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To rapidly return to trade, countries with OIE status, FMD-free country where vaccination is not practised, have destroyed emergency vaccinated animals, raising ethical concerns with respect to social values, the environment, animal welfare and global food security. This two-part review explores whether science could support eligibility to return to previous OIE status in 3 months irrespective of vaccinate-to-live or vaccinate-to-die policies. Here, we examine the benefits of higher potency (≥ 6 PD50 ), high-purity vaccines formulated from antigen banks for emergency use, their efficacy and performance in differentiating infected from vaccinated animals (DIVA) assays for post-outbreak surveillance. From an intensive programme of research, we conclude that high-quality, higher potency vaccines are proven to reduce FMD virus (FMDV) subclinical circulation and the risk of carriers. Broader coverage than predicted by serology suggests the potential to hold a few 'key' vaccine strains improving logistics and reducing the financial burden of antigen banks. The OIE should adopt formal definitions for emergency vaccination and emergency vaccines. In terms of supportive tools, we consider that the lack of OIE recognition of DIVA tests other than those of PANAFTOSA in cattle is a shortcoming. There is need for research on maternal antibody interference with DIVA tests and on the use of such tests to establish whether greater purification of vaccines improves performance. We consider that alignment of waiting periods for vaccinate-to-live and vaccinate-to-die in OIE Code Article 8.5.9 1 b. and c. is feasible until an acceptable level of statistical certainty for surveillance or target probability of freedom is established to substantiate the absence of FMDV infection or circulation. It is surveillance intensity rather than waiting periods that establishes the risk of residual FMDV. EU Directive 2003/85/EC implicitly recognizes this, permitting derogation of the OIE waiting periods., (© 2013 Blackwell Verlag GmbH.)

For countries with OIE status, FMD free country where vaccination is not practised, vaccinate-to-live policies have a significant economic disincentive as the trade restriction waiting period is double that of vaccinate-to-die policies. The disposal of healthy vaccinated animals strictly for the purpose of regaining markets with debatable scientific justification is a global concern. The feasibility of aligning the waiting periods to facilitate vaccinate-to-live is explored. The first article of this two-part review (Barnett et al., 2015) explored the qualities of higher potency Foot-and-Mouth Disease (FMD) vaccines, performance of differentiating infected from vaccinated animals (DIVA) diagnostic assays particularly in vaccinates and carriers, as well as aspects of current limitations of post-outbreak surveillance. Here, the history behind the OIE waiting periods for FMD free status is reviewed as well as whether the risk of vaccinated animals and their subsequent products differ appreciably at 3 versus 6 months. It is concluded that alignment is feasible for vaccinate-to-live using higher potency FMD vaccines within the current OIE waiting period framework of 3 and 6 months blocks of time. These waiting periods reflect precedence, historical practicalities and considered expert opinion rather than a specific scientific rationale. The future lies in updated epidemiological and diagnostic technology to establish an acceptable level of statistical certainty for surveillance or target probability of freedom of FMDV (infection or circulation) not time restricted waiting periods. The OIE Terrestrial Code limits trade from a FMD free country where vaccination is not practiced to animal products and live non-vaccinated animals. The risk of FMDV in products derived from higher potency vaccinated animals is appreciably less than for countries with infected FMD status or even from a FMD free country where vaccination is practised for which the Code has Articles with guidelines for safe trade with time restrictions of 3 months or less. All these presume that key requirements in the implementation of emergency vaccination including appropriate vaccine match, vaccine application, susceptible population coverage, etc. are addressed., (© Her Majesty the Queen in Right of Canada 2013 Reproduced with the permission of the Minister of Agriculture.)

