Theme Shigellae infections. Salmonellae infections. Escherichia infections. Yersiniosis. Rotaviral infection Theme Viral hepatitis A, B, С, d et al. Gastrointestinal infections: guidance, data and analysis
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- Bu səhifədəki naviqasiya:
- Auxiliary therapy of an acute intestinal infection Probiotics
- Key words and phrases
- Features of Rotavirus infection in new-borns
- Differential diagnosis
- Treatment
- Arthralgias or arthritis
- Hepatomegaly
- Glomerulonephritis
- Yersiniosis, peculiarities in infants
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Diet Cancelling of water-tea pauses is an important moment in organization of feeding of sick children, as it is well-proven that the digestive function of a greater part of intestine is saved even in severe forms of diarrhea, and pauses will decelerate reparation, reduce intestine tolerance to a food, and considerably weaken immunity of a patient. A volume and composition of a meal depends on a child’s age, weight and diarrhea severity, and a character of concomitant diseases. Rational feeding is important for a rapid restoration of the intestinal function. It is recommended to diminish a daily volume of the meal on 1/2-1/3 in an acute period of gastroenteritis, and on 1/2-1/4 – in an acute period of colitis. It is possibly to increase a number of meals up to 8-10 daily for infants, especially at urges to vomiting. An early, but gradual renowation of an age-appropriate food is considered to be the most physiological nowadays. It should be done in a short period after the rehydration (in 4-5 days). A fatty, fried, smoked food and other like that is eliminated from a ration of an elder children. If a child is breast fed, it is recommended to continue breastfeeding. Children on the adopted formulas are fed with lactose free formulas by the same chart. Products with a high amount of lactose should be eliminated (milk-based formulas, milk, fruit juices). This will decrease a course of secretory diarrhea. Lactose free diet should last individually from 1-4 weeks to 1.5-2 months. Porridges prepared with water are recommended, meet puree should be given earlier. Fermented milk formulas are recommended after 8 month of age. Soya containing formulas are not recommended because of intestine excessive sensitivity to soy proteins in diarrhea. It is risky for the development of protein entheropathy. Apples prepared in the oven, bananas, apple and carrot puree that contain a large amount of pectins are recommended in case of colitis.
antibacterial therapy is not indicated) or as additional medicine during antibacterial therapy. Probiotics, which contain lacto-, bifidobacteria and propionebacteria, are recommended. Self eliminative probiotics (contain saccharomycets) or probiotics which contain lactobacteria are used in invasive diarrhea on a background of antibacterial therapy. The last ones are stable to antibiotics. Probiotics aren’t given to children with the immune deficiencies, who are treated in the intensive care units. The course of therapy lasts for 5-10 days.
microbes are ruined and deleted from a sick organism. Except bacteria from the intestine, enterosorbents fix rotaviruses on their surface. They also absorb bacterial toxins and products of metabolism. They transform toxic substanses in less toxic. "White", alumsilicate enerosorbents are the most perspective in the treatment of an acute intestinal infections in children. Unlike coal sorbents, they do not require input of a high dose of medicine for therapeutic effect. Also coal sorbents can affect submucous layer of the intestine when come into it. Zinc is recommended by WHO (2006) as an auxiliary therapy of an acute intestinal infections during 10-14 days (10 mg daily for children under 6 months, 20 mg daily for children elder than 6 months).
• Water and food epidemiologic control. • Isolation and sanitation of ill person. • Convalescent may be discharged from hospital after one negative feces culture (taken 2 days after the course of antibiotic therapy is finished). • Dispensary supervision of convalescents for 3 months. • Feces culture taken in contacted and carriers. • Supervision of contacted for 7 days, quarantine. • Disinfection of the focus of infection.
Escherichia Coli (ETEC), Enteroinvasive E. Coli (EIEC), Enterohemorrhagic E. Coli (EHEC), Enteroaggregative (enteroadherrent) E. Coli (EAEC) enterosorption, rehydration, eubiotics, probiotics.
