Lyme Disease in Emergency Medicine 

  • Author: William E Caputo, MD; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: May 24, 2011
 

Background

Lyme disease is a multisystem illness caused by the spirochete Borrelia burgdorferi sensu lato. It is a vector-borne disease transmitted to humans by infected ticks of the Ixodes genus. Lyme disease is the most common vector-borne illness in the United States, accounting for 29,959 reported cases in 2009. It is also endemic in the rest of North America, Europe, and Asia.[1]

Normal and engorged Ixodes ticks. Normal and engorged Ixodes ticks.

Although various parts of the syndrome were described in Europe more than 100 years ago, the full spectrum had not begun to be identified until 1975, when a cluster of statistically improbable cases of juvenile arthritis occurred in Connecticut. This outbreak stimulated intensive clinical and epidemiologic research that led to the discovery of the causative agent, the ecology, an expanding list of clinical manifestations, and the geographic range. Furthermore, the initial antibiotic responsiveness of the cutaneous manifestations described in the European literature was confirmed and extended.[2]

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Pathophysiology

The pathophysiology of Lyme disease is incompletely understood. While active infection by the spirochete causes many manifestations, others may be caused by immunopathogenic mechanisms. Although any body part can be involved, the organism shows a distinct tropism for the skin, CNS, heart, joints, and eyes.

The bacterium is introduced into the skin with a bite from an infected Ixodes tick. In the northeastern and upper midwestern United States, Ixodes scapularis is the vector. In other parts of the country and world, other Ixodes species serve that function. Other ticks (eg, Amblyomma americanum) and insects can carry B burgdorferi, but Ixodes tick bites are thought to cause the vast majority of cases. In the southern and mid-central United States, a Lymelike illness has been reported; the vector appears to be A americanum, and the causative organism or organisms is likely to be a related spirochete.[3, 4] One such organism, named Borrelia lonestarii, has been cultured in a single case.

Once in the skin, the spirochete can (1) be overwhelmed and eliminated by host defense mechanisms; (2) remain viable and localized in the skin where it produces the pathognomonic skin lesion, or erythema migrans (EM); or (3) disseminate through the lymphatics or blood. Hematogenous dissemination can occur within days to weeks of initial infection; the organism can travel to the skin, heart, joints, CNS, and other parts of the body.

Study findings show that in roughly 10% of patients with isolated EM and no systemic symptoms, B burgdorferi can be cultured or that its DNA can be detected in the bloodstream. Using high volume (9 mL) of plasma for culture, one 2005 study suggests that nearly 44% of patients are spirochetemic, some of them with a single skin lesion and no systemic symptoms.[5] Also, early in the course of the disease when EM is still present, the spirochete and its DNA have been isolated from the cerebrospinal fluid (CSF), indicating early CNS penetration. This penetration can occur even in the absence of neurologic symptoms.

Data published in November 2008 show that some genotypes of B burgdorferi are responsible for the large majority of cases of disseminated disease.[6] At the present time, this information likely has greater significance for future vaccines or diagnostic tests than it does in routine practice.

The organism can also persist in skin (and possibly in the CNS) for years without causing symptoms. Experimentally, the spirochete can penetrate human fibroblasts and live intracellularly, even when the extracellular medium contains ceftriaxone well above bacteriocidal levels for the spirochete. Clinically, organisms have been cultured from skin many years after primary infection. This mechanism may allow the spirochete to elude the normal host defense mechanisms directed against it.

Stages of Lyme disease

As with syphilis, the disease classically is divided into stages: early localized, early disseminated, and late. However, distinct cutoff points between the stages are frequently unclear.

Stage 1 is also known as primary or early localized infection. It generally occurs within 30 days of the tick bite. Most patients present with a characteristic expanding rash (erythema migrans) at the site of the tick bite 7-14 days after the tick is removed. Several other nonspecific symptoms can occur and include fatigue, myalgias, arthralgias, headache, fever, chills, and neck stiffness.

Stage 2 is also known as early disseminated disease, occurring generally weeks to months after the bite. Musculoskeletal and neurologic symptoms are the most common; less common symptoms are cardiac and dermatologic.

