Members of the genus Vibrio cause a number of important infectious syndromes. Classic among them is cholera, a devastating diarrheal disease caused by V. cholerae that has been responsible for seven global pandemics and much suffering over the past two centuries. Epidemic cholera remains a significant public health concern in the developing world today. Other vibrioses caused by other Vibrio species include syndromes of diarrhea, soft tissue infection, or primary sepsis. All Vibrio species are highly motile, facultatively anaerobic, curved gram-negative rods with one or more flagella. In nature, vibrios most commonly reside in tidal rivers and bays under conditions of moderate salinity. They proliferate in the summer months when water temperatures exceed 20°C. As might be expected, the illnesses they cause also increase in frequency during the warm months.
Cholera is an acute diarrheal disease that can, in a matter of hours, result in profound, rapidly progressive dehydration and death. Accordingly, cholera gravis (the severe form of cholera) is a much-feared disease, particularly in its epidemic presentation. Fortunately, prompt aggressive fluid repletion and supportive care can obviate the high mortality that cholera has historically wrought. While the term cholera has occasionally been applied to any severely dehydrating secretory diarrheal illness, whether infectious in etiology or not, it now refers to disease caused by V. cholerae serogroup O1 or O139—i.e., the serogroups with epidemic potential.
Microbiology and Epidemiology
The species V. cholerae is classified into more than 200 serogroups based on the carbohydrate determinants of their lipopolysaccharide (LPS) O antigens. Although some non-O1 V. cholerae serogroups (strains that do not agglutinate in antisera to the O1 group antigen) have occasionally caused sporadic outbreaks of diarrhea, serogroup O1 was, until the emergence of serogroup O139 in 1992, the exclusive cause of epidemic cholera. Two biotypes of V. cholerae O1, classical and El Tor, are distinguished. Each biotype is further subdivided into two serotypes, termed Inaba and Ogawa.
The natural habitat of V. cholerae is coastal salt water and brackish estuaries, where the organism lives in close relation to plankton. Humans become infected incidentally but, once infected, can act as vehicles for spread. Ingestion of water contaminated by human feces is the most common means of acquisition of V. cholerae. Consumption of contaminated food also can contribute to spread. There is no known animal reservoir. While the infectious dose is relatively high, it is markedly reduced in hypochlorhydric persons, in those using antacids, and when gastric acidity is buffered by a meal. Cholera is predominantly a pediatric disease in endemic areas, but it affects adults and children equally when newly introduced into a population. In endemic areas, the burden of disease is often greatest during “cholera seasons” associated with high temperatures, heavy rainfall, and flooding, but cholera can occur year-round. For unexplained reasons, susceptibility to cholera is significantly influenced by ABO blood group status; persons with type O blood are at greatest risk of severe disease if infected, while those with type AB are at least risk.
Cholera is native to the Ganges delta in the Indian subcontinent. Since 1817, seven global pandemics have occurred. The current (seventh) pandemic—the first due to the El Tor biotype—began in Indonesia in 1961 and spread throughout Asia as V. cholerae El Tor displaced the endemic classical biotype. In the early 1970s, El Tor cholera erupted in Africa, causing major epidemics before becoming a persistent endemic problem. Currently, >90% of cholera cases reported annually to the World Health Organization (WHO) are from Africa (Fig. 156-1), but the true burden in Africa as well as in Asia is unknown since diagnosis is often syndromic and since many countries with endemic cholera do not report cholera to the WHO. It is possible that >3 million cases of cholera occur yearly (of which only ∼200,000 are reported to the WHO), resulting in >100,000 deaths annually (of which <5000 are reported to the WHO).
World distribution of cholera in 2009. (Adapted from WHO: Cholera, 2009.)
The recent history of cholera has been punctuated by severe outbreaks, especially among impoverished or displaced persons. Such outbreaks are often precipitated by war or other circumstances that lead to the breakdown of public health measures. Such was the case in the camps for Rwandan refugees set up in 1994 around Goma, Zaire; in 2008–2009 in Zimbabwe; and in 2010 in Haiti. Since 1973, sporadic endemic infections due to V. cholerae O1 strains related to the seventh-pandemic strain have been recognized along the U.S. Gulf Coast of Louisiana and Texas. These infections are typically associated with the consumption of contaminated, locally harvested shellfish. Occasionally, cases in U.S. locations remote from the Gulf Coast have been linked to shipped-in Gulf Coast seafood.
After a century without cholera in Latin America, the current cholera pandemic reached Central and South America in 1991. Following an initial explosive spread that affected millions (Fig. 156-2), the burden of disease has markedly decreased in Latin America, although, as it did in Africa two decades earlier, the epidemic El Tor strain proved capable of establishing itself in inland fresh waters rather than in its classic niche of coastal salt waters. In 2010, cholera reappeared in Haiti after a century-long absence.
Spread of Vibrio cholerae O1 in the Americas, 1991–1994. (Courtesy of Dr. Robert V. Tauxe, Centers for Disease Control and Prevention, Atlanta; with permission.)
In October 1992, a large-scale outbreak of clinical cholera caused by a new serogroup, O139, occurred in southeastern India. The organism appears to be a derivative of El Tor O1 but has a distinct LPS and an immunologically related O-antigen polysaccharide capsule. (O1 organisms are not encapsulated.) ...