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Biomedical subjects

R O Jacoby

Publications and source records attributed to R O Jacoby.

At least 55 records · Page 3Linked to original sources
PubMed1990

Infection of SDAV-immune rats with SDAV and rat coronavirus.

Infection of rats with sialodacryoadenitis virus (SDAV) or rat coronavirus (RCV) is acute and self-limiting, and elimination and control of either virus is based on the assumption that recovered rats are immune to reinfection. To test this hypothesis, we examined whether SDAV-immune rats could be infected with RCV or reinfected with SDAV. Sprague Dawley (SD) rats were inoculated intranasally with SDAV or with culture medium alone and serial SDAV antibody titers were obtained. Eleven months after inoculation, when antibody titers had stabilized, SDAV-immune and nonimmune rats were challenged with SDAV or RCV, and euthanatized 3 or 6 days later. SDAV-immune rats challenged with SDAV or RCV manifested acute rhinitis associated with virus antigen by 3 days after inoculation, but no lesions or antigen were subsequently found in the lower respiratory tract, salivary glands or lacrimal glands. There was also a marked anamnestic increase in antibody titer by 6 days after challenge. SDAV-immune rats challenged with SDAV or RCV also transmitted infection to nonimmune cage mates. This study indicates that 11 months after primary infection with SDAV, rats can be infected with SDAV or RCV, but that the severity of disease is significantly reduced.

Animals↗
PubMed1989

Persistence of rat parvovirus in athymic rats.

Euthymic (SD or outbred rnu/+) and athymic (rnu/rnu) rats were inoculated oronasally or intraperitoneally with the RV-Y strain of rat virus when they were 2 days or 4 weeks old. Clinical signs of infection in athymic infants were similar to those in euthymic infants, but significantly more athymic infants died. Some infants developed anemia and thrombocytopenia. After inoculation of infants. RV-Y was detected in surviving euthymic rats for 7 weeks and in surviving athymic rats for at least 10 weeks. After oronasal inoculation of 4 week-old rats no clinical illness was observed. RV-Y persisted less than 6 weeks in juvenile euthymic rats but at least 12 weeks in athymic juvenile rats. Intraperitoneal inoculation of juveniles resulted in infection for at least 6 weeks. The antibody response of athymic rats to RV-Y was significantly reduced compared to that of euthymic rats. These studies indicate that T cell deficiency increases the severity and duration of RV infection and imply that T cells are required for the full expression of resistance to RV infection. They also suggest that RV-Y induced anemia could serve as a model for human parvovirus-induced anemia.

Aging↗
PubMed1989

Evidence that NK cells and interferon are required for genetic resistance to lethal infection with ectromelia virus.

C 57 BL/6 mice developed resistance to lethal intravenous challenge with virulent (Moscow strain) ectromelia virus between 2 and 3 weeks of age. The fraction of C57 BL/6 mice in which virus was detected in spleen was significantly lower than for DBA/2 mice by day 3. Thereafter, C 57 BL/6 mice had significantly reduced virus titers in spleen compared with those of DBA/2 mice. Resistance was abrogated by treatment with anti-asialo GM1 gammaglobulin, which blocks NK cell activity, or with anti-interferon (IFN) alpha, beta. C 57 BL/6 mice carrying the bg/bg mutation, associated with a deficiency of NK cells, were highly susceptible to lethal infection as were athymic mice derived from a resistant genetic background. Virus titers in spleens of C 57 BL/6 mice treated with anti-asialo GM1 or anti-IFN alpha, beta were significantly higher 4 days after virus challenge than were titers in C 57 BL/6 mice treated with normal rabbit serum. The results strongly suggest that genetic resistance to lethal ectromelia virus infection requires non-specific host defenses such as NK cells and IFN alpha, beta that are activated during the first 3 to 4 days of infection.

Aging↗
PubMed1989

Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. V. Genetics of resistance to the Moscow strain.

The genetics of resistance to the Moscow strain of ectromelia virus was examined in crosses derived from resistant C57BL/6 (B6) and susceptible DBA/2 (D2) mice. Infection with 10(1) to 10(5) PFU of virus resulted in mortalities of 90 to 100% of D2, 0% of B6 and 0 to 3% of (B6 x D2) F1 mice by day 21. Among F1 x D2 backcross progeny, 49% of male and 18% of female mice died. Reciprocal backcrossing did not alter male or female mortality rates. These data are consistent with a single autosomal dominant gene controlling resistance to ectromelia in male mice and at least one additional dominant sex-limited gene controlling resistance in female mice. Fewer male F2 mice died than were predicted based on single-locus control and 32% of recombinant inbred (RI) strains derived from B6 and D2 progenitors expressed non-parental phenotypes. Therefore, additional resistance genes, not expressed in backcross mice, were apparently expressed in F2 mice and RI strains.

