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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Differential diagnosis should be performed with: Functional Diarrhea, Shigella infection, Escherichiosis, Klebsiellosis, Typhoid fever, and Sepsis of different etiology. Diagnosis example: •
(enterocolitis), moderate severity, isotonic dehydration of 1st degree, acute course, uncomplicated. •
(enterocolitis, meningitis, bilateral pneumonia, osteomyelitis of the left humeral bone), severe, subacute course. Complicated by malnutrition, 2nd degree. Treatment: see treatment of Salmonella infection below Prophylaxis • 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.
Key words and phrases: nosocomeal Salmonella infection, gastrointestinal form, typhoid form, sepsis, bacillus carrying.
ESCHERICHIA COLI Escherichia coli infections are acute Infectious Diseases of infants and toddlers mainly, caused by different pathogenic strains of Escherichia coli, and are characterized by localization of pathological process in gastro-intestinal tract with development of toxic and diarrheal syndromes, possible generalization of the process with development of sepsis or malnutrition.
major component of the normal intestinal flora and ubiquitous in the human environment. They well grow in ordinary environments, ave a difficult antigen structure. Microbes contain a somatic O- antigen, flagellate Н-antigen and superficial somatic S-antigen. Distinctions in an O-antigen devide bacteria into number of O-groups (serological groups). Enthero-, cyto- and verotoxins, and an adhesive and invasive activity of bacteria cause different pathogenic effects of Е. coli.
Five pathotypes have of diarrheagenic E coli have been recognized; each pathotype has a distinct pathogenesis. The pathotypes are as follows: Enterotoxigenic E coli (ETEC) Enterohemorrhagic E coli (EHEC) Enteropathogenic E coli (EPEC) Enteroinvasive E coli (EIEC) Enteroaggregative E coli (EAEC) Epidemiology: •
•
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Pathogenesis: ETEC adheres to the small bowel mucosa by means of several different fimbrial colonization factor antigens (CFAs). Once colonization is achieved, one or both of the enterotoxins are released (ie, heat labile toxin [LT] and heat stable toxin [ST]). These toxins draw fluid and electrolytes from the small bowel mucosa. ST is reportedly the more virulent of the toxins.
LTs are closely related in structure and function to the enterotoxin severe by Vibrio cholerae. Immunity develops to ETEC surface antigens, confining most disease to immunologically naïve travelers and weaning infants. EHEC, also known as Shiga-toxin producing E coli (STEC), induces an attaching and effacing (AE) lesion in the large bowel. Once established in the colon, EHEC releases one or more toxins known as Shiga-like toxin (Stx). Stx is related to the Shiga toxin of Shigella dysenteriae and is cytotoxic to the vascular endothelium. The systemic circulation of Stx accounts for the potential development of HUS but is not required for EHEC hemorrhagic colitis to occur. E coli O157:H7 is the most virulent of the EHEC.
microangiopathic hemolytic anemia, thrombocytopenia, and renal insufficiency. HUS typically develops in the second week of illness (range, 2-14 d), often after the diarrhea has resolved. Patients present with pallor, weakness, irritability, and oliguria or anuria. EPEC also produce AE lesions; however, it does so in the absence of Shiga toxin production. The pathogenesis includes colonization of the small intestine, followed by the formation of AE lesions and a subsequent net secretory state.
The pathogenesis of EIEC mimics that of the Shigella species. The EIEC invades the large bowel epithelial cells, producing secretogenic enterotoxins and subsequent colonic epithelial cell death. These enterotoxins are typically lactose nonfermenting and are responsible for the local colonic inflammatory response.
Invasiveness derives from a virulence plasmid closely related to that possessed by Shigella species. EAEC adheres to the small and large bowel by means of aggregative adherence fimbriae (AAFs), and colonization ensues. This colonization produces enterotoxins and cytotoxins, which, in turn, damages the intestinal mucosa.
means of vertical or horizontal transmission. The characteristic serotype of this pathogenic E coli displays the K1 antigen, which is responsible for 40% of the cases of bacteremia and 80% of the cases of meningitis caused by E coli.
The virulent activity of the K1 antigen reduces the ability of the host to develop an antibody specific response and to activate the alternative complement system. In addition, S fimbriae have been associated with many of the E coli of patients with CNS infections. S fimbriae enhance the ability of E coli to adhere to vascular epithelium as well as the spread of the bacterium within the CNS.
1.
Invasion of bacteria in GIT 2.
Reproduction of bacteria, selection of toxins • EPEC on the enterocytes surface • ETEC on the enterocytes microvilli surface • EIEC, EHE in the colon epithelial cells 3. Local inflammatory process (EPEC, EIEC), toxemia (EPEC, EIEC) 4. Violation of the digestion, absorption (EPEC, EIEC); hypersecretion; violation of water and electrolytes absorption (ETEC) 5.
