic syndrome were identified in the majority of patients. The most common types were: petechial rash, subconjunctival hemorrhages and post-injection hematomas, which corresponds to grade 1–2 bleeding according to the WHO classification. At the same time, petechial rash on the skin, post-injection hematomas, gastrointestinal bleeding, pulmonary hemorrhage, macrohematuria or a combination of 3 or more signs of hemorrhagic syndrome are statistically significantly associated with death.
A herpetic rash often appears (on the lips, wings of the nose). With manifest hemorrhagic syndrome, the contents of herpetic vesicles may be hemorrhagic.
Sclera are injected in 50% of patients, but without signs of conjunctivitis.
In more severe cases of leptospirosis, from the 3rd to 5th day of illness, jaundice of the sclera appears, and then jaundice of the skin. The intensity of jaundice varies widely.
Hyperemia of the pharynx is recorded in a third of patients: moderate hyperemia of the arches, tonsils, and soft palate. There may be petechiae on the mucous membrane of the soft palate, but this is not very characteristic of leptospirosis.
The tongue is dry and covered with a brown coating.
Cases of leptospirosis with the appearance of edema of the lower extremities and face have been described. However, in general, peripheral edema is not typical for leptospirosis.
In some patients, the submandibular and posterior cervical lymph nodes are enlarged.
Bradycardia, hypotension, muffled heart sounds, and sometimes arrhythmia may be observed; in more severe cases, a clinical picture of specific leptospirotic myocarditis may be observed.
Hard breathing (31%) and dry wheezing (31%) can be heard in the lungs.
Almost all patients from the 3rd-5th day of the disease have an enlarged liver, and in half of the patients the spleen is enlarged. The liver is moderately painful on palpation.
Pain in the lumbar region, positive Pasternatsky symptom, oliguria (up to anuria) during the peak period are typical. In severe cases of the disease, signs of uremia may appear (ulcerative lesions of the colon, pericardial friction rub, convulsions, disturbances of consciousness up to the development of uremic coma).
If the central nervous system is affected, headaches, insomnia, agitation and anxiety are possible. Sometimes meningism is possible in the initial period of the disease. During the peak period, 5.2-15% of patients develop serous meningitis. This causes dizziness, delirium, insomnia, headache, stiff neck, Kernig's sign, upper middle and lower Brudzinski's symptoms.
Oligoanuria may be followed by a polyuric crisis.
Acute renal failure, toxic shock, acute liver failure, hemorrhages in the lungs or adrenal glands, bleeding, meningitis, encephalitis, iridocyclitis, myocarditis, uveitis.
Nonspecific: pneumonia, abscess.
Gastrointestinal bleeding is one of the most serious symptoms in patients with severe leptospirosis (associated with death).
Pulmonary hemorrhage is currently a fatal complication of leptospirosis. Abundant hemorrhagic sputum appears in the first 5 days of illness and may indicate the development of acute respiratory distress syndrome (ARDS) of the type of total hemorrhagic pulmonary edema.
With the development of DIC syndrome, hemorrhages in the subcutaneous tissue, muscles of the lower back and abdominal wall, gastric, intestinal and uterine bleeding, and hemoptysis are possible. Hemorrhages under the mucous membranes of the gastrointestinal tract can manifest as abdominal pain, nausea and vomiting, abnormal stool, and heaviness in the right hypochondrium.
Leptospira can sometimes be detected in the blood in the first days of illness using dark-field microscopy; from 7-8 days, urine sediment can be microscoped, and if meningeal symptoms appear, cerebrospinal fluid can be examined. Leptospira can be detected in biopsy specimens of the calf muscles (silver stained). In the dead, leptospira can be found in the kidneys and liver. The sensitivity of the method is very low.
Culturing of blood, urine, and cerebrospinal fluid is more sensitive, but requires special media, and leptospira grows slowly.
Biological method: infection of guinea pigs followed by microscopy of sections of various organs stained with silver nitrate.
Serological methods (complement fixation reaction, microagglutination reaction) are highly sensitive. Studies are carried out using the method of paired sera (the first study is on the 5-7th day of illness, the second - 7-10 days later). The minimum diagnostic titer in CFR and IRH is 1:100. The diagnostic titer of RMA is 1:100 or higher.
A more reliable confirmation of the diagnosis is considered to be an increase in titer by 4 or more times, since in endemic regions antibodies to Leptospira are often found in healthy people who have previously had leptospirosis.
The Bairam-Ali slide agglutination reaction (BASA) - macroagglutination on glass with a genus-specific slide antigen - is close in sensitivity and specificity to the microagglutination reaction. Used as a screening.
PCR of blood serum is an early diagnosis and is effective in the first 7-10 days; has high specificity and is superior in sensitivity to microscopy.
For the diagnosis of leptospirosis, the parallel use of serological analysis and PCR is optimal, regardless of the phase of the disease.
CBC:
neutrophilic leukocytosis (12-20×10^9/l), lymphopenia, during the peak period the level of eosinophils decreases. Moderate leukocytosis in the range of 11.6–17.9×10^9/l occurs in 18.7% of patients;
significant increase in ESR (up to 40-60 mm/h). Most patients experienced an increase in ESR to 30±2 mm/h;
thrombocytopenia is detected in 43.7% of patients;
an inverse correlation between the levels of platelets and leukocytes was revealed (leukocytosis in the group of patients with thrombocytopenia below 50*10^9/l reached its maximum at the height of infection);
moderate hyporegenerative anemia.
Changes in urine analysis are more often recorded from days 1–7 of illness.
Urine is saturated yellow or dark, cloudy, the reaction is slightly acidic.
Erythrocyturia (2–40 elements per field of view) is detected in some patients.
Proteinuria is recorded in 56.2% of patients (“traces of protein” - in 12.5% of cases, in the remaining 43.7% of patients - proteinuria ranging from 0.15-1 g/l).
Leukocyturia is observed in 18.6% of patients (10–12 in visual field).
Microscopy can reveal hyaline and granular casts, renal epithelial cells (a large number).
At the height of the disease, urine analysis according to Zimnitsky in 40.6% of patients shows hypoisosthenuria in the range of 1003–1008 units. rel. den.
The content of residual nitrogen, urea (9.1±0.8 mmol/l), and creatinine (146±2 µmol/l) increases in the blood. In patients with a severe form of the disease, the values of creatinine and urea increase, respectively, to 460 µmol/l and to 30.2 mmol/l and higher.
Bilirubin increases (80-200 µmol/l or more) due to both fractions (mainly due to direct).
Transaminases are elevated (on average AlAt 87.4 U/l, AsAt up to 65.6 U/l). In patients with anicteric forms of leptospirosis, the increase in transaminases is slightly lower.
Alkaline phosphatase is elevated.
Hypoproteinemia develops (61.3±1.8 g/l), dysproteinemia due to a decrease in albumin content (42.8±2.1%), an increase in α1- and α2-globulins (7.8±0.5 and 11. 9±0.7%, respectively), hypergammaglobulinemia (20.9±1.9%).
Cholesterol concentration is decreased.
Glucose concentration may increase.
When muscles are damaged, creatine phosphokinase increases sharply. In patients with severe thrombocytopenia, already in the initial period, a significantly sharper increase in CPK levels was noted (1339 ± 320 units/l), increasing during the peak period and remaining high in convalescence. And in patients without severe thrombocytopenia at the height of the disease, CPK activity was 3 times less and returned to normal during the period of convalescence.
A marked increase in the level of amylase in the blood serum was noted in 100% of the examined patients with a fatal outcome.
Procalcitonin: sharply positive in 35% of patients (≥ 10 ng/ml), in 10% of patients – ≥ 2 ng/ml; 30% – ≥ 0.5 ng/ml; in 25% of cases a negative result was recorded (≤ 0.5 ng/ml). Patients with sharply positive PCT are characterized by hemorrhagic syndrome and significantly more profound changes in the coagulogram.
During the polyuric phase of the disease, hypercalcemia may develop. A hypercalcemic crisis, which develops when the level of calcium in the blood increases to 2 times the upper limit of normal, is fatal in 30–60% of cases.
The breakdown of muscle tissue leads not only to an increase in the activity of AST and CPK, but also the level of uric acid, potassium, and phosphates.
When examining the cerebrospinal fluid, cytosis is noted (usually within 400-500 cells in 1 μl) with a predominance of neutrophils. Sometimes the cerebrospinal fluid changes as in purulent meningitis: with cytosis up to 3-4 thousand in 1 μl and more with a predominance of neutrophils.
ECG: signs of diffuse myocardial damage, signs of hypercalcemia: rounded bimodal T wave, shortening of the QT interval to 0.30 ms due to the absence of the ST segment.
CT: signs of dystrophy of the lumbar muscles, which can be considered as an indirect sign of waxy necrosis.
During morphological examination of the biopsy, focal changes typical of leptospirosis in the form of waxy (glassy) or Zenker's necrosis are found in the muscles.
In 2004-2018, compared to 1985-1998, complaints of headaches and retroorbital pain, sleep disturbances, adynamia, decreased appetite, and joint pain became less common.
Leptospirosis, icteric form, severe, complicated by toxic shock.
Loa loa (seu African eye worm) is endemic to Central African countries, where the main vectors occur (Chrysops silacea and Chrysops dimidiata).
Loa loa is mainly recorded from south-eastern Benin in the west to southern Sudan and Uganda in the east, and from Chad in the north to Zambia in the south, mainly in tropical forest regions.
The risk of infection of travelers increases with the duration of stay in an endemic region, but cases of the disease have been described when the stay in an endemic region was less than 30 days.
The source of infection is an infected person.
The development of the parasite into L3 larvae takes 10-12 days at a temperature of 20–30°C (tropical forest zones in the Niger Delta) or about 3-4 weeks at lower temperatures (mountain valleys and forests of British Cameroon).
Loa loa is transmitted by deer flies in the genus Chrysops, primarily C. silaceus and C. dimidiata. flies deposit L3 larvae at the bite site when taking a blood meal, and the larvae penetrate the wound.
Flies most often live in thickets along river banks, but can fly into houses as they are attracted to wood smoke.
The incubation period usually lasts several years, sometimes reducing to 4 months.
Acute infection can be asymptomatic for several days or even years. The clinical picture of manifest loalosis is often mild, and the symptoms are transient.
Chronic loalosis is characterized by a wide range of symptoms: from itching, episodic angioedema (Calabar edema) or subconjunctival migration of worms, to severe renal, cardiac and neurological complications.
Loa loa migrates from the blood into tissues, including the skin, at night, causing itching or burning sensation.
The adult parasite can be seen in the eyes or subcutaneous tissue as itchy swellings called "Calabar swellings".
Calabar swellings are painless formations of oval or round shape, up to 8 cm in diameter, slightly inflamed, leaving no pits when pressed and usually disappearing spontaneously after 3-4 days.
Skin lesions may also appear as papules and nodules.
Calabar swellings can occur anywhere on the body, but is most commonly found on the ankles, wrists, or face, and especially around the eyes.
When the worm dies, a painful lump first forms under the skin, then its central part is rejected, forming an ulcer with indurated edges.
Spontaneous allergic reactions (associated with the natural death of worms) with loalosis occur rarely.
General symptoms may include subfebrile temperature, fatigue, pain in the limbs, and paresthesia.
A mobile long thread-like worm can be seen in the subconjunctival space. Usually there are no pathological changes in the anterior chamber and posterior segment.
Such patients complain of photophobia, lacrimation and itching in the eye.
The conjunctiva is hyperemic, the eyelids may be edematous, without ulceration.
Adult worm can move 2 to 3 cm per minute.
The parasite's lifespan can reach 20 years.
Cases of abscess development (arising as a result of secondary infection at the sites of death of adult parasites) and hydrocele in men have been described.
Loiasis can provoke autoimmune glomerulonephritis: proteinuria appears, and morphological examination of the kidney can reveal total glomerular sclerosis. In some patients, kidney function is preserved, while others require hemodialysis.
Prolonged periods of eosinophilia in loalosis may lead to endomyocardial fibrosis.
Ophthalmologic complications of loalosis include chronic uveitis, cataracts, glaucoma, and corneal edema.
A case of bone marrow infection by L. loa is described in a 57-year-old Gabonese patient with T-cell leukemia: microfilariae were found in his bone marrow biopsy.
Neurological manifestations of loalosis have been described: impaired consciousness, asthenia, headache, chills, blurred vision, speech impairment. It is believed that high concentrations of microfilariae in the blood and concomitant infections with Trypanosoma spp., Treponema pallidum and Plasmodium spp. predispose to damage to the blood-brain barrier.
Most cases of encephalitis associated with loiasis have been described in patients with microfilarial concentrations in blood greater than 30,000/ml, but neurological symptoms have also been observed in patients with lower concentrations of the parasite.
Neurological and psychiatric sequelae have been described among the survivors.
Chronicity of the disease has been associated with excess mortality.
The adult parasite can be seen in the eyes. The larval stage "microfilariae" can be found in the blood.
The causative agent of the disease Loa loa is a white translucent nematode 30-70 mm long, the length of the microfilariae is 0.25-0.3 mm.
The main diagnostic method is the detection of microfilariae in thick and thin blood films stained with Giemsa, Wright, Wright-Giemsa, or hematoxylin stains.
The microfilariae of L. loa are 231 to 250 mm long, with a relatively short head and tail with nuclei (irregularly arranged at a tapering tip); the worm's sheath is colourless when stained with Giemsa.
To detect microfilariae, blood microscopy must be performed both during the day and at night. The method is more effective during the daytime (between 10:00 and 14:00).
Microfilariae can also be recovered from urine and spinal fluid.
Automated microscopy systems (CellScope) can improve the efficiency of microscopic diagnostics.
Loa loa may also be diagnosed by the examination of adult worms removed from the eye or in histopathologic examination of skin biopsy specimens. In both instances, the adults need to be differentiated from zoonotic filarids in the genus Dirofilaria. The adults of both worms are similar in size and macroscopic appearance.
A distinguishing difference is that the adult Loa loa has small irregularly spaced bumps (bosses) on the surface of the cuticle, while the adult Dirofilaria has a thick cuticle with multiple longitudinal ridges.
The worm can be removed alive and intact from the subconjunctival space under local anesthesia and sent for histopathological examination.
A simple eye examination or slit lamp examination may be ineffective due to the rapid migration of the worm into the retrobulbar space.
Serological tests do not differentiate between current and past infection. In addition, the presence of cross-filariasis antigens reduces the specificity of serology.
A method for detecting worm’s antigen in urine samples using the luciferase immunoprecipitation system is under investigation.
Qualitative PCR allows confirmation of the loiasis, and quantitative PCR allows an approximate estimate of the concentration of microfilariae.
The material for PCR can be a tissue biopsy from the Calabar tumor.
A complete blood count may reveal eosinophilia.
IgE levels may be elevated.
The adult worm can be detected by optical coherence tomography of the anterior segment of the eye.
Computed tomography may reveal lymphadenopathy.
Ultrasound examination of the Calabar tumor reveals a long formation in the tissue, indicating the presence of a nematode.
Scanning electron microscopy allows differentiation of L. loa from other filarial nematodes.
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Acute loalosis
The incidence of meningococcal infection in the world over the past decade stays at a constant level, and its periodic rises are associated with a change in the leading serogroup of the pathogen that causes generalized forms of meningococcal infection (GFMI) and a decrease in collective immunity.
Higher incidence rates in certain developed countries may be associated with the influx of refugees and migrants.
