EQUINE VETERINARY EDUCATION / AE / MAY 2019


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S. equi infection. Palpation per rectum and thoracic and abdominal ultrasound examinations were within normal limits making metastatic S. equi abscess formation unlikely. All of these findings ruled S. equi out as the primary pathogen involved in this case. Culture and sensitivity results of a fine needle aspirate


sample obtained at presentation, available on Day 5, revealed a heavy growth of Staphylococcus aureus. Antimicrobial susceptibility testing indicated sensitivity to several antimicrobial agents that included tetracycline. Since the mare was receiving oxytetracycline3 at therapeutic dosages, antibiotic therapy was not changed.


Additional therapeutics


In this case, S. aureus cellulitis was implicated in the manifestation of suspect infarctive purpura haemorrhagica causing rhabdomyolysis,


IMHA and myocarditis.


Dexamethasone2 was administered at 0.2 mg/kg bwt i.v. q. 12 h for 2 days (beginning Day 2), then tapered to 0.1 mg/kg bwt i.v. q. 12 h for 2 days, then 0.1 mg/kg bwt i.v. q. 24 h for 3 days. When clinical improvement was noted and the mare appeared to stabilise, the dose was reduced to 0.1 mg/kg bwt q. 24 h intramuscularly. Cryotherapy was implemented on Day 3 for the prophylactic management of potential laminitis, as elevated digital pulses in the forelimbs were noted while the mare received the highest dose of dexamethasone. As the dexamethasone dose was reduced, cryotherapy was subsequently discontinued on Day 6. Digital pulses returned to normal, and shifting limb lameness was not present. The mare was continued on phenylbutazone2 as needed for pain associated with her cellulitis and primary disorder, oxytetracycline3 for septic cellulitis and prevention of secondary infection, vitamin E (Elevate W.S.)5 for anti-oxidative properties (20 IU/kg bwt per os q. 24 h), and omeprazole6 (4 mg/kg bwt per os q. 24 h) for treatment of gastric ulceration. Gastric ulcer risk was considered extremely high due to anorexia, stress and concurrent administration of corticosteroids and NSAIDs. The mare demonstrated a favourable response to 10 days


of hospitalised care, at which time the owner elected to take her home for further management. At the time of hospital discharge, ventral and limb oedema was markedly improved, PCV was stable at 25%, heart rate was consistently between 50–60 beats/min, and CK had decreased to 24,000 U/L. The mare was maintained on a 3-week tapering course of dexamethasone4 (initially 0.5 mg/kg bwt down to 0.35 mg/kg bwt) intramuscularly and trimethoprim- sulfamethoxazole4 960 mg (20 mg/kg bwt per os q. 12 h). Follow-up telephone communication approximately 6 weeks following hospital discharge confirmed that the oedema was completely resolved, but the mare appeared stiff at the walk. Dexamethasone had been discontinued, and the mare was bright and eating well, however further veterinary examination and blood work had not been performed at that time. The referring veterinarian moved to another practice, and the patient was subsequently lost to follow-up.


Discussion


Purpura haemorrhagica, a type III hypersensitivity reaction, is an aseptic necrotising vasculitis that results from immune complex (IgA) deposition in vascular walls (Galen and Timoney 1985; Valberg 2015). Although it is most commonly


associated with Streptococcal sp. infection, the reported case demonstrates that purpura haemorrhagica may develop as a sequela to Staphylococcal sp. infection (Timoney 1993; Pusterla et al. 2003; Kaese et al. 2005; White et al. 2009; Duffee et al. 2015; Valberg 2015; Boyle 2016). Further complications may include myocarditis, endocarditis, panophthalmitis, periorbital abscesses, ulcerative keratitis, paravertebral abscesses, septic arthritis, tenosynovitis and immune-mediated complications such as IMHA, IMTP and myopathies (Pusterla et al. 2003; Kaese et al. 2005). Medical therapy, regardless of inciting cause, is centred around dampening the immune and inflammatory responses and eliminating the inciting cause. Infarctive purpura haemorrhagica is a more severe form of


purpura characterised by necrotising leukocytoclastic vasculitis in addition to subsequent infarction in numerous tissues such as skeletal and cardiac muscle, skin, gastrointestinal tract and lungs (Kaese et al. 2005; Valberg 2015; Durward-Akhurst and Valberg 2017). Clinically, horses may demonstrate muscle swelling, abdominal pain, tachycardia and sloughed necrotic skin. Blood work may reveal neutrophilia with a left shift, hypoalbuminaemia and markedly elevated serum CK activity (Kaese et al. 2005; Durward-Akhurst and Valberg 2017). Prognosis in these patients tends to be guarded. In a case series by Kaese et al. (2005), among five horses diagnosed with infarctive purpura haemorrhagica, only one horse survived. All horses in this series had evidence of infarctions within the skeletal muscle, and had a history of S. equi infection. Furthermore, there seemed to be a breed predilection, specifically the Quarter Horse. While definitive diagnosis is established by skin and/or muscle biopsy and histopathology, the authors of the current report felt that performing a biopsy in this mare was contraindicated in the acute stages of disease based on the deterioration of condition, degree of pain, severity of oedema and marked anaemia. While considered later in the course of disease, skin or muscle biopsy testing was not performed based on concern for impaired wound healing and potential secondary sepsis due to the degree of therapeutic immune suppression required to stabilise her myositis and myocarditis. When combined with her apparent favourable response to therapy, invasive diagnostics were not considered imperative for the successful management of this patient. Based on clinical signs of severe limb and ventral oedema, severe lameness and serum chemistry abnormalities that included marked increases of CK and AST, a presumptive diagnosis of infarctive purpura haemorrhagica was made. The mare in the current report had no history or clinical


signs of a Streptococcal exposure or infection. Henoch- Sch€


onlein purpura, which occurs in human patients, is an


immune complex disease sharing resemblance to purpura haemorrhagica observed in horses and is typically associated with Streptococcal disease (Mills et al. 1990; Duquesonoy 1991; Salsbury 2001; Durward-Akhurst and Valberg 2017). Henoch-Sch€


onlein purpura is characterised by circulating IgA


immune complexes and high serum concentrations of C3d that are deposited within the blood vessels, creating a type III hypersensitivity reaction and vasculitis (Eftychiou et al. 2006). The most common form is seen in children, however there is a more severe adult manifestation. Clinical signs include a rash on the legs and buttocks, arthritis of the knees and ankles (75%), nephritis (40%) and gastrointestinal tract inflammation and bleeding (50–75%). The predominant difference between


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