DOI: 10.1183/09031936.00200210
CopyrightERS 2012
REVIEW
ABSTRACT: From the first descriptions of HIV/AIDS, the lung has been the site most frequently
affected by the disease. Most patients develop a pulmonary complication during the history of HIV
infection, mainly of infectious aetiology.
Important changes in the epidemiology of HIV-related pulmonary infections have occurred.
Overall, prescription of Pneumocystis jirovecii prophylaxis and the introduction of highly active
antiretroviral therapy (HAART) are the main causes.
Currently, the most frequent diagnosis in developed countries is bacterial pneumonia,
especially pneumococcal pneumonia, the second most frequent cause is Pneumocystis
pneumonia and the third is tuberculosis. However, in Africa, tuberculosis could be the most
common pulmonary complication of HIV.
Pulmonary infections remain one of the most important causes of morbidity and mortality in these
patients, and the first cause of hospital admission in the HAART era. Achieving an aetiological
diagnosis of pulmonary infection in these patients is important due to its prognostic consequences.
KEYWORDS: AIDS, bacterial pneumonia, HIV, Pneumocystis pneumonia, pulmonary infections,
tuberculosis
VOLUME 39 NUMBER 3
AFFILIATIONS
*Infectious Diseases Unit, Internal
Medicine Service, Hospital de la
Santa Creu i Sant Pau, Universitat
Autonoma de Barcelona,
#
Infectious Diseases Service,
"
Pneumology Service, Hospital
Clnic-IDIBAPS, Universitat de
Barcelona, and
+
CIBERES, Barcelona, Spain.
CORRESPONDENCE
N. Benito
Infectious Diseases Unit, Internal
Medicine Service
Hospital de la Santa Creu i Sant Pau
Sant Antoni Maria Claret
167
Barcelona 08025
Spain
E-mail: nbenito@santpau.cat
Received:
Dec 28 2010
Accepted after revision:
Aug 15 2011
First published online:
Sept 01 2011
N. BENITO ET AL.
TABLE 1
Aetiology#
Cumulate incidence
Infectious aetiology
Bacterial pneumonia"
with diagnosis
of infectious aetiology
Streptococcus pneumoniae
Haemophilus influenzae
Staphylococcus aureus
9% of bacterial pneumonia
Legionella pneumophila
6% of bacterial pneumonia
Gram-negative bacillus
5% of bacterial pneumonia
PCP
Mycobacteriosis
of infectious aetiology
of infectious aetiology
Mycobacterium tuberculosis
80% of mycobacteriosis
20% of mycobacteriosis
Mycobacterium fortuitum
and Mycobacterium xenopi
Virus
5% of pulmonary infiltrates
of infectious aetiology
Cytomegalovirus
Influenza virus
Parainfluenza virus
Respiratory syncytial virus
Fungus
2% of pulmonary infiltrates
of infectious aetiology
Cryptococcus
Aspergillus fumigatus
Endemic fungal infections
Parasite
Toxoplasma gondii
Strongyloides stercoralis
Multiple organisms
7% of pulmonary infiltrates
Other+
3% of pulmonary infiltrates
Noninfectious aetiology
3% of pulmonary infiltrates
of infectious aetiology
of infectious aetiology
with diagnosis
Pulmonary oedema
Lung cancer
Other
PCP: Pneumocystis pneumonia; MAC: Mycobacterium avium complex. #: incidence
of different aetiologies can vary in different geographical areas; ": percentage of
each microorganism causing bacterial pneumonia is estimated among cases of
bacterial pneumonia with identification of aetiology;
: bronchiectasis and
pulmonary abscess. Data are based on results from [10, 11, 24].
VOLUME 39 NUMBER 3
Bacterial pneumonia
Currently, bacterial pneumonia is the most frequent infection in
HIV-infected patients, as well as the most common admission
731
VOLUME 39 NUMBER 3
N. BENITO ET AL.
N. BENITO ET AL.
Early studies in the USA showed PCP as the most frequent cause
of pulmonary infections (accounting for 85% of cases) and the
first cause of hospital admission in HIV patients [7, 63]. It was
estimated that 75% of these patients would develop PCP during
their lifetime [64]. The rate of PCP greatly decreased in developed
VOLUME 39 NUMBER 3
733
VOLUME 39 NUMBER 3
N. BENITO ET AL.
N. BENITO ET AL.
reverse transcriptase inhibitors (NNRTIs) leading to sub-therapeutic levels of these antiretroviral drugs. Rifampin should not be
used in patients on PI-based regimens; although rifampin lowers
levels of both the NNRTIs (efavirenz and nevirapine), the former
is less affected. Rifabutin is an alternative to rifampin that can be
administered with PIs or NNRTIs with appropriate dose
adjustments. Recent studies suggest that rifampin plays a key
role in the treatment of HIV-associated TB: recurrence rates are
two to four times higher when rifampin is not included in the
continuation phase (after the first 2 months of therapy) [85, 100].
