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Tick, tick, tick, tick ... boom! The explosion of tick-borne diseases.


Becky Sanders woke up in the morning with a throbbing headache, a low-grade fever, virus-like symptoms, and a circular rash on her thigh that had enlarged overnight. That afternoon, her physician identified the rash as erythema migrans (EM), the distinctive bull's-eye or target-pattern rash associated with Lyme disease.

Shocked, Becky assured her doctor she never went near the woods and that her only outside activity in the past month had been gardening at her sister's house in Westchester County, N.Y.

The doctor explained Westchester County had become an endemic area and that if her gardening had been done where numerous deer reside, or if her sister's vegetable patch is located next to brush on the verge of a forest, she was in an at-risk environment. Becky was probably bitten by an infected tick awaiting its next blood meal. The tick does not jump, hop, or fly (it has no wings) but simply sits and waits for something warm and exhaling carbon dioxide to brush up against it.

Diseases spread by tick bites are being reported more frequently than ever before. Lyme disease, for instance, has progressed from only a handful of cases in the early 1980s to become the most common arthropod-borne disease in the U.S. The emergence of this disease is thought to be intimately tied to changes in the use of land that dates back more than two centuries (see "Reforestation offers breeding ground for Lyme disease," p. 46).

Of the more than 800 known species of ticks in existence, nearly 100 of them transmit either bacterial, viral, or protozoal infectious agents to humans. Some tick-associated illnesses have acute presentations and are life-threatening; others have an indolent course with systemic sequelae appearing months to years after infection. This article will focus on four tick-borne illnesses. Lyme disease and Rocky Mountain spotted fever are the most well-known and established tick-associated diseases. Ehrlichiosis is a recently recognized tick-associated disease afflicting humans, and human babesiosis continues to threaten human health.

Lyme Disease: The Great Imitator

Lyme disease is a multisystem illness caused by a spirochete, Borrelia burgdorferi. The disease manifests in regions harboring Ixodes ticks infected with B. burgdorferi. Lyme disease was first described more than 100 years ago in European literature but remained unrecognized in this country until a 1975 epidemic among children in Old Lyme, Conn. The Centers for Disease Control and Prevention (CDC) initiated surveillance for Lyme disease in 1982, and in 1991 it became nationally reportable. The disease has been reported in 47 states but is found mostly in the Northeast (Massachusetts to Maryland), Midwest (Wisconsin and Minnesota), and West (California and Oregon). Lyme disease has a worldwide distribution as well.

Lyme disease is a zoonotic illness. Infection is transmitted through the insect tick vector from animal reservoirs that include the white-footed mouse and white-tailed deer, in addition to birds, raccoons, horses, dogs, and cats, all of which interact at the forest edge in suburbia. Larval and nymphal ticks feed on small mammals; adult ticks feed primarily on deer. When not feeding, ticks commonly are found on vegetation in wooded areas and old fields common to the animal reservoir.

The bacterial spirochete is transmitted by the deer (black-legged) tick, Ixodes scapularis (formerly known as Ixodes dammini), in the eastern and midwestern U.S. Ixodes pacificus (the western black-legged tick) is the vector in the Western states. In New Jersey, Amblyomma americanum (the Lone Star tick) has been found infected but only a small number of cases can be ascribed to its bite. Ixodes ricinus has been reported as a vector in Switzerland. Transmission of infection occurs through tick salivation and is dependent on the duration of tick attachment. Ticks attached for 24 hours, for example, have a low likelihood of transmission, whereas those feeding greater than 72 hours usually result in transmission. Following injection into the skin, the long narrow spirochete with flagella disseminate to foci in the body via blood and lymph vessels. Dogs, cattle, and horses develop systemic disease that may include articular and cardiac manifestations as seen in human patients.

The incidence of human infection coincides with the tick season (May through September). Most cases are reported in June and July when the nymphal stage of the tick two-year life cycle is most active. About 30%-50% of all Lyme disease patients present with a tick bite history. Children and people who work outdoors are most at risk for infection.

Lyme disease symptoms are intermittent and changing and can be as diverse as arthritis, fatigue, depression, headaches, and poor vision. Further, the disease can affect numerous organ systems, thus mimicking other diseases. Many symptoms are a result of the immune system's protracted battles with the microbe. The spirohete can change its surface proteins to evade the immune system as well as antibiotics.

