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Case Report

Case Report, Global Climate Change and Wound Care: Case Study of an Off-season Vibrio alginolyticus Infection in a Healthy Man

Abstract

Vibrio alginolyticus is a halophilic Gram-negative bacterium normally present in seawater. Vibrios are not capable of cutaneous invasion through intact skin and their isolation from extraintestinal sites is uncommon. However, interruptions in skin integrity (cuts or abrasions) can allow these bacteria to cause complicated skin and soft tissues infections.

This case study describes the clinical assessment and management of a nonhealing traumatic wound, sustained in a coastal area during the winter months, in a healthy 70-year-old man. Culture results were positive for V. alginolyticus. Appropriate antibiotic treatment and topical wound care successfully resolved the infection. V. alginolyticus infections are usually benign; respond well to treatment, even with local therapy only; and tend to result from contact with warm ocean water. The clinical characteristics of the wound prompted a suspicion of a Vibrio infection even though the wound was sustained in the winter time and the patient did not have direct contact with ocean water. Although other case studies of Vibrio infections in the absence of direct contact with ocean water have been published, increased ocean temperatures due to global climate changes may explain the out-of-season infection in this patient. Clinicians should monitor the progression of wound healing and be prepared to modify treatment based on individual circumstances, especially in the case of unusual wound presentation, nonhealing, or a progressing wound infection.

     Vibrio alginolyticus is a halophilic Gram-negative, motile, curved bacterium and one of the 12 Vibrio species responsible for human infections.1-4 It is present in seawater with a worldwide distribution.1 Global warming has resulted in increased marine temperatures with an expected diffusion of these pathogens to northern global regions.5-7 Among Vibrio species, the most commonly related to skin and soft tissues infection are V. vulnificus, V. parahaemolyticus, V. alginolyticus, and V. damsela.8–12

     Patient history of persons infected with Vibrios usually shows a recent exposure to seawater,12-18 although cases without specific exposure have been reported.19-23 Normally, Vibrios are not capable of cutaneous invasion through intact skin; however, the presence of cuts (wounds) or abrasions provides a portal of entry and explains the high incidence of Vibrio-related wound infections in bathers and persons involved in other marine activities.12,14,19,21,24,25 The majority of V. alginolyticus isolates have been found in patients with skin and soft tissues infections,7,12,19,22,24,26-31 including ulcers and abscesses, necrotizing fasciitis,13,15,32,33 cellulitis,12,18,34 and infections of the ear (otitis media and otitis externa).7,12,19,20,22,25,27,35 A case of V. alginolyticus peritonitis associated with peritoneal dialysis also has been reported.36 Other rare complications are gastroenteritis (in immunocompromised patients),37,38 intracranial infection following an injury in saltwater,17 pleural empyema (in an immunocompromised patient),39 and bacteremia.26,39-41 Infections due to V. alginolyticus are usually benign and respond well to local therapy.

Case Study

     Mr. S. presented at the authors’ outpatient service with a post-traumatic wound infection. The 70-year-old healthy Caucasian man had no history of diabetes or smoking and was not taking any prescription medications. He had sustained a limited penetrating trauma of the medial surface of the right leg (distal third) with a lacerated contused wound after a fall from his bicycle during a ride by the Adriatic Sea in the winter. His wound initially was treated by his family physician with surgical debridement, conventional dressings, and no antibiotic therapy (a tetanus booster had been administered within 5 years of the injury) and cleaned daily with an antiseptic solution (povidone iodine). Despite this daily attention, after 10 days the wound developed a central area of necrosis and progressively worsened, developing a wider central necrotic area with hyperemic irregular edges and serosanguinous exudation.

     After more than 2 months with no improvement, Mr. S presented at the authors’ surgical outpatient service. At the time of observation, the wound had a central excavated necrotic area in the shape of a crater with irregular edges and a wide surrounding hyperemic area. It was exuding pus. The leg was functionally impaired and painful both at rest and on walking. No signs of systemic inflammation were present: body temperature was normal and the leukocyte count was within the normal values, with normal proportions of polymorphonuclear cells.

     Color Doppler ultrasonography of the right lower limb was performed to evaluate possible venous insufficiency. An x-ray of the right leg was obtained to exclude osteomyelitis.

