Activation and Transmission in Rats of Infection with Pneumocystis

Hendley, J O; Weller, Thomas H.

doi:10.3181/00379727-137-35798

Cited by 49 publications

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“…Airborne transmission appears likely. Hospital outbreaks have been documented (27), and well-designed animal studies have provided evidence of direct transmission from host to host via airborne infective particles (9,26,41). It has been hypothesized that the main source of P. carinii is patients with PCP.…”

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confidence: 99%

Phylogeny of Pneumocystis carinii from 18 Primate Species Confirms Host Specificity and Suggests Coevolution

Demanche

Berthelemy

Petit³

et al. 2001

J Clin Microbiol

114

104

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Primates are regularly infected by fungal organisms identified as Pneumocystis carinii. They constitute a valuable population for the confirmation of P. carinii host specificity. In this study, the presence of P. carinii was assessed by direct examination and nested PCR at mitochondrial large subunit (mtLSU) rRNA and dihydropteroate synthetase (DHPS) genes in 98 lung tissue samples from captive or wild nonhuman primates. Fifty-nine air samples corresponding to the environment of different primate species in zoological parks were also examined. Cystic forms of P. carinii were detected in smears from 7 lung tissue samples corresponding to 5 New World primate species. Amplifications at the mtLSU rRNA gene were positive for 29 lung tissue samples representing 18 different primate species or subspecies and 2 air samples corresponding to the environment of two simian colonies. Amplifications at the DHPS gene were positive for 8 lung tissue samples representing 6 different primate species. Direct sequencing of nested PCR products demonstrated that a specific mtLSU rRNA and DHPS sequence could be attributed to each primate species or subspecies. No nonhuman primate harbored the human type of P. carinii (P. carinii f. sp. hominis). Genetic divergence in primate-derived P. carinii organisms varied in terms of the phylogenetic divergence existing among the corresponding host species, suggesting coevolution.

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confidence: 99%

Phylogeny of Pneumocystis carinii from 18 Primate Species Confirms Host Specificity and Suggests Coevolution

Demanche

Berthelemy

Petit³

et al. 2001

J Clin Microbiol

114

104

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“…The rat model of P. carinii pneumonia (Pcp) has its roots in studies that showed that P. carinii infections can be provoked by treating rats with chemical immunosuppressants (18,24,38,53). These infections appeared to be caused by growth of P. carinii that was present in the rats at the time of immunosuppression (reactivation of latent infections).…”

Section: Pneumocystis Cariniimentioning

confidence: 99%

“…Most, if not all, commercial rat colonies harbor P. carinii in a latent form, where it can persist for up to a year (103,162,178). It seems most plausible that P. carinii maintains itself in rat colonies via airborne transmission from older rats to neonates, and evidence for airborne transmission has been obtained in laboratory settings (53,55,176). However, other mechanisms of transmission from adults to neonates have not been excluded, and observations suggestive of transplacental transfer have been reported (17).…”

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confidence: 99%

“…Reliance on rats as the source of P. carinii has had its advantages and disadvantages, which have shaped the course of research on antigenic variation. It is important, therefore, to preface this review with a brief description of the general features of rat models of P. carinii infection.The rat model of P. carinii pneumonia (Pcp) has its roots in studies that showed that P. carinii infections can be provoked by treating rats with chemical immunosuppressants (18,24,38,53). These infections appeared to be caused by growth of P. carinii that was present in the rats at the time of immunosuppression (reactivation of latent infections).…”

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Genetics of Surface Antigen Expression inPneumocystis carinii