Meningococcal infection is registered in more than 150 countries around the world, in all climatic zones. Currently, the epidemiological situation in the world is ambiguous and has clearly defined territorial features. In North America and Europe, the incidence is less than 0.5-0.9 cases per 100 thousand population, in African countries - 10-1000 cases per 100 thousand population.
The countries of Central and Western Africa south of the Sahara Desert are called the “meningitis belt”. It includes Benin, Burkina Faso, Gambia, Ghana, Northern Cameroon, Mali, Niger, Northern Nigeria, Senegal, Sudan, Chad, Ethiopia.
The age structure of meningococcal infection depends on a number of factors and differs in regions.
About 80% of cases of the disease occur in children, half of which are children aged 1 to 5 years. Among adults, the largest number of cases of the disease occurs at a young age – 15–30 years.
The age structure of carriage differs significantly from the structure of incidence of manifested forms: most of the carriers are adults, and the majority of patients are children.
An increase in the proportion of adult patients with generalized forms of meningococcal infection is considered an unfavorable prognostic factor for a possible increase in morbidity.
In more than 50% of cases, there is family contact, when several children come from the same family, sometimes together with their parents.
Any situation that leads to stress and significant crowding of people in poor living conditions is characterized by a high risk of meningococcal infection. Traditionally, the disease is classified as a “military” infection, since the increase in incidence directly correlates with wars, as well as major disasters and accidents.
The source of infection is a sick person or a bacteria carrier. Patients with meningococcal nasopharyngitis are the most contagious.
The transmission mechanism is aerogenic. The contagiousness of patients is low due to the instability of the pathogen, so the disease requires close contact (for example, crowding). The infectiousness index is 10-15%.
Factors that reduce immunity (mental and physical stress, hypothermia, exposure to radiation) contribute to the development of the disease.
Seasonality: winter and spring. More than 60% of all cases of disease throughout the year are registered in this period. The peak incidence occurs in February-March, and during epidemics - in April-May.
Periodic increases in incidence in developed countries occur every 8-30 years.
The epidemic threshold for meningococcal infection is an incidence of 2.0 per 100 thousand population.
There is a vaccine to prevent meningococcal infection.
The incubation period ranges from 1 to 10 days (usually 2-6 days).
There are localized forms (carriage and acute nasopharyngitis), generalized forms (meningococcemia, meningitis, meningoencephalitis and mixed form), rare forms (endocarditis, polyarthritis, pneumonia, iridocyclitis).
It has been proven that clinically manifest forms of the disease appear, if the number of meningococcal carriers in a group reaches 20% or more.
Among the manifest forms of generalized MI, the most often recorded is a mixed form (57.6% of patients). At the same time, different clinical forms are found evenly in all age groups.
Acute nasopharyngitis is often a form of the disease, but it can also be a stage preceding the development of a generalized form.
It is characterized by low-grade fever (lasts 1-4 days), moderate intoxication (weakness, headache, dizziness) and nasopharyngitis (nasal congestion with scanty discharge, slight cough, sore throat).
Skin is pale.
Sclera are injected.
The back wall of the pharynx is hyperemic, mucus can be seen. On days 2-3, hypertrophy of lymphoid follicles appears (lasts up to 2 weeks after the disappearance of hyperemia).
Meningococcal meningitis in 45% of cases is preceded by symptoms of nasopharyngitis lasting for 1 to 5 days.
Body temperature with severe chills rises to febrile levels in the first hours of the disease. A feature of fever is its resistance to the prescription of antipyretics: even if it decreases by 1–2 degrees, after a while it again reaches high numbers.
Patients complain of intense diffuse headaches of a bursting or pressing nature, aggravated by changes in body position, sudden movements, bright light or loud sounds (61-72.7%), hyperesthesia of the skin of the extremities and abdomen (72.8%; in children - sensitivity to light, any touch), vomiting (13.6 %), not bringing relief (64.4%), weakness, lack of appetite, pain in the eyeballs, especially when moving.
In children, hyperthermia is accompanied by changes in behavior and sleep disturbances, pronounced psychomotor agitation (in 10.6% of cases, more often in children of the first year of life); a shrill monotonous cry is common in children under the age of 3 years.
Most patients experience lethargy and adynamia (in children under 3 years of age - in 100% of cases), in severe cases - somnolence, stupor, coma.
After 12-14 hours from the onset of the disease, physical symptoms of irritation of the meninges appear (stiffness of the neck muscles, Kernig’s sign, Brudzinski’s, Guillain’s symptoms), which can be combined with symptoms of tension (Nery, Lasegue). Most patients experience a decrease in abdominal, periosteal and tendon reflexes, as well as their asymmetry (anisoreflexia).
From the 3-4th day of the disease, patients (especially children) can take a forced position: on their side with their head thrown back and legs tucked towards their body (pointing dog pose).
Reversible lesions of the cranial nerves can be detected in the first days of the disease. Most often, the facial nerve is affected, as well as the oculomotor nerves (III, IV and VI pairs), less often the hypoglossal and trigeminal nerves. Also on the 2-3rd day, pyramidal signs, sometimes paresis of the limbs, and pelvic disorders are possible.
Relative bradycardia and increased blood pressure, especially systolic, are possible.
In children, general cerebral symptoms come to the fore: headache (65%), repeated vomiting (60%), change from periods of anxiety and excitement to lethargy (90%), short-term convulsions (24%), general hyperesthesia (100%).
Meningeal symptoms are detected in 48% of children. The most pronounced are stiff neck in older people and Lessage's symptom in young children. In more than half of young children, meningeal symptoms are mild and are characterized as doubtful (36%) or negative (16%).
In 58.8% of adult patients, pain is detected upon percussion of the skull.
Meningococcal meningoencephalitis is characterized by a severe course, pronounced encephalitic manifestations in combination with severe meningeal and intoxication syndromes.
General cerebral symptoms increase rapidly. By the end of the first - beginning of the second day of the disease, disturbances of consciousness develop in the form of deep stupor, accompanied by psychomotor agitation, convulsions, and often visual or auditory hallucinations.
In parallel, meningeal symptoms increase. A day after the onset of the disease, most patients experience a characteristic meningeal posture (the patient lies on his side with his legs bent and his head thrown back). In the first hours of the disease, some meningeal symptoms (stiff neck muscles, Kernig's sign, etc.) may be absent.
Signs of encephalitis come to the fore as intoxication and cerebral oedema decrease.
Focal cerebral symptoms are often present in the form of pyramidal insufficiency: paresis of facial muscles of the central type, pronounced anisoreflexia of tendon and periosteal reflexes, sharp pathological symptoms, spastic hemi- and paraparesis, less often - paralysis with hyper- or hypoesthesia, coordination disorders. Focal lesions of the brain substance are also detected in the form of damage to the cranial nerves.
Cortical disorders are possible: mental disorders, partial or complete amnesia, visual and auditory hallucinations, euphoria or depression.
Meningococcemia is often (up to 20%) recorded in combination with meningitis or previous nasopharyngitis.
The disease develops suddenly (the temperature reaches high levels within several hours). Chills, body aches (100%), moderate hyperesthesia (mainly sound and light), vomiting (39.7-55.4%), weakness, lethargy (31-41.4%), dry cough (29.4%), runny nose (10.3-26.5%), headache (5.2-12.3%), severe restlessness/moody (6.2-10.3%), leg pain (1.7 %), abdominal pain (1.5%), speech impairment (1.5%), paresthesia (1.7%) and impaired consciousness (1.7%) appear.
Copious loose stools (1-2 times a day) are recorded in 51.4% of young patients (17-27 years old) with a fatal outcome, abdominal pain - in 80%, shortness of breath - in 51.4%, drowsiness - in 60%.
6-12 hours after the onset of chills, a polymorphic (usually star-shaped) hemorrhagic rash can be detected. The speed of appearance and size of the rash elements correlate with the severity of the disease. During the 1st day, new elements may appear.
The size of the rash elements is 2-7 mm, in severe cases they can reach 5-15 cm or more. Large elements of the rash are dense and sensitive to palpation, rising above the surrounding skin.
In the first hours of the disease, a scanty petechial rash with a few stellate elements appears on the skin of the lower extremities and torso. As the hemorrhagic rash gets worse, its amount increases, petechial and stellate elements appear on the skin of the legs, thighs, in the groin and axillary areas, on the abdomen and chest.
Hemorrhagic elements are observed with toxic shock somewhat more often than in its absence (98.3% and 83.1% of patients, respectively); they acquire a “cherry” color against the background of pale skin with an enhanced venous pattern (“marble skin”), significantly more often necrosis is formed (29.5% versus 6.2%). In toxic shock grades II–III, the rash first appears on the face and upper torso and then spreads to the extremities.
Small elements turn into pigmentation, large ones become necrotic: a crust forms, after it falls off, erosive and ulcerative defects are formed, and then scars.
The appearance of hemorrhages may be preceded by the appearance of papules or roseolas, which subsequently disappear or turn into hemorrhages. A maculopapular rash is typical for older patients.
In lethal cases exanthema always appears on the first day of the disease (often in the first 5-8 hours), capturing extensive regions of the skin on the trunk, limbs and head. The appearance of rash coincides with shortness of breath, violation of consciousness and in some patients - with vomiting and diarrhea.
There are hemorrhages in the sclera, conjunctiva, and mucous membranes of the nasopharynx. Other hemorrhagic manifestations also may present: nasal, gastric, uterine bleeding, micro- and macrohematuria, subarachnoid hemorrhages.
In children, pneumonia (9.8%), arthritis (2.4%), and osteomyelitis (0.8%) are sometimes regestered.
Cerebral edema; toxic shock, often combined with acute adrenal insufficiency (Waterhouse-Friderichsen syndrome); endocarditis, myocarditis and pericarditis; thrombosis of large vessels with subsequent gangrene of fingers and limbs.
Cerebral edema more often develops at the end of the first - beginning of the second day of the disease. It may develop before the appearance of typical changes in the cerebrospinal fluid (fulminant form).
Against the background of severe intoxication, disturbances of consciousness appear. Patients do not respond to strong stimuli.
Meningeal symptoms fade, previously increased cerebrospinal fluid pressure decreases. Hemiparesis develops. General clonic-tonic convulsions appear and increase. Corneal reflexes, constriction of the pupils and their sluggish reaction to light fade away.
Bradycardia gives way to tachycardia. Blood pressure is initially labile, with a tendency to significantly decrease, in the terminal stage it is high, up to 150/90-180/110 mm Hg.
Shortness of breath quickly increases, breathing becomes noisy, shallow, with the participation of auxiliary muscles, and then arrhythmic.
Involuntary bowel movements and urination may occur.
Toxic shock remains the most common early complication of meningococcemia (61% of patients). I grade shock prevails (63.8%), less often - grade II or III shock (27.7% and 8.3% of patients, respectively).
Body temperature drops critically to normal or subnormal levels. In the first hours, patients are fully conscious, excited, and complain of severe hyperesthesia. Then excitement gives way to lethargy, and convulsions may appear.
The skin is pale, and cyanosis increases as shock progresses.
The pulse is frequent, weak filling, hypotension, tachypnea are noted, and with decompensation of shock - anuria.
In severe cases of meningococcemia, deep necrosis may appear, resulting in the formation of skin scars and requiring repeated plastic surgery.
The risk of death is higher in children under 1 year of age, in men, and also when seeking medical help late.
Death most often occurs on the 5-7th day (in the absence of treatment in a specialized hospital - on the 3rd day); death can occur even 24-48 hours after the onset of the disease or 5-20 hours after the appearance of the rash.
As a result of generalized forms of meningococcal infection, hypertensive-hydrocephalic syndrome is more often recorded: diffuse headache, periodic dizziness, decreased memory, attentiveness, fatigue, as well as sensorineural hearing loss (3.3%), frontocerebellar ataxia (5%), residual encephalopathy (11.8%), symptomatic epilepsy (3.3%).
Bacteriological method allows you to obtain a culture of the pathogen, determine its serogroup by identifying a group-specific antigen (capsular polysaccharide) and sensitivity to antibiotics.
The material can be cerebrospinal fluid, blood, scrapings from hemorrhagic elements of the rash, mucus from the nasopharynx.
The disadvantages of bacteriology are the time it takes to obtain results, high requirements for taking material, and decreased sensitivity due to early antibiotic therapy. The sensitivity of the bacteriological method for meningococcal infection varies, according to various authors, from 6 to 70%, depending on the equipment of the laboratories.
On bacterioscopic examination of mucus from the nasopharynx and blood smears (“thick drop”), gram-negative diplococci can be detected, located predominantly intracellularly.
Using reaction of direct haemagglutination with an erythrocyte diagnosticum, you can determine the concentration of antimeningococcal antibodies and track its increase.
PCR allows you to detect meningococcal DNA fragments in the material. Meningococcal DNA can be detected in samples that do not contain live pathogens, but only fragments of their genetic material (for example, after starting antibiotic therapy).
A case of postmortem diagnosis using PCR of CSF taken from the decomposed body of a 27-year-old man is also described.
The sensitivity of PCR is higher than that of the bacteriological and bacterioscopic methods, however, it is not a replacement for traditional microbiological methods, but a complement to them: the use of PCR can increase the frequency of confirmation of the diagnosis of meningococcal infection.
In CBC in patients with nasopharyngitis, an increase in ESR to 10-30 mm/hour is possible, although in severe cases neutrophilic leukocytosis may appear (9.7-12.4*10^9/l).
In patients with meningitis, the CBC reveals high neutrophilic leukocytosis and increased ESR.
In the CBC for meningococcemia: neutrophilic leukocytosis up to 11.6–54.0*10^9/l; appearance of myelocytes and promyelocytes is possible; thrombocytopenia (22-150*10^9/l).
In children, CBC shows mild anemia (in 50% of cases), moderate leukocytosis (11.2±2*10^9/l) with neutrophilia, a shift in the leukocyte count to the left, and an increase in ESR to 18–25 mm/hour.
In patients with toxic shock, significantly lower levels of leukocytes, hemoglobin, platelets, neutrophils and ESR, fibrinogen protein A and PTI and higher levels of urea, creatinine, aPTT, lactate and procalcitonin are recorded.
In uranalysis, with severe infection, proteinuria, hematuria, and decreased density are possible.
In patiennts with meningitis, cerebrospinal fluid flows out under increased pressure (with frequent vomiting, cerebrospinal fluid hypotension is possible). By the end of the first day of the disease, as a rule, it is already cloudy, cell-protein dissociation is observed, globulin reactions (Pandey, Nonne-Appelt) are sharply positive.
Glucose concentration quickly drops to 2.9-4.5 mmol/l; on the 3-4th day, glucose levels may drop to undetectable. The content of chlorides in the liquor decreases.
In 72.7% of patients, within a few hours/the first day, the number of neutrophils increases to 1.6-41 thousand per μl (up to 42,240 cells/μl in adults). The average level of pleocytosis is 7947.92 cells/μl, neutrophils make up 91-100%. Sanitation of the cerebrospinal fluid often occurs on days 7–10, and in mixed forms at an earlier date.
An increase in CRP is observed in 50 -100% of patients: 66–407 mg/l.
The increase in procalcitonin on the first day is 18.2-100 ng/ml, later - up to 200 ng/ml.
In uncomplicated forms, there is a tendency to increase fibrinogen (with the development of consumption coagulopathy, its decrease).
Morphological examination reveals leukocyte-fibrinous thrombi containing diplococci in various vessels.
