Acute diarrhea is usually mild and self-limited in normally healthy individuals. Further diagnostic evaluation is indicated in patients with severe diarrhea. We present a case of a 46-year-old woman who presented with dehydration and acute renal failure due to acute severe diarrhea. Initial stool study was suggestive of Aeromonas. Further stool test revealed offending bacteria, which led to appropriate antibiotic use. This paper emphasizes the importance of complete history and correlation between clinical data and laboratory tests. 1. Introduction Cholera is an acute intestinal infectious disease caused by gram-negative bacterium Vibrio cholerae and has variable manifestations. It has been responsible for several pandemics and is endemic in over 50 countries. In 2011, a total of 58 countries from all continents reported cholera cases to World Health Organization (WHO). The total number of cases reported in 2011 worldwide was 5,89,894 with total deaths 7816 [1]. It is estimated that at least 3–5 million persons develop clinical cholera each year, resulting in approximately 100,000 to 120,000 deaths [2]. In the United States, incidence of cholera is very low (0–5 cases per year) primarily due to ingestion of contaminated food, and about half of these cases are imported [3]. The most recent outbreak was reported in Haiti in 2010. Early recognition based on the history and clinical features is vital. More than 80% of cholera cases respond to oral rehydration therapy. If left untreated, 25–50% of typical cholera cases are fatal [3]. 2. Case Report A 46-year-old Dominican woman presented to emergency room with complaints of five hours of vomiting and profuse diarrhea in summer 2011. Symptoms started within 3 hours after eating chicken sandwich and salad, which were prepared at home. While frequency of vomiting decreased, she reported diarrhea, which later occurred and was too often to count. Subsequently, her urine output decreased. The patient denied fever or blood in the stool. She had previously been healthy and was not taking any medications. She had no known allergies. Her last travel to Dominican Republic or outside the US was more than 3 years ago. She lived with her husband and son. She consumed alcohol occasionally and did not smoke or use illicit drugs. Her family and friends who had the dinner together had been well. She had no history of similar symptoms in the past. She denied recent use of antibiotics or hospitalization. She had gastric bypass surgery in 2005 and abdominoplasty in 2007. At presentation, she was afebrile with pulse rate of 103
References
[1]
World Health Organization, “Weekly epidemiological report,” 2012.
[2]
World Health Organization, “Cholera,” 2012, http://www.who.int/mediacentre/factsheets/fs107/en/index.html.
[3]
Centers for Disease Control and Prevention (CDC), “Cholera,” 2011, http://www.cdc.gov/cholera/epi.html.
[4]
O. Schiraldi, V. Benvestito, C. Di Bari, R. Moschetta, and G. Pastore, “Gastric abnormalities in cholera: epidemiological and clinical considerations,” Bulletin of the World Health Organization, vol. 51, no. 4, pp. 349–352, 1974.
[5]
J. G. Morris Jr., T. Takeda, B. D. Tall et al., “Experimental non-O group 1 Vibrio cholerae gastroenteritis in humans,” Journal of Clinical Investigation, vol. 85, no. 3, pp. 697–705, 1990.
[6]
R. A. Giannella, S. A. Broitman, and N. Zamcheck, “Influence of gastric acidity on bacterial and parasitic enteric infections. A perspective,” Annals of Internal Medicine, vol. 78, no. 2, pp. 271–276, 1973.
[7]
S. Gitelson, “Gastrectomy, achlorhydria and cholera,” Israel Journal of Medical Sciences, vol. 7, no. 5, pp. 663–667, 1971.
[8]
W. B. Greenough, “Vibrio cholerae,” in Principles and Practice of Infectious Disases, G. L. Mandell, R. G. Douglas, and J. E. Bennett, Eds., p. 1680, John Wiley & Sons, New York, NY, USA, 1979.
[9]
C. W. Howden and R. H. Hunt, “Relationship between gastric secretion and infection,” Gut, vol. 28, no. 1, pp. 96–107, 1987.
[10]
T. R. Hendrix, “The pathophysiology of cholera,” Bulletin of the New York Academy of Medicine, vol. 47, no. 10, pp. 1169–1180, 1971.
[11]
D. R. Nalin, M. M. Levine, J. Rhead et al., “Cannabis, hypochlorhydria, and cholera,” The Lancet, vol. 2, no. 8095, pp. 859–862, 1978.
[12]
J. W. Tappero and R. V. Tauxe, “Lessons learned during public health response to cholera epidemic in Haiti and the Dominican Republic,” Emerging Infectious Diseases, vol. 17, no. 11, pp. 2087–2093, 2011.
[13]
M. J. Albert, M. Neira, and Y. Motarjemi, “The role of food in the epidemiology of cholera,” World Health Statistics Quarterly, vol. 50, no. 1-2, pp. 111–118, 1997.
[14]
K. L. MacDonald, M. Eidson, C. Strohmeyer et al., “A multistate outbreak of gastrointestinal illness caused by enterotoxigenic Escherichia coli in imported semisoft cheese,” Journal of Infectious Diseases, vol. 151, no. 4, pp. 716–720, 1985.
[15]
W. L. George, M. M. Nakata, J. Thompson, and M. L. White, “Aeromonas-related diarrhea in adults,” Archives of Internal Medicine, vol. 145, no. 12, pp. 2207–2211, 1985.
[16]
A. M. Carnahan and G. Andrews, “Vibrio, Aeromona, Plesiomonas and Campylobacter species,” in Textbook of Diagnostic Microbiology, C. R. Mahon and G. Manuselis, Eds., p. 524, WB Saunders, Philadelphia, Pa, USA, 2nd edition, 2000.
[17]
D. Saha, M. M. Karim, W. A. Khan, S. Ahmed, M. A. Salam, and M. L. Bennish, “Single-dose azithromycin for the treatment of cholera in adults,” The New England Journal of Medicine, vol. 354, no. 23, pp. 2452–2462, 2006.
[18]
E. J. Nelson, D. S. Nelson, M. A. Salam, and D. A. Sack, “Antibiotics for both moderate and severe cholera,” The New England Journal of Medicine, vol. 364, no. 1, pp. 5–7, 2011.
[19]
A. K. Mukhopadhyay, S. Garg, G. B. Nair et al., “Biotype traits and antibiotic susceptibility of Vibrio cholerae serogroup O1 before, during and after the emergence of the O139 serogroup,” Epidemiology and Infection, vol. 115, no. 3, pp. 427–434, 1995.