- Email: [email protected]
Multiple Salmonella isolates from same patient
systemfor the study of HUS: comparison of human umbilical vein and human renal glomerular endothelial cells, p. 337-340. In M.A. Karmali and A.G. Goglio (eds.), Recent advances in verocytotoxin-producing Escherichia coli infections. Elsevier Science, New York
34. van de Kar, N.C.A.J. 1992. Tumor necrosis factor and interleulcm-1 induce expression of the verocytotoxin recep tor globotriaosylceramide on human endothelial cells: implications for the pathogenesis of the hemolytic uremic syndrome. Blood 80:2755-2764.
27. Obrig, T.G., et al. 1993. Endothelial heterogeneity in Shiga toxin receptors and responses. J. Biol. Chem. 268:1548415488.
35. Louise, CB., et al. Binding of [“‘I] Shiga-like toxin-l to human endothelial cells: implications for the pathogenesis of Shiga toxin-associated hemolytic uremic syndrome. Endothelium (in press).
29-37. In B.S. Kaplan, et al. (eds.). Hemolytic uremic syndrome and thrombotic thrombocytopcnic purpura. Marcel Dekker, New York 20. Cimolai, N., et al. 1992. Risk factors for the central nervous system manifestations of gastroenteritis-associated hemolytic uremic syndrome. Pediatrics 9Oz61ti21. 21
Obrig, T.G. 1992. Pathogenesis of Shiga toxin(vemuXin)mducedcndothelialcellin&, p. 405419. In B.S. Kaplan et al. (cds.), Hcmolyuc-uremic syndmme and thlunboticthlun~cpurpumMarccl De&r, New York.
22. Richardson, SE., et al., 1992. Experimental verocytotoxunia in rabbits. Infect. Immun. 6oz4154-4157. 23. Zoja, C., and G. Remuzzi. 1992. The pivotal role of the endothelial cell in the pathogen&s of HUS, p. 389Xl4. In B.S. Kaplan, et al. (eds.), Hemolyticuremic syndrome and thrombotic thrombocytopenic purpura. Marcel Dekker, New York. 24. Obrig, T.G., et al. 1994. Shiga toxin-endothelial cell interactions, p. 317-324. In M.A. Kannali and A.G. Goglio, (eds.), Recent advances in verocytotoxin-producing Escherichia coli infections. Elsevier Science, New York. 25. Fontaine, A., et al. 1988. Role of Shiga toxin in the pathogenesis of bacihary dysentery by using a tox- mutant of Shigella dysenteriae type 1. Infect. Immun.56X9%3109. 26. Louise, CB ., et al. 1994. A cell culture
28. Lingwood, C.A. 1993. Verotoxins and their glycolipid receptors. Adv. Lipid Res. 25:189-211. 29. Jackson, M.P. 1990. Structure-function of Shiga toxin and the Shiga-Iike toxins. Microbial. Path. 8:235-242. 30. Marques, R.M.. et al. 1986. Production of Shiga-like toxin by Escherichia coli. J. Infect. Dis. 154:338-341. 31. Obrig, T.G., et al. 1988. Direct cytotoxic action of Shiga toxin on human vascular endothelial cells. Infect. Immun. 56:237%2378. 32. Kaye, S.A., et al. 1993. Shiga toxin-associated hemolytic uremic syndrome. Interleukin-1B enhancement of Shiga toxin cytotoxicity toward human vascular endothelial cells in vitro. Infect. Immun. 61:3886-3891. 33. Louise, C.B., and T.G. Obrig. 1991. Shiga toxin-associated hemolytic uremic syndrome: combined cytotoxic effects of Shiga toxin, interleukin-lB, and tumor necrosis factor alpha on human vascular endothelial cells in vitro. Infect. Immun. 59:41734179.
37. Wojta, J., et al. 1989. Vascular origin determines plasminogen activator expression in human endothelial cells. J. Cell Biol. 264:2846-2852. 38. Sandvig, K., et al. 1994. Retrograde transport from the golgi complex to the ER of both Shiga toxin and the nontoxic Shiga B-fragment is regulated by butyric acid and CAMP. J. Cell. Biol. 126:53-64. 39. Boyd, B.. and C.A. Lmgwood. 1989. Verotoxin receptor glycolipid in human renal tissue. Nephron 51:207-210. 40. Wadolkowski, E.A., et al. 1990. Acute renal tubular necrosis and death of mice orally infected with Escherichiu coli strains that produce Shiga-like toxin type II. Infect. Immun. 58:3959-3965. 41. Louise, CB., and T.G. Obrig. 1994. Human renal microvascular endothelial cells as a potential target in the development of the hemolytic uremic syndrome as related to fibrinolysis factor production, in vitro. Microvasc. Res.47:377-387.
