BackgroundThree flaviviruses (equine pegivirus [EPgV]; Theiler's disease–associated virus [TDAV]; non‐primate hepacivirus [NPHV]) and equine parvovirus (EqPV‐H) are present in equine blood products; the TDAV, NPHV, and EqPV‐H have been suggested as potential causes of serum hepatitis.ObjectiveTo determine the prevalence of these viruses in horses with equine serum hepatitis.AnimalsEighteen horses diagnosed with serum hepatitis, enrolled from US referral hospitals.MethodsIn the prospective case study, liver, serum, or both samples were tested for EPgV, TDAV, NPHV, and EqPV‐H by PCR.ResultsBoth liver tissue and serum were tested for 6 cases, serum only for 8 cases, and liver only for 4 cases. Twelve horses received tetanus antitoxin (TAT) 4‐12.7 weeks (median = 8 weeks), 3 horses received commercial equine plasma 6‐8.6 weeks, and 3 horses received allogenic stem cells 6.4‐7.6 weeks before the onset of hepatic failure. All samples were TDAV negative. Two of 14 serum samples were NPHV‐positive. Six of 14 serum samples were EPgV‐positive. All liver samples were NPHV‐negative and EPgV‐negative. EqPV‐H was detected in the serum (N = 8), liver (N = 4), or both samples (N = 6) of all 18 cases. The TAT of the same lot number was available for virologic testing in 10 of 12 TAT‐associated cases, and all 10 samples were EqPV‐H positive.Conclusions and Clinical ImportanceWe demonstrated EqPV‐H in 18 consecutive cases of serum hepatitis. EPgV, TDAV, and NPHV were not consistently present. This information should encourage blood product manufacturers to test for EqPV‐H and eliminate EqPV‐H–infected horses from their donor herds.

Summary A 6‐year‐old Quarter Horse gelding was presented for bilateral uveitis resulting in vision loss as well as icterus. Anaemia with autoagglutination was consistent with a presumptive immune‐mediated haemolytic anaemia. Urinary PCR was positive for Leptospira spp. and microscopic agglutination test (MAT) titres were elevated to multiple serovars supportive of a diagnosis of leptospirosis. Treatments included broad spectrum antibiotics and aggressive anti‐inflammatory medications. While the horse was hospitalised, the development of bilateral corneal ulcers precluded the use of topical ophthalmic anti‐inflammatories for a number of days. The corneal ulceration resolved, vision returned in both eyes and the immune‐mediated haemolytic anaemia resolved. After 9 days of hospitalisation, oral minocycline was administered for 2 weeks at home as well as low dose oral flunixin meglumine and topical ophthalmic diclofenac and atropine. This case represents the first published case of haemolytic anaemia associated with leptospirosis in a horse.

Background Streptococcus equi subspecies equi infection elicits M protein antibody titers in equids. Interpretation of titers is not generally accepted.HypothesisThe magnitude of S. equi M protein (SeM) antibody titer after infection (titer ≥1:12 800) will be useful to monitor for the presence of complications or the risk of development of complications.AnimalsForty‐eight horses on 1 farm involved in strangles outbreak.MethodsClinical and observational study. S. equi M protein antibody titers were measured on all horses 8 weeks after infection and select horses 12 and 28 weeks after infection. Horses were categorized: no disease, uncomplicated case, persistent guttural pouch (GP) infection, or complicated cases (metastatic abscesses, purpura hemorrhagica, secondary infections, and dysphagia). Category was compared to titer.ResultsTwenty‐eight of 48 (58%) developed clinical signs of S. equi infection. Of those, 11 (39%) had uncomplicated strangles, 9 (21%) had persistent GP infection, 5 (18%) were complicated cases, and 3 (11%) had both persistent GP infection and complications. Thirty‐three percent of horses (16 of 48) had SeM antibody titers ≥1:12 800 eight weeks after infection. Of horses with titers ≥1:12 800, 6 of 16 had evidence of complications. Of complicated cases, 6 of 8 had titers ≥1:12 800. In this outbreak, the sensitivity (75%; 95% CI [confidence interval] 45‐105) for a SeM antibody titer ≥1:12 800 detecting complications was higher than the specificity (43%; 95% CI 23‐64).Conclusions and Clinical ImportanceThis outbreak demonstrates that SeM antibody titers can be increased after infection (≥1:12 800) in the absence of complications of strangles.

