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Pneumocystis (carinii) jiroveci Pneumonia

Author: Nicholas John Bennett, MB, BCh, PhD, Fellow in Pediatric Infectious Disease, Department of Pediatrics, State University of New York Upstate Medical University
Coauthor(s): Shelley A Gilroy, MD, Clinical Professor of Medicine, State University of New York Upstate; Medical Director, Infection Control, University Hospital and Crouse Hospital, Syracuse; Frederick Burton Rose, MD, FACP, Professor, Department of Medicine, University Hospital Epidemiologist, State University of New York Upstate Medical University; Joseph C McLean, MD, Staff Physician, Department of Internal Medicine, William Beaumont Army Medical Center; Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium; Tanya S Schreibman, MD, Consulting Staff, Department of Internal Medicine, Bach and Godofsky; Michael Rigsby, MD, Director of HIV Care Program, VA Connecticut Healthcare System, West Haven Campus; Associate Professor, Department of Internal Medicine, Yale University School of Medicine
Contributor Information and Disclosures

Updated: Nov 20, 2009

Introduction

Background

Pneumocystis carinii pneumonia (PCP), as the condition is commonly termed (although the causative organism has been renamed Pneumocystis jiroveci [pronounced "yee-row-vet-zee"]), is the most common opportunistic infection in persons with HIV infection.

Pneumocystis is a genus of unicellular fungi found in the respiratory tracts of many mammals and humans. Distinct genomic variability exists between host-specific members of the genus. The organism was first described in 1909 by Chagas and then a few years later by Delanöes, who ultimately named the organism in honor of Dr. Carini after isolating it from infected rats. Years later, Dr. Otto Jirovec and his group isolated the organism from humans, and the organism responsible for PCP was renamed after him.

Pneumocystis first came to attention when it was found to cause interstitial pneumonia in Central and Eastern Europe during World War II in severely malnourished and premature infants. Prior to the 1980s, fewer than 100 cases of PCP per year were reported in the United States, occurring in immunosuppressed patients such as patients with cancer treated with chemotherapy and solid-organ transplant recipients receiving immunosuppressive agents. In 1981, the Centers for Disease Control and Prevention (CDC) reported PCP in 5 previously healthy homosexual males residing in the Los Angeles area.

P jiroveci is now one of several organisms known to cause life-threatening opportunistic infections in patients with advanced HIV infection worldwide. Well over 100,000 cases of PCP were reported in the first decade of the HIV epidemic in the United States in people with no other cause for immunosuppression.

Microbiology

The taxonomic classification of the Pneumocystis genus was debated for some time. It was initially mistaken as a trypanosome and then later as a protozoan. In the 1980s, biochemical analysis of the nucleic acid composition of Pneumocystis rRNA and mitochondrial DNA identified the organism as a unicellular fungus rather than a protozoa. Subsequent genomic sequence analysis of multiple genes including elongation factor 3, a component of fungi protein synthesis not found in protozoa, further supported this notion. The organism is found in 3 distinct morphologic stages, as follows:

  • The trophozoite (trophic form), in which it often exists in clusters
  • The sporozoite (precystic form)
  • The cyst, which contains several intracystic bodies (spores)

Pathophysiology

Pneumocystis organisms are commonly found in the lungs of healthy individuals. Most children are believed to have been exposed to the organism by age 3 or 4 years, and its occurrence is worldwide.

Animal studies have suggested that Pneumocystis organisms are communicable; airborne transmission has been reported. Human evidence of this is provided by molecular analysis of Pneumocystis isolates obtained from groups of patients involved in hospital outbreaks.1,2 Further evidence of human transmission has been found in cases of recurrent pneumonia in which the genotype of Pneumocystis organisms in the same person differed in prior episodes. Despite this, barrier precautions are not required for patients hospitalized with PCP except to protect other patients with depressed immunity.

Disease occurs when both cellular immunity and humoral immunity are defective. Once inhaled, the trophic form of Pneumocystis organisms attach to the alveoli. Multiple host immune defects allow for uncontrolled replication of Pneumocystis organisms and development of illness, including the following:

  • Activated alveolar macrophages without CD4+ cells are unable to eradicate Pneumocystis organisms.
  • Increased alveolar-capillary permeability is visible on electron microscopy.
  • Physiologic changes include the following:
    • Hypoxemia with an increased alveolar-arterial oxygen gradient
    • Respiratory alkalosis
    • Impaired diffusing capacity
    • Changes in total lung capacity and vital capacity

There have been reports of PCP occurring as part of the immune reconstitution syndrome.3,4

Frequency

United States

Prior to the widespread use of PCP prophylaxis, the frequency of Pneumocystis infection in lung transplant patients alone was as high as 88%. Now, with the routine use of prophylaxis, PCP is very rare in solid-organ transplant patients and has significantly decreased in patients infected with HIV.

  • Prior to the widespread use of highly active antiretroviral therapy (HAART), PCP occurred in 70-80% of patients with HIV infection.
  • The frequency of PCP is decreasing with the use of PCP prophylaxis and HAART.
  • PCP is still the most common opportunistic infection in patients with HIV infection.
  • Patients with HIV infection are more prone to PCP recurrence than patients not infected with HIV.

