|Pneumocystis jirovecii pneumonia|
Pneumocystis jirovecii cysts from bronchoalveolar lavage, stained with Toluidine blue O stain
|Classification and external resources|
Pneumocystis pneumonia is not commonly found in the lungs of healthy people, but, being a source of opportunistic infection, it can cause a lung infection in people with a weak immune system. Pneumocystis pneumonia is especially seen in people with cancer undergoing chemotherapy, HIV/AIDS, and the use of medications that suppress the immune system.
Signs and symptoms 1
- Disease course 1.1
- Diagnosis 2
- Prevention and treatment 3
- PCP and AIDS 4.1
- Nomenclature 5
- References 6
Signs and symptoms
Pneumothorax is a well-known complication of PCP. An acute history of chest pain with breathlessness and diminished breath sounds is typical of pneumothorax.
The risk of PCP increases when CD4 positive T-cell levels are less than 200 cells/μL. In these immunosuppressed individuals the manifestations of the infection are highly variable. The disease attacks the interstitial, fibrous tissue of the lungs, with marked thickening of the alveolar septa and alveoli, leading to significant hypoxia which can be fatal if not treated aggressively. In this situation LDH levels increase and gas exchange is compromised. Oxygen is less able to diffuse into the blood, leading to hypoxia. Hypoxia, along with high arterial carbon dioxide (CO2) levels, stimulates hyper-ventilatory effort, thereby causing dyspnea (breathlessness).
The diagnosis can be confirmed by the characteristic appearance of the sputum or bronchio-alveolar lavage (lung rinse). Staining with toluidine blue, silver stain, periodic-acid schiff stain, or an immunofluorescence assay will show the characteristic cysts. The cysts resemble crushed ping-pong balls and are present in aggregates of 2 to 8 (and not to be confused with Histoplasma or Cryptococcus, which typically do not form aggregates of spores or cells). A lung biopsy would show thickened alveolar septa with fluffy eosinophilic exudate in the alveoli. Both the thickened septa and the fluffy exudate contribute to dysfunctional diffusion capacity which is characteristic of this pneumonia.
Pneumocystis infection can also be diagnosed by immunofluorescent or histochemical staining of the specimen, and more recently by molecular analysis of polymerase chain reaction 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 in the general population.
Prevention and treatment
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 trimethoprim/sulfamethoxazole, 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, pafuramidine maleate (under investigation), and clindamycin. Treatment is usually for a period of about 21 days.
Pentamidine is less often used as its major limitation is the high frequency of side effects. These include acute pancreatic inflammation, kidney failure, liver toxicity, decreased white blood cell count, rash, fever, and low blood sugar.
The disease PCP is relatively rare in people with normal immune systems, but common among people with weakened bone marrow transplantation and after surgery. Infections with Pneumocystis pneumonia are also common in infants with hyper IgM syndrome, an X-linked or autosomal recessive trait.
The causative organism of PCP is distributed worldwide and Pneumocystis pneumonia has been described in all continents except Antarctica. Greater than 75% of children are
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Regarding nomenclature, when the name of Pneumocystis pneumonia (PCP) changed from P. carinii pneumonia to P. jirovecii pneumonia, it was at first felt that "PJP" should replace "PCP". However, because the term PCP was already used among physicians that managed patients with Pneumocystis infection, it was rationalized that the term PCP could continue to be used, as it could stand for PneumoCystis (jirovecii) Pneumonia.
The older species name Pneumocystis carinii (which now applies only to the Pneumocystis species that is found in rats) is still in common usage. As a result, Pneumocystis pneumonia (PCP) is also known as Pneumocystis jiroveci[i] pneumonia and (incorrectly) as Pneumocystis carinii pneumonia.
Both Pneumocystis pneumonia and pneumocystis pneumonia are orthographically correct; one uses the genus name per se and the other uses the common noun based on it. (This is the same reason, for example, why "group A Streptococcus" and "group A streptococcus" are both valid.) Synonyms for PCP include pneumocystosis (pneumocystis + -osis), pneumocystiasis (pneumocystis + -iasis), and interstitial plasma cell pneumonia.
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 (Bactrim / Septra) to prevent the disease in people with CD4 counts less than 200/μL. In populations that do not have access to preventive treatment, PCP continues to be a major cause of death in AIDS.
Since the start of the pentamidine, was the first clue to the existence of AIDS in the early 1980s.
PCP and AIDS
, it was suggested as likely, but not proven, that human-to-human spread may have occurred.Leiden For example, in one outbreak of 12 cases among transplant patients in  was originally described as a rare cause of Pneumocystis jirovecii