Biomedical subjects

R O Jacoby

Publications and source records attributed to R O Jacoby.

90 records · Page 5Linked to original sources

PubMed1978

An outbreak of cecal mucosal hyperplasia in hamsters.

Cecal mucosal hyperplasia associated with diarrhea, runting, and high mortality in suckling and weanling hamsters occurred as a natural disease outbreak in a production colony. Young hamsters were runted, and their perineal hair was stained and matted with liquid feces. Their ceca were thickened, contracted, congested, and had scant luminal content. There were severe hyperplasia of cecal crypts, accompanied by increased mitotic activity, inflammation, and focal mucosal erosion. A variety of bacteria was isolated, but none was considered pathogenic. No relationship of cecal hyperplasia to transmissible ileal hyperplasia of hamsters was found. Hyperimmune serum from hamsters with transmissible ileal hyperplasia did not react by immunofluorescence against hyperplastic cecal mucosa. Electron microscopy did not reveal a caustive agent. Transmission attempts have been unsuccessful. Cecal mucosal hyperplasia is apparently a newly discovered disease entity in hamsters with the clinical sign of diarrhea.

Animals↗

PubMed1977

Experimental infection of adult axenic rats with Parker's rat coronavirus.

The pathogenesis of Parker's Rat Coronavirus (PRCV) was studied in axenic CD rats. Three to four 9 to 10 week old rats were euthanized daily for eight days after intranasal inoculation. Rats remained free of clinical disease. Virus was recovered from the nasopharynx and trachea after twenty-four hours and from the lung by day three but was not detected in respiratory tract after seven days. Viral antigen was detected by indirect immunofluorescence in the mucosal epithelium of upper respiratory tract and in pulmonary alveolar septae from day two to six postinoculation. Acute rhinitis developed by day two and was associated with mild focal necrosis of respiratory mucosal epithelium. Mild nonsuppurative tracheitis and multifocal interstitial pneumonia appeared by day five and persisted through day eight. Dacryoadenitis did not occur, sialoadenitis was detected in only three rats and virus was recovered from only one submaxillary salivary gland. This experiment indicates that PRCV can be a primary pathogen for the respiratory system of adult rats. In contrast to sialodacryoadenitis (SDA) virus the tropism of PRCV for salivary and lacrimal glands is low.

Animals↗

PubMed1977

Respiratory infection in mice with sialodacryoadenitis virus, a coronavirus of rats.

Sialodacryoadenitis virus (SDAV), a coronavirus of rats, evoked both serum neutralization and complement fixation antibody responses when inoculated intranasally in mice. Weanling gnotobiotic CD-1 mice inoculated intranasally with 10(3.0) mean tissue culture infective doses of SDAV remained asymptomatic. Virus was recovered from the nasopharynx, trachea, and lung from day 2 to day 7. Viral antigen was readily detected by indirect immunofluorescence in the lung but rarely in the nasopharynx. Infected mice developed interstitial pneumonia. Susceptible mice contact exposed to experimentally infected mice developed antibody to SDAV. Epizootiological studies indicated that retired breeder mice can have complement-fixing antibody to SDAV and mouse hepatitis virus (MHV) in the absence of MHV infection. These studies show that SDAV is infectious for mice and can be a pathogen for the respiratory system. Thus, SDAV infection of mice may be responsible for spurious seroconversions to MHV.

Animals↗

PubMed1976

A canine distemper model of virus-induced anergy.

For development of an animal model of virus-induced anergy, the effect of canine distemper virus (CDV) upon cell-mediated immunity in dogs was investigated. First, canine cutaneous reactions and in vitro lymphocyte responses to soluble protein antigens were characterized. Dogs immunized with picryl guinea pig albumin and with keyhole limpet hemocyanin (both in complete Freund's adjuvant) responded reproducibly to intracutaneous challenge with these antigens. Reactivity peaked in 20-40 days (maximal induration, 6-50 mm). Lymphocytes from these animals responded in vitro to stimulation with keyhole limpet hemocyanin or purified protein derivative. This stimulation was antigen-specific and was maximal on day 6 of culture. Infection with CDV depressed cutaneous reactivity and lymphocyte response in vitro to antigens and mitogens. This effect was transient in animals previously vaccinated with attenuated CDV; however, gnotobiotic puppies (susceptible to CDV) had prolonged depression of cell-mediated immunity and lymphopenia. Some of these animals developed neurologic symptoms and died. The findings indicate that CDV infection is a potentially useful model for study of virus-induced depression of T (thymus)-cell responses and support the hypothesis that there is more than one mechanism responsible for this phenomenon.

Animals↗

PubMed1976

Genetic resistance to lethal flavivirus encephalitis. I. Infection of congenic mice with Banzi virus.

Adult C3H/RV mice were highly resistant and adult C3H/He mice were highly susceptible to lethal encephalitis after intraperitoneal inoculation of Banzi virus (flavivirus), but the infectivity of the virus was the same for both strains of mice. Yields of virus were similar from lymphoid tissues of C3H/He and C3H/RV adult mice, but titers of virus in the brain were significantly lower in C3H/RV mice. Lesions of encephalitis developed in both strains but remained mild and self-limiting in C3H/RV mice, whereas widespread necrosis occurred in the brains of C3H/He mice. Resistance to lethal infection after intraperitoneal inoculation developed postnatally in C3H/RV mice and did not reach significant levels until mice were at least four weeks old. Mortality rates among C3H/RV and C3H/He mice were comparable after intracerebral inoculation of virus. Yields of virus, brain lesions, and immunofluorescent staining patterns for viral antigen were similar in intracerebrally inoculated C3H/He and C3H/RV mice. Results indicate that tissues of resistant and susceptible mice in vivo can support replication of Banzi virus about equally well. Thus, genetic resistance to lethal infection with Banzi virus in these strains of mice does not seem to be solely dependent on resistance of tissues to viral replication.

