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Hepatic fibrosis is commonly diagnosed in dogs, often as a sequela to chronic hepatitis (CH). The development of fibrosis is a crucial event in the progression of hepatic disease that is of prognostic value. The pathophysiology of hepatic fibrosis in human patients and rodent models has been studied extensively. Although less is known about this process in dogs, evidence suggests that fibrogenic mechanisms are similar between species and that activation of hepatic stellate cells is a key step. Diagnosis and staging of hepatic fibrosis in dogs requires histopathological examination of a liver biopsy specimen. However, performing a liver biopsy is invasive and assessment of fibrotic stage is complicated by the absence of a universally accepted staging scheme in veterinary medicine. Serum biomarkers that can discriminate among different fibrosis stages are used in human patients, but such markers must be more completely evaluated in dogs before clinical use. When successful treatment of its underlying cause is feasible, reversal of hepatic fibrosis has been shown to be possible in rodent models and human patients. Reversal of fibrosis has not been well documented in dogs, but successful treatment of CH is possible. In human medicine, better understanding of the pathomechanisms of hepatic fibrosis is leading to the development of novel treatment strategies. In time, these may be applied to dogs. This article comparatively reviews the pathogenesis of hepatic fibrosis, its diagnosis, and its treatment in dogs. [ABSTRACT FROM AUTHOR]

Background: Although the basic pathophysiology is the same in both cervical and thoracolumbar intervertebral disk (IVD) extrusions, there are considerable clinical differences that have only been partially explained. Hypothesis/Objectives: The epidural inflammatory response differs between cervical and thoracolumbar IVD extrusions. Animals: Fifty‐five dogs with cervical and 80 dogs with thoracolumbar IVD extrusions. Methods: Clinical data and histopathologic variables were investigated. Associations between severity of epidural inflammation and clinical and pathologic variables, impact of chondrodystrophic phenotype, and localization (cervical versus thoracolumbar) were evaluated statistically. Results: Dogs with cervical IVD extrusion were significantly older (P < 0.001), had less severe and longer duration of neurologic signs (both P < 0.001), were more painful (P = 0.038), and had a better outcome (P = 0.005) than dogs with a thoracolumbar IVD extrusion. On histopathology, cervical epidural material had less severe calcification (P = 0.002) and inflammation (P < 0.001). No significant differences regarding chondrodystrophic phenotype were found. Conclusion and Clinical Importance: There was significantly less intensive inflammatory response in the cervical epidural space. This observation correlated positively with less nucleus pulposus calcification in cervical extrusions indicating biochemical, metabolic, and biomechanical differences between the 2 locations, which remain to be characterized in future studies. [ABSTRACT FROM AUTHOR]

Background: Chiari‐like malformation (CM) and syringomyelia (SM) cause a pain syndrome in Cavalier King Charles spaniels (CKCS). Clinical signs are not consistently apparent on neurologic examination, and owner reporting of signs provides vital clinical history. However, owner questionnaires for this disease are not well developed. Objectives: To develop a tool to capture owner‐reported clinical signs for use in clinical trials and to compare owner‐reported signs with the presence of pain on neurologic examination and SM on magnetic resonance imaging (MRI). Animals: Fifty client‐owned CKCS. Methods: Owners completed a questionnaire and pain/scratch map. Each dog underwent a neurologic examination and craniocervical magnetic resonance imaging (MRI). Questionnaire responses were developed into scores, area of shading for pain/scratch maps was measured, and consistency of responses between these tools was assessed. Owner‐reported findings were compared with neurologic examination findings and presence and severity of SM on MRI. Results: Thirty‐three dogs were symptomatic and 17 asymptomatic; 30 had SM. The most common sign of pain was crying out when lifted (n = 11). Extent of shaded areas on maps positively correlated with questionnaire scores for pain (r2 = 0.213, P = 0.006) and scratch (r2 = 0.104, P = 0.089). Owner‐reported findings were not significantly associated with presence or severity of SM or neurologic examination findings. Owner‐reported lateralization of signs was significantly associated with SM lateralization (P < 0.0001). Conclusions: The questionnaire and maps may be useful for clinical trials. Lack of association of owner‐reported signs with SM highlights our lack of understanding of the pathophysiology of pain in this disease. [ABSTRACT FROM AUTHOR]

A 10-h-old Thoroughbred foal presented with clinical signs consistent with neonatal encephalopathy including absent suckling behaviour, lack of affinity for the mare and seizures. The foal was provided supportive care and treated with broad-spectrum antimicrobials and fed via naso-oesophageal tube. In addition, magnetic resonance imaging (MRI) was performed to investigate for structural changes that might be evident with equine neonatal encephalopathy. Notable findings on MRI included hyperintensity of the basal nuclei and superficial layers of the ventral cerebral hemispheres as well as the ventral thalamic nuclei and rostral aspect of the ventral midbrain. These imaging changes were consistent with the counterpart disease in infants and are the first to document MRI changes in a foal with neonatal encephalopathy. This report serves as an initial description of MRI findings associated with the presumed diagnosis of equine neonatal encephalopathy and also serves to solicit future diagnostic imaging studies that may help elucidate the pathophysiology and prognosis of equine neonatal encephalopathy. [ABSTRACT FROM AUTHOR]

In this article, 3 cases of an infrequent complication of lower limb trauma that presented as a cellulitis and deteriorating comfort a few days after lower limb laceration are described. All 3 horses sloughed the hoof capsule 10 days after initial trauma to that particular limb. Development of subsequent cellulitis/lymphangitis contributed to deterioration of distal limb perfusion. The exact pathophysiological mechanisms remain unknown but clinicians should be aware of this unusual but major complication following limb trauma. [ABSTRACT FROM AUTHOR]

