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| '''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
| | #Redirect[[Pneumocystis jirovecii pneumonia]] |
| {{DiseaseDisorder infobox |
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| Name = Pneumocystis jirovecii pneumonia |
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| ICD10 = {{ICD10|B|20|6|b|20}} |
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| ICD9 = {{ICD9|136.3}} |
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| ICDO = |
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| Image = Pneumocystis.jpg |
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| Caption = '''''Pneumocystis jirovecii''''' cysts from bronchoalveolar lavage, stained with [[Toluidin blue O stain]] |
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| OMIM = |
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| OMIM_mult = |
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| MedlinePlus = 000671 |
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| eMedicineSubj = |
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| eMedicineTopic = |
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| DiseasesDB = 10160 |
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| MeshID = D011020 |
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| }}
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| {{Search infobox}}
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| {{CMG}}
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| ==Overview==
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| '''''Pneumocystis'' pneumonia''' ('''PCP''') is a form of [[pneumonia]] caused by the yeast-like [[fungus|fungal]] ''Pneumocystis jirovecii'' (Jirovecii is pronounced "yee row vet zee eye"). The causal agent was originally described as a protozoan and spelled ''P. jiroveci'' and prior to then was classified as a form of ''Pneumocystis carinii'', a name still in common usage.<ref name=Stringer_2002>{{cite journal | author=Stringer JR, Beard CB, Miller RF, Wakefield AE | title=A new name (''Pneumocystis jiroveci'') for ''Pneumocystis'' from humans | journal=Emerg Infect Dis | year=2002 | pages=891-6 | volume=8 | issue=9 | id=PMID 12194762}}</ref><ref name=Redhead_2006>{{cite journal | author=Redhead SA, Cushion MT, Frenkel JK, Stringer JR | title=''Pneumocystis'' and ''Trypanosoma cruzi'': nomenclature and typifications | journal=J Eukaryot Microbiol | year=2006 | pages=2–11 | volume=53 | issue=1 | id=PMID 16441572}}</ref> These names are discussed below. As a result, '''Pneumocystis pneumonia (PCP)''' has also been known as '''Pneumocystis jiroveci[i] pneumonia''' and as '''Pneumocystis carinii pneumonia''', as is also explained below.<ref name=Cushion_1998>{{cite journal | author=Cushion MT .| title = Chapter 34. ''Pneumocystis carinii''. In: Collier, L., Balows, A. & Sussman, M. (ed.), Topley and Wilson's Microbiology and Microbial Infections 9th ed. Arnold and Oxford Press, New York. | year = 1998 | pages = 645–683}}</ref><ref name=Cushion_1998b>{{cite journal | author=Cushion MT | title = Taxonomy, genetic organization, and life cycle of ''Pneumocystis carinii'' | | journal = Semin. Respir. Infect | year = 1998 | volume = 13 | issue =4 | pages = 304–312}}</ref><ref name=Cushion_2004>{{cite journal | author=Cushion MT | title = ''Pneumocystis'': unraveling the cloak of obscurity | | journal = Trends Microbiol | year = 2004 | volume = 12 | issue =5 | pages = 243–249}}</ref>
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| It is relatively rare in people with normal immune systems but common among people with
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| weakened [[immune system]]s, such as premature or severely malnourished children, the elderly, and especially [[AIDS]] patients, in whom it is most commonly observed today.<ref name=Sherris>{{cite book | author = Ryan KJ; Ray CG (editors) | title = Sherris Medical Microbiology | edition = 4th ed. | publisher = McGraw Hill | year = 2004 | id = ISBN 0838585299 }}</ref> PCP can also develop in patients who are taking [[Immunosuppressive drug|immunosuppressant medications]] (e.g. patients who have undergone [[Organ transplant|solid organ transplantation]]) and in patients who have undergone [[bone marrow transplantation]].
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| The organism is distributed worldwide<ref name=Morris_2004>{{cite journal | author=Morris A et al | title= Current Epidemiology of Pneumocystis Pneumonia | journal=Emerg Infect Dis | year=2004 | pages=1713-1720 | volume=10 | issue=10 | id=PMID 15504255}}</ref>[http://www.cdc.gov/ncidod/eid/vol10no10/03-0985.htm].