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Meningococcal infection, generalized form: meningococcemia, severe
Opisthorchis felineus is recorded mainly in the basin of the Ob and Irtysh rivers (Western Siberia, Kazakh Republic), less often - the Volga, Dnieper (some regions of Ukraine), Don, Donets, Kama (Perm region), Neman, Oka, Northern Dvina rivers.
The main focus of civet opisthorchiasis is Thailand; O. viverrini and C. sinensis are also registered in Vietnam, Hong Kong, India, Cambodia (in the Mekong River basin), China, Laos, Taiwan, and South Korea.
Data on the gender structure of patients with opisthorchiasis are contradictory.
The age of patients varies from 3.5 to 70 years.
A human can remain a source of infection for up to 20 years.
The route of transmission is food: eating insufficiently heat-treated fish (lightly salted, sliced, dried, poorly fried). The most commonly affected species are ide, dace and roach; bream and asp are also dangerous. Moreover, opisthorchid metacercariae are preserved for up to 7 hours at a temperature of -40°C and for up to 32 hours at -28°C.
Seasonality: summer-autumn. A total of 90.2% of cases become infected in June-July.
There are acute (typhoid-like, hepaocholangiolytic and gastroenterocolitic forms) and chronic opisthorchiasis.
Acute manifest opisthorchiasis usually develops in persons arriving from non-endemic areas. In the local population, the disease usually has a primary chronic course. Acute opisthorchiasis is practically not observed among the indigenous peoples of the North (Khanty, Mansi), in whom the frequency of chronic opisthorchiasis reaches 100%.
The incubation period for acute opisthorchiasis lasts from 1 to 6 weeks (on average about 14 days).
In 83.5–100% of patients, the onset is acute: body temperature with chills rises to 38.5–39.5ºС (61.5–78%), subfebrile level (15.4–22%) or above 39.5ºС (18 -23.1%). In 11.5% of patients, body temperature remains normal.
In most cases, the temperature remains elevated for 3-10 days, but prolonged low-grade fever is possible. Fever may become remitting or continued.
Patients complain of chills, fatigue, aching joints, headache, loss of appetite, sweating, and weakness.
Also typical are discomfort, moderate or severe pain in the upper abdomen and right hypochondrium, bitterness in the mouth, nausea, vomiting, unstable stools, and bloating.
In 14.6% of patients, a sore throat, dry cough, chest pain, and attacks of suffocation may appear against the background of fever.
In 87.1% of patients with febrile fever, autonomic dysfunction is observed with autonomic crises, fatigue, dizziness, palpitations, lability of pulse and breathing, angiodystonic headaches, and difficulty breathing.
According to various sources, yellowness of the sclera, and sometimes the skin, occurs in 7.3-66.7% of cases.
Allergic rashes (7.9-15.4%), skin itching (9%) are possible.
Palpation of the pancreas area is painful; in some patients, hyperesthesia of the skin on the left is detected.
Pain and enlargement of the liver (by 2-3 cm) are common (up to 50% of cases), and sometimes the spleen is enlarged.
In chronic opisthorchiasis, dyspepsia (80%) predominates in the form of discomfort or moderate pain in the right hypochondrium, often radiating to the back (27-65%), loss of appetite, periodic nausea (60%), decreased tolerance to food load, unstable stool (25%), flatulence (20%), bitterness in the mouth (17.5%), heartburn (12.5%).
Long-term low-grade fever (more than a year) is observed in 14.3% of patients.
15% of patients experience periodic rashes on the face, torso, and lower extremities; 7.5% have itchy skin.
The chronic phase is characterized by a decrease in the severity of allergic reactions, but the torpidity of their course. Urticaria often takes a recurrent course. Transformation of urticarial rash into papular and vesicular is often observed. Sometimes urticaria has hemorrhagic component.
Patients complain of headaches, dizziness, weakness, sweating, sleep disturbances, and become emotionally labile.
Tachycardia, dullness of tones, expansion of the borders of the heart, systolic murmur at the apex are possible.
The liver is often enlarged and dense.
The death of the parasite is not always accompanied by clinical recovery: in persons who have suffered from opisthorchiasis for more than 5 years, complaints and objective changes that took place during the chronic phase can persist.
Obstruction of the bile ducts, recurrent cholangitis, liver abscesses, acute pancreatitis, rupture of dilated bile ducts with subsequent development of bile peritonitis, primary liver cancer.
Coproovoscopy (with ether-formalin sedimentation, the Kato-Miura method and the Stoll dilution egg counting method) is the “gold standard” for diagnosing opisthorchiasis. Parasite eggs can be found in feces, bile and duodenal contents.
Opisthorchis eggs are found in stool and bile 1–1.5 months after infection. If the result is negative, coproovoscopy is recommended to be repeated several times with an interval of 5–7 days. With a low intensity of invasion, eggs are more likely to be found in the duodenal contents.
Sometimes opisthorchises themselves are found in the bile with negative results of coproovoscopy. The diagnosis is also confirmed by the extraction of parasites during surgery on the liver or biliary tract.
Serological examination for antibodies is an auxiliary method. Interestingly, the ELISA method can give negative results for the presence of IgM and/or IgG in more than half (57%) of patients with a positive stool microscopy result.
Antibodies are usually detected 3-8 weeks after infection (the period depends on the intensity of the infection). In some patients, IgM is detected already from 6-10 days of illness.
At the same time, with ELISA, false-positive reactions with antigens of other helminths (echinococcus, toxocara, clonorchis, roundworm, etc.) are possible. Therefore, negative ELISA results do not allow us to exclude the diagnosis of opisthorchiasis, while positive results do not allow us to confirm the diagnosis.
Detection of opisthorchiasis antigens in feces using monoclonal antibodies has greater diagnostic value in chronic opisthorchiasis.
The sensitivity of PCR depends on the concentration of opisthorchis eggs in feces: 68.5% in the presence of 200–1000 eggs per 1 g of feces, 50% with a lower concentration.
In CBC in 83-100% of cases there is eosinophilia (from 10% to 90% - leukemoid eosinophilic reaction) and leukocytosis (up to 18-60 thousand) with a shift in the leukocyte formula to the left.
Eosinophilia is detected from the end of the 1st week of illness and reaches a maximum by the 3rd week. Even by the end of the 4th month, the number of eosinophils may remain elevated.
ESR is moderately increased.
Moderate normo- or megaloblastic anemia is often observed.
Biochemical tests: the level of alkaline phosphatase fluctuates in the range of 243-2736 mmol/l (with the norm up to 129), gamma-GTP - 184-542 (with the norm up to 16), AsAt - 83-128 mmol/l, AlAt - 98-225 mmol/l; bilirubin levels often do not exceed normal values, but can increase to 279 µmol/l.
In half of the patients, there is a correlation between the severity of clinical symptoms and the severity of eosinophilia and cholestasis.
Insufficiency of the exocrine function of the pancreas is indicated by an increase in the concentration of trypsin, antitrypsin, amylase, lipase in the blood, and diastase in the urine. Some patients experience disturbances in the endocrine function of the pancreas in the form of fasting hyperglycemia.
Duodenal probing: microscopy of duodenal contents reveals an increase in the number of leukocytes, epithelial cells, as well as detritus, bilirubin crystals and cholesterol in all portions (especially in portion “C”). The concentration of trypsin, amylase, and lipase is reduced.
In chronic opisthorchiasis, a leukemoid reaction of the eosinophilic type is rarely detected, usually eosinophilia does not exceed 10%. Also, in 24% of patients, a moderate increase in transferase activity was recorded, but no more than twofold, and the level of alkaline phosphatase in all patients remained within normal limits.
X-ray can detect eosinophilic infiltrates in the lungs.
In 75% of patients with radiographically established gallbladder motility disorders, a hypokinetic type of dyskinesia is observed.
Endoscopy: some patients develop erosive and ulcerative gastroduodenitis.
An instrumental examination (ultrasound of the abdominal cavity in dynamics, RPCG, CT with contrast, MRI) may reveal transient choledocholithiasis (“heterogeneous suspension in the distal section”), slight dilatation of the intra- and extrahepatic bile ducts, an increase in the size of the gallbladder, and papillitis.
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Acute opisthorchiasis, moderate
The incidence of paratyphoid fever is declining in Europe, Central Asia, Latin America and the Caribbean, but increasing in Southeast Asia, the Pacific and Africa.
74.2% of patients are aged 16-40 years.
Men and women get sick equally often (52.9% and 47.1%, respectively).
Sources of infection in paratyphoid A are sick people and carriers of bacteria (especially chronic - more than 3 months - carriers of bacteria). 5-7% of those who have had paratyphoid fever become carriers.
Bacteria are excreted in feces and urine from the first days of the disease, but the peak of bacterial excretion is reached in the 2nd-3rd week of the disease.
Transmission mechanism is fecal-oral. Waterborne outbreaks are more typical for paratyphoid A.
Seasonality is associated with bathing, drinking unboiled water, poorly washed berries, fruits and vegetables. At a low level of morbidity, there is no seasonality.
Incubation period is 8-10 days.
Paratyphoid A usually occurs as a moderate disease, but can also result in severe forms of the disease.
The disease begins acutely, with a rise in temperature; the fever is often accompanied by chills, and then profuse sweating.
Patients complain of nasal congestion, sore throat, weakness, and dry cough.
There may be discomfort in the abdomen (more on the right side and in the navel area), loose stools without pathological impurities with increasing frequency.
In the initial period, hyperemia of the face, injection of scleral vessels, runny nose, and cough are observed.
Polymorphic rash (roseola, macular, maculopapular and even petechial) appears on the 4th-7th day of illness in 50-60% of patients. The rash is not itchy, more abundant than in typhoid fever, often the number of rash elements increases over time.
During the peak period, the skin is pale.
The mucous membrane of the posterior wall of the oropharynx is hyperemic, there is no plaque on the tonsils. The tongue is coated with a white plaque at the root.
Muffled heart sounds and tachycardia are described.
The abdomen is soft, there is pronounced flatulence, dullness of percussion sound in the right iliac region, moderate pain is possible during palpation of the cecum. Hepatomegaly is moderate, the liver is elastic.
Complications and relapses are observed less frequently than with typhoid fever.
The bacteriological method is the "gold standard" of diagnostics. The material can be feces, urine, blood, vomit or gastric lavage.
The following are widely used as accumulative media for salmonella: magnesium medium, selenite broth, Rappaport-Vassiliadis broth, Müller-Kaufman medium, etc. Among dense selective differential diagnostic nutrient media, such media as Levin medium, Endo agar, bismuth sulfite agar, XLD agar, etc. are usefull.
After the isolation of a pure culture of the pathogen, its identification is carried out based on the characteristics of its enzymatic properties. For example, it is possible to distinguish strains of salmonella typhi that give a positive reaction with lysine from strains of salmonella paratyphi A that do not utilize lysine.
The average diagnostic sensitivity of blood culture is estimated at 61.1% (it decreases with late admission of patients, uncontrolled use of antibacterial drugs, and concomitant chronic diseases of the gastrointestinal tract).
The sensitivity of the bacteriological method correlates with the severity of the disease: in severe cases of paratyphoid A, blood culture is isolated 2.7 times more often, and coproculture 2.4 times more often than in mild cases.
The Widal reaction with paratyphoid diagnosticum may remain negative throughout the disease (or positive in very low titers). The Widal reaction is especially relevant in mild cases of paratyphoid A, when the sensitivity of bacteriology is reduced.
CBC: 63.8% of patients have a moderate decrease in red blood cells, and 36.7% have a decrease in hemoglobin. A decrease in hemoglobin is more often observed after 21 days of illness and in severe cases.
In 49.2% of patients, leukocytes are normal, in 23.2% - leukopenia, in 27.6% - leukocytosis. Moreover, in the first 10 days, leukopenia is recorded less often, and then the frequency of its detection increases slightly.
Eosinophils are absent in 31.8% of patients and decreased in 45.8%; a decrease in the eosinophil level is observed already in the initial period of the disease. The severity of eosinopenia clearly correlates with the severity of paratyphoid A.
Lymphocytosis is observed in 87.5% of patients, and its frequency increases with the duration of the disease. Monocytosis is not typical for paratyphoid A.
Ultrasound of abdomen: hepatosplenomegaly.
X-ray of the abdominal cavity: aerocolia.
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Paratyphoid A, moderate
The most relevant source of infection are chronic (more than 3 months) carriers of the bacteria. In addition to people, sources of infection for paratyphoid B can be animals (cattle, pigs, poultry).
Bacteria are excreted in feces and urine from the first days of the disease, but the peak of bacterial excretion is reached in the 2nd-3rd week of the disease.
The transmission mechanism is fecal-oral. Foodborne outbreaks are particularly typical for paratyphoid B.
Seasonality is absent with a low incidence rate.
Immunity is usually stable, the relapse rate is 1-2%. At the same time, 5-7% of those who have had paratyphoid fever become carriers.
The incubation period is usually 5-10 days, but can be longer.
Paratyphoid B is milder than typhoid fever and paratyphoid A, although severe forms also occur.
The disease often begins suddenly with symptoms of acute gastroenteritis and only then symptoms similar to the clinical features of typhoid fever appear.
Fever is accompanied by severe chills, muscle pain and sweating. The temperature curve is characterized by a large daily range, often undulating. Intoxication symptoms disappear within 3-5 days.
The rash appears on the 4th-6th day of the disease, mainly roseola, but polymorphic and more abundant than in typhoid fever.
Intestinal perforation (0.2%), intestinal bleeding (0.4-2%), bronchopneumonia, cholecystitis, cystitis and other non-specific complications are possible.
Bacteriological examination of feces, urine, blood, vomit or gastric lavage is the main diagnostic method.
The following are widely used as accumulative media for salmonella: magnesium medium, selenite broth, Rappaport-Vassiliadis broth, Müller-Kaufman medium, etc. Among dense selective differential diagnostic nutrient media, the following media are used: Levin medium, Endo agar, bismuth sulfite agar, XLD agar, etc.
Serological studies are also used, especially when they are carried out dynamically.
CBC: neutrophilic leukocytosis.
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Paratyphoid B, moderate
Rotavirus infection is widespread in many countries of the world, accounting for about half of all intestinal disorders in children in the first two years of life in developing countries. The incidence of viral intestinal infections in adults is 5-6 times lower than in children.
Rotavirus infection accounts for 25% of cases of so-called "traveler's diarrhea."
The source of infection is a sick person (with manifest or inapparent form). A sick person is infectious from the end of incubation and then for 2-4 weeks, but from the 4-5th day of illness, the virus excretion rapidly decreases. Asymptomatic virus excretion is possible for several months.
Patients are highly contagious, so the disease usually occurs in groups. In families, the child usually gets sick first, then the adults.
Transmission mechanism is fecal-oral, but airborne transmission of the pathogen is also possible. Among food transmission factors, milk and dairy products are the most dangerous.
Children from 6 months to 2-3 years old are most susceptible to rotavirus infection.
In countries with a temperate climate, seasonality is quite pronounced, with the highest incidence in the winter and spring months. An increase in incidence is noted during the rainy season. Sporadic incidence is year-round.
Immunity is unstable and type-specific.
The incubation period lasts from 15 hours to 7 days (usually 1-2 days).
There is a typical and atypical (erased and asymptomatic) rotavirus infection; typical is divided by severity. The severity is determined by the severity of intoxication and dehydration.
The disease begins acutely. The clinical picture fully develops within 24 hours (only 10% of patients experience vomiting and diarrhea on the 2nd-3rd day of the disease).
