Studies on the pathology of experimental viral disease
Başlık:
Studies on the pathology of experimental viral disease
Yazar:
Wright, Norman G., author.
ISBN:
9780438052727
Yazar Ek Girişi:
Fiziksel Tanımlama:
1 electronic resource (230 pages)
Genel Not:
Source: Dissertation Abstracts International, Volume: 76-08C.
Advisors: J. W. Emelie.
Özet:
The work was divided into two parts. Part 1 dealt with the pathogenesis and pathology of experimental infectious canine hepatitis (ICH) infection in the guinea-pig and a comparison was made with the natural disease of dogs. Following intraperitoneal inoculation of ICH virus into young guinea-pigs, a non-fatal, highly cellular fibrinous peritonitis developed particularly on the serous surfaces of the liver, spleen, omentum and urinary bladder. Typical basophilic ICH intranuclear inclusion bodies, which were shown to contain deoxyribonucleic acid by the fluorescent Feulgen method and to contain specific ICH virus antigen by means of immunofluorescence, were found in peritoneal macrophages in the fibrinous exudates, in hepatic and Kupffer cells and in the vascular endothelium of the kidney. Suckling guinea-pigs were noted to be more susceptible than were young weaned or adult animals. After intracardiac administration of the virus, a more severe, often fatal, disease developed and some infected guinea- pigs showed nervous signs prior to death. Inclusion bodies were widely disseminated throughout the vascular endothelium but were particularly prevalent in that of the central nervous system. The influence of cortisone acetate on experimental ICH infection in the guinea-pig was studied. The steroid was administered by intramuscular injection prior to inoculation of the virus. Enhancement of infection, as indicated by increased mortality and a higher incidence of nervous signs, was noted. Similar results were obtained when infected guinea-pigs were exposed to a low environmental temperature. The mechanisms by which cortisone and cold temperature may aggravate experimental virus infection in the guinea-pig were discussed and it was postulated that both exerted their effect by a depressant action on the reticuloendothelial system (EES). Further work showed that the administration of colloidal thorium dioxide, a known inhibitor of the EES, caused similar enhancement of experimental ICH in the guinea-pig as that shown by both cortisone and low environmental temperature. Part 2 of the work was concerned with certain aspects of natural and experimental ICH infection in dogs. A survey of the renal pathology in 82 natural cases of ICH showed that interstitial nephritis occurred in 29.2% of cases. Typical ICH inclusion bodies were found in the cellular lesions in 33 per cent of the nephritic dogs. An investigation of the pathogenesis and pathology of interstitial nephritis in experimental ICH was then carried out. A high incidence of focal nephritis was found in the convalescent stage of the disease (70.8%). In the cortex, the cellular infiltration was mainly lymphocytic but a characteristic feature of the lesions in the medulla was the presence of tubular necrosis and large numbers of polymorphonuclear leucocytes. Intranuclear inclusion bodies and specific ICH virus antigen were demonstrated in those lesions up to 30 days after infection. In the course of the latter work, some of the experimental dogs showed nervous signs similar to those noted in infected guinea-pigs and that finding prompted a study of the serial pathology of the brain of experimentally infected dogs.
Notlar:
School code: 0547
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Yer Numarası | Demirbaş Numarası | Shelf Location | Lokasyon / Statüsü / İade Tarihi |
---|---|---|---|
XX(684418.1) | 684418-1001 | Proquest E-Tez Koleksiyonu | Arıyor... |
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