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Vibrio vulnificus is a rare cause of necrotising fasciitis. The organism can be found in warm, shallow coastal waters, as well as on shellfish, such as crab, and also filter-feeding molluscs, such as oysters, clams, and scallops. In the USA, it is the leading cause of shellfish related deaths. In individuals with major underlying illnesses, such as liver disease, diabetes mellitus, malignancy, alcoholism, haemochromatosis or chronic renal disease, the organism can lead to a fulminant course with a high degree of mortality. Early antimicrobial treatment and timely surgical interventions can be potentially life preserving in serious infections with V vulnificus. We report a case of an elderly patient with end stage renal disease on haemodialysis who developed necrotising fasciitis with V vulnificus following a puncture injury while cleaning crabs.
An 81-year-old Caucasian Italian American man was admitted for acute, severe left hand pain and swelling for 24 h. The previous day he had incurred a puncture injury to the dorsum of the left hand while cleaning crabs. Over the last 24 h he had been febrile with a temperature of 38.8°C (101°F), with subjective chills, and worsening pain to the point that he was unable to move the left hand and decided to come to the emergency department.
The patient’s past medical history was significant for end stage renal disease (on haemodialysis three times per week), hypertension, seizure disorder, coronary artery disease with stents, deep vein thrombosis (DVT) with inferior vena cave (IVC) filter placement, and gout. He reported a penicillin allergy of itching. Social and travel history were unremarkable.
Vital signs were significant for temperature (39.6°C, 103.3°F), blood pressure (98/46 mm Hg), pulse (103/min), and respiration (18/min). The patient was in moderate distress due to pain. Physical examination was notable for significant left hand swelling and erythema with severe pain elicited upon passive movement. There was a bluish discoloration of the dorsum of the left hand with minimal drainage. Distal pulses and neurological examination of the left hand were normal.
Initial laboratory results revealed a white blood cell (WBC) count of 14.3×103 cells/mm3 with 91% polymorphonuclear leucocytes. The patient’s blood urea nitrogen (BUN)/creatinine values were 26 mg/dl (9.3 mmol/l) and 3.8 mg/dl (336.3 mmol/l), respectively, with a glomerular filtration rate (GFR) of 15 ml/min (baseline creatinine, 4.2 mg/dl (371.7 mmol/l) 1 month earlier). Chest x-ray and ECG were normal. Radiograph of the left hand revealed extensive soft tissue swelling with no fracture. Fluid resuscitation was started, blood cultures were drawn, and the patient was started on intravenous clindamycin.
Subsequently, the patient was taken to the operating room for emergent surgical debridement and fasciiotomy for suspected necrotising fasciitis complicated by compartment syndrome. The procedure was significant for extensive necrotic tissue in the dorsum of the hand, while the palmar aspect was essentially unaffected. Pulse irrigation with antibiotics was used to remove the necrotic tissue. Surgical wound cultures were taken. Pathological examination of the surgical specimen showed significant ulcerative necrosis, acute and chronic inflammation, and granulomatous tissue reaction. Antibiotics were empirically changed to intravenous meropenem, doxycycline, and vancomycin.
Interim blood culture was negative for growth. Gram stain of the surgical specimen revealed curved, gram-negative rods. Subsequent wound culture was significant for Vibrio vulnificus with pan-sensitivity. Antibiotics were changed to intravenous ceftriaxone, ciprofloxacin, and doxycycline.
Over the next several days, the patient required numerous incision and drainage procedures, surgical debridements, as well as a full thickness skin graft to the dorsum of the left hand. These all resulted in clinical improvement of the hand, with notably less swelling and pain. After a 14 day hospitalisation, the patient was discharged with an indwelling catheter on intravenous ceftriaxone and oral doxycycline, with outpatient follow-up for further debridements.
The cutaneous injury from the crab shell suggested a complication from exposure to marine life, and surgical wound cultures grew a gram-negative, curved rod identified as V vulnificus (figs 1 and and22).
V vulnificus can cause serious soft tissue infections and sepsis. The organism can be found in warm, shallow coastal waters, as well as on shellfish, such as crab, and also filter feeding molluscs, such as oysters, clams, and scallops. In the USA it is the leading cause of shellfish related deaths. In recent years, wound infections with V vulnificus have become more common. V vulnificus was reported as an important pathogen of wound infections effecting survivors of the December 2004 Indian Ocean tsunami.1 Following Hurricane Katrina in 2005, 18 cases of wound infection caused by vibrios were reported; 14 (82%) were caused by V vulnificus, with three deaths.2
Numerous bacteria can be found in the exterior slime of shellfish and fish, which can be transmitted to humans via a penetrating injury. There bacteria include Aeromonas hydrophila, Streptococcus iniae, Edwardsiella tarda, Mycobacterium marinum, Vibrio vulnificus, and Erysipelothrix rhusiopathiae.3 In the case of our patient, he described a piercing-type cutaneous injury following exposure to a crab likely colonised with V vulnificus.
Human infection from V vulnificus can occur in two ways: exposure to contaminated seafood, such as raw oysters, or through an open wound or penetration injury exposed to contaminated seawater or shell fragments. Many patients infected with V vulnificus have bullous skin lesions which can progress to necrotic ulcers, which require surgical debridement. V vulnificus is a rare cause of necrotising fasciitis, which can be fatal.4
The virulence of V vulnificus is related to its polysaccharide capsule, which allows the organism to be resistant to serum killing and also stimulates release of inflammatory cytokines, such as tumour necrosis factor α (TNF-α).5 In addition, the organism produces several extracellular enzymes and cell wall lipopolysaccharide which may play adjunctive roles in pathogenicity. One of these proteins, a thermolysin-like metalloprotease, activates the bradykinin pathway, resulting in increased vascular permeability. This metalloprotease has been shown to be much more efficient at inducing human enzymes compared to other Vibrio species, and may explain why V vulnificus causes severe skin damage and rapidly progressive necrotising fasciitis.6
V vulnificus is a halophilic gram-negative bacillus, which has been described as “comma-shaped”. Because bacteraemia frequently occurs with V vulnificus, routine blood cultures should be taken. Bullae, ecchymoses, abscesses, as well as frozen section analysis of tissue are often productive sites to rapidly visualise the bacteria and diagnose necrotising fasciitis.7,8
In individuals with major underlying illnesses, such as liver disease, diabetes mellitus, malignancy, alcoholism, haemochromatosis, or chronic renal disease, the organism can lead to a fulminant course with a high degree of mortality, as well as potential limb threatening complications. Our patient had been on haemodialysis for end stage renal disease for 3 years before presentation, placing him at increased risk for serious infection with V vulnificus, as manifested by the rapid onset of necrotising fasciitis within 24 h of sustaining the injury to his hand.
Mortality rates have been shown to significantly increase when antibiotic treatment is delayed in V vulnificus infections. Patients with septicaemia or serious wound infections should be promptly treated with a combination of either minocycline or doxycycline plus either cefotaxime or ceftriaxone. Early surgical consultation should be obtained as debridement of all devitalised tissue or even amputation may be life preserving.
Competing interests: None.
Patient consent: Patient/guardian consent was obtained for publication.