This is the first study to provide a comprehensive insight into the molecul
ar epidemiology of endemic Clostridium difficile and particularly that asso
ciated with a recently recognized epidemic strain. We DNA fingerprinted all
C. difficile isolates from the stools of patients with symptomatic antibio
tic-associated diarrhoea and from repeated samples of the inanimate ward en
vironment on two elderly medicine hospital wards over a 22-month period. No
tably, C. difficile was not recoverable from either ward immediately before
opening, but was found on both wards within 1-3 weeks of opening, and the
level of environmental contamination rose markedly during the first 6 month
s of the study period. C. difficile infection (CDI) incidence data correlat
ed significantly with the prevalence of environmental C. difficile on ward
B (r = 0(.)76, P < 0(.)05) but not on ward A (r = 0(.)26, P > 0(.)05). We f
ound that RAPD and RS-PCR typing had similar discriminatory power, although
, despite fingerprinting over 200 C. difficile isolates, we identified only
six distinct types. Only two distinct C. difficile strains were identified
as causing both patient infection and ward contamination. Attempts to dete
rmine whether infected patients or contaminated environments are the prime
source for cross-infection by C. difficile had limited success, as over 90%
of C. difficile isolates were the UK epidemic clone. However, a non-epidem
ic strain caused a cluster of six cases of CDI, but was only isolated from
the environment after the sixth patient became symptomatic. The initial abs
ence of this strain from the environment implies patient-to-patient and/or
staff-to-patient spread. In general, routine cleaning with detergent was un
successful at removing C. difficile from the environment. Understanding the
epidemiology and virulence of prevalent strains is important if CDI is to
be successfully controlled.