Case Reports
Multiple Salmonella Isolates from Same Patient Marcel A. Behr Jack Mendelson Department of Microbiology SMBD-Jewish General Hospital Montreal, Canada H3T 1 E2
While infection due to antibiotic-reWant Salmonellu isolates is increasingly recognized (l-3), we report here an unusual case where at least two organisms with three susceptibility patterns were present in the same patient.
Clinical History An 82-yr-old woman was admitted 52
0196-4399/96)6/50.00+ 15.00
with a l-d history of vomiting and six to seven liquid bowel movements, with no DUS or blood. The Datient lived alone, was not on antibiotic therapy, and no dietary history was available. Her past medical history included pemicious anemia, acute angle glaucoma, cataractsurgery 7 wk prior to admission, and a resolved cerebrovascularaccident 10 yr previously. She had had a cholecystectomy 24 yr earlier followed by symptomatic choledocholithiasis requiring surgical intervention 4 yr prior to admission. There were no previous 1
0 19% Elsevier Science Inc.
stool or biliary tract cultures available. On admission, her temperaturewas 38.4’C, BP 190192, and abdominal examination was negative. Rectal exam revealed guaiac-positive liquid stool.
Laboratory Laboratory investigations revealed a WBC count of 6,900/mm3, hemoglobin of 11.9 g/dl, and normal serum chemistry and liver enzyme values. A urine culture grew 1.6 x l@/ml lactose-fermenting enteric organisms susceptible to ampicillin, and the day after admisClinical Microbiology Newsletter 18:7,1996
sion she was begun on ampicillin 1 gm q6h intravenously along with one dose of gentamicin 100 mg. Stool samples sent from the day after admission were negative for C. d#kile toxin. Three sequential stool samples were collected on days 1.2, and 3 of therapy with ampicillin and plated on sheep blood, MacConkey, XLD, SS, and Campylobacter agars, and also placed into Selenite broth from which a 24-h subculture onto SS agar was done. The first sample grew two morphologically different colonies of Sulmonellu identified as groups B and D (BBL Salmonella 0 antiserum, Becton Dickinson, Cockeysville, MD). Disk diffusion susceptibility test and h4IC re sults are reported in Table 1. The sample ftom day 2 grew only ampicillin-resistant group D Salmunellu, and the sample from day 3 again grew Salmonella groups B and D. Susceptibility studies were done twice. The strains were sent to the provincial reference laboratory where they were identified as Sulmunellu choleraesuis, serogroups B and D. The patient’s diarrhea stopped and she defervesced after 48 h of ampicillin therapy. She was discharged home on oral amoxicillin but did not return for follow-up.
Discussion A literature search failed to uncover other reports of the isolation of multiple strains of Salmonellu from a single patient. However, since an asymptomatic carriage state is well recognized, she may have had symptoms from only one of the two strains and been a carrier of the other. With regard to the differing suscepti-
TABLE 1. Isolate susceptibility results* Day
Isolate
Ampicillin
Day 1
Salmonella B Salmonella D
S(MICl8)
Day
Sabnonella D
R (MIC 2
2 Day 3
Salmonella B Salmonella D
S(MICl8)
32)
S(MJC<8)
R (MIC2 32)
*All isolates were suscqtiblc to ceftriaxone,
imipenem. ciprofloxacin. ticarcillinklavulanic acid, andtrimethoprim-sutfametboxaxole.
bilities of the group D strain, it may be that heteroresistant Salmonella D was present from the beginning and antibiotic therapy selectively eliminated the susceptible organisms. A multiresistant Salmonella sp. has previously been shown to be associated with host exposure to penicillins within 4 wk of illness (4). An outbreak of Salmonella newport has been described in which 12 persons treated with penicillins for pharyngitis or o&is developed gastrointestinal illness due to penicillinase-producing S. newport within 24 to 48 h of taking the antibiotic. In this case, it was postulated that the patients were asymptomatically colonized with the resistant strain before taking the antibiotic, therefore allowing it a selective advantage to cause disease (5). Another explanation for our patient’s findings is that resistance was induced by the presence of antibiotic. However, the short delay of 24 h between stool isolates makes this unlikely. One can speculate whether she initially had three organisms or whether the serogroup D isolate manifested new resistance within 24 h of ampicillin ther-
apy. In either scenario, this case demonstrates several points, beginning with the importance in the microbiology laboratory of a diligent search for multiple stool pathogens, since mote than one strain may be present at one time. With regard to pathogenicity, it is notable that in this patient with resistant iso lates, there was clinical improvement on ampicillin, bringing into question whether the resistant isolates were involved in her enteritis and whether she even required treatment of her diarrhea. Since surveillance of in-vitro resistance patterns is often cited to guide changing therapeutic recommendations (6), such as the use of quinolones, efforts should be made to study clinical outcomes in order to support these recommendations. References 1.
