Purpura hemorrhagica in Horses (Equis) | Vetlexicon
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Purpura hemorrhagica

ISSN 2398-2977


Introduction

  • Cause: hypersensitivity to streptococcal antigen; secondary to respiratory tract bacterial or viral infection, eg Streptococcus equi (S. equi var equi) Strangles (Streptococcus equi infection), vaccination with S. equi M-protein equine influenza Equine influenza, wound infection Wound: complications or idiopathic.
  • Signs: variable severity; edematous plaques 2-10 cm diameter over neck, chest, thigh → edema of distal limbs, head, ventral mid-line → serous exudation, fissures, necrosis and cellulitis Cellulitis; +/-pyrexia; petechial/ecchymotic hemorrhages on mucous membranes.
  • Diagnosis: hematology, blood biochemistry, histopathology.
  • Treatment: resolve underlying infection; corticosteroids, diuresis.
  • Prognosis: fair to poor depending on severity; complications may → death.

Presenting signs

  • Urticarial edematous plaques, particularly on the head, ventrum and distal limbs.
  • Petechial or eccymotic hemorrhages on mucous membranes.
  • Severe edema can lead to respiratory distress, anorexia, lethargy and weight loss.
  • Secondary to edema - exudations, ulceration, crusting and eventually sloughing.
  • Tachycardia, tachypnoea, stiffness and reluctance to move.
  • Multi-organ failure can occur due to systemic vasculitis.
  • Recent history of infection, especially strangles.
  • Recent history of administration of a bacterin or M-protein vaccine.

Acute presentation

  • Usually develops in 2-4 weeks after a respiratory infection.

Age predisposition

  • Over 2 years of age.

Cost considerations

  • Duration of therapy can be weeks.
  • Treatment of underlying disease can be expensive, especially if chondroid removal is required.

Pathogenesis

Etiology

Predisposing factors

General

Specific

  • Previous respiratory tract infection.
  • Repeated use of streptococcal bacterins.
  • Low dose penicillin over short periods during strangles outbreaks.

Pathophysiology

  • Hypersensitivity reaction to streptococcal, bacteria or viral antigens. Antigen-antibody complexes bind to endothelial cells on blood vessels and activate complement and IL-8 → chemotaxis induces a localized neutrophilia, reactive oxygen radicle release and subsequent vasculitis → increased capillary permeability → extravasation of blood cells and serum into adjacent mucosa, skin, subcutaneous tissue and internal organs, including heart and muscle.
  • Overproduction of IgA compared with IgG appears to be a predisposing factor. It is unknown why some horses have high IgA values compared with others.

Timecourse

  • Usually about 2-4 weeks following infection.
  • May occur without history of infection.

Epidemiology

  • PH will often follow the outbreak of strangles.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Kaese H J, Valberg S J, Hayden D W, Wilson J H, et al (2005) Infarctive purpura hemorrhagica in five horses. JAVMA 226 (11), 1893-1898 PubMed.
  • Sweeney C R, Timoney J F, Newton J R & Hines M T (2005) Streptococcus equi infections in horses: guidelines for treatment, control and prevention of strangles. J Vet Int Med 19 (1) 123-132 PubMed.
  • Pusterla N, Watson J L et al (2003) Purpura haemorrhagica in 53 horses. Vet Rec 153 (4), 118-121 PubMed.
  • Larsson V L, Perman V & Stevens J B (1983) Idiopathic thrombocytopenic purpura in two horses. JAVMA 183 (3), 328-330 PubMed.
  • Roberts M C & Kelly W R (1982) Renal dysfunction in a case of purpura hemorrhagica in a horse. Vet Rec 110 (7), 144-146 PubMed.

Other sources of information

  • Felippe M J B (2015) Ed. Equine Clinical Immunology. John Wiley & Sons, USA.
  • Newton J R (1999) Strangles - Diagnosis and Treatment of Sequelae. In: Proc 38th BEVA Congress. pp 120-121.