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Letter
Multidrug-Resistant Shiga
Toxin–Producing Escherichia coli O118:H16 in Latin America
Antonio Fernando Pestana de Castro,* Beatriz Guerra,† Luciana Leomil,*
Leila Aidar-Ugrinovitch,‡ and Lothar Beutin§
*Universidade de São Paulo, São Paulo, Brazil; †Federal Institute for
Risk Assessment, Berlin, Germany; ‡Universidade de Campinas, Campinas,
Brazil; and §Robert Koch-Institute, Berlin, Germany
Suggested citation for this article: Poikonen
E, Lyytikäinen O, Anttila V-J, Ruutu P. Multidrug-resistant shiga
toxin–producing Escherichia coli O118:H16 in Latin America. Emerg
Infect Dis [serial online] 2003 Aug [date cited]. Available from:
URL: http://www.cdc.gov/ncidod/EID/vol9no8/03-0062.htm
To the Editor: We report the first isolation of a multiple antimicrobial
drug–resistant strain of Shiga toxin–producing Escherichia coli
(STEC) O118:H16 from cattle in Latin America. The strain was isolated
during a study of fecal STEC in 205 healthy and 139 diarrheic cattle on
12 beef farms in the state of São Paulo, Brazil, in February 2000; one
case of STEC was found in a 1-month-old calf with diarrhea. This bovine
STEC O118:H16 strain showed resistance to eight antimicrobial substances;
the following resistance (R)-genes were detected: ampicillin (blaTEM1-like),
kanamycin and neomycin (aphA1), streptomycin (strA/B), sulphametoxazol
(sul2), tetracyclin (tet[A]), trimethoprim (no dfrA1,
A5, A7, A12, A14, or A17), and trimethoprim/sulphamethoxazol.
The STEC O118:H16 strain from Brazil was found to be similar for virulence
genes (Shiga toxin 1 [stx1], intimin beta 1 [eae β1],
and EHEC-hemolysin [E-hlyA]) and for antimicrobial drug resistance
to STEC O118:H16 strains, which were isolated in different countries of
Europe (1). Beginning in 1986, STEC O118:H16 was identified
as an emerging pathogen for calves and humans in Belgium and Germany (2–4).
Cattle and human STEC O118:H16 isolates were similar in virulence attributes
and antimicrobial drug resistance and belonged to a distinct genetic clone
(1). Transmission of these pathogens from cattle to humans
on farms was observed (5).
Beginning in 1996, STEC O118:H16 has become important as an emerging
pathogen in humans and has been associated with bloody diarrhea and hemolytic
uremic syndrome (2). Analysis of the antimicrobial resistance
profiles showed that >96% of the European STEC O118:H16 strains showed
resistance to one or more antimicrobial drugs in contrast to the 10% to
15% drug-resistant strains that were detected among STEC belonging to
other serotypes (1,6,7). STEC O118:H16 showing multiresistance
in up to eight different antimicrobial drugs predominated among younger
isolates, indicating that drug resistance genes have accumulated over
time in STEC O118:H16 strains. The frequency of antimicrobial drug resistance
in STEC and Stx-negative E. coli in humans and animals was compared
in a study by Schroeder et al. (8). Among human clinical
E. coli isolates, antimicrobial resistance was less frequently
observed in STEC than in Stx-negative strains, whereas in cattle, antibiotic-resistant
strains were found at similar frequencies in both groups of E. coli.
The relatively higher frequency of antimicrobial-resistant STEC in cattle
was explained by the use of antimicrobial drugs in cattle production,
whereas human infections with STEC are generally not treated with antibiotics
(8). Cattle could thus be an important source of new
emerging antibiotic-resistant STEC strains such as O118:H16.
The genetic basis of antimicrobial resistance in STEC O118:H16 is broad,
including R-plasmids, integrons, transposons, and chromosomally inherited
drug-resistance genes. Fluoroquinolone resistance has also been acquired
by some STEC O118:H16 strains (1). The heterogenicity
of antimicrobial drug–resistance patterns, the increase of multidrug-resistant
strains over time of isolation, and the evidence for multiple aquisition
and genetic location of R-determinants indicate that strains belonging
to the STEC O118:H16 clone have a propensity to acquire and accumulate
R-genes. The finding that multidrug-resistant STEC O118:H16 is isolated
from cattle in South America indicates the global spread of this new emerging
EHEC type.
References
- Maidhof H, Guerra B, Abbas S, Elsheikha HM, Whittam
TS, Beutin L. A
multiresistant clone of shiga toxin–producing Escherichia coli
O118:[H16] is spread in cattle and humans over different European countries.
Appl Environ Microbiol 2002;68:5834–42.
- Beutin L, Zimmermann S, Gleier K. Human
infections with Shiga toxin–producing Escherichia coli other
than serogroup O157 in Germany. Emerg Infect Dis 1998;4:635–9.
- Mainil J. Shiga/verocytotoxins
and Shiga/verotoxigenic Escherichia coli in animals. Vet
Res 1999;30:235–57.
- Wieler LH, Vieler E, Erpenstein C, Schlapp T, Steinruck H, Bauerfeind
R, et al. Shiga
toxin–producing Escherichia coli strains from bovines: association
of adhesion with carriage of eae and other genes. J Clin
Microbiol 1996;34:2980–4.
- Beutin L, Bulte M, Weber A, Zimmermann S, Gleier K. Investigation
of human infections with verocytotoxin-producing strains of Escherichia
coli (VTEC) belonging to serogroup O118 with evidence for zoonotic
transmission. Epidemiol Infect 2000;125:47–54.
- Kobayashi H, Shimada J, Nakazawa M, Morozumi T, Pohjanvirta T, Pelkonen
S, et al. Prevalence
and characteristics of Shiga toxin–producing Escherichia coli
from healthy cattle in Japan. Appl Environ Microbiol 2001;67:484–9.
- Schroeder CM, Zhao C, DebRoy C, Torcolini J, Zhao S, White DG, et
al. Antimicrobial
resistance of Escherichia coli O157 isolated from humans, cattle,
swine, and food. Appl Environ Microbiol 2002;68:576–81.
- Schroeder CM, Meng J, Zhao S, DebRoy C, Torcolini J, Zhao C, et al.
Antimicrobial
resistance of Escherichia coli O26, O103, O111, O128, and O145
from animals and humans. Emerg Infect Dis 2002;8:1409–14.
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