Letter
First Shiga Toxin-Producing
Escherichia coli Isolate from a Patient with Hemolytic Uremic
Syndrome, Brazil
To the Editor: Infection by Shiga toxin (Stx)-producing
Escherichia coli (STEC), particularly strains of serotype
O157:H7, can cause sporadic cases and outbreaks of diarrhea, hemorrhagic
colitis (HC), and hemolytic uremic syndrome (HUS) (1).
Some other serotypes (e.g., O26:H11, O111:H8, O111:NM, and O113:H21)
share a similar pathogenic potential. STEC are distributed worldwide,
but most of the HC and HUS cases were reported from industrialized
nations of the Northern and Southern hemisphere (2).
In South America, HUS is a major cause of acute renal failure in
infants in Argentina (3) and Chile (4).
However, in Brazil human STEC infections have been restricted to
sporadic cases of nonbloody diarrhea (5,6). Although
a high frequency of STEC strains was recently found in foods and
animal reservoirs (7,8), only some of the serotypes
identified in animals (8) were recognized as causes
of human illness (e.g., O157:H7, O22:H16, O82:H8, and NT:H21). Moreover,
there is currently no nationwide surveillance system for HUS in
Brazil, and STEC-associated HUS has not been previously reported
in our country.
We describe the case of an 8-month-old boy from a northeastern
state in Brazil, who was admitted to the emergency room of Hospital
São Paulo, São Paulo, on March 17, 2001; the boy had anemia, oliguria,
and edema of lower extremities. He had an acute diarrheal prodromal
illness 3 weeks before hospital admission. On the same day as admission,
respiratory failure developed, and the child was transferred to
the pediatric intensive-care unit of the hospital. The boy had hemolytic
anemia (hemoglobin level 11.9 g/dL at admission, and 9.1 g/dL several
days later), renal failure (blood urea nitrogen 43.8 mg/dL and serum
creatinine 1.5 mg/dL), and thrombocytopenia (platelet count of 70,000/mm3),
leading to a diagnosis of HUS. The patient received treatment with
fresh frozen plasma and needed renal support (peritoneal dialysis)
for 7 days. Once renal function was reestablished, the patient’s
outcome was good.
Feces were collected as soon as HUS was suspected and plated onto
MacConkey Sorbitol Agar (Difco, Becton Dickinson Microbiology Systems,
Sparks, MD). Only sorbitol-positive colonies grew and were biochemically
identified as E. coli by standard procedures. The E. coli
isolates expressed Stx1, as identified by cytotoxicity and neutralization
assays on Vero cells (5). Presence of stx1
and intimin (eae) gene sequences was confirmed by polymerase
chain reaction (9,10). The E. coli strain
belonged to serotype O26:H11 and produced enterohemorragic E.
coli hemolysin (enterohemolysin).
This report is the first on the isolation of an STEC strain in
a HUS patient in Brazil. The serotype O26:H11 has been described
as agent of HC and HUS in other countries and was the second most
frequent serotype found in STEC strains isolated from diarrheal
cases in our settings (6). Moreover, expression
of Stx1 and enterohemolysin and the presence of eae are virulent
characteristics usually found in the human STEC strains isolated
so far in Brazil. These findings show the importance of looking
for non-O157 STEC strains besides O157:H7 in patients with HC and
HUS in Brazil. Surveillance for HUS, either nationally or in sentinel
population-based studies, should be performed in Brazil, and studies
on the occurrence of HUS and its association with STEC infections
are under investigation in our laboratory.
Beatriz Ernestina C. Guth, *Renato Lopes de Souza,† Tânia Mara
I. Vaz,‡ and Kinue Irino‡
*Universidade Federal de São Paulo—Escola Paulista
de Medicina, São Paulo, Brazil; †Hospital São Paulo, São Paulo,
Bazil; and ‡Instituto Adolfo Lutz, São Paulo, Brazil
Acknowledgments
We thank Dr. Tânia A.T. Gomes for encouragement on this subject.
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