Progression of the disease can be divided into three stages, and like its distant cousin syphilis, can subside during a long latency period and reappear to attack joints, the heart, or the nervous system.

In Stage 1, Early Localized Infection, a red lesion on or near the site of a tick, known as EM, develops in about 60% of cases within three to 30 days following a tick bite. The lesion typically starts at the site of the bite and radiates slowly in a circular pattern. It may reach 5-50 cm in diameter and generally clears centrally within a few weeks, hence the name "bull's-eye rash."

The lesion, unfortunately, cannot be relied upon for the clinical diagnosis of Lyme disease. Additionally, because of the very small size of the tick (1 mm-2 mm) and the painlessness of its bite, as many as 80% of tick bites are unrecognized. Usually present during this period are symptoms of headache, malaise, myalgia, fever, arthralgia, fatigue, and lymphadenopathy.

During Early Disseminated Infection (Stage 2), neurological, cardiac, and musculoskeletal involvement can occur. Generally these symptoms appear weeks to months following the first stage. Stage 2 is characterized by symptoms of dizziness, irregular heartbeat, meningitis, inflamed nerve roots in the neck, and Bell's palsy.

Arthritic symptoms, typically involving pain and swelling of the large joints, occur during Stage 3, Chronic Disease. Other symptoms include mood swings, loss of memory, inability to concentrate, poor motor coordination, and somnolence. Arthritic attacks can occur for months, even years.

Lyme disease can be diagnosed by noting a patient's clinical signs and symptoms compatible with Lyme disease, history of travel, and/or exposure to an endemic region for Lyme disease and an elevated antibody titer to B. burgdorferi. Only half of infected individuals demonstrate the classic bull's-eye rash, however, and even fewer remember being bitten by a tick.

While serological methods are the most common and practical for lab confirmation, they are complicated due to lack of standardization among individual labs, intra-laboratory variations, and false-negative and -positive results. Additionally, cross-reactivity may be seen in patients with syphilis, yaws, relapsing fever, leptospirosis, HIV infection, Rocky Mountain spotted fever, infectious mononucleosis, lupus or rheumatoid arthritis. Serologic tests also are insensitive during the first several weeks of infection and may remain negative in people treated early with antibiotics.

While test sensitivity increases when patients progress to later stages of the disease, patients with chronic Lyme disease may remain seronegative. Enzyme immuno-assay (EIA) and indirect immunofluorescence assay (IFA) procedures have been employed. (Of the two, the EIA is considered more sensitive.) A Western Blot (WB) is useful in characterizing the specificity of antibody response to B. burgdorferi and is believed to have a greater sensitivity than either the EIA or IFA procedure. The visual discrimination used in WB analysis can distinguish significant antibody band patterns from nonsignificant bands. This discrimination is not possible with the IFA or EIA, where only total antibody response is measured. To date, none of these assays are standardized.

At the Oct. 1994 Second National Conference on Serological Diagnosis of Lyme Disease, sponsored by the Association of State and Territorial Public Health Laboratory Directors, the CDC, and the Michigan Department of Health, the current state of serodiagnostic testing was reviewed and a set of recommendations developed for test performance and interpretation, quality assurance practices, new test evaluation and clearance, and disseminating information regarding developments in Lyme disease testing.[1] These recommendations are initial steps toward the standardization of serologic testing for this illness. Among the recommendations for test performance and interpretation is a two-step protocol for testing serum specimens. First, a sensitive EIA or IFA should be performed. Then specimens found positive or equivocal can be tested with a standardized WB procedure. Negative specimens need no further testing.

Isolating B. burgdorferi from skin biopsy, blood, serum, and spinal fluid has been reported, yet due to the lack of numbers of spirochetes, their slow growth rate and complicated growth requirements, and microbial overgrowth of media, direct culture from these specimens is not clinically useful to diagnose Lyme disease. Polymerase chain reaction (PCR) procedures have detected B. burgdorferi genetic material in synovial fluid, CSF, skin and other tissues, blood, and urine; however, sensitivity of the assay predisposes to false-positive results in a poorly controlled assay or inadvertently contaminated sample. Testing ticks for the presence of the organism is not a definitive diagnosis but merely serves as an adjunct in diagnosis for the physician.

