Mortality In HIV-infected Patients Research Articles

Mortality of HIV-infected patients in the first year of antiretroviral therapy: comparison between low-income and high-income countries

Mortality of HIV-infected patients in the first year of antiretroviral therapy: comparison between low-income and high-income countries

Incidence of, Risk Factors for, Clinical Presentation, and 1-Year Outcomes of Infective Endocarditis in an Urban HIV Cohort

Previous studies described infective endocarditis (IE) in the era before highly active antiretroviral therapy (HAART); however, IE has not been well studied in the current HAART era. We evaluated the incidence of, risk factors for, clinical presentation, and 1-year outcomes of IE in HIV-infected patients. We evaluated all cases of IE diagnosed between 1990 and 2002 in patients followed at the Johns Hopkins Hospital outpatient HIV clinic. To identify factors associated with IE in the current era of HAART, a nested case-control analysis was employed for all initial episodes of IE occurring between 1996 and 2002. Logistic regression analyses were used to assess risk factors for IE and factors associated with 1-year mortality. IE incidence decreased from 20.5 to 6.6 per 1000 person-years (PY) between 1990 and 1995 and 1996 and 2002. The majority of IE cases were male (66%), African American (90%), and injection drug users (IDUs) (85%). In multivariate regression, an increased risk of IE occurred in IDUs (AOR, 8.71), those with CD4 counts <50 cells/mm, and those with HIV-1 RNA >100,000 copies/mL (AOR, 3.88). Common presenting symptoms included fever (62%), chills (31%), and shortness of breath (26%). The most common etiologic organism was Staphylococcus aureus (69%; of these 11 [28%] were methicillin resistant). Within 1 year, 16% had IE recurrence, and 52% died. Age over 40 years was associated with increased mortality. IE rates have decreased in the current HAART era. IDUs and those with advanced immunosuppression are more likely to develop IE. In addition, there is significant morbidity and 1-year mortality in HIV-infected patients with IE, indicating the need for more aggressive follow-up, especially in those over 40 years of age. Future studies investigating the utility of IE prophylaxis in HIV patients with a history of IE may be warranted.

Episodic HIV Treatment: Not a SMART Idea

Continuous antiretroviral therapy (ART) markedly reduces morbidity and mortality in HIV-infected patients, but it has potential adverse effects, is

Arzneimittelnebenwirkungen bei antiretroviraler Therapie

The introduction of highly active antiretroviral therapy (HAART) has resulted in tremendous improvements in morbidity and mortality in HIV-infected patients. However, the use of these drugs has coincided with an increasing number of reports of gastrointestinal, hepatic or metabolic side effects. Soon after beginning antiretroviral treatment drug rashes, hypersensitivity reactions, immune reconstitution syndrome or injection site reaction are frequently seen. Under HAART dyslipidemia, impaired glucose metabolism and elevated liver function are observed. In the later treatment phase, lipodystrophy, a combination of peripheral lipoatrophy and central fat accumulation, occurs.

Metabolic and Skeletal Complications of HIV Infection

Over the past 10 years, in conjunction with the broad availability of potent antiretroviral regimens, the care of human immunodeficiency virus (HIV)-infected patients has shifted from prevention and treatment of opportunistic infections and malignancies to management of the metabolic and related complications associated with HIV infection and its treatment. Metabolic disorders, including lipodystrophy, dyslipidemia, and insulin resistance, occur at a high rate in HIV-infected individuals receiving highly active antiretroviral therapy (HAART). These disorders are associated with increased risk of cardiovascular disease and have become an important cause of morbidity and mortality in HIV-infected patients. Herein, we present the case of a patient with HIV infection who responded well to HAART but developed multiple complications potentially related to this therapy. This article reviews the clinical characteristics of the metabolic and skeletal disturbances observed in HIV infection and discusses strategies for their management.

