by Kourosh Ghaeli

Introduction

The death of 20 people in the 1950’s lead to the discovery of the bacterium Vibrio parahaemolyticus (Figure 1). This incident took place in Japan, when the consumption of sardines infected with the foodborne pathogen became fatal. The bacterium prefers to take refuge in warm saltwater, and is naturally found in marine products such as mollusks and oysters.

Figure 1: Scanning electron microscopic image of Vibrio parahaemolyticus (pink). Source: Public Health Image Library (PHIL).

Disease

V. parahaemolyticus is found in raw crustaceans and fish. Shellfish such as oysters that are filter feeders also contain a high amount of this bacterium. The pathogenic bacteria are transmitted to humans by ingestion of uncooked seafood. Contaminated food with said bacteria causes symptoms of gastrointestinal distress such as diarrhea, abdominal cramps, vomiting, nausea, as well as low-grade fever. The bacteria attack the intestinal cell lining  through the use of various pathogenic tools. The neutrophils, which are considered to be the “big eater” cells of the immune system, will then travel to the site of infection and defend our body against the pathogen. It is important to note that in healthy individuals the immune system can overcome the bacteria within 3-4 days. Furthermore, V. parahaemolyticus will also cause infections upon exposure to open wounds by infecting skin cells at the site of infection. This is mostly seen in fishermen, who are routinely exposed to the bacterium. By entering the blood stream of patients this bacterium can lead to the activation of the immune system and subsequently the induction of inflammation throughout the individual’s body. The widespread inflammation then causes widening of blood vessels and increases blood flow throughout the body, which can lead to multiple-organ failure and eventually death. This is mainly seen in immune-compromised individuals, whose immune systems are not able to effectively kill the bacteria.

Epidemiology

In 1950,the first outbreak of V. parahaemolyticcus occurred in Japan, where 272 patients were infected. In countries where eating raw seafood is common, most food-borne infections are associated with V. parahaemolyticcus. The first outbreak to occur in North America was in 1971 in the United States whereby ingestion of contaminated crabmeat was the cause. Since this outbreak, 42 additional outbreaks associated with the bacterium have been reported in the United States and, according to CDC Food Net, V. parahaemolyticus infects approximately 5000 people annually throughout the country. Furthermore, the national mortality rate has been reported to be 4% on average. In general, the majority of V. parahaemolyticcus outbreaks occur between April and October because warmer temperatures promote rapid multiplication of the bacteria, thus initiating its spread. In addition to North America, East and South Asia, outbreaks caused by V. parahaemolyticus have been documented in Europe, including an episode in France in 1997.

Virulence systems

As mentioned earlier, during an intestinal infection by V. parahaemolyticus, neutrophils will travel to the site of infection to pick up and eat the bacteria. This process is known as phagocytosis. However, V. parahaemolyticus also has many other diverse pathogenic tools such as a type 3-secretion system (T3SS), which protects the bacteria against neutrophils. The system does this by forming a pore in the outer layer of the neutrophil by a needle-like structure (Figure 2).  Once the pore is formed, it can then inject molecules, called effector proteins, that enable the bacteria to modify the immune cell so that it can no longer attack it.  In particular, the T3SS directly delivers VopQ inside neutrophils which causes these “big eater” cells to digest themselves and, as a result, the bacteria are protected against attack.  Furthermore, VopS and VPA0450 are additional effector proteins that may be inserted inside intestinal cells by the same T3SS system.  These will cause detachment of the skeleton structure that holds the shape of these cells together, which in turn causes them to become damaged and, ultimately, die.

Figure 2: Transfer of effector proteins from bacterium to inside of host cells by type-3 secretion system. VopQ is red, VPA0450 is pink, and VopS is yellow. Adapted from “Vibrio parahaemolyticus cell biology and pathogenicity determinants” by Boberg et al,2011 .

Treatment/Prevention

The bacteria are vulnerable to heat. Cooking the seafood prior to consumption could prevent further infections by the bacteria.In the majority of the cases the symptoms last up to 3 days. It is suggested that infected patients should rest and drink sufficient amount of liquids in order to replace the water lost by diarrhea. Even though V. parahaemolyticus is susceptible to antibiotic treatments, there is a lack of evidence to show that antibiotics can shorten the period of infection. However, in the case of severe infections, which may include high fever, oral antibiotics such as ampicillin or tetracycline should be used. Vaccines have been developed in order to prevent later vibrio infections. These vaccines were tested on mice, where they were found to be 100% effective. They are currently under investigation for use in humans.

References

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