Chronic High-Fat Diet Exacerbates Sexually Dimorphic Pomctm1/tm1 Mouse Obesity.

Mice with a targeted mutation in the pro-opiomelanocortin (Pomc) gene (Pomctm1/tm1 mice) are unable to synthesize desacetyl-α-MSH and α-MSH and they develop obesity when fed chow diet. In this study, we hypothesized that a chronic high-fat (HF) diet exacerbates Pomctm1/tm1 mouse obesity. Male and female Pomcwt/wt and Pomctm1/tm1 mice were fed low-fat (LF) (10 kcal percent fat) or HF (45 kcal percent fat) diets from weaning for 23 weeks. We show that Pomctm1/tm1 mouse obesity is sexually dimorphic and exacerbated by an HF diet. Male Pomctm1/tm1 mice develop obesity because they are hyperphagic compared with Pomcwt/wt mice when fed an LF or HF diet. Female Pomctm1/tm1 mice develop obesity when feeding on an LF or HF diet because they exhibit signs of reduced energy expenditure (no change in feed efficiency; body weight gained exceeding energy intake) compared with Pomcwt/wt mice. A chronic HF diet exacerbates male Pomctm1/tm1 and Pomcwt/wt mouse obesity, and the increased energy intake fully accounts for increased weight gain. In contrast, female Pomcwt/wt mice are protected from chronic HF diet-induced obesity because they reduce the amount of HF diet eaten, and they appear to increase their energy expenditure (no change in feed efficiency but energy intake exceeding body weight gained). A chronic HF diet exacerbates female Pomctm1/tm1 mouse obesity due to impaired ability to reduce the amount of HF diet eaten and apparent impaired HF diet-induced adaptive thermogenesis. Our data show that desacetyl-α-MSH and α-MSH are required for sexually dimorphic HF diet-induced C57BL/6J obesity. In conclusion, desacetyl-α-MSH and α-MSH play salutary roles in sexually dimorphic melanocortin obesity and sexually dimorphic HF diet-induced C57BL/6J obesity.

Seroprevalence of brucellosis in Mississippi shelter dogs.

Canine brucellosis is an emerging disease and compatible with a One Health management approach. Previous research has found higher prevalence of Brucella canis in stray dog populations than in owned animals, and shelter dogs may represent a zoonotic risk to pet owners. Dogs may also contract other Brucella spp., including Brucella suis, which is carried by some feral swine in the United States and poses a public health risk. Diagnostic tests for Brucella spp. are imperfect. Misclassification of disease status can result in serious repercussions for canine and human health including the unnecessary euthanasia of false positive dogs or failure to identify and remove false negative dogs from susceptible populations. Correct interpretation of any diagnostic test requires knowledge of the pre-test probability of disease in the population, therefore the objective of this cross-sectional study was to estimate the seroprevalence of B. canis and B. suis in Mississippi shelter dogs to guide evidence-based diagnostic testing and inform policy recommendations. Banked serum samples from 571 dogs collected in 2016-2017 as a representative sample of the Mississippi shelter dog population were tested for B. canis using a rapid slide agglutination test (RSAT) and for B. suis using a buffered acidified plate agglutination test. No dogs were seropositive for B. suis antibodies. Twenty-eight dogs (4.9%) were seropositive for B. canis antibodies on the RSAT, with 13 dogs (2.3%) remaining positive when retested with the addition of 2-mercaptoethanol to increase specificity. Test prevalence by shelter ranged from 0 to 8.6%. True prevalence was estimated using stochastic modeling to account for test performance and clustering of dogs by shelter. Approximately 65% of modeled shelters did not have seropositive dogs. For shelters where B. canis was present, the mean modeled seroprevalence was 17.8%. This cross-sectional study reveals important information regarding the distribution of B. canis seroprevalence in Mississippi shelter dogs. Current diagnostic tests lack the sensitivity needed to correctly identify individual infected dogs, but population testing may provide a reasonable estimate of disease. Eradication or control measures may be most efficiently allocated to shelters where canine brucellosis has been identified to effectively minimize transmission among dogs and to humans.

Cost of bovine respiratory disease in preweaned calves on US beef cow-calf operations (2011-2015).

OBJECTIVE To develop a partial budget analysis of direct costs associated with bovine respiratory disease (BRD) in preweaned calves on US beef cow-calf operations and identify factors that strongly influence those costs. DESIGN Risk analysis model. ANIMALS US preweaned beef calf inventory from 2011 through 2015. PROCEDURES A stochastic simulation model was developed by use of a computer spreadsheet and add-in software. Input data were obtained from the USDA, peer-reviewed literature, and a survey of beef cow-calf producers. A simulation consisting of 10,000 iterations was used to account for either uncertainty or variability in model inputs. The median (90% confidence interval) was reported for each output variable. Global and local sensitivity analyses were performed to identify the most influential factors and quantitatively evaluate the effects of inputs on the estimated costs. RESULTS From 2011 through 2015, BRD in preweaned calves cost the US beef cow-calf industry approximately $165 million annually, of which costs associated with the death, treatment, and decreased weaning weight of BRD-affected calves were approximately $126, $25, and $15 million, respectively. CONCLUSIONS AND CLINICAL RELEVANCE Although BRD in preweaned calves may have a fairly small effect on the total gross income for the US beef cow-calf industry as a whole, it can have a substantial adverse effect on the net profit of BRD-affected herds. The model developed provided important information regarding the cost of BRD in preweaned calves on US beef cow-calf operations and identified factors that had an import effect on those costs.