Rifampin-based TB treatment with efavirenz-based ART is
probably the preferred treatment approach for HIV-associated
TB [101]. Regarding the optimal timing of starting ART in these
patients, several clinical trials have demonstrated the clinical
benefit of initiating ART during TB therapy, rather than at later
time intervals [102105]. Early HAART (initiated during the first
2 weeks) reduced the HIV disease progression and death among
HIV-infected HAART-nave patients with TB and a CD4 cell
count of ,50 cells per mm3. In patients with CD4+ T-cells
.50 cells per mm3, HAART can be started within 8 weeks after
the start of TB treatment. HAART should never be delayed until
after the completion of the TB therapy, at least for patients with
CD4 T-cells counts f500 cells per mm3 [102]. The risk of immune
reconstitution inflammatory syndrome (IRIS) was higher among
patients who started ART at earlier time-points, but there were no
deaths related specifically to IRIS. A clinical trial showed that
treatment with prednisone for 1 month reduced the incidence of
IRIS in patients with pulmonary TB who started HAART at the
same time as TB treatment [106]. World Health Organization
(WHO) guidelines recommend that, irrespective of CD4 cell
counts, patients co-infected with HIV and TB should be started on
antiretroviral therapy as soon as TB therapy is tolerated [107].
More detailed information on the treatment of TB in HIV patients
and management of drug interactions can be reviewed in the most
recent guidelines of CDC/IDSA [50, 108].
In developed settings, all persons should be tested for latent TB
infection at the time of HIV diagnosis, and they should be treated
if they have a positive diagnostic test for latent TB infection, no
evidence of active TBs and no prior history of treatment for active
or latent TB [50]. The tuberculin skin test has been the usual
method to determine latent TB infection. Recently, the development of interferon (IFN)-c release assays has been an important
advance in the diagnosis of latent TB infection. However,
sensitivity of INF-c release assays could be diminished by HIV
infection [109, 110]; lower CD4 counts have been associated with
higher rates of indeterminate results of these assays [109]. Recent
WHO guidelines for prevention of TB in HIV-infected patients in
resource limited settings recommend that persons living with HIV
should be screened for TB with a clinical algorithm; those patients
who do not report any of the symptoms of current cough, fever,
weight loss or night sweats are unlikely to have active TB and
should be offered treatment of latent infection [111]. Performing a
tuberculin skin test would not be a requirement for initiating
treatment of latent infection [111]. Treatment options for latent TB
infection include isoniazid daily or twice weekly for 9 months. A
recently published clinical trial shows that a 12-week course of
isoniazid plus rifamycin may be an effective alternative [112].
VOLUME 39 NUMBER 3
735
VOLUME 39 NUMBER 3
N. BENITO ET AL.
.80% of cases, and tracheobronchial disease. The chest radiograph might demonstrate a diffuse, focal or cavitary infiltrate in
patients with invasive pneumonia; the halo and the air
crescent sign on computed tomography of the lung are
suggestive of invasive disease. Several forms of tracheobronchitis
have been described: obstructive bronchial aspergillosis, ulcerative tracheobronchitis and pseudomembranous tracheobronchitis. The chest radiograph may be normal or may reveal areas of
atelectasis or parenchymal infiltration [120]. The diagnosis of
definite invasive aspergillosis requires the detection of Aspergillus
in cultures and histological evidence of tissue invasion.
Aspergillus is ubiquitous, and its presence in nasopharyngeal
secretions, sputum and BAL fluid may represent contamination
or colonisation. Newer tests based on circulating fungal antigen
(mainly the serum galactomannan antigen) have been employed
to diagnose aspergillosis, but they have not been formally
evaluated in patients with HIV infection. Treatment of aspergillosis in the HIV-infected population has not been examined
systematically but, currently, voriconazole is considered the drug
of choice for the treatment of invasive aspergillosis [123]. Lipid
formulations of amphotericin B, echinocandins and posaconazol
are alternatives. The length of therapy is not established but
should continue at least until the CD4 count is .200 cells per
mm3 and there is evidence of clinical response [50]. No data are
available to establish a recommendation of therapy among
patients who have successfully completed an initial course of
treatment [50].
