Food Protection Trends - July/August 2019 - 339

and Drug Administration (FDA) on Vp (VPRA) and by
the United Nations Food and Agricultural Organization
(FAO) and the World Health Organization (WHO) for Vv
(VVRA) that were released in 2005 (23, 50). Vp and Vv
levels in oysters at harvest were based on FDA data on their
relationship to water temperature (10, 16, 40). Levels at the
time of consumption were largely determined by Vp and Vv
growth rates (8, 9, 27) in oysters and time to cool the oysters
below the minimum growth temperatures of 10° and 13°C,
respectively (23, 50), for these two pathogens.
This article examines the factors contributing to escalating
Vibrio illness reporting and emerging practices and mitigations that are driving down illnesses in the most severely
impacted regions of the U.S. The lessons learned in the U.S.
have global implications for shellfish safety.
Perfect Vibrio Storm
Vast estuaries abound on U.S. coasts and create ideal
habitats for growing oysters and vibrios. Forces of nature
and man, including bacterial evolution, global warming,
risky food-handling practices, shifting geographical and
seasonal production and consumption patterns, expanding
globalization, improved recognition/diagnosis and fractured
regulatory oversight have spawned a perfect storm of everincreasing rates of vibriosis reported in the U.S.
Bacterial evolution and emergence of virulent
outbreak strains
Vp grows faster than any other pathogen, and its short
generation time accelerates evolution and genetic diversity
(50). Vibrios also exchange genes with other marine bacteria
and can readily acquire gene clusters from numerous phages
(viruses that can lyse bacteria or be integrated into the
bacterial genome). These processes are a source of genetic
elements that can increase pathogenicity toward humans,
most notably the gene system for the cholera toxin (52).
Although a direct link to phage-acquired pathogenicity in
Vp or Vv has not been established, numerous and diverse
lytic Vv phages occur in oysters (20). A lysogenic phage
has also been identified in the pandemic O3:K6 serotype
(42). Separate human-pathogenic variants have recently
evolved from a benign Vp strain endemic to the NE Atlantic
through acquisition of pathogenicity islands of unknown
sources (53). Many Vp and Vv strains and lineages occur
simultaneously in the same area and even in the same oyster.
Climate change
Remarkable seasonal and regional expansion of Vv and
Vp illnesses and outbreaks have followed the warming
of seawater, especially since 1998. Most striking is the
geographical expansion of Vp outbreaks to Alaska (37) and
Chile (25). An unexpected consequence of geographical
expansion is the increasing risk with increasing latitude.
The attack rate on three consecutive cruise ship outbreaks

in the Prince William Sound, AK was about 30% with
consumption of 1-6 oysters (37), an attack rate >1000-fold
higher than the VPRA predictions (33). The AK outbreak
occurred >1000 Km further north than previously reported
Vp outbreaks (37). In southern Chile, Vp infections reached
epidemic levels for the first time in history (25). A recent
draft Food and Agricultural Organization (FAO)/World
Health Organization (WHO) report on updating Vibrio risk
assessment has identified the introduction or emergence
of Vp outbreak strains to high latitude areas as the greatest
foodborne vibriosis threat.
The Vv risk season historically spanned from May to
October in the U.S. Gulf Coast (46). However, since 1998, the
number of days with water temperatures >20°C have increased
in April and November, and oyster-associated illnesses in these
shoulder months are similarly frequent to those of summer
months (33). During a La Niña anomaly in 1998, water
temperatures were 3-4°C higher than historical averages, and
there were 13 reported Vv septicemia illnesses, the most of
any month on record (33). Less stringent time/temperature
controls outside the historical Vv risk season and higher
consumption likely contributed to this surge in illnesses.
Globalization
Growth of international trade has provided avenues for
introduction of emerging pathogenic vibrios on a global
scale. Cargo ships take on millions of liters of harbor water
as ballast for stabilization on the high seas and discharge
it to facilitate cargo transfer at the destination port. Many
ports are highly polluted and have water temperatures and
salinities that favor Vibrio abundance and survival during the
voyage. This phenomenon was first documented in 1991,
when the Latin American epidemic V. cholerae strain was
discovered in ballast water of a number of ships in Mobile
Bay, Alabama that had taken on water from various Latin
American ports where this strain had become endemic
(36). The same epidemic strain had previously been found
in oysters from several growing areas in coastal Alabama,
but these areas had fortunately been closed to harvest for
purposes of conservation (15, 41). The pandemic O3:K6
Vp strain appears to have been introduced into major ports
in North and South America, Asia, Europe and Africa
in the late 1990s. Many of the resulting outbreaks were
identified retrospectively by analysis of archived isolates
(34). Systematic surveys of ballast water were not conducted
to confirm its role in the spread of Vp. Many countries also
permit wet storage/depuration practices related to bivalve
mollusks from other regions or countries, often with little
oversight. Many consider these risky practices responsible for
the introduction of the O4:K12 (Sequence Type 36) strain
from the U.S. Pacific NW to Oyster Bay, New York and to
Galicia, Spain in 2012 (32). This strain, endemic to the NE
Atlantic coast, remains the dominant cause of illnesses in that
region (6, 53). The outbreak in Galicia was on a cruise ship

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