Lyme Disease and Anaplasmosis

Lyme disease and Anaplasmosis
Chilled EDTA plasma
Lyme disease (or Borreliosis) and Anaplasmosis are recognised increasingly as causes of clinical disease
in horses. Both organisms are transmitted by Ixodes ticks (that are common in many parts of the UK)
and are obligate intracellular organisms that may infect multiple species. Some of the clinical signs are
summarised below.

Lyme disease Anaplasmosis
Mild pyrexia Pyrexia
Lethargy Anorexia/Weight loss
Anorexia/Weight Loss Somnolence/altered mentation
Stiffness/Lameness Ataxia (collapse/recumbency)
Muscle Soreness Ventral oedema
Synovial Effusions Anaemia
Laminitis Petechiae/Ecchymotic haemorrhages
Uveitis
Somnolence/altered mentation
Hyperaesthesia
Ataxia

LYME DISEASE

Lyme disease is caused by the spirochete Borrelia burgdorferi. B. burgdorferi infects leucocytes and
synovial lining cells and triggers an inflammatory (and potentially autoimmune) response. The
persistence of the bacteria within both synovial structures and tendons in humans leads to the
prolonged treatment required.
B. burgdorferi has also been reported to cause neuroborreliosis leading to the clinical signs of ataxia,
hyperaesthesia and mentation changes and this can be diagnosed based on CSF samples.
High rates of Borrelia seropositivity have been recorded in horses from many regions of the UK and it
is likely that seropositivity for Anaplasma is similar. A study performed in 1994 indicated low levels
(<7%) of seropositivity in Newmarket, Ireland, Yorkshire and Scotland but quite high levels (30-35%)
in South Coast areas and East Anglia.

ANAPLASMOSIS

Anaplasmosis is caused by the Rickettsial organism Anaplasma phagocytophilum (formerly Ehrlichia
equi). Anaplasma phagocytophilum infects neutrophils and eosinophils resulting in neutropaenia and
anaemia. Clusters of intracellular organisms may be visible as blue-grey spoke-wheel inclusions during
the initial phase of infection. The presence of visible intracellular organisms tends to correlate with
the presence of pyrexia, which usually lasts for around 10 days after infection. The majority of acute
infections will lead to a marked pyrexia.

DIAGNOSIS

Definitive confirmation of Lyme disease or Anaplasmosis is problematic and currently diagnosis is
based upon finding a positive antibody titre for the suspected organism in a horse with suspicious

clinical signs in an area where the disease, or at least Ixodes ticks, are known to be endemic. This has
several limitations however. Firstly, with standard test methods it may take up to 3 months following
infection for horses to seroconvert – meaning that many early cases will be ‘negative’ on serology.
Secondly, horses may become infected and seroconvert without showing any clinical signs – hence
many healthy horses or horses with other conditions could be misdiagnosed with Lyme disease on the
basis of serology. Thirdly, horses that are successfully treated may still remain seropositive for a very
long time thereafter – complicating interpretation of successful resolution.
The ELISA method used at the LEH for detection of Borrelia targets antibodies against the Borrelia
surface protein V1sE. In experimental infections, animals became seropositive to V1sE within 3-5
weeks of infection, well before clinical signs arose. Additionally, infected horses that were successfully
treated showed waning an body titres more rapidly than with other test methods (although this may
still be a matter of months). Furthermore, the method was able to detect some seropositive cases that
had been missed using standard Western Blot techniques. The diagnostic accuracy of the ELISA
method used at the LEH for the identification of seroconversion to Borrelia has been evaluated in 3
studies with a sensitivity (true positive rate) of 65%-100% and a specificity (true negative rate) of 95%-
100%.
Although a PCR assay targeting Borrelia organisms might indicate a secure diagnosis, we stopped
running this in our lab due to few requests.
The ELISA test used at the LEH to diagnose Anaplasma targets antibodies against peptides derived
from the immunodominant p44 protein of Anaplasma phagocytophilum.

TREATMENT

Intensive treatment for Lyme disease can include 7-10days of oxytetracycline (5 mg/kg IV SID/BID)
followed by either oral doxycycline (10 mg/kg PO BID) or oral minocycline (4mg/kg PO BID) for 1-2
months. Anaplasmosis can be treated with a shorter course of either oxytetracycline, doxycycline or
minocycline. While treating with these antibiotics renal values should be closely monitored. Ceftiofur
(2-4 mg/kg IM BID) has also been recommended.
Total eradication of organisms from clinical cases can be problematic and clinical signs can recur
following apparently successful treatment. Although vaccines are available for Borreliosis in other
countries, there are no licensed products available in the UK. Tick control is also an important
component of management in endemic areas.
FURTHER READING:
Carter, S. D. et al. (1994). Borrelia burgdorferi infection in UK horses. Equine Veterinary Journal 26 (3), 187–190.
Chang, Y-F. et al. (2005). Antibiotic treatment of experimentally Borrelia burgdorferi infected ponies. Veterinary Microbiology, 107 (3-4), 285–294.
Johnson, A. L. et al. (2008). Validation of an In-Clinic Enzyme-Linked Immunosorbent Assay Kit for Diagnosis of Borrelia Burgdorferi Infection in Horses.
Journal of Veterinary Diagnostic Investigation. 20 (3), 321 – 324.
Divers, T. J. et a. (2013). Equine Lyme Disease. Journal of Equine Veterinary Science 33 (7) 488-492.