Studies on the Pathogenicity of Campylobacter Jejuni
Rats experimentally, infected with about 106 CFU or more of Campylobacter jejuni were promptly colonized. Campylobacter jejuni was recovered from faecal cultures of infected rats for up to 17 weeks post infection. The infected rats did not succumb to diarrhoea throughout the experiment. Haemagglutination assay was used to detect adhesins of Campylobacter jejuni isolated locally. Five out of 15 (33 percent) of the strains tested agglutinated erythrocytes of human blood group A + and guinea pig but not sheep RBC"s. The haemagglutination observed was inhibited by mannose and galactose but not glucose. The presence of dhesins and the ability of Campylobacter jejuni to colonize the intestinal tract both enhance the establishment of infection. Two out of five (40 percent) culture filtrates of Campylobacter jejuni showed both cytotonic and cytotoxic activities on Vero, Hela and Hep2 cells. Two out of 18 (11 percent) of the filtrates also caused fluid accumulation in ligated rat ileal loop. The cytotonic toxin may be responsible for diarrhoea induction while the cytotoxc toxins may account for the sydenteric symptoms observed with Campylobacter jejuni infections. Purified endotoxin extracted from Campylobacter jejuni was used for Schwartzman reaction in rats. Localized Schwartzman reaction was observed in rats eight hours after second injection of Campylobacter jejuni purified endotoxin extract. The localized lesion was mainly an erythematous swelling. Animals subjected to generalized reactions manifested wide spread deposition of fibrin thrombi. The thrombi observed resulted from disseminated intravascular coagulation. The lungs, heart, kidneys, liver and spleen were all affected in the generalized reaction. Two out of five Campylobacter jejuni strains were recovered from blood of animals following oral experimental infection. The organisms were also recovered from the liver, spleen and kidney after oral infection. The translocation of the organisms from the gastrointestinal organs denotes invasiveness of the strains studied. Kerato conjunctivitis was examined in this work. This negative sereny test implies that the guinea-pig conjunctival cells may be resistant to invasion by Campylobacter jejuni. Oral infection of rats with Campylobacter jejuni gave rise to distinct histological lesions. The gastrointestinal tract showed focal hyperplasia of lymphoid follicles with prominent germinal centres. There were also focal necrosis of superficial epithelia and focal oedema of villi tips. The necrosis gave rise to "gully ulcers" in the mucosa. The lesions were concentrated at the upper ileum. The liver of infected rats should focal perivascular haemorrhage with prominent diffuse hydropic degeneration of hepatocytes. Rats are very useful in the study of histopathology from experimental Campylobacter jejuni infection despite their resistance to diarrhoea. This is because the lesions observed in experimentally infected rats in this work were comparable to lesions observed in human Campylobacteriosis.