Conservation of rare and local breeds of livestock.

The genetic diversity of domesticated species is contained within breeds, with the result that conserving breeds conserves this diversity. Breeds are predictable genetic resources that allow a match of animals with different environments and production goals. Breeds were developed through a process involving foundation, isolation and selection. Breed types that qualify as genetic resources include 'landraces' (local breeds), standardised breeds, commercial production breeds and feral livestock that have returned to a free-living state. Currently, breeds of all classes are threatened with extinction. The reasons for breed conservation include maintaining breed diversity for future needs, cultural connections between people and breeds, and material for scientific investigation. Several breeds have undergone genetic adaptations that make them uniquely suited to specific challenging environments. Conservation depends upon discovering these genetic resources, securing them with a good genetic structure, and subsequently sustaining them for long-term survival with demand for the breed and its products.

La diversité génétique des espèces domestiquées par l'homme se retrouve dans les différentes races au sein de chaque espèce, ce qui signifie que la conservation des races est une manière de préserver cette diversité. Les races constituent des ressources génétiques prévisibles qui permettent d'apparier des individus issus d'environnement différents et dotés de capacités de production correspondant à des objectifs spécifiques. Les races ont été développées au terme d'un processus basé sur la détermination, l'isolement et la sélection de ces traits. Sont qualifiées de ressources génétiques les races locales, les races standardisées, les races de production commerciale et les espèces domestiquées puis retournées à l'état sauvage (animaux féraux). Des races appartenant à chacune de ces catégories sont aujourd'hui menacées d'extinction. La conservation des races se justifie par la nécessité de préserver leur diversité pour les besoins futurs, mais aussi par les liens culturels qui se nouent entre les sociétés humaines et certaines races animales et par l'impératif de fournir des matériels biologiques à la recherche scientifique. Plusieurs races ont connu des adaptations génétiques qui les ont rendues particulièrement aptes à faire face à des environnements difficiles. La conservation consiste à mettre en lumière ces ressources génétiques, à les sécuriser au moyen d'une structure génétique solide et à les préserver de manière durable afin de répondre à la demande de reproducteurs et de leurs produits.

Las razas son el recipiente que aloja la diversidad genética de las especies domésticas, por lo que conservarlas equivale a conservar esa diversidad. Las razas son recursos genéticos predecibles que permiten aparear a animales con diferentes entornos y objetivos de producción. Las razas aparecieron a resultas de un proceso que entraña fundación, aislamiento y selección. Los tipos de raza que cabe asimilar a recursos genéticos son las «variedades locales¼ (razas autóctonas), las razas normalizadas, las razas de producción industrial y las razas de ganado asilvestrado que ha vuelto a la vida en libertad. Actualmente hay toda clase de razas amenazadas de extinción. Entre los argumentos que justifican la conservación de las razas están el de mantener la diversidad para atender futuras necesidades, el de respetar los vínculos culturales que conectan a la gente con las razas y el de disponer de material para la investigación científica. Varias razas han experimentado adaptaciones genéticas que las han hecho singularmente aptas para vivir en uno u otro entorno especialmente difícil. La conservación de las razas depende de que esos recursos genéticos sean descubiertos y su continuidad quede asegurada gracias a una buena estructura genética, para después sostener su supervivencia a largo plazo con la demanda de la raza en cuestión y de sus derivados.

The legacy of Columbus in American horse populations assessed by microsatellite markers.

Criollo horse populations descend from horses brought from the Iberian Peninsula over the period of colonization (15th to 17th century). They are spread throughout the Americas and have potentially undergone genetic hybridization with other breeds in the recent past. In this study, 25 autosomal microsatellites were genotyped in 50 horse breeds representing Criollo populations from 12 American countries (27 breeds), breeds from the Iberian Peninsula (19), one breed each from France and Morocco and two cosmopolitan horse breeds (Thoroughbred and Arabian). The genetic relationships among breeds identified five clusters: Celtic; Iberian; North American with Thoroughbred influence; most Colombian breeds; and nearly all other Criollo breeds. The group of "all other Criollo breeds" had the closest genetic relationship with breeds originating from the Iberian Peninsula, specifically with the Celtic group. For the whole set of Criollo breeds analysed, the estimated genetic contribution from other breeds was approximately 50%, 30% and 20% for the Celtic, Iberian and Arab-Thoroughbred groups, respectively. The spatial distribution of genetic diversity indicates that hotspots of genetic diversity are observed in populations from Colombia, Ecuador, Brazil, Paraguay and western United States, possibly indicating points of arrival and dispersion of Criollo horses in the American continent. These results indicate that Criollo breeds share a common ancestry, but that each breed has its own identity.