Cohen, ML., and R.V. Tauxe. 1986. Drug-resistant Salmonella in the United States:An epidemiologic perspective. Science 234: 964%9.
2. O’Brien, T.F., et al . 1982. Molecular epidemiology of antibiotic resistance in
Salmonella from animals and human beings in the United States. N. Engl. J. Med. 307:1-6.
3. Munoz, P.. et al. 1993. Antibiotic resistance of Salmonella isolates in a Spanish Hospital. Antimicrob. Agents Chemother. 37:12C&1202.
4. Riley. L.W., et al. 1994. Importance of host factors in human salmonellosis caused by multiresistant strains of Salmonella. J. Infect Dis. 149: 878-883.
5. Hohnberg, S.D., et al. 1984. Drug-resistantSalmonella from animals fed antimicrobials. N. Engl. J. Med. 311: 617.
6. Li, E., and S.L. Stanley. 1992. The role of newer antibiotics in gastroenterology. Gastroenterol. Clin. North Am. 21: 633-619.
Shewanella putrefaciens Bacteremia in an Immunodeficient Patient J.R Barbem J.A. Capdevila A.M. Planes Unit&de Malades Injieccioses and Servei de Microbiologia Hospital General Vail dHebron Barcelona, Spain
CIiiicalMcmbiologyNewsletterl&7,19%
Shewanellu plttrefaciens is recovered rarely from human specimens and has been documented as an opportunistic pathogen in only a few patients. Bacteremia and sepsis by this microorganism are also very unusual. We report a case of S. putrefuciens sepsis of
Q 19% ElsevicrScimce Inc.
skin origin in an immunosuppressed patient with human immunodeficiency virus infection and cirrhosis. Case Report A 32-yr-old male was admitted in the emergency room for fever and right
0196-4399#96/$0.00+ 15.00
53
34. van de Kar, N.C.A.J. 1992. Tumor necrosis factor and interleulcm-1 induce expression of the verocytotoxin recep tor globotriaosylceramide on human endothelial cells: implications for the pathogenesis of the hemolytic uremic syndrome. Blood 80:2755-2764.
27. Obrig, T.G., et al. 1993. Endothelial heterogeneity in Shiga toxin receptors and responses. J. Biol. Chem. 268:1548415488.
35. Louise, CB., et al. Binding of [“‘I] Shiga-like toxin-l to human endothelial cells: implications for the pathogenesis of Shiga toxin-associated hemolytic uremic syndrome. Endothelium (in press).
29-37. In B.S. Kaplan, et al. (eds.). Hemolytic uremic syndrome and thrombotic thrombocytopcnic purpura. Marcel Dekker, New York 20. Cimolai, N., et al. 1992. Risk factors for the central nervous system manifestations of gastroenteritis-associated hemolytic uremic syndrome. Pediatrics 9Oz61ti21. 21
Obrig, T.G. 1992. Pathogenesis of Shiga toxin(vemuXin)mducedcndothelialcellin&, p. 405419. In B.S. Kaplan et al. (cds.), Hcmolyuc-uremic syndmme and thlunboticthlun~cpurpumMarccl De&r, New York.