Exertional rhabdomyolysis represents a syndrome of typically recurrent exercise-associated muscle damage in horses that arises from a variety of aetiologies. Major advances have been made in recent years in our understanding of the pathophysiology of equine rhabdomyolysis syndrome (ERS), and a few specific causative genetic defects have been identified. Despite the fact that there is no single procedure or set of procedures (including diet and management) that can guarantee against further episodes of ERS, appropriate management of susceptible individuals, including nutrition, may help to reduce the likelihood, severity or frequency of future episodes. Whilst the dietary advice can be more specific and targeted for those with a known intrinsic muscle problem, for all affected individuals, regardless of the underlying cause, a balanced diet (which is suitable for the individual), together with a well-designed exercise programme, should be the initial management target. This paper will briefly review the condition and give general nutrition and management advice. [ABSTRACT FROM AUTHOR]

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An electronic survey was conducted to determine the attitudes of veterinary pathologists toward forensic pathology and the adequacy of their training in the discipline. The survey was sent to 1933 diplomates of the American College of Veterinary Pathologists and 311 completed responses were analyzed. Of respondents, 80% report receiving at least 1 type of medicolegal case, with cases from law enforcement received most frequently. Most (74%) of the respondents indicated that their previous training did not prepare them adequately to handle forensic cases and almost half of the respondents (48%) indicated that they needed more training on serving as an expert witness. Relative risk ratios (RRR) and odds ratios (OR) were generated to determine the strength of a statistically significant association. Responses from a free-text entry question determining additional training needs could be grouped into 3 main categories: (1) veterinary forensic pathology science and procedures, (2) documentation, evidence collection and handling, and (3) knowledge of the medicolegal system. Last, a field for additional comments or suggestions regarding veterinary forensic pathology was completed by 107 respondents and many reinforced the need for training in the categories previously described. The survey highlights that a significant proportion of diplomates of the American College of Veterinary Pathologists are currently engaged in veterinary forensic pathology but feel their training has not adequately prepared them for these cases. Hopefully, the survey results will inform the college and residency training coordinators as they address the training requirements for an important emerging discipline. [ABSTRACT FROM AUTHOR]

Background Equine gastric glandular disease ( EGGD) is a term used to classify erosive and ulcerative diseases of the glandular mucosa of the equine stomach. Epidemiologic studies of risk factors for EGGD have not been reported. Objective To determine risk factors for EGGD. Animals Cases ( n = 83) had endoscopic evidence of EGGD; controls ( n = 34) included healthy horses and horses with equine squamous gastric disease ( ESGD) without EGGD. Methods Retrospective case-control study. The data were analyzed by multivariable logistic regression modeling. Analysis was performed on the full dataset. An additional analysis compared horses with glandular lesions ( n = 43) against healthy horses ( n = 22). Results On first analysis, Warmblood breed ( OR = 13.9, 95% CI 2.2-90.9, P = .005) and an increasing number of caretakers ( OR = 7.3, 95% CI 0.98-55.6, P = .053) were associated with an increased risk of EGGD. On analysis of the subset of data, Warmblood breed ( OR = 28.6, 95% CI 2.96-250.0, P = .004) and increasing number of riders ( OR = 12.99, 95% CI 0.94-166.7, P = .056) were risk factors. The presence of sand in the colon appeared to have a protective effect against EGGD ( OR = 0.195, 95% CI 0.04-1.0, P = .051 for sand versus not having sand). Conclusions and clinical importance This study suggests that Warmbloods are predisposed to EGGD and multiple handlers/riders might increase the risk of EGGD. Identification of risk factors allows speculation on potential pathophysiological mechanisms of EGGD. [ABSTRACT FROM AUTHOR]

The primary hyperaldosteronism, an endocrine disease increasingly identified in cats, is characterized by adrenal gland dysfunction that interferes with the renin-angiotensin-aldosterone system, triggering the hypersecretion of aldosterone. Pathophysiological consequences of excessive aldosterone secretion are related to increased sodium and water retention, and increased excretion of potassium, which induce hypertension and severe hypokalemia, respectively. The most common clinical findings in cats include: polydipsia, nocturia, polyuria, generalized weakness, neck ventroflexion, syncope, anorexia, weight loss, pendulous abdomen and blindness. Diagnosis is based on the evidence of hormonal hypersecretion with suppression of renin release, imaging and histopathological evaluation of adrenal glands. Treatment may be curative with adrenalectomy, in cases of unilateral disease, or conservative, through administration of aldosterone antagonists, potassium supplementation and antihypertensives. Prognosis varies from fair to good with the appropriate therapy. This article reviews the main aspects of primary aldosteronism in cats, providing the clinician with important information for the diagnosis of this disease. [ABSTRACT FROM AUTHOR]

Bone structure is modulated by the interaction between receptor activator of nuclear factor–κB (RANK) and RANK ligand (RANKL). Osteoprotegerin (OPG), a decoy receptor for RANKL, modifies osteoclast-mediated bone resorption directly and spares articular cartilage indirectly in rodents with immune-mediated arthritis by preventing subchondral bone destruction. The OPG/RANKL balance also seems to be critical in maintaining joint integrity in osteoarthritis, a condition featuring articular bone and cartilage damage in the absence of profound inflammation. The current study explored the role of OPG in sparing articular cartilage by evaluating joint lesions in adult C57BL/6J mice lacking osteoprotegerin (Opg−/−). At 3, 5, 7, 9, and 12 months of age, both sexes of Opg−/− mice developed severe degenerative joint disease (DJD) characterized by progressive loss of cartilage matrix and eventually articular cartilage. Lesions developed earlier and more severely in Opg−/− mice relative to age-matched, wild-type (Opg+/+), or heterozygous (Opg+/−) littermates (P ≤ .05). The femorotibial joint was affected bilaterally at 3 months, while other key weight-bearing diarthrodial joints (eg, coxofemoral, scapulohumeral, humeroradioulnar) were affected later and unilaterally. Cortical bone in subchondral plates and long bone diaphyses of Opg−/− mice but not Opg+/+ or Opg+/− animals was osteoporotic by 3 months of age (P ≤ .05); the extent of porosity was less than the degree of DJD. Closure of the physes in long bones (P ≤ .05) and cartilage retention in the femoral primary spongiosa (P ≤ .05) affected chiefly Opg−/− mice. These data suggest that OPG plays an essential direct role in maintaining cartilage integrity in the articular surfaces and physes. [ABSTRACT FROM AUTHOR]