Serological evidence for a hepatitis e virus-related agent in goats in the United States.

Hepatitis E virus (HEV) causes an important public health disease in many developing countries and is also endemic in some industrialized countries. In addition to humans, strains of HEV have been genetically identified from pig, chicken, rat, mongoose, deer, rabbit and fish. While the genotypes 1 and 2 HEV are restricted to humans, the genotypes 3 and 4 HEV are zoonotic and infect humans and other animal species. As a part of our ongoing efforts to search for potential animal reservoirs for HEV, we tested goats from Virginia for evidence of HEV infection and showed that 16% (13/80) of goat sera from Virginia herds were positive for IgG anti-HEV. Importantly, we demonstrated that neutralizing antibodies to HEV were present in selected IgG anti-HEV positive goat sera. Subsequently, in an attempt to genetically identify the HEV-related agent from goats, we conducted a prospective study in a closed goat herd with known anti-HEV seropositivity and monitored a total of 11 kids from the time of birth until 14 weeks of age for evidence of HEV infection. Seroconversion to IgG anti-HEV was detected in seven of the 11 kids, although repeated attempts to detect HEV RNA by a broad-spectrum nested RT-PCR from the faecal and serum samples of the goats that had seroconverted were unsuccessful. In addition, we also attempted to experimentally infect laboratory goats with three well-characterized mammalian strains of HEV but with no success. The results indicate that a HEV-related agent is circulating and maintained in the goat population in Virginia and that the goat HEV is likely genetically very divergent from the known HEV strains.

Clinicopathologic features of intracranial central neurocytomas in 2 dogs.

BACKGROUND: In humans, central neurocytomas are rare and typically benign intracranial tumors found within the lateral ventricles, although extraventricular variants have been reported. Intracranial central neurocytomas have not been previously recognized in domestic animals. OBJECTIVES: To describe the clinicopathologic features of canine intracranial central neurocytomas. ANIMALS: Two dogs with spontaneous intracranial and intraventricular neoplasms. RESULTS: Both dogs experienced seizures, rapid neurological deterioration, and death from tumor-associated complications within 5 days of the onset of clinical signs, and had neoplastic masses within the lateral ventricles. A brain MRI was performed in 1 dog, which revealed a T1-isointense, heterogeneously T2 and FLAIR hyperintense, and markedly and heterogeneously contrast-enhancing mass lesions within both lateral ventricles. Histologically, the neoplasms resembled oligodendrogliomas. The diagnosis of central neurocytoma was supported by documenting expression of multiple neuronal markers, including neuron-specific enolase, synaptophysin, neural-cell adhesion molecule, and neuronal nuclear antigen within the tumors, and ultrastructural evidence of neuronal differentiation of neoplastic cells. CONCLUSIONS AND CLINICAL IMPORTANCE: Central neurocytoma should be a differential diagnosis for dogs with intraventricular brain masses. Morphologic differentiation of central neurocytoma from other intraventricular neoplasms, such as ependymoma or oligdendroglioma, can be difficult, and definitive diagnosis often requires immunohistochemical or ultrastructural confirmation of the neural origin of the neoplasm.

A single mid-gestation exposure to TCDD yields a postnatal autoimmune signature, differing by sex, in early geriatric C57BL/6 mice.