In endemic areas, Lyme disease has received tremendous media attention leading to what could be coined "Lyme hysteria." Outdoor activities have been curtailed, enrollments in outdoor organizations such as the Boy Scouts have dropped, and residents have built walls and virtual motes of gravel around their houses to ward off ticks. A small cottage industry sells everything from special tick repellent to home diagnostic tests. People have formed special support groups for chronic Lyme disease sufferers.

A far-from-perfect lab test, underdiagnosis, misdiagnosis, and overdiagnosis have divided the public and the medical community on what Lyme disease truly is. Some physicians believe Lyme disease may be a chronic infectious disease requiring a lifetime of monitoring and antibiotics. Major players in mainstream medicine, including the CDC, researchers, clinicians, and insurers, believe the bacteria is almost always eradicated following two to four weeks of therapy. A prominent physician and researcher located in central New Jersey says he is concerned about the patient who walks into the doctor's office with a hangnail and a positive blood test for Lyme disease and suddenly gets diagnosed with the disease. What is known is the duration of Lyme disease symptoms may be shortened and later illness prevented when antimicrobial treatment is given, especially when administered early on. Doxycycline and amoxicillin are among the most common treatments prescribed for both adults and children.

Prophylactic antibiotic therapy following a deer tick bite is not usually prescribed. Certainly prevention is one of the best methods of control for Lyme disease and other tick-borne illnesses. It is imperative, therefore, the public be educated in how to protect themselves against getting tick bites. (For more on this, see "Tips for avoiding tick infection," p. 48).

RMSF: Beyond the Rockies to the coasts

Rocky Mountain spotted fever (RMSF) is caused by Rickettsia rickettsii, a small gram-negative bacillus that is an obligately intracellular bacterium. It belongs to the Genus Rickettsia, is the prototype disease, and is the most virulent rickettsial disease of the spotted fever group.

RMSF was first identified in 1873 and is the most common rickettsial disease occurring throughout the U.S. It is found primarily in the South Atlantic and West South Central states; the highest incidence rates have been noted in North Carolina and Oklahoma. It also has been documented in Canada, Mexico, Panama, Costa Rica, Colombia, and Brazil. The incidence of RMSF may only appear to be increasing since we are now looking for tick-borne diseases where we've never looked before. The same factors that spread Lyme disease (reforestation, suburban sprawl) help spread RMSF.

Rickettsia are maintained in nature in tick vectors found in high grass, low shrubs, woodlands, fields, and at the forest edge. Infection is transmitted by the bite of an infected tick when at least 4-6 hours of attachment and feeding have occurred. In addition, a tick's crushed tissue or feces may lead to infection if either of these elements come in contact with breaks in the skin/mucous membrane. Rickettsiae can be transmitted to dogs and rodents as well.

The Rocky Mountain wood tick, Dermacentor andersoni, is the common vector in the Southwestern U.S. The American dog tick, Dermacentor variabilis, and, to a lesser extent, Amblyomma americanum transmit infection in Eastern and Southern U.S. Following injection into the skin, Rickettsia disseminate through blood and lymphatic vessels, settling and multiplying in endothelial cells throughout the body to create a generalized vasculitis. They can affect any organ and patients of all ages.

The incubation period is two to 14 days. Occurrence parallels the tick season, which in most endemic regions runs April through October. Only about 54% of patients may recall a tick bite. Symptoms include a classic triad of fever, headache, and rash. A rash, the classic hallmark of RMSF, is present in 14% of patients on the first day of illness and in 49% during the first three days.[2] The reddish-to-black maculo-papular rash (resembling measles) usually appears after three to four days on extremities, including palms and soles, and spreads rapidly to much of the body.

Approximately 10% of patients have no rash, fever, or a delayed onset of rash. Myalgia, arthralgia, conjunctivitis, as well as encephalopathy may occur; patients also may present with abnormal white blood cell counts and develop leukopenia, thrombocytopenia, or elevated liver enzymes. Case fatality is about 4% and higher in patients in cases where there is an absence of specific therapy and/or the patient is more than 40 years of age.

