X-ray of Pneumocystis jiroveci pneumonia There is increased white (opacity) in the lower lungs on both sides, characteristic of Pneumocystis pneumonia
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Pneumocystis jiroveci pneumonia

Pneumocystis jiroveci pneumonia or Pneumocystis pneumonia (PCP) is a form of pneumonia caused by a yeast-like fungal microorganism called Pneumocystis jiroveci (sometimes spelled jirovecii, formerly known as Pneumocystis carinii). It is relatively rare in people with normal immune systems but common among people with AIDS. PCP can also develop in patients who are taking immunosuppressant medications (e.g., patients who have undergone solid organ transplantion) and in patients who have undergone bone marrow transplantation. more...

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Symptoms

Symptoms of PCP include high fever, non-productive cough, shortness of breath (especially on exertion), weight loss and night sweats. There is usually not a large amount of sputum with PCP unless the patient has an additional bacterial infection. The fungus can invade other visceral organs, such as the liver, spleen and kidney, but only in a minority of cases.

Diagnosis

The clinical diagnosis can be confirmed by the characteristic appearance of the chest x-ray which shows widespread pulmonary infiltrates, and an arterial oxygen level (pO2) strikingly lower than would be expected from symptoms. The diagnosis can be definitively confirmed by pathologic identification of the causative organism in induced sputum or bronchial washings obtained by bronchoscopy with coloration by toluidine blue or immunofluorescence assay.

PCP and AIDS

Because PCP rarely occurs without AIDS, it can be one of the first clues to a new AIDS diagnosis, though it does not generally occur unless the CD4 count is less than 200/mm³. An unusual rise in PCP cases in North America, noticed when physicians began requesting large quantities of the rarely used antibiotic pentamidine, was the first clue to the existence of AIDS in the early 1980s.

Prior to the development of more effective treatments, PCP was a common and rapid cause of death in AIDS patients. Much of the incidence of PCP has been reduced by instituting a standard practice of using oral trimethoprim/sulfamethoxazole to prevent the disease in people with CD4 counts less than 200/mm³. In populations that do not have access to preventative treatment, PCP continues to be a major cause of death in AIDS.

Treatments

Antipneumocystic medication is used with concomitant steroids in order to avoid inflammation, which causes an exacerbation of symptoms about four days after treatment begins if steroids are not used. By far the most commonly used medication is a combination of trimethoprim and sulfamethoxazole (co-trimoxazole, with the tradenames Bactrim, Septrin, or Septra), but some patients are unable to tolerate this treatment due to allergies. Other medications that are used, alone or in combination, include pentamidine, trimetrexate, dapsone, atovaquone, primaquine, and clindamycin. Treatment is usually for a period of about 21 days.

Nomenclature

The name P. jiroveci, to distinguish the organism found in humans from variants of Pneumocystis found in other animals, was first proposed in 1976, in honor of Otto Jirovec, who described Pneumocystis pneumonia in humans in 1952. After DNA analysis showed significant differences in the human variant, the proposal was made again in 1999 and has come into common use; P. carinii still describes the species found in rats. The International Code of Botanical Nomenclature would normally require the name to be spelled jirovecii rather than jiroveci; both spellings are currently in use.

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Pneumocystis carinii vs. Pneumocystis jiroveci: another misnomer - response to Stringer et al - Letters - Brief Article
From Emerging Infectious Diseases, 2/1/03 by Walter T. Hughes

To the Editor: The proposal by Stringer et al. to change the name of neumocystis carinii found in humans to Pneumocystis jiroveci requires critical consideration (1). First, their rationale for the choice of Jirovec is not compelling. Principle III of the International Code of Botanical Nomenclature (ICBN) states: "the nomenclature of a taxonomic group is based upon priority of publication" (2). Jirovec's publication in 1952 was not the first to report P. carinii infection in human lungs. In 1942, two Dutch investigators, van der Meer and Brug, described P. carinii as the infecting organism in a 3-month-old infant with congenital heart disease and in 2 of 104 autopsy cases (a 4-month-old infant and a 21-year-old adult) (3). Their description, photomicrographs, and drawings of P carinii are unequivocal. They also described the typical "honeycomb" patterns in alveoil. In 1951, Dr. Josef Vanek at Karls-Universitat in Praha, Czechoslovakia, reported his study of lung sections from 16 children with interstitial pneumonia and demonstrated that the disease was caused by P carinii (4). Vanek notes in his report, "In man the parasite was for the first time established as a cause of pneumonia in a child by G. Meer and S. L. Brug (1942)." In 1952, Jirovec reported P carinii as the cause of interstitial plasmacellular pneumonia in neonates (5). A year later, in a coauthored publication, Vanek, Jirovec, and J. Lukes acknowledged and referenced the earlier reports of van der Meer and Brug and Vanek (6). If principle III is to be followed, as well as fairness to the investigators, both van der Meer and Brug and Vanek hold priority over Jirovec, assuming the designation of the species name should be based on the name of the first person to discover P carinii in humans.

