Learning Objectives

1. Discuss the natural history of HIV infection (Robbins 5th Ed. p. 227-228) or (Robbins 6th Ed. p. 246-247).

2. Discuss the current testing methodology for detecting HIV infection.

a. Enzyme-linked antibody test (ELISA)
b. Western blot
c. HIV antigen test
d. Polymerase chain reaction amplification

3. List the opportunistic infections and neoplasms found in patients with HIV infections (Robbins 5th Ed. p. 228-231, Table 6-10) or (Robbins 6th Ed. p. 247-250).

4. Describe the pathology of the following pulmonary infections typically occurring in patients with HIV infections.

a. Pneumocystis pneumonia (Robbins 5th Ed. p. 357) or (6th Ed. p. 382)
b. Cytomegalovirus pneumonitis (Robbins 5th Ed. p. 352) or (Robbins 6th Ed. p. 376)

5. Recognize that CMV may not only cause pneumonitis, but also gastroenteritis in patients with AIDS. Discuss the pathologic alteration produced by other gastrointestinal opportunistic pathogens, below:

a. Cryptosporidium parvum (cryptosporidiosis) (Robbins 5th Ed. p. 357-358) or (Robbins 6th Ed. p. 382-383)
b. Mycobacterium avium intracellulare (Robbins 5th Ed. p. 324-327) or (Robbins 6th Ed. p. 351-352)

6. Discuss the pathogenesis and pathology of mycobacterial infection with respect to:

a. The pathogenesis relating to immune defects in patients with HIV infection (Robbins 5th Ed. p. 326) or (Robbins 6th Ed. p. 351)
b. The histopathology in patients who are moderately vs. severely immunosuppressed (Robbins 5th Ed. p. 326-327) or (Robbins 6th Ed. p. 353)

7. Describe the morphological changes associated with each of the following opportunistic infections (Robbins 5th Ed. p. 225-227, 351-358, 1321-1323) or (Robbins 6th Ed. p. 244-247, 375-383, 1320-1321)

a. Cytomegalovirus encephalitis (Robbins 5th Ed. p. 352) or (Robbins 6th Ed. p. 376)
b. Progressive multifocal leukoencephalopathy (Robbins 5th Ed. p. 1322-1323) or (Robbins 6th Ed. p. 1321)
c. Cryptococcosis (Robbins 5th Ed. p. 355) or (Robbins 6th Ed. p. 380)
d. Toxoplasmosis (Robbins 5th Ed. p. 358) or (Robbins 6th Ed. p. 383)
e. Primary HIV encephalitis (Robbins 5th Ed. p. 225-227, 1321-1322) or (Robbins 6th Ed. p. 244-246, 1320-1321).

8. List the two EBV-associated proliferations seen in patients with HIV infection listed in the text. Indicate the most common site involved by EBV-associated lymphomas in this population (Robbins 5th Ed. p. 229-231) or (Robbins 6th Ed. p. 248-250).

9. Contrast the epidemiology of Kaposi's sarcoma and non-Hodgkins lymphoma in patients with HIV infection (Robbins 5th Ed. p. 229, 511-512) or (Robbins 6th Ed. p. 247, 535-537). Name the virus, aside from HIV, associated with Kaposi's sarcoma.

Resources

1. (Robbins 5th Ed. p. 225-231, 324-327, 351-358, 511-512, 1321-1323) or (Robbins 6th Ed. p. 244-250, 351-352, 375-383, 535-537, 1320-1321)

2. Images 1-10 relate to the case; Images 11-14 are related to other objectives.

Scenario

Normal Reference Range Table

A 36-year-old homosexual male initially presented to the emergency room with a complaint of malaise and fever of several months' duration. A history of intravenous drug abuse was obtained, although the patient stated that he had been "clean" for the past eighteen months. Physical examination was remarkable for pallor and generalized, nontender lymphadenopathy. A needle aspiration biopsy of one of the enlarged nodes revealed a mixed cell population, consistent with reactive hyperplasia. Subsequent laboratory evaluation revealed the patient to be seropositive for HIV by both ELISA and Western blot. A CD4+ count was 350/ul. The patient was discharged with an appointment to return to AIDS clinic, but was subsequently lost to follow-up.

He returned to the emergency room 16 months later complaining of recurrent fever, persistent dry cough, and dyspnea. Chest X-ray at the time is shown in Image 1. A transbronchial biopsy is shown in Image 2. He was begun on sulfa-trimethoprim with resolution of his infiltrates and symptomatic improvement. He was discharged for follow-up in the hospital AIDS clinic.

The patient failed to keep his subsequent clinic appointments, and presented three months later with recurrent dyspnea, fever, voluminous watery diarrhea, and weight loss. Chest X-ray revealed changes similar to those noted on his previous admission, which again responded to therapy with sulfatrimethoprim. Diarrhea persisted, and smear of a stool specimen revealed numerous acid-fast bacilli. CD4+ counts at that time were 190/ul. He was again discharged, to be followed as an outpatient, and told to continue his medications.

Over the next several months, the patient's course was characterized by memory loss, persistent diarrhea, loss of appetite, and continuing weight loss despite antimicrobial therapy. He became progressively confused and withdrawn, and required almost constant care from friends. He was found unresponsive one morning and brought to the emergency room. Examination revealed a markedly cachectic male responsive only to deep pain. Radiographic imaging plus characteristic pathologic changes are seen in Images 3-5. Funduscopic exam revealed irregular areas of retinal hemorrhage and pale exudate bilaterally (Image 6). Breathing was shallow and labored. While in the emergency room, the patient expired. Attempted cardiopulmonary resuscitation was unsuccessful.

Gross findings at autopsy included cachexia (wasting); bilaterally firm, heavy, poorly aerated lungs; markedly enlarged spleen; and large, soft, pale retroperitoneal and mesenteric lymph nodes. Additional significant findings seen at autopsy were noted in the small bowel (Images 7 and 8); similar changes were seen in the spleen. The colon was also markedly abnormal, and the changes may be seen in Images 9 and 10. Sections of the lungs revealed occasional residual accumulations of frothy eosinophilic intra-alveolar exudate and numerous inclusion-bearing cells similar to those present in the colon. Cytomegalovirus retinitis was seen.

Copyright © 1999 by W. B. Saunders Company
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Produced in the United States of America
ISBN: 0-7216-8462-9