Stringer

Keely

2001

Infect Immun

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This article reviews the molecular genetic data pertaining to the major surface glycoprotein (MSG) gene family of Pneumocystis carinii and its role in surface variation and compares this fungal system to antigenic variation systems in the protozoan Trypanosoma brucei and the bacteria Borrelia spp. PNEUMOCYSTIS CARINIIPneumocystis carinii is a fungus that can cause pneumonia in immunocompromised mammals (100, 174). While P. carinii was recognized nearly a century ago and has been a significant human pathogen since the beginning of the AIDS epidemic, this organism is not well understood. Much of the blame for the lack of basic information about this organism and its natural history can be placed on its failure to grow well in culture. Populations of the organism can be maintained in broth culture, but growth in culture has not been good enough to allow either production of large numbers or derivation of clonally derived stocks (95). Therefore, in vitro culture has been of limited utility for studying the genetics and biochemistry of P. carinii.By contrast, large numbers of organisms can be routinely obtained from laboratory animals. Most of what is known about P. carinii has been learned from studies with animals, and most of what is known about the surface antigen genes was determined from studies on organisms from laboratory rats. Reliance on rats as the source of P. carinii has had its advantages and disadvantages, which have shaped the course of research on antigenic variation. It is important, therefore, to preface this review with a brief description of the general features of rat models of P. carinii infection.The rat model of P. carinii pneumonia (Pcp) has its roots in studies that showed that P. carinii infections can be provoked by treating rats with chemical immunosuppressants (18,24,38,53). These infections appeared to be caused by growth of P. carinii that was present in the rats at the time of immunosuppression (reactivation of latent infections). Most, if not all, commercial rat colonies harbor P. carinii in a latent form, where it can persist for up to a year (103,162,178). It seems most plausible that P. carinii maintains itself in rat colonies via airborne transmission from older rats to neonates, and evidence for airborne transmission has been obtained in laboratory settings (53,55,176). However, other mechanisms of transmission from adults to neonates have not been excluded, and observations suggestive of transplacental transfer have been reported (17).Even though latent infections are common in laboratory rats, simply immunosuppressing rats does not always lead to the production of large numbers of organisms per animal. This observation led to the implementation of a protocol known as the natural transmission method. In this method, rats are bred in colonies known to harbor latent infections. Young animals in such colonies are immunosuppressed and housed in openair cages. Some or all of the immunosuppressed animals develop heavy infections. When new young animals from another source (such as a...

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“…and various protozoa. Vavra and Kucera (182) (12,55,76 (31,49,159), and outbreaks in organ transplant units (72,161,176) suggest person-to-person transmission. A report of increased incidence of Pneumocystis infection in immunosuppressed patients without AIDS in an institution where there was an increased incidence of AIDS is suggestive (74 (101) showed that none of seven infants had antibody specific to P. carinii but that seven of eight normal adults did have specific antibody.…”

Section: Taxonomymentioning

confidence: 99%

Pneumocystis carinii, an opportunist in immunocompromised patients

Bartlett

Smith

1991

Clin Microbiol Rev

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Pneumocystis carinii has been recognized as a cause of pneumonia in immunocompromised patients for over 40 years. Until the 1980s, Pneumocystis pneumonia (pneumocystosis) was most often seen in patients undergoing chemotherapy for malignancy or transplantation. Infection could be prevented by trimethoprim-sulfamethoxazole prophylaxis; thus, it was an uncommon clinical problem. With the onset of the AIDS epidemic, Pneumocystis pneumonia has become a major problem in the United States because it develops in approximately 80% of patients with AIDS and because almost two-thirds of patients have adverse reactions to anti-Pneumocystis drugs. Thus, physicians and laboratories in any community may be called upon to diagnose and provide care for patients with Pneumocystis pneumonia. The classification of the organism is currently controversial, but it is either a protozoan or a fungus. P. carinii appears to be acquired during childhood by inhalation and does not cause clinical disease in healthy persons but remains latent. If the person becomes immunosuppressed, the latent infection may become activated and lead to clinical disease. Damage of type I pneumocytes by Pneumocystis organisms leads to the foamy alveolar exudate which is characteristic of the disease. Diagnosis is established by morphologic demonstration of Pneumocystis organisms in material from the lungs. Current efforts to find better anti-Pneumocystis drugs should provide more effective therapy and prophylaxis.

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Activation and Transmission in Rats of Infection with Pneumocystis

Cited by 49 publications

References 0 publications

Phylogeny of Pneumocystis carinii from 18 Primate Species Confirms Host Specificity and Suggests Coevolution

Phylogeny of Pneumocystis carinii from 18 Primate Species Confirms Host Specificity and Suggests Coevolution

Genetics of Surface Antigen Expression inPneumocystis carinii

Pneumocystis carinii, an opportunist in immunocompromised patients

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