J Clin Pathol 1984;37:1301-1304

Necrotising fasciitis caused by Vibrio vulnificusML WOO,* WGD PATRICK, MTP SIMON,t GL FRENCH*

From the *Chinese University ofHong Kong, Shatin, Hong Kong, and the tUnited Christian Hospital, KwunTong, Hong Kong

SUMMARY A case of necrotising fasciitis caused by Vibrio vulnificus is described. The need forearly recognition and aggressive surgical treatment are highlighted, and the necrotising infectionsdue to V vulnificus described in the published work are reviewed.

Necrotising fasciitis is a rapidly progressing necrotis-ing process involving subcutaneous tissue and fasciabut sparing muscles, and is accompanied by severesystemic toxicity.1 2The syndrome is often caused bygroup A streptococci,' 3 but it is now recognised thatother bacteria may be involved, usually in mixedculture. Organisms that have been implicatedinclude a variety of anaerobes, enterobacteria,non-group A streptococci, pseudomonas, andstaphylococcus.43 Vibrio vulnificus is a recentlydescribed halophilic vibrio which causes necroticskin lesions following wound infection.6 We haverecently seen a child who presented with classicnecrotising fasciitis caused by V vulnificus alone.

Case report

An 8 year old schoolboy was admitted with a highfever (40.2°C), chills and rigors, and a peripheralwhite cell count of 19 x 109/l. On the day beforeadmission he had suffered a small abrasion over hisleft thigh, which he rubbed with dirty water from abasin. On admission, he was toxic and lethargic. Hisleft thigh was swollen and extremely tender andshowed several black blisters (about 1-2 cm indiameter) delimited by necrotic purple-blue skin.His condition deteriorated rapidly despite antibiotictreatment. On the next day he went into sep-ticaemic shock, but he was resuscitated successfully.The skin over the left thigh and upper leg becamedusky with bullous formation. The margin of thelesion progressed rapidly, spreading up to the leftgroin and down to the lower calf (Figs. 1 and 2).Discoloration of the left lower quadrant of theabdominal wall was also noticed on the third day.

Sixty two hours after admission necrotising fas-ciitis was diagnosed and an emergency radical

Accepted for publication 24 July 1984

debridement was performed under general anaes-thesia. Necrotising fasciitis was confirmed at opera-tion. There was extensive necrosis of the skin, sub-cutaneous tissue, and the deep fascia, but muscle wasspared. Vessels in the subcutaneous tissue werethrombosed, and tissue necrosis was more wide-spread than the skin lesions had suggested. Thepatient improved almost immediately after theoperation. The wound required skin grafting, butwas completely healed after two months.

MICROBIOLOGYCultures of blood and debrided tissue yielded a puregrowth of an aerobic, halophilic, oxidase positive,Gram negative bacterium with the characteristics ofV vulnificus. This strain was sensitive to ampicillin,chloramphenicol, co-trimoxazole, gentamicin, andamikacin, but resistant to cephalothin. Theidentification was confirmed by Dr JV Lee of thePublic Health Laboratory Service, Centre forApplied Microbiology and Research, Porton Down,Salisbury, UK.

HISTOPATHOLOGYHistology of debrided tissue showed focal necrosisin the skin and subcutaneous tissue with subepider-mal bulla formation. There was diffuse infiltrationwith polymorphonuclear and mononuclearinflammatory cells. The subcutaneous vasculaturewas congested. Numerous Gram negative vibrioswere seen in necrotic areas and spreading along thedeep fascia. Careful search failed to find any otherorganism.

This strain of V vulnificus was used in the animalmodel of Poole and Oliver.7 The LD5O was about7 x 103 colony forming units. This dose producednecrotic skin lesions in survivors when given to ICRadult mice by intradermal and subcutaneous injec-tion, while control injections of the same dose of

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Woo, Patrick, Simon, French

Figs. 1 and 2 Skin lesions of the left leg.

V parahaemolyticus did not. Tissue sections of theexperimental lesions showed typical appearances ofnecrotising fasciitis, with extensive necrosis of der-mal tissues and numerous polymorphonuclearleucocytes and vibrios spreading along fascialplanes. Muscle tissue was much less affected thanthe dermis, but it too showed some necrotic changes.