Stage 3 or chronic Lyme disease happens months to years after infection, which sometimes involves a period of latency. Musculoskeletal (mainly joints) and neurologic systems are most commonly affected.

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Epidemiology

Frequency

United States

In January 2008, the Council of State and Territorial Epidemiologists (CSTE) approved a revised national surveillance case definition for Lyme disease. This allowed for the addi­tion of probable cases to the total case count, which differs from previous years.

Overall in the United States, incidence is 9.21-11.67 cases per 100,000 population (2007 and 2008 data). The total number of reported cases in 2008 in the US was 35,198 (including 28,921 confirmed and 6,277 probable cases).

The total number of cases have been increasing over time. The total number of cases in 1995,2000, and 2005 were 11,700, 17,730, and 23,305, respectively. The increase in incidence is not simply a result of increased recognition; in states that perform active surveillance, true incidence and geographic range have increased. The likely causes of this increase are expansion of deer herds and the expanded range of the vector.[1]

Epidemiologic data suggest that the actual incidence of Lyme disease could be as much as 10 times higher than the CDC data indicate. This probably is a result of a restrictive case definition from the CDC, inevitable misdiagnosis, and the fact that physicians tend to underreport reportable diseases of all kinds.

The risk of Lyme disease follows a general geographic pattern. More than 90% of cases come from 10 states: Connecticut, Delaware, Maryland, Massachusetts, Minnesota, New Jersey, New York, Pennsylvania, Rhode Island, and Wisconsin.[7]

Lyme disease risk in the United States is shown in the map below.

Approximately 90% of Lyme disease cases are reportApproximately 90% of Lyme disease cases are reported from the northeastern and upper midwestern United States. A rash that can be confused with early Lyme disease sometimes occurs following bites of the lone star tick (Amblyomma americanum). These ticks, which do not transmit the Lyme disease bacterium, are common human-biting ticks in the southern and southeastern United States.

International

Lyme disease exists throughout the world, including Scandinavia; central, southern, and western Europe; the former Soviet Union; Japan; and China. While Lyme disease is far more common in the northern hemisphere, occasional cases have been reported in more tropical locales, and it may exist in Australia. Ecology for the disease differs in various parts of the world. Furthermore, different strains of the organism are present in Europe and very likely account for differences in clinical manifestations; these have implications for diagnostic testing and vaccination strategies.

Mortality/Morbidity

Rare fatalities are reported in patients with Lyme disease, with 5 deaths reported in the United States in 2006.[1] Some fatal cases occur in patients who were simultaneously co-infected with other tick-borne pathogens such as Ehrlichia species and B microti, and in Europe, tick-borne encephalitis.

Morbidity is usually neurologic and rheumatic. Patients with neurologic disease who are not diagnosed and treated promptly can suffer from neurologic and cognitive dysfunction that can be difficult to treat. Some patients may have fixed neurologic deficits that are unresponsive to antibiotics. Patients with cardiac disease rarely exhibit chronic morbidity from their heart involvement. Similarly, some genetically predisposed individuals with arthritis may have ongoing joint inflammation that is not responsive to further antibiotic therapy.

Race

No known differential frequency exists in patients of different races; however, EM maybe more difficult to diagnose in dark-skinned individuals.

Sex

Males compromise 54.8 % of cases of Lyme disease, owing to an increase in males to tick exposure.

Age

As with other tick-borne diseases, the incidence of Lyme disease has a bimodal distribution with respect to age. Rates are highest among children aged 5-9 years and among adults aged 55-59 years. This distribution is also a function of tick exposure, rather than age.

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Contributor Information and Disclosures
Author

William E Caputo, MD  Resident Physician, Department of Emergency Medicine, Kings County Hospital

William E Caputo, MD is a member of the following medical societies: American Medical Association and Emergency Medicine Residents Association

Disclosure: Nothing to disclose.

