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Clinical Characteristics

In the initial stage of the disease the primary genital lesion (discussed above in Pathology) may go unnoticed, especially in women. In the secondary stage there is often a seropurulent discharge from the inguinal buboes in men. With the development of proctocolitis in women, and occasionally in men, the clinical features are those of colitis of varying duration and severity with diarrhea, constipation, rectal bleeding and the discharge of pus and blood in the stools. The mucosa feels coarse and granular on rectal examination. Sigmoidoscopy shows an acute proctitis with intense inflammation and a pseudomembrane over a bleeding, friable mucosa. There are often constitutional symptoms at this stage, including malaise, anorexia, headache and fever. In the rare patient in whom infection has been introduced through the respiratory tract, there may be an acute onset of disease with chills, sweating, fever and arthralgias. Meningoencephalitis has been reported as a complication in a few patients.

The third stage of the disease is most striking in women and is characterized by chronic proctitis and extensive fibrosis leading to anorectal stricture. As the stricture develops, there is rectal pain, tenesmus, constipation and narrow stools. Rectovaginal fistula with incontinent passage of feces through the vagina frequently develops, as well as perianal abscesses and vulvar elephantiasis. In this stenotic phase the rectal ampulla is narrowed by scarring and, on proctoscopy, there is frequently friable, bleeding, ulcerated mucosa overlying the stricture. The perianal skin is often thickened and edematous, and a characteristic lymphorrhoid may be present. The lower edge of the stricture is usually 2.5 to 5 cm (1 to 2 inches) from the anal orifice, within easy reach of the examining finger; it is never more than 10 to 12.5 cm (4 to 5 inches) from the anus. The stricture varies in diameter from slight narrowing to virtual total stenosis, admitting only a small probe.

Laboratory Diagnosis

The diagnosis of LGV is ideally confirmed by isolating one of the serovars from a lesion. Unfortunately, positive isolations are made in less than half the specimens taken from otherwise typical buboes. The complement fixing test is easier to perform and requires only a single visit. A positive test at a dilution of 1:64 is diagnostic. When paired specimens are available, a four-fold rise in titer is also diagnostic. An immunofluorescence test is available and more sensitive than the complement fixing test, but there may be a reaction with non-LGV serovars. Finally, hematoxylin and eosin-stained sections that reveal typical stellate pyogranulomatous lesions (Fig. 20.3) are virtually diagnostic when the histopathological background and clinical features are typical.

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Copyright: Palmer and Reeder

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