Viral infections
Respiratory viruses might contribute to pulmonary complications
in HIV-infected patients, although information on the causes, risk
factors and outcomes of respiratory viral infection in these
patients is very scarce [124126]. Moreover, the respective role of
each agent could vary according to the population and the season
studied [124, 127, 128]. Influenza is a common cause of
respiratory illness in adults with HIV, although HAART seems
to have reduced the number of patients treated for influenza in
hospital [124, 129]. People with HIV are usually considered to be
at increased risk from serious influenza-related complications,
mostly based on studies carried out in the pre-HAART era [130].
However, recent studies have shown that HIV patients with
pandemic influenza virus A/H1N1 infection who are well
controlled on HAART had a similar clinical outcome to that of
non-HIV patients [131, 132]. Annual influenza vaccination for
adults infected with HIV is recommended by the CDC and the
IDSA, although this recommendation has not received universal
support [50]. The only clinical trial showed a 20% absolute
reduction in the risk of respiratory symptoms and 100%
protection against laboratory-confirmed symptomatic influenza
among HIV-infected patients receiving the influenza vaccine
compared with those receiving placebo [133]. Two systematic
reviews concluded that influenza vaccination of adults infected
with HIV might be effective despite variable antibody responses
[134, 135]. However, more information is needed to confirm how
effective and safe vaccination is in these patients, particularly
among those with very low CD4 counts [129]. Recently, the role of
human metapneumovirus infection in adults with HIV infection
has been described [126].
The clinical significance of cytomegalovirus (CMV) as a
pulmonary pathogen in HIV-infected patients is often unclear.
EUROPEAN RESPIRATORY JOURNAL
N. BENITO ET AL.
737
Imaging studies
Plain chest radiography is an appropriate initial imaging study
for a HIV-infected patient with suspected pulmonary infection.
Any new abnormalities, including pulmonary infiltrates, pleural
effusions and/or intrathoracic adenopathy, should be pursued
for a definite diagnosis. Certain radiographic patterns as well as
time of appearance and rate of progression can assist in the initial
diagnosis (table 2, fig. 1) [141].
Chest computed tomography scans have become an important
part of the diagnostic evaluation of HIV patients suspected to
have pulmonary infections as they are more sensitive than plain
chest radiographs in the detection of early interstitial lung
disease, lymphadenopathy and nodules.
Specific diagnostic tests
The high overall yield of the microbiological analysis of
spontaneously expectorated sputum sample (.50%) in HIVinfected patients with pulmonary infiltrates is worth mentioning
[14]. In the case of bacterial pneumonia, the yield of sputum
culture ranges from 35% to 60% [14, 142]. Additionally, its
availability and ease of performance highlight the usefulness of
this technique [142]. Moreover, the need for performing
systematic sputum cultures for mycobacteria in these patients
should be considered.
Induced sputum is not superior to a good expectorated sample
for diagnosing pulmonary TB, but it is helpful in patients who are
suspected of having TB and are unable to produce sputum [143,
144]. Induced sputum, if positive, is diagnostic for PCP. The value
of sputum induction in the setting of other pulmonary infections
is unknown.
TABLE 2
N. BENITO ET AL.
Chronic onset
Mycobacteriosis
Legionellosis
Nocardiosis
Fungi (aspergillosis, endemic fungal infections, cryptococcosis)
Pneumocystis jirovecii
Mycobacteriosis
(influenza, CMV)
Toxoplasmosis
Tuberculosis
Nocardiosis
Fungi
CMV
Nodules
Bacteria
Adenopathy
Tuberculosis
Mycobacteriosis
Endemic fungal infections
Cavitary infiltrate
Tuberculosis
Mycobacteriosis
Nocardiosis
Fungi
Fungi
Anaerobes
Rhodococcus equi
Pseudomonas aeruginosa
Legionellosis
Pleural effusion
Pyogenic bacteria
Fungi
Fungi
Nocardiosis
Tuberculosis
Pneumothorax
Pneumocystis jirovecii
CT: computed tomography; CMV: cytomegalovirus; IDU: intravenous drug users. Patients with acute, subacute or chronic onset have ,1 week, 14 weeks or .4 weeks
of symptoms, respectively.
738
VOLUME 39 NUMBER 3
N. BENITO ET AL.
Diagnosis and/or
clinical or radiological
improvement with
initial treatment
No diagnosis and no
improvement after
initial treatment
Complete treatment
FIGURE 1.
