Cholera, caused by Vibrio cholerae serotype O1, is the archetypal toxin-mediated bacterial cause of acute watery diarrhoea. The enterotoxin activates adenylate cyclase in the intestinal epithelium, inducing net secretion of chloride and water. V. cholerae O1 has two biotypes, classical and El Tor, and each of these has two distinct serotypes, Inaba and Ogawa. Following its origin in the Ganges valley, devastating epidemics have occurred, often in association with large religious festivals, and pandemics have spread worldwide. The seventh pandemic, due to the El Tor biotype, began in 1961 and spread via the Middle East to become endemic in Africa. In 1990, it reached Peru and spread throughout South and Central America. Since 2005, numbers of cases of cholera have been increasing. There are recurrent outbreaks and epidemics in Africa, often related to flooding. El Tor is more resistant to commonly used antimicrobials than classical Vibrio, and causes prolonged carriage in 5% of infections. A new classical toxigenic strain, serotype O139, established itself in Bangladesh in 1992 and started a new pandemic. Infection spreads via the stools or vomit of symptomatic patients or of the much larger number of subclinical cases. Organisms survive for up to 2 weeks in fresh water and 8 weeks in salt water. Transmission is normally through infected drinking water, shellfish and food contaminated by flies, or on the hands of carriers.
Severe diarrhoea without pain or colic begins suddenly and is followed by vomiting. Following the evacuation of normal gut faecal contents, typical ‘rice water’ material is passed, consisting of clear fluid with flecks of mucus. Classical cholera produces enormous loss of fluid and electrolytes, leading to intense dehydration with muscular cramps. Shock and oliguria develop but mental clarity remains. Death from acute circulatory failure may occur rapidly unless fluid and electrolytes are replaced. Improvement is rapid with proper treatment. The majority of infections, however, cause mild illness with slight diarrhoea. Occasionally, a very intense illness, ‘cholera sicca’, occurs, with loss of fluid into dilated bowel, killing the patient before typical gastrointestinal symptoms appear. The disease is more dangerous in children.
Diagnosis and management
Clinical diagnosis is easy during an epidemic. Otherwise, the diagnosis should be confirmed bacteriologically. Stool dark-field microscopy shows the typical ‘shooting star’ motility of V. cholerae. Rectal swab or stool cultures allow identification. Cholera is notifiable under international health regulations. Maintenance of circulation by replacement of water and electrolytes is paramount (p. 307). Ringer-Lactate is the best fluid for intravenous replacement. Vomiting usually stops once the patient is rehydrated, and fluid should then be given orally up to 500 mL hourly. Early intervention with oral rehydration solutions that include resistant starch, based on either rice or cereal, shortens the duration of diarrhoea and improves prognosis. Total fluid requirements may exceed 50 L over a period of 2–5 days. Accurate records are greatly facilitated by the use of a ‘cholera cot’, which has a reinforced hole under the patient’s buttocks, beneath which a graded bucket is placed. Three days treatment with tetracycline 250 mg 4 times daily, a single dose of doxycycline 300 mg or ciprofloxacin 1 g in adults reduces the duration of excretion of V. cholerae and the total volume of fluid needed for replacement.