Pathogenesis Of Experimental Infection Research Articles

Pathogenesis of Korean Type 1 (European Genotype) Porcine Reproductive and Respiratory Syndrome Virus in Experimentally Infected Pregnant Gilts

The aims of this study were to determine (1) the pathogenesis of experimental infection with a Korean type 1 porcine reproductive and respiratory syndrome virus (PRRSV) by defining the viral distribution and the sites of viral replication and (2) the relationship between viral replication and apoptosis in stillborn fetuses and live born piglets from infected pregnant gilts. At 3 weeks ante partum, four pregnant gilts were inoculated intranasally with Korean type 1 PRRSV. Stillborn fetuses from the infected gilts were of crown-to-rump length 25.8-27.1 cm consistent with fetal death between 106 and 110 days of gestation. Type 1 PRRSV was isolated from the fetal tissues and these isolates were shown to be identical to the challenge virus by sequence analysis. Type 1 PRRSV RNA was detected in the lung, lymph node, heart, tonsil, thymus, liver, adrenal gland and spleen of live born piglets and stillborn fetuses from the infected gilts. The mean number of apoptotic cells per unit area of lung (P = 0.003), heart (P = 0.011), thymus (P = 0.003), liver (P = 0.011) and spleen (P = 0.002) was significantly higher in stillborn fetuses than in live born piglets. Dual labelling showed that the majority of cells either contained type 1 PRRSV or were apoptotic, but not both. Apoptotic cells were more numerous than PRRSV(+) cells. The results of the study demonstrated that type 1 PRRSV induces reproductive failure in pregnant gilts. Apoptosis induced by type 1 PRRSV may be associated with the incidence of stillborn fetuses in PRRSV-infected pregnant gilts.

The pathogenesis of experimental infection by Staphylococcus aureus in rabbits

The present study was carried out on experimental infected rabbit with Staphylococcus aureus to study some aspects of pathogenesis of staphylococcal infection. Twelve rabbit were randomly divided into two equal groups: group1 (treated group) were inoculated subcutaneously with (0.5ml) of bacterial inocula contain (30x1010) CFU and group2 (control). Blood samples were taking to evaluate some of blood parameters include: WBC counts,(LYM., Mon.and GRA.) percentage, Mon.#,GRA.#,RBC counts, HB, PCV, MCV, MCH, MCHC, RDW, PLT counts, MPV, PCT and PDW. Most clinical signs noticed in treated group were: mild fever, depression, decreased appetite, respiratory distress and abscess formation in some cases at site of injection. Also the P.M. lesion included: congestion of internal organs (liver, lung) and signs of pneumonia. Histopathological investigations were carried on liver, lung and bone. The statistical analysis revealed that there were significant increased in WBC count and GRA % (P<0.05) in treated group as compared with control. The MCV, MCH, MCHC and RDW (P<0.05) showed significant differences between groups. The PLT counts and PCT (P<0.05) revealed significant decreased in treated group as compared with control. Other parameters studied did not show significant differences between two groups. Histopathological study revealed that there were: hydropic degeneration, necrosis and occluded of bile sinusoid with bile pigment in the livers of infected animals, in lung: there were edema, hemorrhage and necrosis with thickening of the wall of alveoli and infiltration of inflammatory cells and in bone there were sever necrosis of osteoblast, osteoclast and osteocyte cells in the infected animals.

Expression of Prion Protein in the Gut of Mice Infected Orally with the 301V Murine Strain of the Bovine Spongiform Encephalopathy Agent

Transmissible spongiform encephalopathies (TSEs) are characterized by the accumulation of an abnormal, disease-associated prion protein (PrP(d)). Expression of its normal cellular counterpart (PrP(c)) by the host is a pre-requisite for the spread of infection to the central nervous system and the development of disease. Moreover, cells expressing PrP(c) at specific sites such as the gastrointestinal tract might be regarded as the initial point of PrP(c)-PrP(d) conversion after infection by the oral route. In this study, inbred mice of the I/M strain were infected orally with the 301V murine strain of the bovine spongiform encephalopathy agent. The expression of PrP(c) and the accumulation of PrP(d) in the intestine was then investigated immunohistochemically, together with the variations in immunoreactivity that resulted from different pretreatments of the tissue. After proteinase K (PK) pretreatment, abnormal PrP was still detectable only in the gut-associated lymphoid tissue (GALT) of clinically affected mice and, to a much more limited degree, in the enteric nervous system (ENS). Cellular PrP that disappeared after PK treatment was particularly conspicuous in the ENS and present to a lesser extent in the GALT of all mice examined after inoculation with 301V or with normal brain homogenates, as well as in uninoculated controls. These findings suggested that not all PrP found in infected mice was PrP(d) and that part of the PrP(d) was sensitive to PK treatment. Reactivity to PrP antibody 1A8 was consistently found in the absorptive epithelium of the intestinal villi, with or without PK pretreatment. However, epithelial immunolabelling was comparable in inoculated and uninoculated mice and was also consistently seen in PrP "knockout" mice used as controls. It is therefore concluded that immunohistochemically detectable accumulation of PrP(d) in the gut of mice is a relatively late event in the pathogenesis of experimental infection in this model and that the immunoreactivity observed in the intestinal epithelium does not correspond to PrP expression. While enterocytes may still play a role in the uptake of infection from the intestinal lumen, the results do not suggest that these cells are a site of initial accumulation of PrP(d).

Histopathology and Pathogenesis of Experimental Infection with Edwardsiella tarda in Channel Catfish

The histopathology and pathogenesis of Edwardsiella tarda-induced edwardsiellosis in juvenile channel catfish Ictalurus punctatus were characterized. The lateral body surfaces of fish were scraped before infection by immersion in a bath of E. tarda for 30 min. Scattered cutaneous petechiae and ulcerations were seen on the mouth, operculum, isthmus, abdomen, and lateral body after infection. Injured skin developed focal ulcerative necrotizing dermatitis, increased mucus, and irregular areas of skin depigmentation scattered over the entire body. Internal organs were congested, and livers showed patchy discoloration and petechiae. Histologically, the liver, head kidney, trunk kidney, and spleen had severe multifocal necrotizing inflammation. Scraped controls did not show gross or microscopic lesions except for mild dermatitis of injured skin at the scraping site. Bacteria in hepatic lesions were specifically identified by immunohistochemistry that used rabbit anti-E. tarda serum. Colony-forming units of E. tarda per gram of tissue or milliliter of blood peaked 3 d postinfection (PI) in the liver, trunk kidney, and blood. No bacteria were isolated from infected fish after 6 d PI. Clinical signs and internal gross lesions declined by 8 d PI and were absent thereafter. No histological lesions were observed in the intestine, stomach, heart, gills, or brain. Infected fish were sluggish and had rapid opercular movements and pale gills before death. Histological lesions were similar to those caused by E. ictaluri in channel catfish.

Role of serum protective factor and neutralizing antibody in pathogenesis of experimental infection with Langat virus in mice.

Journal Article Role of Serum Protective Factor and Neutralizing Antibody in Pathogenesis of Experimental Infection with Langat Virus in Mice Get access Inderjit S. Thind, Inderjit S. Thind From the Kenneth F. Maxcy Laboratories, Department of Epidemiology, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar Winston H. Price Winston H. Price From the Kenneth F. Maxcy Laboratories, Department of Epidemiology, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, Maryland Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 121, Issue 4, April 1970, Pages 378–382, https://doi.org/10.1093/infdis/121.4.378 Published: 01 April 1970 Article history Received: 17 November 1969 Revision received: 16 January 1970 Published: 01 April 1970