Lyme Disease and the Deadly Tick

The Deadly Tick

Lyme disease is caused by the spirochete Borrelia burgdorferi that is transmitted by Ixodes ticks (hard ticks). Ixodes scapularis (the deer tick) is the primary species in the Northeast that transmits Lyme disease. The highest incidence of Lyme disease is seen with the seasons of greatest tick activity-spring through summer. Approximately 90% of the cases of Lyme Disease occur on the East Coast. The East Coast is a Lyme Endemic area.


The life cycles of the hard ticks involve 4 stages: egg, larva, nymph and adult. Ixodes ticks have a multi-host life cycle. The larval tick feeds on small mammals, particularly the white-footed mouse (Peromyscus leucopus), which serves as the primary reservoir for B. burgdorferi. Nymph and adult ticks parasitize many mammals and may transmit previously acquired spirochetes during feeding. One tick can feed up to 3 days and ingest 9 ml of blood. The preferred host for the adult tick is the white-tailed deer, Odocoileus virginianus. Ticks have various mechanisms to survive such as a long starvation tolerance and a high reproductive capacity (producing up to 22,000 eggs). Ixodids can live for several years.

There is a lag phase in the transmission of Borrelia. The spirochete has two outer surface proteins OspA and OspB, which are imperative for the survival of the organism in the deer tick, which is a cold-blooded invertebrate. When the tick begins taking a blood meal, the spirochete must prepare to enter the warm-blooded vertebrate host so it upregulates another protein called OspC and down regulates Osp A and B-this process can take up to 24 hours. Once in the mammalian host, only the protein OspC is expressed on the spirochete.

Erythema migrans (red bull's eye or target sign) occurs in about 2/3 of the people infected with Borrelia within the first month of infection, but does NOT necessarily occur in animals or their fur covers it up so you don't see it.

Diagnosis of Lyme disease is made by presence of appropriate clinical signs, rule-out of alternate causes of these signs, demonstration of infection with Borrelia burgdorferi and response to antibiotic therapy.
A positive blood titer is an indication of exposure to the organism (via a vaccine or tick bite) and by itself is not diagnostic of Lyme disease. A positive titer can take up to 6 weeks to develop and may remain elevated for months to years without new infection. A Western Blot (specialized blood test) can distinguish antibodies from a vaccine or natural infection.

Response to therapy with antibiotics in the penicillin or tetracycline families is usually seen within 3-5 days and is often quite dramatic. Baytril and Sulfa drugs are ineffective for treatment of Lyme disease. About 10-25% of dogs treated for Lyme arthritis will become chronically affected and have incomplete resolution of signs or recurrent disease.

ONCE INFECTED=INFECTED FOR LIFE Antibiotics will reduce the signs of disease but it does not clear the spirochetes from the body. The larger the number of spirochetes in the tissue, the worse the clinical signs will be in that area of the body. Natural infection does NOT lead to protection against the disease.

Clinical syndromes of Canine Lyme Disease include arthritis, carditis (heart), nephritis (kidney) and neurologic abnormalities (seizures).

Lyme arthritis is characterized by sudden onset of lameness, fever, lethargy, joint swelling and lymph node enlargement. This is the most common syndrome seen in practice.

Lyme nephritis is generally fatal and is characterized by anorexia, vomiting, lethargy, weight loss, elevated kidney values, protein loss from the kidneys, peripheral edema and active urine sediment. Young dogs are usually affected.