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CROSS-INFECTION AND CLOSTRIDIUM DIFFICILE
476
interesting effects on learning, provide a treatment for dementia.
seem
unlikely
to
CROSS-INFECTION AND CLOSTRIDIUM DIFFICILE CASES of pseudomembranous colitis occur with annoying irregularity. This "now you see it, now you don’t" character has featured in several reviews and reports. Pettet et al.were stimulated by a flurry of cases to review records between 1925 and 1952; they found nearly the same frequency before as after 1939. Swartzberg and his colleagues2 saw fourteen patients with pseudomembranous colitis over a brief period; then they prospectively evaluated diarrhoea in a thousand patients given clindamycin and identified not one more case. Tedesco’s well known prospective study revealed pseudomembranes in an astonishing 10% of two hundred consecutive patients given clindamycin over a 6 month period,3 an experience confirmed by some4 but not by others.5 Since then the discovery of Clostridium difficile as a specific aetiological factor has permitted cases which occur under disparate circumstances to be associated. Medical and surgical cases, ampicillin, cephalosporin, and clindamycin associated cases, clinically mild and clinically severe cases-all can be lumped into the same epidemiological pot. The result is a persistent flow of reports with grouped or clustered incidence. Greenfield’s description6 of eight cases in 11 days has been followed by similar accounts from centres in London,’,’ the United States,9 and New Zealand. 10 Testing for faecal toxins has revealed clustering where none had been noted on purely anatomical criteria. ] Can these all be artifacts of observation, the result of increased attention and diagnosis? The correct answer may lie in the epidemiology of C. difficile. Two facts about C. difficile stand in contrast to one another: it is a very common faecal organism in infants and young children and rare in healthy adults. Is the latter a result of insensitive culture methods or is the former a consequence of exposure of an unusually susceptible population to a common environmental contaminant? It is very difficult to prove that an organism is absent from human faeces, no matter how sensitive the methods. In the hamster model for C. difficile colitis, this conclusion can be deduced when animals are enclosed for extended periods within sterile, filter-topped boxes. Non-development of colitis under these conditions JD, Baggenstoss AH, Dearing WH, Judd E. Jr. Postoperative pseudomembranous enterocolitis. Surg Gynecol Obstet 1954; 98: 546-52 Swartzberg JE, Maresca RM, Remington JS Clinical study of gastrointestinal complications associated with clindamycin therapy. J Infect Dis 1977; 135:
1. Pettet 2
S99-S103 FJ, Barton RW, Alpers DH. Clindamycin-associated colitis: study. Ann Intern Med 1974; 81: 429-33.
3. Tedesco 4
a
prospective
Kabins SA, Spira TJ Outbreak of clindamycin-associated colitis. Ann Intern Med 1975;
83: 830-31. 5. Gurwith MJ, Rabin
6. 7.
8.
9.
10.
11
HR, Love K and the Co-operative Antibiotic Diarrhea Study Group Diarrhea associated with clindamycin and ampicillin therapy Preliminary results of a co-operative study J Infect Dis 1977, 135: S104-S110. Greenfield C, Burroughs A, Szawathowski M, Bass N, Noone P, Pounder R. Is pseudomembranous colitis infections? Lancet 1981; i: 371-72. Haji TC, Lewis PS, Sanderson PJ. Pseudomembranous colitis: an infectious disease?