Liver‐related mortality in human‐immunodeficiency‐virus‐infected patients between 1995 and 2003 in the French GERMIVIC Joint Study Group Network (MORTAVIC 2003 Study)*

The objective of the present study was to determine mortality because of end-stage liver disease (ESLD) in a nationwide population of HIV-infected patients, 7 years following the introduction of highly active antiretroviral therapy (HAART). All departments of internal medicine and infectious diseases from the GERMIVIC Study Group prospectively recorded all deaths in HIV-infected patients during 2003. Fifty-nine departments, following a total of 20 940 HIV-infected patients, participated in the study. Results were compared with those of previous surveys conducted using similar methodology in 1995, 1997 and 2001. Among 215 deaths observed during 2003, 101 (46.9%) were related to AIDS, 27 (12.6%) to ESLD and 87 (40.5%) to other causes. Mortality because of ESLD represented 23.7% of non-AIDS-related deaths. Patients dying from ESLD had chronic hepatitis because of hepatitis C virus (HCV) in 92.6% of cases and moderate (30-60 g) or high (>60 g) alcohol consumption (43.5% and 26.0%, respectively). In this population, deaths because of ESLD were 1.5% in 1995, 6.6% in 1997, 14.3% in 2001 and 12.6% in 2003. The prevalence of hepatocellular carcinoma as a cause of death remained high in 2003 but stable when compared with 2001 (25%vs 14.8%). Treatment of hepatitis C in patients who died from ESLD was more frequent in 2003 (44.4%) than in 2001 (26.3%). Seven years after the introduction of HAART, ESLD associated with HCV infections is a leading cause of mortality in HIV-infected patients, which did not increase between the years 2001 and 2003.

Hepatopulmonary syndrome: an emerging complication in HIV-hepatitis C virus co-infected patients

Following the availability of highly active antiretroviral therapy (HAART), chronic liver disease now represents the major cause of morbidity and mortality for HIV-infected patients [1,2]. Among the wide spectrum of end-stage liver disease complications, hepatopulmonary syndrome (HPS) has not been described. We report a fatal case of HPS in a woman with HIV and Child–Pugh B cirrhosis due to hepatitis C virus (HCV). A 40-year-old psychotic woman, who had been followed up for a HIV/HCV co-infection over a period of 10 years, presented at our institution complaining of dyspnoea for 2 weeks. She had interrupted her antiretroviral therapy a year earlier. Her CD4 cell count was 22 cells/μl and her HIV-RNA viral load was 88 000 copies/ml. At presentation, with a temperature of 37°C and a respiratory rate of 25/min, she was cyanotic with clubbing of the fingers. She had hepatomegaly and stigmata of portal hypertension (spider angiomas, splenomegaly). Fine crackles could be heard over both lungs. Analysis (on room air) of arterial blood gases withdrawn while the patient was in a supine position showed hypoxemia (arterial partial pressure of oxygen (PaO2) was 50 mmHg and the arterial partial pressure of carbon dioxide (PaCO2) was 40 mmHg). The arterial blood gases worsened upon standing (PaO2, 42 mmHg; PaCO2, 39.3 mmHg) suggesting orthodeoxia. Blood testing showed the following values: haemoglobin, 12.6 g/dl and platelets, 40 000/μl. The serum transaminases were elevated; serum conjugated bilirubin was 30 μmol/l (normal range, < 17 μmol/l); albumin was low with a value 19 g/l (normal range, 35–45 g/l); and the prothrombin time was 51% (normal range, 75–100%). The serum brain natriuretic peptide level was normal. Microscopic examination and culture of sputum and broncho-alveolar lavage were negative for Pneumocystis jirovecii and other opportunistic pathogens. Chest radiographs showed bilateral basilar reticulonodular opacities and normal lung volumes. Pulmonary computerized tomographic angiography with contrast revealed no evidence of pulmonary emboli. Pulmonary function testing demonstrated a reduced carbon monoxide diffusion capacity. The presence of delayed contrast appearance in the left heart on contrast-enhanced echocardiocardiography confirmed the diagnosis of HPS. Continuous home oxygen therapy (6 l/min) and a new antiretroviral therapy regimen were initiated. After initial improvement of the dyspnoea, she died of a urinary sepsis 3 months later. Hepatopulmonary syndrome is defined as a triad of chronic liver diseases, hypoxemia < 70 mmHg and pulmonary vascular dilation [3]. The estimated prevalence of HPS in patients with chronic liver disease varies between 4 and 29% according to the heterogeneous criteria used for definition of the condition [3,4]. In a recent study among patients with hepatitis B or C infection, the reported prevalence was 1.1% [5]. Little data is available on HIV-infected patients as only two cases have previously been reported in the literature [6,7]. The mechanisms leading to pulmonary vasodilation are complex and multifactorial. There appears to be an imbalance between the vasodilating and vasoconstricting mediators (nitrogen monoxide and endothelin-1). Hypoxemia can be explained by anatomical shunting and a diffusion–perfusion abnormality [3,4,6]. HPS occurs mainly but not exclusively in cirrhotic patients with portal hypertension [3,4]. This increasingly frequent complication is characterized by a delayed diagnosis with a mean duration of respiratory symptoms of 4.8 years before diagnosis. The presence of hypoxemia associated with platypnea and orthodeoxia (decrease in PaO2 > 3 mmHg in the erect position) as in our observation is suggestive of clinically significant HPS [3,4,6,7]. When the diagnosis is suspected, analyses of arterial blood gases should be obtained in both erect and supine positions. Attention in daily practice should be drawn to the presence of basilar interstitial infiltrates on chest radiographs, mimicking interstitial lung diseases or opportunistic pulmonary infections. Moreover, a high-resolution computerized tomography scan of the chest is useful to rule out other causes of hypoxemia and confirm the vascular etiology (dilated lung vessels) of the opacities [8]. Contrast-enhanced echocardiography is the key diagnostic tool [3,4]. HPS represents a significant mortality risk factor (overall mortality of 41% at 3 years after onset of dyspnoea) among cirrhotic patients, even after transplantation [9]. The most relevant prognosis factor is severe hypoxemia, with a baseline PaO2 < 50 mmHg associated with high mortality [10]. Currently, there is no effective medical treatment (methylene blue, inhaled NO, garlic, norfloxacin) for HPS [4,6,9,11]. Orthotopic liver transplantation (OLT), an emerging practice in selected HIV/HCV co-infected patients, is the only efficient treatment since it can reverse oxygenation abnormalities [11–13]. No data is available yet in this group. Thus, HPS should be considered in every case of a HIV patient with associated liver disease, presenting with an unexplained dyspnoea and hypoxemia. Early detection of ‘subclinical HPS’ by systematic arterial blood gas measurements in HIV-associated liver disease improves the prognosis.

