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Journal of Clinical Microbiology, October 2007, p. 3462-3463, Vol. 45, No. 10
0095-1137/07/$08.00+0     doi:10.1128/JCM.01205-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

CASE REPORT

Severe Gastroenteritis and Hypovolemic Shock Caused by Grimontia (Vibrio) hollisae Infection{triangledown}

Federico Hinestrosa,1 Robert G. Madeira,2 and Paul P. Bourbeau3*

Divisions of Medicine,1 Laboratory Medicine, Geisinger Medical Center, Danville, Pennsylvania,3 Division of Medicine, Geisinger Wyoming Valley Medical Center, Wilkes-Barre, Pennsylvania2

Received 15 June 2007/ Returned for modification 26 July 2007/ Accepted 10 August 2007


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ABSTRACT
 
Vibrio hollisae is a halophilic species that was recently reclassified as Grimontia hollisae. This organism is known to cause moderate to severe cases of gastroenteritis. We report a case of an individual who suffered a more severe form of this disease, presenting with profound hypotension and acute renal failure, secondary to hypovolemic shock.


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CASE REPORT
 
A previously healthy, 43-year-old, Vietnamese male presented to the emergency room with several days of persistent severe diarrhea associated with nausea, vomiting, and diffuse, cramping abdominal pain. He denied recent travel, contacts with sick people, or ingestion of raw food. Although initially denying recent consumption of seafood, he later recalled consumption of shellfish. On physical exam, his blood pressure was 60/48 mm Hg, heart rate 120 beats/min, and temperature 98.1°F. He looked acutely ill and was dehydrated. His abdomen had diffuse tenderness to palpation without rebound or guarding, and his stools were positive for occult blood. The remainder of his physical exam was unremarkable. Laboratory results included a leukocyte count of 15,510/mm3 with 67% polymorphonucleocytes and 17% bands. Blood chemistry results were consistent with acute renal failure and anion gap metabolic acidosis. Two blood cultures, a stool culture, an exam for ova and parasites, a Clostridium difficile toxin assay, and a fecal leukocyte exam were ordered. A computerized axial tomography scan of the abdomen revealed diffusely dilated and edematous small bowel wall. The patient was admitted to the hospital, treated initially with intravenous fluids, and prescribed ciprofloxacin (800 mg/day) and metronidazole (1.5 g/day). He improved significantly, his renal failure resolved, and his vomiting and diarrhea stopped. He was discharged 2 days later on oral antibiotics.

Stool test results were positive for fecal leukocytes and negative for ova and parasites and C. difficile toxin A/B. A routine stool culture was negative for Salmonella, Shigella, and Campylobacter spp. However, moderate growth of non-lactose-fermenting gram-negative bacilli on MacConkey agar plates and moderate growth of beta-hemolytic, oxidase-positive gray colonies on sheep blood agar plates were noted after overnight incubation. Poor growth of these colonies was noted upon subsequent subculture to thiosulfate-citrate-bile salts-sucrose (TCBS) agar. An identification of Vibrio hollisae was obtained with a Vitek 2 GNI card (bioMerieux, Inc., Durham, NC) and the BBL Crystal E/NF ID kit (Becton Dickinson Microbiology, Cockeysville, MD). This identification was confirmed by Sharon Abbott, Microbial Disease Laboratory, Division of Communicable Disease Control, California Department of Public Health, Richmond, CA.

Susceptibility testing was performed as described for Vibrio species (3) using a MicroScan (Dade Behring, West Sacramento, CA) negative type 30 MIC panel. The MIC test was initially performed using inoculum water with Pleuronic as specified in the Microscan product insert. When the isolate failed to grow, 0.9% sterile saline was substituted for inoculum water with Pleuronic. MIC results were recorded after 24 h, and the panel was reincubated for an additional 24 h. The MICs recorded at 24 h remained unchanged at 48 h. By using published interpretive criteria (3), the isolate was susceptible to cefazolin, cephalothin, ceftazidime, cefoxitin, cefepime, cefotaxime, ampicillin, amoxicillin-clavulanate, ampicillin-sulbactam, piperacillin, piperacillin-tazobactam, imipenem, meropenem, amikacin, gentamicin, ciprofloxacin, levofloxacin, tetracycline, chloramphenicol, and trimethoprim-sulfamethoxazole.

Vibrio hollisae is a halophilic vibrio species first described by Hickman et al. (6) and recently reclassified as Grimontia hollisae by Thompson et al. (10). It is primarily known to cause moderate to severe cases of gastroenteritis in healthy people and is rarely isolated from extraintestinal sites, such as from blood samples (4). Grimontia hollisae bacteria are gram negative, motile by a polar flagellum, and oxidase positive. Strains are negative for the Voges-Proskauer reaction, arginine dihydrolase, and lysine and ornithine decarboxylase, but indole production and nitrate reduction are positive (10). The organism is reported to not usually grow on TCBS agar or MacConkey agar but does grow well on sheep blood agar and marine agar (6).

In the study by Morris et al. (8), G. hollisae was mainly associated with cases of gastroenteritis. The chief medical complaints included diarrhea and abdominal pain. Most of the patients developed vomiting, low-grade fever, and mild leukocytosis and required admission to the hospital. All patients successfully recovered (8). Gastrointestinal disease associated with Vibrio species is generally associated with consumption of seafood (4). Thirty-two cases of G. hollisae infection have been reported in some detail in the literature. The majority of the cases of enteric disease have involved otherwise healthy individuals who had consumed raw oysters, clams, or shrimp (1, 2, 5-9). In our case, the patient suffered from more severe symptoms, including profound hypotension and acute renal failure due to hypovolemic shock that were corrected successfully with aggressive intravenous hydration.

Only four cases of septicemia associated with V. hollisae have been reported in the literature. Three cases occurred in patients with underlying liver disease (5, 7-9).

Epidemiologically, most of the cases of G. hollisae infection have been restricted to the Atlantic and Pacific coasts of the United States. Only one reported case has occurred in Europe (5). Our case occurred in central Pennsylvania, 150 miles from the Atlantic coast. This report indicates the importance of clinical microbiologists being aware of the possibility of Vibrio and Vibrio-like organisms, including G. hollisae, not only as enteric pathogens but also as possible agents of extraintestinal disease, especially in laboratories serving coastal areas or in individuals with exposure to seafood or shellfish. A second important point is that the incidence of G. hollisae infections is likely underestimated, and further attempts should be made to improve the microbiological diagnosis of intestinal infections. TCBS agar is used as the selective medium for isolation of Vibrio species in most clinical laboratories, but unfortunately, G. hollisae grows poorly on this medium. The best growth of our isolate occurred on a sheep blood agar plate. Microbiologists need to work up beta-hemolytic, oxidase-positive, gram-negative bacilli from stool cultures. Finally, obtaining a thorough patient history and recent culinary habits can often be an invaluable clue to the accurate identification of these organisms and thereby result in the prompt and proper treatment of the patient.


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FOOTNOTES
 
* Corresponding author. Mailing address: Division of Laboratory Medicine, Geisinger Medical Center, Danville, PA 17822-0131. Phone: (570) 271-7467. Fax: (570) 271-6105. E-mail: pbourbeau{at}geisinger.edu Back

{triangledown} Published ahead of print on 17 August 2007. Back


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REFERENCES
 
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Journal of Clinical Microbiology, October 2007, p. 3462-3463, Vol. 45, No. 10
0095-1137/07/$08.00+0     doi:10.1128/JCM.01205-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.




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