Influence of vestibulovaginal stenosis,pelvic bladder,and recessed vulva on response to treatment for clinical signs of lower urinary tract disease in dogs: 38 cases (1990-1999)

OBJECTIVE: To determine influence of vestibulovaginal stenosis, pelvic bladder, and recessed vulva on response to treatment for clinical signs of lower urinary tract disease in dogs. DESIGN: Retrospective study. ANIMALS: 38 spayed female dogs. PROCEDURE: Medical records and client follow-up were reviewed for dogs evaluated via excretory urography because of clinical signs of lower urinary tract disease. Clinical signs, results of radiography, and response to surgical or medical treatment were analyzed. RESULTS: Clinical signs included urinary tract infection (n = 24), urinary incontinence (20), vaginitis (11), pollakiuria or stranguria (10), and perivulvar dermatitis (4). Vaginocystourethrographic findings included vestibulovaginal stenosis (n = 28), pelvic bladder (17), and ureteritis or pyelonephritis (4). Ten dogs had a vestibulovaginal ratio of < 0.20 (severe stenosis), 9 dogs had a ratio of 0.20 to 0.25 (moderate stenosis), 9 dogs had a ratio of 0.26 to 0.35 (mild stenosis), and 10 dogs had a ratio of > 0.35 (anatomically normal). Lower urinary tract infection, incontinence, and pelvic bladder were not associated with response to treatment for recessed vulva. Vestibulovaginal stenosis with a ratio < 0.20 was significantly associated negatively with response to treatment. Dogs without severe vestibulovaginal stenosis that received vulvoplasty for a recessed vulva responded well to treatment. CONCLUSIONS AND CLINICAL RELEVANCE: Vestibulovaginal stenosis is likely an important factor in dogs with vestibulovaginal ratio < 0.20. Vaginectomy or resection and anastomosis should be considered in dogs with severe vestibulovaginal stenosis and signs of lower urinary tract disease.     

Sensitivity of test strategies used in the Voluntary Johne's Disease Herd Status Program for detection of Mycobacterium paratuberculosis infection in dairy cattle herds

OBJECTIVE: To evaluate sensitivities at the herd level of test strategies used in the Voluntary Johne's Disease Herd Status Program (VJDHSP) and alternative test strategies for detecting dairy cattle herds infected with Mycobacterium paratuberculosis. DESIGN: Nonrandom cross-sectional study. SAMPLE POPULATION: 64 dairy herds from Pennsylvania, Minnesota, Colorado, Ohio, and Wisconsin. Fifty-six herds had at least 1 cow shedding M. paratuberculosis in feces; the other 8 herds were free from paratuberculosis. PROCEDURE: For all adult cows in each herd, serum samples were tested for antibodies to M. paratuberculosis with an ELISA, and fecal samples were submitted for bacterial culture for M. paratuberculosis. Sensitivities at the herd level (probability of detecting infected herd) of various testing strategies were then evaluated. RESULTS: Sensitivity at the herd level of the testing strategy used in level 1 of the VJDHSP (use of the ELISA to test samples from 30 cows followed by confirmatory bacterial culture of feces from cows with positive ELISA result) ranged from 33 to 84% for infected herds, depending on percentage of cows in the herd with positive bacterial culture results. If follow-up bacterial culture was not used to confirm positive ELISA results, sensitivity ranged from 70 to 93%, but probability of identifying uninfected herds as infected was 89%. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that the testing strategy used in the VJDHSP will fail to identify as infected most dairy herds with a low prevalence of paratuberculosis. A higher percentage of infected herds was detected if follow-up bacterial culture was not used, but this test strategy was associated with a high probability of misclassifying uninfected herds.     

Differences in metabolic parameters and gene expression related to osteochondrosis/osteoarthrosis in pigs fed 25-hydroxyvitamin D3

Osteochondrosis/osteoarthrosis (OC/OA) are common terms for various joint pathologies that occur in pigs. Pathologies that may contribute to these disorders have been described, but the primary cause(s) remain unknown. We hypothesised that as OC has some similarities to dyschondroplasia, which involves a failure of growth plate chondrocytes to fully differentiate and hypertrophy, treatment with 25-hydroxyvitamin D3 (25-D) might reduce the incidence and/or severity of lesions in pigs, as it does in chickens with dyschondroplasia. Control pigs were fed a commercial diet ad libitum. In the treated group this diet was supplemented with 25-D at 0.1 mg/kg. Ten pigs from each of the control and treated groups were sampled at 7, 12, 16 and 21 weeks. Treatment with 25-D had no effect on the incidence or severity of OC/OA lesions. Cartilage dry weight, total collagen content and proteoglycan content, and plasma levels oftotal calcium, inorganic phosphorous, vitamin C, insuline-like growth factor-I, parathyroid hormone and tumour necrosis factor alpha were unaffected by treatment. In addition, none of these parameters were correlated with the incidence or severity of OC/OA lesions. The mRNA expression levels of 21 out of 23 genes assayed by RT-PCR were unaltered in articular cartilage from OA lesion samples as compared to normal articular cartilage. However, collagen type II was reduced and collagen type X increased in OA lesion and near lesion samples. These results suggest that OA in pigs may share some features of osteoarthritis in other mammalian species.     