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| ==Epidemiology==
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| Pneumocystis pneumonia has been described in all continents except Antarctica.<ref name=Morris_2004/> It was originally described as a rare cause of [[pneumonia]] in [[neonate]]s. It is believed to be an environmental organism, and human-to-human transmission is thought not to occur (although in one outbreak of 12 cases among transplant patients in Leiden it was postulated, but not proven, that human-to-human spread may have occurred).<ref>{{cite journal | author=de Boer M, Bruijnesteijn van Coppenraet L, Gaasbeek A, ''et al.'' | title=An outbreak of Pneumocystis jiroveci pneumonia with 1 predominant [[genotype]]
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| among renal transplant recipients: interhuman transmission or a common environmental source? | journal=Clin Infect Dis |year=2007 | volume=44 | issue=9 | pages=1143–49 | id=PMID 17407029 }}</ref> Greater than 75% of children are seropositive by the age of 4, which suggest a high background exposure to the organism.
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| Since the start of the [[HIV]] pandemic, PCP has been closely associated with AIDS. Because it only occurs in an immunocompromised host, it may be the first clue to a new AIDS diagnosis if the patient has no other reason to be immunocompromised (e.g. taking immunosuppressive drugs for [[organ transplant]]). An unusual rise in the number of 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.<ref>{{cite journal | title=A Cluster of Kaposi's Sarcoma and ''Pneumocystis carinii'' pneumonia among homosexual male residents of Los Angeles and Range Counties, California | author=Fannin S, Gottlieb MS, Weisman JD, ''et al.'' | year=1982 | journal=MMWR Weekly | volume=31 | issue=32 | pages=305–7 }}</ref><ref>{{cite journal | author=Masur H, Michelis MA, Greene JB, ''et al.'' |title=An outbreak of community-acquired Pneumocystis carinii pneumonia |journal=N Engl J Med |year=1981 |volume=305 |pages=1431–8 | url=http://www.cdc.gov/mmwr/preview/mmwrhtml/00001114.htm }}</ref>
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| Prior to the development of more effective treatments, PCP was a common and rapid cause of death in persons living with AIDS. Much of the incidence of PCP has been reduced by instituting a standard practice of using oral [[co-trimoxazole]] 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.
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| In [[immunocompromised]] patients (e.g. cancer patients on [[chemotherapy]], or persons living with [[AIDS]] with a [[T helper cell|CD4+ T-cell]] count below 200/μl), [[prophylaxis]] with regular [[pentamidine]] inhalations or [[sulfamethoxazole]]/[[trimethoprim]] ([[co-trimoxazole]] or [[TMP-SMX]]) may be necessary to prevent PCP.
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| ==Symptoms==
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| Symptoms of PCP include 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.
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| ==Pathophysiology==
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| The risk of pneumonia due to Pneumocystis jirovecii increases when [[CD4]] levels are less than 200 cells/μl. In these [[Immunosuppression|immunosuppressed]] individuals the manifestations of the infection are highly variable.<ref>{{cite book | author = Hughes WT | title = Pneumocystis Carinii. ''In:'' Barron's Medical Microbiology ''(Barron S ''et al'', eds.)| edition = 4th ed. | publisher = Univ of Texas Medical Branch | year = 1996 | id = [http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.4516 (via NCBI Bookshelf)] ISBN 0-9631172-1-1 }}</ref> The disease attacks the interstitial, fibrous tissue of the lungs, with marked thickening of the alveolar septa and [[alveoli]] and leading to significant [[Hypoxia (medical)|hypoxia]] which can be fatal if not treated aggressively; ergo, [[LDH]] levels increase and gas exchange is compromised. Oxygen is less able to diffuse into the blood, leading to [[hypoxia (medical)|hypoxia]]. Hypoxia, along with high arterial [[carbon dioxide]] (CO<sub>2</sub>) levels, stimulates [[ventilation (physiology)|ventilation]], thereby causing [[dyspnea]].
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| ==Diagnosis==
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| The diagnosis can be confirmed by the characteristic appearance of the [[chest x-ray]] which shows widespread pulmonary infiltrates, and an [[arterial blood gas|arterial oxygen level]] (pO<sub>2</sub>) 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 [[bronchia]]l washings obtained by [[bronchoscopy]] with coloration by [[toluidine blue]] or [[immunofluorescence assay]], which will show characteristic [[cyst]]s [http://www.bmb.leeds.ac.uk/mbiology/ug/ugteach/icu8/std/pcp.html].
