A field investigation of kennel cough: Efficacy of different treatments

The efficacy of antibiotics, corticosteroids and antitussives in the treatment of kennel cough was investigated in clinical cases in the field, using information recorded on questionnaires distributed to a random sample of veterinary practitioners in the United Kingdom. Analysis of the results demonstrated a statistically significant difference in the duration of coughing between treated and untreated dogs when a trimethoprim-sulphonamide combination, oxytetracycline, ampicillin/amoxycillin, or corticosteroid were administered alone, and when ampicillin/ amoxycillin-corticosteroid or trimethoprim-sulphonamide-corticosteroid combinations were given. The estimated median duration of coughing between treated and untreated animals when a trimethoprim-sulphonamide combination or ampicillin/amoxycillin were administered alone also differed significantly. The most efficacious drug was trimethoprim-sulphonamide, administered alone.     

Clinical signs of West Nile virus encephalomyelitis in horses during the outbreak in Israel in 2000

Between August and October 2000, 76 horses were reported by veterinary practitioners as having signs of a neurological disorder, varying from an involvement of the spinal cord alone to the entire central nervous system; 15 of the horses died or were euthanased as a result of their grave prognosis or secondary complications. At the same time, an outbreak of West Nile virus infection affected people and birds, principally domestic geese. West Nile virus was isolated from four of the horses with encephalomyelitis and five other horses seroconverted, indicating that the virus was the probable cause of the outbreak in horses. Three of the cases from which the virus was isolated are described briefly and one case is described in detail. This horse behaved abnormally and had general proprioceptive deficits in all four limbs. Its neurological condition deteriorated after two days and severe inspiratory dyspnoea due to a failure to abduct the arytenoids necessitated a tracheostomy. It died on the fourth day and histological lesions were observed in the brain stem and grey matter of the spinal cord.     

Seroprevalence of Neospora spp. among asymptomatic horses, aborted mares and horses demonstrating neurological signs in Israel

Sera from 800 asymptomatic horses were examined for the presence of antibodies to Neospora caninum by immunofluorescence antibody test (IFAT). The presence of antibodies to N. caninum was also tested in sera from 52 mares that had aborted and 40 horses exhibiting neurological signs. A total of 95 (11.9%) of the 800 sera had antibodies for Neospora. Significantly higher seropositivity was obtained from horses that had neurological signs (21.2%) and from aborted mares (37.5%). There was significant linear-by-linear association between age and seropositivity. This is the first serologic survey for Neospora spp. antibodies performed on horses from the Middle East and the first to report significant difference in seropositivity between asymptomatic horses and horses exhibiting neurological signs.     

An unusual incidence of neurological disease affecting horses during a drought

The clinical, pathological and epidemiological factors were investigated in 12 horses presenting with severe neurological signs. Although the cases involved differing central (n = 1), spinal cord (n = 4) and peripheral nerve (n = 7) deficits in a number of instances, there were similar pathological findings. The possibility of a unifying aetiological factor, such as a toxicosis, is discussed because of the pathological similarities and as the cases appeared during an unusually long dry period.     

Evidence that antibodies against recombinant SnSAG1 of Sarcocystis neurona merozoites are involved in infection and immunity in equine protozoal myeloencephalitis

Sarcocystis neurona is the principal etiologic agent of equine protozoal myeloencephalitis (EPM). An immunodominant protein of S. neurona, SnSAG-1, is expressed by the majority of S. neurona merozoites isolated from spinal tissues of horses diagnosed with EPM and may be a candidate for diagnostic tests and prophylaxis for EPM. Five horses were vaccinated with adjuvanted recombinant SnSAG1 (rSnSAG1) and 5 control (sham vaccinated) horses were vaccinated with adjuvant only. Serum was evaluated pre- and post-vaccination, prior to challenge, for antibodies against rSnSAG1 and inhibitory effects on the infectivity of S. neurona by an in vitro serum neutralization assay. The effect of vaccination with rSnSAG1 on in vivo infection by S. neurona was evaluated by challenging all the horses with S. neurona merozoites. Blinded daily examinations and 4 blinded neurological examinations were used to evaluate the presence of clinical signs of EPM. The 5 vaccinated horses developed serum and cerebrospinal fluid (CSF) titers of SnSAG1, detected by enzyme-linked immunosorbent assay (ELISA), post-vaccination. Post-vaccination serum from vaccinated horses was found to have an inhibitory effect on merozoites, demonstrated by in vitro bioassay. Following the challenge, the 5 control horses displayed clinical signs of EPM, including ataxia. While 4 of the 5 vaccinated horses did not become ataxic. One rSnSAG-1 vaccinated horse showed paresis in 1 limb with muscle atrophy. All horses showed mild, transient, cranial nerve deficits; however, disease did not progress to ataxia in rSnSAG-1 vaccinated horses. The study showed that vaccination with rSnSAG-1 produced antibodies in horses that neutralized merozoites when tested by in vitro culture and significantly reduced clinical signs demonstrated by in vivo challenge.     