No diagnosis and no
improvement with empirical
treatment
Specific treatment
Aetiological diagnosis
Diagnostic algorithm of pulmonary infiltrates in HIV-infected patients. MV: mechanical ventilation. #: in patients with a known or suspected CD4 cell count
,200 cells per mm3, serum cryptococcal antigen, and blood and urine cultures for Mycobacterium can be useful; ": the determination of the adenosine deaminase can be
useful for the diagnosis of pleural tuberculosis.
Diagnostic algorithm
A possible diagnostic algorithm for HIV-infected patients with
pulmonary infiltrates is shown in figure 1. However, more
studies are needed in order to establish the best diagnostic
algorithm for these patients, which should take into account
geographic differences in epidemiology.
VOLUME 39 NUMBER 3
739
VOLUME 39 NUMBER 3
N. BENITO ET AL.
STATEMENT OF INTEREST
None declared.
REFERENCES
1 Centers for Disease Control and Prevention (CDC). Pneumocystis
pneumonia Los Angeles. MMWR Morb Mortal Wkly Rep 1981;
30: 250252.
2 Global report: UNAIDS report on the global AIDS epidemic 2010.
www.unaids.org/globalreport/documents/20101123_GlobalReport
_full_en.pdf Date last accessed: July 7, 2011.
EUROPEAN RESPIRATORY JOURNAL
N. BENITO ET AL.
3 Grubb JR, Moorman AC, Baker RK, et al. The changing spectrum
of pulmonary disease in patients with HIV infection on
antiretroviral therapy. AIDS 2006; 20: 10951107.
4 Torres RA, Barr M. Impact of combination therapy for HIV
infection on inpatient census. N Engl J Med 1997; 33: 15311532.
5 Sobrino-Vegas P, Garca-San Miguel L, Caro-Murillo AM, et al.
Delayed diagnosis of HIV infection in a multicenter cohort:
prevalence, risk factors, response to HAART and impact on
mortality. Curr HIV Res 2009; 7: 224230.
6 Mugavero MJ. Improving engagement in HIV care: what can we
do? Top HIV Med 2008; 16: 156161.
7 Afessa B, Greaves W, Gren W, et al. Autopsy findings in HIVinfected inner city patients. J Acquir Immune Defic Syndr 1992; 5:
132136.
8 Masliah E, DeTeresa RM, Mallory ME, et al. Changes in
pathological findings at autopsy in AIDS cases for the last 15
years. AIDS 2000; 14: 6974.
9 Murray JF, Garay SM, Hopewell PC, et al. NHLBI workshop
summary. Pulmonary complications of the acquired immunodeficiency syndrome: an update. Report of the second National
Heart, Lung, and Blood Institute workshop. Am Rev Respir Dis
1987; 135: 504509.
10 Meduri GU, Stein DS. Pulmonary manifestations of acquired
immunodeficiency syndrome. Clin Infect Dis 1992; 14: 98113.
11 Miller R. HIV-associated respiratory diseases. Lancet 1996; 348:
307312.
12 Feikin DR, Feldman C, Schuchat A, et al. Global strategies to
prevent bacterial pneumonia in adults with HIV disease. Lancet
Infect Dis 2004; 4: 445455.
13 Lazarous DG, ODonnell AE. Pulmonary infections in the HIVinfected patient in the era of highly active antiretroviral therapy:
an update. Curr Infect Dis Rep 2007; 9: 228232.
14 Benito N, Rano A, Moreno A, et al. Pulmonary infiltrates in HIVinfected patients in the highly active antiretroviral therapy in
Spain. J Acquir Immune Defic Syndr 2001; 27: 3543.
15 Benito N, Moreno A, Filella X, et al. Inflammatory responses in
blood samples of human immunodeficiency virus infected
patients with pulmonary infections. Clin Diagn Lab Immunol
2004; 11: 608614.
16 Whalen C, Horsburgh CR, Hom D, et al. Accelerated course of
human immunodeficiency virus infection after tuberculosis. Am
J Respir Crit Care Med 1995; 151: 129135.
17 Osmond DH, Chin DP, Glassroth J, et al. Impact of bacterial
pneumonia and Pneumocystis carinii pneumonia on human
immunodeficiency virus disease progression. Clin Infect Dis
1999; 29: 536543.
18 Morris AM, Huang L, Bacchetti P, et al. Permanent declines in
pulmonary function following pneumonia in human immunodeficiency virus-infected persons. The Pulmonary Complications
of HIV Infection Study Group. Am J Respir Crit Care Med 2000;
162: 612616.
