Revisão Revisado por pares

Monomicrobial vs Polymicrobial Clostridium difficile Bacteremia: A Case Report and Review of the Literature

2015; Elsevier BV; Volume: 128; Issue: 9 Linguagem: Inglês

10.1016/j.amjmed.2015.05.014

ISSN

1555-7162

Autores

Noora Kazanji, Mihajlo Gjeorgjievski, Siddhartha Yadav, Amy Mertens, Carl B. Lauter,

Tópico(s)

Nosocomial Infections in ICU

Resumo

Extraintestinal Clostridium difficile (C. difficile) infections account for .05) between monomicrobial and polymicrobial C. difficile bacteremia with regard to recent surgery, presence of bowel perforation, recent antibiotic usage, presence of liver disease, malignancy, or positive stool toxin. The presence of blood in the stool, however, was more common in polymicrobial C. difficile bacteremia (P <.05). Overall mortality was 39%. Underlying liver disease or malignancy was present in 64% of cases. This suggests that C. difficile bacteremia may simply be a prognostic marker of severe underlying immunodeficiency.Several hypotheses have been formulated to understand the etiopathogenesis of C. difficile bacteremia. One familiar mechanism is the direct transfer of polymicrobial gut flora to the bloodstream through a site of injury in the intestinal mucosa.2Durojaie O. Gaur S. Alsaffar L. Bacteraemia and breast abscess: unusual extraintestinal manifestations of Clostridium difficile infection.J Med Microbiol. 2011; 60: 378-380Crossref PubMed Scopus (12) Google Scholar Bacterial translocation is another mechanism; any factor disrupting the normal intestinal mucosal barrier, such as inflammation or immunosuppression, can promote translocation of bacteria from the intestine to the lymph nodes, peritoneum, and blood.3Mattila E. Arkkila P. Mattila P.S. et al.Extraintestinal Clostridium difficile infections.Clin Infect Dis. 2013; 57: e148-e153Crossref PubMed Scopus (54) Google Scholar Given the polymicrobial nature of the intestinal flora, a different method is needed to explain monomicrobial C. difficile bacteremia. In our review, 5 cases of the monomicrobial group were noted to have extraintestinal foci, compared with only one case in the polymicrobial group.2Durojaie O. Gaur S. Alsaffar L. Bacteraemia and breast abscess: unusual extraintestinal manifestations of Clostridium difficile infection.J Med Microbiol. 2011; 60: 378-380Crossref PubMed Scopus (12) Google Scholar, 3Mattila E. Arkkila P. Mattila P.S. et al.Extraintestinal Clostridium difficile infections.Clin Infect Dis. 2013; 57: e148-e153Crossref PubMed Scopus (54) Google Scholar, 4Kaufman E. Liska D. Rubinshteyn V. et al.Clostridium difficile bacteremia.Surg Infect (Larchmt). 2013; 14: 559-560Crossref PubMed Scopus (7) Google Scholar, 5Duthilly A. Blanckaert K. Thielemans B. et al.Clostridium difficile bacteremia.Presse Med. 2001; 30: 1825-1826PubMed Google Scholar, 6Saginur R. Fogel R. Begin L. et al.Splenic abscess due to Clostridium difficile.J Infect Dis. 1983; 147: 1105Crossref PubMed Scopus (36) Google Scholar This important difference suggests that evaluation for further infective foci should be considered as a mechanism for monomicrobial C. difficile bacteremia. Extraintestinal Clostridium difficile (C. difficile) infections account for .05) between monomicrobial and polymicrobial C. difficile bacteremia with regard to recent surgery, presence of bowel perforation, recent antibiotic usage, presence of liver disease, malignancy, or positive stool toxin. The presence of blood in the stool, however, was more common in polymicrobial C. difficile bacteremia (P <.05). Overall mortality was 39%. Underlying liver disease or malignancy was present in 64% of cases. This suggests that C. difficile bacteremia may simply be a prognostic marker of severe underlying immunodeficiency. Several hypotheses have been formulated to understand the etiopathogenesis of C. difficile bacteremia. One familiar mechanism is the direct transfer of polymicrobial gut flora to the bloodstream through a site of injury in the intestinal mucosa.2Durojaie O. Gaur S. Alsaffar L. Bacteraemia and breast abscess: unusual extraintestinal manifestations of Clostridium difficile infection.J Med Microbiol. 2011; 60: 378-380Crossref PubMed Scopus (12) Google Scholar Bacterial translocation is another mechanism; any factor disrupting the normal intestinal mucosal barrier, such as inflammation or immunosuppression, can promote translocation of bacteria from the intestine to the lymph nodes, peritoneum, and blood.3Mattila E. Arkkila P. Mattila P.S. et al.Extraintestinal Clostridium difficile infections.Clin Infect Dis. 2013; 57: e148-e153Crossref PubMed Scopus (54) Google Scholar Given the polymicrobial nature of the intestinal flora, a different method is needed to explain monomicrobial C. difficile bacteremia. In our review, 5 cases of the monomicrobial group were noted to have extraintestinal foci, compared with only one case in the polymicrobial group.2Durojaie O. Gaur S. Alsaffar L. Bacteraemia and breast abscess: unusual extraintestinal manifestations of Clostridium difficile infection.J Med Microbiol. 