Tuesday 4 February 2014

Epidemiology and pathogenesis of Vibrio vulnificus.

Epidemiology and pathogenesis of Vibrio vulnificus.

The authors (Strom and Paranjpye) have presented a very detailed review, I am going to summarise the epidemiology of the virus to prevent an essay style 1,000 word summary. I would be happy to cover the pathogenesis separately.

Vibrio vulnificus was first isolated by the US Centres for Disease Control (CDC) in 1964 and was classified as a distinct species in the 1970s. Vibrio vulnificus is a motile, Gram-negative bacterium. It is present in both marine and estuarine environments. Vibrio vulnificus is responsible for a significant percentage of vibrio related illnesses, is the leading cause of seafood-associated fatalities in the US and causes massive economic harm to the entire shellfish industry.

V. vulnificus is taken up by filter feeders, including oysters and clams where the bacteria concentrate in the gut. It has also been found in fish, and it is believed that this is the method by which the bacteria are transported.

V. vulnificus is a naturally occurring and free-living inhabitant of estuarine and marine environments, predominately in tropical areas. This bacterium is known to have caused illness throughout Northern Europe, the US and Australia. It proliferates in summer months when the water exceeds 18 degrees Celsius. It is believed that an onset of both systemic and wound infections occurs primarily between the months of April and September in the US. When water drops below 10 degrees Celsius, V. vulnificus enters a viable but nonculturable state (VBNC) where following several morphological changes, it becomes more resistant to environmental hardship.

There are two biotypes of V. vulnificus. Biotype 1 strains are typically associated with shellfish colonisation and human illness. Biotype 2 strains are implicated in infections of marine vertebrates, particularly in cultured eels. They have, however, been shown to be virulent in mice and capable of causing opportunistic infections in humans.

This bacterium has the ability to cause serious and often fatal infections. These infections include an invasive septicaemia (through eating raw or undercooked shellfish - cooking shellfish is the only reliable method to completely destroy the bacterium), as well as wound infections acquired through contact with shellfish or waters where the bacteria are prevalent. Both of these acquisition methods are just as common as the other.

  • Wound infections are classified as those where a patient incurred a wound before or during exposure to seawater or seafood drippings and where V. vulnificus was subsequently cultured from that wound.
  • Primary Septicaemia was defined as a systematic illness characterised as fever and shock where V. vulnificus was isolated from blood but no wound infection preceded the illness.

422 infections reported between 1988 and 1996; 45% were wound infections and 43% were primary septicaemia. Of the 181 cases of primary septicaemia, 173 patients reported eating raw oysters in the seven days prior to the symptoms.  Many wound infections appear to be related to occupational exposure with 69% reporting either fishing or handling raw seafood during the seven days preceding illness.

The lethal dose of V. vulnificus is unknown in humans however it is known that host susceptibility is a key factor. People who are most susceptible usually suffer from chronic disease that affects either liver function or the immune system. 97% of those people who had primary septicaemia had pre-existing conditions, as opposed to 67% in those with wound infections. Of the risk factors, liver disease was most common, found in 80% of those with primary septicaemia. It was also a strong indicator for fatality, as liver disease was found in 80% of those who died from the infection.

The fatality rate for V. vulnificus is between 30-48%, however this varies depending on the mode of infection and host factors. For example, fatalities occur in 60-75% of patients with primary septicaemia but only 20-30% in those with wound infection. This may be due to the differing in timing and severity of the symptoms in wound infections when compared to those of primary septicaemia.



M.S. Strom and R.N. Paranjpye, (2000). Epidemiology and pathogenesis of Vibrio vulnificus. Microbes and Infection. Volume 2, Issue 2, Pages 177-188

2 comments:

  1. Hi Ethan,
    you said that Biotype 1 strains are the one that is associated with shellfish and causes the human illnesses and Biotype 2 strains cause infection in vertebrates - are the opportunistic infections in humans caused by Biotype 2 strains similar to the other strain or do they have different effects? I assume that that is described in more detail in the pathogenesis part of this paper that you mentioned in the beginning?

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  2. Indeed it is. The authors, for the sake of keeping this review succinct, talk primarily about biotype 1 except for where the similarities or differences are significant.

    One of the key differences mentioned is the differing LPS types. Biotype 1 strains have variable LPS O-polysaccharide side chains whereas biotype 2 have only one LPS O-polysaccharide side chain type. This singular type in b2 has allowed for the role to be examined and it turns out it appears to be a virulence determinant in the infection of eels.

    This is the only factor they really discuss in detail, perhaps there is a comparison paper between 1 and 2 out there!

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