VS: Pulse 104, regular Respirations 24 BP 110/70 Temperature 37.8, oral
Skin: No lesions noted
Lymph: Small mobile nodes in the anterior cervical chain; small bilateral axillary nodes, nontender and freely mobile
HEENT: Eye grounds clear without exudates or hemorrhages; no oral lesions noted
Neck: Supple; adenopathy as noted
Lungs: Scattered crackles at the bases; no wheezes, rhonchi or consolidation
Cor: Tachycardia without murmurs, rubs or gallops
Abd: Normal bowel sounds; flat; nontender; no hepatosplenomegaly
Ext: No cyanosis, clubbing or edema
Neuro: Normal mental status; cranial nerves II-XII intact; normal strength, reflexes, sensation, and cerebellar exam
Labs: WBC: 10.5 x 103/mm3; no left shift
CXR: Diffuse pulmonary infiltrates
ABG on room air:
Because of concern that the patient was immunocompromised with a pneumonia, he underwent bronchalveolar lavage (BAL). Silver stain demonstrated Pneumocystis carinii organisms:
In patients who have HIV, the most common cause for chest disease is actually the encapsulated organisms, such as Strep. pneumoniae and Hemophilus influenza. The most frequent opportunistic infection in these patients is Pneumocystis carinii. Other important pulmonary infections include mycobacterial disease (typical and atypical), viral infections (e.g., cytomegalovirus), and fungal infections such as Histoplasmosis.
Most patients with AIDS will develop infection with Pneumocystis unless they receive prophylaxis. P. carinii is exclusively a pulmonary pathogen, with no known environmental reservoir. There are rare reports of dissemination. The infection tends to be intra-alveolar, with the development of a frothy proteinaceous exudate without a significant inflammatory component. A monocytic infiltrate develops in the lung interstitium. It appears that P. carinii pneumonia (PCP) results from reactivation of a latent infection as the immune system function declines. The infection appears to result primarily from a cell mediated defect. The infection does not occur in immunocompetent patients. The majority of infections in HIV infected individuals occur when the CD4 count is <100/mm3. Patients will frequently present with fever, nonproductive cough and dyspnea. Pleurisy is unusual. The illness usually progresses gradually, and patients will often present after an extended illness. However, some patients present with a fulminant clinical course that rapidly progresses to respiratory failure.
The physical exam may be normal or the lung exam may reveal fine rales or wheezes. The CXR can be normal in up to 10 percent of patients. The remaining 90 percent most often have:
Less commonly, patients can present with pneumothorax. Even with a normal CXR, hypoxemia with an increased A-a gradient is very common.
Once obtained, the sample is stained with Gomori's methenamine silver stain. The cyst form takes up the stain, and the organism is identified as black rings. P. carinii organisms are of varying sizes, often with indentations leading to the designation of a "helmet shape". The organism is differentiated from Histoplasma capsulatum by its larger size. Cytology preparation of the lavage may also show the amorphous pink material from the alveoli with the appearance of negative images where the organisms are located.
Because the immune defect does not resolve, those patients who survive PCP require suppressive therapy once the acute course of treatment is completed. In patients with HIV who develop respiratory compromise with hypoxemia secondary to P. carinii infection, the use of corticosteroids early in the course increases survival and improves exercise tolerance. It is not entirely known how steroids benefit patients, although it is thought that the anti-inflammatory effects of steroids play a role in improving lung function.
Once the CD4 counts fall below 200/mm3 or after treatment of a primary infection, prophylactic therapy with aerosolized pentamidine is started. Pentamidine is used rather than sulfonamides because of the high incidence of adverse effects to oral Bactrim. These patients can be treated with weekly to monthly pentamidine to prevent the development of PCP.
This review provides an excellent overview of the wide range of pulmonary infections which can occur in this patient population. It also provides a handy reference for therapeutic approaches to the various infections. It does not contain an update of the newer drugs being used for prophylaxis of the infection itself.
2. Masur, H. 1992. Prevention and treatment of pneumocystis pneumonia. N. Engl. J. Med. 327:1853-1860.
A good review of the current therapeutic approaches for both prophylaxis and treatment with a broader discussion of other drug options than in the case history.
3. Zaman, M.K., O.J. Wooton, B. Suprahmanya, W. Ankobiah, P.J.P. Finch, and S.L. Kamholz. 1988. Rapid noninvasive diagnosis of Pneumocystis carinii from induced liquefied sputum. Ann. Int. Med 109:7-10.
Gives a nice perspective for the use of induced sputum in the diagnosis of pneumocystis. Also describes the induced sputum technique.
4. Kovacs, J.A. et. al. 1984. Pneumocystis carinii pneumonia: a comparison between patients with the acquired immunodeficiency syndrome and patients with other immunodeficiencies. Ann. Int. Med. 100:663-671.
Provides some insight into the salient differences in presentation and outcome of different patient population. An early study which continues to have clinical relevance.
5. Mottin, D., M. Denis, and H. Dombret, et al. Role for steroids in treatment of Pneumocystis carinii pneumonia in AIDS. Lancet 2:519, 1987.
Prospective study using steroids in AIDS patients with respiratory failure from PCP.
Listing of Media for Lung Disease in Patients with AIDS
Test for Lung Disease in Patients with AIDS
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