Lancet 1981; ii: 208-09. Rogers TR, Petrou M, Lucas C, Chung JTN, Barrett AJ, Borriello SP, Honour P. Spread of Clostridium difficile among patients receiving non-absorbable antibiotics for gut decontamination. Br Med J 1981; 283: 408-09. Pierce PF, Wilson R, Silva J Jr, Garagusi VF, Rifkin GD, Fekety R, Nunez-Montiel O, Dowell VR Jr, Hughes JM. Antibiotic-associated pseudomembranous colitis: an epidemiologic investigation of a cluster of cases. J Infect Dis 1982; 145: 269-74. Ritchie DBC, Jennings LC, Lynn KL, Bailey RR, Cook HB. Clostridium difficileassociated colitis: Cross infection in predisposed patients with renal failure. N Z Med J 1982; 95: 265-67 Mogg GAG, Arabi Y, Youngs D, Johnson M, Bentley S, Burdon DW, Keighley MRB. Therapeutic trials of antibiotic-associated colitis. Scand J Infect Dis 1980; 22 (suppl): 41-45.
would seem to prove that C. difficile is absent from the hamster’s normal flora. 12 In man prospective evidence for acquisition of C. difficile (i.e., conversion from culture negative to culture positive) would be a strong argument for the advocates of crossinfection. Because the occurrence of adult colitis is patchy, prospective investigation might be difficult. However, the high frequency of infant colonisation would be an asset to this type of study-indeed significant differences in the prevalence of C. difficile between neonatal units have been reported. 13,14 Sherertz and Sarubbi 14 state that these "findings support the notion of nosocomial spread". If so, C. difficile colonisation in neonates reveals a previously unsuspected pattern of cross-infection. There is the intriguing suggestion that C. difficile may be a marker for cross-infection mechanisms that are also factors in outbreaks of neonatal necrotising enterocolitis. Retrospective assessment of apparent outbreaks of pseudomembranous colitis in adults would be facilitated by a reliable system for typing strains of C. difficile. Many physicians now advise that patients with C. difficile colitis be barrier nursed, and there is uncontrolled evidence to support this approach.6,15 Environmental contamination occurs readily, especially if there is incontinence. 15 C. difficile has been isolated from hands,i4,i6 and washing them between patients remains an "appropriate technology", especially perhaps in busy intensive care units. Physicians can control the pool of susceptibles by being circumspect about their use of antibiotics. There remains a nascent incidence of asymptomatic colonisation, a considerable prevalence of isolations from control environments, and, perhaps, unappreciated reservoirs in pets and other animals.15,16 All of these could influence the frequency of cases in hospital, but their importance in initiating clinically significant human infections is unknown. The efficacy of germicidal agents or even of simple cleaning on C. difficile contaminating the environment and medical equipment has not been measured. In the U.K. a growing number of routine microbiology laboratories are capable of culturing and identifying this organism. A correct microbiological diagnosis is likely to be the key to further knowledge about managing these patients and their surroundings. CORONARY VASCULAR STEAL VASCULAR steal syndromes are a familiar topic in cardiovascular circles and various local patterns may be envisaged. In principle, if two parallel vascular systems, with separate feeding arteries, accept blood from a common pressure source, a large increase in flow through one resistance system may lead to a fall in flow through the other. Flow can be "stolen" from one system on account of changes in the other-hence the expression steal syndrome. The reasons for this are simple. If the upstream pressure-head remains constant, and ifa large fall in resistance takes place in 12. Larson HE, Price AB, Borriello SP. Epidemiology of experimental enterocolitis due to Clostridium difficile. J Infect Dis 1980; 142: 408-13. 13. Donta ST, Myers MG. Clostridium difficile toxin in asymptomatic neonates. J Pediatr 1982; 100: 431-34. 14 Sherertz RJ, Sarubbi FA. The prevalence of Clostridium difficile and toxin in a nursery population: a comparison between patients with necrotizing enterocolitis and an asymptomatic group. J Pediat 1982; 100: 435-39. 15. Mulligan ME, George WL, Rolfe RD, Finegold SM. Epidemiologic aspects of Clostridium difficile-induced diarrhea and colitis. Am J Clin Nutr 1980, 33: 2533-38. 16. Kim KH, Fekety R, Batts DH, Brown D, Cudmore M, Silva J Jr, Waters D. Isolation of Clostridium difficile from the environment and contact of patients with antibioticassociated colitis. J Infect Dis 1981; 143: 42-50.
