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Cholera-like presentation in Vibrio fluvialis enteritis.

Abstract: We describe a patient who presented with cholera-like diarrhea seven days after eating shellfish at a seafood buffet on the Gulf Coast. The patient's stool culture grew only Vibrio fluvialis on TCBS agar, and his diarrhea and profound acidosis completely resolved within 24 hours of initiating antibiotics. To our knowledge, a detailed case of V fluvialis diarrhea with cholera-like symptoms has not been reported.

Key Words: Vibrio fluvialis, enteritis


Vibrio fluvialis is a halophilic, polarly-flagellated, Gram negative rod that has been implicated in both outbreaks and sporadic cases of acute gastroenteritis in humans. Vibrio species are concentrated by oysters and other filter feeders and are frequently isolated from brackish surface waters of the coastal United States. V fluvialis was first isolated in Bahrain in 1975 from the stool of a patient with diarrhea. Not until 1981 did the Centers for Disease Control receive its first isolate from a patient who had V fluvialis gastroenteritis residing in the United States. (1) Originally called Group F vibrios by Lee et al in 1977, and EF-6 vibrios by the Centers for Disease Control in 1980, the bacterium was described and named Vibrio fluvialis by Lee et al in 1981. (2)

Case Report

A 72-year-old male with a history of coronary artery disease presented with a four-day history of nausea, vomiting, abdominal cramping, and one to four watery, light-brown stools per hour unrelieved by loperamide or bismuth subsalicylate. He also noted decreased urine output, subjective fevers, and leg cramping two days before admission. He denied any hematochezia, melena, hematemesis, dysuria, antibiotic use, recent travel, prior history of inflammatory bowel disease, or alcohol use. He is a resident of the Mississippi Gulf Coast and had eaten shellfish at a local seafood buffet seven days before admission.

Presenting vitals were pulse of 85 per minute, blood pressure of 118/37 mm Hg, temperature of 35.8[degrees]C, respirations of 18 per minute, and pulse oximetry of 98% on room air. Physical examination revealed dry mucous membranes, regular heart rate, and clear lungs. The patient had normal bowel sounds and a diffusely tender abdomen without rebound or guarding. Rectal examination was unremarkable. Serum chemistry revealed a sodium of 131 mmol/L, potassium of 3.5 mmol/L, chloride of 100 mmol/L, bicarbonate of 12.2 mmol/L, BUN of 55 mg/dL, creatinine of 7.0 mg/dL (baseline 1.0 mg/dL), glucose of 208 mg/dL, an anion gap of 18.8, ALT of 13 IU/L, alkaline phosphatase of 77 IU/L, total bilirubin of 0.3 mg/dL, amylase of 44 U/L, lipase 23.9 U/L, and lactate of 0.9 mmol/L. Arterial blood gas revealed a pH of 7.17, PCO2 of 24.5 mm Hg, PO2 of 110 mm Hg, bicarbonate of 9 mmol/L, and 97% saturation on room air. Complete blood count showed an elevated white blood cell count of 13.1 x [10.sup.9]/L with 42% band forms, a hemoglobin of 14.9 g/dL, hematocrit of 44.5%, and platelets of 468,000/uL. Electrocardiogram was normal sinus rhythm without ischemic changes, and an acute abdominal series displayed a nonobstructive bowel gas pattern. Presenting bicarbonate deficit was approximately 420 mEq.

The patient was admitted to the intensive care unit and his renal function improved with IV hydration of 7 L within the first 5 hours of admission and 12 L within the first 24 hours; however, his diarrhea and acidosis continued despite bicarbonate and electrolyte replacement, fluid replacement, and loperamide. On the evening of hospital day 3, levofloxacin and doxycycline were started empirically on the early report of Gram negative rods in the stool. Stool samples before antibiotics were positive for occult blood and fecal leukocytes, and culture ultimately identified Vibrio fluvialis as the sole pathogen on TCBS agar. Levofloxacin was discontinued after one dose on the preliminary report of V fluvialis. Doxycycline was continued and resulted in the complete resolution of the patient's diarrhea and acidemia on hospital day 4.


The typical clinical picture of patients with diarrhea associated with V fluvialis was described in 500 patients in Bangladesh from 1976 to 1977, and includes vomiting (97%), abdominal pain (75%), moderate to severe dehydration (67%), and significant fever (35%). (3) Bloody diarrhea occurred in 11%, while microscopic evaluation demonstrated leukocytes and erythrocytes in 75%. (3)

Klontz and Desenclos (4) described the largest clinical series of V fluvialis cases in the United States. From 1982 through 1988, the Florida Department of Health and Rehabilitative Services received 10 reports of patients presenting clinically with gastroenteritis and a stool culture positive for V fluvialis. Seven of the 10 patients' stool samples yielded only V fluvialis and no other pathogens. These patients commonly described their diarrhea as watery with a median of 7 episodes per day, but half reported at least one episode of bloody stool during the course of their illness. Eight had eaten seafood in the week before the onset of symptoms with the most common vehicle being raw oysters. In 2002, 36 isolates of V fluvialis were reported to the CDC, with 12 occurring in the Gulf Coast states of Florida, Alabama, Mississippi, Louisiana, and Texas. Of the 36 isolates, 29 were isolated from stool samples. (5)

Though diarrhea in general can cause electrolyte disturbances, none of the cases in the literature associated with V fluvialis has described diarrhea with such severe acidemia requiring bicarbonate replacement as in our patient. The frequency of one to four stools per hour is much greater than typically seen in association with this pathogen. Though our patient did have coronary artery disease, he lacked other significant comorbidities that could have contributed to the severity of his condition. His residence on the Gulf Coast and his history of eating shellfish just 7 days prior suggests the source of his infection. Despite receiving extensive supportive care in an intensive care unit for two days, his acidemia and profound diarrhea did not improve until the administration of antibiotics, with complete resolution within 24 hours of initiation. That his stool culture grew only V fluvialis is significant in that it suggests no confounding pathogens contributed to his condition. In addition, the patient's stool was negative for Clostridium difficile toxin, rotavirus antigen, and adenovirus antigen.