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| ''Pneumocystis'' infection can also be diagnosed by [[immunofluorescent]] or [[histochemical staining]] of the specimen, and more recently by molecular analysis of [[PCR]] products comparing [[DNA]] samples. Notably, simple molecular detection of ''Pneumocystis jirovecii'' in lung fluids does not mean that a person has Pneumocystis pneumonia or infection by [[HIV]]. The fungus appears to be present in healthy individuals also in the general population.<ref name=Medrano_2005>{{cite journal | author=Medrano FJ et al | title= ''Pneumocystis jiroveci''i in General Population | journal=Emerg Infect Dis | year=2005 | pages=245–250 | volume=11 | issue=2 | id=PMID 15752442 }}</ref>
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| [[Image:PCPxray.jpg|thumb|left|250px|'''X-ray of Pneumocystis jirovecii pneumonia''' There is increased white (opacity) in the lower lungs on both sides, characteristic of ''Pneumocystis'' pneumonia]]
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| ==Life-cycle==
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| The complete life-cycles of any of the species of ''Pneumocystis'' are not known, but presumably all resemble the others in the genus. The terminology follows zoological terms, rather than mycological terms, reflecting the initial misdetermination as a protozoan parasite. All stages are found in lungs and because they cannot be cultured, direct observation of living ''Pneumocystis'' is difficult. The trophozoite stage is the vegetative state. It is single-celled and appears amoeboid (multilobed) and closely associated with host cells. Globular cysts eventually form that have a thicker wall. Within these [[ascus]]-like cysts, eight spores form which are released through rupture of the cyst wall. The cysts often collapse forming crescent-shaped bodies visible in stained tissue. It is not known for certain if [[meiosis]] takes place within the cysts, or what the genetic status is of the various cell types [http://www.dpd.cdc.gov/dpdx/HTML/Pneumocystis.htm - see DPDx life-cycle diagram].
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| ==Treatment==
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| 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.
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| [[Pentamidine]] is less often used as its major limitation is the high frequency of [[side effect]]s. These include acute [[pancreatitis]], [[renal failure]], [[hepatotoxicity]], [[leukopenia]], [[rash]], [[fever]] and [[hypoglycaemia]].
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| ==Guidelines==
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| To read about guidelines for prevention and treatment of Pneumocystis pneumonia Infections in HIV-Infected Adults and Adolescents, click [[HIV opportunistic infection pneumocystis pneumonia: prevention and treatment guidelines|'''here''']].
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| ==Nomenclature==
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| The name ''P. jirovecii'', to distinguish the organism found in humans from physiological 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<ref name=Stringer_2002 /> and that name is typified by an isolate from rats.<ref name=Redhead_2006 /> The International Code of Botanical Nomenclature (ICBN) requires that the name to be spelled ''jirovecii'' rather than ''jiroveci''. The latter spelling originated when ''Pneumocystis'' was believed to be a protozoan, rather than a fungus, and therefore was spelled using the International Code of Zoological Nomenclature; both spellings are commonly used. A change in the ICBN in 2005 now recognizes the validity of the 1976 publication, making the 1999 proposal redundant, and cites ''Pneumocystis'' and ''P. jirovecii'' as examples of the change in ICBN Article 45, Ex 8. The name ''P. jirovecii'' is typified (both lectotypified and epitypified) by samples from human autopsies dating from the 1960s.<ref name=Redhead_2006 />
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| The term PCP, which was widely used by practitioners and patients, has been retained for convenience, with the rationale that it now stands for the more general '''P'''neumo'''c'''ystis '''p'''neumonia rather than '''P'''neumocystis '''c'''arinii '''p'''neumonia.
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| ==Pneumocystis Genome Project==
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| ''Pneumocystis'' species cannot be grown in culture. Therefore, there is a limitation to the availability of the human disease causing agent, ''P. jirovecii''. Hence, investigation of the whole genome of a ''Pneumocystis'' is largely based upon true ''P. carinii'' available from experimental rats which can be maintained with infections. The project is described in the site linked here. Genetic material of other species, such as ''P. jirovecii'' can be compared to the genome of ''P. carinii''.
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| [http://pgp.cchmc.org/ Pneumocystis Genome Project]
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| ==References==
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| {{Reflist|2}}
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| {{Mycoses}}
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| [[de:Pneumocystis jiroveci]]
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| [[es:Pneumocystis jiroveci]]
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| [[fr:Pneumocystose]]
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| [[fr:Pneumocystis jiroveci]]
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| [[ja:ニューモシスチス肺炎]]
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| [[pt:Pneumocistose]]
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| [[pl:Pneumocystis jiroveci]]
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| [[Category:Fungal diseases]]
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| [[Category:Ascomycota]]
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| [[Category:Infectious disease]]
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| [[Category:Overview complete]]
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