Ig. First The nine Brazilian strains St Showed bootstrap percentages tze Of 100% with strain Weissella sp. JZ 1L previously from diseased rainbow trout isolated in China. 3.4. NIR analysis of epidemiological thresholds and application of the NRI analysis allows the estimation Tzung the deviations from the mean and the standard for sensitive isolates against four of the five antibiotics Lapatinib EGFR inhibitor tested. All 77 isolates were resistant to Sul. FLO had, the 77 St Strains Fl Between 18mm and 31mm Chen, and they represent only a modal group. NIR analysis of these data led to an epidemic threshold WT St Strains highly anf Llige to 16 mm, wherein the size E of the average of 24.4 gap and the level of 3.1. Therefore, all isolates were classified as WT. The values for COWT ERY, oxy, NOR and were calculated to be 21mm, 10mm and 7mm, respectively.
Based on these limits, there was a burden for FYR NWT, two for OXY, NOR, and three for. There was an overall similarity BMS-387032 CDK inhibitor classified In the distribution of data for these three antimicrobial agents, with at least 96% of the St Strains than for WT and modal group. With the exception of SUL, to which all isolates were resistant, is 09 WS strain was resistant to more than one antibiotic. 3.5. Challenge study and bacteriology, has been successfully reproduced the disease in all experimental conditions in both species. Neither clinical signs nor mortality in fish were in the control groups w Observed during the experimental period.
The main clinical symptoms were observed Masitinib in rainbow trout first patient anorexia and lethargy, and these were ascites, exophthalmos, erratic swimming, rectal prolapse, hyper mie And was followed by bleeding in the eye, pectoral fin, the fin side, and anal area. Intraperitoneally challenged fish in the groups, the high and low doses of pr Sented the first clinical symptoms at 22 and 48 hours after infection or mortality T were reviewed and 48 hpi to 16 days, respectively. The members of the group C pr Sented the first clinical symptoms at 24 HPI, and the only death 48 hpi the fish healthy group D were infected with bacteria after cohabitation with sick fish. The first clinical signs of disease 3 days after the start of cohabitation were observed and Todesf Lle occurred on days 6, 8 and 14 Episodes of clinical manifestations of recovery Fischbest Walls were applied may need during the experimental period, especially in the groups that showed low mortality.
Samples were from bacteria from different organs of all, the rainbow trout died and those who had clinical signs, but recovered sp Isolated ter. Three of the six Nile tilapia fry has also developed clinical signs of disease, such as dark skin, loss of appetite, lethargy and exophthalmia. Tilapia asymptomatic negative results in bacteriology, in contrast to reisolation positive bacteria in the three diseased fish. Bacterial populations of 104 CFU g1 were found in various tissues of dead and call the rainbow trout fry of Nile tilapia and dead. No direct correlation between the average load of bacteria in organs and mortality T observed. Up to 21 days after infection, challenged rainbow trout still had a high bacterial load in the brain, kidneys and intestines. 3.6. Pathological Ver Changes Assoc microscopic evaluation