2011; 60: 378-380Crossref PubMed Scopus (12) Google Scholar, 3Mattila E. Arkkila P. Mattila P.S. et al.Extraintestinal Clostridium difficile infections.Clin Infect Dis. 2013; 57: e148-e153Crossref PubMed Scopus (54) Google Scholar, 4Kaufman E. Liska D. Rubinshteyn V. et al.Clostridium difficile bacteremia.Surg Infect (Larchmt). 2013; 14: 559-560Crossref PubMed Scopus (7) Google Scholar, 5Duthilly A. Blanckaert K. Thielemans B. et al.Clostridium difficile bacteremia.Presse Med. 2001; 30: 1825-1826PubMed Google Scholar, 6Saginur R. Fogel R. Begin L. et al.Splenic abscess due to Clostridium difficile.J Infect Dis. 1983; 147: 1105Crossref PubMed Scopus (36) Google Scholar This important difference suggests that evaluation for further infective foci should be considered as a mechanism for monomicrobial C. difficile bacteremia. Technical AppendixSupplementary Table 1Laboratory Results at Admission of Our PatientLaboratory InvestigationPatient's ResultsReference RangeLeukocyte count6.8 billion cells/L4.00-10.00 × billion cells/LHemoglobin13.0 gm/dL14.3-18.3 g/dLPlatelets131 billion cells/L150-400 × 109/LSodium114 mmol/L136-145 mmol/LPotassium3.7 mmol/L3.5-5.1 mmol/LBicarbonate16 mmol/L23-29 mmol/LUrea8 mmol/L8-22 mg/dLCreatinine1.62 mg/dL0.6-1.4 mg/dLTotal bilirubin17.5 mg/dL0.3-1.2 mg/dLConjugated bilirubin9.5 mg/dL0.0-0.3 mg/dLTotal protein6.4 g/dL6.4-8.6 g/dLAlbumin2.3 gm/dL35-52 g/LAlkaline phosphatase234 U/L40-120 U/LAlanine transaminase83 U/L10-40 U/LAspartate transaminase294 U/L15-40 U/LAmmonia65 μmol/L11-35 μmol/LHepatitis A IgM antibodyNegativeNegativeHepatitis B surface antigenNegativeNegativeHepatitis B core IgM antibodyNegativeNegativeHepatitis C antibodyNegativeNegativeINR2.41 international unitsLactic acid8.2 mmol/L0.5-2.2 mmol/LBlood ethanol level59 mg/dL<10 mg/dLIgM = immunoglobulin M; INR = international normalized ratio. Open table in a new tab Supplementary Table 2Culture DataSourceTime CollectedInitial IdentificationFinal IdentificationTime to Final PositivityBlood venipunctureDay 1Gram-negative bacilliClostridium difficile6 d, 2 hBlood venipunctureDay 1Gram-variable bacilliClostridium difficile5 d, 19 hBlood venipunctureDay 3Gram-variable bacilliClostridium difficile4 dBlood venipunctureDay 3Gram-variable bacilliClostridium difficile4 dUrine cultureDay 3No growthNo growth1 dStool nucleic acid amplificationDay 4Toxigenic C. difficile7 h Open table in a new tab Supplementary Table 3Summary of All Reported Cases of Monomicrobial and Polymicrobial Clostridium difficile BacteremiaFirst Author, Year, ReferencePubMed IDAge, SexPresenting SignsSurgery or PerforationRecent Antibiotic UseOther ComorbiditiesStool ToxinC. diff Recovered from Other SitesTreatmentOutcomeOther Microbes RecoveredReports of Monomicrobial Clostridium difficile bacteremia: Smith, 19627Smith L.D. King E.O. 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Clostridium difficile bacteremia, Taiwan.Emerg Infect Dis. 2010; 16: 1204-1210Crossref PubMed Scopus (38) Google Scholar2067831241, FFevers, dyspneaNoUnknownPulmonary fibrosisNegativeNoceftazidime, gentamycin, vancomycinRecovered Durojaie, 20112Durojaie O. Gaur S. Alsaffar L. Bacteraemia and breast abscess: unusual extraintestinal manifestations of Clostridium difficile infection.J Med Microbiol. 2011; 60: 378-380Crossref PubMed Scopus (12) Google Scholar2112715539, FMenorrhagia and spontaneous bruisingNoYesChronic hepatitis and alcoholic liver diseaseUnknownBreast abscessAmoxicillin-Clavulanate and MetronidazoleRecovered McGill, 201111McGill F. Fawley W.N. Wilcox M.H. 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Extraintestinal Clostridium difficile: 10 years' experience at a tertiary-care hospital.Mayo Clin Proc. 1998; 73: 943-947Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar978774117, MIleus, partial small bowel obstructionNoYesDuchenne muscular dystrophyNot testedUnknownUnknownRecoveredCandida Parapsilosis Wolf, 199818Wolf L.E. Gorbach S.L. Granowitz E.V. Extraintestinal Clostridium difficile: 10 years' experience at a tertiary-care hospital.Mayo Clin Proc. 1998; 73: 943-947Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar978774133, FPelvic abscess and rectovaginal fistulaNoYesMetastatic cervical cancerNot testedUnknownUnknownDiedClostridium cadaveris, Bacteroides melaninogenicus, Fusobacterium spp. Wolf, 199818Wolf L.E. Gorbach S.L. Granowitz E.V. 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Open table in a new tab IgM = immunoglobulin M; INR = international normalized ratio. AAA = abdominal aortic aneurysm; CAD = coronary artery disease; CHF = congestive heart failure; CVA = cerebrovascular accident; ESRD = end-stage renal disease; GI = gastrointestinal; HTN = hypertension; IV = intravenous; Mo = month; PO = oral; UTI = urinary tract infection.

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