We recently observed an autoimmune profile in 24-week-old C57BL/6 mice that received a 2.5 or 5.0µg/kg mid-gestation dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (Mustafa et al., 2008). The clinical signs were consistent with a lupus-like syndrome and included: increased autoantibody levels, renal IgG and C3 immune complex deposition with associated inflammation, and increased peripheral Vß(+) T cells. No studies currently exist following the progression of such disease into middle or advanced ages, when human autoimmune diseases may manifest. Therefore in the present study, littermates of mice from the previous 24 week prenatal TCDD study were allowed to age to 48 weeks, considered early geriatric in mice. Similarities and differences in the disease profile based on age and sex were observed. Peripheral autoreactive Vß(+) T cells were increased in both sexes at 48 weeks, in contrast to males only at 24 weeks. Activated T cells from 48-week-old prenatal TCDD females over-produced the pro-inflammatory cytokine IFN-γ while males over-produced IL-10, effects again not seen at 24 weeks. Splenic transitional-2 B cells (CD21(int)CD24(hi)) were increased in males while transitional-1 B cells (CD23(neg) CD1(neg)) were increased in females at 48 weeks. Autoantibodies to cardiolipin and CD138(+) spleen plasma cells were significantly increased in the aged males but not females. Anti-IgG and anti-C3 immune complex renal deposition were also significantly increased in the prenatal TCDD males but not females. These selective changes in the aged male mice may be noteworthy, in that the prevalence of SLE in humans shifts dramatically toward males with aging. The collective findings in aged mice suggest that prenatal TCDD permanently biases the postnatal immune response in C57BL/6 mice toward autoimmunity, and support a significant B cell component to the induced renal autoimmune disease.

An enhanced postnatal autoimmune profile in 24 week-old C57BL/6 mice developmentally exposed to TCDD.

Developmental exposure of mice to the environmental contaminant and AhR agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), causes persistent postnatal suppression of T cell-mediated immune responses. The extent to which prenatal TCDD may induce or exacerbate postnatal autoimmune disease remains unknown. In the present study, time-pregnant high affinity AhR C57BL/6 mice received a single oral administration of 0, 2.5, or 5 microg/kg TCDD on gestation day (gd) 12. Offspring of these mice (n=5/gender/treatment) were evaluated at 24 weeks-of-age and showed considerable immune dysregulation that was often gender-specific. Decreased thymic weight and percentages of CD4(+)CD8(+) thymocytes, and increased CD4(+)CD8(-) thymocytes, were present in the female but not male offspring. Males but not females showed decreased CD4(-)CD8(+) T cells, and increased Vbeta3(+) and Vbeta17a(+) T cells, in the spleen. Males but not females also showed increased percentages of bone marrow CD24(-)B220(+) B cell progenitors. Antibody titers to dsDNA, ssDNA and cardiolipin displayed increasing trends in both male and female mice, reaching significance for anti-dsDNA in both genders and for ssDNA in males at 5 microg/kg TCDD. Immunofluorescent staining of IgG and C3 deposition in kidney glomeruli increased in both genders of prenatal TCDD-exposed mice, suggestive of early stages of autoimmune glomerulonephritis. Collectively, these results show that exposure to TCDD during immune system development causes persistent humoral immune dysregulation as well as altered cell-mediated responses, and induces an adult profile of changes suggestive of increased risk for autoimmune disease.

Persistent vulvar hemorrhage secondary to vaginal hemangioma in dogs.

Two young female dogs were presented with a chronic history of persistent vulvar hemorrhage. Vaginoscopy was ultimately used to locate bleeding vaginal masses near the urethral papilla. In both cases, episiotomy was performed to resect the mass, and hemangioma was diagnosed histologically. These tumors caused persistent vaginal bleeding; they were difficult to diagnose without vaginoscopy and lavage; and surgical excision was curative in at least one case.

A possible dominant white gene in Jersey cattle.

A white heifer ("Snow") was born in 1991 from coloured registered Jersey parents. She produced six calves sired by coloured Jersey bulls: three white bull calves, two white heifer calves, and one coloured bull calf. One of the white bull calves was mated with 40 Hereford x Friesian yearling heifers (white face, predominantly black body with some white patches). The 38 resulting calves included 16 white and 22 coloured calves. Twelve of the 16 white calves were heifers and four were bulls. Red or black spotting was recorded on some white calves. The results are consistent with an autosomal dominant mutant causing the white phenotype. The mutation appears to have arisen spontaneously in Snow, then passing to her white progeny and white grand-progeny. The white individuals varied from entirely white in a few cases, to most having some residual small areas of red or black pigmentation in patterns not typical of other reported white spotting patterns of cattle.

Evaluation of the bromosulfophthalein 30-minute retention test for the diagnosis of hepatic disease in dogs.

