Page 1051 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

1026 CHAPTER 9

VetBooks.ir 9.28 Prognosis
DIC is a serious complication that can be difficult
to treat and warrants a guarded to grave prognosis.
Additionally, the underlying disease process tends to
be serious and often difficult to treat.

EQUINE ANAPLASMOSIS (EQUINE
GRANULOCYTIC EHRLICHIOSIS)

Definition/overview
Equine anaplasmosis (historically referred to as
equine granulocytic ehrlichiosis [EGE]) is a seasonal
rickettsial disease characterised by haematological,
GI and/or neurological signs. It has been reported in
Fig. 9.28 Small petechial haemorrhages (arrows)
on the oral mucous membranes of a horse with the USA, Canada, northern Europe and Brazil.
thrombocytopenia. (Photo courtesy J Scott Weese)
Aetiology/pathophysiology
Equine anaplasmosis is caused by infection with
Table 9.3 Laboratory abnormalities that support a rickettsial organism called Anaplasma phagocy-
the diagnosis of disseminated
intravascular coagulopathy tophilum. The organism causing disease in horses
was formerly called Ehrlichia equi. This is the same
• Thrombocytopenia organism responsible for human granulocytic
• Prolonged prothrombin time (PT) ehrlichiosis and ehrlichiosis of small ruminants in
• Prolonged activated partial thromboplastin time (APTT) Europe. A. phagocytophilum is transmitted to the
• Fragmented RBCs (shistocytes) horse via tick (Ixodes spp.) bites. The organism has
• Increased fibrin degradation products (FDPs) or d-dimers a tropism for granulocytes, predominantly neutro-
phils. Through a combination of increased demand,
• Decreased antithrombin
• Decreased specific factor activity possible immune-mediated destruction and altered
bone marrow microenvironment, decreases in
• Hypofibrinogenaemia white blood cells (WBC)s, platelets and occasion-
• Prolonged thrombin clotting time (TCT) ally RBCs occur. The disease may also produce
vasculitis.

its development (Table 9.3). Laboratory findings may Clinical presentation
include thrombocytopenia, fragmented RBCs (schis- Clinical signs develop within 14 days of exposure and
tocytes) on the blood smear, decreased fibrinogen con- may be vague and non-specific. Horses over 4 years
centration, prolongation of PT and APTT, decreased of age tend to develop progressive fever, depression,
antithrombin activity and increased FDPs or d-dimers. anorexia, icterus, limb oedema and ataxia. Horses
under 4 years of age tend to develop milder signs,
Management and fever may be the only abnormality present in
Treatment of the underlying disease is imperative. horses under 1 year of age. Signs typically peak by
Specific treatments for DIC include heparin admin- days 3–5 and may persist for 14–16 days. Trauma
istration to minimise further clot formation and occurring because of ataxia is not infrequent.
plasma transfusion to replace consumed clotting
factors. Administration of heparin alone may not be Differential diagnosis
useful because heparin requires adequate antithrom- A variety of other causes of vasculitis, icterus and
bin to be effective. ataxia should be considered. Other infectious