key: cord-0007450-bj99orvp
authors: Pifer, Linda L.
title: Pneumocystis carinii in Germ-Free Rats
date: 1984-10-03
journal: J Infect Dis
DOI: 10.1093/infdis/150.4.619
sha: f977fffe0444b4c9a013fa39c887d51f38d40c18
doc_id: 7450
cord_uid: bj99orvp

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. EM appearance of human enteric coronavirus (strain HECV-35). (le/t), Single virus particle in a fecal specimen; (right), immune aggregate by homologous antiserum.

the antisera to the two HECV strains and, to a lesser extent, antiserum to HCV OC43, reacted with the coronavirus-like particles in stools from all the positive patients by conventional IBM and also by solid-phase IBM [3] .

In summary: (1) In infants and young children with acute 619 gastroenteritis, fecal excretion of HECVs is more frequently detected than in age-matched controls; (2) HECV strains are antigenically related to HCV OC43, and their detection in feces is consistently associated with antibody response to HECV as well as to HCV OC43; (3) our results support the existence of HECV strains [4] and suggest that they could play an enteropathogenic role in infants and young children with acute gastroenteritis. GOIUSEPPE [1, 2] and would like to add a cautionary note from our own experience with "germ-free" Sprague-Dawley rats.

In May 1981, we purchased 70 germ-free, Cesarean-delivered, barrier-sustained Sprague-Dawley rats from the Charles River Company (Wilmington, Mass). These rats were shipped in sterile containers. Five rats that were randomly selected and killed immediately upon arrival in our laboratory were subsequently found to have Pneumocystis carinii organisms in their lung tissue. An order placed to the Harlan Sprague-Dawley Company (Indianapolis, Ind) for gnotobiotic rats yielded the same result -all six of the animals shipped were infected with P. carinii. The methods and the results of this serendipitous investigation have been published in detail and should serve as a warning to those who employ "germ-free" research animals [3] . The Charles River Company refunded us for their "germ-free" rats after I visited their facility and demonstrated appropriate histological techniques for screening for P. carinii. Since then, Dr. Hughes has ascertained that the animals purchased by him for use in his transmission studies [4, 5] were from a different isola-Please address requests for reprints to Dr. Linda Pifer, University of Tennessee Center for the Health Sciences, 956 Court Avenue, Room 3B09, Memphis, Tennessee 38163 tor maintained by the Charles River Company (personal communication) than the ones in which our rats were born.

We still do not know how gnotobiotic rats from two highly reputable breeders became infected with P. carin ii, especially since oral swabs and fecal cultures from the same animals were negative for growth. Possible routes include (1) undetected lapses in technique employed by the companies, (2) unusual resistance of P. carinii to physical and/or chemical agents, or (3) in utero transmission. Whatever the route, this experience underscores the need for great caution when attempting to reach conclusions based upon experiments conducted in gnotobiotic animals, especially when the companies breeding the animals do not screen for the infective organisms in question. LINDA L. PIFER University of Tennessee Center for the Health Sciences, Memphis, Tennessee

Human coronavirus OC43 serum inhibitor and neutralizing antibody by a new plaque-reduction assay

Immune electron microscopy as a method for the detection, identification, and characterization of agents non cultivable in an in vitro system

The use of protein A, from Staphylococcus References

The origin of Pneumocystis carinii (correspondence)

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Pneumocystis carinii infection in germ-free rats: implications for human patients

Natural mode of acquisition for de novo infection with Pneumocystis carinii

A natural source of infection due to Pneumocystis carinii