Beef producer survey of the cost to prevent and treat bovine respiratory disease in preweaned calves.

OBJECTIVE To estimate costs associated with prevention and treatment of bovine respiratory disease (BRD) in preweaned calves on US beef cow-calf operations. DESIGN Cross-sectional survey. SAMPLE 43 beef cow-calf producers whose operations had a history of BRD in preweaned calves. PROCEDURES Mail and electronic surveys were developed and administered to producers in Nebraska, North Dakota, and South Dakota to obtain information regarding costs of BRD prevention and treatment. Descriptive statistics were generated. Mixed linear regression models were used to assess factors associated with the costs of vaccines, medicine, and labor and percentage time spent on prevention and treatment of BRD in cows, replacement heifers, and preweaned calves. RESULTS 7 mail and 36 electronic surveys were completed. Median annual costs for BRD vaccines were $2.25, $4.00, and $6.25/animal, and median annual labor costs for vaccination were $4.58, $3.00, and $5.00/animal for cows, heifers, and preweaned calves, respectively. Median annual costs for medicine and labor to treat preweaned calves for BRD were $11.00 and $15.00/ affected calf, respectively. Adjusted mean annual BRD vaccine cost for preweaned calves ($7.67/animal) was significantly greater than that for cows ($3.18/animal) and heifers ($4.48/animal). CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that labor costs associated with BRD vaccination and treatment were similar to or exceeded the cost of vaccines and medicine, and most of those labor costs were associated with gathering and sorting cattle. Therefore, costs associated with labor as well as medicine and vaccines should be considered during the development of BRD prevention and treatment plans.

Prevalence of canine heartworm infection in Mississippi animal shelters.

Understanding diagnosis of heartworm disease in the context of animal shelters' needs and expectations is crucial for developing guidelines that specifically address the unique shelter population. Accurate and economical heartworm testing strategies are essential. However, current comprehensive guidelines for the management of heartworm disease in dogs are directed toward client-owned animals and do not address needs of animal shelters and other resource-scarce facilities. Additionally, testing recommendations do not take into account regional and local differences in heartworm prevalence across the United States that occur due to abiotic and biotic factors. The objective of this study was to determine the apparent prevalence of Dirofilaria immitis microfilaremia and antigenemia in dogs from Mississippi animal shelters. Further, we compare agreement between microfilaria and antigen testing in this population. We performed a cross-sectional study using canine serum and blood bank samples representative of the Mississippi shelter population. Microfilaria testing of whole blood included a blood smear and modified Knott test. Antigen testing of serum was performed using the DiroCHEK® antigen ELISA test. Analyses included descriptive and analytic statistics as well as Cohen's kappa for test agreement. A total of 283 whole blood samples and 363 serum samples, representing 363 dogs from 18 shelters in 17 Mississippi counties, were utilized in this study. Sixty-four (22.6%) whole blood samples demonstrated D. immitis microfilariae on the modified Knott test and 125 (34.4%) serum samples had detectable D. immitis antigen. Increasing age and low body condition were associated with antigen-positive test results. Only age was associated with microfilaria-positive test results. There was moderate agreement between the antigen ELISA test and the modified Knott microfilaria test and poor agreement between the antigen ELISA and the blood smear. This study provides the first known report of the prevalence of D. immitis microfilaremia and antigenemia in Mississippi shelter dogs. We observed that prevalence of both microfilaremia and antigenemia was significantly higher in these sampled dogs compared to previous reports for the owned canine population in Mississippi. Heartworm infection presents unique management challenges for animal shelters. Knowledge of the expected prevalence in the area can be utilized for management decisions related to prevention, testing, and treatment of dogs in shelter populations.

Desacetyl-α-melanocyte stimulating hormone and α-melanocyte stimulating hormone are required to regulate energy balance.

OBJECTIVE: Regulation of energy balance depends on pro-opiomelanocortin (POMC)-derived peptides and melanocortin-4 receptor (MC4R). Alpha-melanocyte stimulating hormone (α-MSH) is the predicted natural POMC-derived peptide that regulates energy balance. Desacetyl-α-MSH, the precursor for α-MSH, is present in brain and blood. Desacetyl-α-MSH is considered to be unimportant for regulating energy balance despite being more potent (compared with α-MSH) at activating the appetite-regulating MC4R in vitro. Thus, the physiological role for desacetyl-α-MSH is still unclear. METHODS: We created a novel mouse model to determine whether desacetyl-α-MSH plays a role in regulating energy balance. We engineered a knock in targeted QKQR mutation in the POMC protein cleavage site that blocks the production of both desacetyl-α-MSH and α-MSH from adrenocorticotropin (ACTH1-39). RESULTS: The mutant ACTH1-39 (ACTHQKQR) functions similar to native ACTH1-39 (ACTHKKRR) at the melanocortin 2 receptor (MC2R) in vivo and MC4R in vitro. Male and female homozygous mutant ACTH1-39 (Pomctm1/tm1) mice develop the characteristic melanocortin obesity phenotype. Replacement of either desacetyl-α-MSH or α-MSH over 14 days into Pomctm1/tm1 mouse brain significantly reverses excess body weight and fat mass gained compared to wild type (WT) (Pomcwt/wt) mice. Here, we identify both desacetyl-α-MSH and α-MSH peptides as regulators of energy balance and highlight a previously unappreciated physiological role for desacetyl-α-MSH. CONCLUSIONS: Based on these data we propose that there is potential to exploit the naturally occurring POMC-derived peptides to treat obesity but this relies on first understanding the specific function(s) for desacetyl-α-MSH and α-MSH.