Osteochondrosis is defined as a focal disturbance in endochondral ossification. The cartilage superficial to an osteochondrosis lesion can fracture, giving rise to fragments in joints known as osteochondrosis dissecans (OCD). In pigs and horses, it has been confirmed that the disturbance in ossification is the result of failure of the blood supply to epiphyseal growth cartilage and associated ischemic chondronecrosis. The earliest lesion following vascular failure is an area of ischemic chondronecrosis at an intermediate depth of the growth cartilage (osteochondrosis latens) that is detectable ex vivo, indirectly using contrast-enhanced micro- and conventional computed tomography (CT) or directly using adiabatic T1ρ magnetic resonance imaging. More chronic lesions of ischemic chondronecrosis within the ossification front (osteochondrosis manifesta) are detectable by the same techniques and have also been followed longitudinally in pigs using plain CT. The results confirm that lesions sometimes undergo spontaneous resolution, and in combination, CT and histology observations indicate that this occurs by filling of radiolucent defects with bone from separate centers of endochondral ossification that form superficial to lesions and by phagocytosis and intramembranous ossification of granulation tissue that forms deep to lesions. Research is currently aimed at discovering the cause of the vascular failure in osteochondrosis, and studies of spontaneous lesions suggest that failure is associated with the process of incorporating blood vessels into the advancing ossification front during growth. Experimental studies also show that bacteremia can lead to vascular occlusion. Future challenges are to differentiate between causes of vascular failure and to discover the nature of the heritable predisposition for osteochondrosis. [ABSTRACT FROM AUTHOR]

Osteochondrosis arises as a result of focal failure of the blood supply to growth cartilage. The current aim was to examine the pathogenesis of pseudocysts and true cysts in subchondral bone following failure of the blood supply to the articular-epiphyseal cartilage complex in horses. Cases were recruited based on identification of lesions (n = 17) that were considered likely to progress to or to represent pseudocysts or true cysts in epiphyseal bone in histological sections and included 10 horses ranging in age from 48 days to 5 years old. Cases comprised 3 warmbloods, 3 Standardbreds, 1 Quarter horse and 1 Arabian with spontaneous lesions and 2 Fjord ponies with experimentally induced lesions. Seven lesions consisted of areas of ischemic chondronecrosis and were compatible with pseudocysts. Two lesions were located at intermediate depth in epiphyseal growth cartilage, 2 lesions were located in the ossification front, 2 lesions were located in epiphyseal bone and 1 lesion was located in the metaphyseal growth plate (physis). Ten lesions contained dilated blood vessels and were compatible with true cysts. In 2 lesions the dilated blood vessels were located within the lumina of failed cartilage canals. In the 8 remaining lesions areas of ischemic chondronecrosis were associated with granulation tissue in the subjacent bone and dilated vessels were located within this granulation tissue. Failure of the blood supply and ischemic chondronecrosis can lead to formation of pseudocysts or dilatation of blood vessels and formation of true cysts in the epiphyseal bone of horses. [ABSTRACT FROM AUTHOR]

We report coincident sternal segment dislocation and focally extensive right ventricular epicardial fibrosis observed during routine histopathology evaluation of C57BL/6N mice as part of a high throughput phenotyping screen conducted between 4 and 16 weeks of age. This retrospective case series study was conducted to determine whether cardiac fibrosis was a pathological consequence of sternal segment dislocation. We identified sternal segment dislocation in 51 of the total 1103 mice (4.6%) analyzed at 16 weeks of age. Males were more frequently affected. In all cases but 2, the dislocation occurred at the fourth intersternebral joint. In 42 of the 51 cases (82.4%), the dislocation was encased by regenerative cartilaginous callus that protruded internally into the thoracic cavity (intrathoracic callus) and/or externally to the outer aspect of the sternum (extrathoracic callus). Displacement of dislocated ends of the sternum into the thoracic cavity was present in 19 of 51 cases (36.5%). Coincident minimal or mild right ventricular epicardial and subepicardial fibrosis was observed in 22 of the 51 cases (43%) but was not observed in any of the mice in the absence of sternal segment dislocation. Our data suggest that right ventricular fibrosis was likely caused by direct injury of the right ventricle by the dislocated ends of the sternum and/or by intrathoracic callus that develops post dislocation. Potential pathogenesis for the sternal and cardiac lesions and their implication for the interpretation of phenotypes in mouse models of cardiopulmonary and skeletal disease are discussed. [ABSTRACT FROM AUTHOR]

