Summary This is the first report to document transplacental transmission of Anaplasma phagocytophillum in the horse. A 4‐year‐old late‐term pregnant mare presented for a recent onset of pyrexia due to equine granulocytic anaplasmosis (EGA). She was hospitalised for treatment with oxytetracycline and monitoring of high‐risk foaling due to significant thrombocytopenia. Parturition occurred overnight, and the foal was PCR positive for A. phagocytophilum at birth. The foal was slow to stand and nurse, with signs of neonatal encephalopathy and anaplasmosis (thrombocytopenia). Therapy with oxytetracycline resulted in complete clinical recovery of the mare and foal within 5 days. Congenital anaplasmosis should be considered in any foal delivered to a mare suffering from EGA during late‐term pregnancy and guide appropriate antimicrobial therapy.

No abstract

BackgroundThe sarcoid is the most common equine cutaneous neoplasm. Evidence‐based treatment of this condition is often lacking, and selection of treatment modality based on clinical experience or anecdotal evidence.ObjectivesTo assess the quality of the currently available best evidence regarding the treatment of the equine sarcoid.Study designSystematic review.MethodsIn compliance with PRISMA guidelines, literature searches were performed in PUBMED, Web of Science, CAB Abstracts, EMBASE (Ovid) and Scopus in April 2021. Included papers were required to describe an interventional study examining sarcoid treatment strategy, of level 4 evidence or greater. The case definition required confirmation of at least some included lesions on histopathology, and a minimum of 6 months of follow‐up was required on treated cases. Studies were assessed by two independent reviewers (KO, CD). Data extraction was performed manually, followed by risk of bias assessment. Methodological quality was assessed using the GRADE system.ResultsIn total, 10 studies were included in the review. Case definition was confirmed via histopathology in all included lesions in 60% of papers. Time to follow‐up was variably reported. Overall risk of bias ranged from ‘some concerns’ to ‘critical’. Reported sarcoid regression rate ranged from 28% to 100% on an individual sarcoid level, and 9%–100% on a whole horse level. Transient local inflammation was reported following most treatment strategies, with further adverse events reported infrequently.Main limitationsReview methodology excluded a large proportion of available literature regarding the equine sarcoid. Significant heterogeneity between included studies prevented quantitative synthesis and most included papers were at significant risk of bias, indirectness, and imprecision.ConclusionsThere is insufficient evidence currently available to recommend one sarcoid treatment over another. There is an urgent need for sufficiently powered, randomised, placebo‐controlled trials in order to allow more definitive comparison of the efficacy of different treatment strategies.

Airway hyperresponsiveness (AHR) is linked to airway inflammation and is considered a key manifestation of mild/moderate equine asthma (EA). The study purpose was to determine whether two modalities of non-invasive lung function testing (FOM—forced oscillatory mechanics vs. FP—flowmetric plethysmography) establish the same clinical diagnosis of AHR in horses, using histamine bronchoprovocation. Nineteen horses (3–25 years, 335–650 kg) with clinical signs suggestive of mild/moderate equine asthma were enrolled. FOM and FP testing was performed in each horse on two consecutive days, using a randomized cross-over design. AHR was defined by the histamine dose needed to double FOM baseline resistance, or to achieve a 35% increase in FP delta flow. Bronchoalveolar lavage fluid (BALF) was subsequently collected and stained with modified Wright's and toluidine blue stains. Binary statistical tests (related samples T-test, Mann-Whitney U, Chi-square analyses) were performed to compare study groups, with P < 0.05 considered significant. Abnormal BALF cytology confirmed EA in 14/19 (73.7%) horses. Both FOM and FP revealed AHR in 7/14 (50%) of these EA horses. An additional 4/19 (21.1%) horses showed AHR based on FP but not FOM, including two horses with normal BALF cytology. A diagnosis of AHR was more often associated with FP than FOM (P = 0.013), although the prevalence of AHR was significantly higher in EA vs. non-EA horses, regardless of testing methodology. The phase angle between thoracic and abdominal components of breathing did not differ between test groups. In conclusion, FP diagnosed AHR more frequently than did FOM, including horses with no other diagnostic evidence of EA. Without further evaluation, these two testing modalities of AHR cannot be used interchangeably.

JUVENILE nephropathy in the dalmatian may be a familial condition as occurs in other breeds such as wheaten terriers and cocker spaniels (Nash and others 1984, Kelly 1986, Nash 1989. Although one case has been reported in a dalmatian (Lucke and others 1980) the possibilities of inheritance remain unresolved. This short communication reports the clinical findings and pathology from a dalmatian with juvenile nephropathy.A six-month-old, entire male dalmatian presented initially with a vague malaise and intermittent retching and vomiting of food 30 to 60 minutes after eating. Ptyalism and polydipsia (approximately 3 litres daily) were noted and there were frequent borborygmi. Repeated urinalysis showed a urine specific gravity varying between 1015 and 1020 with a trace of protein (+1) on a BM7 test stick (Ames Pharmaceuticals). The patient was small in stature and weighed 23 kg. After symptomatic treatment the clinical symptoms resolved.The patient continued to be intermittently polydipsic but no further diagnosis was pursued. Six months later the patient again presented with vomiting and ptyalism. On this occasion, his weight was 20 kg and there was abdominal pain, borborygmi and flatulence.Haematology showed a non-regenerative anaemia (packed cell volume 15-5 per cent, red blood cell count 2-1 x 109 mm-3) and a leucocytosis (white blood cell count 21-4 x 106 mm-3) consisting mainly of a neutrophilia (segmented neutrophils 19-47 x 106 mm-3). Biochemistry showed a slight increase in alkaline phosphatase (304 iu/litre), azotaemia (urea 73 mmol/litre and creatinine 790 mmol/litre), hypoproteinaemia (total protein 56 g/litre), hypoalbuminaemia (21 g/litre) and hypercholesterolaemia (10.3 mmol/litre). Clinical examination revealed oral ulceration with uraemic halitosis. The dog's condition deteriorated over the following 24 hours and it was therefore euthanased. Post mortem examination showed emaciation and poor musculoskeletal development. The kidneys were small with roughened and pitted cortical surfaces. Bisection revealed a reduced cortical thickness and several areas of radial scarring through the cortex into the medulla. The rest of the urinary tract was normal and all the other internal organs appeared normal.