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Cholera and other Vibrio Infections

Cholera and other Vibrio Infections. Sung Chul Hwang, M.D. Dept. of Pulmonary and Critical Care Medicine Ajou University School of Medicine. Vibrios. Coma shaped gram negative rods with flagella The most common organism in the surface water in the world Halophilic organism

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Cholera and other Vibrio Infections

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  1. Cholera and other Vibrio Infections Sung Chul Hwang, M.D. Dept. of Pulmonary and Critical Care Medicine Ajou University School of Medicine

  2. Vibrios • Coma shaped gram negative rods with flagella • The most common organism in the surface water in the world • Halophilic organism • Grows well in alkaline media • Main pathogens are cholerae , parahemolyticus, vulnificus

  3. Cholera • Acute diarrheal disease caused by enterotoxin from V. cholerae in small intestine • Epidemic or endemic in occurrence : South & Central America, Africa, Southeast Asia, Middle East • May produce massive GI fluid loss acidosis & shock

  4. Etiology • Short , slightly curved, sausage shaped gram negative rod • Rapidly motile with the use of polar flagellum • More than 140 serotypes determined by O Ag on cell surface LPS • Only Serotype O1 and O139 are responsible for the epidemic cholera • Other non-O1 strains cause sporadic cases

  5. Microbiology • V. cholerae is divideed into two biotypes, Classical and El Tor based on on biochemical traits and susceptibility to specific phages • Both are subdivided into ogawa( A, B), inaba(A,C), Hikojima (A,B, C) • Major virulence factor for O1 and O 139 serotype is cholera toxin, multimeric protein with one A subunit and 5 B subunits. (ADP ribosylation factor)

  6. Pathogenesis • Ingestion of viable organisms : 10 11 • Attach to mucosa by the pili(TCP) • Production of enterotoxin(CTX): • (A1~A2)+ (5 B): ADP Ribosylation • CTX stimulates adenyl cyclase in intestinal epithelial cells • Increase in cAMP • Secretion of isotonic fluids

  7. Clinical Features • Increase in peristalsis ( 1st Sx) • Abd. Fullness • Loose stool • “ Rice water ” appearance • Hypotensive within hours • Death within 18 hours to several days

  8. Composition of Cholera Stool

  9. Diagnosis • History of acute onset with watery diarrhea in the absence of fever or abdominal cramp • Darkfield or phase contrast microscopy : most effective and rapid diagnostic test • Cultures from stool or rectal swab (Gelatin, Meat extract, MacConkey, TCBS, Monsur)

  10. V. Cholerae on TCBS Yellow Smooth Opaque

  11. Complications • Altered consciousness or convulsions : especially due to hypoglycemia in children • Electrolyte imbalance : Hypokalemia ( in children) • Renal failure • Aspiration in depressed consciousness and vomiting

  12. Treatment (1) Water and salt replacement • 1) oral replacement in most cases – three finger pinch of salts plus handful scoop of sugar, in half liter or one pint of drinking water • 2) Intravenous replacement therapy – in severe cases, when the volume exceeds 100 l/kg/24hours or 7 L/day in 70 kg person

  13. Treatment (2) • Antibiotics  Shortens the duration of diarrhea and reduce fluid loss • Tetracycline : Drug of choice 250 mg q 6 hrs or others such as Ampicillin, CM, TMP/SFX, Doxycycline

  14. Prophylaxis • Cholera vaccines : 50% effective Primary immunization Booster immunization • Antibiotics : prevents transmission in close contacts tetracycline or CM • Improve standard of living , public health, and sanitation

  15. Oral Rehydration Solution (ORS) • 3.5 g Sodium Chloride • 2.9 g Trisodium Citrate or 2.5 g Sodium Bicarbonate • 1.5 g Potassium Chloride • 20 g Glucose or 40 g Sucrose

  16. Mortality • 50 to 70 % in untreated patients • Children mortality is higher ( ten times) • Pregnant woman : 50 % chance of fetal death during third trimester • Death may happen in 2-3 hours of illness but usually after 18hours to several days

  17. Vibrio parahemolyticus • Major cause of acute diarrheal disease in Japan and Korea • Ingestion of contaminated sea food • Production of enterotoxin and inflammation in small bowel mucosa • Incubation : 23 hrs ( 5 to 92 hrs)

  18. Symptoms and Signs • Acute onset of explosive diarrhea • Abdominal pain, low grade fever, mild chills, headache, vomiting, and electrolyte loss • Very high attack rate

  19. Lab Findings • Diarrheal fluid : Watery, sometimes mucoid, less often bloody ( < 15%) with a few leukocytes 10 – 20 WBCs/HPF) • Stool Culture : TCBS agar • Positive Kanagawa test :b- hemolysis

  20. Clinical Course • Self limited • Mortality : rare • Prevention : Adequately cooking sea food

  21. Vibrio vulnificus • “ vulnificus ” means “wound making” • Gram negative rod in Vibrio family • Causes serious wound infections and septicemia • First identified in 1970s • Common in those with liver disease or chronic illnesses such as DM

  22. Microbiology • Gram negative curved rods with a polar flagellum • Grows well in Salt water : Halophilic vibrio • Epidemic when the temperature of the sea water rises • Exponential growth in the presence of free Iron , tranferrin saturation above 70% • Reason for infecting Liver cirrhosis, splenectomy, hemochromatosis, ESRD

  23. Clinical Types of V. vulnificus Infection • Localized wound infection – cellulitis • Acute gastroenteritis • Septicemia with bullae and gangrene

  24. Predisposing Conditions • Chronic Liver Diseases : Liver cirrhosis, chronic hepatitis • Alcohol abuse • Hemochromatosis • Gastrectomy • Splenectomy • Immune suppressive therapy • DM, RA, Leukemia, Lymphoma • TBC, ESRD

  25. Contaminated foods • 조개 • 홍합 • 맛살 • 산낙지 • 생굴

  26. Clinical Features in Septicemia • Incubation Period : 3 – 14 days • Invasion to blood stream through gut mucosa  abrupt onset of fever, chills, hypotension metastatic cutaneous lesion  Bacteremia DIC  Shock • GI bleeding • High mortality rate

  27. Clinical Features in Healthy Wound Infections Open wound contaminations  Intense cellulitis  necrotizing vasculitis  ulcer formation  occasional bacteremia

  28. Treatment • Antibiotics : Tetracycline or ciprofloxacin • Supportive care for the Sepsis • Early Surgical debridement and wide excision with skin graft • Prevention : avoid eating raw fish

  29. Non-O1 V. cholerae • Diarrheal illness from severe watery diarrhea to milder traveller’s diarrhea • May produce enterotoxin • Small numbers of leukocytes and RBCs in stool • Stool culture on TCBS agar • Usually no treatment required

  30. V. vulnificus in blood agar

  31. Antibiotics for Cholera

  32. Hemorrhagic Bullae

  33. Necrotic Bullae & Gangrene

  34. Pathology of the Bullae

  35. Traveler’s Diarrhea

  36. Vibriobacilli

  37. Vibrio vulnificus

  38. Vibrio

  39. Vesicles of V. vulnificus Infection

  40. Vesicles of V. vulnificus Infection

  41. Erythema of the V. vulnificus infection

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