Discussion

There is no doubt that in this patient necrotisingfasciitis was caused by V vulnificus alone. Thepatient had all the classic clinical, anatomical, andhistological features of the disease: the organismwas isolated in pure culture from both blood andtissue taken at different times; the isolated strainproduced a similar syndrome when injected intomice; and the organism with its characteristic

appearance was seen in tissue sections of lesionsfrom both the patient and experimentally infectedanimals.

Giuliano et a15 suggested that streptococci are themost common single bacterial cause of necrotisingfasciitis, and non-group A streptococci with Bac-teroides fragilis is the most common combination.Numerous other bacteria have also been implicated,including peptostreptococci, peptococci, clostridia,other bacteroides species, fusobacteria,Staphylococcus aureus, Escherichia coli, citrobacter,klebsiella, enterobacter, serratia, Proteus mirabilisand Pseudomonas aeruginosa.5 V vulnificus has notpreviously been given as a cause of necrotising fas-ciitis, but there are a large number of reports notingnecrotic skin lesions associated with Vibriovulnificus (or " lactose-positive halophilic vibrio"8 9)wound infection and septicaemia.

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Necrotising fasciitis caused by Vibrio vulnificus:.. ;. A

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Roland'° reported a case of gangrene of the legwith massive necrosis of adipose and muscular tissueafter sea bathing and "clamming." "Vibno para-haemolyticus" was isolated from the exudate of theleg'0 but was later identified as a lactose fermentinghalophilic vibrio.8 A case of erythema multiformewith fatal fulminating septicaemia was described byZide." Blood culture yielded "Vibrio para-haemolyticus," which was later identified as a lactosefermenting halophilic vibrio.8 Microscopical exam-ination of the skin lesions showed focal acute fatnecrosis in subcutaneous tissues, and the dermis wasinfiltrated by Gram negative bacteria. Thorsteinsonet al'2 reported three cases of halophilic non-cholera vibrio infection. One of the patients had a

non-purulent thumb infection that required fas-ciotomy and another had gangrene of the leg anddied despite amputation. Fernandez and Pankey'3described three cases of severe necrotising cellulitis,two of which yielded a lactose positive, halophilicvibrio. Five patients with septicaemia and woundinfections caused by a similar organism weredescribed by Hollis et al.'4 All five died shortly afteradmission, but details of the skin lesions were notgiven. Matsuo et all5 described a fatal case of sep-ticaemia caused by a lactose positive halophilic vibrio,presenting with bullae on the legs and eruptionsover the arms. Histological examination of the skinlesions showed areas of fibroadipose necrosis in thedermis and subcutaneous tissue. Massive bacterial

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infiltration in the skin was also noted.Blake et al," Mertens et al,'7 and Tacket et al'l

reported altogether 18 patients with V vulnificuswound infections, the lesions being variouslydescribed as bullous, cellulitic, or necrotic. Castillo'9described two patients with V vulnificus septicaemiawho developed haemorrhagic and necrotic skinlesions of the hands that required urgent surgicaldebridement. Finally, Kelly et al20 reported a fatalcase of V vulnificus septicaemia with acute necrotis-ing myositis of the leg. Postmortem dissectionshowed focal necrosis and haemorrhage of the calfmuscles.'7

In all these cases of serious wound infection,spreading necrotic skin lesions appear to have beenregarded as complications of an often fatal Vvulnificus septicaemia. Detailed clinical informationwas not always available, however, and some ofthese patients may have had necrotising fasciitis. Vvulnificus necrotising fasciitis may be part of a rangeof conditions, varying from localised focal necrosisof the dermis to widespread skin and musclenecrosis.Wound infections due to V vulnificus are usually

caused by contamination with sea water or seafood.6 In our case there was no history of suchexposure. The domestic water supply was culturedbut no pathogen was isolated, and the basin of dirtywater which the patient used to rub the abrasion hadbeen poured away.Although caused by an unusual organism, this

case of necrotising fasciitis illustrates the generalprinciples of management of this condition, includ-ing early recognition and immediate aggressive sur-

gical treatment.2

We thank Dr P Yip, Department of Paediatrics,United Christian Hospital, for permission to reportthis patient, who was under her care. We are in-debted to Mr HT Yeung and Mr Eric Ng, DiagnosticLaboratory, United Christian Hospital for technicalhelp.

