In this study, A total of 153 animals at Taif governorate were included (55 diseased sheep, 22 dead lambs, 42 diseased goats and 34 dead kids). The bacteriological examination revealed that E. coli was isolated from diarrheic sheep in percentage of 36.36%. Regarding to dead lambs E. coli was isolated from lung, liver, spleen and intestine in a percentage of 12 (54.55 %), 15 (68.18 %), 16 (72.73 %), 18 (81.82%), respectively. E. coli was isolated from diarrheic goats in percentage of 35.71%. Regarding to dead kids E. coli was isolated from lung, liver, spleen and intestine in a percentage of 15(44.12 %), 20 (58.82 %), 20 (58.82%), 21 (61.76 %), respectively. Serological identification of isolated strains revealed that E. coli O128:H2, E. coli O146:H8 and E. coli O157:H7 were detected in percentage of 33 (44.60%), 28 (37.84%) and 8 (10.81%) respectively. ELISA using LPS as coating antigen revealed that of 69 serum samples collected from culture positive animals for E. coli, 67 (97.10 %) were seropositive. From 79 serum samples obtained from culture negative animals,7 (8.86%) were seropositives. From 69 tested E. coli isolates belonged to 3 serovars, 64(92.75%) were positive for heamolysin test, 65(94.20%) were able to survive in normal serum, 60 (86.96%) were MRHA and 9 (13.04%) were MSHA. All isolates 69 (100%) were positive for verocytotoxine production. All isolates of E. coli serovars were highly sensitive to Ampicillin, ciprofloxacin, ofloxacin and tobramycin (100% each) On the contrary all isolates were resistant to erythromycin. The use of Lactobacillus acidophilus induced inhibitory results on the growth of all isolated E. coli serovars in vitro. Eighty male Wister rats of 10-12 weeks old and weighing approximately 100 gm, the rats were divided into 8 equal groups (infected-with E. coli O128:H2 non treated [1], infected with E. coli O146:H8- non treated [2], infected with E. coli O157:H7 - non treated [3], groups 4 & 5 & 6 infected with above mentioned serovars respectively and treated with Lactobacillus acidophilus. Group 7 administrated the Lactobacillus acidophilus only, group 8 kept as control group). Antibody titre measured by ELISA test in experimental animals increased from 1 st week post infection in infected- treated groups (4 & 5&6) which more than that recorded in infected-non treated groups (1 & 2&3) This increase in antibody titre increase gradually till reach peak at 3 weeks post infection. Mortality rates in infected non treated groups (1 & 2&3) were 60%, 70%and 90% respectively while mortality rates among infected treated groups(4 & 5) were 0 % each and was10% in group (6). Re-isolation of E. coli serovars from different organs of dead rats all over experimental period and sacrificed rats at the end of the experiment gave variable results. In infected-non treated groups (1 & 2&3) E. coli O128:H2 isolated from lungs, liver, spleen and intestine in a percent of 40%, 70%, 80% and100% respectively. While E. coli O146:H8 isolated in a percent of 20%, 50%, and 80% and100% respectively. E. coli O157:H7 isolated in a percent of 40%, 80%, 80% and100% respectively. In rats of infected-treated groups (4 & 5), E. coli O128:H2, E. coli O146:H8 couldn't be isolated from any internal organ E. coli O157:H7 isolated in a percent of 10% from spleen and 20% from intestine. The histopathological examination of naturally infected animals revealed that VTEC had a drastic severe pathological alteration represented by haemorrhagic pneumonia, haemorrhage and necrosis of hepatocytes, hemolytic-uremic syndrome as well as haemorrhagic colitis. The histopathological examination of rats groups (1 & 2&3) which died during the experiment showed nearly the same lesions as naturally infected animal. While the rats of the infectedtreated groups (4 & 5& 6) showed mild pathological changes such as mild necrosis and mild infiltration of mononuclear cells and their cells tend to be in normal state. These results confirmed the probiotic effect of L. acidophilus against the colonization of E. coli serovars in animal tissues as well as enhancing their immune response.
