Cholera El Tor

I.      Definition

An acute bacterial enteric disease of the GIT characterized by profuse diarrhea, vomiting, massive loss of fluid and electrolyte and could result to hypovolemic shock, acidosis and death. The intestinal infection is caused by the bacterium Vibrio cholera serogroups 01 and 0139 in the family Vibrionaceae. Serogroup 01 V. cholerae is subdivided into three serotypes based on specific antigens in the O antigen: Ogawa, Inaba and Hikojima.

Cholera has been a devastating disease for centuries. It is estimated to have 3-5million cholera cases and 100,000-120,000 death caused by cholera in the world annually. Cases mostly occur in Asia and Africa where it has been endemic. The infection is also called as Asiatic Cholera and Epidemic Cholera.

II.     Morphological Description

     Vibrio cholerae/ Vibrio coma – “comma” shaped gram-negative bacteria with a single, polar flagellum. Vibrios are facultative anaerobes that ferment and grow on ordinary or selective media containing bile at 37˚C (22-40˚C). They possess unique O and H antigens and membrane receptor antigens that provide some basis for classifying members of the family. There are two major biotypes, called classic and El tor.

III.   Pathogenesis

  

1.Fluid loss is attributed to the enterotoxin elaborated by the organism as they lie within the lining of the cells of the intestines

2.The toxin stimulates adenylate cyclase, which results in the conversion of ATP to cAMP

3.The mucosal cell is stimulated to increase secretion of chloride, with water and HCO₃ loss.

4.The toxin acts upon the intact epithelium on the vasculator of the bowel, thus, resulting in outpouring of intestinal fluids.

5.Fluid loss of 5-10% of the body wt. resulting in dehydration and metabolic acidosis.

6.If the treatment is delayed, acute renal failure and hypokalemia become secondary problems.

7.Death can occur from hypovolemic shock, metabolic acidosis, and uremia resulting from acute tubular necrosis.

IV.     Mode of Transmission

·         Ingestion of contaminated food, milk or water

·         Vibrio associated with certain plankton, chitinous shelled animals and vegetation is also crucial for its long term survival

·         Raw fish

·         Flies, soiled hands and utensils also serve to transmit infection

·         Contaminated food at room temperature supports the growth of the bacterium

V.      Signs and Symptoms

     After an incubation period of a few hours-days, symptoms begin abruptly with nausea vomiting, followed by a profuse painless diarrhea that is described as “rice-water” stool in nature called secretory diarrhea or rice-watery diarrhea. The intestinal contents are lost very quickly, leaving only secreted fluids. Fluid losses or nearly 1 liter per hour have been reported in severe cases. The diarrhea causes loss of blood volume, acidosis from HCO₃ loss, and potassium depletion, which manifest in muscle cramps, severe thirst, flaccid skin, sunken eyes and in young children, coma and convulsions. In case of cholera gravis, there is a rapid loss of body fluids of 6 liters per hour containing 10⁷ vibrios/mL and has sunken eyes. Secondary circulatory consequences can include hypotension, tachycardia, cyanosis, and collapse from shock within 18-24 hrs. If cholera is left untreated, death can occur in less than 48 hrs, and the mortality rate approaches 55%.

VI.     Diagnosis

      V. cholerae can be readily isolated and identified in the laboratory from stool samples. Direct dark-field microscopic observation reveals the bacterium in groups of similar to “schools of fish” and its serotype is determined by immobilization with Inaba or Ogawa specific anti-serum. Best selective medium is TCBS(Thiosulfate-citrate-bile salts-sucrose agar) on which the organisms grow as a typical opaque yellow colonies.

"schools of fish"

VII.   Period of Communicability

    

      People are infectious during the stool positive stage for a few days after recovery. By the end of the first week, 70% of patients are non-infectious. While at the end of third week, 98% are non-infectious. Carrier state may persist for months and chronic biliary infection with intermittent shedding of organisms may last for years.

VIII. Incubation Period

      Two hours to five days after the ingestion of the bacteria with an average of 2-3 days.

IX.     Prognosis

      The infection manifests a 50-60% mortality rate for untreated cholera. While if properly treated, no patient should die of cholera, but if treatment is delayed or is given too slowly, case fatality rates exceed at 5%

X.      Prevention and Treatment

     Effective prevention is contingent upon proper sewage treatment and water purification. Detecting and treating carriers with mild or asymptomatic cholera are serious goals, but they are difficult to accomplish because of inadequate medical provisions in those countries where cholera is endemic. Control measures include sterilization of water and pasteurization of milk. Seafoods must be thoroughly cooked and vegetables and fruits should be washed before consumption. Washing of hands is the fundamental way of preventing the infection.

     Vaccines are available which contains a sterile suspension of killed Vibrio cholerae of the Inaba and Ogawa strains in NSS or suitable diluents. It contains 8 billion v. cholera per mL and preserved by addition of 0.5% phenol. But it only protects for only 6 months or less. E For infants, passive immunity is feasible through ingestion of breast milk. ORS solution should be considered as the first treatment if the patient is vomiting for rapid replacement of fluids to correct dehydration. Drug of choice is doxycycline for sensitive strains. Other clinically effective antibiotics include tetracycline, cotrimoxazole, chloramphenicol, flurazolidone, erythromycin, azithromycin and ciprofloxacin.