Lyme Disease

Description

Map of the areas where Borrelia burgdorferi is endemic
Copyright Percherie 2006 Wikimedia Commons

Lyme disease descibes the clinical syndrome caused by infection with Borrelia burgdorferi in humans, dogs, horses, cattle and sheep. The disease is named after the town of Lyme[1] in Connecticut, USA where clinical cases were first described in humans in 1975. Since its identification, it has become clear that B. burgdorferi has been present in Europe and North America since at least the start of the twentieth Century. Currently, the bacterium is known to be present in Europe, Asia and North America (see image).

The bacterium is transmitted by ticks of which the most common is Ixodes ricinus in the UK. I. ricinus is a three host tick that acquires B. burgdorferi bacteria when it obtains a blood meal from small rodents as a larva or nymph and then transmits it to large mammals as an adult. Lyme disease therefore occurs when domestic animals and humans enter areas of tick habitat and ticks must be attached for at least 48 hours for the organisms to multiply and transfer to the mammalian host.

Pathophysiology

The virulence of the borreliae is associated with changes in expression of outer membrane proteins (OMP) after introduction into the mammalian host. In the majority of hosts, the bacteria remain at the site of introduction but do not cause clinical disease. Antibodies are produced in response to the bacteria but, despite this, they are not eliminated and they may persist for the life of the host. In a small proportion of infected animals, the bacteria multiply and migrate through the connective tissues and disseminate via the blood stream. The migrant bacteria localise particularly in the skin, joints, brain, nerves, eyes and heart and clinical syndromes may involve any of these organs. The immune response to the bacterial OMPs cross-reacts with epitopes present of host proteins and the lesions that are observed in Lyme disease may in part be caused by this immune response.

It is not currently known why only a small proportion of infected animals develop clinical disease.

Signalment

Affected animals often have a history of exposure to ticks but this may occur months before clinical disease is detected. Ticks are most abundant in particular types of habitat, as discussed here.

Diagnosis

Lyme disease is very rare and care should be taken not to perform specific tests unnecessarily. A positive result on serological or PCR tests also does not necessarily support a diagnosis of Lyme disease as most infections are asymptomatic. A period of 2-5 months usually elapses before clinical signs are observed in infected animals and it is therefore unlikely that animals recently infested with ticks will have Lyme disease.

Clinical Signs

The exact clinical signs shown depend on the species of Borrelia with which the animal is infected and on the area of the World in which infection occurs. Clinical signs are often vague, intermittent and variable between individuals, reasons why the disease was not identified until late in the twentieth Century. The exact clinical manifestation also depends on the site of localisation of the organisms. In the UK, animals infected with Borrelia burgdorferi sensu lato may show the following signs:

• Dogs
  • A local cutaneous reaction may occur at the site of the tick bite but this usually resolves within a week. This is not the equivalent of the erythema migrans described in infected humans.
  • Transient or intermittent pyrexia and lethargy.
  • Generalised lymphadenopathy.
  • Infection of the joints may result in non-erosive arthritis, causing intermittent bouts of shifting lameness.
  • Disease in the heart may cause myocarditis with atrio-ventricular block and dysrhythmias
  • Infection of the kidneys may result in glomerulonephritis and renal failure. This may occur chronically but cases of acute renal failure have been described.
  • Presence of organisms in the brain or spinal cord may cause neurological signs due to meningitis or encephalitis.
• Horses may suffer similar clinical signs of shifting lameness, uveitis, nephritis, hepatitis and encephalitis.
• Cattle and sheep may suffer from shifting lameness.

Other Tests

• Laboratory confirmation difficult due to low numbers of organisms and fastidious growth requirements
• History of exposure to ticks in an endemic region and clinical signs
• Rising antibody titre to Borrelia burgdorferi detected by ELISA
• Immunofluorescence
• Culture in Barbour-Stoenner-Kelly medium for 6 weeks under microaerophilic conditions
• PCR

Treatment

• • • Amoxycillin and oxytetracycline in the acute phase; prolonged treatment in the chronic phase
    • Tick control and removal
    • Vaccines including whole cell bacterins and recombinant subunit vaccines available for dogs