| Tilapia is an important freshwater cultured fish in China. It is very popular in China, which is fast-growing, omnivorous and little inter-muscular bone. In August2011, high mortality of tilapia with typical signs of streptococcosis occurred in fish farms of Guangxi Zhuang Autonomous Region of China, which caused significant economic losses. Diseased fish showed clinical signs of septicaemia, exophthalmia, corneal opacity, spinning swimming, off-feeding, haemorrhagic ulcers inside the operculum and at the base of the pectoral, liver and spleen congested, gallbladder swollen and abdominal fluid (in some fish). Five bacterial strains were isolated from five farms in three districts (Yizhou, Liuzhou, Beihai city) of Guangxi. They were confirmed to be pathogenic by recurrent infections. They were identified as Streptococcus in regular morphological observation, API20strep and16S rRNA gene sequence analysis. The Yizhou isolate was Streptococcus iniae, while the Liuzhou and Beihai isolates were Streptococcus agalactiae. Their sensitivities to45kinds of antimicrobial drugs were determined. The results showed that S. iniae was sensitive to23antibiotics, such as the rifamycins, amide alcohols, nitrofurans, etc.. On the other hand, the four S. agalactiae isolates showed different sensitivity to45antibiotics, though they were both sensitive to11antibiotics, such as piperacillin, cefradine, cefamandole, penicillins, cephalosporins, tetracyclines, glycopeptides, macrolides, quinolones, rifamycins and amide alcohols.Histopathological and ultrastructural pathology characteristics of Tilapia (Oreochromis niloticus) infected with S.iniae were studied. The most consistent gross pathological changes of the diseased fish in the brain, kidney, spleen, liver, intestine, heart, skeletal muscle and gills of diseased fish, particularly in the liver, spleen, kidney and gills were necrosis and inflammatory cell infiltration. Most hepatic cells showed hydropic degeneration, necrosis, hepatic sinusoid dilatation and hyperemia with the pancreatic cells in the liver. The spleen was infiltrated by inflammatory cells; there were more deposits of hemosiderin than the control fish. While in the kidney, edemas were seen in the endothelial cells of renal tubule, accompanied by hyaline degeneration, infiltration of interstitial inflammatory cells. In addition, necrosis was also found in the intestine and brain. The findings of transmission electron microscope in the infected tilapias were studied. The sighs of nuclear atrophy, chromatin emarginated under nuclear inner membrane, enlargement of the pool of rough endoplasmic reticulum, scattering of ribosomal particles on the membrane were seen. Swollen and dissolved cristae were also seen in mitochondrial of the hepatocyte of diseased fish. In the spleen, bacteria were seen in the cell, with broken and dissolved nuclear membrane, marginated and fragmentated chromatin. Edemas occurred and organelles decreased in reticular cells in diseased fish. The myofibrils were broken and disorientated, light and dark bands were blurred, and vacuolization occurrences in the myofibril. Necrosis and fracture were seen in myocardial, mitochondrial reduced, swollen, dissolution, necrosis were seen in the mitochondrial, and myelin structure appeared in cristae. The microglia chromatin in the infected fish was low electron density and many vacuoles were showed in the infected brain. The pathological changes revealed that lesions of systemic organs in tilapia due to S. iniae, causing multiple organ dysfunctions. The infected fish lost normal physiological regulation of metabolism, which eventually led to its death.Evaluation of the blood chemistry of Tilapia (O. niloticus) artificially challenged with S. iniae at28℃and33℃revealed that, after inoculation, serum total protein (TP) content increased with the time, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity increased firstly and then decreased, finally they both increased again. The33℃group peaked in shoter time compared with the28℃group, both groups were significantly higher than the contol group (P<0.05). Urea (UREA) and potassium (K+) content firstly increased and then decreased. Sodium (Na+) content firstly increased and then decreased, and finally it inreased again. Creatinine (CREA) increased with the post-injected time going by. Serum alkaline phosphatase(AKP) activity was increased and then decreased in28℃group, while it showed a rising trend in33℃group. Superoxidedismutase(SOD) activity was increased and then decreased, and finally it inreased again, which in33℃group was always higher than that in28℃group. Globulin (GLO) showed an increasing trend, but showed no significant differences (P>0.05) between the two groups at each time point. The pathological changes of different degree were observed in the liver and kidney of infected tilapia. The hepatocyte and renal tubular epithelial cells were hydropic degeneration in33℃group, while in28℃group, eosinophilic body appeared in hepatocyte, eosinophilic body and granular degeneration appeared in renal tubular epithelial cells. The results indicated that the liver and kidney of tilapia associated with S.iniae damaged, resulting in organs dysfunction and the more serious damage was found in the groups at high temperatures. |
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