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A fatal case associated with shigellosis and Vibrio fluvialis bacteremia
509
DIAGN MICROBIOL INFECT DIS 1991;14:509-510
A Fatal Case Associated with Shigellosis and Vibrio fluvialis Bacteremia M. John Albert, M. Anowat Hossain, K. Alam, I. Kabir, Prodyot K.B. Neogi, and Saul Tzipori
Vibrio fluvialis is a halophilic bacterium normally found in coastal waters and sea foods. Although this organism is mainly associated with gastroenteritis, there has been one report of isolation from an infected wound (Tacket et al., 1982) and another from gall bladder (Yoshii et al., 1987). We describe here a fatal case associated with V. fluvialis bacteremia in a child, which to our knowledge, has not previously been reported. A 5-month-old boy was admitted to the Clinical Research Centre of the International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh, with a history of watery diarrhea, vomiting, and continuous fever for 7 days that was treated with amoxicillin, paracetamol, metronidazole, and chlorpheniramine maleate for 6 days. On examination he appeared to have clinical evidence of hypovolemic shock, respiratory distress, and toxemia. His body weight was 5.5 kg with weight for age and this was 75% of median (National Center for Health Statistics). Lungs had bilateral crepitation with radiological evidence of infiltration. His stool was alkaline and contained trace amounts of mucus. Stool microscopy revealed 20-50 pus cells, 1-10 red cells, and 1-5 macrophages per high-power field. No protozoa or helminths were detected. Blood examination showed a total leukocyte count of 15,500/mm 3. From the International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka, Bangladesh. Address reprint requests to Dr. M.J. Albert, ICDDR,B, GPO Box 128, Dhaka-1000, Bangladesh. Received 18 October 1990; revised and accepted 7 January 1991. © 1991 Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010 0732-8893/91/$3.50
The patient was kept in the intensive care unit, rehydrated intravenously, and treated with three parenteral doses of ampicillin (200 mg/kg body weight/day), two parenteral doses of gentamicin (6 mg/kg body weight/day), and three oral doses of pivmecillinam suspension (60 mg/kg body weight/day), along with other symptomatic management, but his condition deteriorated further and he died 16 hr after admission. Blood drawn on admission for culture grew V. fluvialis, which was identified by standard techniques (Lee et al., 1981) and was susceptible to ampicillin and gentamicin by disk diffusion method. Rectal swab also taken on admission and cultured on MacConkey agar and SalmoneUa-Shigella agar grew Shigella flexneri 6, which was susceptible to pivmecillinam but resistant to ampicillin. The clinical picture suggested that the patient had septicemia with invasive diarrhea, pneumonia, and second-degree malnutrition. Even though the organism that caused bacteremia (V. fluvialis) was susceptible to ampicillin and gentamicin in vitro, the administration of these drugs at the terminal stage failed to save the patient. Before hospitalization, the patient was treated with amoxicillin without improvement, although amoxicillin and ampicillin have a similar spectrum of activity. Yet it is also known that these drugs could have differences in activity against certain organisms although their in vivo action against Vibrio spp. is not known (Neu, 1979). It is also possible that the patient might have been treated with an inadequate dose of the drug, which could explain the treatment failure. Because we did not suspect involvement of V. fluvialis, no attempts were made to isolate it from stool, and, therefore, it is not certain
510
whether the intestinal tract was infected with V. fluvialis, and whether intestinal infection preceded bacteremia. Even though the patient was shedding Shigella flexneri 6, dysentery was not overt, and although a probable contributory factor, it was not considered to have been the cause of death. Bacteremia due to Gram-negative rods is not uncommon in shigellosis
M.J. Albert et al.
and is probably precipitated by colonic damage (Strulens et al., 1985). It is possible that colonic damage caused by shigellosis and the malnutrition that affects immune function might have facilitated the systemic invasion of V. fluvialis. Therefore, V. fluvialis should be added to the list of organisms causing bacteremia complicating shigellosis.
REFERENCES Lee JV, Shread P, Furniss AL, Bryant TN (1981) Taxonomy and description of Vibrio fluvialis sp. nov. (synonym group F vibrios, group EF-6). J Appl Bacteriol 50:73-94. Neu HC (1979) Amoxicillin. Ann Intern Med 90:356-360. Strulens M, Patte D, Kabir I, Salam A, Nath SK, Butler T (1985) Shigella septicemia: prevalence, presentation, risk factors and outcome. J Infect Dis 152:784-790.
Tacket CO, Hickman F, Pierce GU, Mendoza LF (1982) Diarrhea associated with Vibrio fluvialis in the United States. J Clin Microbiol 16:991-992. Yoshii Y, Nishino H, Satake K, Umeyama K (1987) Isolation of Vibrio fluvialis: an unusual pathogen in acute suppurative cholangitis. Am J Gastroenterol 82:903-905.