Due to the combination of diarrhea, fever and vomiting in 90% of patients, the concept of DFV syndrome emerged.
The body temperature of most hospitalized children reaches 37.9°C and above, and in some it may rise above 39°C. According to various authors, in adults, signs of intoxication are observed in 10-95% of patients; in half of the cases, the temperature rises only to a subfebrile level.
Patients complain of severe weakness that does not correspond to the degree of increase in temperature.
Pain in the epigastric region, vomiting and diarrhea appear.
The pains are localized in the upper abdomen, they are moderate and monotonous (less often cramping). Tenesmus is not typical.
Vomiting is the leading manifestation of the disease. It is often repeated, but present only for one day (only in some patients vomiting persist on the 2nd-3rd day of the disease).
Typically, there is abundant, liquid, watery or yellowish stool with a sharp odor without any mucus or blood, sometimes the stool is cloudy-whitish (with a mild course, the stool may be mushy, with a severe course - cholera-like). Blood is not typical. The urge to defecate is imperative, there are no false urges.
Gastrointestinal symptoms persist for 3-6 days. Dehydration in rotavirus gastroenteritis is rarely observed in practice and is mild.
Signs of nasopharyngitis are a fundamental difference between rotavirus infection and bacterial diarrhea. Coughing, runny nose (less often signs of conjunctivitis or catarrhal otitis) are more often observed in children.
In adults with rotavirus infection, catarrh of the upper respiratory tract is observed in 42.3% of cases: patients complain of a dry cough, sore throat and runny nose; hyperemia of the mucous membranes of the soft palate, palatine arches, posterior pharyngeal wall, granularity and swelling of the uvula, hyperemia of the tonsils appear. Teeth marks on the tongue are possible.
Scleritis and enlargment of cervical lymph nodes can also be detected.
Some patients have a tendency to bradycardia and muffled heart sounds.
Palpation of the abdomen reveals pain in the epigastric and umbilical regions, and a rough rumbling sound in the right iliac region. The liver and spleen are not enlarged.
Shock, acute cardiovascular failure, renal failure.
The infection is more severe in children under 3 years of age, elderly patients and patients with concomitant chronic diseases.
The PCR method can detect rotavirus RNA in feces.
Viral antigens can be detected in the coprofiltrate using ELISA, complement fixation reaction, immunofluorescence reaction or latex agglutination reaction on days 1-4 of illness.
Detection of antibodies to rotavirus by ELISA, IHR, and CFR methods is a retrospective diagnosis, since confirmation of the diagnosis is an increase in the antibody titer in serum samples taken in the first days of the disease and after 2 weeks.
CBC: more often without pathology, less often at the beginning of the disease moderate neutrophilic leukocytosis is recorded, which during the peak period is replaced by leukopenia; some patients have eosinophilia; ESR is normal.
Uranalisis: in some patients there is albuminuria, leukocytes, and erythrocytes in the urine.
Coprogram: no signs of pronounced inflammation; starch grains, mucus (28.6%), undigested muscle fibers, undigested plant fiber (42.3%), neutral fat are detected. The pH of feces decreases.
In some patients, creatinine and urea levels increase.
During endoscopy, most patients show moderate hyperemia and swelling of the mucous membrane of the rectum and sigmoid colon. Signs of damage to the GIT persist for 2-6 days.
Microscopic examination of the small intestinal mucosa reveals areas with a smoothed surface, shortened villi, and infiltration of the mucosa by mononuclear cells. After 4-8 weeks, the small intestinal mucosa is completely normalized.
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Rotavirus infection, gastroenteritis syndrome, moderate, grade 1 dehydration.
Salmonellosis is currently a widespread infection in many countries around the world.
Various authors describe the predominance of men or women in the structure of patients with salmonellosis. The age of patients also varies greatly. Apparently, the predominance of certain age and gender categories of patients during outbreaks is determined by their culinary preferences.
The source of infection is animals with manifest or asymptomatic disease, and less often - people.
Birds, pigs, cattle, cats, dogs, rodents excrete Salmonella in urine, feces, and milk; the pathogen is also contained in muscles and inner organs; birds transmit Salmonella transovarially. The asymptomatic course of salmonellosis in animals can last for years. If the carcasses of infected animals are slaughtered and cut up incorrectly, post-mortem infection of the meat with intestinal contents is possible.
Humans as a source of infection are considered especially relevant in hospital outbreaks of salmonellosis (patients excrete salmonella in their feces, sometimes in their urine).
The main route of transmission is nutritional. Transmission factors can be various food products with insufficient heat treatment (usually even pasteurization kills salmonella) or contaminated with salmonella at the stage of preparing ready-made dishes: meat, eggs, milk and dairy products, etc.
Water transmission is also possible, with the transmission factor being water from open reservoirs or tap water in emergency situations.
Contact transmission is usually relevant in hospital outbreaks. Transmission factors include dishes, medical equipment, and household items.
Seasonality is predominantly summer-autumn, but pronounced increases in incidence are also observed during the New Year holidays.
Persons with hypoacid gastritis are more susceptible to salmonellosis. In patients with immunodeficiencies, the infection tends to generalize.Z
Immunity is very short-lived (patient can get sick several times a year).
The incubation period for foodborne infection ranges from 6 hours to 3 days (on average 13 hours). In nosocomial outbreaks, when contact transmission of infection predominates, incubation is extended to 3-8 days.
There are localized (gastrointestinal), generalized forms and carriage.
The localized form includes the following variants: gastritis, enteritis, gastroenteritis, gastroenterocolitis, enterocolitis.
The generalized form occurs in the form of typhus-like or septic variants.
Duration of carriage can be transient, acute (up to 3 months) and chronic (more than 3 months).
The severity of manifest forms is determined by the severity of intoxication and dehydration. Most of cases of nosocomial salmonellosis are moderate (58.2%), mild and/or atypical (36.5%); only 5.3% are severe.
The localized form is the main clinical form of salmonellosis (96-98% of cases).
The gastroenteric variant is the most common, although during some outbreaks described in the literature, the enterocolitic variant of the infection predominated.
The disease begins acutely: body temperature rises with chills (usually fever within 38.5 -39.5 degrees). Patients complain of headache, weakness, malaise, body aches, aching pain in the epi- and mesogastrium, or diffuse pain throughout the abdomen (not associated with bowel movements), nausea and vomiting (about 30% of patients).
Repeated vomiting is observed in 23.8% of patients, more than 5 times a day in 35.7%, up to 3 times a day in 14.3% of patients.
76-86% of patients complain of cramping abdominal pain of varying intensity.
Diarrhea usually occurs after vomiting; it is noted by 88.1% of patients (multiple - in 14.3%, up to 13 times a day - in 19.%, up to 10 times a day - in 40.5%, up to 5 times a day - in 23.8%); in the remaining patients, stool is formed or there is single loose stool.
Stool is enteric: copious watery, green (a type of “swamp mud”) or brown, foamy, foul-smelling (at first the stool is fecal, but soon becomes watery and foamy - like “frog spawn”). With the gastroenterocolitic variant, on the 2-3rd day of illness, the volume of stool decreases, an admixture of mucus and sometimes blood appears in them (hemocolitis is rarely recorded).
The majority of patients have dehydration expressed to varying degrees: in 45% - 2nd degree, in 15% - 3rd degree.
As hypokalemia increases, muscle pain and convulsive muscle contractions (usually the calf muscles) may appear.
The skin is pale; in more severe cases, cyanosis appears.
Heart sounds are muffled, tachycardia; blood pressure is decreased.
The abdomen is swollen, painful in all parts (mainly around the navel, in the iliac regions and sometimes in the epigastric region), rumbling upon palpation; when the large intestine is involved, a spasmodic, painful sigmoid colon is palpated.
The duration of the disease in most cases is from 2 to 10 days.
Hospital infection (usually S. typhimurium) predisposes to a protracted course of salmonellosis. This is characterized by a relatively slow development of the disease with the sequential appearance of clinical symptoms and the formation of persistent dehydration, reaching its maximum severity in a period of two to five days. Hemocolitis is detected quite often (up to 54% of cases), and at the same time, vomiting occurs quite rarely. The severity of the condition is determined more by the underlying disease causing immunosuppression than by the infection itself.
The generalized form of the disease is relatively rare and, as a rule, occurs in individuals with severe immunodeficiency. It includes typhus-like and septic variants.
The typhus-like variant of salmonellosis usually begins acutely with gastrointestinal symptoms (which soon disappear or fade into the background), but can occur from the very beginning without intestinal dysfunction (intoxication syndrome dominates throughout the disease). The body temperature is febrile, often reaching 39-40°C.
There is a disturbance of consciousness with a predominance of lethargy and apathy.
The skin is pale, sometimes roseola appears on the trunk from the 6th-7th day of illness. Heart sounds are muffled, heart rate corresponds to body temperature, or relative bradycardia occurs. blood pressure is reduced.
The abdomen is swollen. Generalization of infection often occurs on days 6-7 of illness, with hepatomegaly and splenomegaly appearing.
The septic variant is clinically similar to the typhus-like one, but purulent foci appear in various organs: lungs, heart, liver, spleen, meninges. Often, lesions occur in those organs and tissues that have lost their anatomical integrity (for example, on a damaged heart valve, in an atheroscleretically altered aortic wall, postoperative stumps of various organs, against the background of infarction-pneumonia, ovarian cysts, etc.).
Sometimes septic foci are found in the subcutaneous fat and dermis. In these cases, they resemble erythema nodosum in appearance, but, unlike it, are localized, more often on the trunk, but not on the extremities.
Body temperature takes on an irregular, remitting, less often hectic character with large daily variations, accompanied by chills and sweats.
Complications of the localized (gastrointestinal) form include shock of mixed origin (toxic and dehydration), acute peritonitis (usually serous), toxic intestinal dilatation, and reactive polyarthritis.
To confirm the diagnosis, bacteriological and serological methods are used.
The material for bacteriological investigation can be: vomit or gastric lavage, feces, urine, bile, blood (in generalized forms), remains of suspicious products.
Among S. typhimurium cultures isolated from patients with nosocomial salmonellosis, only 2.5% are highly sensitive to almost all antibiotics used, and 97.5% are characterized by pronounced antibiotic resistance.
Serological methods: agglutination reaction and IHR. IHR is more informative. Antibodies are detected from the 4-6th day, reaching a maximum at the 2-3rd week. The diagnostic titer is 1:200, but more conclusive is an increase in the antibody titer by 4 or more times with an interval of 5-7 days (paired serum method).
Criteria for transient bacterial carriage: absence of clinical symptoms at the time of examination and in the previous 3 months, single positive culture of salmonella from stool and negative results of repeated subsequent stool cultures, absence of any pathological changes in the intestinal mucosa during sigmoidoscopy, absence of seroconversion according to IHR with salmonella antigens over time.
In the CBC: moderate neutrophilic leukocytosis, increased ESR (in half of the cases it increases to 23±8 mm/h). Due to the increase in hematocrit, the concentration of red blood cells and platelets increases.
In the coprogram: an increase in leukocytes (more than 20 in the field of view) in 50% of patients examined on the first day of the disease, the presence of mucus, red blood cells and epithelial cells.
In 43% of cases, serum amylase is elevated, which suggested the presence of reactive pancreatitis.
Dyslipidemia is noted with an increase in the concentrations of free fatty acids, cholesterol, triglycerides, phospholipids in plasma and erythrocytes, as well as low and very low density lipoproteins in blood plasma.
Sigmoidoscopy can reveal catarrhal and catarrhal-hemorrhagic proctosigmoiditis (if the colon is involved).
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Salmonellosis, gastrointestinal form (gastroenteric variant), moderate.
Shigellosis is widespread, but predominates in backward and developing countries. Outbreaks and epidemics of dysentery are often associated with social disasters (wars, mass migrations, natural disasters), since the intensity of the spread of the microbe directly depends on non-compliance with personal hygiene rules.
Men and women get sick with a similar frequency (women are slightly more likely).
All age groups are affected: from children to the elderly (average age 45-50 years), but children are more severely ill.
Patients with blood type A (II) Rh(-) are considered most susceptible to shigellosis.
Rural residents get sick slightly more often than urban residents (54.8% and 45.2%, respectively).
The source of infection is patients with acute and chronic forms, as well as bacteria carriers. Shigella is excreted in feces from the onset of the disease (sometimes from the end of the incubation period). The infectious dose for Shigella Grigoriev-Shiga (the most pathogenic) is only 6 bacteria; Shigella Sonne has a high infectious dose.
The duration of bacterial excretion, as a rule, does not exceed a week, but can be prolonged.
The mechanism of transmission of infection is fecal-oral.
It is believed that different types of Shigella are characterized by different preferential transmission routes: aquatic - for Flexner's Shigella, alimentary - for Sonne's Shigella, contact - for Grigoriev-Shiga's Shigella. In addition, flies, cockroaches and ants can mechanically transmit the pathogen.
Possible transmission factors are: food (sausages, fish, sour cream, milk), water, dirty hands (contact route is especially important in family settings).
Countries with a temperate climate are characterized by year-round incidence with an increase in the summer-autumn period. The most significant increase in incidence was recorded from July to September (51.3% of patients). The frequency of hospitalization of children with shigellosis does not depend on the time of year (only in the summer is a decline in incidence recorded).
After the disease or asymptomatic infection, short-term type-specific immunity develops.
Specific prevention has not been developed.
The incubation period is usually 2-5 days. It can be reduced to 2-12 hours (the shortest incubation is with Sonne's shigellosis).
Shigellosis can be acute or chronic; asymptomatic bacterial carriage is also possible.
Most often, colitic and gastroenterocolitic variants of acute shigellosis are registered. Colitic variant predominates (62.5-78.8%), especially in cases of dysentery caused by Sh. dysenteriae and Sh. Flexneri.
According to the severity, acute shigellosis can be mild, moderate, severe and very severe.
Chronic shigellosis can have a recurrent or continuous course.
Shigella bacteria carriage is divided into convalescent and transient.
Acute shigellosis
In 3.2% of patients, a prodrome is registered within 3 days in the form of weakness (81.6%), discomfort in the epigastrium (69.4%) and the periumbilical region (54.7%).
The disease begins acutely: body temperature rises (in 38.5% of patients - up to febrile levels, in 35% - only low-grade fever, in the rest it remains normal). An increase in temperature is accompanied by chills, a feeling of heat (56.5%), fatigue, general weakness (100%), drowsiness (36.2%), decreased or lack of appetite, headache (53-98.7%), dizziness (17 .3%, mainly in the elderly).
In 75% of patients, abdominal pain appears: at first in 53% of patients it can be dull and diffuse, then it becomes more acute, cramping and localized in the left iliac region. After defecation, the pain temporarily disappears or decreases. The urge to defecate is accompanied by tenesmus in only 4-9% of patients, while false urges occur in 25% of patients. In 79.1% of patients with gastroenterocolitic dysentery, the pain is diffuse.
With the gastroenterocolitic variant, nausea (41.3%), vomiting (37.5-76.5%), mostly once or twice, appears first.
Diarrhea appears on the first day. Over time, the frequency of stool increases, the volume decreases, the stool loses its fecal character, and impurities of mucus (in 93.3-100%) and blood (in 50.9-94%) appear. In severe cases, a symptom of “rectal spitting” may appear.
The frequency of stool up to 5 times a day is observed in 6.7%, up to 10 times a day - in 65.4%, up to 20 times a day - in 27.9-51.9% of patients.