19 Kohli R, Lo Y, Homel P, et al. Bacterial pneumonia, HIV therapy,
and disease progression among HIV-infected women in the HIV
epidemiologic research (HER) study. Clin Infect Dis 2006; 43: 9098.
20 Del Amo J, Perez-Hoyos S, Hernandez Aguado I, et al. Impact of
tuberculosis on HIV disease progression in persons with welldocumented time of HIV seroconversion. J Acquir Immune Defic
Syndr 2003; 33: 184190.
21 Wallace JM, Hansen NI, Lavange L, et al. Respiratory disease
trends in the pulmonary complications of HIV infection study
cohort. Am J Respir Crit Care Med 1997; 155: 7280.
22 Wolff AJ, ODonnell AE. Pulmonary manifestations of HIV
infection in the era of highly active antiretroviral therapy. Chest
2001; 120: 18881893.
23 Murray F. Pulmonary complications of HIV-1 infection among
adults living in Sub-Saharan Africa. Int J Tuberc Lung Dis 2005; 9:
826835.
EUROPEAN RESPIRATORY JOURNAL
741
VOLUME 39 NUMBER 3
N. BENITO ET AL.
N. BENITO ET AL.
82
83
84
85
86
87
88
89
90
91
92
93
94
95
96
97
98
99
combined antiretroviral therapy era: prevalence of dihydropteroate synthase mutations and prognostic factors of mortality.
Diagn Microbiol Infect Dis 2008; 62: 3443.
Alvarez-Martnez MJ, Miro JM, Valls ME, et al. Prevalence of
dihydropteroate synthase genotypes before and after the
introduction of combined antiretroviral therapy and their
influence on the outcome of Pneumocystis pneumonia in HIV-1infected patients. Diagn Microbiol Infect Dis 2010; 68: 6065.
Lopez Bernaldo de Quiros JC, Miro JM, et al. A randomized trial
of the discontinuation of primary and secondary prophylaxis
against Pneumocystis carinii pneumonia after highly active
antiretroviral therapy in patients with HIV infection. N Engl J
Med 2001; 344: 159167.
Opportunistic Infections Project Team of the Collaboration of
Observational HIV Epidemiological Research in Europe
(COHERE), Mocroft A, Reiss P, et al. Is it safe to discontinue
primary Pneumocystis jiroveci pneumonia prophylaxis in patients
with virologically suppressed HIV infection and a CD4 cell count
,200 cells/mL? Clin Infect Dis 2010; 51: 611619.
Swaminathan S, Padmapriyadarsini C, Narendran G. HIVassociated tuberculosis: clinical update. Clin Infect Dis 2010; 50:
13771386.
Treatment and care: unprecedented progress, remaining challenges. Chapter 5. http://data.unaids.org/pub/GlobalReport/
2008/jc1510_2008_global_report_pp129_158_en.pdf Date last
accessed: July 7, 2011.
Sonnenberg P, Glynn JR, Fielding K, et al. How soon after
infection with HIV does the risk of tuberculosis start to increase?
A retrospective cohort study in South African gold miners.
J Infect Dis 2005; 191: 150.
DeRiemer K, Kawamura LM, Hopewell PC, et al. Quantitative
impact of human immunodeficiency virus infection on tuberculosis dynamics. Am J Respir Crit Care Med 2007; 176: 936944.
Lawn SD, Bekker LG, Wood R. How effectively does HAART
restore immune responses to Mycobacterium tuberculosis?
Implications for tuberculosis control. AIDS 2005; 19: 11131124.
Girardi E, Sabin CA, dArminio Monforte A, et al. Incidence of
tuberculosis among HIV-infected patients receiving highly active
antiretroviral therapy in Europe and North America. Clin Infect
Dis 2005; 41: 1772.
Lawn SD, Badri M, Wood R. Tuberculosis among HIV-infected
patients receiving HAART: long term incidence and risk factors
in a South African cohort. AIDS 2005; 19: 21092116.
Havlir DV, Getahun H, Sann I, et al. Opportunities and
challenges for HIV care in overlapping HIV and TB epidemics.
JAMA 2008; 300: 423430.
Lawn SD, Myer L, Edwards D, et al. Short-term and long-term
risk of tuberculosis associated with CD4 cell recovery during
antiretroviral therapy in South Africa. AIDS 2009; 23: 17171725.
Chaisson RE, Martinson NA. Tuberculosis in Africa combating
an HIV-driven crisis. N Engl J Med 2008; 358: 10891092.
