Vibrio vulnificus
Authors:Wen-Liang Yu, M.D., Yin-Ching Chuang, M.D.
History
Infections of Vibrio vulnificus, as the etiology suggests, have been described in the literature as an infection that could be traced back to the days of Hippocrates (1). In fifth century BC, he described a man, who developed a violent pain in his foot, shivering, nausea, and slight fever that occurred with mental status changes. On the second day, the entire foot became erythematous and swollen with the appearance of small black blisters. The patient died on the second day of his illness. Medical historians hypothesize that the patient had a fatal infection due to V. vulnificus. In 1970, Roland described a 40-year-old patient who developed a generalized papular hemorrhagic rash, the manifestations of which included vomiting, diarrhea and fever that occurred after bathing and clamming in the New England coastal waters (48). He subsequently developed a left leg gangrene and endotoxin shock. Though vesicle exudate grew Vibrio parahemolytics, it is likely that the disease was attributed to V. vulnificus (3).. Vibrio vulnificus was initially identified as a simple halophilic lactose-positive marine vibrio which received its present name in 1979 (18).
Microbiology
Vibrio vulnificus is a gram-negative, pleomorphic, motile, curved, rod-shaped bacteria. Most, if not all vibrio species, are free-living in marine or brackish water, and therefore vibrio-associated illness tends to occur in coastal areas in the summer and fall seasons when the water is warmer and vibrio counts are higher. The disease is always associated with seafood or salt water (2, 5).
Epidemiology
This bacterium can be found worldwide and is part of the natural bacterial flora of estuarial waters. The organism occurs in many varieties of shell fish including oysters and clams. It is a halophilic organism, and its growth is favored in waters with a salinity of 0.7 to 1.6% and warm temperatures higher than 20°C (31). As the water temperature increases during the summer months, the number of shell fish harboring V. vulnificus similarly increases. As many as 50% of oysters (52) and 11% of crabs (17) are positive cultures for the organism during the peak summer months. The incidence of V. vulnificus wound infections and primary septicemia show similar rise during the summer (10). Global warming may cause worldwide increases in the frequency and geographical extent of V. vulnificus infections (46). Infections have been reported worldwide (10, 16, 41, 47 ). Vibrio vulnificus is estimated to account for 90% of all seafood-related deaths in the United States.
Clinical Manifestations
Vibrio vulnificus characteristically produces three distinct syndromes (9, 10, 29, 28 ):
1. Primary sepsis with high fever and chills without an apparent focus of infection. In this condition, V. vulnificus is usually acquired through the gastrointestinal route. Primary septicemia is classically associated with consumption of raw oysters.
2. Wound infection with cellulitis caused by direct inoculation of the microorganism, can result in tissue necrosis with secondary bacteremia. This can result from exposure of abraded skin to salt water containing the microorganism or injuries associated with the cultivation and preparation of seafood.
3. Gastrointestinal illness, characterized by vomiting diarrhea, or abdominal pain. The microorganism is culturable from the stool but not from blood.
Other infections, such as pneumonia and endometritis have also been reported (2, 26, 54 ). The mortality can be 55% in septic patients and 25% in patients with wound infections (1). Risk factors for V. vulnificus infections include liver cirrhosis, hemochromatosis, chronic renal failure, diabetes mellitus, malignancy, human immunodeficiency virus, infection, and corticosteroid consumption.
Laboratory Diagnosis
The genus Vibrio is oxidase positive and ferments glucose. Vibrio vulnificus, which is arginine dehydrogenase negative and lysine decarboxylase and ornithine decarboxylase positive, can be differentiated from most Aeromonas spp. and Plesiomonas spp., which are arginine dehydrogenase positive. Vibrio are sensitive to O129 (2, 4-diamino-6, 7-diisopropylpteridine, vibriostatic compound), but Aeromonas spp. are resistant. Vibrio vulnificus grows on MacConkey agar, heart infusion medium, and thiosulfate citric bile salt sucrose (TCBS) agar. Colonies of most V. vulnificus are green on TCBS agar plate after overnight incubation. It can be distinguished from other vibrios by the Voges-Proskauer test, sodium chloride tolerance, and lactose fermentation.