What Is the Role of GB Virus C Infection in Hepatitis C Virus/HIV Coinfection?

Much has been published over the past 10 years regarding the influence of GB virus C (GBV-C) on HIV infection. Several studies have reported that coinfection with HIV and GBV-C leads to a more favorable outcome in patients with a delay in the development of AIDS compared with the outcome in patients infected with HIV alone. This has led some groups to look for the putative mechanism of this beneficial effect and alterations in the cellular immune response have been implicated. However there is still considerable controversy regarding this interaction because not all studies have shown a beneficial effect of GBV-C infection on the progression of HIV disease. By contrast there is no debate that GBV-C plays little role if any in hepatitis C virus (HCV) infection with no effect on the progression of HCV-related liver disease or on the effectiveness of interferon (IFN)--based therapy. Similarly there is no dispute that the course of liver disease is accelerated in patients with HCV/HIV coinfection. Indeed HCV related liver disease has been a significant cause of morbidity and mortality in HIV infected patients during the era of highly active antiretroviral therapy (HAART). This has stimulated increased interest in HCV therapy in HCV/HIV-coinfected subjects particularly given that HCV clearance rates of >40% are possible with combination pegylated (PEG)--IFN and ribavirin therapy. (excerpt)

Cryptogenic Liver Disease in HIV-Infected Patients

Liver disease has become an important cause of morbidity and mortality in HIV-infected patients. Now, researchers have described the characteristics of

HIV/HCV Coinfection and Normal ALT Levels

Hepatitis C virus (HCV) coinfection is an important cause of liver-related morbidity and mortality in HIV-infected patients. In coinfected patients,

The changing spectrum of pulmonary disease in patients with HIV infection on antiretroviral therapy

The pulmonary manifestations of HIV disease in 2005 can be divided into two sets of presentations. For patients who do not have access to care, and who are not taking antiretroviral or chemoprophylactic drugs, opportunistic infections and neoplasms continue to occur. Pulmonary disease caused by Streptococcus pneumoniae, Pneumocystis carinii (now known as Pneumocystis jiroveci pneumonia; PCP), Mycobacterium tuberculosis, lymphoma, and Kaposi’s sarcoma present much as they did in the 1980s. Management has improved in terms of new diagnostic, therapeutic, and preventive strategies, as reviewed in guidelines issued jointly by the National Institutes of Health, Centers for Disease Control and Prevention, and Infectious Disease Society of America (available online at http://www.aidsinfo.nih.gov).