In addition to causing gastroenteritis, (4,6-8) V fluvialis has been implicated in cerebritis secondary to hemorrhagic cellulitis in an alcoholic who had suffered multiple fire-ant stings and had subsequently waded in brackish water. (9) V fluvialis has also been implicated in wound infections (4) including one associated with medicinal leech therapy, (10) peritonitis in a patient receiving continuous ambulatory peritoneal dialysis, (11) and suppurative cholangitis. (12)

V fluvialis produces several toxins, including cell elongation factor (CEF), cell-killing factor (CKF), a protease, and a hemolysin. (13,14) However, the exact role of each of these toxins in producing the clinical manifestations of V fluvialis-associated diarrhea has been difficult to establish.


Figures suggest that V fluvialis is infrequently implicated in gastroenteritis in the United States. However, only the cholera agents are nationally notifiable; the true number of the remaining Vibrio infections is greater than reported. Though multiple case reports of diarrhea have been reported in the literature, none has described diarrhea with such frequency, dehydration, and severe acidemia requiring bicarbonate replacement. Ingestion of raw or undercooked seafood, especially raw oysters, is an important risk factor. Physicians should consider this organism in the differential diagnosis for diarrhea in patients who have recently ingested raw or undercooked seafood.


We thank Dr. Parisa Ann Suthun for her careful review of this paper.


1. Tacket CO, Hickman F. Peirce GV, et al. Diarrhea associated with Vibrio fluvialis in the United States. J Clin Microbiol 1982;16:991-992.

2. Lee JV, Shread P, Furniss AL, et al. Taxonomy and description of Vibrio fluvialis sp nov (synonym Group F vibrios, Group EF6). J Appl Bacteriol 1981;50:73-94.

3. Huq MI, Alam AK, Brenner DJ. et al. Isolation of Vibrio-like group, EF-6, from patients with diarrhea. J Clin Microbiol 1980;11:621-624.

4. Klontz KC, Desenclos JC. Clinical and epidemiological features of sporadic infections with Vibrio fluvialis in Florida, USA. J Diarrhoeal Dis Res 1990;8:24-26.

5. Centers for Disease Control. Summary of human Vibrio isolates reported to CDC, 1982. Available at: Accessed May 1, 2005.

6. Bellet J, Klein B, Altieri M, et al. Vibrio fluvialis, an unusual pediatric enteric pathogen. Pediatr Emerg Care 1989;5:27-28.

7. Kolb EA, Eppes SC, Klein JD. Vibrio fluvialis: an underrecognized enteric pathogen in infants? South Med J 1997;90:544-545.

8. Hickman-Brenner FW, Brenner DJ, Steigerwalt AG, et al. Vibrio fluvialis and Vibrio furnissii isolated from a stool sample of one patient. J Clin Microbiol 1984;20:125-127.

9. Huang KC, Hsu RW. Vibrio fluvialis hemorrhagic cellulitis and cerebritis. Clin Infect Dis 2005;40:e75-e77.

10. Varghese MR, Farr RW, Wax MK, et al. Vibrio fluvialis wound infection associated with medicinal leech therapy. Clin Infect Dis 1996;22:709-710.

11. Ratnaraja N, Blackmore T, Byrne J, et al. Vibrio fluvialis peritonitis in a patient receiving continuous ambulatory peritoneal dialysis. J Clin Microbiol 2005;43:514-515.

12. Yoshii Y, Nishino H, Satake K, et al. Isolation of Vibrio fluvialis, an unusual pathogen in acute suppurative cholangitis. Am J Gastroenterol 1987;82:903-905.

13. Chikahira M, Hamada K. Enterotoxigenic substance and other toxins produced by Vibrio fluvialis and Vibrio furnissii. Nippon Juigaku Zasshi 1988;50:865-873.

14. Lockwood DE, Kreger AS, Richardson SH. Detection of toxins produced by Vibrio fluvialis. Infect Immun 1982;35:702-708.
The pessimist complains about the wind; the optimist expects it to
change; the realist adjusts the sails.
--William Arthur Ward

David R. Allton, MD, Michael A. Forgione Jr., MD, and Sheila P. Gros, MT (ASCP) SM

From the Departments of Internal Medicine and Infectious Diseases, Keesler Medical Center, Keesler Air Force Base, Biloxi, MS.

Reprint requests to David R. Allton, MD, Keesler Medical Center, 2003 Dixon Court, Godfrey, IL 62035. Email:

Accepted April 5, 2006.


* Vibrio fluvialis is often isolated from brackish waters of the coastal US and has been implicated in gastroenteritis in humans.

* Though most cases are mild, the diarrhea and acidosis experienced by this patient was very severe.

* Ingestion of raw or undercooked seafood is a risk factor for developing V fluvialis diarrhea.
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Title Annotation:Case Report; medical research; includes related article "Key Points"
Author:Gros, Sheila P.
Publication:Southern Medical Journal
Geographic Code:1U600
Date:Jul 1, 2006
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