Coauthor(s)

Richard H Sinert, DO  Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Dan Danzl, MD  Chair, Department of Emergency Medicine, Professor, University of Louisville Hospital

Dan Danzl, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Kentucky Medical Association, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: eMedicine Salary Employment

Jon Mark Hirshon, MD, MPH  Associate Professor, Department of Emergency Medicine, University of Maryland School of Medicine

Jon Mark Hirshon, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Public Health Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD 

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

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This patient's erythema migrans rash demonstrates several key features of the rash, including size, location, and presence of a central punctum, which can be seen right at the lateral margin of the inferior gluteal fold. Note that the color is uniform; this pattern probably is more common than the classic pattern of central clearing.
The thorax and torso are typical locations for erythema migrans. The lesion is slightly darker in the center, a common variation. In addition, this patient worked outdoors in a highly endemic area. Physical examination also revealed a right axillary lymph node.
This patient recalled pulling a tick from the left side of his neck 7 days previously. His rash displays the vesicular variant. Roughly 18 hours after the first dose of doxycycline, he developed a typical Jarisch-Herxheimer reaction.
The Ixodes scapularis tick is considerably smaller than the Dermacentor tick. The former is the vector for Lyme disease, granulocytic ehrlichiosis, and babesiosis. The latter is the vector for Rocky Mountain spotted fever. This photo displays an adult I scapularis tick (on the right) next to an adult Dermacentor variabilis; both are next to a common match displayed for scale. Photo by Darlyne Murawski; reproduced with permission.
In general, Ixodes scapularis must be attached for 24-48 hours to transmit the spirochete to the host mammal. Prophylactic antibiotics are more likely to be helpful if feeding is longer. This photo shows 2 I scapularis nymphs. The one on the right is unfed; the other has been feeding for 48 hours. Note its larger size and the fact that the midgut diverticula (delicate brown linear areas on the body) are blurred. Photo by Darlyne Murawski; reproduced with permission.
This is the classic target lesion of erythema migrans (EM). Although this morphology has been emphasized in the older literature, in North America, it represents only about 40% of all EM lesions. This morphology is more commonly found in Europe. Photo reproduced with permission; Lyme Disease Foundation, Hartford, CT.
Lyme disease frequently affects children. Pictured below is a young girl with no known tick bite in the area. While vacationing with her family on Fire Island in August, this young girl developed the rash shown below. She was treated successfully with amoxicillin. Photo courtesy of Dr John Hanrahan.
This is an ECG from a 21-year-old man with severe weakness and near syncope. Ten days earlier, while in upstate New York, he had a febrile illness without rash. No tick bite was known to occur, and the serologic result for Lyme disease was negative at the time. Seroconversion occurred when this ECG was obtained. He was admitted to a telemetry unit, had a temporary pacemaker inserted, and was given 2 g of intravenous ceftriaxone daily. He was well and did not need the pacemaker after 4 days.
This patient from Nantucket presented in early July with this rash. When the rash started, he had been treated for 1 week with Lotrisone for a presumed tineal infection, but the initial lesion grew, and new ones developed. He worked outside as a carpenter but had no definite tick bite.
This patient from a highly endemic area presented in July with a lesion on his ankle. It was mildly painful and had been present for 2-3 days. Mild tenderness was evident on physical examination. Both cellulitis and erythema migrans were possibilities; therefore, the patient was treated for both. Cefuroxime axetil or amoxicillin-clavulanate is useful in this situation because of their antimicrobial spectra.
Ticks are the most common vectors for vector-borne diseases in the United States. In North America, tick bites can cause Lyme disease, human granulocytic and monocytic ehrlichiosis, babesiosis, relapsing fever, Rocky Mountain spotted fever, Colorado tick fever, tularemia, Q fever, and tick paralysis. Europe has a similar list of illnesses caused by ticks, but additional concerns include boutonneuse fever and tick-borne encephalitis. Lyme disease is one of the most prominent tick-borne diseases, and its main vector is the tick genus Ixodes, primarily Ixodes scapularis. Image courtesy of the US Centers of Disease Control and Prevention.
The bacterium Borrelia burgdorferi (darkfield microscopy technique, 400X; courtesy of the US Centers for Disease Control and Prevention).
Approximate US distribution of Ixodes scapularis. Image courtesy of the US Centers for Disease Control and Prevention.
Amblyomma americanum is the tick vector for monocytic ehrlichiosis and tularemia. An adult and a nymphal form are shown (common match shown for size comparison). Image by Darlyne Murawski; reproduced with permission. Ehrlichiosis is a tick-borne infection of the white blood cells caused by Ehrlichia species. Typical symptoms include fever, headache, malaise, and myalgia, and they occur 5-14 days after the tick bite. It is sometimes referred to as "spotless" Rocky Mountain spotted fever. The treatment of choice is doxycycline, 100 mg twice daily, either orally or intravenously for 10 days. This regimen will also treat Lyme disease and the often mistaken Rocky Mountain spotted fever. Rifampin, 200 mg twice daily for 7 days, is a second-line option because chloramphenicol does not treat Ehrlichia chaffeensis. Tularemia is a zoonosis caused by infection with Francisella tularensis. Typical symptoms include fever, lethargy, anorexia, and in some forms, extensive ulcerating lymphadenopathy. With early diagnosis and treatment, mortality is rare (1%). Antibiotic treatment with streptomycin, 1 g intramuscularly twice daily for 10 days, eradicates the bacteria.
Approximate US distribution of A americanum. Image courtesy of the US Centers for Disease Control and Prevention.