The purpose of this study was to evaluate efficacy of bromosulfophthalein (BSP) retention testing in dogs with and without histopathologically confirmed hepatobiliary disease. Medical records of 150 dogs with hepatobiliary disease having both a BSP test and hepatic biopsy were retrieved. Histopathologic slides of liver tissue were reviewed, and dogs were classified according to 1 of 11 histopathologic categories. Twenty-five clinically normal random-source dogs were used as controls for hepatic biopsy and BSP testing. No dogs suffered adverse effects due to BSP administration. BSP retention was significantly (P < .05) higher in hospitalized (13.9%) than control (3.2%) dogs, but the test could not distinguish between hospitalized dogs with different types of hepatobiliary disease. Sensitivity, specificity, and predictive values of BSP retention as a test for hepatic disease were calculated. Using 5.0% as a cutoff for normal BSP retention resulted in a specificity of 88% and a sensitivity of 76%. Using 6.0% as a cutoff for normal BSP retention resulted in a specificity of 100% and a sensitivity of 70%. Dogs of this study having BSP retention of >6% had at least an 86% chance of having an abnormal liver. We concluded that continued use of BSP retention testing is warranted as a noninvasive diagnostic test for liver disease in dogs.

Diffuse annular fusiform adenocarcinoma in a dog.

Canine colonic intestinal adenocarcinoma typically presents as rectal polypoid or annular stenotic masses causing clinical signs consistent with large bowel disease. This report discusses an unusual case of intestinal adenocarcinoma in an 11-year-old, neutered male German shepherd dog presented for evaluation of anorexia, profuse watery diarrhea, and weight loss. In this dog, colonic adenocarcinoma diffusely infiltrated the entire large bowel and caused an annular fusiform lesion, as confirmed by endoscopic biopsies and postmortem examination. Other unique features included a paucity of desmoplasia associated with the neoplastic lesion and widespread metastasis to regional lymph nodes, lung, and prostate.

Evidence for the involvement of CD44 in endothelial cell injury and induction of vascular leak syndrome by IL-2.

At sites of chronic inflammation seen during infections, autoimmunity, graft-vs-host response, and cytokine therapy, endothelial cell injury is known to occur, the exact mechanism of which is unknown. In the current study we used IL-2-induced vascular leak syndrome (VLS) as a model to investigate whether cytotoxic lymphocytes use CD44 in mediating endothelial cell injury. Administration of IL-2 to wild-type mice triggered significant VLS in the lungs and liver. In contrast, in CD44 knockout (KO) mice, IL-2-induced VLS was markedly reduced in the lungs and liver. IL-2-treated wild-type and CD44 KO mice had similar levels of perivascular infiltration with lymphocytes in the lungs and liver. This suggested that the decrease in VLS seen in CD44 KO mice was not due to the inability of lymphocytes to migrate to these organs. Ultrastructural studies demonstrated extensive endothelial cell damage in the lungs and liver of IL-2-treated wild-type, but not CD44 KO, mice. Moreover, CD44-KO mice exhibited a marked decrease in IL-2-induced lymphokine-activated killer cell activity. The induction of VLS was dependent on the expression of CD44 on immune cells rather than endothelial cells because adoptive transfer of CD44+, but not CD44- spleen cells along with IL-2 into CD44 KO mice triggered VLS. The IL-2-induced VLS was blocked by administration of F(ab')2 of Abs against CD44. The current study demonstrates that CD44 plays a key role in endothelial cell injury. Blocking CD44 in vivo may offer a novel therapeutic approach to prevent endothelial cell injury by cytotoxic lymphocytes in a variety of clinical disease models.

Evaluation of canine lumbosacral stenosis using intravenous contrast-enhanced computed tomography.

The objective of this study was to evaluate intravenous contrast-enhanced computed tomography as a technique for predicting the within-level location(s) of compressive soft tissues in the canine lumbosacral spine. Pre-operative intravenous contrast-enhanced computed tomography of the L5-S3 vertebral levels was performed in 12 consecutive large breed dogs with lumbosacral stenosis. The images were evaluated for enhancement of soft tissues by two radiologists who were unaware of the surgical findings. For each within-level location (dorsal canal, ventral canal, right lateral recess, left lateral recess) enhancement was classified as present, absent or equivocal. The results were compared with the results of surgical exploration and histopathology of excised tissues. The positive predictive values of intravenous contrast-enhanced computed tomography for compressive soft tissues involving the dorsal canal, ventral canal and lateral recesses were 83%, 100%, and 81% respectively. Negative predictive values for compressive soft tissues involving these locations were 29%, 50%, and 40% respectively.