interesting effects on learning, provide a treatment for dementia.
seem
unlikely
to
CROSS-INFECTION AND CLOSTRIDIUM DIFFICILE CASES of pseudomembranous colitis occur with annoying irregularity. This "now you see it, now you don’t" character has featured in several reviews and reports. Pettet et al.were stimulated by a flurry of cases to review records between 1925 and 1952; they found nearly the same frequency before as after 1939. Swartzberg and his colleagues2 saw fourteen patients with pseudomembranous colitis over a brief period; then they prospectively evaluated diarrhoea in a thousand patients given clindamycin and identified not one more case. Tedesco’s well known prospective study revealed pseudomembranes in an astonishing 10% of two hundred consecutive patients given clindamycin over a 6 month period,3 an experience confirmed by some4 but not by others.5 Since then the discovery of Clostridium difficile as a specific aetiological factor has permitted cases which occur under disparate circumstances to be associated. Medical and surgical cases, ampicillin, cephalosporin, and clindamycin associated cases, clinically mild and clinically severe cases-all can be lumped into the same epidemiological pot. The result is a persistent flow of reports with grouped or clustered incidence. Greenfield’s description6 of eight cases in 11 days has been followed by similar accounts from centres in London,’,’ the United States,9 and New Zealand. 10 Testing for faecal toxins has revealed clustering where none had been noted on purely anatomical criteria. ] Can these all be artifacts of observation, the result of increased attention and diagnosis? The correct answer may lie in the epidemiology of C. difficile. Two facts about C. difficile stand in contrast to one another: it is a very common faecal organism in infants and young children and rare in healthy adults. Is the latter a result of insensitive culture methods or is the former a consequence of exposure of an unusually susceptible population to a common environmental contaminant? It is very difficult to prove that an organism is absent from human faeces, no matter how sensitive the methods. In the hamster model for C. difficile colitis, this conclusion can be deduced when animals are enclosed for extended periods within sterile, filter-topped boxes. Non-development of colitis under these conditions JD, Baggenstoss AH, Dearing WH, Judd E. Jr. Postoperative pseudomembranous enterocolitis. Surg Gynecol Obstet 1954; 98: 546-52 Swartzberg JE, Maresca RM, Remington JS Clinical study of gastrointestinal complications associated with clindamycin therapy. J Infect Dis 1977; 135:
1. Pettet 2
S99-S103 FJ, Barton RW, Alpers DH. Clindamycin-associated colitis: study. Ann Intern Med 1974; 81: 429-33.
3. Tedesco 4
a
prospective
Kabins SA, Spira TJ Outbreak of clindamycin-associated colitis. Ann Intern Med 1975;
83: 830-31. 5. Gurwith MJ, Rabin
6. 7.
8.
9.
10.
11
HR, Love K and the Co-operative Antibiotic Diarrhea Study Group Diarrhea associated with clindamycin and ampicillin therapy Preliminary results of a co-operative study J Infect Dis 1977, 135: S104-S110. Greenfield C, Burroughs A, Szawathowski M, Bass N, Noone P, Pounder R. Is pseudomembranous colitis infections? Lancet 1981; i: 371-72. Haji TC, Lewis PS, Sanderson PJ. Pseudomembranous colitis: an infectious disease?
Lancet 1981; ii: 208-09. Rogers TR, Petrou M, Lucas C, Chung JTN, Barrett AJ, Borriello SP, Honour P. Spread of Clostridium difficile among patients receiving non-absorbable antibiotics for gut decontamination. Br Med J 1981; 283: 408-09. Pierce PF, Wilson R, Silva J Jr, Garagusi VF, Rifkin GD, Fekety R, Nunez-Montiel O, Dowell VR Jr, Hughes JM. Antibiotic-associated pseudomembranous colitis: an epidemiologic investigation of a cluster of cases. J Infect Dis 1982; 145: 269-74. Ritchie DBC, Jennings LC, Lynn KL, Bailey RR, Cook HB. Clostridium difficileassociated colitis: Cross infection in predisposed patients with renal failure. N Z Med J 1982; 95: 265-67 Mogg GAG, Arabi Y, Youngs D, Johnson M, Bentley S, Burdon DW, Keighley MRB. Therapeutic trials of antibiotic-associated colitis. Scand J Infect Dis 1980; 22 (suppl): 41-45.
