New Nomenclature for the Genus <i>Pneumocystis</i>

Stringer, James R.; Cushion, Melanie T.; Wakefield, Ann E.

doi:10.1111/j.1550-7408.2001.tb00512.x

Cited by 77 publications

(45 citation statements)

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“…Although our data are in agreement with the lack of vertical transmission in rats, the rat pups included in the study by Hong et al were not collected by cesarean section, and thus, in utero infection cannot be definitively ruled out by their experimental design. Animal inoculation studies and genetic analyses have provided sufficient evidence that Pneumocystis organisms harbored by different mammalian hosts are distinct species (27). To date, few biological differences have been reported among the various Pneumocystis populations, but this is likely due to difficulties in conducting such studies rather than to lack of biological diversity.…”

Section: Vol 1 2002 Early Acquisition Of P Carinii In Rats 417mentioning

confidence: 99%

“…(Changes in the nomenclature of Pneumocystis were recommended at the Seventh International Workshop on Opportunistic Protists in Cincinnati, Ohio, in June 2001; thus, Pneumocystis carinii f. sp. carinii is referred to by its binomial, P. carinii, throughout this report [27].) Amplicons were produced from oral swabs up to 4 weeks after birth, the final time point of the study, suggesting that colonization may occur in neonatal rats and that these neonates could potentially serve as a reservoir of infection for the general rat population.…”

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Early Acquisition of Pneumocystis carinii in Neonatal Rats as Evidenced by PCR and Oral Swabs

et al. 2002

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The complete life cycle of Pneumocystis carinii has not been defined, but accumulating evidence suggests that the mammalian host may acquire this organism early in life. In the present study, the initial time of P. carinii acquisition was determined in rats by amplification of P. carinii DNA in oral swabs from seven sets of pups and dams and from fetal tissue obtained by cesarean section of three gravid female rats. DNA extracted from all samples was amplified by using PCR primers directed to the P. carinii mitochondrial large subunit rRNA. Amplicons were produced from 80% (28 of 35) of pups within 2 h after birth; from 97% (34 of 35) after 24 h, and in all of the serially sampled pups by 48 h. No P. carinii amplicons were produced from 48 fetuses or their placentae taken by cesarean section. Thus, P. carinii is acquired almost immediately after birth, and placental transmission occurs rarely, if ever, in rats.

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Section: Vol 1 2002 Early Acquisition Of P Carinii In Rats 417mentioning

confidence: 99%

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confidence: 99%

Early Acquisition of Pneumocystis carinii in Neonatal Rats as Evidenced by PCR and Oral Swabs

et al. 2002

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“…Pneumocystis pneumonia (PCP) in humans is caused by the opportunistic fungus Pneumocystis jiroveci (16,17). Several studies have demonstrated a significant association between sulfa drug prophylaxis of PCP in human immunodeficiency virus (HIV)-infected patients and the presence of dihydropteroate synthase (DHPS) mutations in samples of P. jiroveci (4,7,8).…”

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Genotypesof Pneumocystis jiroveci Isolates Obtained in Harare,Zimbabwe, and London, UnitedKingdom

Miller

Lindley

Ambrose

et al. 2003

Antimicrob Agents Chemother

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“…However, AIDS and other patients with prolonged immunodeficiency experience recurrent Pneumocystis jiroveci ( Pneumocystis carinii f. sp. hominis ) (3,4) infections. Also, some individuals cannot tolerate these drugs and suffer undesirable side effects.…”

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Comprehensive and definitive structural identities of Pneumocystis carinii sterols

Giner

Zhao

Beach

et al. 2002

Journal of Lipid Research

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Pneumocystis causes a type of pneumonia in immunodeficient mammals, such as AIDS patients. Mammals cannot alkylate the C-24 position of the sterol side chain, nor can they desaturate C-22. Thus, the reactions leading to these sterol modifications are particularly attractive targets for the development of drugs against fungal and protozoan pathogens that make them. In the present study, the definitive structures of 43 sterol molecular species in rat-derived Pneumocystis carinii were elucidated by nuclear magnetic resonance spectroscopy. Ergosterol, ⌬ 5,7 sterols, trienes, and tetraenes were not among them. Most (32 of the 43) were 24-alkylsterols, products of S -adenosyl-L -methionine:C-24 sterol methyl transferase (SAM:SMT) enzyme activity. Their abundance is consistent with the suggestion that SAM:SMT is highly active in this organism and that the enzyme is an excellent anti-Pneumocystis drug target. In contrast, the comprehensive analysis strongly suggest that P. carinii does not form ⌬ 22 sterols, thus C-22 desaturation does not appear to be a drug target in this pathogen. The lanosterol derivatives, 24-methylenelanost-8-en-3 ␤ -ol and ( Z )-24-ethylidenelanost-8-en-3 ␤ -ol (pneumocysterol), previously identified in human-derived Pneumocystis jiroveci , were also detected among the sterols of the rat-derived P. carinii organisms. Pneumocystis pneumonia (PcP) remains among the most prevalent opportunistic infections in immunocompromised individuals such as AIDS patients. It has becoming evident that the high incidence of PcP in AIDS patients is global and that the organism can infect other immunodeficient people such as patients undergoing chemotherapy for cancer or solid organ transplant (1, 2), children prior to becoming fully immunocompetent, and the elderly with diminished immune systems. Pneumocystis can also transiently colonize normal, healthy people and animals without causing overt symptoms of respiratory disorder. The combination of trimethoprim and sulfamethoxazole and other agents (e.g., pentamidine, atovaquone) used for prophylaxis and for clearing PcP has successfully reduced the number of deaths directly attributed to PcP. However, AIDS and other patients with prolonged immunodeficiency experience recurrent Pneumocystis jiroveci ( Pneumocystis carinii f. sp. hominis ) (3, 4) infections. Also, some individuals cannot tolerate these drugs and suffer undesirable side effects. The development of drug-resistant pathogen populations is of serious concern, making it imperative to develop a larger armamentarium of diverse drugs to circumvent these problems (5 Ϫ 7). Although the organism can be maintained in long-term, small-volume axenic cultures (8), growth is very slow and insufficient numbers of organisms are obtained for most biochemical studies. Thus, Pneumocystis remains an organism considered difficult to manipulate for experimental work. Despite this difficulty, much is now known about the organism's lipids from analyses performed on preparations purified from infected rat lungs (9 Ϫ 11...

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New Nomenclature for the Genus Pneumocystis

Cited by 77 publications

References 47 publications

Early Acquisition of Pneumocystis carinii in Neonatal Rats as Evidenced by PCR and Oral Swabs

Early Acquisition of Pneumocystis carinii in Neonatal Rats as Evidenced by PCR and Oral Swabs

Genotypesof Pneumocystis jiroveci Isolates Obtained in Harare,Zimbabwe, and London, UnitedKingdom

Comprehensive and definitive structural identities of Pneumocystis carinii sterols

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