Everything you need to know about Vibrio vulnificus – the ‘flesh-eating bacteria’

The media has recently been awash with news of the 31-year old man who went for a swim in the Gulf of Mexico with a new tattoo featuring the words ‘Jesus Is my Life’. Three days later, he was admitted to hospital and after testing positive for a Vibrio vulnificus infection, died from septic shock a few months later. James Oliver and Dr. Craig Baker-Austin take a close look at this bacterium and the dangers it can pose.

Cryptic virulence

The Gram-negative bacterium Vibrio vulnificus is a naturally occurring and common inhabitant of estuarine and coastal environments. This bacterium is fascinating for a number of reasons – these include its striking pathogenicity, high case fatality rate, interesting and unusual epidemiology, cryptic virulence potential and the increasing incidence of disease.

Globally, V. vulnificus is a significant foodborne pathogen capable of causing primary septicaemia, typically resulting in necrotizing skin lesions, and is the leading cause of seafood-related mortality. Most infections are linked to the consumption of raw or undercooked seafood such as oysters. Perhaps the most striking aspect associated with this bacterium is the extremely high case fatality rate.

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Rare but deadly

In individuals where V. vulnificus progresses to primary sepsis, the mortality rate is around 50%, placing these infections on a par with the most serious viral and bacterial human pathogens such as Ebola, Marburg and bubonic plague. Because of this virulence potential, immediate antibiotic therapy is required – and where infections have not been treated very rapidly, death is almost a certainty. V. vulnificus is a relatively rare cause of infection, but there have been a number of published studies that demonstrate an increase in disease in the USA and more recently in Europe.

Indeed, this pathogen is particularly fascinating because most cases occur in males (~85%), and in patients with underlying conditions resulting in elevated serum iron levels, primarily hepatitis and alcohol-associated liver cirrhosis. Oestrogen appears to reduce the ability of this pathogen to elicit endotoxic shock in women, however, the molecular basis of this protective role remains unclear. These infections progress into visible lesions, typically on the extremities, and result in vesicles or fluid-filled bullae that become necrotic.

glass of wine

Minute portals

In addition to foodborne disease, V. vulnificus causes potentially fatal wound infections. Both food-associated and wound infections involve a short incubation period between exposure and the onset of symptoms (Baker-Austin et al., 2008), typically within 24 hours of exposure. Significantly, as with other vibrios, V. vulnificus requires only minute portals of entry to initiate wound infections, and often appear initially as an insect bite.

Typically, V. vulnificus wound infections are characterized by swelling, erythema and intense pain (Figure 1). An analysis of recent V. vulnificus wound infections reported in the USA over the last 25 years revealed an almost 20% mortality rate.


Highly heterogeneous

This species is highly heterogeneous and is currently subdivided into three biotypes based on genetic, biochemical and serological features, as well as host range. Biotype 1 strains are human pathogens and are responsible for the vast majority of V. vulnificus infections reported worldwide. Biotype 2 contains strains which cause generally fatal infections in aquatic animals such as eels, with occasional human infections. A further biotype (biotype 3) was discovered in 1996 after an outbreak of V. vulnificus infections in an Israeli fish market, and was later found to be a hybrid of biotypes 1 and 2.

Complicating our understanding of the virulence process of V. vulnificus was the finding that biotype 1 strains are comprised of two distinct genotypes, termed ‘C’ (clinical) and ‘E’ (environmental). C-genotype strains are the form most often encountered in human septicaemias (90%), although comprising a much smaller proportion (c. 15%) of the V. vulnificus strains occurring in estuarine waters and shellfish.

The opposite is the case for wound infections caused by this species, with nearly all isolates being of the E-genotype. Numerous individual genes have been suggested to be important in pathogenesis, including those involved in cytotoxicity, haemolysins, iron sequestration pathways, secretion systems and acid neutralization pathways. To date, and in spite of over a decade of efforts utilizing whole-genome sequencing, no single molecular target has been identified to distinguish pathogenic and non-pathogenic V. vulnificus strains, and is a key area of current work.

nice beach

Climate change

Strikingly, the number of reported V. vulnificus infections (particularly wound associated) appears to be increasing in the USA. The factors underlying this increase in cases remain unclear, but changes in population density and demographics in coastal areas (and hence possible exposure), better systems of epidemiology and surveillance, and climate change are likely to be contributing to the numbers of infections seen.

Certainly, warming of low salinity environments as a result of climate warming appears to be playing a significant role in driving disease emergence. For example, the advent of V. vulnificus infections in typically frigid marine waters, such as the Baltic Sea and North Sea during heatwave events serves to illustrate that climate change may be modulating the timing and geographical spread of these pathogens with huge ramifications for the identification, treatment and management of waterborne diseases.

James Oliver (University of North Carolina at Charlotte)

Dr Craig Baker-Austin (Centre for Environment, Fisheries and Aquaculture Science)

This article was first published in Microbiologist December 2016




























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