Porcine epidemic diarrhea virus (PEDV), a member of the genera Alphacoronavirus in the family Coronaviridae , causes acute diarrhea/vomiting, dehydration and high mortality in seronegative neonatal piglets. For the last three decades, PEDV infection has resulted in significant economic losses in the European and Asian pig industries, but in 2013–2014 the disease was also reported in the US, Canada and Mexico. The PED epidemic in the US, from April 2013 to the present, has led to the loss of more than 10% of the US pig population. The disappearance and re-emergence of epidemic PED indicates that the virus is able to escape from current vaccination protocols, biosecurity and control systems. Endemic PED is a significant problem, which is exacerbated by the emergence (or potential importation) of multiple PEDV variants. Epidemic PEDV strains spread rapidly and cause a high number of pig deaths. These strains are highly enteropathogenic and acutely infect villous epithelial cells of the entire small and large intestines although the jejunum and ileum are the primary sites. PEDV infections cause acute, severe atrophic enteritis accompanied by viremia that leads to profound diarrhea and vomiting, followed by extensive dehydration, which is the major cause of death in nursing piglets. A comprehensive understanding of the pathogenic characteristics of epidemic or endemic PEDV strains is needed to prevent and control the disease in affected regions and to develop an effective vaccine. This review focuses on the etiology, epidemiology, disease mechanisms and pathogenesis as well as immunoprophylaxis against PEDV infection. [ABSTRACT FROM AUTHOR]

Actinobacillus pleuropneumoniae is a major cause of respiratory disease in pigs. Many farms are endemically infected without apparent disease, but occasionally severe outbreaks of pleuropneumonia occur. To prevent and control these outbreaks without antibiotics, the underlying mechanisms of these outbreaks need to be understood. Outbreaks are probably initiated by a trigger (common risk factor) changing the host-pathogen interaction, but it is unclear whether this trigger causes all cases directly (trigger mechanism), or whether the first case starts a transmission chain inducing disease in the infected contacts (transmission mechanism). The aim of this study was to identify conditions under which these mechanisms could cause A. pleuropneumoniae outbreaks, and to assess means for prevention and control. Outbreaks were first characterised by data from a literature review, defining an average outbreak at 12 weeks of age, affecting 50% of animals within 4 days. Simple mathematical models describing the two mechanisms can reproduce average outbreaks, with two observations supporting the trigger mechanism: (1) disease should be transmitted 50 times faster than supported by literature if there is a transmission chain; and (2) the trigger mechanism is consistent with the absence of reported outbreaks in young pigs as they have not yet been colonised by the bacterium. In conclusion, outbreaks of A. pleuropneumoniae on endemic farms are most likely caused by a trigger inducing pneumonia in already infected pigs, but more evidence is needed to identify optimum preventive interventions. [ABSTRACT FROM AUTHOR]

Mycoplasma suis is an uncultivable bacterium lacking a cell wall that attaches to and may invade the red blood cells of pigs. M. suis infections occur worldwide and cause the pig industry serious economic losses due to the disease known as infectious anaemia of pigs or, historically, porcine eperythrozoonosis. Infectious anaemia of pigs is characterised predominantly by acute haemolytic or chronic anaemia, along with non-specific manifestations, such as growth retardation in feeder pigs and poor reproductive performance in sows. The fastidious nature of M. suis, as well as the lack of an in vitro cultivation system, has hampered the understanding of the biology and pathogenicity of this organism. Pathogenetic mechanisms of M. suis include direct destruction of red blood cells by adhesion, invasion, nutrient scavenging, immune-mediated lysis and eryptosis, as well as endothelial targeting. Recently published genome sequences, in combination with proteome analyses, have generated new insights into the pathogenicity of M. suis. The present review combines these data with the knowledge provided by experimental M. suis infections. [ABSTRACT FROM AUTHOR]

A rapid and rational clinical reasoning approach will not only help to identify the possible underlying pathology of an epileptic dog, but will also help to give the likely prognosis and allow treatment to be initiated swiftly to ensure the best possible outcome for the patient. This article will provide a step-by-step approach for clinical reasoning to improve clinical efficiency and to maximise patient care. [ABSTRACT FROM AUTHOR]

Epilepsy represents the most common chronic neurological condition in the dog. As our understanding of the underlying pathophysiology improves, we are better able to describe the neuroanatomical diagnosis, select the best medication for an individual patient and predict the potential for pharmacoresistance to antiepileptic drugs (AEDs). An epileptic seizure is a clinical sign of neurological disease (similar to any other neurological abnormality, such as ataxia or paresis), whereas epilepsy is defined as recurrent epileptic seizures (ie, a patient does not have epilepsy until it has had repeated seizures). Epileptogenesis is the process whereby a seizure focus develops or increases in size, with an associated increase in seizure frequency or severity. While the effect of early instigation of treatment with AEDs on epileptogenesis is still to be elucidated, it is apparent that early treatment results in the development of less long term adverse behaviour effects in the patient. The main risk factors for pharmacoresistance to AEDs include breed (in particular the border collie) and severe or progressively worsening seizures. [ABSTRACT FROM AUTHOR]

Canine idiopathic epilepsy has an estimated prevalence of 0.62 per cent in primary veterinary practice (Kearsley-Fleet and others 2013) and as such is one of the most common chronic neurological diseases. Descriptions of 'epilepsy of unknown origin . . . where no symptom characteristic of any other condition has as yet presented' can be found in early veterinary textbooks (Kirk 1922) and although our knowledge is now considerably greater, and we are no longer treating it with arsenic, we are still a long way from preventing or curing this enigmatic disease. This article describes the diagnosis, management and considerations to take when dealing with this condition. [ABSTRACT FROM AUTHOR]

Neurology is often seen as a disengaging subject, with seizures representing a manifestation of the dysfunctional 'black-box' we know as the brain. Seizures in small and fragile juvenile patients can quickly become life-threatening, demanding critical attention and informed intervention. This, when combined with the emotions of the owner, can lead to a very stressful environment in which time is of the essence and clear thinking is the key to success. A structured approach to investigating the problem allows optimal management of these cases, giving these altricial patients every chance of success. This article will discuss some conditions that are specific to these patients, and explain how best to treat and manage them. [ABSTRACT FROM AUTHOR]