Pale skin is observed in 86% of patients, dry skin - in 68.3%, decreased turgor - in 27.9%.
The tongue is covered with a brown coating and is dry.
In severe cases of shigellosis patients develop a gaping anus (due to paresis of the sphincters) from which bloody necrotic masses are continuously released, often looking like “meat slop”.
Tachycardia (72.1%), arrhythmias (3.8%), decreased blood pressure (25%), increased blood pressure (24%) were noted. Expanding the boundaries of cardiac dullness is possible.
Palpation of the abdomen reveals rumbling, sometimes flatulence; spasmodic and painful sigmoid colon is palpated in 51.9% of cases.
In patients with the gastroenterocolitic form, upon palpation of the abdomen, pain is noted in the epigastrium and right hypochondrium, and a dense, painful sigmoid colon is observed in 69.1-87.3% of patients.
In 17% of patients with shigellosis, Padalka's symptom is detected.
94.1% of patients with the gastroenterocolitic form of dysentery are admitted with symptoms of dehydration of varying degrees: degree I - in 25%, degree II - in 71.9%, degree III - in 3.1%.
In elderly patients, in 91.4% of cases, shigellosis occurred in a moderate form; in other cases, a severe form of the disease was noted with signs of severe dehydration and grade I hypovolemic shock.
In elderly patients, the gastroenterocolitic variant of shigellosis predominates (80%).
Gastroenterocolitis in the elderly occurs with low-grade fever or normal body temperature in 84.3% of cases, although in case of an increase the temperature remains elevated longer.
Elderly patients complain of pain longer. Tenesmus and false urges are noted by only 11.4% of elderly patients.
In the structure of nosocomial shigellosis, mild and atypical forms of the disease dominate (60.6% of cases), and moderate severity accounts for 39.4%.
Patients with shigellosis associated with alcoholism significantly later consult a doctor. Mild forms are usually not observed in them; streaks of blood are more often found in their stool.
Convalescent carriage is formed in 4% of patients.
The risk of developing prolonged diarrhea is significantly higher in the colitic variant of the disease compared to the gastroenterocolitic one.
The diagnosis of Хроническая дизентерия is established if the disease lasts more than 3 months.
Chronicity is more typical for Flexner's shigellosis.
There are two types of chronic shigellosis: recurrent (more common) and continuous.
In a relapsing course, exacerbations alternate with periods of complete clinical well-being lasting from several weeks to 2-3 months. Intoxication and colitis during relapse are usually less pronounced than in acute shigellosis: the patient’s well-being is not significantly affected, the body temperature is normal, less often subfebrile, the frequency of stools is usually 3-5 times a day, tenesmus and blood in the stool are usually absent. With a long course, irritability, emotional lability, weakness, and sleep disturbance increase.
With a continuous course, there is a mild general intoxication, unstable mushy stool (sometimes mixed with mucus and pus, rarely blood), as well as symptoms of gastroenteritis (feeling of heaviness in the epigastrium, belching, rumbling and discomfort in the umbilical region). In patients with a continuous course of shigellosis, hepatomegaly can be detected, anemia and hypovitaminosis progresses.
Chronic dysentery lasts up to 2 years (after that the disease is regarded as post-shigellosis colitis, IBS, etc.).
Carriage is diagnosed by bacteriological isolation of Shigella, in the absence of a clinical diagnosis during the last 3 months, and in the absence of changes in the colon mucosa according to endoscopy.
Transient carriage is a single isolation of Shigella with a negative serological test result in a clinically healthy person who has not had intestinal dysfunction over the past 3 months.
Toxic shock, shock of mixed origin (toxic in combination with dehydration), infectious-toxic encephalopathy, paresis and perforation of the intestine with the development of peritonitis, peritiphlitis, toxic dilatation of the colon, pericolitis, anal sphincter fissures, prolapse of the rectal mucosa.
Bacteriological method: according to various estimates, it provides confirmation of the diagnosis in 1.7-90% of patients (depending on the timing and frequency of examination, the severity of the patients and other factors).
The bacteriological method is more effective in the first 3 days of the disease.
To isolate Shigella, 20% bile broth, combined Kauffman nutrient medium, and selenite broth are used.
The material for culture is usually feces. In case of Grigoriev-Shiga shigellosis, blood culture of Shigella can be isolated.
Also it is possible to detect Shigella antigens in the material (ELISA, RIF) or their DNA, using PCR.
Serological methods make it possible to detect antibodies to Shigella using the indirect (passive) hemagglutination reaction (IRHA) and direct hemagglutination reaction (DRHA).
A titer in the IRHA and DRHA of 1:400 or an increase in the titer by 4 or more times is considered diagnostic (the first blood sample is taken on the 6-8th day of the disease, the second - 10 days after the first).
CBC: in 20-25.9% of patients, neutrophilic leukocytosis is observed up to 15×10^9/l, toxic granularity of neutrophils, ESR increases (on average 18.7 mm/h). In 20% of elderly patients, signs of grade I hypochromic anemia are detected.
Urine analysis: moderate proteinuria, the appearance of granular and hyaline cylinders. Normalization of urine analysis parameters occurs on average on the 8th day in patients with the colitic variant, on the 9th day - in patients with the gastroenterocolitic variant.
In the coprogram, pathological changes are determined in all patients. A large amount of mucus and leukocytes is detected (more than 15 cells in the field of view), red blood cells are increased to a lesser extent.
In asymptomatic cases of acute shigellosis, an increased amount of mucus and leukocytes can be detected.
Normalization of the coprogram occurs on the 8th day of the disease in patients with the colitic variant and on the 13th day in patients with the gastroenterocolitic variant.
There are usually no significant changes in the biochemical blood test.
Sigmoidoscopy/fibrocolonoscopy: distal colitis, often sphincteritis. Damage to the mucous membrane is diffuse.
When carrying Shigella, the endoscopic picture is normal.
In mild cases, colitis is catarrhal, less often catarrhal-hemorrhagic or catarrhal-erosive. With catarrhal colitis, hypertrophied lymphoid follicles in the form of granularity are sometimes detected.
In moderate cases there are catarrhal-erosive changes with many hemorrhages, sometimes ulcers.
In severe cases, there is widespread fibrinous inflammation of the mucous membrane, multiple foci of hemorrhage and necrosis (after their rejection - slowly healing ulcers).
For severe shigellosis caused by Sh. flexneri and Sh. dysenteriae (Shigella Grigorieva - Shiga) the formation of pseudomembranes is observed: in 18% of cases with shigellosis caused by Sh. flexneri, and in 66.7% of patients with shigellosis caused by Sh. dysenteriae. In this case, extensive fibrinous lesions of the large intestine appear, starting from the rectum and sigmoid colon.
Ultrasound of the abdomen revealed mesadenitis in 47% of children with shigellosis.
ECG may show signs of diffuse damage to the left ventricular myocardium and overload of the right heart.
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Acute shigellosis, colitic variant, moderate.
The disease is registered all over the world, but is more widespread in hot, humid climates, which is associated with slow wound healing and increased contamination of the soil with the pathogen.
The incidence rate depends on the proportion of vaccinated individuals in the population, as well as on emergency prevention, and in developing countries reaches 10 to 50 cases per 100,000 population. In developed countries, where mass vaccination began in the 1950s, the incidence rate is almost 2 orders of magnitude lower.
Worldwide, 80% of cases occur in newborns who become infected when the umbilical cord is tied with a non-sterile instrument or the umbilical wound is treated with soil/animal excrement. Up to 400,000 newborns die each year.
Source of infection – many species of animals, especially ruminants (spores and vegetative forms of clostridia are found in their gastrointestinal tract). Sometimes clostridia can be found in the human intestine.
In an anaerobic environment, spores can germinate into vegetative forms, which leads to the accumulation of the pathogen in the soil. This is especially true for tropical countries.
Sick people do not pose an epidemiological danger.
Infection occurs when spores penetrate tissue.
Wartime tetanus is associated with wounds. In peacetime, the entry points for infection are domestic injuries (punctures, abrasions, etc.). Infection is possible during illegal abortions, operations, through trophic ulcers.
The entry of exotoxin into the gastrointestinal tract does not lead to the development of the disease.
Susceptibility to tetanus is high.
In countries with a temperate climate, there is a summer seasonality.
Post-infectious immunity do not develop.
There are generalized, localized and bulbar forms of tetanus; according to the rate of development, there are fulminant, acute, subacute and chronic tetanus.
The incubation period varies from 1 to 31 days (on average 1-2 weeks), sometimes more. It has been proven that the shorter the incubation period, the more severe the disease.
Tetanus begins acutely, sometimes preceded by a prodrome in the form of general malaise, chills, irritability, a feeling of stiffness, difficulty swallowing, dull aching pain and/or muscle twitching at the site of entry.
The more severe the tetanus, the faster the clinical picture develops.
The first and most constant symptom is tonic tension (trismus) of the masticatory muscles, which makes it difficult or impossible to open the mouth. At the beginning of the disease, trismus can be detected by tapping on a spatula placed on the teeth of the lower jaw. Trismus is a cardinal sign of the generalized form of tetanus.
The involvement of the facial muscles usually occurs later than trismus: wrinkles appear on the forehead and around the eyes. The mouth stretches, its corners are lowered or raised (sardonic smile).
Dysphagia appears at about the same time as the involvement of the facial muscles.
Trismus, sardonic smile, and dysphagia constitute the typical triad of symptoms of tetanus.
Muscle involvement occurs in a descending manner over 2-4 days. Hypertonicity of the occipital muscles appears with the head being thrown back, the tone of the back muscles increases with hyperextension of the spine, abdomen, proximal parts of the limbs, especially the lower ones with straightening of the legs and bending of the arms. The process does not extend to the hands and feet.
In extremely severe cases of the disease, the body bends backwards (opisthotonus). In addition to opisthotonus, emprostotonus is possible (bending of the body forward with a strongly developed abdominal press).
Involvement of the intercostal muscles, diaphragm and laryngeal muscles leads to respiratory failure and hypoxia.
The clinical features of tetanus are considered to be constant (without relaxation) hypertonicity of muscles, involvement of only large muscles of the limbs in the process, and muscle pain.
Convulsions lasting from a few seconds to minutes are provoked by touch, bright light, a gust of air, knocking, rustling.
The convulsions are painful, accompanied by an increase in body temperature, sweating, hypersalivation, tachycardia and increasing hypoxia. The severity of hyperthermia correlates with the severity of the convulsions.
Consciousness remains clear; insomnia is typical.
Tachycardia and increased blood pressure are observed. As the disease progresses, muffled heart sounds and arrhythmia may occur.
Difficulty in urination and defecation is noted due to spasm of the perineal muscles.
Focal and meningeal symptoms are absent.
There are mild, moderate and severe forms.
Mild tetanus occurs mainly in previously vaccinated individuals. The incubation period exceeds 20 days, the classic triad of symptoms is weakly expressed. Convulsions are absent or occur only a few times a day. Body temperature is normal or subfebrile, tachycardia is rarely detected. Duration of the disease is up to 2 weeks.
In moderate tetanus, the incubation period is 15-20 days. Body temperature is up to 39 degrees, tachycardia. Convulsions are no more than 2 times per hour, but their duration is no more than 30 seconds. Complications do not occur, and the duration of the disease is up to 3 weeks.
In severe tetanus, the incubation period is 7-14 days, the fever is constant and high, convulsions are frequent (every 5-30 minutes) and prolonged (up to 1-3 minutes) with severe hypoxia, damage to the vasomotor center (tachyarrhythmia, unstable blood pressure). Complications are possible.
In a favorable course of tetanus, seizures become less frequent and stop by the 3rd-4th week of the disease, but tonic muscle tension remains for about a week after the disappearance of seizures. Trismus disappears last of all, and vegetative disorders persist for some time.
In the late convalescence period, there are signs of myocarditis (tachycardia, muffled heart sounds, moderate dilation of the heart borders) and asthenovegetative syndrome, persisting for 1-3 months.
Asphyxia, asystole, muscle ruptures, tendon ruptures, bone fractures, muscle contractures, laryngospasm are possible. Sometimes, compression deformations of the spine are formed as a result of the disease.
Some complications are associated with the addition of secondary flora: pneumonia (sometimes with atelectasis), sepsis, pyelonephritis. If tetanus infection occurs as a result of extensive wounds, additional purulent complications often occur in the form of abscesses and phlegmons in the area of the infection portal.
Most often, the cause of death is direct damage to the brain stem with respiratory or cardiac arrest.
The toxin cannot be detected in the blood. Detection of antitoxic antibodies has no diagnostic value, since it can only indicate successful vaccination. In tetanus, there is no increase in antibody titers due to the fact that even lethal doses of exotoxin are an insignificant antigenic irritant and do not cause an immune response.
Bacteriological examination of tissues excised from the suspected infection portals allows for the isolation of clostridia in an anaerobic culture. This confirms the diagnosis, but the sensitivity of the method is low (up to 30%).
In CBC in severe cases of tetanus, an increase in hematocrit can be detected.
A decrease in blood saturation is detected as respiratory failure increases.
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Tetanus, generalized form, severe
Taeniasis is registered in countries with developed pig farming: in South America (especially in the Andean region (Bolivia, Peru, Chile, Ecuador) and Brazil), Central America (Guatemala, Honduras, El Salvador), Mexico, China, the Indian subcontinent, Southeast Asia (Indonesia, especially Bali, Western New Guinea), sub-Saharan Africa (in particular, Burundi, Tanzania, DR Congo, South Africa), in Eastern Europe.
In endemic areas, pork tapeworm is most often detected in individuals aged 10 to 39 years.
The source of infection - the infected person - excretes oncospheres with feces 2-4 months after being infected and for many years (the lifespan of an adult helminth is several years, possibly reaching 25 years).
Several parasites can live in the human body at the same time (usually 1-3, but there are known cases of up to 25).
The released oncospheres remain viable in the environment for several weeks or months (they survive best in a cool, moist environment), but do not tolerate direct sunlight.
The main route of transmission is food.
The main transmission factor is insufficiently heat-treated pork or wild boar meat. Cysticercosis can also develop in bears, rabbits, camels, sheep, deer, dogs, cats, monkeys, marine mammals, etc.
Cysticerci can be found in skeletal muscles, tongue, chewing muscles, brain, heart, liver, kidneys and other tissues. They remain viable in the animal's body for several (3-6) years after the animal was infected.
Infection is possible through water or unwashed hands.
Human susceptibility is high.
Risk groups include workers on pig farms, slaughterhouses, meat processing and production plants, and housewives.
The patient may complain of passage of segments or small fragments of the strobila with feces. Terminal proglottids containing eggs with mature oncospheres are separated from the strobila in chains of 3-6 pieces (up to 8-10 per day).
Dyspeptic and asthenoneurotic symptoms occur relatively frequently.
Dyspeptic symptoms: loss of appetite, nausea, vomiting, loose stools, abdominal pain, rumbling in the abdomen, flatulence.
Asthenoneurotic symptoms: malaise, weakness, dizziness, headaches, sleep disturbances.
If neurological symptoms are present, it is necessary to exclude the presence of cysticercosis of the brain.
Intestinal bleeding, intestinal perforation, appendicitis, cholangitis, pancreatitis, cysticercosis are possible.
If mature segments are thrown from the intestine into the stomach during antiperistaltic movements, autoinvasion by oncospheres is possible with the development of cysticercosis of the brain, eyes, and skeletal muscles.
