Abstract
At the time of admission, the patient was febrile (39.3 °C) and had a blood pressure of 107/60 mmHg. Blood and urine were taken for culture. Haematology reports indicated a white blood cell count of 3.9x109 l–1, a platelet count of 158x1012 l–1, a haemoglobin of 11.5 g dl–1 and a haematocrit of 34.1 %. A differential count revealed 93 % neutrophils, 6 % lymphocytes and 1 % monocytes. Urinalysis showed clear, yellow urine, pH 8.5, specific gravity 1.015, 30 mg dl–1 protein, white cell count 100 cells per low-power field view, red cell count 7 cells per low-power field view, epithelial cell count 7 cells per low-power field view, while glucose, ketone, nitrite, bilirubin and occult blood were undetectable. Urine culture yielded bacteria at >100 000 c.f.u. ml–1. Blood cultures also tested positive for a Gram-negative rod. Biochemical characterization showed the bacterium to grow well on MacConkey agar and nutrient agar at 30 °C and 37 °C. The bacteria produced H2S, hydrolysed urea and ONPG, and did not deaminate phenylalanine or decarboxylate lysine, arginine or ornithine. Little or no gas was produced from fermentation of carbohydrates. It was motile at 22 °C and variable in motility at 37 °C. The bacterium produced enterobacterial common antigen I. The isolate was identified as Budvicia aquatica by the VITEK (bioMérieux) microbial identification system. The bacterial identification was subsequently confirmed by Quest Diagnostics Services. The bacterium was found to be sensitive to several agents. MICs were found to be (in µg ml–1): amikacin (<8), ampicillin (<4), cefzolin (<4), ceftoxin (<4), ceftriaxone (<4), cefuroxime (<4), ciprofloxacin (<0.5), gentamicin (<2), imipenem (<2), piperacillin (<16), ticarcillin/clavulanic acid (<16) and trimethoprim/sulfamethoxazole (<0.5).
The patient was hospitalized with a diagnosis of urosepsis and treated empirically with intravenous levofloxacin. Considering the severity of the infection, azathioprine was discontinued. After the patient's condition improved and culture results became available, her antimicrobial therapy was switched to orally administered ciprofloxacin. The patient responded well to treatment and was discharged home in good condition to complete a 14-day course of antibiotics. Azathioprine was not restarted pending further evaluation as an outpatient.
At the time of admission, the patient was febrile (39.3 °C) and had a blood pressure of 107/60 mmHg. Blood and urine were taken for culture. Haematology reports indicated a white blood cell count of 3.9x109 l–1, a platelet count of 158x1012 l–1, a haemoglobin of 11.5 g dl–1 and a haematocrit of 34.1 %. A differential count revealed 93 % neutrophils, 6 % lymphocytes and 1 % monocytes. Urinalysis showed clear, yellow urine, pH 8.5, specific gravity 1.015, 30 mg dl–1 protein, white cell count 100 cells per low-power field view, red cell count 7 cells per low-power field view, epithelial cell count 7 cells per low-power field view, while glucose, ketone, nitrite, bilirubin and occult blood were undetectable. Urine culture yielded bacteria at >100 000 c.f.u. ml–1. Blood cultures also tested positive for a Gram-negative rod. Biochemical characterization showed the bacterium to grow well on MacConkey agar and nutrient agar at 30 °C and 37 °C. The bacteria produced H2S, hydrolysed urea and ONPG, and did not deaminate phenylalanine or decarboxylate lysine, arginine or ornithine. Little or no gas was produced from fermentation of carbohydrates. It was motile at 22 °C and variable in motility at 37 °C. The bacterium produced enterobacterial common antigen I. The isolate was identified as Budvicia aquatica by the VITEK (bioMérieux) microbial identification system. The bacterial identification was subsequently confirmed by Quest Diagnostics Services. The bacterium was found to be sensitive to several agents. MICs were found to be (in µg ml–1): amikacin (<8), ampicillin (<4), cefzolin (<4), ceftoxin (<4), ceftriaxone (<4), cefuroxime (<4), ciprofloxacin (<0.5), gentamicin (<2), imipenem (<2), piperacillin (<16), ticarcillin/clavulanic acid (<16) and trimethoprim/sulfamethoxazole (<0.5).
The patient was hospitalized with a diagnosis of urosepsis and treated empirically with intravenous levofloxacin. Considering the severity of the infection, azathioprine was discontinued. After the patient's condition improved and culture results became available, her antimicrobial therapy was switched to orally administered ciprofloxacin. The patient responded well to treatment and was discharged home in good condition to complete a 14-day course of antibiotics. Azathioprine was not restarted pending further evaluation as an outpatient.
Autoimmune hepatitis is a chronic inflammatory disease of the liver characterized by histological changes of the liver occurring in the presence of circulating autoantibodies (Czaja, 1995). Immunomodulating drugs such as azathioprine are used to treat this disease. Azathioprine is thought to suppress the immune system at least partially by its effect on T lymphocytes, and this is mediated through blocking the purine-synthesis pathway (Maltzman & Koretzky, 2003). Azathioprine can further compromise the immune system by suppressing the bone marrow and causing neutropenia. Individuals being treated on a long-term basis with this or any immunosuppressive agent are at risk of the development of opportunistic infections.B. aquatica has been reported elsewhere as a surface-water contaminant not associated with human faeces or sewage. As this organism has not been implicated before in human disease, this case presents a concern regarding the exposure risks for immunocompromised patients exposed to the aftermath of Hurricane Katrina.
References
Czaja, A. J. (1995). Autoimmune hepatitis. Evolving concepts and treatment strategies. Dig Dis Sci 40, 435[CrossRef][Medline]
Hausner, O., Kocmoud, Z. & Gabrhelova, M. (1986). The incidence and diagnosis of a new type of bacteria, Budvicia aquatica, in specimens from the laboratory for water study. Cesk Epidemiol Mikrobiol Imunol 35, 336–340. (in Czech)[Medline]
Maltzman, J. & Koretzky, G. (2003). Azathoprine: old drug, new actions. J Clin Invest 111, 1122–1124.[CrossRef][Medline]
Schubert, R. H. & Groeger-Sohn, S. (1998). Detection of Budvicia aquatica and Pragia fontium and occurrence in surface waters. Zentralbl Hyg Umweltmed 201, 371–376.[Medline]
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