Prevention of cholera.

Sir—With modern air-travel, diseases such as influenza and severe acute respiratory syndrome (SARS) can spread across continents and oceans in days. Why, then, did the current (seventh) pandemic of cholera take 10 years to spread across Asia from Indonesia (1961) before causing widespread epidemics in Africa during the 1970s? Subsequently, a further two decades elapsed before Latin America was devastated in the 1990s by this same organism—a haemolysin-negative vibrio, similar to the classical biotype, but sharing properties with the El Tor strain.

In a Seminar on cholera (Jan 17, p 223), David Sack and colleague note, but do not comment on, this slow progression. Does the vibrio first need to colonise the environment (algae and crustaceans)? Sack and colleagues discuss growth of vibrios environmentally; but are they too pessimistic in asserting that cholera “cannot be eradicated; it is part of the normal flora and ecology of the surface water of our planet”? That non-cholera vibrios (NCVs; serogroups O2–O138) thrive in the environment, is true, but do cholera vibrios (serogroup O1) occur there naturally too or only from human excreta? Where have the Latin American epidemics gone? Why do outbreaks of cholera seldom follow the dire warnings evoked by earthquakes or warfare? Until the full enigma of cholera epidemiology is unravelled, it is too early to deny the long-held view that human cases constitute the reservoir of infection—a prerequisite for eradication.

Vaccination and improved sanitation have synergistic roles in preventing cholera. Sack and colleagues, however, seem unduly negative about parenteral vaccine, because of painful local reactions. Like other travellers in the 1980s, I received many injections of cholera vaccine, with minimal discomfort, to meet entry requirements abroad. Moreover, the most impressive protection with cholera vaccine dates back to the 1970s when 88% efficacy was reported with only a single dose of parenteral vaccine containing adjuvant, which enhances the immune response and probably reduces adverse reactions, as with pertussis vaccine. Sack and colleagues mention the Inaba and Ogawa serotypes of O1 vibrios, but not that these produce only type-specific immunity: Ogawa does not protect against Inaba, and vice versa. Despite advocating oral vaccine, they admit uncertain efficacy in the field, although a live oral vaccine (single Inaba strain) was highly protective against Inaba challenge in volunteers.

During the 1990s, a parallel (eighth) pandemic of cholera started around the Bay of Bengal—caused by what various studies showed was an antigenic mutant of the seventh pandemic O1 vibrio, against which neither Inaba nor Ogawa antibody protects. This new Bengal serotype of O1 (sometimes misleadingly designated O139, as though it were yet another NCV) needs to be incorporated in future vaccines (oral or parenteral) alongside Inaba and Ogawa strains, to produce a balanced immune response to all three. Likewise, the rapid-diagnosis antiserum, which stops the motility of vibrios in patients' stools, should immobilise or agglutinate all three serotypes.