Mortality and Morbidity in HIV-Infected Patients Undergoing Coronary Artery Bypass Surgery: a Case Control Study

The use of highly active antiretroviral therapy (HAART) in patients with HIV infection has improved survival. This improvement combined with the metabolic effects of treatment has increased cardiovascular risk and the need for cardiac surgery in these patients. We compared morbidity and mortality in HIV-infected patients (cases, n=7) and non-HIV-infected patients (controls, n=21) who underwent isolated coronary artery surgery between 1997 and 2004. The durations of extracorporeal circulation and aortic cross-clamping were shorter in HIV-infected patients (P=.002 and P=.014, respectively). The percentage of patients who experienced complications was similar, at 57.1% in both groups, but there was a slightly higher number of complications per patient in non-HIV-infected individuals. The mean length of total hospitalization was greater in HIV-infected patients (27.1 [13.3] versus 8.8 [5.3] days; P=.003), as was that of postoperative hospitalization (18.2 [15.4] vs 7.9 [4.2] days; P=.08). No HIV-infected patient died or needed a repeat cardiac operation. No progression of the HIV infection was observed. Isolated coronary artery surgery in HIV-infected patients produces good results, and there is no increase in morbidity or mortality. Extracorporeal circulation did not influence disease progression.

Clinical Presentation and Course of Acute Hepatitis C Infection in HIV-Infected Patients

Hepatitis C virus (HCV) has become a significant source of morbidity and mortality in HIV-infected patients. However, little is known about the clinical presentation and course of acute HCV infection in this population. This study reports the outcomes of acute HCV infection in 9 HIV-infected men. Sex with men was the only reported risk factor for HCV infection in 6 of the subjects. Clinical presentation of acute HCV ranged from incidentally discovered elevated transaminases to severe liver dysfunction requiring hospitalization. At the time of HCV diagnosis, 8 of 9 patients had CD4+ counts >250 cells/mm(3), and 6 had HIV viral loads of < or =5000 copies/mL. Eight patients were receiving antiretroviral therapy. Outcome of these acute HCV infections varied. Five patients experienced virologic clearance, 2 in whom virus cleared spontaneously and 3 who were treated with pegylated interferon and ribavirin. Four patients developed chronic infection, one of whom had a relapse during HCV treatment and 3 of whom were untreated. All 4 patients to whom HCV therapy was administered experienced significant anemia or neutropenia, necessitating dose reduction or support with growth factors. Prompt recognition of acute HCV infection may minimize antiretroviral treatment interruption and will allow early treatment, which may improve virologic clearance. Unexplained transaminase elevations in HIV-infected patients, including men who have sex with men, should trigger an evaluation for acute HCV infection.

Current issues in critical care of the human immunodeficiency virus-infected patient*

To provide current information on the epidemiology of human immunodeficiency virus (HIV)-infected patients admitted to the intensive care unit during the era of combination antiretroviral therapy and to review issues related to the administration of antiretroviral therapy that are relevant to the intensivist. Review of literature related to intensive care of HIV-infected patients. Overall mortality of HIV-infected patients in the intensive care unit has decreased in the era of combination antiretroviral therapy, and patients are more commonly admitted with non-HIV-related illnesses. Use of antiretroviral therapy in the intensive care unit is difficult but may be associated with improved outcomes. HIV-infected patients are less likely to be admitted to the intensive care unit with opportunistic infections but more likely to be admitted with problems unrelated to HIV infection or with conditions related to antiretroviral therapy. With current management strategies, more patients survive intensive care unit admission. Intensivists need to be familiar with antiretroviral therapy to recognize life-threatening toxicities unique to these drugs; to avoid drug interactions, which are extremely common and potentially life-threatening; and to avoid enhancing HIV drug resistance, an occurrence that could have devastating consequences for the patient following intensive care unit discharge.

Natural history and predictors of severity of chronic hepatitis C virus (HCV) and human immunodeficiency virus (HIV) co-infection

Co-infection by the hepatitis C virus (HCV) is observed in up to 30% of HIV-infected individuals. In studies conducted in the 'pre-HAART era', the late consequences of HCV-related chronic liver disease were overshadowed by extra-hepatic causes of deaths, related to severe immune deficiency, and the impact of HCV infection on mortality of HIV-infected patients was low. While the development of HAART has resulted in a significant decrease in morbidity and mortality amongst HIV-infected patients, this clear benefit allowed the expression of liver-related complications associated with HCV chronic infection. The impact of HCV on HIV remains debated but HIV infection significantly modifies the natural history of HCV infection. HIV infection increases levels of HCV viraemia by 2- to 8-fold, resulting in a significant decrease in spontaneous recovery of acute hepatitis. HIV co-infection also worsens the histological course of HCV infection by increasing and accelerating the risk of cirrhosis or leading to rare but lethal fibrosing cholestatic hepatitis. Liver disease is now one of the leading causes of morbidity and mortality in co-infected patients, even if HAART and especially protease inhibitors, may decrease the severity of the liver disease and the liver-related mortality. Several non-exclusive pathogenic processes explain the increasing rate of liver complications associated with HCV-related liver disease.