Pathogenesis
Vibrios produce several extracellular proteases to obtain nutrients via digestion of various protein substrates. However, human pathogenic vibrio species produce extracellular metalloproteases termed vibriolysin (43). The vibriolysin from V. vulnificus is a major toxic factor eliciting an edematous change of skin, an increase in vascular permeability and the hemorrhagic bullous necrotic cutaneous lesions (12, 14, 42 ). V. vulnificus metalloprotease (VVP) encoded by the vvp gene is thought to be a major pathogenic factor for tissue damage (50). Yet the extracellular serine protease expressed in the vvp gene-negative strains may also contribute to pathogenicity of V. vulnificus (56).
Other factors have been implicated as virulence determinants including extracellular hemolysin/cytolysin (VvhA) (19, 27), an elastolytic protease (45), the ability to acquire iron from transferrin (44, 51), a polysaccharide capsule (32, 57)., an endotoxic lipopolysaccharide (40), and resistance to the bactericidal effects of sera (24). Of the putative virulence factors described for this bacterium, its antiphagocytic capsule and LPS endotoxin are considered to be of prime importance in pathogenesis (37).
SUSCEPTIBILITY IN VITRO AND IN VIVO
Single Drug
The antibacterial activities of 25 antimicrobial agents against clinical isolates of V. vulnificus are shown in Table 1. All of the antibiotics tested except for clindamycin had good antibacterial activity against all isolates. Fluoroquinolones are very active against V. vulnificus (8, 53).. In time-kill studies, at the concentration of less than 2x MIC, all of the quinolones were effective in suppressing bacteria growth.
Combination Drugs
Time-kill studies with cefotaxime combined minocycline were highly synergistic against a clinical strain of V. vulnificus (13). In vivo studies in a murine model of severe V. vulnificus infection also showed that combined cefotaxime and minocycline therapy was superior to single antibiotic regimen therapy. In a murine model, the new fluoroquinolones were as active as combined cefotaxine and minocycline in treating severe V. vulnificus infection (23, 53).. In clinical experiences, the most effective antibiotic treatment for V. vulnificus infections includes combination of a third-generation cephalosporin and a tetracyclinc, doxycycline, or minocycline (38). In a retrospective analysis of an 8 year period, fluoroquinolones or third generation cephalosporins plus minocycline are the best option for antibiotic treatment of necrotizing fasciitis caused by V. vulnificus (7).
A salvage therapy with intravenous cefpirome plus tigecycline survived a 12-year-old immunocompetent boy with severe necrotizing fasciitis caused by V. vulnificus (36).
ANTIMICROBIAL THERAPY
General Consideration for the Goal of Treatment
In Taiwan, one hundred cases of necrotizing fasciitis caused by V. vulnificus were retrospectively reviewed. Multivariate analysis showed that treatment delayed beyond 3 days is in independent factor indicating a poor prognosis. Thus early diagnosis and prompt treatment within 3 days post-injury or symptom onset should be the goal for treating patients with necrotizing fasciitis caused by V. vulnificus (34).
General Drug of Choice
Because of the sporadic occurrence of V. vulnificus infection, randomized, comparative trials of different antimicrobial treatments are not feasible. Tetracycline was suggested as the drug of choice based on an in vivo animal study (3). Some authors recommend the addition of aminoglycoside, whereas other authors recommend cephalosporin antibiotics based on their clinical experience (11). We recommend combined cefotaxime-minocycline for severe cases, while Sanford et al recommend doxycycline and ceftazidime (49). As mentioned previously, fluoroquinolones such as ciprofloxacin, moxifloxacin, levofloxacin, gatifloxacin, sparfloxacin, and lomefloxacin may also be efficacious in V. vulnificus infection.
Gastrointestinal Infection:
Vibrio vulnificus gastroenteritis in immunocompetent persons is usually acute but self-limited; therefore antimicrobial therapy is not routinely recommended. Patients with severe symptoms and signs, or with a high risk of systemic infection, especially in immunocompromised patients, administration of antibiotic therapy seems reasonable.
Soft-Tissue Infections:
Skin and soft tissue infections, including cellulitis, infected wounds, and soft tissue abscesses and necrotizing fasciitis are common. Bacteremia and bullous formation are secondary complications. Antibiotic treatment is necessary.