Animals↗
PubMed1988

Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. IV. Studies with the Moscow strain.

The pathogenesis and transmission of infection with the Moscow strain of ectromelia virus were studied in inbred mice. BALB/cAnNcr had high morbidity and mortality and C57BL/6Ncr (B6) mice had high morbidity and low mortality. Virus was detected in B6 mice for 2 weeks after subcutaneous (s.c.) inoculation and infected mice developed lesions compatible with acute mousepox. B6 inoculated by footpad transmitted infection to cagemates for up to five weeks and soiled cages that had housed infected mice were infectious for three weeks. S.c.-inoculated B6 mice also transmitted by contact for 2 weeks. Transmission was attributed to oronasal excretion of virus. Airborne transmission of infection between adjacent cages occurred at a low rate. Ectromelia virus-free progeny were derived from previously infected dams. These studies indicate that the highly virulent and infectious Moscow strain of ectromelia virus caused self-limiting infection in inbred mice and that direct contact is the most efficient means of transmission. These findings support the concept that mousepox can be contained by husbandry practices that minimize or eliminate the spread of infection by direct contact or fomites.

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PubMed1988

The pathology of "sheep-associated" malignant catarrhal fever in the hamster.

Lesions induced in hamsters by inoculation with the "sheep-associated" agents of malignant catarrhal fever (SA-MCF) isolated from a red deer (Cervus elaphus), designated D/1 and of bovine origin (C/2), are described. Clinical signs in hamsters inoculated with the D/1 isolate occurred as early as 13 days after infection although the mean incubation period in animals that developed signs was 27 days. Increased numbers of polymorphonuclear leucocytes were present in the blood of clinically affected hamsters. Gross lesions included erosions of epithelium in the buccal cavity, haemorrhage of the forestomach, dilated fluid-filled intestines and enlargement of the mesenteric lymph node. Microscopic lesions were widespread throughout the body but had a predilection for epithelial surfaces. They consisted of hyperplasia of certain lymph nodes, vasculitis and interstitial accumulations of mononuclear cells of lymphoid appearance in non-lymphoid tissues. Cytolysis was also seen. Lesions produced by the C/2 isolate were similar and both isolates produced disease comparable with that seen in naturally occurring cases in cattle and deer. It is suggested that disease might arise through a dysfunction of the immune system following infection of host large granular lymphocytes by the SA-MCF agent, in a way similar to that suggested for the rabbit.

Animals↗
PubMed1988

Transmission of wildebeest-associated and sheep-associated malignant catarrhal fever to hamsters, rats and guinea-pigs.

Wildebeest-derived malignant catarrhal fever (WD-MCF) was transmitted to hamsters, rats and guinea-pigs by inoculation of rabbit lymphoid cells infected with alcelaphine herpesvirus-1, strain C-500. Sheep-associated MCF (SA-MCF) was transmitted to hamsters by inoculation of lymphoid cells from rabbits affected with SA-MCF derived from deer. Mice were refractory to both forms of the disease. With both forms of MCF, the incubation period during initial transmission varied from 21 to 90 days and disease was readily passaged in rodents by inoculation of live lymphoid cells. Clinical signs in hamsters most closely resembled those described for naturally occurring MCF. Results given here and in two following papers indicate that rodents are useful models to study the aetiology and pathogenesis of both forms of MCF.

Animals↗
PubMed1988

The pathology of wildebeest-associated malignant catarrhal fever in hamsters, rats and guinea-pigs.

Lesions typical of malignant catarrhal fever were found in hamsters, rats and guinea-pigs inoculated with a rabbit-passaged strain (C-500) of alcelaphine herpesvirus-1. Lesions found during primary passage included proliferation of lymphoid tissues, multisystemic mononuclear cell infiltrates, vasculitis and necrosis, especially in the alimentary tract. The character, severity and distribution of lesions remained stable in affected hamsters during serial passage of disease, whereas lympho-proliferation became dominant in rats. The lesions in rats typically affected lymph nodes, heart and kidney and appear similar to those caused by oncogenic herpesviruses. Because rodents are susceptible to malignant catarrhal fever, the prospect is advanced that they can be used to elucidate the pathogenesis of both lymphoproliferative and cytolytic aspects of the disease.

Animals↗
PubMed1988

An animal model for Lyme arthritis.

