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Cholera
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Cholera Presentation Transcript

  • 1. CHOLERACHOLERA Ranjit PandeyRanjit Pandey PharmacistPharmacist ranjitpandey17@gmail.comranjitpandey17@gmail.com
  • 2. Points to discussPoints to discuss  HistoryHistory  BacteriaBacteria  Person to person spreadPerson to person spread  CarriersCarriers  PathogenesisPathogenesis  Clinical featuresClinical features  TherapyTherapy  RecoveryRecovery  PreventionPrevention
  • 3. HistoryHistory  1919thth century: great epidemiologicalcentury: great epidemiological controversy- contagiousness vs. non-controversy- contagiousness vs. non- contagiousness.contagiousness.  1885- John Snow’s monograph- “turn off1885- John Snow’s monograph- “turn off the taps”the taps”  1883- Robert Koch isolates V. cholerae1883- Robert Koch isolates V. cholerae  1894- fulfillment of Koch’s third postulate1894- fulfillment of Koch’s third postulate  1992- discovery of 0139 serotype1992- discovery of 0139 serotype
  • 4. Map of London by John SnowMap of London by John Snow
  • 5. The global spread of cholera during the seventh pandemic, 1961-The global spread of cholera during the seventh pandemic, 1961- 1971. (CDC)1971. (CDC)
  • 6. EpidemiologyEpidemiology
  • 7. The BacteriaThe Bacteria  Vibrios are Gram-negative, highly motile curved rodsVibrios are Gram-negative, highly motile curved rods with a single polar flagellum.with a single polar flagellum.  Classified on the basis of their liposachharide (LPS) OClassified on the basis of their liposachharide (LPS) O antigens.antigens.  155 serotypes now recognized.155 serotypes now recognized.  Until 1992, the vibrios that caused epidemic choleraUntil 1992, the vibrios that caused epidemic cholera were subdivided into two biotypes: classical and El Tor.were subdivided into two biotypes: classical and El Tor.  Classical V cholerae was first isolated by Koch in 1883.Classical V cholerae was first isolated by Koch in 1883. Subsequently, in the early 1900s, some vibriosSubsequently, in the early 1900s, some vibrios resembling V cholerae were isolated from Mecca-boundresembling V cholerae were isolated from Mecca-bound pilgrims at the quarantine station at El Tor, in the Sinaipilgrims at the quarantine station at El Tor, in the Sinai peninsula, that had been established to try to controlpeninsula, that had been established to try to control cholera associated with pilgrimages to Mecca.cholera associated with pilgrimages to Mecca.
  • 8. Vibrio cholerae O1 antigensVibrio cholerae O1 antigens
  • 9. The BacteriaThe Bacteria
  • 10. The BacteriaThe Bacteria  Most El Tor vibrios are Voges-Proskauer positive andMost El Tor vibrios are Voges-Proskauer positive and resistant to polymyxin and to bacteriophage IV, whereasresistant to polymyxin and to bacteriophage IV, whereas classical vibrios are sensitive to them. As both biotypesclassical vibrios are sensitive to them. As both biotypes cause the same disease, these characteristics have onlycause the same disease, these characteristics have only epidemiologic significance.epidemiologic significance.  In 1992, cholera caused by serogroup O139 (synonymIn 1992, cholera caused by serogroup O139 (synonym "Bengal"; the 139th and latest serogroup of V cholerae to"Bengal"; the 139th and latest serogroup of V cholerae to be identified) emerged in epidemic proportions in Indiabe identified) emerged in epidemic proportions in India and Bangladesh.and Bangladesh.  This serovar is identified by 1) absence of agglutinationThis serovar is identified by 1) absence of agglutination in O group 1 specific antiserum; 2) by agglutination in Oin O group 1 specific antiserum; 2) by agglutination in O group 139 specific antiserum; and 3) by the presence ofgroup 139 specific antiserum; and 3) by the presence of a capsule.a capsule.
  • 11. The BacteriaThe Bacteria  Not much resistance to heat or dryingNot much resistance to heat or drying  Can withstand freezing. At 0Can withstand freezing. At 0°C, survives for several°C, survives for several weeks.weeks.  Clean tap water: survives 30 days.Clean tap water: survives 30 days.  Easily destroyed by chemicals e.g. phenol, chlorine.Easily destroyed by chemicals e.g. phenol, chlorine.  Lives in warm salty water, roots of plants, undercookedLives in warm salty water, roots of plants, undercooked shell fish.shell fish.  Man- only known host- contaminates environment.Man- only known host- contaminates environment.  Acute stage disease:- 10Acute stage disease:- 107 -10-109 V. cholerae/cc of stool.V. cholerae/cc of stool.  Asymptomatic person:- 100- 100000 V. choleraeAsymptomatic person:- 100- 100000 V. cholerae per gram of stoolper gram of stool
  • 12. The BacteriaThe Bacteria  Period of excretion:Period of excretion: By end of first weekBy end of first week- 70% no longer- 70% no longer excreted.excreted. By end of second weekBy end of second week- 90% no longer- 90% no longer excreted.excreted. By end of third week-By end of third week- 98% no longer98% no longer excreted.excreted.