Recognizing RMSF early on is critical; diagnosis usually is based on clinical presentation and epidemiologic history. Diagnostic titers of antibodies are not found until 10-14 days post-onset. Serologic tests used to confirm RMSF include an indirect hemagglutination assay (IHA), latex agglutination test, and IFA, all of which use R. rickettsii as antigen. The IFA is the method of choice, and a fourfold or greater increase in titer on paired sera (acute and convalescent) is diagnostic. Direct immunofluorescent staining of biopsy specimens from active skin lesions may confirm diagnosis sooner than serology; however, this technique is not widely available and can result in false negatives.

Culturing R. rickettsii is hazardous and impractical in the clinical setting. PCR currently is investigative. The need for reamplification indicates a lack of sensitivity, which limits the usefulness of this method as a clinical diagnostic test.[3] Ticks can be tested for the presence of the causative agent organism. Important to note, however, is a negative test does not rule out the possibility of infection.

Patients with RMSF can be treated with rickettsial static agents chloramphenicol, tetracycline, or doxycycline. Treatment must be started early. Waiting until the rash is widespread or until serologic results are complete may lead to a poor prognosis. Preventive measures are the same as those described for Lyme disease. Antibiotic prophylaxis is not recommended for asymptomatic patients following a tick bite.

Ehrlichiosis: RMSF without the spots

Ehrlichiosis is a tick-borne disease caused by Ehrlichia species. Two emerging diseases were recently recognized in the U.S.: Human monocytic ehrlichiosis (HME), caused by Ehrlichia chaffeensis, was first recognized in 1986 and was isolated from an Army recruit at Fort Chaffee, Ark.[4] Human granulocytic ehrlichiosis (HGE) was recognized in 1993;[5] its causative agent has not yet been identified, although it is similar to the veterinary pathogen E. equi.

Ehrlichiae are obligately intraleukocytic bacteria. They belong to the Rickettsiaceae family as do the R. rickettsii of RMSF. E. chaffeensis has been observed primarily in monocytes/macrophages and also in lymphocytes and neutrophils. The HGE organism has been seen exclusively in granulocytes, primarily neutrophils.

More than 400 cases of HME have been confirmed in 30 states, primarily in southwestern and south central regions of the country. Fewer than 100 cases of HGE have been confirmed in Connecticut, Massachusetts, Minnesota, Wisconsin, and New York, with suspected cases in Maryland, California, Florida, and New Jersey.[6] Coinfections with Lyme disease have been reported.

The E. chaffeensis bacterium has been identified in the Amblyomma americanum tick. HGE patients have reported being exposed to or bitten by Ixodes scapularis or Dermacentor variabilis ticks. Animal reservoirs of both agents are still being investigated.

White-tailed deer, white-footed mice, and dogs may be potential reservoirs of the HGE agent. Both the white-tailed deer and dogs have been shown to be experimentally susceptible to E. chaffeensis, but more definitive studies are needed.[7]

Incubation periods are not well established, but most patients report tick exposure one to three weeks before onset of illness. Most cases have occurred between April and September. Clinical signs and symptoms for both forms of human ehrlichiosis are identical, the spectrum of disease ranging from mild to a severe, life-threatening or fatal disease.

Fever, headache, myalgia, chills, nausea, and vomiting are the most common symptoms. Less common symptoms include cough, joint pain, confusion, and rash. The rash, found in approximately 30% of patients, can occur anywhere on the body (not necessarily associated with the tick bite site) and can be macular or papular.

Laboratory findings include thrombocytopenia, leukopenia, elevated liver enzymes, and anemia. The most commonly involved organs are bone marrow, liver, spleen, and lymph nodes. The disease may be confused clinically with RMSF but differs by rarity of the prominent rash and often referred to as spotless RMSF.

Diagnosis of human ehrlichiosis infection can be done by serologic or molecular techniques. E. equi is used as surrogate antigen for HGE in the IFA assay since it is a closely related species (99.8% similarity between 16S ribosomal RNA gene sequences).[8]

E. chaffeensis has been grown successfully in vitro and used as the IFA assay antigen. Ideally, acute and convalescent phase serum specimens, drawn at least four weeks apart, should be submitted for testing. A four-fold or greater increase in antibody titer is diagnostic. Because there is no cross-reactivity between antibodies to HGE and E. chaffeensis, a negative test result with this antigen does not exclude a diagnosis of ehrlichiosis.

