| Clostridium perfringens(CP) is a contagious zoonotic pathogen. Many researchers have done a lot of meticulous research on its etiology, epidemiology, diagnosis, and vaccine development.But there is still few reports about the pathogenesis mechanism of CP infection, especially the systematic and profound research of the pathomorpholoical changes of CP infection.This experiment is undertaken to investigate qualitatively and quantitatively CP bacteria distribution and the pathological changes in the predominant organs and tissue of the chickens infected with CP type A standard strains ATCC13124 and F3 field isolate. 135 one-day-old chickens were randomly divided into three groups: control group, CP type A standards strains infection group, CP type A isolated strain infection group. 22-day-old chickens from the two infection groups were orally inoculated with 500 μL CP type A standard strains ATCC13124 and F3 field isolate with the concentration of 109 CFU/m L continuously for five days, respectively;while 45 chickens were inoculated with chopped meat medium as control. Chickens were sacrificed at 1, 3, 5, 7, 9, 11, 14, 21, 35 days after the first infection. Most organs and tissues of infected chickens were taken for the observation of pathological, histopathological, ultrastructural pathological changes. Indirect immunofluorescence assay was used to detect the bacterium distribution and amount in duodenum, jejunum, ileum. The purpose was to explore systematically and completely the pathological lesion of the CP infection for revealing its pathogenesis mechanism. The results were as follows:(1) After infection with CP, chickens began to show listlessness, depression, loss of appetite.Five days after inoculation, the infected chickens appeared gathering together, messy feathers,standing unfirmly and recumbency, diarrhea of brown or black feces with small amount of mucus and blood, and often contaminated feathers around the anus. Some organs, especially the intestinal tract, of chickens infected with CP showed hyperemia, hemorrhage, swollen gas, edema and degeneration and necrosis of parenchyma and other anatopathological changes.(2) Histopathological changes mainly consisted of small intestine hemorrhagic necrotic enteritis; And in other organs, there were shown as the parenchymatous myocarditis,parenchymatous hepatitis, glomerulonephritis, hemorrhagic pneumonia, acute splenitis. The primary target organ of CP was small intestine and showed typical pathological changes. The lesions in the rear section of small intestine, such as distal jejunum, ileum is more serious than thefront section, such as the duodenum, proximal jejunum. Indirect immunofluorescence showed that there were a large number of CP colonization in the jejunum and ileum and less in duodenum. The specific green fluorescence was observed in the enteric cavity and intestinal mucosa.(3) CP isolation and identificantion experiment of small intestine showed that it had the similar fluctuation trends with the pathlogical lesion, that is, 5 to 9 days after inoculation, the number of bacteria and lesion severity in the small intestine arrived the peak point. Isolates strain of F3 has the similar regularity with the standard strain of ATCC13124, but its pathogenicity was a little weaker.(4) Ultrastructural pathological examination found a series of injury in intestine and other parenchymal organs of infected chickens, and mainly occurs in the mitochondria, rough endoplasmic reticulum, nuclear membrane and appearance of abnormal membrane structure.In conclusion, the research demonstrated systematically the pathomorphological changes and bacterium distribution of chickens infected with CP, this would provide important scientific evidences for illumination its pathogenesis mechanism and the comprehensive prevention CP infection. |
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