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The laboratory mouse was domesticated from fancy mice that arose from geographically diverse genetic origins. The diverse origins of the mouse also contributed to a lengthy list of infectious agents that are carried by mice. Despite years of microbial quality control, the burgeoning use of mice for research is causing a resurgence of infectious disease among laboratory mice. Infections can be introduced through mice, but also through biologic products such as serum, hybridomas, and transplantable tumors and through iatrogenic introduction by scientists. Retroviruses represent an important group of agents with significant effects upon mouse research, but the transmissible exogenous viruses are no longer an issue among laboratory mice. The diversity of other infectious agents induce a wide variety of effects upon cancer research, including immunomodulation, tumor graft rejection, misinterpretation of phenotype, modified carcinogenesis, and zoonotic risk. Prudent research practices require that microbial status of research mice does not necessarily have to be standardized among laboratories, but it must be defined so that research results are reproducible and valid.
The laboratory mouse was domesticated from fancy mice that arose from geographically diverse genetic origins. The diverse origins of the mouse also contributed to a lengthy list of infectious agents that are carried by mice. Despite years of microbial quality control, the burgeoning use of mice for research is causing a resurgence of infectious disease among laboratory mice. Infections can be introduced through mice, but also through biologic products such as serum, hybridomas, and transplantable tumors and through iatrogenic introduction by scientists. Retroviruses represent an important group of agents with significant effects upon mouse research, but the transmissible exogenous viruses are no longer an issue among laboratory mice. The diversity of other infectious agents induce a wide variety of effects upon cancer research, including immunomodulation, tumor graft rejection, misinterpretation of phenotype, modified carcinogenesis, and zoonotic risk. Prudent research practices require that microbial status of research mice does not necessarily have to be standardized among laboratories, but it must be defined so that research results are reproducible and valid.
Summary Adult CBA/J mice regularly showed a delayed response to intracerebral inoculation with LCM virus indicating an impaired cellular reactivity toward this agent. Viral antigen titers of spleens and kidneys were about equally high in congenitally infected CBA/J and NMRI mice sacrificed at different age levels, but the former animals, unlike those of the NMRI strain, failed to develop serum antibodies demonstrable either by direct or by indirect complement fixation. This result, together with the rare occurrence of glomerulonephritis in CBA/J carriers supports the concept that antibodies are involved in the pathogenesis of kidney disease in mouse strains with a high incidence of nephritis, for instance, NMRI carriers. Old CBA/J mice persistently infected with LCM virus frequently showed swollen and hemorrhagic mesenteric lymph nodes, a peculiar lesion not seen in uninfected animals of this breed or in NMRI mice of similar age, infected or normal. Thymic, renal and mammary tumors occurred at a very low rate in old CBA/J carriers. Possible correlations betweeen chronic LCM infection, tumor incidence and frequency of glomerulonephritis are discussed making reference to previous own work with different mouse strains and that of other investigators. Zusammenfassung Beobachtungen über “Späterkrankungen” und Tumorauftreten bei unterschiedlichen, congenital mit LCM‐Virus infizierten Labormäusestämmen II. Versuche mit Inzucht CBA/J‐Mäusen Erwachsene CBA/J‐Mäuse erkrankten nach cerebraler Injektion von LCM‐Virus regelmäßig verspätet, was auf eine verminderte zelluläre Reaktionsfähigkeit gegenüber diesem Erreger hinweist. Der Gehalt der Milz und Nieren an Virusantigen war bei congenital infizierten CBA/J‐Mäusen verschiedener Altersstufen ungefähr gleich hoch wie bei altersmäßig vergleichbaren Virusträgern des NMRI‐Stammes, doch bildeten die ersteren im Gegensatz zu NMRI‐Tieren keine, weder durch direkte noch durch indirekte Komplementbindung nachweisbaren Serumantikörper. Dieses Ergebnis, im Verein mit dem seltenen Vorkommen von Glomerulonephritis bei CBA/J‐Virusträgern, stützt die Auffassung, daß Antikörper an der Pathogenese der Nierenerkrankung bei solchen Mäusestämmen beteiligt sind, die eine hohe Nephritisquote aufweisen, so z. B. bei congenital infizierten NMRI‐Mäusen. Ältere persistent infizierte CBA/J‐Tiere zeigten häufig geschwollene und hämorrhagische Darmlymphknoten, eine eigenartige Veränderung, die weder bei nicht infizierten Mäusen dieser Zucht, noch bei infizierten oder normalen NMRI‐Tieren beobachtet wurde. Bei alten CBA/J‐Virusträgern wurden Thymus‐, Nieren‐ und Mammatumoren, jedoch nur in sehr geringer Zahl festgestellt. Mögliche Zusammenhänge zwischen chronischer LCM‐Infektion, Tumorbildung und Häufigkeit von Glomerulonephritis werden an Hand von früheren eigenen Versuchsergebnissen sowie von Befunden anderer Autoren diskutiert. Résumé Observations sur des (maladies retardées) et l'apparition de tumeurs chez différentes souches de souris de laboratoire infectées congénitalement avec un virus LCM II. Es...
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