Background: A large multistate outbreak of equine herpesvirus myeloencephalopathy (EHM) occurred in May 2011 among horses that participated in a competitive event., Objective: To identify EHM risk factors among horses with a common exposure venue., Animals: A total of 123 horses: 19 horses with EHM, 14 equine herpesvirus-1 cases with no reported neurologic signs, and 90 control horses., Methods: EHM case survey data were compared with data from EHV-1 cases with no neurologic signs and healthy controls using univariable and multivariable methods., Results: Significant factors associated with higher risk for EHM compared with EHV-1 cases with no neurologic signs were (1) greater number of biosecurity risks at the event, (2) female sex, (3) increasing number of classes competed in at the event, and (4) an interaction between sex and number of classes competed in. In the EHM versus controls comparison, in addition to sex and biosecurity risks, factors associated with higher EHM risk included EHV-1 vaccination in the 5 weeks before the event and increasing number of events attended in April 2011; zinc dietary supplementation was associated with decreased risk. An interaction between sex and the number of events attended in April 2011 also was significant., Conclusions and Clinical Importance: Findings from this study suggest that dietary zinc supplementation may be associated with decreased risk of EHM. Several factors were associated with increased risk of EHM. Additional investigations of factors associated with risk of EHM are warranted to evaluate the importance of these factors in this complex disease of horses., (Copyright © 2013 by the American College of Veterinary Internal Medicine.)

Objective: To evaluate the feasibility for Rift Valley fever virus (RVFV) to enter the continental United States by various routes as well as to identify states in which domestic and wild ruminant and human populations would be most vulnerable to exposure to RVFV., Study Design: Pathways analysis., Sample Population: Animals, commodities, and humans transported from RVFV-endemic countries to the continental United States between 2000 and 2005., Procedures: Initially, agent, host, and environmental factors important in the epidemiologic aspects of RVFV were used to develop a list of potential pathways for release of RVFV into the continental United States. Next, the feasibility of each pathway was evaluated by use of data contained in governmental and public domain sources. Finally, entry points into the continental United States for each feasible pathway were used to identify the domestic and wild ruminant and human populations at risk for exposure to RVFV., Results: Feasible pathways for entry of RVFV into the continental United States were importation of RVFV-infected animals, entry of RVFV-infected people, mechanical transport of RVFV-infected insect vectors, and smuggling of live virus., Conclusions and Clinical Relevance: Domestic ruminant livestock, ruminant wildlife, and people in 14 states (Alabama, California, Florida, Georgia, Maine, Maryland, Massachusetts, Minnesota, New Jersey, New York, Pennsylvania, South Carolina, Texas, and Virginia) appeared to be most vulnerable to exposure to RVFV. Pathways analysis can provide the requisite information needed to construct an effective targeted surveillance plan for RVFV to enable rapid detection and response by animal health and public health officials.

In neonatal calves metabolic acidosis is a common sequela to diarrhea-induced dehydration and endotoxemia in the aftermath of gram-negative bacterial infections. Without treatment, metabolic acidosis is a prime factor in the death of many of these calves. This article begins with a general discussion about the causes and recognition of metabolic acidosis. The remaining sections detail the subjective and objective methods available to assess the severity of acidosis and treatment options for this metabolic condition.

Objective: To develop an economic model for comparing cost-effectiveness of medical and surgical treatment versus replacement of beef bulls with preputial prolapse., Design: Economic analysis., Sample Population: Estimates determined from medical records of bulls treated for preputial prolapse at our hospital and from information about treatment of bulls published elsewhere., Procedure: Annual depreciation cost for treatment (ADC(T)) and replacement (ADC(R)) were calculated. Total investment for an injured bull equaled the sum of salvage value, maintenance cost, and expected cost of the treatment option under consideration. Total investment for a replacement bull was purchase price. Net present value of cost was calculated for each year of bull use. Sensitivity analyses were constructed to determine the value that would warrant treatment of an injured bull., Results: The decision to treat was indicated when ADC(T) was less than ADC(R). In our example, it was more cost-effective for owners to cull an injured bull. The ADC(R) was $97 less than ADC(T) for medical treatment ($365 vs $462) and $280 less than ADC(T) for surgical treatment ($365 vs $645). Likewise, net present value of cost values indicated that it was more cost-effective for owners to cull an injured bull. Sensitivity analysis indicated treatment decisions were justified on the basis of replacement value or planned number of breeding seasons remaining for the bull., Clinical Implications: The model described here can be used by practitioners to provide an objective basis to guide decision making of owners who seek advice on whether to treat or replace bulls with preputial prolapse.