Rotavirus infection is an acute contagious disease of humans and animals that is caused by Rotavirus, is passed by a fecal-oral mechanism, and is characterized by the affection of gastro-intestinal tract (as gastroenteritis).
an 11 double-stranded RNA genome enclosed in a double-shelled capsid. The outer shell is composed of a major glycoprotein with a molecular weight of 34,000 (ie, viral protein [VP]7) and a minor, trypsin-sensitive protein with a molecular weight of 84,000 (ie, VP4, previously designated VP3). Four proteins (ie, VP1, VP2, VP3, VP6) make up the virus core. Six nonstructural (NS) proteins (ie, NS53, NS34, NS35, NS28, NS26, NS12) are also produced during Rotavirus infection. HRVs belonging to 11 G serotypes have been isolated, but the vast majority have been identified as G1, G2, G3, or G4, and strains belonging to these G types have commonly been designated as serotype 1, 2, 3, or 4, respectively. The severity of illness caused by viruses that belong to these 4 serotypes varies little, if at all. At least 6 different HRV P types have been identified.
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direct contact); •
upper intestine and typically leads to a series of histologic and physiologic changes. The incubation period is brief. Rotaviruses infect cells in the villi of the small intestine (gastric and colonic mucosa are spared). They multiply in the cytoplasm of enterocytes and damage their transport mechanism. One of the rotavirus-encoded proteins, NSP4, is a viral enterotoxin that induces secretion by triggering a signal transduction pathway. Damaged cells may slough into the lumen of the intestine and release large quantities of viruses, which appear in stool. Viral excretion usually lasts 2-12 days in healthy patients but may be prolonged in those with poor nutrition. Diarrhea caused by rotaviruses may be due to impaired sodium and glucose absorption as damaged cells on villi are replaced by nonabsorbing immature crypt cells. Three to 8 weeks may be necessary for normal function to be restored. 1.
Virus invasion to the thin intestine epithelial cells (enterocytes). 2.
Replication of virus and destruction of enterocytes. 3.
Increased growth of immature cells. 4.
Enzymes defficiency. 5.
Violation of digestion and absorbtion of disaccharides. 6.
Accumulation of fluid and electrolytes in the intestine. 7.
Diarrhea. Diagnostic criteria: Infection with human rotavirus (HRV) appears to cause a substantial portion of cases of gastroenteritis in children aged 6 months to 2 years. Infants and young children most commonly have fever, vomiting, diarrhea, and (occasionally) dehydration. Vomiting, usually short-lived, can occur before or after the onset of diarrhea. Symptoms of an apparent respiratory infection may be present. The patient's stools can be watery, green or yellow, and not obviously bloody. Stools rarely contain mucus and number as many as 10 per day. In most cases, diarrhea lessens soon after admission and, in only a few cases, persists longer than 3-4 days. The association of HRV, gastroenteritis, and upper respiratory tract symptoms has been noted frequently. The history should focus on severity and dehydration. The onset, frequency, quantity, and duration of diarrhea and vomiting are important factors in assessing the status. Oral intake, urine output, and weight loss are important considerations. Viruses are the suspected cause of acute gastroenteritis when vomiting is prominent, when the incubation period is longer than 14 hours, and when the entire illness is over in less than 3 days. 1.
Latent period is 1-4 days. 2.
DVF-syndrome (diarrhea, vomiting, fever): • Diarrhea (gastroenteritis, enterocolitis): stools are “sprinkling”, colorless, watery for 3-6 days; • Vomiting for 1-3 days (precedes or appears together with diarrhea); • Fever (moderate to high) for 2-4 days. • In koprogram – lymphocytes, signs of indigestion. The physical findings for Rotavirus infection are often unremarkable except for signs of dehydration. Other findings on examination may include the following: • Hyperactive bowel sounds: Most common finding • Sunken eyes and/or anterior fontanelle • Dry or sticky-appearing mucosa • Rough skin or diarrhea-induced diaper dermatitis • Tachycardia: Can be disproportionate to the temperature • Rectal examination: May stimulate production of watery, heme-negative stools • Depressed sensorium • Weight loss Significantly decreased urine output is an important sign. However, this may be hard to identify in diapered infants. Features of Rotavirus infection in new-borns Often is a hospital infection. Begins with the refuse of breast feeding, vomiting, diarrhea, development of the severe dehydration. Beginning is gradual with increase of dehydration severity. The disease is lethally often.
