Spilling the tea on Lyme disease
by Dr. Carey Hemmelgarn
Lyme disease is caused by a spirochete bacterium of the genus Borrelia. B. burgdorferi is the most commonly blamed, but other Borrelia species in Europe and the Midwestern US have been implicated. This spirochete is carried in ticks, mainly Ixodes scapularis, but other ticks in the same genus are capable of transmitting the disease. Transmission is usually noted in the spring, summer, and fall months when temperature is greater than 40 degrees Fahrenheit.1 A tick needs to feed on a human or animal for more than twenty-four hours to transmit Lyme disease.1
The most common clinical signs of Lyme disease fall into two categories: Lyme arthritis or Lyme nephritis. Other less common manifestations of myositis, myocarditis, and perineuritis have been described in a small number of cases. Many seropositive dogs are asymptomatic.
Cats can be seropositive, but clinical disease has not been noted in them. If it were, many think the signs would be similar to anaplasmosis in cats. Some experts suggest that cats are better at discovering ticks through grooming than dogs, removing them before they can transmit Lyme disease. However, seroconversion occurs in naturally exposed and experimentally infested cats suggesting that infection occurs, which should be blocked if ticks were promptly removed.1
Diagnostic tools available for Lyme disease include serology tests such as Antech Accuplex® 4, Vetscan® Flex4 Rapid, and SNAP 4Dx®, but none of these reliably distinguish between acute and chronic infection.
The Lyme Quant C6® test is not recommended as a screening tool for symptomatic pets. This type of test is looking for antibodies against the C6 peptide, which occurs only with natural exposure to Borrelia species, and this protein is not present in any vaccines. Antibodies indicate exposure but do not prove cause of clinical signs or predict future clinical signs. Antibodies can develop three to four weeks after bites.2
Fever, joint swelling, lameness, and local lymphadenopathy would all be expected clinical signs. Treatment recommended in symptomatic patients is a four-week course of beta-lactams or tetracyclines. Doxycycline is preferred; the response should be rapid.
Lyme nephritis is seen in no more than 1-2% of Lyme-seropositive dogs.3 Nonclinical, nonprogressive renal proteinuria or hypoalbuminemia with no azotemia in seropositive patients should be treated with a course of antimicrobials. Other comorbidities can include hypertension and hypercoagulopathy due to loss of angiotensin.4 These should be treated with RAAS inhibitors, antithrombotics, and anti-hypertensives.
The use of ACE inhibitors is warranted in dogs with Lyme nephritis. The use of ACE inhibitors has been shown to improve renal function and possibly prolong survival.5 The use of ACE inhibitors also was shown to decrease proteinuria, glomerular capillary pressure, hypertrophy and lower mean arterial pressure.5,7 Treatment is thought to preserve renal function by decreasing cellular proliferation and intraglomerular hypertension.4, 8
Pets that are azotemic, progressively proteinuric, and/or clinical should be treated with anti-emetics and gastroprotectants and possibly immunosuppressants if a biopsy has been performed to diagnose Lyme nephritis. Treatment is often started without biopsies. Symptomatic dogs will show signs of nephrotic syndrome such as hypoalbuminemia, proteinuria, hyperlipidemia, and third spacing. Mycophenolate is recommended as the first-line treatment with tapering prednisone.
Prevention:
All dogs in endemic areas should be screened yearly. If seropositive and asymptomatic, evaluation for proteinuria is recommended. Whether seropositive asymptomatic dogs should be treated remains controversial.
The best way to prevent disease is a combination of tick preventatives, environmental modifications, and rapid tick removal. Vaccinations are also available but should be used in conjunction with tick prevention.
References:[1]
1. Littman, M.P., et al. (2018) ACVIM consensus update on Lyme borreliosis in dogs and cats Journal of Veterinary Internal Medicine, May-Jun, 32(3): 887–903.
2. IDEXX: The truth about lyme disease: https://www.idexx.com/files/truth-about-lyme-disease.pdf
3. Littman M.P. (2013) Lyme nephritis. Journal of Veterinary Emergency and Critical Care. Mar-Apr; 23(2):163–173.
4. Protein Losing Nephropathy: Vetfolio: https://www.vetfolio.com/learn/article/protein-
a. losing-nephropathy
5. Vaden, S.L. (2005) Glomerular diseases. In S.J. Ettinger and E.C. Feldman (Eds) Textbook of Veterinary Internal Medicine (pp. 1786–1799). Elsevier Saunders, St. Louis, MO
6. Grauer, G.F., Greco, D.S., Getzy, D.M., et al. (2000) Effects of enalapril versus placebo as a treatment for canine idiopathic glomerulonephritis. Journal of Veterinary Internal Medicine, 14:526–533.
7. Brown SA, Walton CL, Crawford P, et al. Long-term effects of antihypertensive regimens on renal hemodynamics and proteinuria. Kidney Int 1993;43:1210–1218
8. Lee, Justine. Lyme Disease: Treatment of Acute and Chronic Manifestations. 2014. Microsoft Word - Lyme FINAL 10 8 2014.docx (vetgirlontherun.com)