The nomenclature of P. carinii has actually been fraught with errors from the beginning. In the earliest publications, Carlos Chagas and Antonio Carini mistook the organism for stages in the life cycle of trypanosomes. Chagas placed it in a new genus, Schizotrypanum (7,8). In 1912, Delanooe and Delanoe at the Pasteur Institute in Paris published the first description of the organism as a new entity unrelated to trypanosomes (9). They proposed the name "Pneumocystis carinii" as a tribute to Carini. The Delanoe paper has remained unchallenged as the original description of P. carinii. Both Chagas and Carini later acknowledged their errors and the validity of the Delanoes' conclusion. By current ICBN principles, P. carinii is acceptable nomenclature because the authors of the first publication proposed the name of Carini, rather than their own.

In addition, changing the name to P. jiroveci will create confusion in clinical medicine where the name P carinii has served physicians and microbiologists well for over half a century. I was moved to write this letter because of a call from a knowledgeable oncologist asking for information on "the new strain of P. carinii that has just been reported from the Centers for Disease Control and Prevention," referring to the report by Stringer et al (1).

AIDS patients are well informed about P carinii pneumonia and avidly monitor medical news about their disease. Without doubt, the name change will cause confusion and undue anxiety among the many thousands of HIV-infected patients who attend clinics. Health-care workers will have an added burden of explaining why the name was changed, but the organism and infection are unchanged. Also, versions of the pronunciation of jiroveci (yee row vet zee) by American patients, physicians, and health-care workers will be interesting to hear.

The tone of the article by Stringer et al. implies that the change of P carinii to P jiroveci is final, which is not the case. The nomenclature of fungi is governed by ICBN under the auspices of the International Botanical Congress and is not based solely on molecular genetics. Neither P carinii nor P jiroveci have been submitted for ICBN scrutiny. In another paper, Stringer et al. outline the mechanics for submission, but indicate that no application has been submitted for their proposal (10). In fact, P carinii has not been acknowledged as a fungus by ICBN or any other authoritative taxonomic system. Only when nomenclature is registered in ICBN, can a name be referred to as "formally accepted." In the meantime, the workable terminology proposed earlier by Stringer et al. in 1994 (11) will suffice for clinical use.

Walter T. Hughes, St. Jude Children's Research Hospital, Memphis, Tennessee, USA

References

(1.) Stringer JR, Beard CB, Miller RF, Wakefield AE. A new name (Pneumocystis jiroveci) for Pneumocystis from humans. Emerg Infect Dis 2002;8:891-6.

(2.) Editorial Committee, International Botanical Congress. International Code of Botanical Nomenclature (St. Louis Code). Konigstein, Germany: Koeltiz Scientific Books; 2000.

(3.) van der Meer MG, Brug SL. Infection a neumocystis chez l'homme et chez les animaux. Amer Soc Beige Med Trop 1942;22:301-9.

(4.) Vanek J. Atypicka (interstitialni) pneumonie deti vyvolana Pneumocystis carinii (atypical interstitial pneumonia of infants produced by Pneumocystis carinii). Casop lek cesk 1951;90:1121-4.

(5.) Jirovec O. neumocystis carinii puvodce t. zv intertitialnich plasmocelulamich pneumonii kojencw (Pneumocystis carinii, the cause 6f interstitial plasmacellular pneumonia in neonates) Csl. Hyg epid mikrob 1952;1:141.

(6.) Vanek J, Jirovec O, Lukes J. Interstitial plasma cell pneumonia in infants. Ann Paediatrici 1953;180:1-21.

(7.) Chagas C. Uber eine neue Trypoanosomiasis des Menschen. Mere Inst Oswaldo Cruz 1909;3:1-218.

(8.) Carini A. Formas des eschizogonia do Trypanosoma lewisi. Soc Med Cir Sao Paulo 1910;38:8.

(9.) Delanoe P, Delanoe M. Sur les rapports des kystes de Carini du poumon des rats avec le Trypanosoma lewisi. Comptes rendus de "l'Academie des sciences. 1912;155:658-61.

(10.) Stringer JR, Cushion MT, Wakefield AE. New nomenclature for the genus Pneumocvstis. J Eukaryot Microbiol 2001;Suppl:184-9.

(11.) Stringer J and the Pneumocystis Workshop. Revised nomenclature for neumocystis carinii. J Eukaryot Microbiol 1994;41:121-2.

Address for correspondence: Walter T. Hughes, Emeritus Member, Department of Infectious Diseases, St. Jude Children's Research Hospital, 332 N. Lauderdale St., Memphis, TN 381052794, USA; fax: 901-495-5068; e-mail: walter, hughes@stjude.org

COPYRIGHT 2003 U.S. National Center for Infectious Diseases
COPYRIGHT 2003 Gale Group

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