     Two biopsy samples of the lesion were taken for microbiological investigation and empirical antibiotic treatment with levofloxacin (500 mg twice daily) was started, together with local medication with salicylic acid plus sodium iodide (Fertomcidina, Theriaca Srl, Italy). Both biopsy samples produced pure cultures of Gram-negative, oxidase-positive organisms that grew on thiosulfate-citrate-bile salts-sucrose agar. The isolates presumptively were identified as V. alginolyticus by the Vitek® 2 system (bioMérieux, Inc, Hazelwood, MO). Species-level identification was further confirmed with manual tests (growth at high concentration of NaCl [up to 8%] and reactions to urea, indole, arginine, ornithine, lysine, glucose, sucrose, lactose, threalose, arabinose, gelatine, acetate, and the Voges-Proskauer test). Bacterial DNA was extracted from culture isolates using a QIAmp® DNA Mini kit (Qiagen, Hilden, Germany). Sequence analysis of the PCR-amplified 16S rRNA genes revealed 99% homology with the prototype strain sequence of V. alginolyticus ATCC 177497. In vitro antimicrobial susceptibility testing using the Etest® (AB Biodisk, Solna, Sweden) confirmed susceptibility to levofloxacin (minimum inhibitory concentration [MIC], 0.38 mg/L 0.38 mg/L) and additionally yielded the following MICs: amoxycillin-clavulanic acid, 4 mg/L; cefotaxime, 0.19 mg/L; ceftazidime, 0.25 mg/L; ciprofloxacin, 0.38 mg/L; doxycycline, 0.38 mg/L; meropenem, 0.125 mg/L; tetracycline, 0.5 mg/L; and trimethoprim-sulphamethoxazole, 0.19 mg/L. Cultures for anaerobes and mycobacteria yielded no growth.

     On the basis of these results, levofloxacin therapy was continued for a total of 20 days (500 mg twice daily for 7 days, followed by 750 mg once daily). After the first week, Mr. S’s condition improved (see Figure 1). The pain resolved, leg functionality returned, and purulent exudation lessened. After the second week, necrosis decreased slightly and local inflammation was responding favorably to treatment (see Figure 2). After 1 month, the slow healing process resulted in wound remargination with the complete disappearance of the hyperemic area (see Figure 3).

Discussion

     The different micro-organisms in any wound are influenced by various wound (type, depth, location) and host (tissue perfusion, efficacy of the immune response) characteristics. Wound contaminants usually originate from three main sources: the environment (exogenous micro-organisms in the air or introduced by traumatic injury), the surrounding skin (involving members of the normal skin microflora such as Staphylococcus epidermidis, micrococci, skin diphtheroids), and endogenous factors involving mucous membranes (gastrointestinal, oropharyngeal, genitourinary mucosa). In Mr. S’s case, initial wound management reflected the family physician’s supposition that the wound contaminants were common micro-organisms belonging to the surrounding skin and to soil. Thus, the clinician applied standard wound management: normal and compressive dressing, disinfection with antiseptic solution, wound cleansing, and repeated surgical debridement.

     V. alginolyticus was the only invasive pathogen isolated after 2 months. No other micro-organisms were identified. In this case study, the infection was directly related to neither previous swimming nor any direct contact with seawater, although the wound was incurred near the beach. Presentation was unusual because the injury/contamination occurred during the winter months, when water temperature and levels of Vibrio species are generally lower. The wound characteristics on presentation (emergence of a new area of hyperemia, with irregular edges, central necrosis, disability, and lack of sensation near the trauma site) were unusual and prompted an investigation to identify the pathogen, resulting in definitive therapy of a simple but prolonged and painful wound infection.

Conclusion

     Infections due to V. alginolyticus are usually benign and respond well to local therapy. However, in any patient with a nonhealing wound infection associated with swimming or trauma occurring in coastal areas, V. alginolyticus should be considered among the possible suspected causative organisms, not only in warm seasons but throughout the year, considering the increased marine temperature due to global warming.

