BackgroundRecent research has demonstrated that many swine and swine farmers in the Netherlands and Canada are colonized with MRSA. However, no studies to date have investigated carriage of MRSA among swine and swine farmers in the United States (U.S.).MethodsWe sampled the nares of 299 swine and 20 workers from two different production systems in Iowa and Illinois, comprising approximately 87,000 live animals. MRSA isolates were typed by pulsed field gel electrophoresis (PFGE) using SmaI and EagI restriction enzymes, and by multi locus sequence typing (MLST). PCR was used to determine SCCmec type and presence of the pvl gene.ResultsIn this pilot study, overall MRSA prevalence in swine was 49% (147/299) and 45% (9/20) in workers. The prevalence of MRSA carriage among production system A's swine varied by age, ranging from 36% (11/30) in adult swine to 100% (60/60) of animals aged 9 and 12 weeks. The prevalence among production system A's workers was 64% (9/14). MRSA was not isolated from production system B's swine or workers. Isolates examined were not typeable by PFGE when SmaI was used, but digestion with EagI revealed that the isolates were clonal and were not related to common human types in Iowa (USA100, USA300, and USA400). MLST documented that the isolates were ST398.ConclusionsThese results show that colonization of swine by MRSA was very common on one swine production system in the midwestern U.S., suggesting that agricultural animals could become an important reservoir for this bacterium. MRSA strain ST398 was the only strain documented on this farm. Further studies are examining carriage rates on additional farms.
In this study, we investigated the effects of 192 IgG saporin injections into the medial septal area (MSA), or nucleus basalis magnocellularis (NBM), and combined injections into the MSA and NBM, on water maze and radial arm maze performance in the male rat. The results of the present study reveal a dissociation between the effects of 192 IgG saporin injections into the basal forebrain on the performance of two tasks of spatial learning in the rat. Bilateral injections of 192 IgG saporin into the NBM, MSA or combined MSA/NBM failed to disrupt water maze performance when compared to controls. In contrast, injections of 192 IgG saporin into the MSA, NBM or MSA/NBM induced mild impairments on a radial arm maze task. Overall, the disruption of spatial learning observed in this study was, however, relatively mild compared to deficits in spatial learning reported using less selective lesions of the cholinergic basal forebrain. Consequently, the results of this study suggest that a selective reduction in cholinergic transmission in the basal forebrain is, by itself, insufficient to account for the functional impairments observed in spatial learning in the rat. Although our data do support the use of 192 IgG saporin as a selective cholinergic toxin in the basal forebrain, they further suggests that assessment of spatial learning in the rat following 192 IgG saporin lesions of the basal forebrain in combination with lesions to other neurotransmitter systems, may be a more viable approach to the elucidation of the neuropathological mechanisms that are associated with the cognitive deficits seen in Alzheimer's disease.
The present study examined the long-term (2 years) effects of estrogen loss or estrogen replacement therapy (ERT) on cholinergic neurons in the nucleus basalis of Meynert and on cholinergic fibers in the prefrontal and parietal cortex of adult female cynomolgus monkeys. Cholinergic fiber density in layer II of the prefrontal cortex was decreased in monkeys who were ovariectomized and treated with placebo for 2 years. In contrast, ovariectomized monkeys receiving ERT for 2 years had fiber densities that were comparable to those of intact controls. No differences in parietal cholinergic fiber density or nucleus basalis cholinergic neuron number or volume were found among intact, ovariectomized, or ERT monkeys. Our results suggest that ERT is effective in preventing region-specific changes in cortical cholinergic fibers that result from the loss of circulating ovarian hormones. These modest but appreciable effects on cholinergic neurobiology following long-term estrogen loss and ERT may contribute to changes in visuospatial attention function that is mediated by the prefrontal cortex.
Many postmenopausal women question whether to start or continue hormone therapy because of recent clinical trial negative results. However, evidence from other studies of postmenopausal women, and from studies in menopausal monkeys, indicate that estrogen has neurocognitive protective effects, particularly when therapy is initiated close to the time of menopause before neural systems become increasingly compromised with age. In this review, we present studies of menopausal women and female monkeys that support the concept that estrogen therapies protect both cognitive function and neurobiological processes. Keywords monkeys; hormones; menopause; neurobiology; memoryResults from the Women's Health Initiative Memory Study (WHIMS) [Espeland et al., 2004;Rapp et al., 2003a;Shumaker et al., 2003;Shumaker et al., 2004] has caused many postmenopausal women to question whether to start or to continue hormone therapy (HT) to decrease the risk of developing dementia and has caused many others to question the role of estrogen in protecting cognitive function from age-related decline in general. However, several critical factors likely influenced the WHIMS negative results, including the advanced age of the subjects, delayed timing of HT initiation in relation to when menopause occurred, and the presence of pathological states (e.g., diabetes, hypertension, obesity) [Ancelin and Ritchie, 2005;Genazzani et al., 2007;Maki, 2006;Sherwin, 2005]. In conjunction with the positive results of estrogen obtained in randomized clinical trials in younger women [Sherwin and Henry 2008], multiple factors have led to the development of the "critical period hypothesis" in which it is theorized that estrogen exerts protective effects on cognition only when it is initiated closely in time to menopause, before neural systems become increasingly challenged by age-related changes and/or neurons become less sensitive or responsive to HT.Animal models have proven useful in investigating different parameters of HT neuroprotection in ways that otherwise are not possible in women. Over the last 15 years, our laboratory has used surgically menopausal macaque monkeys as models of postmenopausal women in studies to investigate the neuroprotection by HT of both [Steger and Peluso, 1987], female macaques have 28 day menstrual cycles and patterns of ovarian hormone fluctuations that are similar to those of human females [Goodman et al., 1977;Jewitt and Dukelow, 1972]. These monkeys experience a menopause that closely resembles that of women [Gilardi et al., 1997;Johnson and Kapsalis, 1995], and they also have physiological responses to surgical menopause and estrogen therapy (ET) that are similar to women [Adams et al., 1990;Jayo et al., 1998;Jerome et al., 1994].In the following sections, we present studies of menopausal women and female monkeys that support the concept that estrogen therapies protect both cognitive function and neurobiological processes. Neuroprotection of Cognitive Function Evidence in Postmenopausal WomenSeveral lines of evid...
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