Diagnosis example: Rota-viral infection typical form, severe course, hypotonic dehydration of moderate severity. Differential diagnosis is performed with other Viral gastroenteritis, Cholera, Salmonella infection, enterotoxigenic Escherichiosis; Acute intestinal infections caused by ubiquitous intestinal microflora.
• Rotavirus may be identified by several means (ie, enzyme immunoassay being the most common, latex agglutination, electron microscopy, culture). • Electrolyte levels should be measured with severe dehydration, alterations in mental status, associated seizures, or oral replenishment with excessive water or salt.
• Bedside glucose levels should be measured in very young infants and in any age child with associated lethargy.
• Intime diagnosis and treatment of patients; • final and current disinfection; • sanitary-epidemic regime in child’s collectives, hospitals; • supervision for contacted; • There are two vaccines for the specific prophylaxis of Rotavirus infection. Both are given orally and contain a weak living virus of 1-4th types. YERSINIOSIS Yersiniosis is an acute infectious disease caused by Yersinia enterocolitica that causes enterocolitis, acute diarrhea, terminal ileitis, mesenteric lymphadenitis, and pseudoappendicitis but, if it spreads systemically, can also result in fatal sepsis.
belongs to the family Enterobacteriaceae. Y enterocolitica is non–lactose-fermenting, glucose-fermenting, and oxidase-negative facultative anaerobe that is motile at 25°C and nonmotile at 37°C. Most, but not all, Y enterocolitica isolates reduce nitrates. Y enterocolitica is classified according to various distinct biochemical and serologic reactions. Based on biochemical characteristics, 6 biotypes of the bacterium have been described. Biotypes 2, 3, and 4 are most common in humans. The serotyping is based on O and H antigens. More than 60 serotypes of Y enterocolitica have been described. The serotypes most clearly pathogenic to humans include O:3, O:5,27, O:8, O:9, and O:13.
H-antigen typing can be a valuable supplement to O-antigen typing and biochemical characterization in epidemiologic investigations. Accurate identification of pathogenic strains requires consideration of both the biotype and the serotype because some strains can contain multiple cross-reacting O antigens. Epidemiology: •
enterocolitica include swine (principle reservoir), dogs, cats, cows, sheep, goats, rodents, foxes, porcupines, and birds. Fecal-oral transmission among humans has not been proven. •
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and milk products, raw pork, tofu, meats, oysters, and fish. Outbreaks have been associated with raw vegetables; the surface of vegetables can become contaminated with pathogenic microorganisms through contact with soil, irrigation water, fertilizers, equipment, humans, and animals. Pasteurized milk and dairy
products can also cause outbreaks because Yersinia can proliferate at refrigerated temperatures. •
infection appears to occur predominantly in cooler climates, being much more common in northern Europe, Scandinavia, and Japan.
Y enterocolitica can efficiently colonize and induce disease in the small intestine. Following ingestion, the bacteria colonize the lumen and invade the epithelial lining of the small intestine, resulting in the colonization of the underlying lymphoid tissues known as Peyer patches. A direct lymphatic link between the Peyer patches and mesenteric lymph nodes may result in bacterial dissemination to these sites, resulting in mesenteric lymphadenitis or systemic infection. The enterotoxin produced by Y enterocolitica is similar to that produced by the heat-stable Escherichia coli; however, it likely plays a minor role in causing disease, as diarrheal syndromes have been observed in the absence of enterotoxin production. In addition, the toxin does not appear to be produced at temperatures higher than 30°C. The plasmid-mediated outer membrane antigens are associated with bacterial resistance to opsonization and neutrophil phagocytosis. After an incubation period of 4-7 days, infection may result in mucosal ulceration (usually in the terminal ileum and rarely in the ascending colon), necrotic lesions in Peyer patches, and mesenteric lymph node enlargement. In severe cases, bowel necrosis may occur, as a result of mesenteric vessel thrombosis.