Degenerative mitral valve disease (DMVD) is the most common cardiovascular disease in dogs and is a major cause of congestive heart failure (CHF) in this species. This article reviews the pathophysiology and natural history of the disease and provides a summary of current recommendations for diagnosis and treatment of dogs with advanced DMVD and CHF. [ABSTRACT FROM AUTHOR]

Summary: GM2 gangliosidosis (Tay–Sachs disease) was diagnosed in 6- to 8-month-old pedigree Jacob lambs from two unrelated flocks presenting clinically with progressive neurological dysfunction of 10 day's to 8 week's duration. Clinical signs included hindlimb ataxia and weakness, recumbency and proprioceptive defects. Histopathological examination of the nervous system identified extensive neuronal cytoplasmic accumulation of material that stained with periodic acid–Schiff and Luxol fast blue. Electron microscopy identified membranous cytoplasmic bodies within the nervous system. Serum biochemistry detected a marked decrease in hexosaminidase A activity in the one lamb tested, when compared with the concentration in age matched controls and genetic analysis identified a mutation in the sheep hexa allele G444R consistent with Tay–Sachs disease in Jacob sheep in North America. The identification of Tay–Sachs disease in British Jacob sheep supports previous evidence that the mutation in North American Jacob sheep originated from imported UK stock. [ABSTRACT FROM AUTHOR]

Summary: This paper reports a newly described form of skeletal dysplasia affecting Brazilian hair sheep of the Cabugi breed. This breed is characterized by having a short head and in some cases the animals are smaller and more compact than sheep of similar breeds. Lambs born with craniofacial abnormalities and dwarfism that die at 2–6 months of age are frequent in this breed. In a flock of 68 ewes and three rams of the Cabugi breed, 134 lambs were born over a 4-year period. Of these, 14 (10.4%) had marked cranial abnormalities and dwarfism and died or were humanely destroyed, 43 (32%) had a normal face and 77 (57.5%) had the short face characteristic of the breed. Dwarf lambs were much smaller than normal, with short legs, a domed head with retruded muzzle and protruded mandible, sternal deformities and exophthalmic eyes situated more laterally in the face than normal. Microscopical examination of long bones of the limbs, bones of the base of the skull and vertebrae showed no lesions. Bones from four affected lambs and one control lamb were macerated for morphometric examination. Although the length of the spinal cord was similar, there was disproportionate shortening of the appendicular bones, particularly the distal segments. Thus the disease was defined as a skeletal dysplasia characterized by craniofacial deformity and disproportionate dwarfism. It is suggested that the disease is inherited as an incomplete dominant trait. The shortened face, which is a feature of the Cabugi breed, may represent the heterozygous state and the more severe, often lethal, dwarfism may occur in homozygotes. [ABSTRACT FROM AUTHOR]

Objective--To assess the feasibility and reproducibility of longitudinal tissue Doppler ultrasonographic imaging with regard to determination of velocity, strain, and strain rate (SR) of the left atrium (LA) and use those data to characterize LA synchrony (LAS) for a group of healthy dogs. Animals--15 healthy dogs. Procedures--For each dog, apical 4- and 2-chamber echocardiographic views were obtained. Peak velocity, strain, and SR and time to peak value during systole, early diastole, and late diastole were measured for each of the 4 LA walls. To characterize LAS, mean and SD maximal late diastolic time difference (LAD) among the 4 walls were calculated on the basis of time to peak for velocity, strain, and SR; for each, the 95% confidence interval (mean ± 2SD) was calculated. Within-day and between-day intraobserver variability was calculated. Results--For all dogs, tissue velocity and SR had peak positive values during systole and 2 negative peaks during early and late diastole. Atrial strain had a peak positive value during systole, positive values during early diastole, and a negative peak value during late diastole. Reproducibility was acceptable for most variables. Diastolic strain and SR had the highest variability, but times to peak values were always reproducible. For velocity, strain, and SR, the 95% confidence interval for the maximal LAD was < 50 milliseconds and that for the SD of the LAD was < 23 milliseconds. Conclusions and Clinical Relevance--Longitudinal tissue Doppler imaging of LA deformation was feasible in healthy dogs, and its application may be useful for understanding atrial pathophysiologic changes associated with various cardiac diseases in dogs. [ABSTRACT FROM AUTHOR]

Neuropathic pain is a form of pain caused by a lesion or disease of the somatosensory nervous system. It is usually chronic and difficult to treat, affecting quality of life. Mechanisms of neuropathic pain are not yet fully understood. New ways to assess pain in chronically affected patients are described in the medical literature, but the use of these tools for diagnosis and assessment of neuropathic pain is not as frequent in veterinary analgesia compared to humans. Treatment options consist of multimodal analgesia and adjuvant therapy. Here current knowledge of pathophysiology, diagnosis and treatment of neuropathic pain in dogs is briefly reviewed. [ABSTRACT FROM AUTHOR]

The article discusses the pathophysiology and diagnosis of tooth traumas in domestic animals and the available treatment options. It notes that untreated tooth trauma could result to pain, pulpitis or pulp necrosis, root resorption and periodontitis. It describes trauma to the crown with and without pulp exposure, trauma to the root and trauma to the periodontal ligament. Treatment options include extraction, endodontic treatment, and treatment for teeth with damage to the periodontal ligament.

