Vectorborne diseases are infectious diseases transmitted to people via blood sucking arthropods, like mosquitos, flies and ticks. Lyme disease, caused by spirochete bacteria of the genus Borrelia, is the most common such disease in North America. In the US, more than 20,000 cases have been reported annually in the years since 2002. 94% of cases occur in New England, the Mid-Atlantic, and the upper Midwest. (CDC, 2010) Every year, 1-3% of people living in endemic regions of the US become infected. Cumulatively, you can see infection rates of as high as 15%. (Tugwell 1997)
Most people with Lyme are diagnosed in early disease. A hallmark erythema migrans (EM) rash, commonly called the Bull’s eye rash, is found at the site of the tick bite in the majority of Lyme patients. Accompanying symptoms include fever and headache. However, up to 16% of patients never develop a rash. In the absence of this rash, many people think they had a virus and do not seek treatment. (Steere 2003)
Lyme disease has three distinct phases:
- Early localized infection. This is the initial presentation of viral type symptoms, like headache, soreness, fever, tiredness, and often the Bull’s eye rash. At this point, the infection is in the skin where the tick bite occurred. (Auwaerter 2004)
- Early disseminated infection. This is when the bacteria enter the bloodstream and spread. The EM rash may occur in places other than the site of the bite. In Europe, patients may develop borrelial lymphocytomas, which are darkly colored bumps. This symptom is specific to the European species of Borrelia. Neurologic problems affect 10-15% of patients in this stage. It can cause meningitis, facial palsy, memory loss, shooting pains, psychiatric changes and sleep disturbances. Some patients may also experience cardiac problems such as atrioventricular block (AV block.) (Stanek 2012)
- Late disseminated infection. Untreated or undertreated patients can progress to this stage after several months. About 5% of untreated patients develop chronc neurologic problems, including polyneuropathy and Lyme encephalopathy. (Seltzer 2000) Encephalomyelitis can cause cognitive impairment, weakness in the legs, difficulty walking and balance disturbances, among other things. Psychosis, panic attacks and anxiety can all occur. Lyme arthritis can occur, usually in the knees, but sometimes elsewhere. (Puius 2008)
Early localized or early disseminated infection (without neurologic or cardiac symptoms) is treated with short courses of antibiotics: doxycycline 100mg twice daily; or amoxicillin 500mg three times a day; or cefuroxime axetil 500mg twice daily, for 14 days. In the presence of neurologic symptoms of early disseminated disease, the recommended treatment is ceftriaxone 2gm daily IV for 14 days; or cefotaxine 2gm IV every 8 hours, or penicillin G 18-24 million units per day, in divided doses every 4 hours, for 14 days; or oral doxycycline 200-400 mg daily in 2 divided doses for 10-28 days. These recommendations are for adults. Patients with cardiac issues secondary to Lyme should be treated with either oral or IV antibiotics for 14 days while hospitalized. Ceftriaxone is usually used for this purpose. (Wormser 2006)
In late disseminated infection, Lyme arthritis can be treated successfully with doxycycline, amoxicillin or cefuroxime axetil as detailed above. Adults with arthritis and evidence of neurologic disease should receive IV ceftriaxone for 2-4 weeks. If joint swelling recurs, retreatment for 4 weeks of oral antibiotics or 2 weeks of IV antibiotics is recommended. Late neurologic disease can be treated with IV ceftriaxone for 2-4 weeks. Existing inflammation may take some time to wane and response to treatment may be slow. (Wormser 2006)
About 10-20% of patients treated for Lyme disease with 2-4 weeks of antibiotics continue to have fatigue and joint/muscle pain for some time after treatment is completed. These ongoing symptoms can last upwards of six months and indeed can last for years. This is termed Post-Treatment Lyme Disease Syndrome (PTLDS) and the exact reason for this is unknown. Many people also refer to this as “chronic Lyme disease.” (Aucott 2012) We are going to go through the competing theories on “chronic Lyme” and the evidence presented for both sides in the upcoming posts.
John N Aucott, Ari Seifter and Alison W Rebman. Probable late lyme disease: a variant manifestation or untreated Borellia burgdorferi infection. BMC Infectious Diseases 2012, 12:173.
Wormser, Gary P. The Clinical Assessment, Treatment, and Prevention of Lyme Disease, Human Granulocytic Anaplasmosis, and Babesiosis: Clinical Practice Guidelines by the Infectious Diseases Society of America. Clin Infect Dis. (2006) 43 (9): 1089-1134.
Seltzer EG, Gerber MA, Cartter ML, Freudigman K, Shapiro ED (February 2000). “Long-term outcomes of persons with Lyme disease”. JAMA 283 (5): 609–16.
Puius YA, Kalish RA (June 2008). “Lyme arthritis: pathogenesis, clinical presentation, and management”. Infect. Dis. Clin. North Am. 22 (2): 289–300, vi–vii.
Auwaerter PG, Aucott J, Dumler JS (January 2004). “Lyme borreliosis (Lyme disease): molecular and cellular pathobiology and prospects for prevention, diagnosis and treatment”. Expert Rev Mol Med 6 (2): 1–22.
Stanek G, Wormser GP, Gray J, Strle F (February 2012). “Lyme borreliosis”. Lancet 379 (9814): 461–73.
Tugwell P, Dennis DT, Weinstein A, Wells G, Shea B, Nichol G, Hayward R, Lightfoot R, Baker P, Steere AC: Laboratory evaluation in the diagnosis of Lyme disease. Ann Intern Med 1997, 127(12):1109-1123.
Steere AC, Dhar A, Hernandez J, Fischer PA, Sikand VK, Schoen RT, Nowakowski J, McHugh G, Persing DH: Systemic symptoms without erythema migrans as the presenting picture of early Lyme disease. Am J Med 2003, 114(1):58-62.
Centers for Disease Control. Lyme disease data, 2010.