Diarrhea 6.
In severe cases: bacteremia (sepsis)
Diarrhea Classification Diarrhea's type Diagnostic's criteria Severity Main clinical syndrome Invasive (bacterial) Liquid
excrements with
pathological admixture (mucus, verdure, blood)
Mild
Moderate
Severe
Primary toxicosis (neurotoxicosis)
Toxicosis with dehydration I, II and III degree
Infectious-toxic shock
Toxic-dystrophic syndrome
syndrome
Excrements are liquid, massive, without pathological admixtures Prolonged Long-lasting diarrhea (more 2 weeks) with pathological admixtures
Watery, don’t fermentated excrements without signs of the inflammation in koprogram, associated with food ingredients Criteria of the Diarrhea Severity Criteria Mild current Moderate current Severe current Local manifestations
regurgitation, vomiting 1-2 times per day, excrements less than 7-
Multiple vomiting, as a rule after receiving the food, excrements
Multiple vomiting not only after receiving the food, but also 8 times per day, changed nature with small amount of mucus, but with increase of
stools, moderate metheorism to 15 times per day, liquid, with much mucus, can be bloody mucus, metheorism independent, can be with bile, sometimes - as coffee lees, excrements - more 15 times per day, sometimes - with each diaper, much mucus, there is blood, sometimes - an intestinal bleeding General manifestations
General condition is broken little, falls
appetite, body
temperature is
normal or
subfebrile, deceleration or delay of the body weight, visible signs of toxicosis and dehydration are absent
General condition is moderately broken, malaise or excitement, appetite is reduced, poor sleeping, moderate signs of toxicosis and dehydration, body temperature is 38-39º С, body weight decreases
General condition is
sharply worsened, changes in all organs and systems, quite often - sopor, loss of the consciousness, cramps, expressed toxicosis and dehydration, significant weight loss
vomiting, seizures and voluminous diarrhea without blood and mucus are common. Diarrhea lasting 2 weeks or longer in infants. Enterotoxigenic diarrhea includes nausea, vomiting, seizures and frequent watery stools. There no fecal leukocytes in the stool. This syndrome is usually self – limited and lasts about 5 days.
with shigella. Nausea and vomiting frequently accompany abdominal pain. The diarrhea is less in volume than that seen with ETEC strains and contains mucus and blood. Fever, headache, and myalgia are common. Enterohemorrhagic Escherichiosis is associated with severe abdominal cramps, low – grade fever, grossly bloody stools, nausea and vomiting. This organism also has been found in association with hemolytic uremic syndrome (HUS). Symptoms of E coli HUS range from asymptomatic to nonbloody diarrhea to bloody diarrhea, renal failure, microangiopathic hemolytic anemia, thrombocytopenia, and CNS manifestations.
• Latent period is 5-8 days, in new-borns it is up to 1-2 days. • Beginning of illness is gradual or acute. • Feces are yellow-orange watery with a bit of mucus, greenish admixtures sometimes (Pic.203) up to 10-15 times daily. • Vomiting, regurgitation from the beginning of the disease. • Symptoms have gradual development up to 5-7 days. • Temperature is subfebrile. • Toxicosis with dehydration of 2-3 degree is typical. • An acute renal or adrenal failure, DIC-syndrome, infectious-toxic shock may occur. Massive yellow-orange feces Enteropathogenic E.coli infection, peculiarities in the newborns • Hospital infection caused by antibioticresistant strains. • Generalization of the infection with sepsis development. • Meningitis is typical, with the development of complications (hydrocephalus). • Diarrhea is rare. • Lethality is high. Criteria of Enteroinvasive E.coli infection • Latent period is 1-3 days. • Acute beginning with a severe toxic syndrome, fever (1-3 days), vomiting is rare. • Diarrhea from the 1st day of the disease: feces 3-5 times daily with the admixtures of greenish mucus and blood. • Abdomen is tender by the colon way, sigmoid colon is infiltrated, tenesmus are absent. • Rapid recovery, stool normalization in 3-5 days. Enteroinvasive E.coli infection, peculiarities in infants • Gradual beginning. • Severe toxic syndrome that increases for 5-7 days. • Enteritic or enterocolitic character of stools. • Dehydration is frequent. • Moderate or severe course of the disease. • The fever lasts for 5-7 days, sometimes up to 2 weeks. • Stool normalization delays up to 1-2 weeks. Criteria of Enterotoxigenic E.coli infection • Latent period lasts from few hours up to 1-2 days. • Beginning is acute from the repeated vomiting, watery diarrhea. • Intoxication is absent; body temperature is normal or subfebrile. • Palpation of a thin intestine reveals grumbling sound. • Feces 15-20 times daily, as a rice-water without pathological admixtures. • Severe dehydration develops. • The disease lasts not more than 5-10 days. Criteria of Enterohemorrhagic Е. coli infection • Latent period is 1-7 days, rarely is up to 9-10 days. • A disease has moderate or severe course. • Beginning is acute. • Cramps in the epigastrium or all over the abdomen are typical. • Secretory diarrhea develops from the first days of the disease. • Hemocolitis with frequent defecation (in severe cases up to 20-30 times daily) develops later. •