Animals↗

PubMed1976

Genetic resistance to lethal flavivrus encephalitis. II. Effect of immunosuppression.

Genetic resistance of C3H/RV mice to lethal infection with Banzi virus (flavivirus) was severely compromised by immunosuppression with cyclophosphamide, sublethal X-irradiation, or thymus (T-) cell depletion. The mortality rate among immunosuppressed mice was usually 100%, but average survival times were shorter for mice treated with cyclophosphamide or for X-irradiated mice (10 days) than for T-cell-depleted mice (17 days). Mice treated with cyclophosphamide had high titers of virus in brain, lymphoid tissues, pancreas, and serum. Viral antigen was widespread in brain and pancreas, and mice developed nonsuppurative meningoencephalitis and pancreatitis. Yields of virus, spread of viral antigen, and lesions in T-cell-depleted mice were similar but less severe. Mice treated with cyclophosphamide did not have detectable hemagglutination-inhibiting antibody. T-cell-depleted mice developed hemagglutination-inhibiting antibody but were not protected from lethal infection. These results indicate that genetic resistance of C3H/RV mice to Banzi virus requires immunological factors, and that T-cells play a significant role in resistance to infection with Banzi virus.

Animals↗

PubMed1976

Keratoconjunctivitis associated with sialodacryoadenitis in rats.

A high incidence of keratoconjunctivitis was observed in a closed colony of inbred Lewis/Wistar rats. Clinical signs including blinking, ocular discharge, circumcorneal flush, corneal opacity, ulceration, pannus, hypopyon, and hyphema were observed at about three weeks of age. Acute disease subsided by six weeks of age, but some lesions progressed to low-grade chronic keratitis. Six per cent of affected rats developed megaloglobus, which usually appeared by three weeks of age. Lesions included focal or diffuse interstitial keratitis, corneal ulceration, anterior synechia, and inflammatory exudate in the anterior chamber. A high incidence of lenticular and retinal degeneration was associated with megaloglobus. Most affected rats also had harderian dacryoadenitis. Sialodacryoadenitis virus (SDA) was recovered from nasal washes, but not from affected eyes. Serological evidence indicated that SDA virus infection was widespread in the colony.

Animals↗

PubMed1975

Pathogenesis of sialodacryoadenitis in gnotobiotic rats.

The pathogenesis of sialodacryoadenitis was studied in gnotobiotic CD rats inoculated intranasally with the causal virus. Virus replication was detected sequentially in the nasopharynx, tracheobronchial tree, cervical lymph nodes, submaxillary and parotid salivary glands, exorbital gland, and Harderian gland. Acute rhinitis appeared within 2 days after inoculation, and salivary glands had lesions in 4 days. Early changes in salivary and exorbital glands were characterized by necrosis of ductal epithelium, which rapidly progressed to widespread acinar necrosis, marked inflammation, edema and total effacement of glandular architecture. Harderian glands also had massive necrosis of tubuloalveolar units. Repair in all glands was characterized by marked squamous metaplasia of tubuloalveolar units. Repair in all glands was characterized by marked squamous metaplasia of ducts. Neutralizing and complement-fixing antibodies were detected in 7 days, and there was a concomitant decrease in tissue-virus titers. There was no detectable evidence for hematogenous spread of virus or for retrograde infection by way of major salivary ducts.

Animals↗

PubMed1975

Experimental transmission of atypical ileal hyperplasia of hamsters.

Conditions for oral transmission of atypical ileal hyperplasia (AIH) in weanling hamsters were established and 22 passages were made. AIH was transmitted by feeding whole cell-free supernatants of ileal homogenates. The etiologic agent(s) was retained by 0.22 mum pore-size filters and was inactivated by chloroform treatment or by heating at 56 degrees C for 30 min. Enteric bacteria from affected animals also induced AIH, but with a lower morbidity and mortality than following inoculation with ileal extracts. Experimentally induced lesions progressed from marked segmental hyperplasia of ileal mucosa to granulomatous inflammation in underlying connective tissue and muscle tunics. Hyperplastic mucosal epithelium penetrated the muscularis mucosa, but metastases were not detected. Serum antibody from exposed animals reacted specifically, by indirect immunofluorescence, with an intracytoplasmic mucosal cell antigen(s) of autologous and homogolous ileal lesions, but antibody did not react with normal ileal mucosa or with unaffected portions of intestine from animals bearing ileal lesions.

Administration, Oral↗

PubMed1975

A new form of hereditary retinal degeneration in Wag/Rij rats.

A spontaneous, hereditable, bilateral retinal degeneration affecting all adult animals in a closed, imbred colony of Wag/Rij rats has been discovered. The disorder is characterized by early onset and a slow progressive course. Early lesions are detected by one month in retinas which are otherwise fully developed. Destruction of the photoreceptor layer proceeds as more and more cells degenerate. Degeneration appears to begin in the photoreceptor cell body and only secondarily affects the outer segment. Futhermore, phagocytic activity of pigment epithelium remains intact until late in the disease. Endstage lesions include retinal disorganization, proliferation and vascularization of pigment epithelium, and migration of pigment epithilial cells into the retina. The temporal and structural characteristics of this retinopathy indicate it may serve as a useful model for study of retinitis pigmentosa in man.

Age Factors↗

PubMed1973