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Friday, July 10, 2009

Identification from stool culture can be confirmed by latex agglutination with specific antiserum

elderly. Diag. - Identification from stool culture can be confirmed by latex agglutination with specific antiserum. Tr - Fluid replacement. Ciprofloxacin if severe or prolonged disease for adults, ampicillin or co-trimoxsazole for children Vibrio cholerae -the causative organism of cholerae, is a short, curved motile Gram-negative bacillus. The major pathogenic strain possesses a somatic antigen (01) with two biotypes - classical El Tor. More recently, a strain with somatic antigen 0139, the Bengal strain has appeared. Pathogenesis - The major factor distinguishing 01 and 0139 serotypes from other 'non-cholera' vibrios is the ability to produce an enterotoxin. This consists of a ring of five 'B'subunits around a central 'A' unit. This pentameric ring structure binds to GM1 ganglioside on the enterocyte cell membrane and the A subunit stimulates enterocyte adenylate cyclase, leading to conspicuous secretion of small intestinal fluid and ultimately diarrhoea. Cl. Fs. - (a) Stage of evacuation - Sudden onset with frequent loose stools, first yellow soon become colourless, watery and copious with flakes of mucus (rice water stools). Copious and incessant watery vomit. Subnormal temperature. (b) Stage of collapse - Depletion of water and salts occurs rapidly, leading to severe dehydration and hypovolemic shock, and ultimately to death. Diag - is mainly clinical. The organism can be grown from stool either directly or after alkaline enrichment. Tr - (a) Fluid and electrolyte replacement: Mild case - Oral rehydration therapy with glucose-electrolyte solution. Constituents (g/litre): Sodium chloide 3.5 Sodium bicarbonate 2.5 Potassium chloride 1.5 Glucose 20 Other solutions containing glucose polymers (e. g. rice water) and electrolytes are highly effective Severe case -IV fluids. Rate of infusion determined by skin tugor, whether eyes are sunken, pulse volume, auscultation of lung bases, measurement of urinary output. Antibiotics, - shortern duration of diarrhoea. Tetracycline 100 mg. i. v. q6h for 24 hrs, then 500 mg p.o. for 3 days. Amoxycillin preferred in pregnant women. Doxycycline 300 mg single dose for contacts Immunization-Vaccine containing suspension of 8000 organisms/ml, 0.5 ml followed after 7 days by 1 ml. Clostridium difficile - is a Gram-positive, anaerobic spore-forming bacillus, and produces a syndrome ranging from a mild diarrhoea to pseudomembranous colitis and is often associated with antibiotic use (broad-spectrum cephalosporins and penicillin) Cl. Fs. - Symptoms usually begin 4-9 days after starting antibiotic therapy to 6 weeks after finishing. Profuse watery diarrhoea, abdominal tenderness, fever and leucocytosis indicate probable colitis. The condition can progress to toxic megacolon and ultimately colonic perforation and death. Diag - (a) Colonoscopy. yellow-white plaques of fibrin, mucus and epithelial cells. (b) Detection of cytotoxin in faecal filtrate applied to fibroblasts in tissue culture The cytotoxic effect is inhibited by C. sordelli-specific antitoxin. Tr - Stoppage of antibiotics. If severe colitis or if antibiotic needs to be continued, specific therapy with oral vancomycin or metronidazole Cholestyramine and ion exchange resins which bind the toxins are alternatives. 5. TYPHOID FEVER Epidemiology - Causative organism - Gram negative bacillus Salmonella typhi a human pathogen which depends on man-to-man transfer for continued existence, and can survive for many weeks in sewage. Transmission - S typhi is present in stools anc urine during the acute illness, but the chronic asymptomatic carrier is mainly responsible for persistence of the disease. Prolonged carrier states are usually due to biliary infection, but an infected pelvis of the kidney can also retain the infection. Contamination of drinking water by sewage has been responsible for epidemic disease. Milk is a rare cause of epidemic spread. Contamination of food may occur from flies, or rarely during growing of crops if there is use of human excreta as fertiliser for 'nightsoil PATHOGENESIS - After penetrating the intestinal mucosa the organisms multiply silently in the reticuloendothelial tissues until, at the end of the incubation period, invasion of blood stream marks the onset of clinical illness Secondary invasion of the intestine, via the liver and biliary passages multiply rapidly and re-enter the intestinal tract Incubation period - 10-15 days. Clinical Features - 1 Invasion. (1st week) - (a) Onset - insidious. Lassitude, frontal headache, bodyache, anorexia, abdominal discomfort (bi) Gl system -Tongue coated with raw tips and edges (typhoid V tongue). Abdomen becomes distended and uncomfortable. Initially there may be either diarrhoea or constipation, but by the end of the week there is usually diarrhoea (pea soup stools). (c) Fever - May show step-ladder rise, higher in evening At end of 1st week it usually reaches, 39.5°C (103°F).Shivering attacks may occur. (d) Signs of bronchitis common Epistaxis may occur. (e) Pulse-At times relative bradycardia and dicrotic pulse. 2. Advance (2nd week) - if untreated (a) General state - Listlessness and apathy, no headache, prostration. (b) Abdomen - (a) Spleen becomes palpable at end of first week Soft and at times tender. (b) Increased abdominal distension and discomfort. Pulse rate quickens B. P. tends to fall. Usually there is diarrhoea. (c) Temperature - high, with slight morning remissions. (d) Rash - Rose spots on 7th to 10th, day Usually

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