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Section 2
Section 3
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Section 5
Appendices

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Section 3. Summaries of Infectious Diseases

Pneumocystis jiroveci Infections

Clinical Manifestations
Etiology
Epidemiology
Diagnostic Tests
Treatment
Isolation of the Hospitalized Patient
Control Measures

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CLINICAL MANIFESTATIONS: Infants and children develop a characteristic syndrome of subacute diffuse pneumonitis with dyspnea at rest, tachypnea, oxygen desaturation, nonproductive cough, and fever. However, the intensity of these signs and symptoms can vary, and in some immunocompromised children and adults, onset can be acute and fulminant. The chest radiograph often shows bilateral diffuse interstitial or alveolar disease; rarely, lobar, miliary, and nodular lesions or even no lesions are seen. The mortality rate in immunocompromised patients ranges from 5% to 40% if treated and approaches 100% if untreated.


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ETIOLOGY: Nomenclature for Pneumocystis species is in evolution. Pneumocystis jiroveci has been proposed, denoting the fact that Pneumocystis carinii only infects rats and not humans. At present, Pneumocystis carinii or P carinii f. sp. hominis continue to be used. Pneumocystis jiroveci is classified as a fungus on the basis of DNA sequence analysis. However, P jiroveci retains several morphologic and biologic similarities to protozoa, including susceptibility to a number of antiprotozoal agents but resistance to most antifungal agents. The 5- to 7-µm-diameter cysts contain up to 8 intracystic bodies.


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EPIDEMIOLOGY: Pneumocystis jiroveci is ubiquitous in mammals worldwide, particularly rodents, and has a tropism for growth on respiratory tract surfaces. Pneumocystis jiroveci isolates recovered from mice, rats, and ferrets are diverse genetically from each other and from human P jiroveci; isolates from one animal species do not cross-infect other animal species. Asymptomatic infection occurs early in life, with more than 85% of healthy children acquiring antibody by 20 months of age. Pneumocystis jiroveci often is found postmortem in lungs of infants with a diagnosis of sudden infant death syndrome, but a causal relationship is uncertain. In resource-limited countries and in . . . [Go to Full Text]


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This topic has been referenced by these articles:

  • Goldman, A. S., Goldman, L. R., Goldman, D. A. (2005). What Caused the Epidemic of Pneumocystis Pneumonia in European Premature Infants in the Mid-20th Century?. Pediatrics 115: e725-e736 [Abstract] [Full Version]  
  • Church, J. A. (2004). LETHAL T CELL IMMUNODEFICIENCY INDUCED BY CHRONIC COSTIMULATION VIA CD27-CD70 INTERACTIONS. Pediatrics 114: 552-553 [Full Version]  
  • King, S. M., Committee on Pediatric AIDS, , Canadian Paediatric Society, Infectious Diseases a, (2004). Evaluation and Treatment of the Human Immunodeficiency Virus-1--Exposed Infant. Pediatrics 114: 497-505 [Abstract] [Full Version]