Evidence for the involvement of Fas ligand and perforin in the induction of vascular leak syndrome.

Endothelial cell injury resulting in vascular leak syndrome (VLS) is one of the most widely noted phenomenons in a variety of clinical diseases. In the current study we used IL-2-induced VLS as a model to investigate the role of cytolytic lymphocytes in the cytotoxicity of endothelial cells. Administration of IL-2 (75,000 U/mouse, three times a day for 3 days) into BL/6 wild-type mice triggered significant VLS in the lungs, liver, and spleen. Interestingly, perforin-knockout (KO) mice exhibited a marked decrease in IL-2-induced VLS in all three organs tested. Also, Fas ligand-defective (gld) mice and Fas-deficient (lpr) mice exhibited decreased VLS in the liver and spleen, but not in the lungs. The decreased VLS seen in perforin-KO, gld, and lpr mice was not due to any defect in lymphocyte migration or homing to various organs because histopathologic studies in these mice demonstrated significant and often greater perivascular infiltration of lymphocytes compared with the IL-2-treated wild-type mice. Ultrastructural studies of the lungs demonstrated significant damage to the endothelial cells in IL-2-treated wild-type mice and decreased damage in perforin-KO mice. IL-2 administration caused up-regulation of CD44 in all strains of mice tested and triggered increased LAK activity against an endothelial cell line in wild-type and gld mice, but not in perforin-KO mice. The current study demonstrates for the first time that perforin and Fas ligand may actively participate in endothelial cell injury and induction of VLS in a variety of organs.

Multicentric lymphosarcoma with ovarian involvement in a Nubian goat.

Multiple lymph node enlargement and an intra-abdominal mass were diagnosed in a 6-year-old doe. Necropsy revealed lymphosarcoma involving multiple organs, including the ovaries. Lymphosarcoma is rare in goats; ovarian involvement has not previously been reported.

Systemic and local effects associated with long-term epidural catheterization and morphine-detomidine administration in horses.

OBJECTIVE: The purpose of this study was to determine the systemic and local effects associated with long-term epidural catheterization and epidural morphine-detomidine administration in horses. STUDY DESIGN: Development of systemic or local effects was assessed by placing caudal epidural catheters in study horses and administering injections through the catheters every 12 hours for 14 days. ANIMALS: Ten horses with epidural catheters that received daily injections; six uncatheterized horses presented for euthanasia. METHODS: Horses received either 0.2 mg/kg morphine sulfate and 30 micrograms/kg detomidine hydrochloride or an equivalent volume of physiologic saline solution through epidural catheters. Systemic effects were compared between control and treatment horses by measuring physical parameters and hay and water consumption, as well as by evaluating major organs after euthanasia. Local effects were studied by examining cerebrospinal fluid and by grading representative samples of the spinal cord and surrounding tissues histologically for inflammation and fibrosis. Local effects were compared between control and treatment horses, as well as between catheterized (control plus treatment) horses and uncatheterized horses. RESULTS: No significant difference was identified in daily variables or hay and water consumption between control and treatment horses. No growth was obtained from cerebrospinal fluid cultures. No significant difference in cerebrospinal fluid values or spinal tissue inflammation or fibrosis grades was shown between control and treatment horses. However, when compared with uncatheterized horses, cerebrospinal fluid red blood cell values were marginally higher and protein concentrations were significantly higher in the catheterized group. Lumbosacral and sacral spinal tissue segment inflammation grades, and sacral segment fibrosis grades were significantly higher in catheterized horses. CONCLUSIONS: Long-term epidural administration of a morphine-detomidine combination is not associated with apparent adverse systemic effects in horses. Localized inflammation and fibrosis seem to be catheter-related. CLINICAL RELEVANCE: Potential systemic and local effects are important considerations with long-term administration of a morphine-detomidine combination through indwelling epidural catheters for alleviation of chronic musculoskeletal pain in horses.