NB! Cysticercosis in patients infected with mature helminths is considered a complication of taeniasis, and in the absence of mature individuals, as an independent nosological entity.
The diagnosis is confirmed by detecting mature segments of the pork tapeworm in the feces. The segments are 12-15 mm long and 6-7 mm wide. Counting the lateral branches of the uterus allows differentiating between teniarinhosis and teniasis: Taenia solium is characterized by the presence of 7-13 branches of the uterus from the central trunk.
The diagnosis can also be made by examining the heads of the tapeworms released during deworming.
Pork tapeworm eggs can be found in feces.
Oncospheres of the pork tapeworm are practically indistinguishable from oncospheres of the bovine tapeworm (therefore, when they are detected, the conclusion is formulated as “taenia oncospheres detected”).
PCR allows detection of genetic material of pork tapeworm in feces.
ELISA allows to detect antibodies in blood serum and pork tapeworm coproantigens. The concentration of coproantigen can be used to monitor the effectiveness of treatment: after successful sanitation, it decreases rapidly (usually within 5-15 days).
CBC may show eosinophilia. Sometimes taeniasis causes hypochromic anemia.
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Teniosis
The source of infection is dogs.
Contaminated soil may be a transmission factor.
Risk groups: a relatively high incidence of toxocariasis has been established among veterinarians, workers at dog kennels, drivers and mechanics, utility workers, owners of private plots, psychiatric patients, and hunters who own dogs.
Men get sick more often than women (61% and 39% respectively).
Clinical manifestations of toxocariasis depend on the localization of parasites and the intensity of invasion. There are acute and chronic (exacerbation/remission phase) toxocariasis, visceral and ocular toxocariasis.
In case of toxocara invasion, an allergy to animal hair is often detected.
Visceral toxocariasis is characterized by recurrent fever, lung damage, hepatomegaly, lymphadenopathy, eosinophilia, and hypergammaglobulinemia.
Recurrent increases in body temperature can be observed over several weeks and even months, with the temperature often being subfebrile, less often febrile.
Patients complain of weakness and sweating.
In 24-33% of patients, the disease is accompanied by recurrent small-spotted, erythematous, papular, papulovesicular or urticarial rashes on the skin of the face, trunk, and limbs. In the group of children under 14 years of age, 27% had a history of recurrent urticaria.
In 50-65% of patients with visceral toxocariasis, lung involvement is observed in the form of recurrent bronchitis, pneumonia, and broncho-obstructive syndrome. In some cases, bronchial asthma may develop.
In the group of children under 14 years of age, a prolonged unproductive cough is most often recorded (46%). At the same time, a prolonged cough is statistically significantly 4 times more common (p = 0.023) in boys than in girls, and recurrent obstructive bronchitis is not typical for girls.
Patients complain of dry, paroxysmal cough, which intensifies at night, and inspiratory dyspnea.
On auscultation: diffuse dry and wet wheezing (disappears within a few days, then appears again).
Percussion can reveal dullness of sound over the infiltrates.
Enlargement of lymph nodes up to systemic lymphadenopathy is observed in 67% of patients; lymph nodes are small (0.5-2 cm), painless, and not fused with surrounding tissues.
60% of patients show abdominal syndrome: abdominal pain, bloating, nausea, sometimes vomiting, diarrhea.
In 40-80% of patients, an enlarged liver is detected, in 20-50% - an enlarged spleen.
In some cases, toxocariasis occurs with the development of myocarditis and pancreatitis.
Migration of larvae into the central nervous system can lead to the development of meningitis, encephalitis, myelitis, arachnoiditis, which can manifest as convulsions of the "petit mal" type, epileptiform seizures, paresis and paralysis. With toxocariasis, behavioral changes can be observed: hyperactivity and affects.
Ocular toxocariasis occurs when a person is infected with a small number of toxocara larvae and can progress to granuloma, uveitis, pars planitis, chronic endophthalmitis, vitreous abscess, optic neuritis, keratitis, or the presence of migrating larvae in the vitreous.
Almost always, the eye damage is unilateral.
Strabismus, decreased vision, and leukocoria are observed.
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There are no reliable methods for specific diagnosis of ocular toxocariasis.
In a living person, parasitological diagnosis of toxocariasis is practically impossible, since it is difficult to detect migrating larvae in the body. Histological examination of biopsies only sometimes allows to detect toxocara larvae.
ELISA (specificity 92%, sensitivity 78%): confirmation is considered to be detection of IgG in a titer of 1:800 or higher (titers correlate with severity); titers of 1:200 – 1:400 may indicate infection. Serological response in ocular toxocariasis is less pronounced (antibody titers are lower).
Antibody titers decrease very slowly and are therefore not suitable for monitoring the effectiveness of treatment and establishing the fact of chronicity.
Immunoblotting may be performed.
In CBC: high eosinophilia with leukocytosis up to eosinophilic-leukemoid reactions, increased ESR; with prolonged course, anemia increases.
In the group of children under 14 years of age, anemia occurs in 52% and is mainly mild. Eosinophilia is observed in 79% of patients, while the level of eosinophils is within 6-10% in 27% of children, 11-20% in 24%, 21-30% in 27% of patients. Leukocytosis is detected in 36% of children, and ESR is elevated in 39%.
Morphological examination of bone marrow puncture allows to identify eosinophilic hyperplasia.
Biochemical blood tests often show a moderate increase in bilirubin and liver transaminases. In the group of children under 14, a moderate increase in transaminases is observed in 21% of patients.
The level of total protein is increased due to gamma globulins.
IgE levels are greatly elevated (IgE concentrations can be used to monitor recovery).
On radiographs of the chest: increased pneumatization, equally expressed on both sides, multiple or single infiltrates, increased pulmonary pattern. Sometimes - Löffler syndrome: transient "flying" infiltrates in a patient with pronounced eosinophilia.
In the group of children under 14 years of age, X-ray examination of the chest organs reveales increased pulmonary pattern and signs of bronchitis in 60%.
Ophthalmologic examination may reveal larvae in the macula area.
If ocular toxocariasis is suspected, CT of the eye is recommended.
In the group of children under 14 years of age, ultrasound of the abdominal cavity reveals hepatosplenomegaly in 58% of patients, diffuse changes in the liver in 30%, and reactive changes in the pancreas in 27%. Eosinophilic ascites is possible.
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Toxocariasis
Natural foci are found in all latitudes of the globe and on all continents except Australia.
The introduction of Trichinella from natural foci leads to the formation of temporary synanthropic foci. In synanthropic foci, the spread of invasion in rats and pigs is closely related: pigs readily eat rodent carcasses. Humans become infected in synanthropic foci as a result of eating undercooked pork (in more than 95% of cases).
The age of patients ranged from 23 to 72 years (average 39 years).
60% of those infected are men, 40% are women.
The group nature of the disease is associated with a common source of infection (slaughter of individually fattened pigs or shooting of wild boars during hunting).
Transmission factors: meat of bear, wild boar, deer, badger, elk and walrus; horse meat, pork, lard. In Siberia and the Far East, more than half of the cases of trichinellosis in recent years have been associated with the consumption of dogs and wild game meat.
Trichinella larvae found in animal muscles are resistant to freezing (in large pieces of meat, larvae remain viable and invasive at a temperature of minus 15-17°C for 30 days, and at a temperature of minus 10-14°C - up to two months).
At +70°C, trichinella larvae die, but it should be taken into account that when boiling and frying meat, the temperature in the depths of large pieces does not rise high enough and the larvae may remain alive. When boiling a piece of meat 8 cm or more thick, all trichinella larvae die only after 2-2.5 hours.
When salting and smoking meat, the larvae die only in the surface layers. When vacuum drying (plus 55-58°C), the larvae die within 4 hours.
Pork fat may contain layers of muscle fibers that contain live Trichinella larvae.
Usually, with seeding of less than 1 larva per 1 g of meat, clinical symptoms do not develop. With the presence of 10 larvae per 1 g of meat, some people develop mild forms of the disease, with a number of 50 or more larvae, moderate and severe cases occur. With the same source of infection, the severity depends on the amount of meat eaten.
Seasonality: Most outbreaks of trichinellosis occur between November and February, which is associated with the hunting season for wild animals and the mass slaughter of pigs.
During outbreaks, up to 45% of cases occur in urban residents.
The incubation period for human trichinellosis lasts from 5 to 80 days (the more intense the infection, the shorter the incubation period). The average incubation period for severe cases is 7.4 days, for moderate cases - 15.9, for mild cases - 21 days.
Symptoms develop over 2-4 days, peak by the end of the first week of illness and persist for 1-3 weeks.
From the first days of the disease, weakness (100%), headache and dizziness (30%), insomnia, myalgia, nausea and vomiting (more than 25%), loose stools (rarely), and fever (above 38.5°C, sometimes up to 40°C) are observed.
Myalgias in most patients appear from the 1st to the 3rd day of illness or later (the more severe the trichinellosis, the earlier they appear). At first, pains appear in the muscles of the lower extremities, then in other muscle groups - gluteal, back, abdomen, arms, neck, chewing, tongue, pharynx, eyes.
Most often, pain is observed in the muscles of the eyeballs, chewing, calf muscles, and flexors of the limbs.
80% have facial puffiness (pronounced edema - moon face), less often - edema of the extremities. In severe cases, edema can spread to the neck, trunk, and extremities.
In 20% of patients, there is a small-point spotted, maculopapular, urticarial, and sometimes hemorrhagic rash on the skin of the trunk and arms.
The frequency of myalgia, edema, and rash depends on the type of trichinella.
Conjunctivitis and conjunctival hemorrhages are often observed. Facial edema combined with conjunctivitis is one of the constant signs of trichinellosis.
Muscle pain and swelling may recur periodically. Sometimes relapses occur with a rise in temperature.
An "enteropathic" variant of the disease course has been described, manifested by prolonged diarrhea (5-6 weeks) with a short period of myalgia and myasthenia (4-5 days) and a classic "myopathic" variant with a predominance of myalgia and edema. It is believed that the "enteropathic" variant occurs in people previously infected with trichinella, and the "myopathic" variant - during primary infection.
Chronic trichinellosis usually occurs subclinically, but paresthesia, numbness, and decreased muscle strength may be observed; the duration of chronic trichinellosis can reach 10 years.
Myocarditis (the most common cause of death), pneumonia, meningoencephalitis.
Serological reactions with trichinellosis diagnosticums reveal antibodies from the end of the 2nd week after infection (4-6 weeks in case of infection through meat of wild animals). A 4-fold or more increase in titers in paired sera taken at intervals of 14-20 days is considered diagnostic.
The antibody level reaches its maximum in the 2nd-4th month after invasion and then gradually decreases (up to 10 years or more). In the case of invasion caused by T. pseudospiralis, antibody titers increase faster than in the case of invasion caused by T. spiralis.
CBC shows eosinophilia from the first days of the disease (on average 17.7%, maximum - up to 80-93%) against the background of leukocytosis up to 10-30 thousand in 1 μl. There is a direct relationship between the number of eosinophils and the severity of the clinical picture, especially myalgia, but extremely severe forms of the disease, on the contrary, occur with hypoeosinophilia.
As organ damage increases, the level of eosinophilia decreases with a simultaneous increase in neutrophilia. A drop in the level of eosinophils below 10-15% in severe cases of the disease is an unfavorable sign.
Eosinophilia reaches its maximum level in mild cases on the 4th week of the disease, and in moderate and severe cases on the 3rd week. Eosinophilia up to 10-15% can persist for 2-3 months or more after recovery.
ESR averages 14.2 mm/h.
In urinalysis in severe trichinellosis, moderate proteinuria and cylindruria appear.
An increase in liver enzyme levels is often observed (average values of ALT 51.9 mmol/l, AST 46.2 mmol/l).
Dysproteinemia is determined (hypoalbuminemia, hypergammaglobulinemia, hypoproteinemia).
The level of LDH and CPK is increased.
ECG: with moderate trichinellosis, moderate changes of a dystrophic nature appear.
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Acute trichinellosis, moderate
The source of infection is only a person (patient with manifested form or bacteria carrier). Carriage of Salmonella typhus can last for decades.
The transmission mechanism is fecal-oral. Routes of transmission: water, food and contact.
Since salmonella cannot withstand high temperatures, water and foods that have not been sufficiently processed become transmission factors. Salmonella can get into water bodies with wastewater, and into food if the person preparing the food does not comply with sanitary rules.
The infectious dose is quite high, so the contact route of transmission occurs through prolonged close contact with an active bacterial excretor (for example, a mother takes care of a sick child, changing his underwear and bed linen and not being able to regularly wash her hands).
The risk group consists of people with hypoacid conditions, since the main barrier to pathogens of intestinal tract is the hydrochloric acid of gastric juice.
Seasonality: the warm season, when people are more likely to drink water from untested water sources, and in products at room temperature salmonella multiplies faster, reaching an infectious dose in a few hours.
The duration of immunity is debated. Before the widespread use of antibiotics and antipyretics, immunity was considered to be lifelong. Currently, the duration of immunity is estimated by many authors at 6-10 years.
The incubation period depends on the dose of the infection and the patient's vaccination status and ranges from 7 to 25 days (usually 9-14 days). A short incubation period is typical for unvaccinated individuals and for those with a high dose of salmonella received. At a low dose of infection and in vaccinated people, it lengthens.
The clinical picture of typhoid fever is cyclical, that is, periods can be distinguished: initial, height, extinction of the disease, convalescence.
From the initial period, typhoid fever has a number of clinical features.
In the classic course of the disease, body temperature rises gradually, that is, it reaches a maximum within 8-9 days.
Patients complain of diffuse monotonous headache, sleep inversion (insomnia at night combined with daytime sleepiness), weakness, decreased or lack of appetite.
Some patients develop enteric-type diarrhea (pea-soup-type stool).
On physical examination, lethargy is noted.
Despite the high body temperature, the skin of patients is pale and dry (the classic appearance of the patient is “pale, hot and dry”).
The tongue may be thickened (due to regional lymphostasis), with tooth marks on the lateral surfaces, and also covered with a thick coating (a “chop cutlet” tongue).
In some patients, enlargement and hyperemia of the palatine tonsils can be detected.
Relative bradycardia and hypotension are often observed.
Dullness of percussion sound in the ileocecal region is determined (Padalka's symptom).
From 4-5 days of illness, splenomegaly can be detected (in a small percentage of patients), from 7-8 days - hepatomegaly (detected much more often).
The height period occurs when, on days 8-9th, in 55-65% of patients a rash appears.
The elements of the rash are scanty small, dim roseolas, slightly raised above the surrounding healthy skin (roseola elevata). They are located on the chest and abdomen. Day by day, the number of elements of the rash increases slightly.
Body temperature reaches maximum values. Against the background of such pronounced intoxication, the development of typhoid status is possible: apathy, adynamia, impaired consciousness, sometimes delirium, and hallucinations appear.
Diarrhea gives way to constipation and severe flatulence (in fact, dynamic intestinal obstruction develops associated with impaired innervation of the gastrointestinal tract).
Previous physical symptoms persist or worsen.
Some patients have carotene hyperchromia of the skin of the palms and feet (Filippovich's symptom).
You can detect dicrotism of the pulse - a bifurcation of the pulse wave (by palpation or on a sphygmogram).
During the period of extinction, a lytic decrease in temperature and a gradual decrease in intoxication occur.
During the period of convalescence, asthenia persists for a long time.
As a result of the disease, 3-5% of patients develop Salmonella carriage.