would seem to prove that C. difficile is absent from the hamster’s normal flora. 12 In man prospective evidence for acquisition of C. difficile (i.e., conversion from culture negative to culture positive) would be a strong argument for the advocates of crossinfection. Because the occurrence of adult colitis is patchy, prospective investigation might be difficult. However, the high frequency of infant colonisation would be an asset to this type of study-indeed significant differences in the prevalence of C. difficile between neonatal units have been reported. 13,14 Sherertz and Sarubbi 14 state that these "findings support the notion of nosocomial spread". If so, C. difficile colonisation in neonates reveals a previously unsuspected pattern of cross-infection. There is the intriguing suggestion that C. difficile may be a marker for cross-infection mechanisms that are also factors in outbreaks of neonatal necrotising enterocolitis. Retrospective assessment of apparent outbreaks of pseudomembranous colitis in adults would be facilitated by a reliable system for typing strains of C. difficile. Many physicians now advise that patients with C. difficile colitis be barrier nursed, and there is uncontrolled evidence to support this approach.6,15 Environmental contamination occurs readily, especially if there is incontinence. 15 C. difficile has been isolated from hands,i4,i6 and washing them between patients remains an "appropriate technology", especially perhaps in busy intensive care units. Physicians can control the pool of susceptibles by being circumspect about their use of antibiotics. There remains a nascent incidence of asymptomatic colonisation, a considerable prevalence of isolations from control environments, and, perhaps, unappreciated reservoirs in pets and other animals.15,16 All of these could influence the frequency of cases in hospital, but their importance in initiating clinically significant human infections is unknown. The efficacy of germicidal agents or even of simple cleaning on C. difficile contaminating the environment and medical equipment has not been measured. In the U.K. a growing number of routine microbiology laboratories are capable of culturing and identifying this organism. A correct microbiological diagnosis is likely to be the key to further knowledge about managing these patients and their surroundings. CORONARY VASCULAR STEAL VASCULAR steal syndromes are a familiar topic in cardiovascular circles and various local patterns may be envisaged. In principle, if two parallel vascular systems, with separate feeding arteries, accept blood from a common pressure source, a large increase in flow through one resistance system may lead to a fall in flow through the other. Flow can be "stolen" from one system on account of changes in the other-hence the expression steal syndrome. The reasons for this are simple. If the upstream pressure-head remains constant, and ifa large fall in resistance takes place in 12. Larson HE, Price AB, Borriello SP. Epidemiology of experimental enterocolitis due to Clostridium difficile. J Infect Dis 1980; 142: 408-13. 13. Donta ST, Myers MG. Clostridium difficile toxin in asymptomatic neonates. J Pediatr 1982; 100: 431-34. 14 Sherertz RJ, Sarubbi FA. The prevalence of Clostridium difficile and toxin in a nursery population: a comparison between patients with necrotizing enterocolitis and an asymptomatic group. J Pediat 1982; 100: 435-39. 15. Mulligan ME, George WL, Rolfe RD, Finegold SM. Epidemiologic aspects of Clostridium difficile-induced diarrhea and colitis. Am J Clin Nutr 1980, 33: 2533-38. 16. Kim KH, Fekety R, Batts DH, Brown D, Cudmore M, Silva J Jr, Waters D. Isolation of Clostridium difficile from the environment and contact of patients with antibioticassociated colitis. J Infect Dis 1981; 143: 42-50.