In immunocompromised hosts, especially patients with liver cirrhosis, soft tissue infections can be fulminant and the patient may die within days. Typically, patients have unrecognized wounds on their extremities when handling seafood or being exposed to seawater. Within 24 hours, pain, erythema, swelling and hemorrhagic bullae can develop rapidly. Septic shock with multiple organ failure is common. Early surgical debridement is often necessary. The above-mentioned clinical presentations are indistinguishable from Aeromonas-associated soft tissue infections (29). We have shown that cefotaxime and minocycline are not only synergistic against V. vulnificus, but also Aeromonas hydrophila in both in vitro and and in vivo animal studies (15, 30 ). We recommend combined cefotaxime (2 g every 6 h) with minocycline (i. v. or p. o. 100 mg every 12 h, with a 200 mg loading dose). High doses (double the standard dose) of the new fluoroquinolones are promising in treating severe V. vulnificus infections based on our published data (53).
Bacteremia:
Vibrio vulnificus bacteremia usually occurs in patients with underlying illnesses, such as liver cirrhosis, hemochromatosis, alcoholism, chronic renal disease, diabetes mellitus, cancer, immunodeficiency syndromes, and those taking immunosuppressive drugs. Primary bacteremia is not uncommon, although some cases were reported to be caused by eating raw seafood. In the early phase, sepsis syndrome caused by V. vulnificus, is clinically indistinguishable from that caused by other Gram-negative bacilli. A history of exposure to seawater or consumption of raw or semi-cooked seafood may be an important clue for diagnosis. Tetracyclines are recommended as the first line agent, while cefotaxime and ciprofloxacin are recommended as alternatives. In severe cases, we recommended the combination of cefotaxime (2 g every 6 h) with minocycline (100 mg i. v. every 12 h, with 200 mg loading). Instituting antibiotic therapy before development of hypotension has been shown to decrease mortality.
Special Infections
Meningitis:
Meningitis caused by V. vulnificus is extremely rare. Meningitis has been described in a child with thalassemia and who became ill three days after he ate raw oysters (29). He was successfully treated with three weeks of chloramphenicol treatment. We recommend high dose cefotaxime (2 g every 4 h), with minocycline (100 mg i. v. every 12 h, with 200 mg loading).
Ocular Infections:
V. vulnificus ocular infections are very rare and usually related to exposure to seafood or seawater. The infections respond well to topical use of tetracycline ointment (39).
Endocarditis:
A case of V. vulnificus endocarditis has been reported in a patient with liver cirrhosi. He was successfully treated within 42 days of ampicillin plus aminoglycoside (55).
Acute cardiac injury:
Acute V. vulnificus–related nonthrombotic myocardial damage has been reported in a diabetic patient. He acquired V. vulnificus infection via a fish-stunning wound on the right foot and developed acute cardiac injury with low cardiac output. He recovered well by dobutamine inotropic therapy with combination of cefpirome and ciprofloxacin or minocycline (4)
ADJUNCTIVE THERAPY
Considering the fulminant course and high morbidity and mortality of V. vulnificus infection, early recognition is essential for effective treatment. Because of widespread obliterative vasculitis with vascular necrosis, penetration of antibiotics to the affected area may be severely hindered. Hence, early surgical debridement of the lesion may be critically important (43, 58). Since most patients who die do so within 48 hours of hospitalization, an urgent decision is required within the first 24 hours as to whether the infected areas should be resected. Early surgical exploration and debridement correlated with shortened stay in the intensive care unit. There were beneficial effects of surgical treatment within 12 hours of admission for V. vulnificus-related necrotizingfasciitis. Interestingly, there was no difference in mortality risk between patients who underwent surgery 12 to 24 hours after admission and those who had surgery more than 24 hours after admission (5). However, another 10-year retrospective study showed that patients receiving prompt surgical treatments within 24 hours after admission have better prognoses (7). Similarly, early fasciotomy within 24 hours remains the highest priority and decreased mortality rate (33). Amputation of affected extremities should be considered in severe cases refractory to antibiotics. However, some investigators believe that the infection tends to confine itself to the skin and subcutaneous tisssue (27, 35), and thus routine amputation may be overly aggressive (16, 21).
