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common symptoms of STEC disease. Interestingly, STEC patients do not
develop bacteremia. Thus, patients with acute and painful bloody diarrhea
without fever are considered to have a possible STEC infection.
In most cases, diarrheal disease is self-limiting, but some individuals
develop severe complications, the most lethal of which is HUS, defined as
a triad of microangiopathic anemia, thrombocytopenia, and acute renal fail-
ure (
Scheiring et al., 2008
;
Pennington, 2010
). HUS associated with Stx
accounts for 90% of all the HUS cases (
Ray and Liu, 2001
). The onset of
HUS occurs typically between 5-13 days of the infection and generally
starts as thrombocytopenia followed by hemolysis, anemia, and decrease in
packed cell volume, and finally elevated serum creatinine level, which is
often used as a guide for the clinical management. HUS causes renal fail-
ure in 15% of STEC-infected children younger than 10 years old (
Ostroff
et al., 1989
;
Bell et al., 1997
), and can develop even in the absence of pre-
ceding diarrhea. In addition to young age, administration of anti-motility
drugs or antibiotics and elevated white blood cell count are correlated with
an increased risk of HUS (
Pavia et al., 1990
;
Bell et al., 1997
;
Wong et al.,
2000
). The hematologic manifestations of HUS usually disappear within
1-2 weeks (
Tarr et al., 2005
).
The characteristic histopathologic lesions of HUS include microvascular
thrombi and swollen endothelial cells, reflecting the thrombotic nature of this
disorder. The renal disease is marked by hematuria, proteinuria, oliguria, and in
severe cases renal failure (
Tarr et al., 2005
;
Pennington, 2010
). Increased activ-
ity of plasminogen activator inhibitor 1 (PAI-1) results in inhibition of fibrino-
lysis in HUS patients leading to increased intravascular generation of fibrin and
thrombin, which are manifested as high plasma levels of D-dimer and thrombin
fragment 1+2, respectively (
Nevard et al., 1997
). Consequently, high concentra-
tions of D-dimer and fragment 1+2 when presented with diarrhea are believed
to be risk factors for the development of HUS.
While most patients recover from acute renal disease, they retain a long-
term risk of renal failure even many years after recovery. Furthermore, in cer-
tain cases, STEC toxicity affects other organ systems such as the pulmonary,
cardiovascular, and central nervous system (CNS). Fluid overload, pleural
effusions, and adult respiratory distress are frequent pulmonary complications.
Adult HUS patients are more prone to congestive heart failure whereas other
cardiac disorders are common in children. Additionally, complications such as
intestinal perforations and necrosis, acidosis, pancreatitis, and glucose intoler-
ance can develop during HUS (
Tarr et al., 2005
). Importantly, CNS complica-
tions, which develop in 25% of the HUS cases, are the most perilous and are
the main precedent of HUS lethality (
Eriksson et al., 2001
). Ischemia-hypoxia
resulting from cerebral microvascular thrombi, along with direct CNS toxicity
of Stx, can lead to irritability, lethargy, and confusion. Approximately, 10%
of the patients develop stroke, seizures, and coma (
Taylor et al., 1986
;
Brandt
et al., 1994
).
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