Tor Classics
Uncategorized July 7th. 2011, 12:54pmTor Classics
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Vibrio cholera etiology and pathogeneis
Cholera is due to infection with the Gram-negative bacillusVibrio cholerae, which causes acute secretory diarrhoeawith death due to dehydration.AetiologyV. cholerae is a curved Gram-negative motile bacillus. Twobiotypes are recognized, the classic biotype and the El Torbiotype. The organism is present in vast numbers in thefaeces of infected patients. The El Tor biotype tendsto cause more asymptomatic and mild infections, whichresolve spontaneously and leave the patient excretingvibrios to infect others. The organism is sensitive to desiccationbut survives in saline waters. Vibrio cholerae 0.139has been recently recognized in India and Bangladesh.Until that time the 0.1 serotype was the sole pathogenicorganism and 0.2 to 0.138 were non-pathogenic.
Distribution and incidenceCholera has been imported into European countries but no outbreaks have resulted, apart from that in Naples in1974.Transmission and epidemiologyOrganisms are ingested in contaminated food and water.In India, Bangladesh and Pakistan, where cholera isendemic, it is predominantly a paediatric disease. Inepidemic cholera all ages are affected. Individual susceptibilityis governed by the infecting dose and by the gastricacid barrier. The 0.139 serotype affected adults andchildren in India and Bangladesh, indicating that there wasno cross-protection between the usual serotype and thenew one.PathogenesisV. cholerae secretes an exotoxin which binds to the GM1ganglioside, a glycolipid on the surface membrane ofjejunal enterocytes. The effects of choleratoxin are mediated by several mechanisms, one ofwhich may be accumulation of cyclic AMP in the cell.Local neurohumoral stimuli may also contribute to thediarrhoea.The outcome is that the upper small intestine becomesa site of net secretion, with the accumulation of isotonicfluid containing Na+, Cl-, HCO3- and water. This fluidpasses down the intestine and in the colon K+ exchangesfor Na+ under the influence of aldosterone. Stooling ratesof 500mL/h are common, and up to 1 L/h may be produced.The effect of cholera toxin lasts for the duration of the lifeof the enterocyte, which is 3-4 days; during this time thecell migrates from the crypt to villous tip, where it isdesquamated into the gut lumen.There are no histological changes in the affectedmucosa. Cholera is a secretory diarrhoea with no mucosalinflammation. Secondary changes in a range of tissues, e.g.kidney, occur as a result of hypovolaemia and shock.Clinical featuresThe incubation period is about 2 days. Diarrhoea begins suddenly, with vomiting during the first 24 hours of illness.Faecal residues disappear, and opalescent rice-waterstools are passed. There are no pus cells in faecal smears.The abdomen may be distended and bowel sounds areincreased. Stool losses are maximal within the first 48hours of the illness and decline spontaneously thereafter,but death can occur from dehydration within 24 hours inthe most severe cases.The clinical features are due to isotonic volume depletion. Haematocrit and plasma specificgravity rise with haemoconcentration. Hypoglycaemiamay occur in young children and may be associated withconvulsions. Loss of bicarbonate causes acidosis. There isprerenal uraemia. Colicky abdominal pain and slight feverare features of infection with the serotype 0.139.There is a considerable range in the severity of diarrhoeain cholera, particularly the El Tor biotype, which is thecause of many mild cases.Diagnosis Severe diarrhoea causing rapid progression to dehydrationsuggests that cholera is the cause in severe cases. Mildercases will not be diagnosed unless a stool is cultured orimmediate dark-ground microscopy of a fresh faecal smearshows the characteristic morphology of V. cholerae.Differential diagnosis All the acute infective causes of diarrhoea need to be considered,including ingestion of staphylococcal enterotoxin,invasive bacteria such as Salmonella, Shigella and Campylobacter,which are usually readily distinguished because ofthe presence of systemic upset and colicky abdominal pain,and enterotoxigenic strains of E. coli. Rotavirus infectionmay also be difficult to distinguish from cholera.ManagementMild to moderate dehydration can be managed with oralrehydration solution (ORS) , but patients withsevere dehydration need intravenous infusions, e.g.Ringer's lactate, to restore blood volume. The aims ofrehydration are:• To replace estimated fluid losses in the first 4 hours afterpresentation;• To replace continuing intestinal fluid losses with equalvolumes until diarrhoea stops.Frequent small amounts of ORS are better tolerated thanless frequent large volumes, especially if the patient isvomiting. Additional fluid, such as water, fruit juice, teaor breast milk, but not ORS, should be given to allow forinsensible losses and obligatory urinary losses. The glucosein ORS is not sufficient to counter hypoglycaemia and soextra sugar should be given orally.A solution prepared using rice flour as the source ofglucose is capable of reducing faecal fluid losses byproducing net absorption of sodium, glucose and waterfrom the gut.Bowel sedatives merely paralyse smooth muscle, leavingfluid containing organisms and the toxin in the intestinallumen, and should not be used in management. Tetracycline,250 mg four times daily for 3-5 days, will reduce the duration of both diarrhoea and faecal excretion ofVibrio cholerae. In pregnancy and childhood ampicillinor furazolidone may be given. Co-trimoxazole is alsoeffective.Prevention and control Adequate clean water supplies and the safe disposal offaecal waste would do much to prevent the occurrence ofcholera. Concurrent education of the population about therelationship between infective diarrhoeal disease andpersonal and general sanitation practices is essential. Thewidespread use of ORS early in the course of all diarrhoealillness reduces mortality.Vaccination with the current killed vaccine is of nobenefit, either for prophylaxis in the traveller or for thecontrol of epidemics.
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