Efficacy of an epidural combination of morphine and detomidine in alleviating experimentally induced hindlimb lameness in horses.

Amphotericin B-induced synovitis of the left tarsocrural joint was used to create a grade 3 of 4 lameness in 11 horses. Caudal epidural catheters were placed and advanced to the lumbosacral region. Baseline heart and respiratory rates were recorded and horses were videotaped at a walk and trot. Morphine sulphate (0.2 mg/kg) and detomidine hydrochloride (30 micrograms/kg) were administered to treated horses (n = 8) through the epidural catheter; an equivalent volume of physiologic saline solution was administered to control horses (n = 3) through the catheter. At hourly intervals after epidural injection for a total of 6 hours, heart and respiratory rates were recorded, and horses were videotaped walking and trotting. At the end of the observation period, video recordings were scrambled onto a master videotape. Lamenesses were scored by three investigators unaware of group assignment or treatment time. Lameness scores, heart rates, and respiratory rates were compared between groups using repeated measures analysis of variance. There was a significant decrease in lameness score after treatment with epidural morphine and detomidine (P = .0003); average lameness scores of treated horses were less than grade 1 at each hourly observation for 6 hours after drug administration. Early in the observation period, heart rates significantly increased in control horses and decreased in treated horses (P = .03). A similar trend occurred for respiratory rates (P = .07). Results of this study demonstrate that epidural administration of a combination of morphine and detomidine is capable of providing profound hindlimb analgesia in horses.

Inheritance of goat coat colors.

Goat color inheritance was evaluated based on color description of 218 kids and their parents (10 sires, 178 dams) from mixed crosses between several goat populations in an experiment on cashmere fiber production. Altogether 10 color patterns were observed. They were postulated to be caused by 10 alleles at the Agouti locus, with the allele for white or tan color being the top dominant allele, and the nine others codominant. The bottom recessive allele, for nonagouti color, was the 11th allele at this locus. The postulated alleles are white or tan (A(wt)), black mask (A(blm)), bezoar (A(bz)), badgerface (A(b)), grey (A(g)), lightbelly (A(lb)), swiss markings (A(sm)), lateral stripes (A(ls)), mahogany (A(mh)), red cheek (A(rc)), and nonagouti (Aa). Two types of eumelanin pigment were observed, black and light brown, the latter being dominant. Recessive brown was not observed.

Spontaneous uterine infections are associated with elevated prostaglandin F(2)alpha metabolite concentrations in postpartum dairy cows.

Postpartum Holstein (n=21) and Jersey (n=4) cows were used to determine if uterine infections are associated with elevated plasma concentrations of 13,14-dihydro-15-keto-prostaglandin F(2)alpha (PGFM). Based upon clinical examinations and bacterial content of intrauterine fluid samples, cows detected with uterine infections between 21 and 28 d post partum were used (infected; n=14). These cows were matched with herdmates that were free of infection (control; n=11). Beginning on the day the cows were assigned to the experiment (Day 1), blood samples were collected on alternate days for the next 14 to 15 d. Plasma samples were stored at -20 degrees C until assayed. From Day 1 until the end of the experiment, uterine fluid samples were collected transcervically twice weekly for aerobic bacterial culture. Endometrial biopsies were collected between Days 6 and 8 and Days 13 and 15. Control cows did not show signs of uterine infection throughout the trial, and bacterial cultures indicated that there were no significant bacterial populations in the uteri of the control cows. The uteri of infected cows harbored numerous microbes. Actinomyces pyogenes was most prominent. Various species of Streptococcus and Pasteurella were also prevalent in the infected cows. Escherichia coli was present in the uterus of both infected and control cows. Biopsies showed that infected cows had more (P<0.05) neutrophils, plasma cells and lymphocytes in the endometrium than did the control cows. As determined by plasma progesterone concentrations, 83% of the control and 50% of the infected cows had functional luteal tissue during the 2-wk sampling period. Plasma PGFM profiles were linear (P<0.03) and did not differ between treatment groups (P>0.01). However, average plasma PGFM concentrations were greater (P<0.0001) in infected than in control cows. These data indicate that plasma PGFM concentrations are greater in postpartum cows with spontaneous uterine infections then in herdmates free of infection.