Surgical procedure and postoperative management of a perineal urethrostomy in a chimpanzee (Pan troglodytes).

A chimpanzee (Pan troglodytes) with traumatic loss of the distal penis developed a gradually enlarging ventral urethral swelling and progressive dysuria. Endoscopy identified a urethral diverticulum, and endoscopic resection of the diverticulum wall was performed. Postoperative infection caused extensive necrosis of the penis, which necessitated a perineal urethrostomy. Complications of the urethrostomy included urethral obstruction from recurrent urethral stricture. The stricture was managed by regular dilatation using urethral bougies. Because of considerable postoperative swelling, catheterization was required to allow micturition following both the diverticular resection and polyp debulking. A shortened catheter sutured to the skin was tolerated for up to 10 days. Four yr after the urethrostomy, the animal is healthy and asymptomatic with endoscopic examinations performed at 12 mo intervals. This case demonstrates that with appropriate aftercare, perineal urethrostomy is an effective technique in the treatment of chronic distal urethral obstruction in the chimpanzee and probably other primate species.     

Implications of simian retroviruses for captive primate population management and the occupational safety of primate handlers.

Nonhuman primates can be naturally infected with a plethora of viruses with zoonotic potential, including retroviruses. These simian viruses present risks to both captive nonhuman primate populations and persons exposed to nonhuman primates. Simian retroviruses, including simian immunodeficiency virus, simian type D retrovirus, simian T-lymphotropic virus, and gibbon ape leukemia virus, have been shown to cause clinical disease in nonhuman primates. In contrast, simian foamy virus, a retrovirus that is highly prevalent in most nonhuman primates, has not been associated with clinical disease in naturally infected primates. Although it has been shown that human retrovirus infections with human T-lymphotropic virus and human immunodeficiency virus originated through multiple independent introductions of simian retroviruses into human populations that then spread globally, little is known about the frequency of such zoonotic events. In this article, exogenous simian retroviruses are reviewed as a concern for zoo and wildlife veterinarians, primate handlers, other persons in direct contact with nonhuman primates, and other nonhuman primates in a collection. The health implications for individual animals as well as managed populations in zoos and research institutions are discussed, the cross-species transmission and zoonotic disease potential of simian retroviruses are described, and suggestions for working safely with nonhuman primates are provided.     

Gut growth and glucose tolerance in newborn pigs subjected to prenatal protein restriction and postnatal Glucagon-like Peptides

Fetal protein restriction is potentially associated with organ dysfunctions after birth (e.g. impaired gut growth, glucose tolerance and pancreatic β-cell function). Just after birth, gut growth and maturation is stimulated by enteral food intake, and inhibited by total parenteral nutrition (TPN), in part mediated via differential release of insulino- and intestino-tropic hormones like the Glucagon-Like Peptides 1 and 2 (GLP-1, GLP-2). We hypothesized that short-term co-infusion of GLP-1 and GLP-2 would stimulate pancreatic and intestinal growth in newborn TPN-fed pigs subjected to prenatal protein restriction. Two sows were fed a protein-restricted diet (PR: 8% crude protein during last 50% of gestation) while a third sow was fed a control diet (C: 15% crude protein). PR pigs were killed either at birth (n = 7) or after 3 days TPN with (n = 6) or without (n = 4) intravenous infusion of a mixture of synthetic human GLP-1_7–37 and GLP-2_1–33 (each 50 μg/kg/d). At birth, PR piglets did not show reduced body weight, relative to controls (1.45 vs. 1.50 kg), but significantly reduced weight of the small intestine (18.0 ± 0.6 vs. 21.9 ± 0.5 g/kg, P < 0.001) and a marginally reduced pancreas weight (0.85 ± 0.02 vs. 0.93 ± 0.04 g/kg, P = 0.10). Co-infusion GLP-1 and GLP-2 into PR pigs resulted in increased basal glucose levels (5.3 vs. 4.0 mM), and glucose-stimulated insulin release, but did not have any significant effect on body weight, or weight of internal organs (heart, lungs, spleen, kidneys, adrenals, stomach, colon, liver, intestine, pancreas). We conclude that short-term (3 days) infusion of native GLP-1 and GLP-2 does not stimulate gut growth or glucose tolerance in TPN-fed piglets born from protein-restricted mothers. Moderate maternal protein restriction does however cause significant reduction in intestinal growth in newborn piglets which may decrease the neonatal digestive capacity.