- Email: [email protected]
This letter was shown to Dr Sanderson and Ms Richardson whose reply follows:
334
Letters
to the
Editor
9. Starr JM, Rogers TR, Impallomeni M. Hospital-acquired Clostridium difficile diarrhoea and herd immunity. Lancet 1997; 349: 426-428. 10. Fekerty R, Kim KH, Batts DH, Cudmore M, Silva J Jr. Epidemiology of antibioticassociated colitis; isolation of Clostridium difficile from the hospital environment. Am J Med 1981; 70: 906-908.
This reply
letter was follows:
shown
to Dr
Sanderson
and
MS Richardson
whose
Sir, Thank you for the opportunity to reply to the interesting letter from Wilcox et al. We were unable to fingerprint the strains of C. dijjicile recovered from our patients. However a collection of strains from 20 patients in the study wards obtained over a period of some months for a separate project were typed by pyrolysis mass spectrometry by Dr J. S. Brazier; three different types were identified. Of four patients from whom sequential isolates were recovered three yielded a second strain different from the first. If an epidemic strain had been present the question arises as to why its prevalence should reduce since spores are difficult to eliminate from the environment and isolation nursing had been abandoned. Environmental cleaning and disinfection usage remained similar during the three year (and now four year) study period and no additional cleaning for infected patients took place. It is possible that infection control awareness increased over the years. Infected patients remained in the open ward and used commodes and toilets like other non-isolated patients. The average length of stay of patients decreased over the study period and this may have meant that some courses of antibiotics were shortened, but we have no details of this. The marginal relative decrease of cefuroxime usage seems an unlikely explanation for the lack of clinical outbreaks. We agree that there is a complex interplay between the organism and antibiotics and feel that this, rather than cross-infection, is the main cause of overt clinical illness. We accept that cross infection may take place but suggest that this does not determine clinical illness, the onset of disease depending on the interplay of antibiotics with the current intestinal flora of the patient. Fingerprinting and close correlation of the use of antibiotics in individual patients will help elucidate this infection. We look forward to more results from Leeds. P. J. Sanderson D. M. Richardson
Barnet
General Hospital, Wellhouse Lane, Barnet, Herb EN5 3DJ
Letters
to the
Editor
9. Starr JM, Rogers TR, Impallomeni M. Hospital-acquired Clostridium difficile diarrhoea and herd immunity. Lancet 1997; 349: 426-428. 10. Fekerty R, Kim KH, Batts DH, Cudmore M, Silva J Jr. Epidemiology of antibioticassociated colitis; isolation of Clostridium difficile from the hospital environment. Am J Med 1981; 70: 906-908.
This reply
letter was follows:
shown
to Dr
Sanderson
and
MS Richardson
whose
Sir, Thank you for the opportunity to reply to the interesting letter from Wilcox et al. We were unable to fingerprint the strains of C. dijjicile recovered from our patients. However a collection of strains from 20 patients in the study wards obtained over a period of some months for a separate project were typed by pyrolysis mass spectrometry by Dr J. S. Brazier; three different types were identified. Of four patients from whom sequential isolates were recovered three yielded a second strain different from the first. If an epidemic strain had been present the question arises as to why its prevalence should reduce since spores are difficult to eliminate from the environment and isolation nursing had been abandoned. Environmental cleaning and disinfection usage remained similar during the three year (and now four year) study period and no additional cleaning for infected patients took place. It is possible that infection control awareness increased over the years. Infected patients remained in the open ward and used commodes and toilets like other non-isolated patients. The average length of stay of patients decreased over the study period and this may have meant that some courses of antibiotics were shortened, but we have no details of this. The marginal relative decrease of cefuroxime usage seems an unlikely explanation for the lack of clinical outbreaks. We agree that there is a complex interplay between the organism and antibiotics and feel that this, rather than cross-infection, is the main cause of overt clinical illness. We accept that cross infection may take place but suggest that this does not determine clinical illness, the onset of disease depending on the interplay of antibiotics with the current intestinal flora of the patient. Fingerprinting and close correlation of the use of antibiotics in individual patients will help elucidate this infection. We look forward to more results from Leeds. P. J. Sanderson D. M. Richardson
Barnet
General Hospital, Wellhouse Lane, Barnet, Herb EN5 3DJ