The severity of the disease is determined by the severity of intoxication and the presence/absence of complications.
Toxic shock develops during the height of the disease. Against the background of a sharp increase in intoxication, the temperature decreases, blood pressure drops, tachycardia appears, and diuresis decreases.
Intestinal bleeding often develops at 2-4 weeks of the disease: body temperature decreases rapidly, and relative bradycardia gives way to tachycardia, pallor increases, blood pressure decreases, peristalsis increases, and dark stools appear.
A decrease in temperature with an increase in heart rate, accompanied by a worsening in the condition of a patient with typhoid fever, is called the “devil’s cross”.
Perforation and peritonitis most often develop in the 2-4th week of illness. In 80% of patients, pain appears, but it is mild, since the endotoxin of Salmonella typhi, acting on the central nervous system, also suppresses pain sensitivity. Therefore, the appearance of even slight abdominal pain in a patient with typhoid fever is a reason for urgent consultation with a surgeon.
Symptoms of peritoneal irritation, muscle defance appear, and hepatic dullness is no longer detectable by percussion.
As in the case of intestinal bleeding, relative bradycardia is replaced by tachycardia. “Devil’s cross” can be seen in patients.
Nonspecific complications can also occur with typhoid fever. Their development is due to the addition of secondary bacterial flora. Nonspecific complications are pneumonia, pyelonephritis, etc.
The bacteriological method is the “gold standard” for diagnosing typhoid fever.
Blood culture can be isolated from the 1st day of illness. Venous blood is taken during all periods of the disease (5 ml in the 1st week, 10 ml in the 2nd week, 15 ml after 2 weeks) and inoculated in 50-100 ml of bile broth or Rappoport medium.
Coproculture and urine culture are effective no earlier than the 5th-6th day of illness (they are most often performed starting from the 2nd week of illness).
Biculture is often performed 7-10 days before discharge. Early biculture is dangerous: to obtain bile it is necessary to perform duodenal intubation, and this can provoke bleeding or perforation of the intestine.
Serological methods: agglutination reaction (Vidal reaction), indirect hemagglutination reaction.
The Vidal reaction allows for the differential determination of antibodies to the O-, H- and Vi-antigen.
Detection of antibodies to the O-antigen in a high or increasing titer confirms the presence of the disease. Diagnostic titer is 1:200 and above; a more reliable confirmation of the diagnosis is an increase in titer by 4 or more times when implementing the method of paired sera.
Detection of antibodies only to the Vi-antigen may indicate carriage of Salmonella typhus, and the guidelines do not specify what titer of antibodies to the Vi-antigen confirms the diagnosis - carriage must be confirmed for any positive result.
Antibodies to the H-antigen are detected in vaccinated patients.
Immunofluorescence in coprofiltrate can also confirm the diagnosis, however, this method is technically difficult and relatively expensive.
In the CBC, moderate neutrophilic leukocytosis is often observed in the first 2-5 days, but then pancytopenia occurs: leukopenia with relative lymphomonocytosis, eosinopenia, anemia and thrombocytopenia. ESR is often moderately elevated.
Urinalysis: proteinuria.
Biochemical tests: AST and ALT are moderately increased; in case of complications, bilirubin, urea, and creatinine may be increased.
Abdominal ultrasound can confirm the presence of hepatosplenomegaly and helps in differential diagnosis.
X-ray of the chest is necessary for differential diagnosis, ruling out pneumotyphoid fever and monitoring of the addition of a nonspecific secondary bacterial infection.
X-ray of the abdominal organs in case of perforation can detect a “gas sickle” between the liver and the diaphragm.
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Typhoid fever, typical form, moderate
Acute carriage of S. typhi
The virus is widespread in Africa, southern Europe and Asia. In 1999, the virus was brought to New York, caused a large outbreak and quickly spread throughout the United States and southern Canada, and in 2006-2007 began to be registered in South American countries.
Cases of the disease have been registered in Serbia, Italy, Greece, Hungary and Romania. Natural foci of the disease have been described in Armenia, Turkmenistan, Tajikistan, Azerbaijan, Kazakhstan, Moldova, Ukraine and Belarus.
The spread of West Nile virus is facilitated by various climatic (higher than usual temperatures, abundant rainfall, river floods) and environmental factors (seasonal migration of migratory birds, high numbers of synanthropic birds in populated areas).
Heavy rainfall reduces the flow of water from irrigation reservoirs, which increases the number of mosquito breeding sites.
The age of those infected varies widely (from 18 to 80 years). Moderate and severe forms of the disease often develop in people over 50 years of age.
In different studies, the gender structure of diseased groups is assessed differently, but men usually predominate.
68-77.4% of patients are city dwellers who went out into nature.
The main source of infection is migratory birds (coots, mallards, cormorants, herons, gulls) and non-migratory birds (crows, rooks, jackdaws, starlings, rock doves, cuckoos).
In sick people, the concentration of virus in the blood is usually insufficient to infect mosquitoes, so an anthroponotic cycle of infection is unlikely.
Transmission route - the bite of an infected insect. The main carriers of the virus are mosquitoes that feed on infected birds. The virus has been detected in 65 species of mosquitoes, but it is most often found in mosquitoes of the genus Culex.
Transmission of the virus by some other species of mosquitoes of the genus Aedes and Anopheles, as well as ixodid and argasid ticks, is not excluded.
The virus adapts to local species of argasid and ixodid ticks, which participate in maintaining the viral population during the interepizootic period. However, patients usually do not have a history of tick bites.
A mosquito is considered infectious 10 to 14 days after feeding on an infected bird.
The virus has two main types of circulation:
Rural cycle (wild birds living in wetlands and ornithophilous mosquitoes).
Urban cycle (synanthropic, ecologically associated with humans, bird species and mosquitoes that feed on the blood of birds and humans, mainly Culex pipiens/molestus).
In some cases, people become infected through blood transfusions, but transmission of the virus is also possible in the laboratory, through breastfeeding and organ transplants.
Seasonality is distinct: from July to October. The peak incidence rate is annually in the second half of August – early September (63.1% of patients).
Human susceptibility is high.
Risk groups include fishermen, hunters, and people engaged in agricultural activities.
Information on immunity after the disease is contradictory. There is currently insufficient data on the protective properties of antibodies. In low-endemic areas, re-infection of older people with another serovar of the virus is possible.
It is believed that up to 80% of cases of infection are subclinical.
Patients with manifest forms are hospitalized on average on the 6th-7th day of the disease.
There are flu-like variant and neuromeningeal form.
The influenza-like form of the disease is recorded in 50-75.8% of patients, the meningeal form - in 24.2-50%.
Among patients with the neuromeningeal form, 61.9-71.4% are diagnosed with serous meningitis, 28.6-35.8% with meningoencephalitis, and 7.1% with lower motor neuron damage (meningoencephalopolyradiculopathy syndrome, Guillain-Barré syndrome, or poliomyelitis syndrome).
The prevalence of neuromeningeal (more severe) forms over the influenza-like variant in the structure of confirmed cases of the disease is considered as evidence of the low alertness of doctors in the region regarding West Nile fever.
The incubation period lasts from 2 days to 3 weeks (usually 3–8 days).
The clinical picture of the disease is very variable.
The frequency of arthralgia varies depending on the age of the patients and the year the study was conducted in the same area.
Roseola rash is detected in an average of 13.4% of patients. But exanthema can be registered with different frequencies in one region in different years (for example, an increase in the frequency of rashes from 5% to 30-53.8% in the Volgograd region), which may be associated with a change in the dominant genotype of the virus.
Jaundice is detected in 13.8% of patients.
Polylymphadenopathy is detected in an average of 27.6% of patients.
Hepatomegaly is detected in an average of 63.2%, splenomegaly – in 18.2% of patients. The frequency of detection of hepatomegaly also varies depending on the age of patients and the year of the study in the same area.
Flu-like variant
In 16.7% of patients, a rise in temperature is preceded by short-term weakness, loss of appetite, muscle and joint pain, and headaches.
Most often, the disease begins acutely: in 69.6% - with a rise in temperature to febrile values, and in 30.4% - with subfebrile temperature. The duration of febrile temperature is 4-10 days. In 50% of patients, the temperature curve is constant, in 9.5% of patients - a remitting type.
The second wave of fever is observed in 21.7% of patients. The total duration of the disease is on average 20-23 days.
Patients complain of weakness (100%), malaise (91.3%), chills (21.7%), headache (47.8%), retro-orbital pain (4.3%), dizziness (26.1%), nausea (26.1%), single or double vomiting (21.7%), drowsiness (8.7%), sweating (8.7%), decreased appetite (8.7%), muscle pain (4.3%), body aches (39.1%), skin hyperesthesia, moderate arthralgia (50%), pain or a sinking feeling in the heart (28.6%).
In 83.3% of patients myalgia is generalized. Particularly severe pain is noted in the muscles of the neck and lower back.
Subjective intoxication is severe even with short-term and mild fever. After normalization of temperature, asthenia persists for a long time in all patients.
In the initial stage, catarrhal symptoms are possible in 21.4-63.9% of patients (of which tonsillitis is described in 49.8% of patients, pharyngitis in 35.6%, rhinitis in 31.2%, conjunctivitis and scleritis in 4.5% each). 21.4% of patients complain of a dry cough.
45.2% of patients experience enteritis-type diarrhea without abdominal pain.
The skin is hyperemic.
Exanthema is detected in 21.4-73.9% of patients. The rash appears on the 4th-5th day of the disease and is more often (81%) roseolous, maculopapular, less often roseolous-papular. In severe cases, the rash may acquire a hemorrhagic character.
The rash may be located everywhere or be sparse, with a predominant localization on the upper and lower extremities.
The rash lasts from 2 to 13 days (in 88.1% of patients - 5-6 days), then disappears without a trace.
In 90.5% of patients, severe hyperemia of the conjunctiva of the eyelids and uniform injection of the vessels of the conjunctiva of the eyeballs are detected.
The tongue is coated with a thick grayish-white coating and is dry. All patients have hyperemia and granularity of the mucous membranes of the soft and hard palate.
In 34.8-76.2% of patients, enlargement of the submandibular, lateral cervical, axillary and peripheral lymph nodes is detected.
Heart sounds are often muffled, and a tendency toward arterial hypotension is noted. A rough systolic murmur is heard at the apex in 42.9% of patients.
When palpating the abdomen, 47.6% of those examined experienced diffuse pain in the muscles of the anterior abdominal wall.
In 8.7-50% of cases, moderate hepatomegaly is detected; splenomegaly is often absent.
Weakly positive meningeal symptoms may be detected.
Meningeal form
In 76.8-100% of patients with the meningeal form, the disease begins acutely with a febrile temperature lasting 5 days, followed by subfebrile temperature. The temperature remains elevated for 6-13 days. In 23.2% of cases, the disease proceeds with a subfebrile temperature from the very beginning.
In 31.6%, there is a second wave of subfebrile temperature lasting 3-4 days after a short period of normalization of temperature.
Patients complain of weakness (100%), malaise (73.7%), chills (36.8%), headache (96.8%), retro-orbital pain (12.6%), dizziness (74.7%), nausea (55.8%), vomiting (36.8%), drowsiness (24.2%), sweating (14.7%), decreased appetite (26.3%), muscle pain (17.9%), arthralgia, body aches (27.4%).
The headache is excruciating, without clear localization and with maximum intensity on the 4th–6th day.
Weakness persists even after the temperature returns to normal.
Rhinitis is not typical for the meningeal form.
In 14.7% of cases, there is a disturbance of balance, in 13.7% - disturbances of consciousness, less common: tremor of the limbs (6.3%), cerebellar ataxia (5.3%), speech disorders (3.2%), weakness in the limbs (2.1%), visual impairment (2.1%), hearing impairment (1.1%), tongue deviation (1.1%) and loss of control over the function of the pelvic organs (1.1%).
Rash is present in 12.6% of patients, predominantly maculopapular (less often with a hemorrhagic component), located everywhere. Exanthema appears mainly in the first three days of the disease and lasts from 2 to 13 days, then disappears without a trace.
Enlargement of the cervical lymph nodes is detected in 3.2% of patients.
In 12.6% of cases, hepatomegaly is detected, in 2.1% - splenomegaly.
Typical scattered and transient focal neurological microsymptoms (usually appear on the 2nd-3rd day): anisoreflexia, pyramidal signs, presence of cerebellar ataxia, horizontal nystagmus, proboscis reflex, slight asymmetry of the eye slits, decreased tendon reflexes, absence of abdominal reflexes, diffuse decrease in muscle tone, flaccid paresis.
Meningeal symptoms are detected in 98.9% of patients. The peculiarity of meningeal syndrome is the predominance of rigidity of the occipital muscles with weakly expressed Brudzinsky and Kernig symptoms. The reverse development of meningeal symptoms occurs within 7-10 days.
The disease in patients with serous meningitis is relatively severe, but fatal outcomes are rare.
The meningoencephalitic form is severe, with severe intoxication. From the 3rd-4th day of the disease, confusion, agitation, convulsions, and muscle tremors appear against the background of moderately expressed meningeal syndrome.
У данной группы пациентов длительно сохраняется общая слабость, потливость, тремор кончиков пальцев, подавленное состояние психики, ослабление памяти, бессонница.
Cerebral edema.
Mortality is 10% of all hospitalized patients. The risk group includes patients over 60 years of age with an unfavorable premorbid background and immunosuppression.
Mortality in patients with severe forms of meningoencephalitis reaches 40%.
ELISA allows to detect IgM and IgG.
The diagnosis is considered confirmed by a single detection of IgM in a titer of 1:800 or higher. When examining paired blood sera for the presence of IgG, the diagnosis is considered confirmed by a 4-fold increase in titer. The absence of an increase in antibody titer indicates a post-infection.
IgM usually appear in the blood on the 2nd–5th day of illness and reach maximum level after 1.5–2 weeks.
According to various authors, IgM persists for 2-8 months after the disease. Even after a year, IgM can be detected in low concentrations in 13-17% of patients.
Confirmation of the diagnosis based on a 4-fold increase in IgG titer is not always possible, since the antibody concentration in West Nile fever increases quite quickly after the onset of the disease and then stabilizes.
It is necessary to examine paired blood samples, even if the results of the first ELISA are negative, if there are clinical and anamnestic indications: seroconversion can be detected dynamically, which also confirms the diagnosis.
Additionally, it is possible to determine the avidity of IgM and IgG: low-avidity antibodies circulate in the blood for the first 2-3 months, and high-avidity antibodies are detected later. That is, in the absence of IgM and viral RNA, determining the avidity of antibodies helps to establish the duration of the infection.
IgM in the cerebrospinal fluid appears on the 3rd-5th day of the disease, and in the blood serum - 2-3 days later (in severe forms of the disease). IgM in the cerebrospinal fluid persists up to 200 days after infection.
PCR allows to detect viral RNA.
The material for PCR can be blood (sensitivity on the 8th-9th day of illness is 16.7% for the meningeal form and 42.9% for the influenza-like form) and CSF (sensitivity on the 8th-9th day of illness is 3.6% for the meningeal form).
Viral RNA cannot be detected in urine.
PCR testing of autopsy material (liver, lungs, spleen, kidneys, brain and spinal cord, blood) is possible.
The sensitivity of PCR is highly dependent on compliance with the rules for delivering the material to the laboratory.
RNA is detected in the patient’s blood within 2–3 to 14–18 days from the onset of the disease.