DIAGN MICROBIOL INFECT DIS 1991;14:509-510
A Fatal Case Associated with Shigellosis and Vibrio fluvialis Bacteremia M. John Albert, M. Anowat Hossain, K. Alam, I. Kabir, Prodyot K.B. Neogi, and Saul Tzipori
Vibrio fluvialis is a halophilic bacterium normally found in coastal waters and sea foods. Although this organism is mainly associated with gastroenteritis, there has been one report of isolation from an infected wound (Tacket et al., 1982) and another from gall bladder (Yoshii et al., 1987). We describe here a fatal case associated with V. fluvialis bacteremia in a child, which to our knowledge, has not previously been reported. A 5-month-old boy was admitted to the Clinical Research Centre of the International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh, with a history of watery diarrhea, vomiting, and continuous fever for 7 days that was treated with amoxicillin, paracetamol, metronidazole, and chlorpheniramine maleate for 6 days. On examination he appeared to have clinical evidence of hypovolemic shock, respiratory distress, and toxemia. His body weight was 5.5 kg with weight for age and this was 75% of median (National Center for Health Statistics). Lungs had bilateral crepitation with radiological evidence of infiltration. His stool was alkaline and contained trace amounts of mucus. Stool microscopy revealed 20-50 pus cells, 1-10 red cells, and 1-5 macrophages per high-power field. No protozoa or helminths were detected. Blood examination showed a total leukocyte count of 15,500/mm 3. From the International Centre for Diarrhoeal Disease Research, Bangladesh, Dhaka, Bangladesh. Address reprint requests to Dr. M.J. Albert, ICDDR,B, GPO Box 128, Dhaka-1000, Bangladesh. Received 18 October 1990; revised and accepted 7 January 1991. © 1991 Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010 0732-8893/91/$3.50
The patient was kept in the intensive care unit, rehydrated intravenously, and treated with three parenteral doses of ampicillin (200 mg/kg body weight/day), two parenteral doses of gentamicin (6 mg/kg body weight/day), and three oral doses of pivmecillinam suspension (60 mg/kg body weight/day), along with other symptomatic management, but his condition deteriorated further and he died 16 hr after admission. Blood drawn on admission for culture grew V. fluvialis, which was identified by standard techniques (Lee et al., 1981) and was susceptible to ampicillin and gentamicin by disk diffusion method. Rectal swab also taken on admission and cultured on MacConkey agar and SalmoneUa-Shigella agar grew Shigella flexneri 6, which was susceptible to pivmecillinam but resistant to ampicillin. The clinical picture suggested that the patient had septicemia with invasive diarrhea, pneumonia, and second-degree malnutrition. Even though the organism that caused bacteremia (V. fluvialis) was susceptible to ampicillin and gentamicin in vitro, the administration of these drugs at the terminal stage failed to save the patient. Before hospitalization, the patient was treated with amoxicillin without improvement, although amoxicillin and ampicillin have a similar spectrum of activity. Yet it is also known that these drugs could have differences in activity against certain organisms although their in vivo action against Vibrio spp. is not known (Neu, 1979). It is also possible that the patient might have been treated with an inadequate dose of the drug, which could explain the treatment failure. Because we did not suspect involvement of V. fluvialis, no attempts were made to isolate it from stool, and, therefore, it is not certain
510
whether the intestinal tract was infected with V. fluvialis, and whether intestinal infection preceded bacteremia. Even though the patient was shedding Shigella flexneri 6, dysentery was not overt, and although a probable contributory factor, it was not considered to have been the cause of death. Bacteremia due to Gram-negative rods is not uncommon in shigellosis
M.J. Albert et al.
and is probably precipitated by colonic damage (Strulens et al., 1985). It is possible that colonic damage caused by shigellosis and the malnutrition that affects immune function might have facilitated the systemic invasion of V. fluvialis. Therefore, V. fluvialis should be added to the list of organisms causing bacteremia complicating shigellosis.
REFERENCES Lee JV, Shread P, Furniss AL, Bryant TN (1981) Taxonomy and description of Vibrio fluvialis sp. nov. (synonym group F vibrios, group EF-6). J Appl Bacteriol 50:73-94. Neu HC (1979) Amoxicillin. Ann Intern Med 90:356-360. Strulens M, Patte D, Kabir I, Salam A, Nath SK, Butler T (1985) Shigella septicemia: prevalence, presentation, risk factors and outcome. J Infect Dis 152:784-790.
Tacket CO, Hickman F, Pierce GU, Mendoza LF (1982) Diarrhea associated with Vibrio fluvialis in the United States. J Clin Microbiol 16:991-992. Yoshii Y, Nishino H, Satake K, Umeyama K (1987) Isolation of Vibrio fluvialis: an unusual pathogen in acute suppurative cholangitis. Am J Gastroenterol 82:903-905.