Patients with human immunodeficiency virus (HIV) are at risk for a number of pulmonary infections. Pneumocystis jirovecii (formerly Pneumocystis carinii) remains the most common opportunistic infection in this group, while the incidence of mycobacterial infections has decreased significantly. [6]

HIV causes dysfunction of cell-mediated and humoral immunity. CD4 T cells principally help other cells achieve their effector function. Low CD4 counts, which correlate with the degree of immunosuppression, cause a disruption of B-cell differentiation. Impaired B-cell functions, particularly memory cells, are correlated with increased risk of infection. [7]

Despite the advances in the development of highly active antiretroviral therapy (HAART), pulmonary disease remains an important cause of mortality and morbidity in persons with HIV/AIDS. [8, 9, 10]

Tuberculosis

HIV is considered to be the greatest risk factor for TB. [11] Patients with HIV are more likely not only to contract TB, but progress from latent to active TB. [12] In addition, they have a higher mortality risk from TB.

Chest radiograph in a patient with HIV infection and focal infiltrates due to tuberculosis. View Media Gallery

The clinical manifestations of TB in persons with HIV depend on the degree of immunosuppression. In severely immunocompromised individuals, the typical presentation of TB becomes less frequent. Instead of upper lobe cavitary disease, some of these patients present with lower lobe primary pneumonias, nonspecific patterns, or even no chest radiograph findings. [13]

Tuberculin skin test (TST) is more likely to be negative in persons with HIV. Typically, interferon-gamma release assays (IGRAs) are the gold standard for identification of TB-infected individuals; however, in HIV patients, the sensitivity of IGRAs is diminished. In studies, IGRAs perform similarly to the TST. Since both methods have a modest predictive value and suboptimal sensitivity, the choice of test should be based on country guidelines and resource considerations. [14]

Recent studies have shown that the timing of HAART and tuberculosis therapy is important in those concurrently infected. Withholding HAART until the third week of anti-tuberculosis therapy likely reduced TB mortality. [15]

Bacterial pneumonia

The most common bacterial causes of community-acquired pneumonia (CAP) in patients with HIV are the same as those in the general population [16] , the top three being Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus. [17, 18, 19]

However, the risks of contracting Streptococcus pneumonia are increased 10,000-fold in a patient with HIV. [20] Protease inhibitor (PI)­ containing ART regimens show great effect in lowering this risk. [21]

In a nosocomial setting, Pseudomonas aeruginosa, Staphylococcus aureus, Klebsiella pneumoniae, and Enterobacter species are common.

Fungal pneumonia

Fungal pneumonias are divided into opportunistic (i.e. PCP, Candida, Aspergillus, Mucor species) and endemic (Histoplasma capsulatum, Coccidioides immitis, Cryptococcus neoformans).

Opportunistic: Pneumocystis jirovecii pneumonia (PJP)

Pneumocystis jirovecii infection remains the most common opportunistic infection among patients with HIV.

It becomes a concern in individuals when CD4 count drops below 200, which is when prophylaxis with Trimethoprim-sulfamethoxazole (TMP-SMX) is recommended. When the A-a gradient is >35 or a room air arterial blood gas pO2< 70, adjuvant corticosteroids are recommended.

Transmission and infectivity of P. jirovecii is incompletely understood, in most cases attributed to reactivation of latently colonized patients. [22]

Opportunistic: Aspergillus

Invasive aspergillus pneumonia is one of the four aspergillosis syndromes that primarily affects immunosuppressed individuals.

In solid organ and hematopoietic transplant patients, there is a bimodal distribution of incidence with peaks during 1. prolonged neutropenia before engraftment and 2. in later stages with corticosteroid therapy in treatment of graft-versus-host disease.

Patients with leukemia and lymphoma have a higher incidence of invasive aspergillosis which is associated with a higher mortality rate. [23]

Invasive aspergillosis is also being increasingly observed in patients with severe COPD who remain on long-term corticosteroid therapy. [24]

There are no reliable biomarkers for detection of fungal cell wall constituents or other specific measures, thus, the recommendation continues to be close monitoring of clinical signs and symptoms for prevention and prophylaxis of opportunistic fungal pneumonias. [25]

Endemic: Cryptococcus neoformans

Cryptococcal pneumonia is more severe in patients with HIV. Patients with pulmonary disease frequently progress to disseminated disease.​ [26]

Most cases are the result of the reactivation of a latent infection.

Endemic: Histoplasma capsulatum

For the immunocompetent host, histoplasmosis is frequently asymptomatic or self-­limited. In the setting of HIV/AIDS, this infection is much more common and frequently progresses to disseminated disease.

This infection is endemic to certain areas of the United States, particularly in states bordering the Ohio River valley and the lower Mississippi River.

Spores of the mold phase are inhaled and cause a localized or patchy bronchopneumonia. CD4 lymphocytes normally activate macrophages to control the infection. [27]

Endemic: Coccidioides immitis

Coccidioides immitis is an organism endemic to large parts of the southwestern United States.

Spores are inhaled and then ingested by pulmonary macrophages. Impaired cell­-mediated immunity in persons with HIV accounts for an increased risk of infection in these patients. [28]

Viruses

Varicella ­zoster virus

Visceral dissemination of primary varicella, especially pneumonitis, has been reported in persons with HIV. [29]

Parasites

Strongyloides stercoralis

Strongyloides is an human intestinal nematode which can reproduce and persist in the body indefinitely, and affects millions of people worldwide. In immunocompromised individuals, this autoinfective cycle can be amplified into a hyperinfection syndrome. Increased parasite burden migrates rom the gastrointestinal tract, where it causes GI bleeding, into a systemic process. Filariform larvae have been found in the respiratory system, where they cause respiratory distress and sepsis secondary to pneumonia, and the neurological system causing meningitis.

Though the two conditions most often shown to trigger hyperinfection are glucocorticoid treatment and human T-lymphotropic virus type 1 infection, it is also associated with HIV/AIDS and hematologic malignancy. Anthelmintic agents such as ivermectin have been used successfully in both treatment as well as primary and secondary prevention in patients with risk factors. [30]

Chest radiograph demonstrating diffuse bilateral infiltrates in a patient with Pneumocystis carinii pneumonia. View Media Gallery

High-resolution computed tomography scan obtained through the upper lobes in the prone position in a patient with a history of Pneumocystis carinii pneumonia. This image shows parenchymal and subpleural cysts and patchy fibrosis that resulted from the Pneumocystis carinii infection. View Media Gallery