VACCINES
There are no vaccines available for the prevention of V. vulnificus.
PREVENTION
Patients with underlying liver disease and other illness should avoid eating raw or undercooked seafood. Exposure of open wounds to seawater should be avoided. Workers handling seafood should wear protective gloves.
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Tables
Table 1. Susceptibilities of Clinical Isolates of V. vulnificus to 25 Antimicrobial Agents
| Antimicrobial agents (No. of isolates tested) | MIC (μg/ml) (n=19)a |
|
MIC (μg/ml) (n=42)b |
|
MIC (μg/ml) (n=46)c |
||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| 50 | 90 | Range | 50 |
90 |
Range |
50 |
90 |
Range |
|||
Ampicillin |
1.0 |
1.0 |
0.5-1.0 |
1.0 |
1.0 |
0.25-2.0 |
- |
- |
- |
||
Carbenicillin |
4 |
4 |
4-8 |
- |
- |
- |
- |
- |
- |
||
Piperacillin |
<0.03 |
<0.03 |
<0.03 |
- |
- |
- |
- |
- |
- |
||
Cephalothin |
4 |
4 |
2-8 |
- |
- |
- |
- |
- |
- |
||
Cefamandole |
1 |
2 |
1-4 |
- |
- |
- |
- |
- |
- |
||
Cefotaxime |
<0.03 |
<0.03 |
<0.03 |
<0.03 |
0.06 |
<0.03-1.0 |
- |
- |
- |
||
Ceftriaxone |
<0.03 |
<0.03 |
<.03 |
<0.03 |
<0.03 |
<0.03-0.12 |
- |
- |
- |
||
Ceftazidime |
0.25 |
0.25 |
0.125-0.25 |
1.0 |
2.0 |
1.0-32.0 |
- |
- |
- |
||
Aztreonam |
2 |
8 |
2-8 |
- |
- |
- |
- |
- |
- |
||
Imipenem |
<0.03 |
<0.03 |
<0.03-0.06 |
0.12 |
0.12 |
0.06-0.12 |
- |
- |
- |
||
Gentamicin |
1.0 |
4.0 |
0.5-4.0 |
2.0 |
4.0 |
1.0-8.0 |
- |
- |
- |
||
Amikacin |
4 |
8 |
1-8 |
- |
- |
- |
- |
- |
- |
||
Tetracycline |
0.25 |
0.25 |
0.25 |
- |
- |
- |
- |
- |
- |
||
Minocycline |
0.06 |
0.06 |
0.06 |
0.06 |
0.25 |
0.06-0.25 |
- |
- |
- |
||
Chloramphenicol |
0.5 |
0.5 |
0.25-0.5 |
- |
- |
- |
- |
- |
- |
||
Clindamycin |
>256 |
>256 |
>256 |
- |
- |
- |
- |
- |
- |
||
Ofloxacin |
<0.03 |
<0.03 |
<0.03 |
0.12 |
0.12 |
0.06-8.0 |
- |
- |
- |
||
Ciprofloxacin |
<0.03 |
<0.03 |
<0.03 |
- |
- |
- |
0.03 |
0.03 |
0.015-0.03 |
||
Moxalactam |
- |
- |
- |
0.25 |
0.5 |
0.25-32.0 |
- |
- |
- |
||
Cefoperazone |
- |
- |
- |
0.06 |
0.12 |
<0.03-2.0 |
- |
- |
- |
||
Moxifloxacin |
- |
- |
- |
- |
- |
- |
0.06 |
0.06 |
0.03-0.06 |
||
Gatifloxacin |
- |
- |
- |
- |
- |
- |
0.03 |
0.06 |
0.015-0.06 |
||
Sparfloxacin |
- |
- |
- |
- |
- |
- |
0.06 |
0.06 |
0.015-0.06 |
||
Levofloxacin |
- |
- |
- |
- |
- |
- |
0.03 |
0.03 |
0.015-0.03 |
||
Lomefloxacin |
- |
- |
- |
- |
- |
- |
0.12 |
0.12 |
0.06-0.12 |
||