ABSTRACT
Some 90 years ago, Carlos Chagas the discoverer of Chagas’ disease, American trypanosomiasis, made an observation of pulmonary cysts in Schizotrypanum cruzi-infected individuals (Chagas 1909). This finding was followed up by Carinii working on rats infected with Trypanosoma lewisi. In these rats suffering from trypanosomiasis, lungs contained cysts similar to those observed by Chagas, which were considered as the schizogonic stage of the trypanosome. In 1912 the Delanoë couple in Paris redescribed and reached a different conclusion on the origin of the ‘pulmonary cysts of Carinii’ in the lungs of T. lewisi-infected rats. The ‘pneumocysts of Carinii’ were identified as a new parasite of rats by Delanoë and Delanoë and were called by them as Pneumocystis carinii in their 1912 publication (Delanoë and Delanoë 1912). This significant contribution is acknowledged in the current classification (Haase 1997). It took another 10 years before Vavra in Prague associated P. carinii with the severe plasma cell pneumonia affecting undernourished children in postwar Europe (Vavra and Kucera 1970; see also Gajdusek 1957). The original publication was followed by an article by Vavra and Jirovec a year later. However, for more than a decade the etiological link between pneumocystis and plasma cell pneumonia was disputed. Not only in the United States where only a few cases were seen, but also in European countries like Finland there was a reluctance to accept Pneumocystis as the etiological agent of plasma cell pneumonia (Stenbäck et al. 1968). Despite the fact that the high standards of neonatology brought down neonatal mortality to a record low, a premature baby only had a 50-50 chance of avoiding a deadly Pneumocystis infection at the Children’s hospital in Helsinki at that time. The seriousness of ‘plasma cell pneumonia’ in prematurely born babies in the 1950s (Vanek and Jirovec 1952; Gajdusek, 1957) can be compared to pneumocystis pneumonia (PCP) in AIDS 30 years later (Figure 12.1).
