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Biomedical subjects

M C Jordan

Publications and source records attributed to M C Jordan.

At least 73 records · Page 4Linked to original sources
PubMed1981

Modification by adoptive humoral immunity of murine cytomegalovirus infection.

The effects of specific antiviral antibody on several aspects of infection with murine cytomegalovirus (CMV) were examined. Administration of immune serum 24 hr before subcutaneous inoculation of 10(5) plaque-forming units of murine CMV prevented detectable viral replication in the tissues of 92% of animals. Protection was associated with the immune globulin fraction and not with normal serum or heterologous antiviral serum. However, the development of latent murine CMV infection was not prevented by prior administration of antibody since immunosuppression with antilymphocyte serum and cortisone 16 weeks later unmasked dormant virus in 17 of 20 animals. In normal animals murine CMV-immune serum administered six days after acute virus infection had been initiated did not influence the outcome; however, in immunosuppressed mice, virus dissemination during acute infection was substantially reduced by specific antibody. These results demonstrate a significant effect of humoral immunity on the course of experimental CMV infection.

Animals↗
PubMed1980

Adverse effects of cytomegalovirus vaccination in mice.

Studies of live attenuated cytomegalovirus (CMV) vaccine have recently been initiated in man. The possibilities of latent infection and disease resulting from reactivation of vaccine virus are major concerns. Because markers for attenuation of tissue culture-passaged mouse CMV (MCMV) exist, studies of potential adverse effects of vaccination were initiated in mice. Plaque-purified MCMV was passed 12 times in cell culture ("vaccine virus") and shown to be attenuated by virtue of loss of lethality and diminished replication in reticuloendothelial organs of normal mice. Although subcutaneous inoculation of 10(5) plaque-forming units of wild virus was lethal for mice immunosuppressed with antilymphocyte serum (18/18 died), "vaccine MCMV" killed only 3/18 (P < 0.05) and was thus shown to be highly attenuated even in immunosuppressed animals. 4 mo after subcutaneous inoculation of vaccine MCMV, no infectious virus was detectable in the tissues of normal C(3)H mice. However, immunosuppression with anti-lymphocyte serum and cortisone caused MCMV reactivation, dissemination, and wide-spread cytomegalic inclusion disease in 19 of 20 animals. Characterization of the reactivating virus recovered from salivary glands indicated that reversion to virulence had occurred. Thus, vaccine MCMV, although markedly attenuated initially, established latent infection, reactivated after immunosuppression, and reverted to virulence, at least in salivary gland tissue. These data from the murine model substantiate the need for careful surveillance and virologic study of patients given experimental CMV vaccine.

Animals↗
PubMed1980

Clinical aspects of CNS cysticercosis.

Central nervous system cysticercosis, caused by infection with the larva of the pork tapeworm, is common throughout the world. Infection occurs after ingestion of fecal contaminants containing the ova of Taenia solium. The clinical manifestations depend on the number, age, and location of the larval cysts disrupting neural tissues. Several disease patterns are apparent: (1) basilar cysticercosis resulting in chronic meningitis or progressive hydrocephalus, (2) parenchymal cysts with focal symptoms, (3) diffuse parenchymal cysts with intracranial hypertension, (4) ventricular localization with episodic acute hydrocephalus, and (5) spinal cord cysticercosis mimicking mass lesions. Mixtures of these basic patterns may occur, and asymptomatic infections are common. In the United States, meningeal cysticercosis is often mistaken for tuberculous or fungal meningitis. A diagnosis of CNS cysticercosis should be considered in any patient with these syndromes who has resided in an area of high prevalence of T solium.

Adult↗
PubMed1979

Pathogenesis of reactivated latent murine cytomegalovirus infection.

Sixteen weeks after inoculation, murine cytomegalovirus (MCMV) can no longer be detected in the tissues of mice. However, a 2-week course of immunosuppression with antilymphocyte serum and cortisone acetate results in reactivation and dissemination of the latent virus in all animals. In this study of reactivation, MCMV was first detected in the liver, usually during the first week of immunosuppression, and virus replication was shown to be restricted to hepatocytes. Subsequently, a viremia occurred, with spread of infection to other organs. The highest titers of virus were reached in salivary glands in which replication occurred in serous acinar cells. In the lung, virus-specific abnormalities were difficult to detect because of superimposed bacterial and fungal infections. However, interstitial pneumonitis could be produced when cortisone acetate was deleted from the immunosuppressive regimen. Although the site of virus latency has not been defined, this model system will be useful for study of reactivation of latent cytomegalovirus infection.