• Complications: - hemolytic-uremic syndrome in 2-7 %, in the end of the first – beginning of the second week of the disease, - acute renal failure, - hemolytic anaemia, - thrombocytopenia, - seizures and other neurological disorders (up to blindness development). • In the fecal test large amount of erythrocytes and small amount of l eucocytes. • Letality is 1-2 %. In HUS – 5-10 %. Laboratory test -
-
-
-
elder than 1 year if fecal culture is negative. Differential diagnosis should be performed among acute non infectious diarrheas, Salmonella infection, Shigella infection, Staphylococcal diarrhea, Viral diarrhea, and Colera. Diagnosis example: Enterotoxigenic E.coli infection, typical form, severe course, hypertonic dehydration, 3rd degree. Treatment Therapy of an acute intestinal infection for children has 4 constituents: diet, rehydration therapy, antibacterial therapy and auxiliary therapy (enerosorption, probiotics).
Dehydration can be caused by fluid loss (through vomiting, diarrhea or excessive urination), inadequate intake, or a combination of both. The most common cause of dehydration in infants and children is acute gastroenteritis, with its associated vomiting and diarrhea.
1. Rehydration Timely and adequate rehydration is the most essential direction in treatment of an acute intestinal infection, either secretory or invasive. Early beginning of an adequate rehydration therapy is the main warranty of a rapid and successful treatment. Rehydration therapy corresponds to the severity of child’s dehydration (Table 1). Table 1
Clinical signs of dehydration severity (present 2 or more from the noted signs) Sign Mild (1 st degree) Moderate (2 nd degree) Severe (3 rd degree) Loss
of the
body weig
ht Children younger than 3 yrs 3-5 % 6-9 %
10 % and more Children of 3-14 years
Up to 3 % 3-6 %
6-9 % General condition Anxiety Anxiety or sleepiness Languor, sleepiness Thirst Drinks
voraciously Drinks voraciously Does not drink Anterior fontanel Not changed Slightly sunken Sunken Eyeballs Not changed Soft
Deeply sunken Mucous membranes of the mouth Moist
Slightly dry Dry
Skin fold Disappears at once
Disappears slowly It can disappear slowly (> 2 sec.) or does not disappear at all Arterial pressure Normal Hypotonia Severe hypotonia Urination Normal
Decreased Considerably decreased to 10 ml/kg day Oral rehydration (by mouth) Oral rehydration is the most effective from the first hours of the disease. Oral rehydration should be the first aid at home when the disease begins. It doesn’t have any contraindications. In accordance with recommendations of WHO, an optimal composition of solutions for oral rehydration is: sodium – 60 mmol/l; potassium – 20 mmol/l; bicarbonates – 10 mmol/l; glucose – 110 mmol/l; osmolarity is – 250 mosmol/l. Content of sodium and potassium in solutions for oral rehydration have to correspond to their average losses in acute intestinal infection. The concentration of glucose in them must help to resorb water not only in the intestine but also in kidneys. It is not recommended to give fruit juices, sweet drinks (Coca-cola, and others like that) during the oral rehydration because of their high osmolarity. Oral rehydration should be started immediately, because dehydration begins after the first liquid, watery emptying, a long before the first clinical sign of dehydration will appear. An avaluable rehydration therapy is performed in 2 steps.
volume of 30-50 ml/kg in case of mild dehydration, 60-100 ml/kg in case of moderate dehydration.
calculat ion of oral rehydra tion solution s volume Table 2
Body weight in kg An amount of solution for 4-6 hours (ml) mild dehydration moderate dehydration 5 250 400 10
500 800
15 750
1 200 20
1 000 1 600
25 1 250
2 000 Criteria of the 1st stage of rehydration efficacy: (are evaluated in 4-6 hours) • thirst disappears, • turgor of tissues improves, • mucous membranes become moist, • diuresis increases, • microcirculation normalizes. Choice of a subsequent tactic: 1. If signs of dehydration have disappeared, you should start the 2nd step of rehydration; 2. If signs of dehydration have reduced, but still are present, it is needed to continue the 1 st
step of rehydration for the next 4-6 hours in a previous regimen; 3. If signs of dehydration have increased, parenteral rehydration should be started.
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