Indinavir impairs endothelial function in healthy HIV-negative men

Potent antiretroviral treatment has drastically reduced mortality in HIV-infected patients but may accelerate atherosclerotic disease, which could be partially mediated via endothelial dysfunction. In 8 HIV-negative healthy males, leg blood flow responses to intraartery infusions of methacholine chloride (Mch), sodium nitroprusside, and NG-mono-methyl-L-arginine (L-NMMA) were measured before and after 4 weeks of daily oral indinavir. In the same subjects, we also assessed the effect of indinavir on lipids, insulin sensitivity, markers of inflammation, as well as oxidative stress. After 4 weeks of indinavir, the endothelium-dependent response to methacholine chloride was impaired (195% +/- 38% vs 83% +/- 13%, P < .05), the response to NG-mono-methyl-L-arginine (nitric oxide-dependent tone) was nearly abrogated (-30% +/- 4% vs -1% +/- 11%, P < .05), whereas the endothelium-independent response to sodium nitroprusside remained unchanged. Fasting insulin levels increased from 5.8 +/- 1.2 to 7.0 +/- 1.4 microU/mL (P < .05), and HOMA-IR scores increased from 1.3 +/- 0.3 to 1.6 +/- 0.3 U (P < .05). There were no changes in blood pressure, lipids, markers of inflammation, or oxidative stress. Four weeks of the HIV-1 protease inhibitor indinavir, in the absence of HIV-1 infection, causes vascular dysfunction most likely at the level of endothelial nitric oxide production. The vascular dysfunction may be mediated partially by the concomitant induction of insulin resistance but other mechanisms cannot be ruled out.

Structured treatment interruptions (STI) in chronic suppressed HIV infection in adults

Although antiretroviral treatment (ART) has led to a decline in morbidity and mortality of HIV-infected patients in developed countries, it has also presented challenges. These challenges include increases in pill burden; adherence to treatment; development of resistance and treatment failure; development of drug toxicities; and increase in cost of HIV treatment and care. These issues stimulated interest in investigating the short-term and long-term consequences of discontinuing ART, thus providing support for research in structured treatment interruptions (STI). Structured treatment interruptions of antiretroviral treatment involve taking supervised breaks from ART. STI are defined as one or more planned, timing pre-specified, cyclical interruptions in ART. STI are attempted in monitored clinical settings in eligible participants. STI have generated hopes of reducing drug toxicities, decreasing costs and total time on treatment in HIV-positive patients. The first STI was attempted in the case of a patient in Germany, who later permanently discontinued treatment. This successful anecdotal case report led to several trials on STI worldwide. The objective of this systematic review was to assess the effects of structured treatment interruptions (STI) of antiretroviral therapy (ART) in the management of chronic suppressed HIV infection, using all available high-quality studies. Nine databases covering the time period from January 1996 to March 2005 were searched. Bibliographies were scanned and experts contacted in the field to identify unpublished research and ongoing trials. Two reviewers independently extracted data, and evaluated study eligibility and quality. Disagreements were resolved in consultation with a third reviewer. Data from 33 studies were included in the review. STI is a planned, timing pre-specified experimental intervention. In our review, we decided to include all available intervention trials in HIV-infected patients, with or without control groups. We reviewed evidence from 18 randomized and non-randomized controlled trials, and 15 single arm trials. Single arm trials were included because these pilot studies made significant contribution to the early development and refutation of hypotheses in STI. Trials included in this review varied in study participants, methodology and reported inconsistent measures of effect. Due to this heterogeneity, we did not attempt to meta-analyse them. Results were tabulated and a qualitative systematic review was done For the purpose of this review, STI strategies were classified either as a timed-cycle STI strategy or a CD4-guided STI strategy. In timed-cycle STI strategy, a predetermined period of fixed duration (e.g. one week, one month) off ART was attempted followed by resumption of ART, while closely monitoring changes in CD4 levels and viral load levels. Predetermined criteria for interruption and resumption were laid out in this strategy. Timed-cycle STI fell out of favor due to reports of development of resistance in many studies. Moreover, there were no significant immunological and virological benefits, and no reduction in toxicities, reported in these studies. In CD4-guided STI strategy, ART was interrupted for variable durations guided by CD4 levels. Participants with high nadir CD4 levels qualified for this approach. A reduction in costs of ART, a reduction in mutation, and a better tolerability of this CD4-guided STI strategy was reported. However, concerns about long-term safety of this strategy on immunological, virological, and clinical outcomes were also raised. Timed-cycle STI have not been proven to be safe in the short term. Although CD4-guided STI strategy has reported favorable outcomes in the short term, the long-term safety, efficacy and tolerability of this strategy has not been fully investigated. Based on the studies we reviewed, the evidence to support the use of timed-cycle STI and CD4-guided STI cycles as a standard of care in the management of chronic suppressed HIV infection is inconclusive.

