Introduction

• Cause: infection with Borrelia burgdorferi Borrelia burgdorferi via biting ticks. End-stage incidental hosts.
• Also known as Lyme Disease.
• Proliferation at bite site migration of bacteria and localization elsewhere in body especially joints Arthritis: borrelial.
• Signs: pyrexia, lymphadenopathy, swollen joints, lameness, glomerular nephritis, uveitis.
• Diagnosis: C6 peptide, rising antibody titers or PCR.
• Treatment: Doxycycline Doxycycline , Amoxicillin Amoxicillin.
• Prognosis: good in many cases.
  Print off the owner factsheet on Lyme disease Lyme disease to give to your client.

Pathogenesis

Etiology

• Spirochete: Borrelia burgdorferi Borrelia burgdorferi.
• Primary agent in the United States is Borrelia burgdorferi sensu stricto.
• Borrelia afzelii andBorrelia garinii are also reported as causing clinical disease in Europe and Asia.
• Virulence can vary depending on certain variable detectable antigens including outer surface proteins (Osp) A and B.

Specific

• Infection with tick vector:
  • Ixodes ricinus (Europe) Ixodes ricinus.
  • Ixodes scapularis Ixodes scapularis/Ixodes pacificus Ixodes pacificus (USA).
  • Ixodes persulcatus (Asia).

Pathophysiology

• Borreliosis affects primarily dogs and people.
• It occasionally infects horses, cattle and rarely cats.
• Ticks initially feed on the first host, which is usually a rodent (mice, voles and rats), although birds and some lizard species have also been reported. If the host is infected with the bacteria, then the tick larvae become infected.
• The tick larvae lay dormant over the winter and molt to the nymph stage the following spring. The nymphs then may infect more mice and other susceptible hosts when they feed.
• Nymphs may also become infected if they feed on an infected host.
• Nymphs mature into adults in the fall and attach to deer and other mammals at that time. After engorging on the hosts blood, the females drop off. The males may remain attached throughout the winter.
• During engorgement the bacteria migrate from the tick into the mammalian host (over 48 hours).
• Although many people and animals are bitten only a few develop clinical disease.
• In endemic areas infection rate may be around 75% in dogs but clinical signs are seen in only 5-10%.
• Borrelia spirochetes multiply in the skin before migratory spread of the spirochetes, and eventual localization of the bacteria in certain target organs.
• Infection may be prevented by the host's immune response at this stage. However once the organism has settled in tissues the inflammatory response causes clinical disease.
• The peripheral joints are the primary target, with the first joint affected usually the one closest to the tick bite.
• The bacteria may also infect the lymph nodes, muscles, eyes, kidneys, brain and meninges, heart and pericardium.
• Arthritis is often acute in onset and may occur weeks to months after exposure.
• A Lyme-specific immune-complexing form of glomerulonephritis Glomerulonephritis has been documented in some dogs in the USA, but is rarely reported in Europe.
• Dissemination in the blood is rare.

Timecourse

• Arthritis may not occur until weeks or months after the acute phase of the disease.

Epidemiology

• Acute onset of lameness and painful, swollen joints.
• Pyrexia.
• Lethargy, myalgia.

Diagnosis

Treatment

Prevention

Outcomes