COMPANION ANIMALS

Lyme borreliosis in a Labrador retriever  

Andrew Brooks

In October 2013, a 7-year-old Labrador retriever from the Ottawa region was euthanized due its worsening lameness and renal disease and poor prognosis, and was presented to the AHL for postmortem examination.  The clinical history included lameness and pain affecting multiple limbs, lethargy, reduced appetite, enlarged peripheral lymph nodes, edema of the face and limbs, azotemia, hypoproteinemia, anemia, proteinuria and thrombocytopenia.  The clinical signs began in late summer 2013 and a tick had been observed on the dog prior to the onset.  The vaccination status (including Lyme disease) was up to date.  The IDEXX SNAP® 4Dx® Plus Test was positive for Borrelia burgdorferi, indicating natural exposure to this agent.

At postmortem examination, every major joint in all 4 limbs contained increased amounts of watery synovial fluid consistent with polyarthritis.  There was peripheral lymphadenopathy with enlargement of the prescapular, popliteal and submandibular lymph nodes and there was prominent subcutaneous edema of the head and all 4 limbs.

Although there was autolysis and freezing artifact, arthritis was observed histologically in most of the joints.  The lesions varied from very mild mononuclear (lymphocytic) inflammation of the synovium or surrounding connective tissues to fibrinous arthritis (Figure 1).  Some joints also had mild perineuritis and periarteritis, with rare acute fibrinoid vasculitis.  The lymph nodes contained mild lymphoid hyperplasia.  The adrenal glands also exhibited acute multifocal necrosis and mild lymphocytic inflammation.  There was multifocal glomerulonephritis with vasculitis which explained the clinical renal problems in this dog. The vasculitis appeared to involve the afferent or efferent arterioles located at the hilar region of the glomeruli (Figure 2).  Similar renal lesions have been described in a protein-losing nephropathy (Lyme nephropathy) encountered in a small percentage of seropositive dogs which develop clinical signs.  Other components of Lyme nephropathy, such as diffuse tubular necrosis, were not evident in this case.  The cause and pathogenesis of Lyme nephropathy are not understood, but an immune-mediated pathogenesis is suspected and Labrador and Golden retrievers may be predisposed.

A PCR assay for detection of B. burgdorferi and Anaplasma phagocytophilum was performed at the AHL on tissue from 2 inflamed joints, kidney, and skin.  Positive and suspicious-positive PCR reactions for B. burgdorferi were detected in joint tissue and skin.

A final diagnosis of Lyme borreliosis was derived from the combination of clinical signs, history of tick exposure, positive SNAP® 4Dx® Plus Test, compatible gross and histological lesions, and the positive PCR results.

In Ontario, B. burgdorferi is transmitted by the bite of the blacklegged tick Ixodes scapularis.  Established populations of this tick vector are located in the Long Point, Turkey Point, and Rondeau Provincial Parks, Point Pelee National Park, the Wainfleet Bog Conservation Area, the Prince Edward Point National Wildlife Area, and the Thousand Island region of the St. Lawrence River.  Vector ticks feeding on migratory birds may be transported to other locations in the province.  Once transmitted by the tick bite, B. burgdorferi has a predilection for skin, joints and connective tissues.  Most exposed dogs (up to 95%) remain subclinical but some may develop clinical illness which usually involves arthritis, fever, lethargy and lymphadenopathy.