Prendergast A, Tudor-Williams G, Jeena P, et al. International
perspectives, progress, and future challenges of paediatric HIV
infection. Lancet 2007; 370: 6880.
Markowitz N, Hansen N, Hopewell PC, et al. Incidence of
tuberculosis in the United States among HIV-infected persons.
Ann Intern Med 1997; 126: 123132.
Kirk O, Gatell JM, Mocroft A, et al. Infections with Mycobacterium
tuberculosis and Mycobacterium avium among HIV-patients after
the introduction of highly active antiretroviral therapy. Am J
Respir Crit Care Med 2000; 162: 865872.
Nahid P, Pai M, Hopewell PC. Advances in the diagnosis and
treatment of tuberculosis. Proc Am Thorac Soc 2006; 3: 103110.
Boehme CC, Nabeta P, Hillemann D, et al. Rapid molecular
detection of tuberculosis and rifampin resistence. N Engl J Med
2010; 363: 10051015.
743
VOLUME 39 NUMBER 3
N. BENITO ET AL.
N. BENITO ET AL.
155 Powell K, Davis JL, Morris AM, et al. Survival for patients with
HIV admitted to the ICU continues to improve in the current era
of combination antiretroviral therapy. Chest 2009; 135: 1117.
156 Alves C, Nicolas JM, Miro JM, et al. Reappraisal of the aetiology
and prognostic factors of severe acute respiratory failure in HIV
patients. Eur Respir J 2001; 17: 8793.
157 Barbier F, Coquet I, Legriel S, et al. Etiologies and outcome of
acute respiratory failure in HIV-infected patients. Intensive Care
Med 2009; 35: 16781686.
158 Dickson SJ, Batson S, Copas AJ, et al. Survival of HIV infected
patients in the intensive care unit in the era of highly active
antiretroviral therapy. Thorax 2007; 62: 964968.
159 Olaechea PM, Alvarez-Lerma F, Sanchez M, et al. Evaluation of the
status of patients with severe infection, criteria for intensive care
unit admittance. Spanish Society for Infectious Diseases and
Clinical Microbiology. Spanish Society of Intensive and Critical
Medicine and Coronary Units. Enferm Infecc Microbiol Clin 2009; 27:
342352.
160 Masur H. Caring for AIDS patients in the ICU: expanding
horizons. Chest 2009; 135: 12.
161 Walzer PD, Evans HE, Copas AJ. Early predictors of mortality
from Pneumocystis jirovecii pneumonia in HIV-infected patients:
1985-2006. Clin Infect Dis 2008; 46: 625633.
162 Safrin S, Finkelstein DM, Feinberg J, et al. Comparison of three
regimens for treatment of mild to moderate Pneumocystis carinii
pneumonia in patients with AIDS. A double-blind, randomized,
163
164
165
166
167
168
trial of oral trimethoprim-sulfamethoxazole, dapsone-trimethoprim, and clindamycin-primaquine. ACTG 108 Study Group.
Ann Intern Med 1996; 124: 792802.
Gagnon S, Boota AM, Fischl MA, et al. Corticosteroids as
adjunctive therapy for severe Pneumocystis carinii pneumonia
in the acquired immunodeficiency syndrome. A doubleblind, placebo-controlled trial. N Engl J Med 1990; 323:
14441450.
Fei MW, Kim EJ, Sant CA, et al. Predicting mortality from HIVassociated Pneumocystis pneumonia at illness presentation: an
observational cohort study. Thorax 2009; 64: 10701076.
Tumbarello M, Tacconelli E, de Gaetano K, et al. Bacterial
pneumonia in HIV-infected patients. Analysis of risk factors
and prognosis indicators. J Acquir Immune Defic Syndr 1998; 16:
3945.
Cordero E, Pachon J, Rivero A, et al. Community-acquired
bacterial pneumonia in human immunodeficiency virus-infected
patients: validation of severity criteria. Am J Respir Crit Care Med
2000; 162: 20632068.
Christensen D, Feldman C, Rossi P, et al. HIV infection does not
influence clinical outcomes in hospitalized patients with
bacterial community-acquired pneumonia: results from the
CAPO international cohort study. Clin Infect Dis 2005; 4: 554556.
Feldman C, Klugman KP, Yu VL, et al. Bacteraemic pneumococcal pneumonia: impact of HIV on clinical presentation and
outcome. J Infect 2007; 55: 125135.
VOLUME 39 NUMBER 3
745