Applied Evidence

Beyond the bull's eye: Recognizing Lyme disease

J Fam Pract. 2016 June;65(6):373-379

From The Journal of Family Practice | 2016;65(6):373-379.

References

1. Centers for Disease Control and Prevention. Lyme disease data. Available at: http://www.cdc.gov/lyme/stats. Accessed April 19, 2016.

2. Lantos PM, Nigrovic LE, Auwaerter PG, et al. Geographic expansion of Lyme disease in the Southeastern United States, 2000-2014. Open Forum Infect Dis. 2015;2:ofv143.

3. Gerstenblith TA, Stern TA. Lyme disease: a review of its epidemiology, evaluation and treatment. Psychosomatics. 2014;55:421-429.

4. Wright WF, Riedel DJ, Talwani R, et al. Diagnosis and management of Lyme disease. Am Fam Physician. 2012;85:1086-1093.

5. Marques AR. Lyme disease: a review. Curr Allergy Asthma Rep. 2010;10:13-20.

6. Borchers AT, Keen CL, Huntley AC, et al. Lyme disease: a rigorous review of diagnostic criteria and treatment. J Autoimmun. 2015;57:82-115.

7. Shapiro ED. Clinical practice. Lyme disease. N Engl J Med. 2014;370:1724-1731.

8. Cook MJ. Lyme borreliosis: a review of the data on transmission time after tick attachment. Int J Gen Med. 2014;8:1-8.

9. Tibbles CD, Edlow JA. Does this patient have erythema migrans? JAMA. 2007;29:2617-2627.

10. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of lyme disease, human granulocytic anaplasmosis and babesiosis: clinical practice guidelines by the Infectious Disease Society of America. Clin Infect Dis. 2006;43:1089-1134.

11. Khalil S, Padala SK, Hui CC, et al. Lyme carditis in the fast lane: from alternating bundle branch block to asystole in 12 hours. Conn Med. 2015;79:517-520.

12. Sigal LH. Early disseminated Lyme disease: cardiac manifestations. Am J Med. 1995;98:25S-28S.

13. Blaut-Jurkowska J, Jurkowski M. [Post-Lyme disease syndrome.] Pol Merkur Lekarski. 2016;40:129-133.

14. Steere AC, McHugh G, Damle N, et al. Prospective study of serologic test for lyme disease. Clin Infect Dis. 2008;47:188-195.

15. Carris NW, Pardo J, Montero J, et al. Minocycline as a substitute for doxycycline in targeted scenarios: a systematic review. Open Forum Infect Dis. 2015;2:ofv178.

16. Marques AR. Lyme Neuroborreliosis. Continuum (Minneap Minn). 2015;21:1729-1744.

17. American Academy of Neurology. Treatment of nervous system Lyme disease. Available at: https://www.aan.com/Guidelines/home//241. Accessed May 13, 2016.

18. Berende A, ter Hofstede HJ, Vos FJ, et al. Randomized trial of longer-term therapy for symptoms attributed to Lyme disease. N Eng J Med. 2016;374:1209-1220.

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Ixodes ticks are also vectors for human granulocytic anaplasmosis (HGA) and babesiosis, which can cause a variety of symptoms. Keep these diseases in mind when a patient presents with severe or atypical features of Lyme disease.⁵ The benefit of antibiotics after a tick bite to reduce the incidence of HGA or babesiosis is unclear.¹⁰

Late manifestations of Lyme disease can occur within one to 2 months of infection or even months to years after tick exposure, often resulting in substantial morbidity.^3-7,11 Musculoskeletal symptoms are the most common manifestations of late, disseminated disease, usually presenting as transient asymmetrical oligoarticular arthralgias or myalgia. Arthritis also occurs in 60% of untreated patients with late disease.^4,5 Large joint effusions are typical, with synovial fluid studies showing high quantities of polymorphonuclear leukocytes (25,000/mm³).⁵ Joint symptoms that persist after antibiotic treatment are called antibiotic-refractory Lyme arthritis.^4-7

Neurologic involvement affects 10% to 15% of untreated patients.^3,4 It can present as lymphocytic meningitis (most common), cranial neuropathies, motor or sensory radiculoneuropathy, mononeuritis multiplex, cerebellar ataxia, or myelitis. Late neurologic Lyme disease may also present as a subacute mild encephalopathy affecting memory and concentration. When cranial neuropathies are involved, it is usually as unilateral facial nerve palsy (but may be bilateral). Always consider Lyme disease in endemic areas when patients have severe Bell's palsy.

Patients may present with altered mental status, neck stiffness, pain, and headaches.^4-7 The classic triad (known as Bannwarth syndrome) consists of lymphocytic meningitis, cranial neuritis, and radiculoneuritis. However, these conditions do not always occur together.^3,4

Cardiovascular complications occur in 4% to 8% of untreated patients,^4,5usually one to 2 months following infection. Varying degrees of atrioventricular (AV) block can be seen, but third-degree block is most common. A less frequent complication is Lyme carditis, seen in 4% to 10% of patients.¹² The pathophysiology of Lyme carditis is not well understood.¹¹ It may present as chest pain, dyspnea on exertion, fatigue, palpitations, or syncope, often involving an AV block. Less frequent complications include myopericarditis, bundle branch block, and heart failure.