Neurological disease associated with EHV-1-infection in a riding school: clinical and virological characteristics

An outbreak of neurological disease caused by EHV-1 infection is described with emphasis on diagnosis and prognosis for recumbent horses. In April 1995, an outbreak of the neurological form of Equine herpesvirus type 1 (EHV-1) occurred in a well-managed riding school with 41 horses: 34 horses showed a temperature spike and 20 some degree of neurological signs, of which 10 were nursed intensively in the indoor arena of the riding school for 3 to 20 days, 8 having to be maintained in slings for 2-18 days, while 9 needed bladder catheterisation b.i.d. for 2-16 days. Within the first 3 days, one horse was subjected to euthanasia and another horse died. Postmortem examination revealed a mild vasculitis with perivascular mononuclear cuffing and axonal degeneration in the central nervous system. Clinical diagnosis was confirmed by serology and virology: 28 horses seroconverted in one or more tests during the outbreak, whereas 12 had already high CF and SN titres in the first sample, suggestive of recent infection. Virus was isolated from nasal swabs of 4 horses, and identified as EHV-1 with type-specific monoclonal antibodies. Restriction enzyme analysis revealed that the EHV-1 strains from this outbreak belonged to genome type EHV-1.IP. The electropherotypes were identical to those from another, epidemiologically unrelated, outbreak of neurological disease 2 months earlier. The timing of the temperature spikes and seroconversions indicated that the infection was probably introduced by a horse purchased 3 weeks before neurological signs occurred. At follow-up one year later, the 10 horses that showed mild neurological signs had recovered completely. Of the 8 horses that survived intensive care, 3 had returned to around their former performance level (2 of which had been in slings), while the other 5 had become pasture-sound. At follow-up 4 years later, all pasture-sound horses had been subjected to euthanasia because of persistent mild ataxia and incontinence. In conclusion, the prognosis for recumbent horses due to EHV-1 infection is grave. For virological diagnosis, extensive and strategic sampling of febrile in-contact horses is required, and the EHV-1-specific glycoprotein G (gG) ELISA is a valuable tool for specific serological diagnosis of EHV-1 infection causing neurological disease.     

Large pituitary adenoma in an 8‐year‐old Arabian stallion

An 8‐year‐old Arabian stallion weighing 361 kg presented to Louisiana State University Veterinary Teaching Hospital with a 3‐month history of weight loss, exercise intolerance, long hair coat and recent history of seizures and aimless wandering in the pasture. An initial presumptive diagnosis of pituitary pars intermedia dysfunction (PPID) was made based on clinical signs. The initial examination revealed weight loss and loss of body condition (BCS 3/9), hypertrichosis, muscle wasting and reluctance to move when prompted. A neurological examination revealed dull mentation with no evidence of proprioceptive deficits in the limbs. Mild hyperglycaemia and a stress leucogram were noted on initial biochemical panel and haematology, respectively. Plasma adrenocorticotrophic hormone (ACTH) concentrations before and after thyrotropin releasing hormone (TRH) stimulation were markedly increased. Rapid slice computed tomography (CT) scan of the head before and after contrast revealed a large mass in the region of the pituitary gland suggestive of macroadenoma causing PPID. Prior to imaging, treatment consisted of supportive nursing care. Due to size of the pituitary gland (measuring 4.6 × 4.6 × 3.8 cm) and the presence of seizure‐like activity and dull mentation, the stallion was subjected to euthanasia. A necropsy was not performed. Pituitary macroadenomas in horses affected with PPID, who show neurological signs such as seizure‐like activity, dull mentation and aimless wandering, might have a poor prognosis and treatment with pergolide mesylate might not reduce pituitary gland size or relieve clinical signs. A CT scan is indicated in horses with neurological signs suspected of PPID to further evaluate pituitary gland size and surrounding structures and rule out other causes to better assess prognosis.     