There is limited information in the literature regarding the clinical use of formalin for the treatment of haemorrhage in horses. This uncontrolled retrospective study summarises 11 cases that were treated with intravenous formalin at the Veterinary Health Center at Kansas State University from 2009 to 2019. The objective of this study was to describe signalment, clinical and laboratory findings, treatment and outcome of horses treated with intravenous formalin for potentially life-threatening haemorrhagic conditions. This study does not attempt to prove efficacy of intravenous formalin, but rather to report its clinical use and the associated details of those cases. Horses ranged in age from 2 to 23 years old. There were nine Quarter Horses, one Thoroughbred and one Appaloosa. Treated conditions included haemoabdomen (4/11), uterine haemorrhage (1/ 11), epistaxis (3/11), haemorrhage secondary to a mandibular laceration (2/11) and haemothorax (1/11). The most utilised dose was 0.476% formalin (50 mL 10% neutral buffered formalin diluted in 1 L of isotonic fluid). Some horses were also treated with aminocaproic acid, Yunnan Baiyao, whole blood transfusions and surgery. Ten out of the 11 horses survived to discharge with one horse reported by the owner to have died 2 weeks later of an unknown cause.

Background: While there is a commercially-available vaccine for Streptococcus equi subsp. equi

Summary A 7‐year‐old Quarter Horse mare was presented for severe left hindlimb oedema and nonweightbearing lameness that was progressive over approximately 48 h. The mare subsequently developed marked and worsening oedema, immune‐mediated haemolytic anaemia (IMHA), myositis and myocarditis. The marked oedema, degree of pain and severity of myositis were consistent with infarctive purpura haemorrhagica. Fine needle aspiration of affected tissue resulted in positive bacterial culture of Staphylococcus aureus. Purpura haemorrhagica and associated complications are typically associated with Streptococcal sp. infection or exposure, and have not been previously reported in association with Staphylococcus aureus in the horse. The mare responded favourably to long‐term, high‐dose corticosteroid therapy, antimicrobials and supportive care.

Summary A 3‐year‐old Gypsy Vanner stallion was presented for evaluation of intermittent recumbency, muscle fasciculations, weakness, low head carriage, shifting of weight between the hindlimbs and an elevated tail head. History, physical examination and serum alpha tocopherol concentrations were suggestive of vitamin E deficiency and equine motor neuron disease (EMND). Sacrocaudalis dorsalis medialis muscle biopsy identified myositis secondary to sarcocystosis. Treatment with alpha tocopherol, ponazuril and sulfadiazine/pyrimethamine resulted in significant improvement in muscle weakness and body condition with resolution of sarcocystosis and inflammation on repeat muscle biopsy. This case illustrates the importance of muscle biopsy in horses with neuromuscular disease as concurrent diseases may be present that require specific treatment for a positive outcome.

Background: Neonatal foals are born essentially agammaglobulinemic and therefore must ingest colostrum or receive immunoglobulins to maintain health. Failure of passive transfer treatment involves administration of equine colostrum, plasma or commercial powdered colostrum (CPC). Anecdotal reports suggest a risk of anaphylaxis associated with plasma transfusion in neonates that received CPC prior to gut closure. Bovine serum albumin (BSA) in CPC may serve as a target for BSA-specific immunoglobulin E (IgE) in donor equine plasma. Objectives: To determine presence of BSA-specific IgE in samples collected post-routine vaccination in healthy horses, horses experiencing adverse vaccine reactions and commercial equine plasma. Study Design: Prospective Observational Methods: Serum was collected from 65 healthy horses at day 0, 14, 28, 90, 180, 270 and 365 post-vaccination, 26 horses after vaccine reaction at day 1, 180 or 270 post-vaccination, 4 horses not vaccinated and 10 horses from a commercial plasma donor herd. BSA-specific IgE was determined using enzyme-linked immunosorbent assay (ELISA). Results: BSA-specific IgE was not detected in non-vaccinated horses and was identified in all vaccinated horses. Younger horses demonstrated higher fold changes in post-vaccination BSA-specific IgE expression compared to older horses. No significant difference in BSA-specific IgE levels between commercial plasma donors and healthy horses was identified. No significant difference in post-vaccination anti-BSA IgE levels between reactor and healthy horses at day 180 and 270 post-vaccination were identified. Main Limitations: Small number of reactor horses at day 180 and 270 post-vaccination with most samples being collected 24 hours. There were no healthy horse samples for 24 hours post-vaccination; therefore, it was not possible to compare the two groups at this timepoint. Conclusions: Horses may express BSA specific IgE following vaccination. There may be risk of hypersensitivity type reaction when veterinarians administer commercial plasma to neonatal foals that have consumed CPC prior to gut closure.