Abstract: |
DNA amplification has identified P. carinii DNA in diverse biologic specimens, including the serum of patients with P. carinii pneumonia. To further examine the relationship between P. carinii DNA in serum and P. carinii infection, the corticosteroid-treated rat model of pneumocystosis was studied. By 4 weeks ofimmunosuppression, P. carinii DNA was detected in rat lungs and by 6 weeks, in their serum. P. carinii DNA persisted in lung tissue as long as 5 months after the withdrawal of steroids. Serum DNA disappeared 2 weeks after steroids were withdrawn. Nonimmunocompromised, sentinel rats housed near immunocompromised, P. carin;;-infected rats also were studied. Within 6 weeks, P. carin;;DNA became detectable in lung and by 8 weeks, in serum. P. cariniiDNA disappeared rapidly from lungs and sera after sentinel rats were isolated away from corticosteroid-treated rats. These findings support the contagious transmission of P. carinii and suggest facile development of P. carinii carrier states. © 1993 by The University of Chicago. |
Keywords: |
nonhuman; prospective study; polymerase chain reaction; animal; animal tissue; gene amplification; animal experiment; animal model; molecular sequence data; rat; lung; base sequence; rats; rats, sprague-dawley; immune deficiency; immunosuppressive treatment; dihydrofolate reductase; disease transmission; opportunistic infection; dna, fungal; dna template; lung homogenate; pneumocystosis; pneumocystis carinii; disease carrier; female; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; pneumonia, pneumocystis carinii
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