The soft-bodied tick of the genus Ornithodoros transmits various Borrelia species that cause relapsing fever. Photo courtesy of Julie Rawlings, MPH, Texas Department of Health. Relapsing fever is characterized by recurrent acute episodes of fever (usually >39°C). It is a vector-borne illness spread by lice and ticks. The spirochete species Borrelia is responsible. For tick-borne relapsing fever, treatment is with tetracycline, 500 mg orally every 6 hours, or doxycycline, 100 mg orally twice daily, for 10 days. The louse-borne illness usually only requires a single dose of tetracycline or erythromycin, 500 mg orally.
Approximate US distribution of Dermacentor andersoni. Image courtesy of the US Centers for Disease Control and Prevention.
Rhipicephalus ticks are vectors for babesiosis and rickettsial infections, among others. Image courtesy of Dirk M. Elston, MD. In typical practice, testing ticks for tick-borne infectious organisms is not generally recommended. However, healthcare practitioners should become familiar with the clinical manifestations of tick-borne diseases (eg, Lyme disease, especially those practicing in endemic areas) and maintain a high index of suspicion during warmer months. Ticks can be placed in a sealed container with alcohol if they need to be transported and identified.
A rarely reported noninfectious complication for tick bites is alopecia. It can begin within a week of tick removal and typically occurs in a 3- to 4-cm circle around a tick bite on the scalp. A moth-eaten alopecia of the scalp caused by bites of Dermacentor variabilis (the American dog tick) has also been described. No particular species appears more likely to cause alopecia. Hair regrowth typically occurs within 1-3 months, although permanent alopecia has been observed.
To remove a tick, use fine-tipped forceps and wear gloves. Grasp the tick as close to the skin surface as possible, including the mouth parts, and pull upward with steady, even traction. Do not twist or jerk the tick because this may cause the mouth parts to break off and remain in the skin; however, note that the mouth parts themselves are not infectious. When removing, wear gloves to avoid possible infection. Children, elderly persons, and immunocompromised persons may be at greater risk for infection and should avoid removing ticks if possible. A common misperception is that pressing a hot match to the tick or trying to smother it with petroleum jelly, gasoline, nail polish, or other noxious substances is beneficial. This only prolongs exposure time and may cause the tick to eject infectious organisms into the body. Additionally, using lidocaine (subcutaneously or topically) may actually irritate the tick and prompt it to regurgitate its stomach contents. Finally, do not squeeze, crush, or puncture the body of the tick because its fluids (saliva, hemolymph, gut contents) may contain infectious organisms. Once the tick is removed, wash the bite area with soap and water or with an antiseptic to destroy any contaminating microorganisms. Additionally, the person who removed the tick should wash his or her hands.
Tick-borne disease prevention can be divided into environmental and personal measures. Patients exposed to tick-endemic areas should wear long-sleeved, light-colored clothing when outside. Lighter colors allow for easier identification of ticks. Chemical repellents with DEET (N,N-diethyl-3-methylbenzamide) and picaridin are available in numerous over-the-counter skin preparations as sprays or lotions. Permethrin is an acaricide that can be applied to clothing and is used in conjunction with chemical repellents. All individuals should perform regular skin checks. Ticks prefer warm, moist areas, such as the beltline, groin, and axilla, although in children, the hairline is a common site. Environmental prevention involves clearing underbrush and spraying acaricides in the spring around property sites. These measures prevent both mice and ticks from encroaching on properties. Studies involving the treatment of wild deer and mice have not been conclusive in reducing tick-borne diseases in humans. Currently, no Lyme disease vaccines are available in the United States. Lyme disease vaccine (Lymerix™) was discontinued in 2002, so some patients may still have residual protective antibodies. Image courtesy of the National Library of Medicine.
Hematoxylin and eosin stained section from a biopsy performed at the periphery of an eruption. Note the perivascular lymphocytic infiltrate, a pattern that is not specific for, but is characteristic of, erythema migrans.
Borrelial lymphocytoma of the earlobe, which shows a bluish red discoloration. The location is typical in children, as opposed to the nipple in adults. This manifestation of Lyme disease is uncommon and occurs only in Europe. Courtesy of Lyme Disease Foundation, Hartford, Conn.
Acrodermatitis chronica atrophicans is found almost exclusively in European patients and comprises an early inflammatory phase and a later atrophic phase. As the term suggests, the lesion occurs acrally and ultimately results in skin described as being like cigarette paper. Courtesy of Lyme Disease Foundation, Hartford, Conn.
Multiple lesions of erythema migrans occur in approximately 20% of patients. This patient, a carpenter from Nantucket who worked predominantly outside, had been treated with Lotrisone for 1 week prior to presenting to the emergency department with this rash. The patient had no fever and only mild systemic symptoms. He was treated with a 3-week course of oral antibiotics.
Blood smear showing likely babesiosis. Babesiosis can be difficult to distinguish from malaria on a blood smear.
Magnified ticks at various stages of development.
Typical appearance of erythema migrans, the bull's-eye rash of Lyme disease
Lyme rash. Courtesy of M. Fergione, B. Tucker, and L. Zernel; Pfizer Laboratories.
Normal and engorged Ixodes ticks.
Erythema migrans, the characteristic rash of early Lyme disease.
Bulls-eye rash
MMWR June 25, 2010 LymeDisease. Incidence (Per 100,000 population) of reported cases, by county — United States, 2008
Clinical presentation and therapy for the stages of Lyme Disease
Adult and Pediatric treatment options, dosages, and routes of administration
Approximately 90% of Lyme disease cases are reported from the northeastern and upper midwestern United States. A rash that can be confused with early Lyme disease sometimes occurs following bites of the lone star tick (Amblyomma americanum). These ticks, which do not transmit the Lyme disease bacterium, are common human-biting ticks in the southern and southeastern United States.
Table 1. Clinical presentation and therapy for the stages of Lyme Disease
Disease