Dr. Sganga is Associate Professor of Surgery, Department of Surgery; Dr. Cozza is a General Surgery Resident, Department of Surgery; Dr. Spanu is a Research Fellow, Department of Microbiology; Dr, Spada is a Research Fellow, Department of Surgery; and Dr. Fadda is Professor and Chairman of Microbiology, Department of Microbiology, Catholic University of Sacred Heart, Rome, Italy. Please address correspondence to Gabriele Sganga, Catholic University of Sacred Heart, Department of Surgery, Policlinico “A. Gemmelli”, Largo A. Gemmelli 8, 00168 Roma, Italy; email: gsganga@tiscali.it.

1. Chakraborty S, Nair GB, Shinoda S. Pathogenic vibrios in the natural aquatic environment. Rev Environ Health. 1997;12(2):63–80.

2. West PA. The human pathogenic vibrios — a public health update with environmental perspectives. Epidemiol Infect. 1989;103(1):1–34.

3. Farmer JJ, Hickman-Brenner F. The genera Vibrio and Photobacterium. In: Balows A, Truper HG, Schleifer KH, et al (eds). The Prokaryotes: A Handbook of the Biology of Bacteria. New York: Springer-Verlag; 1992:2952–3011.

4. Schmidt U, Chmel H, Cobbs C. Vibrio alginolyticus infections in humans. J Clin Microbiol. 1979;10(5):666–668.

5. Hornstrup MK, Gahrn-Hansen B. Extraintestinal infections caused by Vibrio parahaemolyticus and Vibrio alginolyticus in a Danish county, 1987-1993. Scan J Infect Dis. 1993;25(6):35–740.

6. Schijven JF, de Roda Husman AM. Effect of climate changes on waterborne disease in the Netherlands. Wat Sci Techn. 2005;51(5):78–87.

7. Schets FM, van den Berg HH, Demeulmeester AA, van Dijk E, Rutjes SA, van Hooijdonk HJ, de Roda Husman AM. Vibrio alginolyticus infections in the Netherlands after swimming in the North Sea. Euro Surveill. Available at: www.eurosurveillance.org/ViewArticle.aspx?ArticleId=3075. Accessed March 27, 2009.

8. Auerbach PS, Yajko DM, Nassos PS, et al. Bacteriology of the marine environment: implications for clinical therapy. Ann Emerg Med. 1987:16(6):643–649.

9. Blake PA, Merson MJ, Weaver RE, Hollis DG, Heublein PC. Disease caused by a marine vibrio: clinical characteristics and epidemiology. N Engl J Med. 1979;300(1):1–5.

10. Blake PA, Weaver RE, Hollis D. Diseases of humans (other than cholera) caused by vibrios. Annu Rev Microbiol. 1980;34:341–367.

11. Joseph SW, Colwell RR, Kaper JB. Vibrio parahaemolyticus and related halophilic vibrios. Crit Rev Microbiol. 1983;10(1):77–124.

12. Dechet AM, Yu PA, Koram N, Painter J. Nonfoodborne vibrio infections: an important cause of morbidity and mortality in the United States, 1997–2006. Clin Infect Dis. 2008;46(7):970–976.

13. Ho PL, Tang WM, Lo KS, Yuen KY. Necrotizing fasciitis due to Vibrio alginolyticus following an injury inflicted by a stingray. Scand J Infect Dis. 1998;30(2):192–193.

14. Hoge CW, Watsky D, Peeler RN, Libonati JP, Israel E, Morris JG Jr. Epidemiology and spectrum of vibrio infections in a Chesapeake Bay community. J Infect Dis. 1989;160(6):985–993.

15. Howard RJ, Pessa ME, Brennaman BH, Ramphal R. Necrotizing soft-tissue infections caused by marine vibrios. Surgery. 1985;98(1):126–130.

16. Lessner AM, Webb RM, Rabin B. Vibrio alginolyticus conjunctivitis. First reported case. Arch Ophthalmol. 1985;103(2):229–230.

17. Opal SM, Saxon JR. Intracranial infection by Vibrio alginolyticus following injury in salt water. J Clin Microbiol. 1986;23(2):373–374.

18. Patterson TF, Bell SR, Bia FJ. Vibrio alginolyticus cellulitis following coral injury. Yale J Biol Med. 1988;61(6):507–512.