A model of Lyme arthritis has been developed in laboratory rats. Intraperitoneal inoculation of a low-passage tick isolate of B. burgdorferi into neonatal and weanling LEW/N rats resulted in multisystemic infection and arthritis. Spirochetes were isolated from blood, liver, kidney, spleen, brain, and joints of inoculated rats. Arthritis, associated with the presence of spirochetes, developed in multiple joints by day 14 and persisted through day 90 after inoculation. Arthritic lesions resembled those found in human Lyme disease lesions. Lesions were not found in other organs, although spirochetes were present. Neonatal F344 and SD rats were also susceptible to infection and induction of arthritis. Three different isolates of B. burgdorferi were shown to be pathogenic. Pathogenicity of one isolate was retained after at least 11 in vitro passages. Formalin-killed spirochetes were not pathogenic. Other features of the Lyme disease complex have yet to be seen in the rat, but long-term studies are required to completely define the rat model. This highly reproducible model should allow in-depth studies on the pathogenetic mechanisms of this important human disease.

Animals↗
PubMed1988

Transmission of experimentally-induced rat virus infection.

The duration of transmission of rat virus (RV) infection was determined using Sprague-Dawley rats inoculated oronasally as juveniles (4 weeks old) or as infants (2 days old). Contact transmission from rats inoculated as juveniles was detected for 3 weeks, whereas transmission from rats inoculated as infants occurred for 10 weeks. Transmission continued for at least 7 weeks after seroconversion occurred in rats inoculated as infants. Two of three rats that had ceased to transmit infection harbored infectious virus as detected by explantation of kidney. Intrauterine transmission occurred only after pregnant dams were inoculated with large doses of virus and was more efficient when virus was inoculated intravenously than by the oronasal route. Enzyme immunoassay antibody titers to RV in offspring of previously infected dams decreased steadily during the first 13 weeks of life and 27 of 29 offspring tested by immunofluorescence assay at 12 or 13 weeks of age were seronegative. These results indicate that RV was transmitted by rats inoculated as infants for long periods after seroconversion occurred. They also suggest that the offspring of previously-infected dams were not infected. In utero transmission of RV-Y is unlikely to occur after oronasal inoculation unless rats are exposed to large doses of virus.

Animals↗
PubMed1987

The pathogenesis of rat virus infection in infant and juvenile rats after oronasal inoculation.

The pathogenesis of rat virus (RV) infection was studied in random-bred Sprague-Dawley rats after oronasal inoculation of a recent RV isolate designated RV-Yale (RV-Y). RV-Y was pathogenic for rats inoculated as infants (2 days) whereas rats inoculated as juveniles (4 weeks) had asymptomatic infection and no lesions. Rats inoculated as infants developed pantropic infection accompanied by hepatic necrosis, granuloprival cerebellar hypoplasia and hemorrhagic encephalopathy. Virological and serological studies showed that virus could persist in inoculated rats for at least 35 days and for at least 28 days after seroconversion was first detected. Immunohistochemical results indicated that RV-Y infects tissues conducive to virus excretion including kidney and lung. RV-Y also was found in genital tissues of some rats. Athymic juvenile rats inoculated intraperitoneally with RV-Y had a poor humoral immune response and harbored infectious virus for at least 3 weeks, whereas infection in euthymic control rats was detected for 1 week. These studies indicate that RV-Y can persists in the presence of humoral immunity and suggest that transmission of infection could occur for a substantial period after seroconversion. They also suggest that immunodeficient rats have increased susceptibility to persistent infection.

Aging↗
PubMed1987

Effect of vaccination on the clinical response, pathogenesis and transmission of mousepox.

The effects of vaccination with the IHD-T strain of vaccinia virus on the course and severity of ectromelia virus infection was investigated in BALB/c mice. Protection from lethal mousepox occurred when mice were vaccinated and challenged on the same day and protection persisted for at least 9 months. Vaccinated mice were not protected from infection or from lesions, but necrotic lesions in vaccinated mice were usually mild and were accompanied by inflammation, whereas necrosis in unvaccinated mice was severe and not accompanied by inflammation. Inoculated feet of previously vaccinated mice contained infectious ectromelia virus for at least 28 days. Vaccinated-challenged mice transmitted infection to non-immune cagemates for up to 2 weeks, but only rarely transmitted virus to vaccinated cagemates. These results emphasize that vaccination protects mice against lethal mousepox, but it does not prevent infection. In addition, vaccination reduces, but does not eliminate, transmission of infection to non-immune and immune mice.

Animals↗
PubMed1987

Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. I. Clinical responses.