22. Richardson, SE., et al., 1992. Experimental verocytotoxunia in rabbits. Infect. Immun. 6oz4154-4157. 23. Zoja, C., and G. Remuzzi. 1992. The pivotal role of the endothelial cell in the pathogen&s of HUS, p. 389Xl4. In B.S. Kaplan, et al. (eds.), Hemolyticuremic syndrome and thrombotic thrombocytopenic purpura. Marcel Dekker, New York. 24. Obrig, T.G., et al. 1994. Shiga toxin-endothelial cell interactions, p. 317-324. In M.A. Kannali and A.G. Goglio, (eds.), Recent advances in verocytotoxin-producing Escherichia coli infections. Elsevier Science, New York. 25. Fontaine, A., et al. 1988. Role of Shiga toxin in the pathogenesis of bacihary dysentery by using a tox- mutant of Shigella dysenteriae type 1. Infect. Immun.56X9%3109. 26. Louise, CB ., et al. 1994. A cell culture
28. Lingwood, C.A. 1993. Verotoxins and their glycolipid receptors. Adv. Lipid Res. 25:189-211. 29. Jackson, M.P. 1990. Structure-function of Shiga toxin and the Shiga-Iike toxins. Microbial. Path. 8:235-242. 30. Marques, R.M.. et al. 1986. Production of Shiga-like toxin by Escherichia coli. J. Infect. Dis. 154:338-341. 31. Obrig, T.G., et al. 1988. Direct cytotoxic action of Shiga toxin on human vascular endothelial cells. Infect. Immun. 56:237%2378. 32. Kaye, S.A., et al. 1993. Shiga toxin-associated hemolytic uremic syndrome. Interleukin-1B enhancement of Shiga toxin cytotoxicity toward human vascular endothelial cells in vitro. Infect. Immun. 61:3886-3891. 33. Louise, C.B., and T.G. Obrig. 1991. Shiga toxin-associated hemolytic uremic syndrome: combined cytotoxic effects of Shiga toxin, interleukin-lB, and tumor necrosis factor alpha on human vascular endothelial cells in vitro. Infect. Immun. 59:41734179.
37. Wojta, J., et al. 1989. Vascular origin determines plasminogen activator expression in human endothelial cells. J. Cell Biol. 264:2846-2852. 38. Sandvig, K., et al. 1994. Retrograde transport from the golgi complex to the ER of both Shiga toxin and the nontoxic Shiga B-fragment is regulated by butyric acid and CAMP. J. Cell. Biol. 126:53-64. 39. Boyd, B.. and C.A. Lmgwood. 1989. Verotoxin receptor glycolipid in human renal tissue. Nephron 51:207-210. 40. Wadolkowski, E.A., et al. 1990. Acute renal tubular necrosis and death of mice orally infected with Escherichiu coli strains that produce Shiga-like toxin type II. Infect. Immun. 58:3959-3965. 41. Louise, CB., and T.G. Obrig. 1994. Human renal microvascular endothelial cells as a potential target in the development of the hemolytic uremic syndrome as related to fibrinolysis factor production, in vitro. Microvasc. Res.47:377-387.
Case Reports
Multiple Salmonella Isolates from Same Patient Marcel A. Behr Jack Mendelson Department of Microbiology SMBD-Jewish General Hospital Montreal, Canada H3T 1 E2
While infection due to antibiotic-reWant Salmonellu isolates is increasingly recognized (l-3), we report here an unusual case where at least two organisms with three susceptibility patterns were present in the same patient.
Clinical History An 82-yr-old woman was admitted 52
0196-4399/96)6/50.00+ 15.00
with a l-d history of vomiting and six to seven liquid bowel movements, with no DUS or blood. The Datient lived alone, was not on antibiotic therapy, and no dietary history was available. Her past medical history included pemicious anemia, acute angle glaucoma, cataractsurgery 7 wk prior to admission, and a resolved cerebrovascularaccident 10 yr previously. She had had a cholecystectomy 24 yr earlier followed by symptomatic choledocholithiasis requiring surgical intervention 4 yr prior to admission. There were no previous 1
0 19% Elsevier Science Inc.
stool or biliary tract cultures available. On admission, her temperaturewas 38.4’C, BP 190192, and abdominal examination was negative. Rectal exam revealed guaiac-positive liquid stool.
Laboratory Laboratory investigations revealed a WBC count of 6,900/mm3, hemoglobin of 11.9 g/dl, and normal serum chemistry and liver enzyme values. A urine culture grew 1.6 x l@/ml lactose-fermenting enteric organisms susceptible to ampicillin, and the day after admisClinical Microbiology Newsletter 18:7,1996
sion she was begun on ampicillin 1 gm q6h intravenously along with one dose of gentamicin 100 mg. Stool samples sent from the day after admission were negative for C. d#kile toxin. Three sequential stool samples were collected on days 1.2, and 3 of therapy with ampicillin and plated on sheep blood, MacConkey, XLD, SS, and Campylobacter agars, and also placed into Selenite broth from which a 24-h subculture onto SS agar was done. The first sample grew two morphologically different colonies of Sulmonellu identified as groups B and D (BBL Salmonella 0 antiserum, Becton Dickinson, Cockeysville, MD). Disk diffusion susceptibility test and h4IC re sults are reported in Table 1. The sample ftom day 2 grew only ampicillin-resistant group D Salmunellu, and the sample from day 3 again grew Salmonella groups B and D. Susceptibility studies were done twice. The strains were sent to the provincial reference laboratory where they were identified as Sulmunellu choleraesuis, serogroups B and D. The patient’s diarrhea stopped and she defervesced after 48 h of ampicillin therapy. She was discharged home on oral amoxicillin but did not return for follow-up.
