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Pneumonia
in the immunocompromised host is often caused by unusual pathogens.
Symptoms and signs depend on the pathogen. Diagnosis is based on
blood cultures and bronchoscopic sampling of respiratory secretions,
sometimes with quantitative cultures. Treatment depends on the host
defect and pathogen.
The potential pathogens in patients with compromised defenses are legion. Likely pathogens based on the type of defect in host defenses are listed in
Table 7: Pneumonia: Pneumonia in the Immunocompromised Host . However, respiratory symptoms and changes on chest x-rays in immunocompromised hosts may be due to a variety of processes other than infection, such as pulmonary hemorrhage, pulmonary edema, radiation injury, pulmonary toxicity due to cytotoxic drugs, and tumor infiltrates.
Symptoms,
Signs, and Diagnosis
Symptoms and signs may be the same as those found with community-acquired pneumonia or hospital-acquired pneumonia in immunocompetent patients, though immunocompromised patients may have no fever or respiratory signs and are less likely to have purulent sputum if they are neutropenic. In some patients, the only sign is fever.
An immunocompromised patient with respiratory symptoms, signs, or fever should undergo chest x-ray. If an infiltrate is present, diagnostic studies should include sputum Gram stain and culture and blood cultures. Optimally, firm diagnosis is made with induced sputum and/or bronchoscopy, especially in patients with chronic pneumonia, atypical presentation, severe defects in immune function, and failure to respond to broad-spectrum antibiotics.
Likely pathogens can often be predicted on the basis of symptoms, x-ray changes, and the type of immunodeficiency. In patients with acute symptoms, likely diagnoses are bacterial infection, hemorrhage, pulmonary edema, a leukocyte agglutinin reaction, and pulmonary emboli. A subacute or chronic presentation is more suggestive of a fungal or mycobacterial infection, an opportunis- tic viral infection, Pneumocystis
jiroveci (formerly P.
carinii) pneumonia, tumor, a cytotoxic drug reaction, or radiation injury.
X-rays showing localized consolidation usually indicate an infection involving bacteria, mycobacteria, fungi, or Nocardia sp. A diffuse interstitial pattern is more likely to represent a viral infection, P. jiroveci pneumonia, drug or radiation injury, or pulmonary edema. Diffuse nodular lesions suggest mycobacteria, Nocardia sp, fungi, or tumor. Cavitary disease suggests mycobacteria,
Nocardia sp, fungi, or bacteria.
In organ or marrow transplantation recipients with bilateral interstitial pneumonia, the usual cause is cytomegalovirus, or the disease is idiopathic. A pleural-based con-solidation is usually aspergillosis. In AIDS patients, bilateral pneumonia is usually P. jiroveci pneumonia. About 30% of patients with HIV infection have P.
jiroveci pneumonia as the initial AIDS-defining diagnosis, and > 80% of AIDS patients have this infection at some time if prophylaxis is not given (see Human Immunodeficiency Virus (HIV): Prevention of opportunistic infections). Patients with HIV infection become vulnerable to P.
jiroveci pneumonia when the CD4+ helper cell count is < 200/μL.
Treatment
In neutropenic patients, empiric treatment depends on the host defect, x-ray, and severity of illness. Generally, broad-spectrum drugs are needed to cover gram-negative bacilli, Staphylococcus aureus
, and anaerobes, as for hospital-acquired pneumonia (see Pneumonia: Treatment).
Pneumocystis
jiroveci
pneumonia
P. jiroveci (formerly P. carinii) is a common cause
of pneumonia in immunosuppressed patients, especially in those infected
with HIV. Symptoms include fever, dyspnea, and cough. Diagnosis
requires demonstration of the organism in a sputum specimen. Treatment
is with antibiotics, usually trimethoprim-sulfamethoxazole or pentamidine,
and corticosteroids for patients with Pao2 < 70 mm Hg. Prognosis is generally
good with timely treatment.
P.
jiroveci is a ubiquitous organism transmitted by aerosol route and causes no disease in immunocompetent patients. Patients with HIV infection and CD4+ counts < 200/μL, organ transplant recipients, those who have hematologic malignancies, and pa-tients taking corticosteroids are at risk of developing P. jiroveci pneumonia. Most have fever, dyspnea, and a dry, nonproductive cough that evolves subacutely over several weeks (HIV infection) or acutely over several days (other causes of compromised cell-mediated immunity). The chest x-ray characteristically shows diffuse, bilateral perihilar infiltrates, but 20 to 30% of patients have normal x-rays. ABGs show hypoxemia, with an increase in the alveolar-arterial O2 gradient, and pulmonary function tests show altered diffusing capacity (although this is rarely done as a diagnostic test). Diagnosis requires histopathologic demonstration of the organism with methenamine silver, Giemsa, Wright-Giemsa, modified Grocott, Weigert-Gram, or monoclonal antibody stain. Sputum specimens are usually obtained by induced sputum or bronchoscopy. Sensitivity ranges from 30 to 80% for induced sputum and is > 95% for bronchoscopy with bronchoalveolar lavage.
Treatment is with trimethoprim-sulfamethoxazole (TMP-SMX) 4 to 5 mg/kg IV or po tid for 14 to 21 days. Treatment can be started before diagnosis is confirmed because P. jiroveci cysts persist in the lungs for weeks. Adverse effects more common in patients with AIDS include skin rash, neutropenia, hepatitis, and fever. Alternative regimens are pentamidine 4 mg/kg IV once/day, atovaquone 750 mg po bid, TMP-SMX 5 mg/kg po qid with dapsone 100 mg po once/day, or clindamycin 300 to 900 mg IV q 6 to 8 h with primaquine base 15 to 30 mg/day po, also for 21 days. The major limitation of pentamidine is the high frequency of toxic adverse effects, including renal failure, hypotension, and hypoglycemia. Adjunctive therapy with corticosteroids is advocated for those with a Pao2 < 70 mm Hg. The suggested regimen is prednisone 40 mg bid (or its equivalent) for the first 5 days, 40 mg/day for the next 5 days (as a single dose or as 20 mg bid), and then 20 mg once/day for the duration of treatment.
HIV-infected patients who have had P. jiroveci pneumonia or who have a CD4+ count < 200/μL should receive prophylaxis with TMP-SMX 80/400 mg once/day; if this treatment is not tolerated, dapsone 100 mg po once/day or aerosolized pentamidine 300 mg once/month can be used. These prophylactic regimens are also probably indicated for non-HIV-infected patients at risk of P. jiroveci pneumonia.
Overall mortality for P. jiroveci pneumonia in hospitalized patients is 15 to 20%. Risk factors for death may include previous history of P. jiroveci pneumonia, older age, and, in HIV-infected patients, CD4+ cell count < 50/μL.
Last full review/revision November 2005
Content last modified November 2005
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