  • 13. Person to person spreadPerson to person spread  Inoculums required to cause disease- highInoculums required to cause disease- high ingestion of 10ingestion of 106 inoculums- 70 to 80% becomeinoculums- 70 to 80% become diseased.diseased.  El Tor or 0139 does not spread readily.El Tor or 0139 does not spread readily.  Hut or primitive habitation- 5% household mayHut or primitive habitation- 5% household may get infected; others- 4 to 20%.get infected; others- 4 to 20%.  Aquatic reservoir more important.Aquatic reservoir more important.  Asymptomatic carriers important in introducingAsymptomatic carriers important in introducing cholera into non-endemic areas.cholera into non-endemic areas.  Ratio of asymptomatic: symptomatic infectionsRatio of asymptomatic: symptomatic infections El Tor- 5:1El Tor- 5:1 Classical- 25:1 to 100:1
  • 14. CarriersCarriers  Incubatory: 1-5 daysIncubatory: 1-5 days  Convalescent: 2-3 weeksConvalescent: 2-3 weeks  Asymptomatic carriers: 5-20%Asymptomatic carriers: 5-20%  Chronic: only one authenticated case.Chronic: only one authenticated case.
  • 15. PathogenesisPathogenesis  Cholera is transmitted by the fecal-oral route.Cholera is transmitted by the fecal-oral route.  Vibrios are sensitive to acid, and most die in theVibrios are sensitive to acid, and most die in the stomach. Acid forms a formidable barrier.stomach. Acid forms a formidable barrier.  Surviving virulent organisms adhere to and colonizeSurviving virulent organisms adhere to and colonize the small bowel(duodenum & jejunum), where theythe small bowel(duodenum & jejunum), where they secrete the potent cholera enterotoxin (CT, also calledsecrete the potent cholera enterotoxin (CT, also called "choleragen"). CT consists of two sub-units A & B."choleragen"). CT consists of two sub-units A & B.  Mucosa not destroyed, a few inflammatory cells inMucosa not destroyed, a few inflammatory cells in lamina proprialamina propria  Fluid loss is isotonic with plasmaFluid loss is isotonic with plasma  Some impairment of jejunal disachharidases, butSome impairment of jejunal disachharidases, but glucose absorption is preserved.glucose absorption is preserved.
  • 16. Cholera toxin(CTX)Cholera toxin(CTX)  This toxin binds to the plasma membrane ofThis toxin binds to the plasma membrane of intestinal epithelial cells and releases anintestinal epithelial cells and releases an enzymatically active subunit –A, that causes aenzymatically active subunit –A, that causes a rise in cyclic adenosine 5,1-monophosphaterise in cyclic adenosine 5,1-monophosphate (cAMP) production.(cAMP) production.  The resulting high intracellular cAMP levelThe resulting high intracellular cAMP level causes massive secretion of electrolytes(causes massive secretion of electrolytes(↓active↓active absorption of Na & Cl and ↑active secretion ofabsorption of Na & Cl and ↑active secretion of Cl)Cl) and water into the intestinal lumen.and water into the intestinal lumen.
  • 17. OTHER TOXINSOTHER TOXINS 1.1. Zonula occludens toxin (ZOT)-Zonula occludens toxin (ZOT)- decreases strand complexity of ZO and causesdecreases strand complexity of ZO and causes leak back of already absorbed water &leak back of already absorbed water & electrolytes into the lumen.electrolytes into the lumen. 2.2. Accessory cholera enterotoxin(ACE)Accessory cholera enterotoxin(ACE)  Virulence cassette of Vibrio cholerae-term usedterm used for all the mechanisms operating infor all the mechanisms operating in pathogenesis of cholera.pathogenesis of cholera.
