Pneumocystis Pneumonia

 Pneumocystis Pneumonia.

P. K. Ghatak, MD

In 1980 the medical community was challenged by an outbreak of a new disease that was rampant in homosexual communities in the major US cities. Within a few months, it was found to be a viral infection. The patients were in the immune suppressed individuals and the virus was called HIV (human immunodeficient virus). An interstitial pneumonia was almost a constantly coexisted with the HIV infection. The organism was Pneumocystis jirovecii, a unicellular fungus, and the pneumonia was called PJP pneumonia.

The history of Pneumocystis interesting.

In 1090 Dr. Chagas was in pursuit for the causative organisms of Trypanosomiasis of South America. He discovered a few tiny organisms in the respiratory tract of some of the victims. He thought those were immature Trypanosome trophozoites. In 1909 Antonio Carnii found 3 cysts in the lung of children which were similar to Chagas' trypanosome but he did not think they were trypanosomes. In 1910 Delano of Pasture institute discovered similar cysts in a rat's lung and found that the organism had many features of a protozoan and named it Pneumocystis carnii. In 1999 molecular analysis of mRNA and mitochondria of the pneumocystis was conducted by Otto Jiroveci, a parasitologist from Czechoslovakia. He identified Galactosaminogalactan a signature for a fungus. The organism now classified as a unicellular fungus. Pneumocystis exists in nature in three morphological stages – Protozoite, Sporozoite and Cysts (spores). Distinct genomic variability exists between host specific member of the genera. For the humans, the pathogenic organism is called pneumocystis jirovecii. It was so named to, honor Otto Jiroveci's work.

PJP pneumonia.

This fungus in ubiquitous, and exists as a parasite in lungs of mammals and humans. The children acquire this fungus by 3 to 4 years of age. It spreads from person to person by being airborne. In good health, no adults or children show any ill effects of this parasitic fungus.

In severely immunodeppressed individuals, with a CD4 cell count of less than 200 micro L, the pneumocystis becomes an opportunist pathogen. In the lung, it produces an interstitial pneumonia. The infiltrates are perihiliar distribution is called a bat wing pattern. Like a viral interstitial pneumonia, the patients become severely hypoxic due to low oxygen diffusion capacity with a wide A-a gradient. Most severe infections produce acute respiratory syndrome. Various systemic symptoms develop due to tissue hypoxemia, specially cerebral manifestations. Other non-pulmonary features are – a. severe bone marrow depression producing pancytopenia, b. lymphadenopathy. c. cotton-wool exudates in the retina, d. thyroid gland enlargement and gastrointestinal symptoms.

Common symptoms are – fever, unproductive cough, chest pain, shortness of breath, cyanosis and tachycardia.

Diagnosis:

High LDH is a characteristic feature. Pneumocystis trophozoites and cysts are recovered by warm saline induced sputum and from Broncho alveolar lavage fluids.

Treatment:

Severely ill patients requires tracheal intubation and mechanical ventilation.

PJP are very sensitive to Trimethoprim-Sulfa-Methoxazol(TMP-SMX). Usually given by IV in acute situation. In tablet form, is used as chemoprophylaxis. Alternative to TMP-SMX chemoprophylaxis are Dapsone, Atovaquone and aerosolized Pentamidine.

Prognosis:

Before Retroviral therapy, the mortality from PJP pneumonia was 80-90 %.  The mortality is 10 to 20%.at present.

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