Stage



Clinical



Manifestations



Treatment Duration
Early localizedErythema migransOral14-21 days
Early disseminatedMultiple erythema migransOral14-21 days
Isolated cranial nerve palsyOral14-21 days
MeningoradiculoneuritisOral14-28 days
MeningitisIntravenous or oral14-21 days
Carditis
-AmbulatoryOral 14-21 days
-HospitalizedIntravenous followed by oral14-21 days
Borrelial lymphocytoma Oral14-21 days
LateArthritisOral28 days
Recurrent arthritis after oral therapyOral or intravenous28 days or 14-28 days
EncephalitisIntravenous14-28 days
Acrodermatitis chronica atrophicansOral14-28 days
Table 2. Adult and Pediatric treatment options, dosages, and routes of administration
TreatmentAdult DosePediatric Dose
Oral TherapyDoxycycline



(patients ≥8 y)



100 mg twice a day4 mg/kg (up to 100 mg)



twice a day



Amoxicillin500 mg three times a day50 mg/kg (up to 500 mg)



three times a day



Cefuroxime axetil500 mg twice a day30 mg/kg (up to 500 mg)



twice a day



Intravenous therapyCeftriaxone2 g once a day50-75 mg/kg (up to 2 g)



once a day



Cefotaxime2 g every 8 h 150-200 mg/kg (up to 2 g) every 8 h
Penicillin G18-24 million U/d divided



every 4 h



200,000-400,000 mg/kg



(up to 2 g) every 8 h



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