A 5-day-old Simmental Heifer was evaluated for excessive bleeding from the skin following horse fly bites. A coagulation profile and platelet numbers were normal. In vitro platelet function, measured by whole blood aggregometry, was found to be abnormal when compared with age-matched controls. Therefore, this defect in hemostasis was attributed to a qualitative defect in platelet function.

This article contains a brief overview of the magnitude and causes of perinatal calf mortality (PCM). A PATH model chart of the risk factors of PCM is presented as a foundation for preparation of herd-management programs to prevent PCM, for herd investigations to control excessive PCM, or to plan seminars for livestock producers on control of PCM. The financial impact of PCM is explored through discussions of expenses associated with PCM, management decisions after calf deaths, and a comparison of the financial losses of PCM with losses incurred through pregnancy failure.

The peak time period for the average beef producer to experience the majority of calf losses has consistently been from the time of birth through the first seven days of life. Weakness is a principal clinical sign of diseases or conditions responsible for mortality including birth trauma, prematurity or dysmaturity, congenital malformations, metabolic defects, intrauterine infection, anoxia or hypoxia, hypothermia, starvation, extremes in birth weight, and post-natal infection. This article discusses anoxia/hypoxia and septicemia in greater detail because of their involvement as a common cause of weakness in the newborn calf.

At the moment the umbilicus separates from the fetus during the birthing process, several physiologic functions formerly supported by the dam must become operational in the neonate to ensure survival of the calf. These functions include the ability to maintain adequate oxygen saturation of blood, to regulate acid-base balance, to engage endogenous metabolic pathways for energy production, and to preserve body temperature within critical limits. This article reviews cardiopulmonary function, acid-base balance, and energy metabolism in the fetus and neonate.

In a 2-month-old crossbred calf with paraplegia, results of neurologic evaluation were suggestive of a spinal cord lesion caudal to L3. The calf bled from the blood sampling site for an extended period after venipuncture. Leukocytosis, anemia, and thrombocytopenia were observed. The leukocytes were predominantly atypical blast cells. Postmortem examination revealed petechial hemorrhages throughout the internal organs. Bone marrow was pale tan, with no red marrow seen. Atypical leukocytes were diffusely distributed throughout the body, with penetration of the spinal cord and spinal roots, particularly in the lumbar region. Atypical leukocytes stained positively for alpha-naphthyl acetate esterase and chloracetate esterase, and stained with Sudan black B. Atypical leukocytes expressed class-1 and class-2 major histocompatability antigens, but did not express specific T-, B-, or null-cell surface antigens. The final diagnosis was myelomonocytic leukemia. Differential diagnosis of leukemia in calves should include myelogenous leukemia, and requires use of various techniques to make a definitive diagnosis.

Osteolytic defects were detected radiographically in the distal sesamoid bone of a 16-month-old Bralers heifer, in the middle phalanx of a 14-month-old American Gray Brahman bull, and in the distal phalanx of a 3-year-old American Gray Brahman bull. The articular cartilage was damaged in each animal because of osteolysis or pathologic fracture. After each animal was anesthetized and positioned in lateral recumbency, the lesions were curetted and packed with cancellous bone harvested from the same animal's tuber coxae. Basic postoperative management involved stall rest and immobilization of the graft site with a fiberglass cast (42 to 79 days), after which a support bandage was used for approximately 2 weeks. Recurrence of lameness has not been observed in these animals for 60 months, 58 months, and 21 months, respectively. These cases exemplify the benefit of using an autogenous cancellous bone graft for treatment of severe osteolysis of a digit in cattle.

A diagnosis of beta-mannosidosis, a lysosomal storage disease caused by a deficiency of beta-mannosidase, was made in 12 purebred Salers calves. Affected neonatal calves were unable to rise and had intention tremors, hidebound skin, slightly domed calvaria, slight prognathism, and narrow palpebral fissures. Postmortem findings included variable dilatation of the lateral cerebral ventricles, marked pallor and paucity of white matter of the cerebrum and cerebellum, and mild to marked bilateral renomegaly. Microscopic lesions consisted of clear, intracytoplasmic vacuoles, which were especially prominent in neurons, thyroid follicular cells, proximal renal tubular epithelium, and reticuloendothelial cells. By ultrastructural examination, the intracytoplasmic vacuoles were identified as membrane-bound lysosomes distended by lucent material. The serum of affected calves was profoundly deficient in beta-mannosidase. Oligosaccharides, principally a trisaccharide with a terminal hexose in the beta-anomeric configuration, accumulated in tissues of affected calves. The percentage (37.2) of affected calves from groups of siblings, the approximately equal sex ratio, and the phenotypic normalcy of the parents of affected calves are compatible with an autosomal recessive mode of inheritance typical of other glycoproteinoses.