While PCR and nested PCR of patient's blood have been used to detect these organisms, these assays are research tools. Occasionally the HGE agent can be observed in cytoplasmic inclusions in peripheral granulocytes, especially neutrophils. The round, dark-blue-stained inclusion bodies, called morulae, are diagnostic of ehrlichiosis.

On routine examination of blood during differential blood counts, these inclusions may be observed. E. chaffeensis is rarely detected by this method. PCR and nested PCR testing of ticks for these agents remain under investigation.

Treatment should not be delayed until laboratory confirmation is obtained. Patients presenting with signs and symptoms consistent with ehrlichiosis should be treated empirically. Doxycycline or other tetracyclines are recommended for adults. Fevers generally subside 24-48 hours following treatment.

Chloramphenicol is the treatment of choice in young children. Post-exposure treatment following a tick bite is not recommended. Prevention is the same as that described for Lyme disease and RMSF.

Babesiosis: Malaria-like illness

Babesiosis is a malaria-like illness caused by an intraerythrocytic protozoan parasite. Babesia microti, a rodent parasite and the most frequent species infecting humans in the U.S., is transmitted by the Ixodes scapularis - the same tick that transmits B. burgdorferi, the causative agent of Lyme disease. Dual infections of babesiosis and borreliosis do occur.[9]

Babesiosis, a zoonotic disease involving humans only accidentally, was first recognized in 1957 in Yugoslavia. Similar to Lyme disease, it emerged from New England, the old whaling center of Nantucket Island off the Massachusetts coast in 1969 out of the same ecosystem of reforestation with scrub and heavy underbrush after tourism replaced sheep farming and cranberry farms. The reintroduction of deer in the 1920s brought the deer tick to replace local tick species. The mixture of forest, wildlife, and tourism offered a new home for both Lyme disease and babesiosis, the latter of which now occurs primarily in the Northeastern U.S. and Minnesota, Wisconsin, California, and Washington. In Europe, human infections are caused by B. divergins, a bovine parasite whose vector is another Ixodes tick, I. ricinus.

B. microti is transmitted during the summer months by the bite of the Ixodes tick. The tick feeds on infected deer mice, other small mammals, and deer. Occasionally, cases of babesiosis have been transmitted by blood transfusion from asymptomatic but parasitemic donors. Babesia live in erythrocytes and, in severe infections, can produce massive hemolysis. The incubation period is variable: one week to 12 months.

The clinical spectrum ranges from asymptomatic to a rapidly progressive and fatal disease, with increased severity in the elderly, asplenic, or immunologically suppressed. The clinical syndrome may include fever, chills, myalgia, fatigue, nausea, vomiting, and weight loss. A patient may develop hemolytic anemia, jaundice, and lymphadenopathy. No consistent dermatologic manifestations have been reported. Laboratory manifestations are dependent on the level of parasitemia and may include thrombocytopenia and leukopenia.

Diagnosing Babesia infection is made by observing parasites within red blood cells on a thick or thin blood smear. A morphologic diagnosis is essential for critically ill patients, who must be diagnosed and treated rapidly. In subacute or chronic illnesses, serologic analysis is diagnostic because the three to four weeks that are needed to produce a diagnostic rise in antibody titer may transpire months before the patient consults a physician.

Serologic analysis is used most frequently in epidemiologic studies but useful in subacute or chronic illnesses where blood smears can be negative. The IFA assay using B. microti antigen has been found to be a sensitive, specific, and reproducible method for diagnosing babesiosis; unfortunately, it is not available in many laboratories.

A titer of greater than 1:64 is considered consistent with infection and can rise to greater than or equal to 1:1,024 during the first few weeks of illness.[10] The serologic test can be compromised by the cross-reactivity that can occur with other Babesia species and malaria. Inoculation of susceptible animal hosts can be performed to isolate and confirm diagnosis. PCR has permitted the molecular diagnosis and monitoring of babesial infection. It appears to be sensitive and specific for diagnosis of acute cases but remains available only at a few research labs.

Specific treatment for human babesiosis is the co-administration of clindamycin and quinine. This combination has been efficacious in animal studies and patients; however, these drug regimens on occasion have failed and not shown consistent benefit. Methods of control include preventive measures as described for the other tick-borne diseases, including educating the public on the mode of transmission, means for personal protection, as well as control of rodents around human habitats.