Animal models have historically informed veterinary and human pathophysiology. Next-generation genomic sequencing and molecular analyses using analytes derived from tissue require integrative approaches to determine macroanalyte integrity as well as morphology for imaging algorithms that can extend translational applications. The field of biospecimen science and biobanking will play critical roles in tissue sample collection and processing to ensure the integrity of macromolecules, aid experimental design, and provide more accurate and reproducible downstream genomic data. Herein, we employ animal experiments to combine protein expression analysis by microscopy with RNA integrity number and quantitative measures of morphologic changes of autolysis. These analyses can be used to predict the effect of preanalytic variables and provide the basis for standardized methods in tissue sample collection and processing. We also discuss the application of digital imaging with quantitative RNA and tissue-based protein measurements to show that genomic methods augment traditional in vivo imaging to support biospecimen science. To make these observations, we have established a time course experiment of murine kidney tissues that predicts conventional measures of RNA integrity by RIN analysis and provides reliable and accurate measures of biospecimen integrity and fitness, in particular for time points less than 3 hours post–tissue resection. [ABSTRACT FROM AUTHOR]

Schmallenberg virus (SBV) infection is an emerging infectious disease of ruminants first described in Germany in November, 2011. Since then it has spread very rapidly to several European countries. The disease is characterised by fever, reduced milk production and diarrhoea in cattle and abortions, stillbirths and foetal abnormalities in sheep and goats. SBV is an enveloped, negative-sense, segmented, single-stranded RNA virus, classified in the genus Orthobunyavirus of the Bunyaviridae family, and is closely related to Akabane, Ainoa and Shamonda viruses. As of now there is no vaccine available for SBV, which poses a serious threat to naive ruminant population. Owing to its recent discovery, our understanding of Schmallenberg viral disease and its pathology and pathogenesis is limited. This article reviews the data reported so far on this emerging disease with regard to aetiology, epidemiology, pathogenesis, pathology, diagnosis and control and discusses the future scenario and implications of the disease. [ABSTRACT FROM AUTHOR]

Epileptogenesis is the process by which a normal brain develops into an epileptic brain. There are 3 distinct phases of epileptogenesis--the latent period before seizures occur, the occurrence of recurrent seizures, and in about 30% of patients, the development of refractory epilepsy Understanding the basic epileptic circuit abnormalities associated with recurrent seizures via aberrations in glutamate, gamma-aminobutyric acid, and ligand- and voltage-gated ion channel activity can help the small-animal practitioner understand the mechanism of action of the antiepileptic drugs currently used for dogs and cats for new-onset and refractory epilepsy Understanding the latest research results and theories about the pathophysiology of the latent period of epileptogenesis, where recurrent seizures have not yet developed, would help the practitioner understand possible target areas for future treatments to treat epilepsy by preventing it rather than just symptomatically preventing recurrent seizures. The current areas of focus of research on the latent period include neurodegeneration, neurogenesis, axonal sprouting, glial cell activatioa invasion of inflammatory cells, angiogenesis, and subclinical alteration of ligand- and receptor-gated ion channels. [ABSTRACT FROM AUTHOR]

To review the human and veterinary literature on the pathophysiology of myasthenia gravis (MG) and describe treatment options for clinical use in people and animals. Human and veterinary clinical reports, studies and reviews, textbooks, and recent research findings in MG from 1996 present, with a focus on treatment and patient management. MG is a well-described condition in people with new research and treatment options available. Many of the newest therapeutic options available in veterinary medicine for MG are based on current strategies used in people with this condition. Seronegative MG is well described in people and provides insight to clinical cases encountered in veterinary medicine when the index of suspicion is high though serologic tests are negative. Previous studies in veterinary medicine focused on the use of acetylcholinesterase inhibitors as the main form of treatment in canine MG. Recent studies, mainly case series and case reports, emphasize the use of immunomodulatory treatments as an alternative for long-term treatment. However, there are no randomized, controlled studies on treatment with immunomodulatory therapy for MG in dogs available to assess the efficacy of this treatment strategy. Although early recognition of clinical signs is most important in the outcome of patients with MG, further understanding the pathophysiology of MG may lead to earlier diagnosis and novel treatment strategies. The discovery of additional autoantibodies against striated muscle proteins in dogs, should enhance our understanding of diseases affecting the neuromuscular junction. In addition, clinical data for canine MG could be applied to other autoimmune disorders. [ABSTRACT FROM AUTHOR]

Summary: The pathological findings in nine cases of pneumonia associated with infection by felid herpesvirus-1 (FeHV-1) are presented. The animals affected were five kittens, two subadult cats and two adult cats. The microscopical changes included fibrinonecrotic pneumonia and severe necrosis of the bronchial and bronchiolar epithelium. FeHV-1 antigen was detected immunohistochemically in pneumocytes, alveolar macrophages and necrotic bronchial and bronchiolar epithelial cells. In the youngest kitten viral antigen was also found in the liver. FeHV-1 infection should therefore be considered as a differential diagnosis in cats with fibrinonecrotic pneumonia and demonstration of viral antigen by immunohistochemistry is a useful diagnostic procedure in such cases. [Copyright &y& Elsevier]

The article discusses a study which examined the occurrence of a very virulent infectious bursal disease virus (vvIBDV) in Northern California commercial brown pullets. Particular focus is given to flock mortality from the affected house at two neighboring ranches. IBD-affected birds exhibited lethargy, ruffled feathers, as well as postmortem lesions. The economic implications of IBD include a decrease in egg production and egg quality, immunosuppression in young chickens and impaired efficacy of vaccination. Results of the study showed that mortality in specific-pathogen-free leghorns inoculated with vvIBD strain can range between 25% and 100%. It also found a possible correlation between the degree of pathogenecity and lesion production in nonbursal organs.