Two cows, 1 with diarrhea and 1 with signs of forestomach outflow obstruction, were treated in part with repeated doses of a commercially available antacid/cathartic preparation containing magnesium hydroxide. Both cows subsequently were determined to have hypermagnesemia, along with severe metabolic alkalosis. In addition, each cow was comatose at the time of death. A clinical study was initiated to investigate the causal relationship between the ingestion of magnesium hydroxide and the generation of hypermagnesemia and metabolic alkalosis in adult cows. Twelve healthy mature cross bred beef cows were allotted at random to a fed or fasted (simulated anorexia) group, with 2 untreated and 4 treated cows in each group. A single dose of magnesium hydroxide (1.5 g/kg of body weight, suspended in 3.8 L of warm water) was administered per os to each treated cow, whereas each control cow was given only water. Individual determinations of selected venous blood gas values (plasma bicarbonate ion [HCO3-] concentration, and base excess [BE]), serum magnesium (Mg) concentration, and urine magnesium fractional clearance ratio (Mg-FCR) were made immediately before drug administration, and at 2, 4, 8, 12, 24, and 36 hours after treatment. Compared with control values at the conclusion of the study, mean serum Mg concentration, urine Mg-FCR, plasma HCO3- concentration, and BE were significantly higher (P = 0.0001, P = 0.0015, P = 0.028, and P = 0.021, respectively) in treated cows.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic acidosis is one of the prime factors responsible for the death of many diarrheic calves. This article begins with a general discussion about the recognition of metabolic acidosis. The remaining sections detail the utilization of certain subjective and objective methods to assess the severity of acidosis as well as the approach to treatment of this metabolic condition.

A nine year old Hereford crossbred cow with a history of progressive neurological signs was referred to the Western College of Veterinary Medicine, Saskatoon. A large intracranial mass, histologically identified as a schwannoma, was found to be compressing the left brain stem and appeared to have arisen from the left fifth cranial nerve.

Acquired megaesophagus of suspected neuromuscular origin was diagnosed in a six year old Holstein cow. The dilatation was restricted to the lower cervical esophagus. Signs included projectile regurgitation of chewed ingesta at variable periods of time after swallowing, nasal discharge of mucus and feed particles, and a cough. A secondary aspiration pneumonia was associated with this condition. The dilated portion of the esophagus was detected utilizing positive contrast radiography and fiberoptic endoscopy. Treatment consisted of feed management and antibiotics. Deglutition in the cow returned to normal over a three month period despite radiographic and fiberoptic endoscopic evidence of a persistent dilatation of the esophagus.

The effects of feeding supplementary dietary copper to a herd of 400 beef cows, were studied over a two year period. In the first year of the trial, the calves showed clinical signs of copper deficiency. There was improved growth following subcutaneous injection of copper ethylenediamine tetraacetate, and the treated calves had a 2.8% increase in adjusted weaning weights. In the second year of the trial pregnant cows were fed a basal ration of bromegrass silage, barley and minerals over the winter feeding period. The feed was supplemented with copper so that half received 5.5 mg/kg of copper on a dry matter basis and half 40 mg/kg. Calving occurred in the spring and half the calves were treated with injectable copper at birth and again at 12 weeks of age. There was no evidence of copper deficiency in the calves and there was no effect of high level copper supplementation on calf birth weight, or neutrophil candidacidal activity. Susceptibility to diarrhea varied in a complex fashion; morbidity was lowest in calves born to dams fed supplementary copper and highest in calves born to supplemented dams and injected with copper at birth. The cows and calves grazed the same copper deficient pasture over the summer. The average daily gain for calves born to supplemented cows was 0.999 +/- 0.010 kg/day (x +/- SEM) which was significantly greater than the 0.972 +/- 0.009 kg/day for calves from nonsupplemented dams (p = 0.044). The benefit of copper supplementation on 200 day weaning weight was estimated at 4.8 kg. Evidence of copper deficiency was seen when a herd test showed mean serum levels below 9 mumol/L and liver values below 0.09 mmol/kg wet matter.

