CHOLERA AND BACILLARY DYSENTERY Year 4 Internal Medicine

CHOLERA AND BACILLARY DYSENTERY Year 4 · Internal Medicine Collection: 4TH YEAR ALL NOTES / IMED / IMED 4.1 / ALEX -- Slide 1 CHOLERA/BACILLARY DYSENTRY Dr. Alex Mogere Consultant physician Slide 3 CHOLERA Infection in the small intestine caused by Vibrio cholerae. Gram negative, comma shaped bacillus. Aerobic,or facultative anaerobic bacillus Several strains do exist, commonest being Vibrio cholerae O1 and O139(serogroups) Serotype O1 – 2 biotypes (classical and El Tor) Each biotype classified as( Inaba or Ogawa) El Tor now more,common mild illness, more carriers V cholerae is a saltwater organism Other types e.g. V.parahemolyticus Slide 4 Epidemiology Affects 3-5 million people world wide; 100 to 150,000 deaths per year. Remains an epidemic and endemic in many areas of the world (Developing) Slide 5 History Probably originated from Indian sub continent(Ganges ),\nReported in Ganges delta since ancient times. Russia -1817, Europe, and then Africa with the arrival of Europeans and other traders in 10 th century. Seven pandemics, seventh1961reached Africa 1971, Americas 1991 Slide 6 Pathophysiology Its antigenic structure consists of: Flagellar H antigen Somatic O antigen Slide 7 Pathophysiology Slide 8 Virulence /pathogenicity Ingestion of V. cholera Resistant to gastric acid Colonize the small intestine Virulence of non toxigenic v.cholera 01 strain not well understood Slide 9 Cont virulence/pathogenicity Secrete enterotoxin Enterotoxin binds to intestinal cells\nChloride channels activated Release large quantities of electrolytes & HCO3-s Fluid hypersecretion Diarrhoea dehydration Slide 10 Risk Factors More than 100 million bacteria to cause cholera in normal adults.\nIncreased incidence;\nin low gastric acid states.\nChildren especially below 5 years.\nBlood group type O.(AB relative protection)(O B A AB).\nPeople with low immunity eg HIV or malnourished children Slide 11 Cont. risks Poor sanitary conditions-developing world Raw or undercooked food-contaminated sea food,esp shell fish Hypochlorhydria-low levels of gastric acid eg in children,older adults,some meds Slide 12 Selective advantage Cystic fibrosis gene (heterozygous carriers) Slide 13 Transmission Feco-oral spread Humans the only reservoir Contaminated food or water Lack of proper sanitation - in the developing world Africa, Asia, S.America etc Overcrowding eg refugee camps, pilgrims, slums but can occur in any environment. Eating sea food (shell fish and plankton) – in the West Others Slide 14 Incubation period Few Hours to 5 days after ingestion of the bacteria Average is 1-3 days Shorter incubation period: -High gastric pH(from antacid use) -Consumption of high inoculum of cholera For every infected person, 3-100 people do not develop disease. Slide 15 Infectious dose Water,the infectious dose is 1000-1000000 Ingested with food,fewer organisms 100-10000 Slide 16 Period of communicability During acute stage A few days after recovery By end of week, 70% of pts non infectious By end of 3rd week,98 %non-infectious Slide 17 Symptoms Sudden onset of profuse painless diarrhea and vomiting (10-20 litres of water per day) Rice water stools with fishy odour Vomiting Cramps w/o tx,death in 18 hrs-several days Slide 18 Signs Severe dehydration Kidney failure\nOther organ failure Slide 19 Pathogenesis Ingestion of bacteria - mostly killed by stomach acid Surviving bacteria – stop activity while passing through stomach In small intestine, they penetrate mucus to the intestinal wall Vibrio cholerae produce toxins which give infected person watery diarrhea Slide 20 Cholera toxin Made up of 6 sub units 1 type A sub unit ( A1 &A2) 5 type B sub units A1 A2 B B B B B B s s Slide 21 MECHANISM Cholera toxin has 5B subunits surrounding A subunit A subunit cleaved into A1 A2 segments. B subunits binds ganglioside receptors on intestinal epithelial cells. This leads to internalisation of the A subunit Slide 22 In the Cell The A1 A2 subunits separate A1 stimulates ADP breakdown increasing production cAMP Increased cAMP change Na/Cl flux across the cell membrane Chloride flux followed by massive outflow of water and electrolytes from the cell Leading to profuse (secretory) diarrhea. Slide 23 Diagnosis History Clinical picture Specimens: fresh stools and swab samples Rapid dip stick test determines presence of V. cholera Culture and sensitivity (antibiotic) Slide 24 Other lab findings Deranged rfts-\nHigh hematocrit & wbc due to hemoconcentration Metabolic acidosis with wide –anion gap Total body K+ is depleted,but serum level may be normal due to effect of acidosis Slide 25 Enrichment media Alkaline peptone water at PH 8.6 Monsur’s taurocholate tellurite peptone water at PH 9.2 Slide 26 Plating media Alkaline bile salt agar (BSA) Monsur’s gelatin tauro cholate trypticase tellurite agar (GTTA) medium: TCBS medium: This is the mostly widely used medium; it contains thiosulphate, citrate, bile salts and sucrose. Cholera vibrios produce flat, 2-3 mm diameter, yellow-nucl