Discussion A literature search failed to uncover other reports of the isolation of multiple strains of Salmonellu from a single patient. However, since an asymptomatic carriage state is well recognized, she may have had symptoms from only one of the two strains and been a carrier of the other. With regard to the differing suscepti-
TABLE 1. Isolate susceptibility results* Day
Isolate
Ampicillin
Day 1
Salmonella B Salmonella D
S(MICl8)
Day
Sabnonella D
R (MIC 2
2 Day 3
Salmonella B Salmonella D
S(MICl8)
32)
S(MJC<8)
R (MIC2 32)
*All isolates were suscqtiblc to ceftriaxone,
imipenem. ciprofloxacin. ticarcillinklavulanic acid, andtrimethoprim-sutfametboxaxole.
bilities of the group D strain, it may be that heteroresistant Salmonella D was present from the beginning and antibiotic therapy selectively eliminated the susceptible organisms. A multiresistant Salmonella sp. has previously been shown to be associated with host exposure to penicillins within 4 wk of illness (4). An outbreak of Salmonella newport has been described in which 12 persons treated with penicillins for pharyngitis or o&is developed gastrointestinal illness due to penicillinase-producing S. newport within 24 to 48 h of taking the antibiotic. In this case, it was postulated that the patients were asymptomatically colonized with the resistant strain before taking the antibiotic, therefore allowing it a selective advantage to cause disease (5). Another explanation for our patient’s findings is that resistance was induced by the presence of antibiotic. However, the short delay of 24 h between stool isolates makes this unlikely. One can speculate whether she initially had three organisms or whether the serogroup D isolate manifested new resistance within 24 h of ampicillin ther-
apy. In either scenario, this case demonstrates several points, beginning with the importance in the microbiology laboratory of a diligent search for multiple stool pathogens, since mote than one strain may be present at one time. With regard to pathogenicity, it is notable that in this patient with resistant iso lates, there was clinical improvement on ampicillin, bringing into question whether the resistant isolates were involved in her enteritis and whether she even required treatment of her diarrhea. Since surveillance of in-vitro resistance patterns is often cited to guide changing therapeutic recommendations (6), such as the use of quinolones, efforts should be made to study clinical outcomes in order to support these recommendations. References 1.
Cohen, ML., and R.V. Tauxe. 1986. Drug-resistant Salmonella in the United States:An epidemiologic perspective. Science 234: 964%9.
2. O’Brien, T.F., et al . 1982. Molecular epidemiology of antibiotic resistance in
Salmonella from animals and human beings in the United States. N. Engl. J. Med. 307:1-6.
3. Munoz, P.. et al. 1993. Antibiotic resistance of Salmonella isolates in a Spanish Hospital. Antimicrob. Agents Chemother. 37:12C&1202.
4. Riley. L.W., et al. 1994. Importance of host factors in human salmonellosis caused by multiresistant strains of Salmonella. J. Infect Dis. 149: 878-883.
5. Hohnberg, S.D., et al. 1984. Drug-resistantSalmonella from animals fed antimicrobials. N. Engl. J. Med. 311: 617.
6. Li, E., and S.L. Stanley. 1992. The role of newer antibiotics in gastroenterology. Gastroenterol. Clin. North Am. 21: 633-619.
Shewanella putrefaciens Bacteremia in an Immunodeficient Patient J.R Barbem J.A. Capdevila A.M. Planes Unit&de Malades Injieccioses and Servei de Microbiologia Hospital General Vail dHebron Barcelona, Spain
CIiiicalMcmbiologyNewsletterl&7,19%
Shewanellu plttrefaciens is recovered rarely from human specimens and has been documented as an opportunistic pathogen in only a few patients. Bacteremia and sepsis by this microorganism are also very unusual. We report a case of S. putrefuciens sepsis of
Q 19% ElsevicrScimce Inc.
skin origin in an immunosuppressed patient with human immunodeficiency virus infection and cirrhosis. Case Report A 32-yr-old male was admitted in the emergency room for fever and right
0196-4399#96/$0.00+ 15.00
53