A syndrome of metabolic acidosis of unknown etiology was diagnosed in twelve beef calves 7 to 31 days old. Principal clinical signs were unconsciousness or depression concomitant with weakness and ataxia. Other signs included weak or absent suckle and menace reflexes, succussable nontympanic fluid sounds in the anterior abdomen, and a slow, deep thoracic and abdominal pattern of respiration. The variation in clinical signs between calves was highly correlated (r = 0.87, P less than 0.001) with their acid-base (base deficit) status. Abnormal laboratory findings included reduced venous blood pH, pCO2 and bicarbonate ion concentration as well as hyperchloremia, elevated blood urea nitrogen, increased anion gap and neutrophilic leukocytosis with a left shift. Sodium bicarbonate solution administered intravenously effectively raised blood pH and improved demeanor, ambulation and appetite. All calves did well following a return to a normal acid-base status.

Metabolic acidosis without clinical signs of dehydration was diagnosed in four calves between nine and 21 days of age. In each calf either coma or depression with weakness and ataxia was observed. Two calves had slow deep respirations. Treatment with intravenous administration of solutions of sodium bicarbonate was accompanied by a rise in blood pH and a return to normal demeanor, ambulation and appetites, allowing these calves to return to their respective herds.

A 20-month-old Charolais bull was referred for evaluation of progressive hind limb ataxia. Clinical findings suggested a neuroanatomic lesion caudal to T2. Postmortem histologic examination revealed multifocal, acellular, pale, eosinophilic plaques throughout the cerebellum, which were diagnostic for the disease progressive ataxia of Charolais cattle. This disease is presumed to have a hereditary transmission and is not commonly recognized in the United States.

Thirty-six dehydrated diarrheic neonatal calves were used to study the effects of various alkalinizing compounds on acid-base status, the changes in central venous pressure (CVP) in response to rapid IV infusion of large volumes of fluid, and the correlation of acid-base (base deficit) status, using a depression scoring system with physical determinants related to cardiovascular and neurologic function. Calves were allotted randomly to 4 groups (9 calves/group). Over a 4-hour period, each calf was given two 3.6-L volumes (the first 3.6 L given in the first hour) of a polyionic fluid alone (control group) or were given the polyionic fluid with sodium bicarbonate, sodium L-lactate, or sodium acetate added (50 mmol/L). Acid-base status, hematologic examination, and biochemical evaluations were made immediately before infusion of each fluid (at entry) and after 3.6, 4.8, and 7.2 L of fluid had been given. Compared with control values, bicarbonate, lactate, and acetate had significantly greater alkalinizing effects on pH (P less than 0.01) and base deficit (P less than 0.01) after 3.6, 4.8, and 7.2 L of fluid were given. Bicarbonate had the most rapid alkalinizing effect and induced greater changes in base deficit (P less than 0.01) than did acetate or lactate at each of the 3 administered fluid volumes evaluated. Acetate and lactate had similar alkalinizing effects on blood. Rehydration alone did not improve acid-base status. The CVP was elevated in 10 (28%) of the 36 calves after 1 hour of fluid (3.6 L) administration, but significant differences in body weight, PCV, and clinical condition or depression score at entry were not found between calves with elevated CVP and those with normal CVP.(ABSTRACT TRUNCATED AT 250 WORDS)

A 4-year-old beefmaster cow was examined for a left hind leg lateral claw lameness due to septic arthritis of the distal interphalangeal joint and associated osteomyelitis of the second and third phalanges. Actinomyces pyogenes and Fusobacterium necrophorum, which have been demonstrated previously to act synergistically in ovine heel abscesses, were isolated from the affected digit. A claw amputation was performed because of the advanced destructive nature of the lesion.