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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 />

26

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