Mortality in Patients With Successful Initial Response to Highly Active Antiretroviral Therapy Is Still Higher Than in Non-HIV-Infected Individuals

Mortality in HIV-infected patients has decreased dramatically since the introduction of highly active antiretroviral therapy (HAART). We analyzed progression to death in a population of 3678 antiretroviral treatment-naive patients from the ATHENA national observational cohort from 24 weeks after the start of HAART. Mortality was compared with that in the general population in the Netherlands matched by age and gender. Only log-transformed CD4 cell count (hazard ratio [HR] = 0.50, 95% confidence interval [CI]: 0.40 to 0.61 per unit increase) and plasma viral load (HR = 0.30, 95% CI: 0.15 to 0.60, HIV RNA level <100,000 vs. > or = 100,000 copies/mL) measured at 24 weeks and infection via intravenous drug use (IDU) (HR = 0.16, 95% CI: 0.10 to 0.26, non-IDU vs. IDU) were significantly associated with progression to death. For non-IDU patients with 600 x 10 CD4 cells/L and an HIV RNA level <100,000 copies/mL at 24 weeks, mortality was predicted to be 5.3 (95% CI: 3.5 to 8.4) and 10.4 (95% CI: 6.4 to 17.4) times higher than in the general population for 25-year-old men and women, respectively, and 1.15 (95% CI: 1.08 to 1.25) and 1.29 (95% CI: 1.16 to 1.50) times higher for 65-year-old men and women, respectively. Hence, mortality in HIV-infected patients with a good initial response to HAART is still higher than in the general population.

Interaktionen kardialer und antiretroviraler Medikation

New therapeutic options such as the highly active antiretroviral therapy (HAART) have significantly improved morbidity and mortality of HIV-infected patients. Consequently, age-related diseases become more manifest. In addition, HIV infection itself causes certain cardiovascular morbidity. Therefore, treatment of cardiovascular symptoms of HIV-positive patients becomes more and more important. Pharmacotherapy in these patients is complex and requires polypharmacy with drugs carrying a high risk of drug-drug interactions.

Pneumonia associated with HIV infection

Pneumonia occurs commonly in HIV-infected patients and this review highlights some of the recent findings in the epidemiology, pathogenesis, clinical features, treatment and prevention of this condition. Pneumonia remains an important cause of morbidity and mortality in HIV-infected patients. A number of factors have been identified that increase the risk of pneumonia. Cigarette smoking increases the risk of lung colonization, as well acute pneumonia due to Pneumocystis jiroveci, and has been documented to produce significant depression of the phagocytic function of alveolar macrophages in HIV-infected patients, which may underlie this risk. Legionella pneumophila infections appear to be uncommon in HIV-infected patients, while pneumonia with Streptococcus pneumoniae continues to occur with regularity, including infections with antibiotic-resistant isolates. Pneumocystis pneumonia occurs with a low incidence in patients receiving HAART, once the CD4 count increases to over 200 microl. Studies of invasive pneumococcal infections (predominantly pneumonia) indicate that in critically ill cases, including HIV-seropositive patients, combination antibiotic therapy is associated with a lower mortality than monotherapy. The 23-polyvalent pneumococcal vaccine has been shown to reduce the risk of pneumococcal infection in HIV-infected adults receiving HAART, and a 9-valent conjugate pneumococcal vaccine has been shown to reduce the incidence of radiologically confirmed pneumonia in HIV-seropositive and HIV-seronegative children. Pneumonia remains an important condition in HIV-infected patients, but recent studies demonstrate that antibiotic prophylaxis, the introduction of HAART, recognition of specific risk factors, new antibiotic treatment strategies and effective vaccines should serve to decrease its impact.