Clinical and reproductive consequences of using BVDV-contaminated semen in artificial insemination in a beef herd in Argentina.

The current report was prompted by an atypical outbreak of mucosal disease that occurred in a beef herd in the southwestern part of Buenos Aires Province, Argentina, where a total of 9/41 (21.9%) yearling bulls died. Blood samples from 73 bulls and 189 heifers were tested for evidence of persistent BVDV infection with Bovine Viral Diarrhea Virus (BVDV). Non-cytopathic BVDV was isolated from 7 (9.6%) 24- to 36-month-old bulls, and 3 (1.6%) 36-month-old heifers. Non-cytopathic BVDV was also detected in the seminal plasma of three of six persistently infected (PI) bulls. Furthermore, a 171 bp genomic fragment of BVDV was consistently detected by nested RT-PCR in one of the two samples of the commercial semen used for artificial insemination, indicating that this semen could be a possible source of infection for the whole herd. To evaluate the possible reproductive consequences of PI heifers and bulls, ovaries and semen were obtained from PI cattle for in vitro assays. The in vitro fertilization of oocytes with semen from PI bulls was associated with decreased cleavage and embryo development rates. Additionally, non-cytopathic BVDV was isolated from the follicular fluid of PI heifers. Genetic typing revealed that all isolates BVDV from the present study had a high percentage of homology and that all of the fragments from the RT-PCR clearly fit with the BVDV 1b cluster. These findings confirm the negative impact that BVDV can have on the reproductive performance of cattle and the importance of applying the proper sanitary controls to minimize the risk of BVDV infection.

Extinction and reacquisition of a fear-motivated memory require activity of the Src family of tyrosine kinases in the CA1 region of the hippocampus.

Evidences indicate that extinction represents a NMDA receptor (NMDAr)-dependent learning rather than erasure of previously stored information. Several members of the Src family of tyrosine kinases are activated by stimulation of the NMDAr and are involved in both induction of hippocampal long-term potentiation and consolidation of hippocampal-dependent, NMDAr-sensitive, memories. Here we analyzed the role of the Src family within the CA1 region of the hippocampus in extinction and reacquisition of the memory for step-down, inhibitory avoidance learning task (IA). Rats trained in IA were submitted to 5 daily extinction sessions during which the avoidance response was elicited in the absence of the unconditioned stimulus. Immediately or 180 min after each extinction session animals received intra-CA1 infusions of either 0.1% DMSO, the Src-family inhibitor PP2 or its inactive analog, PP3. PP2 blocked extinction of the IA response which was otherwise evident in DMSO and PP3-treated animals. After being submitted to a new training session the animals reacquired the avoidance response; however, they failed to do so if they received intra-CA1 infusions of PP2 immediately following retraining. Our results indicate that, like the original learning, extinction and reacquisition of the IA response require activity of the Src family in the CA1 region of the hippocampus.

Endemic human plague in New Mexico: risk factors associated with infection.

A retrospective case-control study was conducted to identify risk factors, other than contact with infected animal tissues, for infection caused by Yersinia pestis in non-Indian residents of areas with endemic sylvatic plague in New Mexico. The study group consisted of 16 persons who had bacteriologically confirmed cases of plague in the period 1975-1976 and 45 controls who were matched by age, sex, and location of residence. Participants were questioned about outdoor activities, environmental conditions in and around the home, procedures of pet care, exposure to animals and insects, and medical history. The availability of harborage and food sources for wild rodents as a result of human activity in the immediate home environment was associated with risk of infection. Failure to take steps to control fleas on dogs and cats also appeared to be a possible risk factor. No other significant differences were found between patients and controls. Plague in New Mexico appears to result primarily from entry of the reservoir host into the habitat of the human rather than from entry of the human into the sylvatic habitat of the reservoir host.

Epidemiologic and clinical features of an outbreak of bubonic plague in New Mexico.

An outbreak of seven cases of bubonic plague in New Mexico was investigated. Clinical features were studied and correlated with field studies in an attmept to determine the source of infection in patients with indefinite histories of exposure. Most patients presented with fever, malaise, and an acute painful lymphadenitis (bubo). One death occurred in a patient with bubonic-septicemic plague complicated by meningitis due to Yersinia pestis. All patients lived in rural or semirural areas, and most had been in the general vicinity of their usual residence during the six days prior to onset of symptoms. The outbreak was associated with probable epizootics in rodents in two different areas of the state. One case was traced to direct hand contact with plague-infected rabbits. One patient developed insect bites after sleeping in the same bed with a flea-infested cat. Three of the other five patients had insect bites, presumably flea bites, but none of the five recalled contact with rodents or rabbits. Four of the five, however, had been in contact with dogs or cats that were later shown to have titers of antibody to Y. pestis. These findings provide further support for the hypothesis that contact with domestic dogs and cats may result in direct or indirect transmission of Y. pestis to humans.