In OAK, 8.7% of patients with influenza-like form showed moderate leukocytosis, 9% - leukopenia, relative lymphocytosis (30.4%), relative monocytosis (43.5%) and increased ESR (30.4-50%), left shift of the formula (13.0%), in 23% of cases hypochromic anemia was detected, in 4.5% of cases - thrombocytopenia.
In the OAC, 6-28.4% of patients with the meningeal form show moderate leukocytosis, 6% have leukopenia; 7.4% have a left shift, 5.3% have relative lymphocytosis, 11.6% have relative monocytosis, and 12.6-31% have an increased ESR.
Hyperbilirubinemia is recorded in 13.4% of cases.
An increase in ALT activity to 1.5 normal values was detected in 4.3% of patients with influenza-like illness, an increase in AST was detected in 4.3% of patients, and an increase in C-reactive protein was detected in 8.7% of patients.
An increase in ALT activity to 1.5–3 norms was detected in 14.7% of patients with the meningeal form, an increase in AST – in 13.7% of patients, an increase in C-reactive protein – in 13.7% of patients.
Increased concentrations of creatinine and glucose are present in 6% of cases.
Examination of cerebrospinal fluid in the flu-like variant reveals increased cerebrospinal fluid pressure in the absence of cytosis.
In the meningeal form, transparent or opalescent CSF flows out under increased pressure. CSF is colorless in 95.8% of cases, xanthochromic in 3.1%, and pink in 1.1%; it is completely transparent in 70.5% of cases, and cloudy in the rest.
The cellular composition depends on the timing of the study: on the first day of illness, lymphocytic pleocytosis, in some patients - mixed or with a predominance of neutrophils. Pleocytosis varies widely: 5-600 cells in 1 μl (on average, 89-114 cells). In 81.1% of studies, lymphocytes predominate, in 18.9% - neutrophils.
The protein level is moderately elevated: on average 0.63-0.71 g/l (0.125-2.930 g/l), 55.8% have a positive Pandy reaction. The glucose level remains normal (average 3.15-3.31 mmol/l). In 30.5% of patients, the chloride level is reduced below 120 mmol/l, and in 5.3% it is increased above 128 mmol/l.
In the meningoencephalitic form, CSF pleocytosis is within 50-150 cells in 1 μl, the protein content increases to 2 g/l. Protein sedimentation tests (Pandy, Nonne-Apelt reactions) are weakly positive.
ECG shows signs of myocardial hypoxia in the apex and septum region, focal changes, and slowing of atrioventricular conduction.
Examination of the fundus in the meningoencephalitic form reveals edema (congestive papillae) of the optic nerves, and sometimes hemorrhages.
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West Nile fever, meningoencephalitic form, severe
weakness, fatigue, decreased or loss of appetite, dry mouth, monotonous moderate headache, sleep disturbance, aches in muscles and/or joints, chills, fever.
change in skin color (usually hyperemia, less often pallor), scleral injection, tachycardia, sometimes hypotension.
an increase in body temperature is usually part of an inflammatory response. Depending on the nature of the inflammation, leukocytosis, leukopenia, or a normal level of leukocytes can be detected in a CBC; erythrocyte sedimentation rate often increases. C-reactive protein is often elevated.
the most objective criterion for the severity of intoxication is the degree of temperature rise (usually the highest temperature during the illness is taken into account). With mild intoxication, low-grade fever is observed (different authors designate this concept as a temperature of up to 38.0 or 38.5 degrees), with moderate intoxication - up to 39.5, with severe - above 39.5 degrees. For some infectious diseases, fever is not typical or is limited to low-grade fever; in such cases, one has to focus on subjective manifestations of intoxication or the severity of other syndromes. It should also be remembered that with the development of shock of any origin, body temperature usually decreases, so body temperature should not be taken as the only criterion for the severity of intoxication.
heaviness in the right hypochondrium, a feeling of bitterness in the mouth, decreased or lack of appetite.
yellowness (icterus) of the skin, sclera and visible mucous membranes, darkening of urine, hepatomegaly (in acute disease, the liver is usually slightly enlarged (1-3 cm), sensitive to palpation, elastic, with smooth surface), sometimes splenomegaly.
an increase in the concentration of bilirubin mainly due to the conjugated (direct) fraction, transaminases (in case of infectious liver damage, ALT is mainly increased, in case of toxic damage - AST); an increase in the thymol test (synonymous with the level of globulins) and a decrease in the level of albumin.
Ultrasound of the abdominal organs can reveal moderate hepatomegaly, and in some cases splenomegaly; the echogenicity of the liver in acute disease is usually reduced, in chronic disease it is increased, and as liver cirrhosis develops, portal hypertension increases (dilatation of the portal vein, splenomegaly, ascites). Please note that detection of ascitic fluid on ultrasound is possible not only with cirrhosis, but also with extremely severe acute hepatitis, as well as with an intact liver (for example, cancer metastases in the peritoneum).
nausea, vomiting of eaten food, which brings relief, epigastric pain (usually nagging).
coated tongue, abdominal pain in the epigastrium.
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hyperemia of the gastric mucosa is detected during fibrogastroduodenoscopy.
discomfort and rumbling along the small intestine (mainly in the mesogastrium), loose stools without admixtures or mixed with greens (bile) up to 10 times a day, copious. In severe cases of infectious enteritis, the frequency of stool may be higher, and blood may sometimes appear in the stool.
palpation determines pain and “small-caliber” rumbling along the small intestine (mainly in the mesogastrium).
in the coprogram, a moderate increase in the level of leukocytes can be detected, as well as signs of digestive disorders (undigested fibers, fats, etc.).
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nagging pain in the right (proximal colitis) or left (distal colitis) iliac region with irradiation to the perineum. The pain may be perceived as an urge to defecate (tenesmus). Loose stools more than 10 times a day in small portions mixed with mucus, blood or pus. In mild cases of colitis, the frequency of stool may be low and the volume of portions significant; in severe cases, on the contrary, stools can be observed “without counting” (more than 25 times a day), and stool portions are so reduced that the phenomenon of “rectal spitting” is possible. Proximal colitis is characterized by a predominance of blood in the stool ("raspberry jelly" type stool), and distal colitis is characterized by pus ("meat slop" type stool).
a spasmodic, painful cecum (with proximal colitis) or sigmoid (with distal colitis) colon is palpated, the abdomen is swollen, and a “large-caliber” rumbling is detected along the course of the large intestine.
in the coprogram, you can detect a pronounced increase in the level of leukocytes (prevail in distal colitis) and erythrocytes (prevail in proximal colitis), as well as signs of digestive disorders (undigested fibers, fats, etc.).
sigmoidoscopy allows you to detect hyperemia of the mucous membranes of the rectum and sigmoid colon; Examination of the entire colon is possible with fibrocolonoscopy. In addition to hyperemia, petechiae or larger hemorrhages in the submucosa, erosions and ulcers, which are often covered with plaque, can be detected.
thirst, dry mouth, weakness. With the development of decompensated dehydration shock, oligoanuria and loss of consciousness are noted.
dry skin and visible mucous membranes, decreased skin turgor (usually checked by the time of straightening of the skin fold collected on the abdomen or the back of the hand). As dehydration progresses, hoarseness of the voice is noted, then aphonia; the skin pattern on the fingers may become emphasized (symptom of “washerwoman’s hand”). In the most severely ill patients, the skin “hangs like a suit from someone else’s shoulder,” and you can notice wrinkling and sunken eyeballs. There is a progressive decrease in body weight.
The most objective criteria for the severity of dehydration are hematocrit and relative plasma density.
Weighing the patient reveals progressive weight loss.
hiccups, rapid heartbeat, spastic pain in the calf muscles, forearm muscles (other muscle groups are less often involved).
you can see forced flexion of the fingers (the “obstetrician’s hand” symptom), plantar flexion of the feet (the “horse foot” symptom); Tachycardia and tachyarrhythmias are observed.
decrease in potassium concentration in blood plasma.
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sore throat that gets worse when swallowing.
an increase in the size of the tonsils (due to edema and/or hypertrophy), their hyperemia, the presence of suppurating follicles, plaque or areas of necrosis.
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nasal congestion, often with discharge; for viral infections and allergic reactions, serous or mucous discharge is more typical; for bacterial inflammation, the discharge is grayish, yellowish or greenish.
in infections accompanied by severe rhinorrhea, macerations often form on the skin of the upper lip or in the area of the wings of the nose.
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during rhinoscopy, hyperemia of the mucous membranes of the nasal passages can be revealed; in some infections, plaque on the mucous membranes can be revealed (for example, nasal diphtheria)
presence of rashes/erythema, pain, burning, itching in the area of the rash elements.
the size and shape of elements, clarity of boundaries, skin temperature in the area of erythema, the presence of edema, infiltration, hemorrhages, areas of epidermal detachment, erosions, ulcers and crusts/eschar are assessed.
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to verify some dermatological diagnoses, a morphological (and sometimes immunohistochemical) examination of a skin biopsy from the area of erythema/rash is necessary.
pain in the lymph nodes, foreign body sensation
the size, consistency, mobility of the lymph nodes, the presence of periadenitis (redness of the skin over the lymph node, adhesion of the lymph nodes to each other and to surrounding tissues) are assessed; all groups of peripheral lymph nodes are examined.
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examination of the structure of the lymph node can be carried out using ultrasound or be invasive (morphological examination of a biopsy specimen). CT, MRI and ultrasound can detect enlarged intrathoracic lymph nodes and abdominal lymph nodes.
intense diffuse squeezing or bursting headache, at the height of which vomiting of stomach contents, and then mucus and bile often appears without relief.
you can see a forced position (the “pointing dog” pose), reveal meningeal symptoms (Kernig, Brudzinsky, stiff neck, etc.).
microscopic examination of the cerebrospinal fluid can reveal an increase in the level of leukocytes (depending on the etiology of meningitis, cytosis can be moderate or severe, neutrophilic or lymphocytic), a decrease in glucose, and an increase in protein. Detection of the bacteria that causes meningitis is also possible.
MRI of the brain usually reveals thickening of the meninges.
nasal and/or gingival bleeding, spontaneous appearance of subcutaneous hemorrhages or their appearance with minor bruises; rectal, uterine bleeding, black tarry stools, reddish urine.
petechiae on the skin and visible mucous membranes, subcutaneous hemorrhages, hemorrhage in the sclera (cherry brown symptom), positive symptoms of a pinch.
thrombocytopenia, increased clotting time and bleeding time, decreased PTI and increased INR; hematuria; positive stool occult blood test result.
the presence of hemorrhages under the mucous membranes of the gastrointestinal tract (during FGDS, FCS) and airways (during rhinoscopy, bronchoscopy).
Various secretions (feces, urine, vomit, sputum), internal media (blood, cerebrospinal fluid), biopsies and scrapings can be used as material. Optical microscopy allows you to study objects larger than 0.2 microns (bacteria, protozoa, fungi, helminth eggs, their fragments and larvae, as well as arthropods). The method is most effective in the early stages of the disease (and before the start of etiotropic therapy) or during exacerbation of the disease. Microscopy is one of the express diagnostic methods, since the analysis conclusion can be obtained within a couple of hours after the material is delivered to the laboratory. A trained laboratory technician is expected to be able to identify the microbe, but in practice errors do occur. The quality of diagnostics can be improved by using differentiating methods of staining, sedimentation and flotation of material. The disadvantages of light optical microscopy are very low sensitivity of the method and the inability to determine the sensitivity of bacteria to antibiotics. Electron microscopy allows you to study viruses and individual structures of microorganisms. Due to the high cost of equipment, electron microscopy has not become widespread in clinical practice.
The material can be various secretions (feces, urine, vomit, sputum), internal media (blood, cerebrospinal fluid), biopsies and scrapings. Swabs from environmental objects, remains of suspicious products, etc. can also be used. The bacteriological method is the “gold standard” in the diagnosis of bacterial infections. It allows you to determine the pathogen and its sensitivity to antibiotics and bacteriophages. The sensitivity of bacteriology is significantly superior to microscopy, but is still very far from 100%. Bacteriology is one of the early diagnostic methods: as the duration of the disease increases, the sensitivity of bacteriology usually decreases. The disadvantage of the method is the duration of bacteriological tests: in most cases, the result can be obtained in 2-3 days, but some bacteria grow very slowly (for example, Yersinia); to isolate others, special nutrient mediums (enriched, selective, selective) or anaerobic conditions (use of an anaerostat) are required.
Infection of laboratory animals in some cases makes it possible to identify the pathogen, as well as to verify its pathogenicity. The method is relevant for infections, the pathogens of which are contained in low concentrations in the studied fluids and tissues of the human body and grow poorly or slowly on nutrient media. During an autopsy of an infected animal, microscopy or tissue culture of parenchymal organs can be performed (that is, a biological sample is also a way of accumulating the pathogen - it increases the sensitivity of bacteriology and bacterioscopy). Using a bioassay, you can also verify the presence of very low concentrations of specific toxins in the patient’s blood (for example, with botulism). Disadvantages of the method: the need to maintain a vivarium; increasing the time to confirm the diagnosis.
The material for analysis is selected based on the type of pathogen and the form of the disease. Isolation of viruses on tissue culture or chicken embryos is considered to be the “gold standard” in the diagnosis of viral infections. Viruses pathogenic to humans grow better on human tissue cultures, and most of them are characterized by tissue specificity. Some viruses must be grown in very specific tissue cultures, which increases the complexity and cost of virological testing. To identify an unknown virus, it is advisable to infect 3-4 different cell cultures. The virus is identified by its cytopathogenic effect: specific changes in cells, the appearance of specific inclusions. The complexity of implementation and high cost of the method make it impossible to use it in routine clinical practice, but it remains relevant in scientific work.
Usually blood is tested, but sometimes other biological fluids are used (for example, so-called intrathecal antibodies can be detected in cerebrospinal fluid) Serological tests are based on the interaction of antigens with antibodies. Antigens can be detected not only in the early stages of the disease, but sometimes even during the incubation period. Antibodies are detected at a later date: for most infections - after 5-7 days of illness (usually the more severe the disease, the faster antibodies appear), for some - after 2-3 weeks (for example, borreliosis) or even several months (HIV). Because of this, serological diagnosis is often retrospective. A single detection of antibodies to the desired pathogen does not always confirm the diagnosis (it may indicate a past infection or vaccination). As a rule, it is preferable to repeat the determination of antibodies after 7-10 days (paired serum method). For most infections, the diagnosis is considered to be confirmed when the antibody titer increases by 4 times or more. The specificity of serological methods does not reach 100%: false-positive results are possible, especially if the patient has concomitant rheumatological and oncological diseases, or pregnancy.
The material can be various secretions (feces, urine, vomit, sputum), internal biological fluids (blood, cerebrospinal fluid), biopsies and scrapings. PCR is based on identifying specific nucleotide sequences of pathogens, therefore it allows you to determine the species of the pathogen, has high specificity, high sensitivity and gives false positive results only when the test material is contaminated or the laboratory technician makes a mistake. It is not included in the examination standards for most infectious diseases, therefore it is relatively rarely used in outpatient practice. Laboratories in infectious diseases hospitals are usually better equipped, so PCR is used much more widely in hospitals.
The use of skin allergy tests is currently very limited (tuberculosis, tularemia, anthrax, brucellosis). The method is based on the injection of an antigen of the suspected pathogen to a person, followed by assessment of the local allergic reaction. Usually the result is assessed after 24 and 48 hours. The method often gives false-positive results, so its specificity is low.
