Borrelliaburgdoferi(Bb) was first discovered in the county of Lyme, Connecticut and therefore is not described in the possessive as it was not named after a person. It is a small spirochete that can only be visualized using dark field microscopy. There are 4 genomic species groups, but the only one that occurs in the US is group one, B. bergdorferi sensu stricto.   It cannot survive as a free-living organism and can only be found in the vertebrate host or the arthropod vector, Ixodesscapularis, commonly referred to as the deer tick or the black legged tick. Although this tick occurs almost nationwide, there are only three endemic regions from which the organism has been cultured. 85% of human cases occur in the coastal northeast, while 10% in the upper Midwest and 4% in northern California. As the tick and potential host species inhabit additional areas of the country, however, potential for spread should always be considered. In the north, the reservoir host is mostly small animals, particularly the white footed mouse. Before the tick attaches to the dog, B. bergdorferi expresses the protein Osp A which adheres the organism to the midgut of the tick. With the warmth and presence of a blood meal, Bb switches from the expression of Osp A to Osp C. This allows migration and adherence to the salivary tissue of the tick. Experimentally, this takes 53 hours. The tick must therefore be attached for some time before Bb will be able to be transferred to a dog or person. Once it is in the dog, there is local proliferation. This may produce the classic target lesion that is often seen in people, but often missed in dogs due to their furry covering. The organism then migrates through tissue and blood.¹

We have all seen the classic signs of Lyme in our patients: fever, lethargy, anorexia, polyarthritis, and lymphadenopathy. The pathogenesis of Lyme disease in dogs, however, is still somewhat elusive. Koch's postulates have partially been satisfied, but only in young dogs. In an experimental study of putting infected Ixodes ticks on Beagles, the adult dogs seroconverted, but remained asymptomatic. It was only the 6-12 week old puppies that showed clinical signs including decreased appetite, lethargy and arthropathy 2-5 months after exposure. In contrast, people that are exposed to Bbshow an acute illness including flu-like signs, erythema migrans rash, subsequent arthritis and possibly cardiac, neurologic, or chronic skin changes. Only 10% of people remain asymptomatic.

  

The most clinically used method of diagnosis of Lyme disease is serology. Interestingly, in people there can be cross reactivity with certain autoimmune diseases, syphilis, periodontal disease, and leptospira. This, however, has not been documented in dogs.¹  There are 4 antibody types to different antigens commonly tested for through commercial laboratories: Osp A, Osp C, Osp F and C6. Osp A is generally found when the organism is within the gut of the tick. After a warm blood meal, Bb changes its expression to OspC and migrates to the salivary tissue in the tick. Although OspA is mostly expressed while in the tick, early in the animal exposure, some OspA may still be present.After entering into the animal, Bb then changes its expression to OspF. However, in the chronic carrier, random and spontaneous mutations and recombinations allow for many antigens to be expressed as the organism goes through its antigenic repertoire to avoid the host immune system. The 4DX Snap test from IDEXX^atests for anti-C6 antibodies. C6 is a synthesized protein which mimics an antigen which is only expressed by Bb organism when it is within the host, the variable major protein like sequence (VIsE). IDEXX also offers the Lyme Quant C6,^b which gives a quantitative result that can be compared over time. The value does not predict illness as many asymptomatic dogs have very high values.² Dogs in endemic areas (such as Massachusetts) have rates of 70-90% seropositive, while only 5% of seropositive animals develop clinical signs. There are hypotheses of why some dogs become ill while others do not, but the bottom line is that we do not know why. What we do know is that it is very difficult to document an active infection. What we can do is correlate clinical signs and seroposivity (as a polyarthropathy caused by Lyme will be positive on serology as it has been shown experimentally to take 2-5 months after exposure to develop clinical sings) to help our decisions on when to treat.^2,3 Unlike other tick borne diseases, thrombocytopenia is not a common finding on a CBC. If it is present, it is likely due to a co-infection or another disease process. A hyperglobulinemia is seen commonly on chemistry. If an arthrocentesis is performed, the synovial fluid is often grossly turbid with decreased viscosity. Fluid analysis of the synovial fluid reveals an increased protein and cell count with non degenerate neutrophils predominating. The organism is not seen. In experimentally induced infection in dogs, tests show viable organisms in the skin biopsies of previous tick bite sites in untreated dogs and in 10% or more of treated dogs. In clinical medicine, however, cultures and PCRs are rarely positive even when sampling joint fluid, synovium, or kidneys. This phenomenon is a result of the pathology of the disease process: the signs are caused by an immune-mediated response in predisposed individuals.^2,3