Abstract: We consider evidence that crustaceans might experience pain and stress in ways that are analogous to those of vertebrates. Various criteria are applied that might indicate a potential for pain experience: (1) a suitable central nervous system and receptors, (2) avoidance learning, (3) protective motor reactions that might include reduced use of the affected area, limping, rubbing, holding or autotomy, (4) physiological changes, (5) trade-offs between stimulus avoidance and other motivational requirements, (6) opioid receptors and evidence of reduced pain experience if treated with local anaesthetics or analgesics, and (7) high cognitive ability and sentience. For stress, we examine hormonal responses that have similar function to glucocorticoids in vertebrates. We conclude that there is considerable similarity of function, although different systems are used, and thus there might be a similar experience in terms of suffering. The treatment of these animals in the food industry and elsewhere might thus pose welfare problems. [Copyright &y& Elsevier]

Abstract: To correlate the clinical course of mycoplasma mastitis with its immune response, right mammary glands of 15 lactating goats were inoculating with 1010 colony-forming units (cfu) of Mycoplasma agalactiae (Ma). Before sacrificing the animals at 5, 15 or 45 days post-inoculation (dpi), blood Ma antibody titres and milk mycoplasma colony and somatic cell counts were monitored. Ma colonised the mammary gland and milk counts increased to over 1012 cfu/ml within 5dpi. During this period, an innate immune response involving neutrophils and macrophages was observed, and Ma antigen appeared in the degenerated acinar epithelium. From 7dpi, a specific antibody response coincided with reduced viable mycoplasmas in milk. The humoral immune response was limited; by 37dpi, all animals scored negative for anti-Ma antibodies, and around 108 cfu/ml were shed. Results indicate an early immune response to Ma inoculation unable to control mycoplasmal invasion. An ensuing humoral response, despite reducing the mycoplasma burden, leads to chronic, persistent infection. [Copyright &y& Elsevier]

The article focuses on therapeutic targets and scientific progress toward the development of appropriate animal models by utilizing novel strategies that will help in understanding the pathogenesis and pathophysiology of anorexigen-induced valvulopathy and pulmonary arterial hypertension (PAH). According to the author, various safety issues, such as valvulopathy with fenfluramine and PAH with aminorex, were initially not predicted by routine preclinical toxicology studies. The author also discusses the translatability challenges of drug effects from animals to humans.

The article discusses the case of an 11-year-old male Australian Shepherd dog that was diagnosed with focal atrial tachycardia (FAT). Particular focus is given to the dog's physical examination and laboratory tests. Also discussed are the dog's first-degree atrioventricular (AV) block, possible reasons behind AV block, and mechanisms underlying FAT.

Epizootics (nonhuman animal disease epidemics) can have detrimental impacts on livelihoods through a complex interaction of demographic trends, food production, and animal disease. Differences in the rate of demographic shifts, including rates of population growth, economic growth, urbanization, environmental sustainability, and role of women in society, are strong driving forces that will determine to what extent food demand will be matched by food production capacity. Epizootics can negatively affect commerce and trade in all countries, and in low-income countries limited infrastructure and resources as well as competing priorities provide additional disincentive to controlling or eradicating animal diseases. Economic growth is critical to overcoming disparities among countries and is best supported by integrated animal health, public health, labor, and foreign policies. The adverse impacts of epizootics can be largely overcome through programs that support job growth along the value-added chain of food production and will require significant investments in science- (risk-) based education. [ABSTRACT FROM AUTHOR]

Abstract: Transcranial magnetic stimulation (TMS) has opened important perspectives on the pathophysiological bases and potential targets of treatment strategies for idiopathic Parkinson’s disease (IPD). Studies have been mainly focusing on motor cortical inhibitory phenomena. However, differences in patients and methods caused several discrepancies, particularly on the so-called long-latency cortical inhibition (LICI). We wanted to challenge such controversies by studying early, drug-naïve patients, and by reproducing the original method that detected a pathologic LICI in IPD. We studied the motor potentials evoked in the first dorsal interosseous muscle on the more and the less parkinsonian side of the body in 18 asymmetrical untreated IPD patients in the early stages of their disease. We had 12 healthy controls. The TMS variables were the active motor threshold, the size of the motor-evoked potential, the cortical silent period and LICI. Average active motor threshold was similar in patients and controls, but its variability was significantly higher among patients (P<0.05). There was a trend for the cortical silent period to be shorter on the more affected side of the patients (P=0.1). Patients, especially on their more affected side, exhibited a late LICI peak, which was absent among controls (P<0.05). This effect was independent of the silent period duration. However, patients and controls having a short silent period also had a shorter LICI (P<0.05). Changes in LICI had a strong trend to correlate to the severity of the parkinsonian signs (P=0.1). Thus, the present study definitely reinforced several previous TMS findings in IPD as a feature of the “pure” disease pathophysiology. The pathologic enhancement of late LICI can act as a candidate physiological hallmark of IPD, to be tested in various diagnostic or therapeutic circumstances. [Copyright &y& Elsevier]

Abstract: It has been suggested that bipolar disorder is associated with altered immune function. Monocyte chemoattractant protien-1 (MCP-1) is a chemokine that influences both neural and immune functions. We thus hypothesized that MCP-1 may be related to the development or pathophysiology of bipolar disorder. In this case–control study, we investigated the association between the A-2518G single nucleotide polymorphism (SNP) of the MCP-1 promoter and bipolar disorder. Patients with bipolar disorder (n =183; bipolar I=145, bipolar II=38) and healthy controls (350) were recruited for the study. No significant allelic or genotypic association was detected between the A-2518G polymorphism and any sample of bipolar disorder patients. When we pooled the healthy controls and the cases of bipolar I disorder from previous Korean studies and this study, we again found no significant association. No significant difference in either allele frequency or genotype distribution was observed between bipolar I and bipolar II disorders. There was no difference in the age at onset of bipolar disorder among the three genotype groups. Our data suggest that the A-2518G polymorphism of MCP-1 is not a major susceptibility factor for bipolar disorder in the Korean population. However, the physiological role of MCP-1 is highly suggestive of its being associated with bipolar disorder, and further analyses of other SNPs of MCP-1 remain to be performed. [Copyright &y& Elsevier]

The article discusses the underlying pathophysiology and principal differential diagnoses for canine immune-mediated thrombocytopenia. It is a disorder of accelerated platelet destruction and can be classified as primary or secondary immune-mediated thrombocytopenia. Treatment includes initial supportive therapy, transfusions and immunosuppressive therapy. Vaccination should be avoided in dogs affected with immune-mediated thrombocytopenia.