References

'Meleney FL. Hemolytic streptococcus gangrene. Arch Surg1924;9:317-64.

Woo, Patrick, Simon, French2 Janevicius RV, Hann SE, Batt MD. Necrotising fasciitis (collec-

tive review). Surg Gynecol Obstet 1982; 154:97-102.3 Leppard BJ, Seal DV. The value of bacteriology and serology in

the diagnosis of necrotising fasciitis. Br J Dermatol1983; 1"9:37-44.

4 Swartz MN. In: Mandell GL, Douglas RG, Bennett JE, eds.Principles and practice ofinfectious diseases. New York: WileyMedical Publications, 1979:813-6.

5 Giuliano A, Lewis F, Hadley K, Blaisdell FW. Bacteriology ofnecrotising fasciitis. Am J Surg 1977;134:52-7.

6 Blake PA, Weaver RE, Hollis DG. Diseases of humans (otherthan cholera) caused by vibrios. Ann Rev Microbiol1980;34:357-60.

7 Poole MD, Oliver JD. Experimental pathogenicity and mortalityin ligated ileal loop studies of the newly reported halophiliclactose-positive vibrio sp. Infect Immun 1978;20: 126-9.

Weaver RE, Ehrenkranz NJ. Vibrio parahemolyticus sep-ticaemia. Arch Intern Med 1975;135:197.

Farmer JJ III. Vibrio ("Beneckea") vulnificus, the bacteriumassociated with sepsis, septicemia and the sea. Lancet1979;ii:903.

'° Roland FP. Leg gangrene and endotoxin shock due to Vibrioparahemolyticus-an infection acquired in New Englandcoastal waters. N Engl J Med 1970;282: 1306.

Zide N, Davies J, Ehrenkranz NJ. Fulminating Vibrio para-hemolyticus septicemia. Arch Intern Med 1974; 133:479-81.

12 Thorsteinson SB, Minuth JN, Musher DM. Clinical manifesta-tions of halophilic non-cholera vibrio infections. Lancet1974;ii: 1283-4.

3 Fernandez CR, Pankey GA. Tissue invasion by unnamed marinevibrios. JAMA 1975;233:1173-6.

'4 Hollis DG, Weaver RE, Baker CN, Thornsberry C. Halophilicvibrio species isolated from blood cultures J Clin Microbiol1976;3:425-31.

"5 Matsuo T, Kohno S, Ikeda T, Saruwatari K, Nonomiya H. Ful-minating lactose-positive vibrio septicemia. Acta Pathol Jap1978;28:937-48.

16 Blake PA, Merson MH, Weaver RE, et al. Disease caused by amarine vibrio (clinical characteristics and epidemiology). NEngl J Med 1979;300: 1-5.

7Mertens A, Nagler J, Hansen W, Gepts-Friedenreich E.Halophilic lactose-positive vibrio in a case of fatal septicemia.J Clin Microbiol 1979;9:233-5.

18 Tacket CO, Barrett TJ, Mann JM, Roberts MA, Blake PA.Wound infections caused by Vibrio vulnificus, a marine vibrioin inland areas of the United States. J Clin Microbiol1984; 19:197-9.

9 Castillo LE, Winslow DL, Pankey GA. Wound infection andseptic shock due to Vibrio vulnificus. Am J Trop Med Hyg1981;30: 844-8.

20 Kelly MT, McCormick WF. Acute bacterial myositis caused byVibrio vulnificus. JAMA 1981;246:72-3.

Requests for reprints to: Professor GL French, UniversityDepartment of Microbiology, 1/F, Clinical Sciences Build-ing, Prince of Wales Hospital, Shatin, New Territories,Hong Kong.

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