Animals↗
PubMed1978

Interstitial pneumonia and subclinical infection after intranasal inoculation of murine cytomegalovirus.

Although cytomegalovirus (CMV) infections are common throughout the world, little is known about the means of person-to-person transmission. To determine whether infection could be established by a respiratory route, studies were conducted in a murine CMV (MCMV) model by using intranasal inoculation. The infectious dose which resulted in pulmonary and systemic infection of half the mice was 100 plaque-forming units of MCMV. Here, infection was subclinical, but virus replicated in the lungs and subsequently disseminated via the blood to other organs within 7 days. The serum immunofluorescence antibody titer peaked by day 21. None of these mice died, although focal peribronchial interstitial pneumonitis was found in infected animals. In mice given greater than or equal to 10(4) plaque-forming units of MCMV intranasally, severe diffuse interstitial pneumonitis resulted uniformly, closely resembling that seen in immunocompromised patients and in newborn infants, and 20% of the animals died. Normal pulmonary architecture was obliterated by sheets of histiocytes, many containing MCMV intranuclear inclusions, and by accumulation of proteinaceous fluid in the interstitial and alveolar spaces. Of relevance to human disease, these experiments show that MCMV as a sole pathogen can cause severe interstitial pneumonitis in normal mice and that subclinical systemic infection results from respiratory inoculation of small amounts of virus.

Animals↗
PubMed1978

Immunosuppression reactivates and disseminates latent murine cytomegalovirus.

When searched for by standard virological methods, murine cytomegalovirus (MCMV) becomes undetectable by four months after inoculation of mice. However, a two-week regimen of immunosuppression with antilymphocyte serum and corticosteroid results in reactivation and dissemination of the virus in virtually all animals. This system should be useful in defining the pathogenesis of generalized cytomegalic disease resulting from reactivation of latent virus in immunocompromized individuals.

Animals↗
PubMed1977

Allescheria boydii infections in the immunosuppressed host.

Allescheria boydii, a true fungus frequently isolated from soil, is best known as a causative agent of maduromycosis of the foot. In our report we describe two patients under treatment for acute leukemia who died from rapidly progressive A. boydii infections. One patient had signs of central nervous system infection and was found at autopsy to have had a large brain abscess. The second patient had a cavitary necrotizing pneumonia with thoracic inlet obstruction (Pancoast's syndrome) and failed to show improvement despite treatment with amphotericin B. The clinical spectrum of allescheriasis is reviewed with particular emphasis on its role as a pathogen in the compromised host. Since A. boydii may resemble other fungi morphologically in tissue sections and may produce infections clinically similar to other mycoses, culture of the organism is required for definitive diagnosis. Based on recently reported in vitro susceptibility studies, miconazole may have a future role in the therapy of A. boydii infections which are resistant to presently available antifungal agents.

Adult↗
PubMed1977

Immunosuppression reactivates and disseminates latent murine cytomegalovirus.

When searched for by standard virological methods, murine cytomegalovirus (MCMV) becomes undetectable by 4 months after inoculation of mice. However, a 2-week regimen of immunosuppression with antilymphocyte serum and corticosteroid results in reactivation and dissemination of the virus in virtually all animals. This system should be useful in defining the pathogenesis of generalized cytomegalic disease resulting from reactivation of latent virus in immunocompromised individuals.

Animals↗
PubMed1975

Reactivation of latent Herpes simplex virus after pneumococcal pneumonia in mice.

In attempts to reactivate latent herpes simplex virus, we instilled Diplococcus pneumoniae intratracheally into mice harboring latent infections in sacrosciatic spinal ganglia. All mice developed a severe pneumonia within 24 h and were given penicillin therapy. Representative mice that survived the penumonia were sacrificed at daily intervals, and appropriate tissues were examined for evidence of viral reactivation. Herpes simplex virus was reactivated in the ganglia and appeared to travel both proximally and distally in associated nerve trunks. Clinically apparent disease due to the virus was not detected in any mice.

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