International

The prevalence of PCP was once thought to be much lower in developing regions of the world,5 but studies have shown that the lower reported incidence is likely a failure to accurately diagnose PCP. An accurate diagnosis requires access to modern medical care not available worldwide. Currently, the frequency of documented Pneumocystis infection is increasing in Africa, with Pneumocystis organisms found in up to 80% of infants with pneumonia who have HIV infection. In sub-Saharan Africa, tuberculosis is a common co-infection in persons with PCP.6

Mortality/Morbidity

  • In patients with HIV infection
    • In this population, PCP once carried a mortality rate of 20-40%, depending on disease severity at presentation. Currently, mortality rates of 10-20% are reported.
    • PCP is still a major cause of death in patients with AIDS in the United States.
  • In patients without HIV infection
    • PCP carries a worse prognosis in persons without HIV infection7 ; this has not changed significantly in the past 20 years.
    • Mortality rates of 30-50% have been documented in several large studies.
    • The higher mortality rate is likely a result of delayed diagnoses and initiation of appropriate treatment.

Clinical

History

The symptoms of P carinii pneumonia (PCP) are nonspecific. PCP in patients with HIV infection tends to run a more subacute indolent course and tends to present much later, often after several weeks of symptoms, compared with PCP associated with other immunocompromising conditions. Symptoms of PCP include the following:

  • Progressive exertional dyspnea (95%)
  • Fever (>80%)
  • Nonproductive cough (95%)
  • Chest discomfort
  • Weight loss
  • Chills
  • Hemoptysis (rare)

Physical

The physical examination findings of PCP are nonspecific and include the following:

  • Tachypnea
  • Fever
  • Tachycardia
  • Pulmonary symptoms: Pulmonary examination may reveal mild crackles and rhonchi but may yield normal findings in up to half of patients.
  • Additional findings in children with severe disease
    • Cyanosis
    • Nasal flaring
    • Intercostal retractions
  • Extrapulmonary manifestations: Although Pneumocystis infection rarely causes extrapulmonary manifestations, they may be present in patients receiving aerosolized pentamidine for prophylaxis or in patients with advanced HIV infection who are not taking any prophylaxis. They may also occur in the absence of lung involvement. Based on most well-documented findings, Pneumocystis infection may present in almost any organ system, as follows:
    • CNS
    • Bone marrow (may have necrosis with resultant pancytopenia)
    • Lymphadenopathy
    • Eyes (may have retinal cotton-wool spots)
    • Thyroid (may present as a rapidly enlarging thyroid mass)
    • GI tract

Causes

PCP is caused by infection with P jiroveci. The following groups are at risk for PCP:

  • Persons with HIV infection whose CD4+ cells fall below 200/µL and who are not receiving PCP prophylaxis (In addition, in patients with HIV infection, findings of other opportunistic infections [eg, oral thrush] increases the risk of PCP, regardless of CD4+ count.)
  • Persons with primary immune deficiencies, including hypogammaglobulinemia and severe combined immunodeficiency (SCID).
  • Persons receiving long-term immunosuppressive regimens for connective-tissue disorders, vasculitides, or solid-organ transplantation (eg, heart, lung, liver, kidney)
  • Persons with hematologic and nonhematologic malignancies, including solid tumors and lymphomas
  • Persons with severe malnutrition

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References
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Further Reading

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Keywords

Pneumocystis carinii pneumonia, PCP, P carinii pneumonia, Pneumocystis jiroveci pneumonia, P jiroveci pneumonia, Pneumocystis pneumonia, PCP prophylaxis, PCP prevention, opportunistic respiratory infection, opportunistic pneumonia, HIV, AIDS

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Contributor Information and Disclosures

Author

Nicholas John Bennett, MB, BCh, PhD, Fellow in Pediatric Infectious Disease, Department of Pediatrics, State University of New York Upstate Medical University
Nicholas John Bennett, MB, BCh, PhD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Shelley A Gilroy, MD, Clinical Professor of Medicine, State University of New York Upstate; Medical Director, Infection Control, University Hospital and Crouse Hospital, Syracuse
Shelley A Gilroy, MD is a member of the following medical societies: American College of Physicians, American Medical Association, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Frederick Burton Rose, MD, FACP, Professor, Department of Medicine, University Hospital Epidemiologist, State University of New York Upstate Medical University
Frederick Burton Rose, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Joseph C McLean, MD, Staff Physician, Department of Internal Medicine, William Beaumont Army Medical Center
Joseph C McLean, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium
Clinton Murray, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Tanya S Schreibman, MD, Consulting Staff, Department of Internal Medicine, Bach and Godofsky
Disclosure: Nothing to disclose.

Michael Rigsby, MD, Director of HIV Care Program, VA Connecticut Healthcare System, West Haven Campus; Associate Professor, Department of Internal Medicine, Yale University School of Medicine
Disclosure: Nothing to disclose.

Medical Editor

Klaus-Dieter Lessnau, MD, FCCP, Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital
Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Artificial Internal Organs, American Thoracic Society, Physicians for Social Responsibility, and Society of Critical Care Medicine
Disclosure: sepracor Ownership interest None

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Harold L Manning, MD, Associate Professor, Departments of Medicine, Anesthesiology and Physiology, Section of Pulmonary and Critical Care Medicine, Dartmouth Medical School
Harold L Manning, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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