Antimicrobial resistance in Yersinia pestis is rare, yet constitutes a significant international public health and biodefense threat. In 1995, the first multidrug resistant (MDR) isolate of Y. pestis (strain IP275) was identified, and was shown to contain a self-transmissible plasmid (pIP1202) that conferred resistance to many of the antimicrobials recommended for plague treatment and prophylaxis. Comparative analysis of the DNA sequence of Y. pestis plasmid pIP1202 revealed a near identical IncA/C plasmid backbone that is shared by MDR plasmids isolated from Salmonella enterica serotype Newport SL254 and the fish pathogen Yersinia ruckeri YR71. The high degree of sequence identity and gene synteny between the plasmid backbones suggests recent acquisition of these plasmids from a common ancestor. In addition, the Y. pestis pIP1202-like plasmid backbone was detected in numerous MDR enterobacterial pathogens isolated from retail meat samples collected between 2002 and 2005 in the United States. Plasmid-positive strains were isolated from beef, chicken, turkey and pork, and were found in samples from the following states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York and Oregon. Our studies reveal that this common plasmid backbone is broadly disseminated among MDR zoonotic pathogens associated with agriculture. This reservoir of mobile resistance determinants has the potential to disseminate to Y. pestis and other human and zoonotic bacterial pathogens and therefore represents a significant public health concern.

Biotype 2 (BT2) variants of the bacterium Yersinia ruckeri are an increasing disease problem in U.S. and European aquaculture and have been characterized as serovar 1 isolates that lack both peritrichous flagella and secreted phospholipase activity. The emergence of this biotype has been associated with an increased frequency of enteric redmouth disease (ERM) outbreaks in previously vaccinated salmonid fish. In this study, four independent specific natural mutations that cause the loss of both motility and secreted lipase activity were identified in BT2 strains from the United States, United Kingdom, and mainland Europe. Each of these was a unique mutation in either fliR, flhA, or flhB, all of which are genes predicted to encode essential components of the flagellar secretion apparatus. Our results demonstrate the existence of independent mutations leading to the BT2 phenotype; thus, this phenotype has emerged separately at least four times. In addition, BT2 strains from the United Kingdom were shown to have the same mutant allele found in U.S. BT2 strains, suggesting a common origin of this BT2 lineage. This differentiation of distinct BT2 lineages is of critical importance for the development and validation of alternative vaccines or other treatment strategies intended for the control of BT2 strains.

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The influence of illumination and prey contrast on survival, growth, and feeding of larval yellow perch fed Artemia sp. nauplii was tested in an experimental upfiow culture system. The treatment with high light level and high prey contrast (205 lux, black background) supported the best survival (mean, 44.2%) and growth (mean total length, 8.9 mm; mean wet weight, 5.0 mg) from hatching to age 14 d. Mean survival was 37.2% when light was low and prey contrast high (75 lux, black background). In the remainder of the tests, survival to age 14 d ranged from 0 to 6.9%. Low light and low prey contrast caused a 1-2 d delay in initial feeding. Visibility of the prey resulting from contrast with the surroundings, rather than light level, accounted for most of the variation in the ability of yellow perch larvae to acquire adequate food. Although poorly equipped for vision, most fish larvae rely on visual stimuli to obtain food (Blaxter 1969). Successful food location by visually dependent larvae is a function of the volume ofwater searched and the concentration and visibility of edible prey. The visibility of prey items generally depends on contrast, and, therefore, on the optical properties of the prey, the medium, the background, and the direction and intensity of light (Hemmings 1966). Low light intensity in culture systems has reduced survival or growth of fish larvae (Tandler and Mason 1983). Decreased survival of larval sea bass Dicentrarchus labrax occurred in tanks exposed to strong light intensities (Barahona-Fernandes 1979), and of larval striped bass

Gravid brown trout (Salmo trutta) females were injected with various doses of a synthetic gonadotropin-releasing hormone analog (GnRHa), given with or without an injection of triiodothyronine (T3), in order to investigate the potential of T3 (a) to enhance the stimulatory effect of GnRHa on ovulation, and (b) to enhance the growth and survival of the produced progeny. From the time the hormonal treatments were initiated until ovulation was detected 5-38 days later, endogenous plasma T3 levels increased from an average of 3.6 to 11.6 ng ml(-1). Injection with 20 mg T3 kg(-1) body weight, further elevated plasma T3 levels at ovulation (16.0 ng ml(-1). Mean time to ovulation was reduced significantly in fish injected with 10 μg kg(-1) of GnRHa, whereas treatment with lower doses was ineffective. Injection with T3 did not enhance the ovulatory response of brown trout to GnRHa. Unfertilized eggs obtained from T3-injected females had a higher T3 content, suggesting a transfer of T3 from the maternal circulation into the oocytes. Maternal T3 injection had no effect on egg fertilization rates, embryo survival to eyeing and hatching, or the prevalence of abnormal larvae at the time of hatching. Length and weight gain of the progeny during yolk absorption was also not influenced by maternal T3 treatment. At the completion of yolk-sac absorption, progeny from females injected with T3 had a higher prevalence of skeletal abnormalities than controls. The results suggest that in teleosts like brown trout, which have high endogenous circulating T3 levels, treatment of females with T3 does not enhance responsiveness to GnRHa and it has the potential for deleterious effects on their offspring.