  

 The treatment of choice for Lyme disease in dogs is doxycycline at 10mg/kg SID or 5 mg/kg BID for 4-6 weeks.  Doxycycline is a bacteriostatic drug that requires an intact cellular immunity in order for it to be effective. It is lipid soluble and crosses cell membranes in order to attack intracellular organisms. It inhibits bacterial protein synthesis by binding to the 30s subunit of the ribosome. It is preferred over amoxicillin as it also has anti-inflammatory and chondroprotective effects through the inhibition of matrix metalloproteinases. Although generally well tolerated, there are side effects of doxycycline that should preclude its indiscriminant use. Technically it should be given on an empty stomach, but can cause significant gastrointestinal upset. In cats and humans it has been well documented to cause esophageal erosions leading to potential stricture formation. In young animals, it can cause permanent discoloration of the teeth (although of all of the tetracyclines, it is the least likely to do so). Hypersensitivity reactions have been seen. Elevations of ALT and ALP can occur in 1/3 of patients andcanlead to hepatotoxicity. Finally, it can cause acute renal injury or a Fanconi-like syndrome, especially if the drug has started to degrade.⁴ Drug resistance is a huge concern in the entire medical profession. Overuse of any antimicrobial will contribute to bacterial resistance. Doxycycline use in non-tick borne related diseasecauses continued exposure of other bacteria to this drug and will contribute to long term resistance patterns. Given the seroprevelance of Lyme in our area and the potential dangers of bacterial resistance, careful consideration that the current clinical signs are caused by Lyme disease before starting antibiotics is warrented.

Although it is considered the second most common canine syndrome, the incidence of Lyme nephritis is actually unknown. It seems to affect Labrador retrievers more than other breeds, but the association between Lyme and the resultant glomerulonephritis has never been a very strong correlation.   These dogs have a severe protein losing nephropathy that is believed to be immune mediated in origin. Koch's postulates have never been fulfilled with this clinical syndrome and the presence of Bb in affected renal tissues either through culture or PCR techniques has never been demonstrated.⁵Despite this, many experts in the veterinary community believe in a relationship between some cases of protein losing nephropathy (PLN) and Lyme disease. These reported cases are clinically ill dogs presenting mostly in the summer or fall months with a presentation that would range in severity from chronic weight loss and protein losing nephropathy to acute renal failure. They will have variable abnormalities including vasculitis, edema, effusions, hypertension (with possible blindness), and thromboembolic events. Seizures and other neurological signs can be seen secondary to the vasculitis, hypertension, thromboembolic events, uremic encephalopathy, or meningitis.^1-3 Dogs with this syndrome often require 24 hour care with careful attention to fluid therapy and aggressive management of hypertension. Treatment with immunosuppressive medications have anecdotally resulted in improvement in some cases, but unfortunately many dogs do not respond. Due to the severity of this possible sequelae, it is recommended that all lyme positive dogs (regardless of clinical signs) be routinely screened for proteinuria.^2,3   

        

When we think about other diseases that we routinely vaccinate against (Distemper, Parvovirus) they carry a high rate of morbidity and mortality and are expensive to treat. The most common condition associated with Lyme is that of polyarthritis which is readily treatable with an inexpensive medication. The disease process behind the syndrome of Lyme nephritis is an immune-mediated one. Vaccines are meant to stimulate the immune system so as to create a level of immunoglobulins that may protect the animal from getting that disease. By vaccinating for Lyme, we may actually be adding fuel to the fire. Borrelia has developed a clever way of evading the host immune system by changing its antigen to avoid detection. It is unknown which of these antigens is the offending one that ultimately may result in either the arthropathicornephropathicsyndromes of the disease.²Vaccination for Lyme should be carefully considered and discussed with clients with attention to the potential risks and benefits for each patient given their breed and exposure risks.