19. Pien F, Lee K, Higa H. 1977. Vibrio alginolyticus infections in Hawaii. J Clin Microbiol. 1977;5(6):670–672.

20. Hansen W, Crockaert F, Yourassowsky E. Two strains of vibrio species with unusual biochemical features isolated from ear tracts. J Clin Microbiol. 1979;9(1):152–153.

21. Spark RP, Fried ML, Perry C, Watkins C. Vibrio alginolyticus wound infection-case report and review. Ann Clin Lab Sci. 1979;9(2):133–138.

22. Von Graevenitz A, Carrington GO. Halophilic vibrios from extraintestinal lesions in man. Infection. 1973;1(1):54–58.

23. Morris JG, Black RE. Cholera and other vibrios in the United States. N Engl J Med. 1985;312(6):343–350.

24. Rubin SJ, Tilton RC. 1975. Isolation of Vibrio alginolyticus from wound infections. J Clin Microbiol. 1975;2(6):556–558.

25. McSweeney RJ, Forgan-Smith WR. Wound infections in Australia from halophilic vibrios. Med J Aust. 1977;1(24):896–897.

26. English VL, Lindberg RB. 1977. Isolation of Vibrio alginolyticus from wounds and blood of a burn patient. Am J Med Technol. 1977;43(10):989–993.

27. Ryan WJ. Marine vibrios associated with superficial septic lesions. J Clin Pathol. 1976;29(11):1014–1015.

28. Prociv P. 1978. Vibrio alginolyticus in Western Australia. Med J Aust. 1978;2:296.

29. Bonner JR, Coker AS, Berryman CR, Pollock HM. 1983. Spectrum of vibrio infections in a Gulf Coast community. Ann Intern Med. 1983;99(4):464–469.

30. Pezzlo M, Valter PJ, Burns MJ. 1979. Wound infection associated with Vibrio alginolyticus. Am J Clin Pathol. 1979;71(4):476–478.

31. Hansen W, Hennebert N, Seynave D, Glupczynski Y. Isolation of Vibrio alginolyticus from a leg ulcer. Acta Clin Belg. 1990;45(1):4–8.

32. Gomez JM, Fajardo R, Patiño JF, Arias CA. Necrotizing fasciitis due to Vibrio alginolyticus in an immunocompetent patient. J Clin Microbiol. 2003;41(7):3427–3429.

33. Patiño JF, Castro D, Valencia A, Morales P. Necrotizing soft tissue lesions after a volcanic cataclysm. World J Surg. 1991;15(2):240–247.

34. Aelvoet G, Kets R, Pattyn SR. Cellulitis caused by Vibrio alginolyticus. Acta Derm Venereol. 1983;63(6):559–560.

35. Mukherji A, Schroeder S, Deyling C, Procop GW. An unusual source of Vibrio alginolyticus-associated otitis: prolonged colonization or freshwater exposure? Arch Otolaryngol Head Neck Surg. 2000;126(6):790–791.

36. Taylor R, McDonald M, Russ G, Carson M, Lukaczynski E. Vibrio alginolyticus peritonitis associated with ambulatory peritoneal dialysis. Br Med J (Clin Res Ed). 1981;283(6286):275.

37. Caccamese SM, Rastegar DA. 1999. Chronic diarrhea associated with Vibrio alginolyticus in an immunocompromised patient. Clin Infect Dis. 1999; 29(4):946–947.

38. Uh Y, Park JS, Hwang GY, Jang IH, Yoon KJ, Park HC, Hwang SO. Vibrio alginolyticus acute gastroenteritis: report of two cases. Clin Microbiol Infect. 2001;7(2):104–106.

39. Chien JY, Shih JT, Hsuch PR, Yang PC, Luh KT. Vibrio alginolyticus as the cause of pleural empyema and bacteremia in an immunocompromised patient. Eur J Clin Microbiol Infect Dis. 2002;21(5):401–403.

40. Hollis DG, Weaver RE, Baker CN, Thornsberry C. Halophilic vibrio species isolated from blood cultures. J Clin Microbiol. 1976;3(4):425–431.

41. Janda JM, Brenden R, DeBenedetti JA, Constantino MO, Robin T. Vibrio alginolyticus bacteremia in an immunocompromised patient. Diagn Microbiol Infect Dis. 1986;5(4):337–340.

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