A CLINICO.PATHOLOGICAL STUDY OF ANAL FISTULAE
A CLINICO.PATHOLOGICAL STUDY OF ANAL FISTULAE
A CLINICO.PATHOLOGICAL STUDY OF ANAL FISTULAE
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AnalFkruh<br />
Revlprt olLiterutwrc<br />
Pathosenesis<br />
Primant Infeetion and Latencv<br />
Most CMV infections are acquired either in the pErinatal period and<br />
infancy or in adulthood through sexual contacts (HO, 1990. )<br />
#<br />
Although congenital infections due to primary CMV infection in<br />
pregnaricy af,e a cause of substantial morbidity and death (Demmler, I99I),<br />
Most primary CMV infections in immunologically healthy adults are<br />
asymptomatic or are associf,ted with a mild mononucleosis like syndrome.<br />
Serious gastrointestinal disease due to primary infection is rare (see below<br />
in "Healthy persons"). All primary infections resolve and enter a state of<br />
latency in which live virus is sequestered in a non replicative state. Persons<br />
with latent infection have no symptoms but do have antibody to CMV.<br />
s<br />
The predominantissue site of viral latency is not known (Rabin<br />
1990) but circulating lymphocytes, monocytes, and polymorphnuclear<br />
leukocytes all probably contrilin latent vinrs (Merigan 1990).<br />
#<br />
Organs. at risk for subsequent CMV disease, including the<br />
gashointestinal ttact, may contain latent virus that may cause local disease<br />
with reactivation (Tyms et atr., 1989)<br />
Inf'ect ion C ompared with Disease<br />
t<br />
Because most patients previously exposed to CMV have latent vinrs in<br />
various organs without evidence of organ damage, infection with CMV is<br />
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