A survey of neurological diseases in horses

SUMMARY: Case records of 450 horses with signs of neurological disease are reviewed. One hundred and nineteen horses with neurological disease due to trauma were examined, of which 60 were due to spinal cord trauma, 47 to brain or cranial nerve trauma and 12 to peripheral nerve trauma. Cervical vertebral fractures/trauma were the most common injury. Basisphenold/basloccipital bone fractures were the most common form of cranial trauma and facial nerve paralysis the most common cranial nerve injury. Eighty-nine horses with neurological disease due to malformation were examined. Cervical vertebral malformation occurred in 83 horses and congenital defects in 6 foals. Neurological disease due to inflammation or infection occurred in 30 horses. The most common disease of this type was meningitis, which occurred in 11 horses and foals. Neoplasms in the CNS caused neurological disease in 8 horses. The final category was miscellaneous neurological disease, which was diagnosed in 204 horses. Diseases in this category included neonatal (28 cases), toxic/metabolic (27 cases), idiopathic (133 cases), degenerative (3 cases) and other neurological diseases (13 cases). The most common condition was idiopathic laryngeal hemiplegia (116 cases).
Where possible, diagnosis relied on a thorough neurological examination with use of ancillary tests in selected cases including rhinolaryngoscopy, radiography, myelography, ophthalmoscopy and cerebrospinal fluid analysis when indicated. In many cases necropsy and histopathological confirmation or diagnosis was necessary.     

Management of equine ataxia caused by cervical vertebral stenotic myelopathy: A European perspective 2010–2015

The diagnosis and therapy of cervical vertebral stenotic myelopathy (CVSM) are challenging and have been most frequently described in racehorses. We aimed to analyse CVSM cases presented for diagnostic work‐up and treatment in a nonracing horse population. We hypothesised that our diagnostic work‐up protocol including clinical/orthopaedic/neurological/radiographic and myelographic examinations may provide practical reference points for in vivo diagnosis/prognosis and adequate CVSM management. Medical records from 2010 to 2015 were reviewed retrospectively. Cases were included if our standardised work‐up protocol was followed, there was no evidence of any infectious diseases causing the neurological signs, and native cervical radiographs and myelograms confirmed CVSM. Age/breed/sex/type of performance/degree of neurological deficits and number/sites/quality/therapy of stenosis were recorded. Sixty‐two horses met the inclusion criteria. The majority of the horses were aged 5–10 years (44%) or >10 years (35%); nine horses (15%) were 1–4 years and four <1 year (6%) old. Forty‐six horses were Warmbloods (73%), 10 ponies (16%) and six of other breeds (11%). Males were more affected (69%) than females (31%). Sixty‐one percent were pleasure‐horses, 26% were sport‐horses and no information was available for 13%. Most cases presented with mild–moderate neurological signs (grade 2/5 = 18%, grade 2–3/5 = 31%). On myelograms, 23 horses (37%) had single‐level, 22 (35%) had double‐level, and eight (13%) triple‐level stenosis, while nine cases (15%) did not have stenosis. Fifty horses (55%) showed dynamic and 41 (45%) static stenosis. Dynamic stenosis was more common (46%) than static (29%) stenosis and/or combined stenosis (25%). Stenoses were more frequently observed in the mid‐to‐caudal vertebrae. Static stenoses tended to be located more caudally. Based on our protocol, 15% of horses were subjected to euthanasia without therapy, 62% treated conservatively and 23% underwent cervical ventral interbody fusion. In conclusion, our diagnostic work‐up protocol provided practical reference points for in vivo diagnosis/prognosis and adequate management of CVSM in a nonracing horse population.     

