Page 140 - AIDSBK23C

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macrophages, polymorphonuclear leukocytes, or lymphocytes may be seen. Diagnosis is made
by finding the 5 to 7 micron cysts with special stains in biopsy or cytologic specimens.[602]
Most PCP cases are "typical" in that pink foamy to granular alveolar exudate is present
and interstitial or inflammatory changes are minimal to absent. This exudate is found in most
alveoli throughout the lung, though it may be more pronounced in some. A patchy pattern of
alveolar involvement is seen in a few cases. However, one or more "atypical" features may be
found in over half of PCP cases and can include: a plasma cell interstitial pneumonitis with
round cells--including many plasma cells; a necrotizing granulomatous pattern of inflammation
with giant cells, epithelioid macrophages, and caseation; prominent microcalcifications; absence
of foamy exudate; interstitial or intraluminal fibrosis; bronchiolitis obliterans; or desquamation
of type II pneumonocytes. A "pneumocystoma" may develop and consist of a localized mass
lesion containing sheets of foamy to granular pink exudate without an intervening alveolar
framework.[603,609,612,613]
Pulmonary cavitation may occur in association with PCP in less than 5% of cases, either
alone or within an area of pulmonary consolidation, mass, or nodule. Patients with cavitation
may present with hemoptysis. Cavitation may be promoted by vascular invasion by P jiroveci
(carinii) and subsequent vasculitis and necrosis or by alveolar septal invasion and
necrosis.[602,615]
Extrapulmonary spread of P jiroveci (carinii) occurs in less than 5% of cases of AIDS in
which P jiroveci (carinii) infection is diagnosed. The most common site is hilar lymph nodes,
followed by spleen and liver.[417] The microscopic appearance is often similar to that of the
alveoli, but in widely disseminated cases, P jiroveci (carinii) can produce numerous small 0.1 to
0.3 cm calcified granulomas that give cut surfaces of parenchymal organs the gross appearance
of rough sandpaper. A GMS stain reveals the organisms, even in densely calcified areas.
Immunohistochemical staining for P jiroveci (carinii) in extrapulmonary sites is very
useful.[415] In the rare cases of PCP accompanied by pleural effusion, typically in association
with aerosolized pentamidine therapy, pleural fluid cytologic examination with GMS stain helps
to reveal the organisms.[616]

CYTOMEGALOVIRUS.-- Cytomegalovirus (CMV) involvement of lung varies from an
insignificant and incidental microscopic finding without extensive gross or microscopic changes
to a florid pneumonitis with numerous inclusion bodies. Cytomegalovirus may not always be
diagnosed pre mortem either because a long latent incubation period is present without
characteristic morphologic changes, infection develops agonally, or there is sampling error with
tissue biopsy or cytologic methods caused by the patchy distribution of cells with characteristic
CMV inclusions.[617]
The finding of CMV in bronchoalveolar lavage or sputum specimens or by culture may
not necessarily indicate that a pneumonitis is present.[418] Cytomegalovirus can frequently be
detected in bronchoalveolar lavage fluid from HIV-infected patients and does not necessarily
correlate with pulmonary symptoms nor predict outcome.[618] Cytomegalovirus inclusions in
tissue biopsy specimens, along with the absence of other pathogens, may represent pneumonitis
that can be treated with ganciclovir. Though CMV is the most common viral infection of lung in
AIDS, it occurs frequently in conjunction with other opportunistic infections, so CMV is rarely
the sole cause for a symptomatic pneumonitis.
In cases of CMV pneumonitis, the most frequent clinical findings are fever, dyspnea, and
non-productive cough. Concomitant extrapulmonary evidence for CMV accompanies half of