Clinical responses to infection with ectromelia virus strain NIH-79 were determined in several strains of inbred mice. All mice were equally susceptible to infection, but mortality was strain dependent. BALB/c AnNCr, A/JNCr, DBA/2NCr and C3H/He/NCr MTV- mice were highly susceptible to lethal infection whereas AKR/NCr and SJL/NCr mice were moderately susceptible and C57BL/6NCr mice were highly resistant. Death rates were influenced strongly by virus dose and by route of inoculation. High doses were associated with early and high mortality. For a given dose, intraperitoneal inoculation resulted in the highest mortality and death rates were progressively reduced in mice inoculated by the footpad, subcutaneous and intranasal routes. Footpad swelling was prominent in resistant mice and in survivors among susceptible strains. Deaths among AKR and SJL mice were sporadic and often occurred late irrespective of virus dose. It is suggested that this pattern could be influenced by secondary contact infections or by immunologic injury associated with host responses to ectromelia virus.

Animals↗
PubMed1987

Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. II. Pathogenesis.

The pathogenesis of mousepox due to infection with ectromelia virus strain NIH-79 was characterized in genetically susceptible (BALB/cAnNCr) and genetically resistant (C57BL/6NCr) mice. BALB/c mice inoculated subcutaneous (s.c.) or intranasally (i.n.) had high mortality. Most mice died within 7 days from severe necrosis of the spleen and liver. Necrotic foci in livers of BALB/c mice that survived beyond 7 days often were accompanied by mononuclear cell infiltrates and by hyperplasia of lymphoid tissues. C57BL/6 mice inoculated by either route remained asymptomatic and necrotic lesions were mild or absent, whereas focal non-suppurative hepatitis and lymphoid hyperplasia were prominent. Infectious virus and viral antigen were distributed widely in tissues of BALB/c mice, but had limited distribution in C57BL/6 mice. Both mouse strains had infection of the respiratory tract, genital tract, oral tissues and bone marrow, and BALB/c mice also had infection of the intestines. Both strains also developed serum antibody to vaccinia virus antigen after infection. The results show that ectromelia virus occurs in tissues conducive to mouse to mouse transmission and that the severity and character of mousepox lesions correlate directly with resistance and susceptibility to infection. They also support the concept that cellular immunity contributes to survival from infection.

Animals↗
PubMed1987

Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. III. Experimental transmission of infection and derivation of virus-free progeny from previously infected dams.

The incidence and duration of transmission of infection with ectromelia virus strain NIH-79 was tested in innately resistant (C57BL/6) and innately susceptible (BALB/c) inbred mice. Transmission by C57BL/6 index mice occurred through 3 weeks and by BALB/c index mice through 4 weeks, although the duration of infection in individual index mice was often shorter. Soiled caging that previously housed infected mice was inconsistently infectious. Transmission was high in cages where infected mice died and were cannibalized by cagemates, but was low to moderate in cages where there was no cannibalism. Infected mice that were bred 6 weeks after they were infected, delivered virus-free progeny and did not transmit infection to their non-immune breeding partners. Sentinel mice housed in the room with experimentally infected mice were seronegative for antibody to ectromelia virus and to other murine viruses. These results support the view that infection with NIH-79 virus is typically short-lived. They also indicate that breeding of recovered mice can save valuable colonies that have been exposed to ectromelia virus.

Animals↗
PubMed1987

Stability of ectromelia virus strain NIH-79 under various laboratory conditions.

Ectromelia virus strain NIH-79 was suspended in fetal bovine serum (FBS), minimum essential medium, Hanks' base plus 10% FBS (MEMH + FBS), phosphate-buffered saline (PBS) or PBS plus 50% glycerol (PBS + G). Suspensions were held as liquids or as dry spots at various temperatures. Virus was most stable in FBS and least stable in PBS + G at 4 degrees C, room temperature (23-25 degrees C) or 37 degrees C. Virus held at 4 degrees C was more stable than virus held at higher temperatures, irrespective of supporting medium. Dried spots of blood or serum from ectromelia virus-infected mice remained infectious at room temperature for 11 days and 4 days, respectively. Dried spots of FBS that contained virus were infectious for 5 days, whereas virus retained infectivity for 1 day after drying in other media. Virus was inactivated completely in 10% serum in PBS exposed to 60 degrees C for 30 minutes. Virus was inactivated completely in slices of infected liver and spleen immersed in 10% neutral buffered formalin for 20 hours. These results show that the stability of ectromelia virus strain NIH-79 is medium and temperature dependent and that rapid inactivation occurs after treatments routinely used in diagnostic and research procedures.

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