Abstract: The role for growth restriction in the multifactorial pathophysiology of developing white-matter damage remains debated. We studied rat pups with prenatal growth restriction (GR) induced by unilateral ligation of the uterine artery. Pups with severe GR exhibited white-matter damage that persisted to adulthood [Olivier, P., Baud, O., Evrard, P., Gressens, P.,Verney, C., 2005. Prenatal ischemia and white matter damage in rats. J. Neuropathol. Exp. Neurol. 64, 998–1006]. Moderate GR was associated with diffuse white-matter lesions, microglial activation, and astrogliosis. Loss of pre-oligodendrocytes on postnatal day 7 was followed by a delay in myelination. Following a cortical excitotoxic insult on postnatal day 5, the size of the induced white-matter lesion was smaller in pups with moderate GR and larger in pups with severe GR, compared to normal pups. The increased pre-oligodendrocyte proliferation seen in the white matter of pups with moderate GR subjected to this “double-hit” injury may constitute a heretofore-undescribed neuroprotective mechanism of immature white matter. [Copyright &y& Elsevier]

Objective: To evaluate the effect of increased intra-abdominal pressure (IAP) on the systolic and pulse pressure variations induced by positive pressure ventilation in a porcine model.Design and Setting: Experimental study in a research laboratory.Subjects: Seven mechanically ventilated and instrumented pigs prone to normovolaemia and hypovolaemia by blood withdrawal.Intervention: Abdominal banding gradually increased IAP in 5-mmHg steps up to 30 mmHg.Measurements and Main Results: Variations in systolic pressure, pulse pressure, inferior vena cava flow, and pleural and transmural (LVEDPtm) left-ventricular end-diastolic pressure were recorded at each step. Systolic pressure variations were 6.1+/-3.1%, 8.5+/-3.6% and 16.0+/-5.0% at 0, 10, and 30 mmHg IAP in normovolaemic animals (mean+/-SD; p<0.01 for IAP effect). They were 12.7+/-4.6%, 13.4+/-6.7%, and 23.4+/-6.3% in hypovolaemic animals (p<0.01 vs normovolaemic group) for the same IAP. Fluctuations of the inferior vena cava flow disappeared as the IAP increased. Breath cycle did not induce any variations of LVEDPtm for 0 and 30 mmHg IAP.Conclusions: In this model, the systolic pressure and pulse pressure variations, and inferior vena cava flow fluctuations were dependent on IAP values which caused changes in pleural pressure swing, and this dependency was more marked during hypovolaemia. The present study suggests that dynamic indices are not exclusively related to volaemia in the presence of increased IAP. However, their fluid responsiveness predictive value could not be ascertained as no fluid challenge was performed. [ABSTRACT FROM AUTHOR]

To compare economic outcome for herds not exposed to Neospora caninum with that for herds with various seroprevalences of N caninum infection and evaluate 3 control strategies. For a 5-year period with low prices for feeder claves, endemic N caninum infection decreased mean return to fixed assets by 22.2% when true seroprevalence was 10% and by 29.9% when true seroprevalence was 70%. Percentage decrease in return to fixed assets was less dramatic when a 5-year period with high prices for feeder calves was evaluated. Analysis indicated that 2 control strategies (culling females that fail to give birth to a calf and selling seropositive female cattle and purchasing seronegative replacement female cattle) were not likely to be economically beneficial. The third control strategy (testing the entire herd for N caninum infection and excluding the female offspring of seropositive dams as replacements) appeared to be a reasonable control strategy. For the assumptions in the model, endemic N caninum infection decreases return to fixed assets for cow-calf herds. Of the potential control strategies evaluated, testing the entire herd for N caninum infection and excluding the daughters of seropositive dams as potential replacements provided the best economic return. [ABSTRACT FROM AUTHOR]

Examines a dog that characterizes clinical signs associated with Fanconi syndrome. Detection of promixal renal tubular acidosis in the dog consistent with Fanconi syndrome in humans; Clinical signs of Fanconi syndrome; Transience of the Fanconi syndrome in the dog as indicated by the resolution of clinical signs and laboratory results within reference ranges or reevaluation.

To evaluate characteristics of a large epidemic of sporotrichosis in cats. Lesions varied from small papules to extensive zones of necrosis. Ten cats had no skin lesions, 114 had skin lesions at a single site, 86 had skin lesions in 2 sites, and 137 had skin lesions in 3 or more sites. Respiratory tract signs were observed in 154 cats were the most frequent extracutaneous sign. Anemia, leukocytosis with neutrophilia, hypoalbuminemia, and hyperglobulinemia were the main blood abnormalities. Antibodies against FIV were detected in 28 cats, FeLV antigen was detected in 2 cats, and both were detected in 1 cat among 142 cats tested. During the study, 118 cats were lost to follow-up and 124 died. Of 266 cats that were treated, 68 were cured. Complete healing of the lesions was observed regardless of the presence of extracutaneous signs, general condition, treatment schedule, or coinfection with FIV. Feline sporotrichosis was evident in subclinical to severe forms; however, cats can respond well to regular and prolonged antifungal treatment. [ABSTRACT FROM AUTHOR]