What is Lyme disease? |

Causes and Symptoms

Lyme disease is the most common tick-borne disease in the United States and Europe. It is caused by spirochete bacteria of the species complex Borrelia burgdorferi sensu lato. (This name refers to all bacteria causing Lyme disease.) Borrelia burgdorferi sensu stricto is the predominant cause of Lyme disease in the United States, while Borrelia afzelii and Borrelia garinii more often cause Lyme disease in Europe. The hard-bodied (Ixodes) tick transmits Borrelia burgdorferi to humans. Lyme disease is endemic in parts of New England, the upper Midwest, and Northern California. The tick species Ixodes scapularis (the black-legged tick or deer tick) transmits Lyme disease in the East and Midwest, while Ixodes pacificus (the Western black-legged tick) is the vector for Lyme disease in the West. In Europe, Ixodes ricinus (the sheep tick) is the vector.

Ticks are arachnid, obligate, blood-feeding ectoparasites with mouth parts that pierce the host skin. The tick saliva contains analgesics, anti-inflammatories, antihistamines, and anticoagulants that make it less likely that the tick bite will be detected. A tick takes three blood meals—as a larva, a nymph, and an adult—typically from different host species. The spirochete does not pass from the adult tick into the tick eggs. When a tick larva feeds on a host infected with Borrelia burgdorferi, that larva becomes infected, molts to the nymph stage, and passes on the spirochete when it takes its next blood meal. In the eastern United States, the hosts infected with Borrelia burgdorferi on which the tick feeds are white-footed mice (the reservoirs of infection) and deer. There is a receptor that binds an outer membrane
protein of the bacterium to maintain the bacteria in the tick gut. When the tick begins feeding on another host, a bacterial protein is produced that aids in detaching the bacteria from the receptor, and bacteria begin multiplying. The bacteria then go to the salivary glands and via saliva go to the host
skin. Initially, there is little or no transmission of bacteria to the host. It takes at least twelve hours and perhaps as long as three days before the efficient transfer of bacteria. Even though the adult tick is twice as likely as the nymph to be infected with the Lyme spirochete, most cases of Lyme disease are noted in the late spring and summer, when nymphs seek blood meals from hosts. This may be because the smaller nymph is more difficult to notice.

Within a month after Borrelia burgdorferi bacteria enter the skin, a bull’s-eye-shaped, rapidly expanding rash may form at the bite site. Bacteria travel through the bloodstream to other organs. Viral infection-like symptoms may develop, such as fatigue, headache, and neck pain. Respiratory symptoms, such as coughing, and vomiting or diarrhea do not occur. Not all who have the viral infection-like symptoms develop the rash or note a tick bite. About 60 percent of those who had the skin rash and were not treated develop arthritis, usually of the knee. About 10 percent develop neurological problems, usually facial nerve
palsy. About 5 percent develop a cardiac complication as a result of atrioventricular block. The eyes may also be affected.

Lyme disease experts disagree about other possible effects. In some individuals, months after initial infection and treatment, symptoms such as muscle pain and fatigue seem to develop. Bacteria in some parts of the body may be resistant to antibiotic treatment, causing a persistent infection. Such infections would benefit from additional antibiotic treatment. A Lyme infection may be more severe because of coinfection from the tick with other pathogens, such as the rickettsial infection human granulocytic anaplasmosis and the protozoan disease babesiosis.

Treatment and Therapy

To prevent Lyme disease, avoiding exposure to ticks is key. In a tick-infected area, one should wear protective clothing, use tick repellent such as DEET, check daily for ticks, and promptly remove any ticks. To reduce the population of ticks around a house, the lawn should be kept mowed and brush cleared.

The rash of Lyme disease is treated with antibiotics such as doxycycline, amoxicillin, or cefuroxime axetil. For those under eight years of age and pregnant women, however, doxycycline is not recommended.

In the late 1990s, a vaccine against Lyme disease was available. This vaccine induced the production of antibodies to a Borrelia burgdorferi outer cell membrane surface lipoprotein. In 2002, the manufacturers of the vaccine withdrew it from the market because of problems involving postvaccination fatigue. In its 2012 report to the Africa, Global Health and Human Rights Subcommittee’s Hearing on Global Challenges in Diagnosing and Managing Lyme Disease, the Infectious Diseases Society of America (IDSA) stated that the withdrawal of the vaccine had been misguided and was caused by what it considers to be unsubstantiated claims about the vaccines' side effects; currently, there is no human vaccine available. In 2008, the National Institutes of Health and the Center for Disease Control started a serum reference repository to house serum samples that can be used to compare different tests for the diagnosis of Lyme disease; in 2011, the samples became available to the scientific community at large.

Perspective and Prospects

The clinical symptoms of Lyme disease have been documented in European medical literature as early as the 1880s, but each clinical sign was considered a separate illness. In the 1970s, an outbreak of apparent juvenile rheumatoid arthritis, in some cases preceded by a rash, occurred in Old Lyme and Lyme, Connecticut. In 1975, this range of different symptoms was recognized as a single illness. Borrelia burgdorferi was identified in 1982 by Willy Burgdorfer, a tick-borne disease expert from the Rocky Mountain Labs in Montana.

In 2006, the IDSA released updated diagnosis and treatment guidelines for Lyme disease. These guidelines recommend a bull’s-eye, or erythema migrans (EM), rash or positive laboratory tests to diagnose Lyme disease. The IDSA guidelines do not recognize a chronic form of Lyme disease, nor do they recognize seronegative Lyme disease except in early infections. This stance has generated a great deal of controversy. Both the International Lyme and Associated Disease Society (ILADS), a professional medical society, and the Lyme Disease Association, an all-volunteer association, have expressed concern about the stricter guidelines. They worry that patients with chronic Lyme disease will continue to suffer. However, as of 2013, the IDSA continues to stand behind its initial diagnosis guidelines, stating that there is not sufficient evidence for the existence of "chronic Lyme disease." There is much more to learn about the Lyme bacteria in order to aid patients.

Bibliography

American Lyme Disease Foundation. http://www.aldf .com.

Edlow, Jonathan A. Bull’s-Eye: Unraveling the Medical Mystery of Lyme Disease. 2d ed. New Haven, Conn.: Yale University Press, 2004.

Edlow, Jonathan A., and Robert Moellering, Jr., eds. “Tick-Borne Diseases, Part 1: Lyme Disease.” Infectious Disease Clinics of North America 22, no. 2 (June, 2008).

Horowitz, Richard. Why Can't I Get Better? Solving the Mystery of Lyme and Chronic Disease. New York: St. Martin's Press, 2013.

International Lyme and Associated Disease Society. http://www.ilads.org.

Lyme Disease Association. http://www.lymedisease association.org.

Plotkin, Stanley A. The Need for a New Lyme Disease Vaccine. Chicago: University of Chicago Press, 2011.

Stricker, Raphael B., Andrew Lautin, and Joseph J. Burrascano. “Lyme Disease: The Quest for Magic Bullets.” Chemotherapy 52 (2006): 53–59.

Wormser, Gary P., et al. “The Clinical Assessment, Treatment, and Prevention of Lyme Disease, Human Granulocytic Anaplasmosis, and Babesiosis: Clinical Practice Guidelines by the Infectious Diseases Society of America.” Clinical Infectious Diseases 43, no. 9 (2006): 1089–134.