Vibrio cholerae and Asiatic Cholera (page 2)
(This chapter has 4 pages)
© Kenneth Todar, PhD
History and spread of epidemic cholera
Cholera has smoldered in an endemic fashion on the Indian subcontinent
for centuries. There are references to deaths due to dehydrating
dating back to Hippocrates and Sanskrit writings. Epidemic cholera was
described in 1563 by Garcia del Huerto, a Portuguese physician at Goa,
India. The mode of transmission of cholera by water was proven in 1849
by John Snow, a London physician. In 1883, Robert Koch successfully
the cholera vibrio from the intestinal discharges of cholera patients
proved conclusively that it was the agent of the disease.
The first long-distance spread of cholera to Europe and the Americas
began in 1817, such that by the early 20th century, six waves of
had spread across the world in devastating epidemic fashion. Since
until the 1960s, the disease contracted, remaining present only in
Asia. In 1961, the "El Tor" biotype (distinguished from classic
biotypes by the production of hemolysins) reemerged and produced a
epidemic in the Philippines to initiate a seventh global pandemic
(See map below). Since then, this biotype has spread across Asia, the
East, Africa, and parts of Europe.
There are several characteristics of the El Tor strain that confer
it a high degree of "epidemic virulence" allowing it to spread across
world as previous strains have done. First, the ratio of cases to
is much less than in cholera due to classic biotypes (1: 30-100 for El
Tor vs. 1: 2 - 4 for "classic" biotypes). Second, the duration of
after infection is longer for the El Tor strain than the classic
Third, the El Tor strain survives for longer periods in the
environment. Between 1969 and 1974, El Tor replaced the classic strains
in the heartland of endemic cholera, the Ganges River Delta of India.
The global spread of cholera
during the seventh pandemic, 1961-1971. (CDC)
El Tor broke out explosively in Peru in 1991 (after an absence of
there for 100 years), and spread rapidly in Central and South America,
with recurrent epidemics in 1992 and 1993. From the onset of the
in January 1991 through September 1, 1994, a total of 1,041,422 cases
9,642 deaths (overall case-fatality rate: 0.9%) were reported from
in the Western Hemisphere to the Pan American Health Organization. In
the numbers of reported cases and deaths were 204,543 and 2362,
In 1982, in Bangladesh, a classic biotype resurfaced with a new
to produce more severe illness, and it rapidly replaced the El Tor
which was thought to be well-entrenched. This classic strain has not
produced a major outbreak in any other country.
In December, 1992, a large epidemic of cholera began in Bangladesh,
and large numbers of people have been involved. The organism has been
as V. cholerae O139 "Bengal". It is derived genetically
the El Tor pandemic strain but it has changed its antigenic structure
that there is no existing immunity and all ages, even in endemic areas,
are susceptible. The epidemic has continued to spread. and V.
has affected at least 11 countries in southern Asia. Specific totals
numbers of V. cholerae O139 cases are unknown because affected
do not report infections caused by O1 and O139 separately.
In April 1997, a cholera outbreak occurred among 90,000 Rwandan
residing in temporary camps in the Democratic Republic of Congo. During
the first 22 days of the outbreak, 1521 deaths were recorded, most of
occurred outside of health-care facilities.
In the United States, cholera was prevalent in the 1800s but has
virtually eliminated by modern sewage and water treatment systems.
as a result of improved transportation, more persons from the United
travel to parts of Latin America, Africa, or Asia where epidemic
is occurring. U.S. travelers to areas with epidemic cholera may be
to the bacterium. In addition, travelers may bring contaminated seafood
back to the United States. A few foodborne outbreaks have been caused
contaminated seafood brought into this country by travelers. Greater
90 percent of the cases of cholera in the U.S. have been associated
V. choleraemay also live in the environment in brackish
and coastal waters. Shellfish eaten raw have been a source of cholera,
and a few persons in the United States have contracted cholera after
raw or undercooked shellfish from the Gulf of Mexico.
Antigenic Variation and LPS Structure in Vibrio
Antigenic variation plays an important role in the epidemiology and
of cholera. The emergence of the Bengal strain, mentioned above, is an
example. The flagellar antigens of V. cholerae are shared with
water vibrios and therefore are of no use in distinguishing strains
epidemic cholera. O antigens, however, do distinguish strains of
cholerae into 139 known serotypes. Almost all of these strains of V.
cholerae are nonvirulent. Until the emergence of the Bengal strain
(which is "non-O1") a single serotype, designated O1, has been
for epidemic cholera. However, there are three distinct O1 biotypes,
named Ogawa, Inaba and Hikojima, and each
may display the "classical" or El Tor phenotype. The Bengal strain
is a new serological strain with a unique O-antigen which partly
the lack of residual immunity.
Antigenic Determinants of Vibrio
||A, B, C
Endotoxin is present in Vibrio cholerae as in other
bacteria. Fewer details of the chemical structure of Vibrio cholerae
LPS are known than in the case of E. coli and Salmonella,
but some unique properties have been described. Most importantly,
in LPS occur in vivo and in vitro, which may be correlated with
in nature of nonepidemic strains to classic epidemic strains and vice