Typical clinical signs of V. vulnificus infections include fever, chills, diarrhea, nausea, vomiting, septic shock, and characteristic skin lesions [15]. These characteristic skin lesions include lower extremity cellulitis with ecchymosis and bullae. Since the organism can cross the intestinal mucosa rapidly, development of bullous skin lesions of the lower extremities can occur within the first 24 hours after onset of illness [16]. This onset if often thought of as an early manifestation of sepsis. The clinical signs can vary depending on which way the person was infected by V. vulnificus. Symptoms typically occur within 7 days, although they may be delayed up to 14 days in cases of the ingestion of raw or undercooked seafood [17] V.
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Once the organism attaches, it uses several other virulence factors to evade host immune system, such as a polysaccharide capsule, OmpU, and siderophores. The polysaccharide capsule allows the organism to evade opsonization and phagocytosis due to its slippery property as well as allows the organism to be resistant to bactericidal properties of serum and hide its immunogenic structures from the host nonspecific defenses [25]. An outer membrane protein, called OmpU, allows the organism to bind to host fibronectin, thus improving its chances of adhering to the host [26]. V. vulnificus further produces two siderophores, vulnibactin and deferoxamine, which allow the bacterium to sequester iron for survival through the use of heme receptors (HupA) [27]. Vulnibactin specifically uses HupA to steal iron from host transferrins and holotransferrins due to it having a higher affinity for iron, and deferoxamine promotes organism growth and iron uptake [28]. Variation between virulent and avirulent forms of V. vulnificus depends on the presence of these three virulence factors. Virulent forms are almost always encapsulated, serum resistant, and possessing the ability to acquire iron from iron-saturated transferrin, while avirulent variants lack these characteristics
Once the organism attaches, it uses several other virulence factors to evade host immune system, such as a polysaccharide capsule, OmpU, and siderophores. The polysaccharide capsule allows the organism to evade opsonization and phagocytosis due to its slippery property as well as allows the organism to be resistant to bactericidal properties of serum and hide its immunogenic structures from the host nonspecific defenses [25]. An outer membrane protein, called OmpU, allows the organism to bind to host fibronectin, thus improving its chances of adhering to the host [26]. V. vulnificus further produces two siderophores, vulnibactin and deferoxamine, which allow the bacterium to sequester iron for survival through the use of heme receptors (HupA) [27]. Vulnibactin specifically uses HupA to steal iron from host transferrins and holotransferrins due to it having a higher affinity for iron, and deferoxamine promotes organism growth and iron uptake [28]. Variation between virulent and avirulent forms of V. vulnificus depends on the presence of these three virulence factors. Virulent forms are almost always encapsulated, serum resistant, and possessing the ability to acquire iron from iron-saturated transferrin, while avirulent variants lack these characteristics