  • 18. Clinical featuresClinical features  Incubation period of 6 to 48 hoursIncubation period of 6 to 48 hours  Abrupt onset of watery diarrheaAbrupt onset of watery diarrhea  The initial stool may exceed 1 L, and several liters of fluidThe initial stool may exceed 1 L, and several liters of fluid may be secreted within hours, leading to hypovolemic shockmay be secreted within hours, leading to hypovolemic shock  Vomiting usually accompanies the diarrheal episodesVomiting usually accompanies the diarrheal episodes  Muscle crampsMuscle cramps  Loss of skin turgor, scaphoid abdomen, and weak pulse areLoss of skin turgor, scaphoid abdomen, and weak pulse are characteristic of cholera.characteristic of cholera.  Various degrees of fluid and electrolyte loss are observed.Various degrees of fluid and electrolyte loss are observed.  The disease runs its course in 2 to 7 daysThe disease runs its course in 2 to 7 days  The outcome depends upon the extent of water andThe outcome depends upon the extent of water and electrolyte loss and the adequacy of water and electrolyteelectrolyte loss and the adequacy of water and electrolyte repletion therapy.repletion therapy.
  • 19. Clinical featuresClinical features
  • 20. Metabolic & systemic manifestationsMetabolic & systemic manifestations 1.1. Severe dehydrationSevere dehydration 2.2. Hypoglycemia (mortality up to 15%) due toHypoglycemia (mortality up to 15%) due to ↓food↓food intake, exhaustion of glycogen storage & defectiveintake, exhaustion of glycogen storage & defective gluconeogenesis.gluconeogenesis. 3.3. Acidosis due to loss of bicarbonate inAcidosis due to loss of bicarbonate in stools;accumulation of lactate due to decreasedstools;accumulation of lactate due to decreased perfusion of peripheral tissues & hyperphosphatemia.perfusion of peripheral tissues & hyperphosphatemia. 4.4. Hypokalemia-initial K normal, decreased whenHypokalemia-initial K normal, decreased when acidosis corrected. Most severe in malnourished.acidosis corrected. Most severe in malnourished. 5.5. Hypocalcemia- while rehydrating with fluidHypocalcemia- while rehydrating with fluid containing bicarbonatecontaining bicarbonate 6.6. Prerenal azotemia →renal failurePrerenal azotemia →renal failure 7.7. HypothermiaHypothermia 8.8. Leucocytosis- stress response rather thanLeucocytosis- stress response rather than inflammatory.inflammatory.
  • 21. Cholera stools Na mmol/L Cl mmol/L K mmol/L HCO3 mmol/L Osmolality mOsmol/L Adults 130 100 20 44 300 Children 100 90 33 30 300 Hydration solutions WHO ORS 90 80 20 30 220 Ringer lactate 130 109 4 28 251 DACCA 5/4/1 133 99 14 48 Normal plasma 136-145 95-105 3.8-5 24-32 280-300 •DACCA 5/4/1- 5 g NaCl, 4 g NaHCO3, 1 g KCl per litre •ORS- 5 g NaCl, 4 g NaHCO3, 1.5 g KCl, 20 g glucose
  • 22. FluidsFluids  IV Fluids- if purging more than 10 ml/kg/hrIV Fluids- if purging more than 10 ml/kg/hr  Oral- if purging less than 10 ml/kg/hrOral- if purging less than 10 ml/kg/hr
  • 23. THERAPYTHERAPY  AgentAgent DoxicyclineDoxicycline TetracyclineTetracycline FurazolidineFurazolidine CiprofloxacinCiprofloxacin  Co-trimoxazole, ampicillin,Co-trimoxazole, ampicillin, erythromycin: not evaluated inerythromycin: not evaluated in children.children. Single doseSingle dose 7 mg/kg, max:300 mg7 mg/kg, max:300 mg 25 mg/kg, max dose: 1 gm25 mg/kg, max dose: 1 gm 7 mg/kg, max:300 mg7 mg/kg, max:300 mg 30 mg/kg, max dose: 1 gm30 mg/kg, max dose: 1 gm Non-antimicrobial therapy: not useful
  • 24. RecoveryRecovery  Diarrhoea in cholera stops abruptly.Diarrhoea in cholera stops abruptly.  V. cholerae does not cause systemic infection andV. cholerae does not cause systemic infection and does not damage intestinal epitheliumdoes not damage intestinal epithelium  Recovery- not complicated by late sequelaeRecovery- not complicated by late sequelae  Malnutrition is not a major problemMalnutrition is not a major problem  Anorexia not persistentAnorexia not persistent  Intestinal enzyme activity remains intactIntestinal enzyme activity remains intact  Severely malnourished children- prolonged courseSeverely malnourished children- prolonged course of diseaseof disease