Polyneuropathy associated with forage sources in Norwegian horses

BACKGROUND: Cases of hindlimb digital extensor weakness of unknown etiology have been observed in Norway since 1995. HYPOTHESIS: We hypothesized that the observed bilateral extensor weakness was attributable to neuropathy of the distal nerves and that this was related to environmental factors, possibly dietary. ANIMALS: Seventy-five horses with digital extensor weakness occurring from 1995 to 2004 are described. METHODS: Eleven horses were examined at The Norwegian School of Veterinary Science, and the medical records of 64 horses seen in ambulatory practice were reviewed. RESULTS: There was no apparent sex, age, or breed predilection, but the majority were horses kept for pleasure or breeding purposes. Clinical signs varied from intermittent knuckling of the hindlimbs to paraplegia. Some horses showed no or only slow progression of signs, whereas others developed severe signs within hours. No other neurologic deficits were detected in any of the horses. Epidemiologic data and laboratory results were not supportive of an infectious etiology. The only common factor for all affected horses seemed to be feeding big bale silage or, occasionally, hay of poor microbiologic quality. Forty of the 75 horses were euthanized. Histopathologic examination of peripheral nervous tissue was performed in 22 horses, all of which had neuronal fiber degeneration. The majority of horses with mild signs recovered after 5-6 months of rest. CONCLUSIONS AND CLINICAL IMPORTANCE: Clinical signs correlated with polyneuropathy involving sciatic nerves.     

Aujeszky's disease in horses fulfils Koch's postulates

Aujeszky's disease virus was isolated from the brain of a horse which had shown severe neurological signs, including excessive sweating, muscle tremors and periods of mania. Pathological examination revealed a non-suppurative meningoencephalitis. The virus was propagated in cell culture and inoculated into the conjunctiva and nostrils of two ponies. The ponies developed fever seven days after inoculation and subsequently started to behave abnormally, showing severe neurological signs on the ninth day after inoculation. One pony became excited and the other was depressed. One pony died on the ninth day after inoculation and the other was euthanased on the 10th day. Both ponies had a significant increase in serum antibody titre against the virus. The virus was recovered from several parts of the brains and the eyes of the ponies. Aujeszky's disease in horses therefore fulfils Koch's postulates. Although horses do not appear to be very susceptible to the virus, Aujeszky's disease should be included in the differential diagnosis of horses with fatal or transient neurological signs of disease in areas where the virus is endemic.     

Fractures of the withers in horses

The objective was to determine the prognostic features and long‐term outcome of withers fractures in horses. Medical records and radiographs of 14 horses with withers fractures from 2 veterinary teaching hospitals were reviewed. Case details, presentation, clinical signs, radiographs, treatment and outcome were assessed. In all cases, withers fractures were found to occur following a fall on the back. Although horses were often presented with severe acute clinical signs, the long‐term prognosis was good, in the absence of neurological signs, and following extended conservative management (an approximate 6 month rest period).     

Suspected venous air embolism in three horses

Venous air embolism was suspected in 3 hospitalised horses on the basis of an inadvertently open jugular venous line. Subsequently the 3 horses developed clinical signs including cardiovascular collapse, cardiac dysrhythmia, pulmonary oedema, behavioural abnormalities and neurological signs consistent with central nervous system injury. Treatment included intranasal oxygen therapy, i.v. fluid administration and anti‐inflammatory therapy. Specific therapy aimed at treating air embolism in man is reviewed, with pertinent therapy potentially applicable to horses emphasised.     

Polyneuropathy of Finnish horses characterised by inflammatory demyelination and intracisternal Schwann cell inclusions

REASON FOR PERFORMING STUDY: A neurological disorder characterised by pelvic limb metatarsophalangeal joint extensor paresis has been observed in numerous horses in Scandinavia for the last decade. Very little has been formally reported and there have been no detailed assessments of the neurological signs or neuropathological lesions. OBJECTIVES: To describe the epidemiological and pathological features of an outbreak of 'Scandinavian knuckling syndrome' in a riding stable in southern Finland. METHODS: Clinical neurological examination of 4 cases and neuropathological assessment of tissues of one case were performed. RESULTS: Eleven out of 17 horses fed on ryegrass from a common source showed progressive clinical signs of metatarsophalangeal extensor paresis necessitating euthanasia of 7 horses. Nervous system lesions in one horse consisted of a novel demyelinating, mildly inflammatory peripheral neuropathy, with BiP/GRP positive rough endoplasmatic reticulum Schwann cell inclusions. CONCLUSIONS: The clinical signs and lesions documented differ from any previously described equine polyneuropathy and suggest a primary Schwann cell lesion. POTENTIAL RELEVANCE: The classification of this disease as a novel demyelinating polyneuropathy may assist focused epidemiological investigations.     