Focal abscesses may occur. In persons with human leukocyte antigen (HLA)–B27, reactive arthritis is not uncommon, possibly because of the molecular similarity between HLA-B27 antigen and Yersinia antigens. The pathogenesis of Yersinia -associated erythema nodosum is unknown. 1. Entering the bacilli to gastrointestinal tract. An atrium is a small intestinum (terminal part) and appendix. 2. Enteral phase: invasion of bacteria to enterocytes, development of local inflammation, diarrhea, enterotoxin secretion. 3. Regional lymphadenitis (regional infection). 4. Generalization (bacteriemia, toxemia) in severe cases. 5. Parenhymatous phase: hematogenous distribution of bacteria with forming of secondary foci (lungs, liver, spleen, bones). 6. Immunological response, recovering from the disease. 7. May be secondary bacteriemia (exacerbations and relapses), because of possible persistance in the lymph nodes. Diagnostic criteria: • Latent period is 4-7 days with a range of 1-14 days. • Acute (72.2 %) or gradual (27.8 %) beginning. • Polymorphism of clinical picture. • Enterocolitis. The usual presentation of Y enterocolitica infection includes diarrhea (the most common clinical manifestation of this infection), low- grade fever, and abdominal pain lasting 1-3 weeks. Diarrhea may be bloody in severe cases. Vomiting is present in approximately 15-40% of cases. The diarrhea generally has duration of 1 day to 3 weeks.
20-30% of infants younger than 3 months. • Complications of enterocolitis include appendicitis,
diffuse ulceration and inflammation of the small intestine and colon, peritonitis,
meningitis, intussusception,
and cholangitis. • Moderate toxic syndrome, prolong fever up to 1-2 wks. • The existence of extraintestinal symptoms after the gastrointestinal illness may also indicate the possibility of Yersiniosis.
• Mesenteric adenitis, mesenteric ileitis, and acute pseudoappendicitis. Pseudoappendicitis syndrome is more common in older children and young adults.These manifestations are characterized by the following symptoms (although nausea, vomiting, diarrhea, and aphthous ulcers of the mouth can also occur): • Fever • Abdominal pain • Tenderness of the right lower quadrant • Leukocytosis • Mild respiratory syndrome (pharyngitis, rhinitis). • Rashes for 6-14 days: macular or macular-papular, located in skin folds, around the joints, on a lateral surfaces of the trunk and chest; • Hyperemia of the face, hands and feet (“hood”, “gloves”,”socks” symptom). • “Strawberry” tongue. •
on the patient’s legs and trunk. Lesions appear 2-20 days after the onset of fever and abdominal pain and resolve spontaneously in most cases in about a month. The female-to-male ratio of erythema nodosum is 2:1, and it is more common in adults than in children. •
which occur in approximately 2% of patients, typically arise 1-2 weeks after gastrointestinal illness. The large joints of the lower extremities are involved most commonly, and symptoms usually persist for 1-4 months •
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with the HLA-B27) •
focal abscesses in the liver, kidneys, spleen, and lungs. Cutaneous manifestations include cellulitis, pyomyositis, pustules, and bullous lesions. Pneumonia, meningitis, panophthalmitis, endocarditis, infected mycotic aneurysm, and osteomyelitis may also occur.
illness; 5. Frequent respiratory syndrome; 6. Hepatitis develops rarely; 7. Arthritis is absent. Classification Form: • typical: - gastro-interstinal, - pseudo appendicitis, - nodular erythema, - arthralgic form, - hepatic, - septic (generalized), • atypical (subclinical). Severity: • mild • moderate • severe
Course (duration): • acute: - uncomoplicated - relapsed, complicated (not smooth) • chronic
Diagnosis example: •
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• Complete blood analysis: leucocytosis, neutrophilia with left shift, eosinophilia, ESR is increased. • Urinalysis: slight proteinuria, leucocituria, casts in a small amount (in case of toxic affection of kidneys). • Bacteriological – Yersinia enterocolitica may be found in feces, urine, blood, pus, lymph nodes and pharyngeal mucus. The culture result is usually positive within 2 weeks of onset of disease. • Coprogram: Increasing of red blood sells and leukocytes, mucus. • Serodiagnosis – increasing of special antibodies 4 times and more in 2-4 wks in paired sera (tube agglutination, enzyme-linked immunosorbent assays, and radioimmunoassays 1:200).
Cross-reactions with
other organisms can occur
— including with Brucella, Morganella, and Salmonella — and a background seroprevalence rate among different populations may confound the diagnosis by acting as a false-positive result. However, elevated levels can be found for years after infection, which also limits the usefulness of serodiagnosis.
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