Studies on Coccidia in Experimental Infection with Eimeria spp in Rose-Cobb Broiler Chicken

Out of 400 examined samples 45 suspected Salmonella isolates (11.25%) were obtained 19 (9.5%) out of apparently healthy and 26 (13%) from diseased chickens. Intestinal samples had more isolates (29, 14.5%) more than liver (16, 8%). Identified S.Enteritidis from suspected salmonella was 16/45 (35.6%) with a rate of 8% out of the examined 400 samples, 6 (3.0%) out of apparently healthy and 10 (5.0%) from diseased chickens. Intestinal samples had more isolates (11, 5.5%) than liver (5, 2.5%). The Antibiotics susceptibility profile of S. Enteritidis isolates revealed 100% resistance to trimethoprim/sulfamethoxazole, followed by oxacillin (62.5%), 56.3% for each of ampicillin, clindamycin, enrofloxacin and doxycycline, 50% for chloramphenicol, 43.8% for streptomycin, 37.5% to cephalosporins and 18.8% for colistin. Tested S. Enteritidis isolates are classified into 11 profiles and are resistant to two - nine antibiotic classes with resistant index 0.2- 0.9. Only two isolates are NDR (12.5%), most of isolates 10/16 (62.5%) are MDR and 25% are EDR to 8-9 antibiotics. Clinical signs in experimentally infected chickens appeared at 2nd dpi, mortality started at the 4th to reach 27.5% in infected nontreated and 5% in colistin treated. Signs and lesions were markedly severe in infected nontreated than treated. S. Enteritidis was re-isolated from dead infected birds. S. Enteritidis intestinal count in sacrificed infected nontreated was higher than treated. Colistin treated group showed higher FCR, EEF and CV% (1.52, 402.8 and 6.12%) than infected non-treated (1.73, 222.6 and 14.83%). It could be concluded that S. Enteritidis is prevalent in broiler chicken flocks. Most of the isolates are MDR. Experimental infection of broiler with S. Enteritidis field isolates resulted in high mortality and the addition of colistin sulphate in drinking water controlled the infection and restores the productivity of infected broiler chickens.

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Labelling of non-A, non-B hepatitis infected chimpanzee hepatocytes with nuclease-gold conjugates

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100111367 ◽

1984 ◽

Vol 42 ◽

pp. 250-251

Author(s):

G. D. Gagne ◽

M. F. Miller ◽

D. A. Peterson

Keyword(s):

Endoplasmic Reticulum ◽

Experimental Infection ◽

Uranyl Acetate ◽

Type I ◽

Cellular Injury ◽

Type Ii ◽

Tubular Structures ◽

Type Iii ◽

Type Iv ◽

Infected Chimpanzee

Experimental infection of chimpanzees with non-A, non-B hepatitis (NANB) or with delta agent hepatitis results in the appearance of characteristic cytoplasmic alterations in the hepatocytes. These alterations include spongelike inclusions (Type I), attached convoluted membranes (Type II), tubular structures (Type III), and microtubular aggregates (Type IV) (Fig. 1). Type I, II and III structures are, by association, believed to be derived from endoplasmic reticulum and may be morphogenetically related. Type IV structures are generally observed free in the cytoplasm but sometimes in the vicinity of type III structures. It is not known whether these structures are somehow involved in the replication and/or assembly of the putative NANB virus or whether they are simply nonspecific responses to cellular injury. When treated with uranyl acetate, type I, II and III structures stain intensely as if they might contain nucleic acids. If these structures do correspond to intermediates in the replication of a virus, one might expect them to contain DNA or RNA and the present study was undertaken to explore this possibility.

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