Cerebellar abiotrophy in a 6‐year‐old Arabian mare

Cerebellar abiotrophy (CA) is an uncommon neurological disease that most commonly affects Arabian horses. Affected horses are typically identified within the first 6 months of life. Intention tremor, wide based stance and ataxia are common clinical signs observed in affected individuals. No treatment is available for resolution of clinical signs. Definitive diagnosis is based on histopathological examination of cerebellar tissue, which is characterised by loss of Purkinje cell layer. This report describes a case of cerebellar abiotrophy that had a delayed diagnosis until 6 years of age.     

Head trauma in two horses

The initial clinical signs displayed by two horses with head trauma are described and related to the pathology and management of the condition, to illustrate the diversity of signs that may result from similar events. It is suggested that careful repeated neurological investigations are more reliable prognostic indicators in cases of equine head trauma than a reliance on the initial assessment.     

Conservative Management of a Cervical Vertebral Fracture in a Gelding

The presentation, diagnostic evaluation, treatment, and 5 years follow-up of a 12-year-old Arabian-Saddlebred cross gelding with neck pain and stiffness, attributable to a fracture of the third cervical vertebrae (C3), is described. Initial cervical spinal radiographs revealed a concave defect in the ventral aspect of the cranial end plate of C3. However, both this finding and ultrasonographic imaging of the area were inconclusive for a fracture. Nuclear scintigraphy revealed that the lesion was metabolically active, prompting computed tomographic imaging that revealed a fracture of C3. Sequential radiographs documented progressive fusion of C2-C3 and no neurological deficits developed over the 5 years after the injury. Cervical vertebral injuries in horses can lead to various clinical signs including ataxia, weakness, and neck stiffness or pain. Diagnosis with cervical radiographs alone can be challenging and, in some cases as the horse in this report, multiple imaging modalities may be required to establish a definitive diagnosis. Horses without neurological signs may recover successfully with conservative medical management, which was performed in this case.     

Ceratohyoidectomy for treatment of equine temporohyoid osteoarthopathy (15 cases)

This study investigated 15 horses diagnosed with temporohyoid osteoarthopathy (THO) and treated by ceratohyoidectomy between 2004 and 2012. The presenting complaint, duration and nature of the clinical signs, additional diagnostic procedures, and complications were reviewed retrospectively. Long-term follow-up on horses was used to determine prognosis. All horses were diagnosed by guttural pouch endoscopy. Follow-up was available for 14 horses that survived to discharge. Eight of 10 horses that were used athletically prior to surgery returned to previous levels of use. Persisting clinical signs included mild facial nerve paralysis (3/14; 21.4%) or head tilt (6/14; 42.8%) but these were not functionally limiting. It was concluded that equine THO affects a wide range of breeds, disciplines, and ages of horses, and has a variety of presenting clinical signs most commonly associated with vestibular and facial nerves. Prognosis following ceratohyoidectomy is good for resolution of ataxia but some cranial nerve deficits may persist.     

Serological markers of Bornavirus infection found in horses in Iceland

Background

In a stable of eight horses in Northern Iceland, six horses presented with clinical signs, such as ataxia and reduced appetite, leading to euthanasia of one severely affected horse. Serological investigations revealed no evidence of active equine herpes virus type 1 infection, a common source of central nervous system disease in horses, nor equine arteritis virus and West Nile virus. Another neurotropic virus, Borna disease virus, was therefore included in the differential diagnosis list.

Findings

Serological investigations revealed antibodies against Borna disease virus in four of five horses with neurological signs in the affected stable. One horse without clinical signs was seronegative. Four clinically healthy horses in the stable that arrived and were sampled one year after the outbreak were found seronegative, whereas one of four investigated healthy horses in an unaffected stable was seropositive.

Conclusions

This report contains the first evidence of antibodies to Borna disease virus in Iceland. Whether Borna disease virus was the cause of the neurological signs could however not be confirmed by pathology or molecular detection of the virus. As Iceland has very restricted legislation regarding animal imports, the questions of how this virus has entered the country and to what extent markers of Bornavirus infection can be found in humans and animals in Iceland remain to be answered.