Since the early 1980s, many investigators have examined pulmonary complications in the HIV-infected population (1
). Special attention has been focused on infectious pulmonary diseases in this patient group, including PCP, tuberculosis and bacterial pneumonia. In December 1992, the CDC expanded their definition of AIDS to include recurrent bacterial pneumonia as an AIDS-defining illness (4
). This was promptly added to the Canadian definition (5
An etiological diagnosis of pneumonia is key to appropriate treatment. Multiple prospective studies have examined the etiologies of CAP and found that 43% to 56% of pneumonias were of unknown etiology (6
). In our retrospective study, 73% of the non-HIV-infected and 34% of the HIV-infected patients had no etiological diagnosis for their pneumonia.
Bacterial pulmonary infections appear to occur at an increasing frequency in HIV-infected individuals. The incidence varies from 3% to 31% in hospitalized patients, the higher incidence involving intravenous drug users (1
). Pneumococcus and Haemophilus influenzae
are the most common bacterial causes of CAP in HIV-infected patients (15
). Other common bacterial pathogens that cause pneumonia in this group include Staphylococcus aureus, Klebsiella pneumoniae, Rhodococcus equi, Moraxella catarrhalis
and Legionella pneumophila
). The incidence of pneumococcal pneumonia among HIV-infected persons has been reported to be up to 17.5 times the rate in the general population (19
). In our patients infected with HIV, only one was found to have S pneumoniae
infection. Although our total number of HIV-infected patients studied was small, it appears that pneumococcus is not as common a bacterial pathogen at our centre as in other geographical areas. It has been recommended that the 23-valent pneumococcal vaccine be administered to persons with HIV to prevent invasive pneumococcal disease (20
). The efficacy of the pneumococcal vaccine is unknown (19
). All HIV-infected persons seen at our centre are offered pneumococcal vaccine at their first visit. Whether vaccination resulted in the low rate of pneumococcal disease in our HIV-infected population is speculative.
Our data indicate that PCP remains the most common etiology of CAP in HIV-infected patients requiring hospital care for this illness. In the United States and in the United Kingdom, PCP remains an important illness in the HIV-infected patient (2
). In France and Edinburgh, however, the number of patients with PCP appears to be decreasing (3
). Caiaffa et al (14
) found that a low T helper cell count, low socioeconomic status and intravenous drug use were the most significant risk factors for bacterial CAP in HIV-infected patients. In a large population of HIV-infected intravenous drug users, bacterial pneumonia was the most common cause of CAP (3
). This was not the case in a population consisting mostly of homosexual males, in which PCP was the most common etiological diagnosis (21
). Similarly, our population consists mostly of homosexual males with only 11% intravenous drug users. It is noteworthy that both patients with P aeruginosa
pneumonia were intravenous drug users.
From 1982 to 1990, 4% (54 of 1350) of patients with CAP admitted to our institution were HIV-positive, and 61% (33 of 54) of these had a diagnosis of PCP. This compares with the current rate of 50% (16 of 32) for PCP among our HIV patients with pneumonia. A question that remains is whether the rate of PCP is decreasing as a result of increasing antiretroviral drug use and PCP prophylaxis. The rate of PCP in our hospitalized HIV-infected patients, despite prophylaxis, remains high. Our study may be biased by including only hospitalized patients with CAP and by our inability to assess compliance with PCP prophylaxis. Current regimens have failure rates of 4% to 18% and up to 9% for secondary and primary prophylaxis, respectively (23
). Failure rates for PCP prophylaxis are higher when T helper cell count falls below 75 to 100 cells/mm3 and are more frequently encountered with AP use than with TMP/SMX or dapsone/TMP (24
Clinical manifestations of pneumonia did not differ in our two populations. This comparison is limited by the nature of a retrospective study and information available in charts. The review of chest radiographs did show a difference between the two groups. The predominance of interstitial patterns in the HIV-infected patients can be explained by the etiology profiles with a large majority having a diagnosis of PCP.
The use of laboratory tests was essentially the same in both groups. HIV-infected patients had more chemistry tests done, which may be explained by our pentamidine protocol, which requires regular verification of blood glucose and renal function. Our HIV-infected population underwent a more intensive diagnostic work-up than the non-HIV infected group, including blood cultures and bronchoscopy. This is not surprising because empirical therapy has been advocated in the non-HIV-infected patient with CAP. Initial antimicrobial management guidelines for CAP have been established by the Canadian Community-Acquired Pneumonia Consensus Group (25
). No such guidelines exist for the HIV-infected patient with CAP, nor should there be such guidelines. The range of diagnoses in this population is vast, with the potential need for toxic and prolonged courses of therapy and possible lifelong prophylaxis. An etiological diagnosis should therefore be sought whenever possible (26
As expected in our population with moderately advanced disease, the HIV-infected group had a high in-hospital and postdis-charge mortality. Studies predicting death from CAP have identified factors that allow stratification of patients into various levels of risk for poor outcome. Farr et al (27
) concluded that tachypnea, diastolic hypotension and elevated blood urea nitrogen were independently associated with death from pneumonia. These factors have not been studied in HIV-infected patients with CAP. No significant differences were found in these parameters in our two patient groups, although a marked difference in survival was noted between the two groups.
A decrease in mortality from PCP in HIV-infected patients has been observed with the introduction of prophylaxis (see above), glucocorticoids as adjuvant therapy (23
) and more aggressive supportive treatment (26
). Survival rates for a first episode of PCP with early diagnosis and initiation of treatment are approximately 90%. These can fall precipitously to 10% if there is a lack of response to therapy necessitating a change in treatment regimen (26
). Although a low T helper cell count (less than 200 cells/mm3
) is an excellent predictor of the risk of developing PCP, hypoxemia appears to be the best prognostic factor of mortality in HIV-infected patients with PCP (28
). The consensus statement on the use of corticosteroid therapy for PCP issued in 1990 reviewed five randomized trials evaluating the use of corticosteroids as adjuvant therapy. It was found that when given early in the course of treatment (24 to 72 h), in patients with moderate to severe disease, corticosteroids could decrease failure of oxygenation, need for mechanical ventilation and death by approximately 50% (28
It has been more difficult to show that supportive therapy such as mechanical ventilation in the face of respiratory failure favourably affects survival in this population. Five per cent to 30% of first PCP episodes will lead to death from acute respiratory failure (ARF) (30
). Survival of PCP with mechanical ventilation as a treatment for ARF was felt to be less than 15% (31
). With improvement of supportive care, in-hospital survival of HIV-infected patients requiring mechanical ventilation for PCP and ARF is 25% to 50%. Long term survival rates one year post-discharge in patients with PCP and ARF requiring mechanical ventilation are as high as 80% (31
). Unfortunately, there are no good prognostic indicators to predict who will develop ARF or require mechanical ventilation. Brooks et al (26
) found high mortality rates in patients with multiple admissions, multiple pulmonary infections, leukocytosis, elevated serum lactate dehydrogenase, decreased PaO2, decreased CO2 tension and diminished serum albumin levels. The decision to admit to an intensive care unit and to use mechanical ventilation in patients with PCP, AIDS and ARF remains a complex one, which must involve the patient, the physician and up-to-date knowledge of data concerning the issue.
In-hospital mortality in our group of 32 HIV-infected patients was 25%, while from 1982 to 1990 the in-hospital mortality rate for HIV-infected patients with CAP was 17% (nine of 54, not significant). Although this difference in mortality is not significant, it may suggest that the patients admitted to hospital in the 1990s have more advanced disease.