All about ticks

The ticks implicated in the four tick-borne illnesses outlined above belong to the Ixodidae (hard ticks) family as opposed to the soft tick Argasidae family. They have a hard dorsal plate or scutum, and mouth parts are clearly visible from above. Ticks are blood-sucking arachnids that are ectoparasites of many vertebrates, such as reptiles, birds, mammals, and human.

Ticks have a four-stage life cycle: 1) egg; 2) six-legged larva; 3) eight-legged, sexually immature nymph; and 4) eight-legged, sexually mature adult. Generally a blood meal is necessary for larva to molt and become a nymph and another blood meal is needed for the nymph to molt before becoming an adult. Hard ticks have one nymphal stage, whereas soft ticks may have more.

Testing ticks for the causative organism of disease is not conclusive. For example, the nonobservance of spirochetes does not rule out the presence of spirochetes in the tick or the presence of disease in patients. On the other hand, detecting spirochetes does not automatically mean transmission has occurred since not all ticks carry an infectious organism. Hence, species identification and tick testing only serve as adjuncts to diagnosing physicians. Tick analyses can be used in epidemic measures or ecological survey studies to identify tick species involved and what organism it might be carrying. Additionally, the distribution of tick species and their vertebrate hosts can identify areas of greatest risk for particular infections.

Primary resource for clinicians

The more rare an infectious disease, the more thorough and accurate laboratory testing must become. Many facilities maintain a small personal library of helpful literature to help guide physicians in interpreting laboratory tests. Some labs also have added a more extensive information section to their test reports or to their on-line directory of services.

Laboratorians must become a primary resource for clinicians where tick-borne diseases are concerned by continually communicating the limitations and problems associated with this testing. Conscientious lab workers can make all the difference in the world.


1. ASTPHLD. Proceedings from the Second National Conference on Serologic Diagnosis of Lyme Disease. Association for State and Territorial Public Health Laboratory Directors. Washington, DC, 1995.

2. Walker DH. Rocky Mountain spotted fever: A seasonal alert. CID. 1995; 20: 1,111-1,117.

3. Sexton DJ, Kanj SS, Wilson K, et al. The use of polymerase chain reaction as a diagnostic test for Rocky Mountain spotted fever. Am J Trop Med Hyg. 1994; 50(1): 59-63.

4. Dawson JE, Anderson BE, Fishbein DB, et al. Isolation and characterization of an Ehrlichia sp. from a patient diagnosed with human ehrlichiosis. J Clin Microbiol. 1991; 29: 2,741-2,745.

5. Bakken JS, Dumlar JS, Chen SM, et al. Human granulocytic ehrlichiosis in the upper Midwest United States. JAMA. 1994; 272: 212-218.

6. Fishbein DB, Dawson JE, Robinson LE. Human ehrlichiosis in the United States, 1985-1990. Ann Inter Med. 1994; 120: 736-743.

7. Dumler JS, Bakken JS. Ehrlichial diseases of humans: Emerging tick-borne infections. CID. 1995; 20: 1,102-1,110.

8. Chen SM, Dumler JS, Bakken JS, Walker DH. Identification of a granulocytotropic Ehrlichia species as the etiologic agent of human disease. J Clin Microbiol. 1994; 32: 589-595.

9. Pruthi RK, Marshall WF, Wiltsie JC, Persing DH. Subspecialty clinic: Infectious diseases, human babesiosis. Mayo Clin Proc. 1955; 70: 853-862.

10. Krause PJ, Telford III SR, Ryan R, et al. Diagnosis of babesiosis: Evaluation of a serologic test for the detection of Babesia microti antibody. JID. 1994; 169: 9.

RELATED ARTICLE: Objectives for this article:

1. Discuss factors that have contributed to an increased incidence of Lyme disease.

2. Describe transmission mechanism and laboratory identification procedures for Lyme disease.

3. Compare and contrast the transmission, the clinical presentation, and the lab investigation of Rocky Mountain Spotted Fever (RMSF) and ehrlichiosis.

4. Discuss the geographic and pathologic characteristics of human babesiosis.

RELATED ARTICLE: Reforestation offers breeding ground for Lyme disease

In the nearly 1800s, the eastern U.S. was rendered virtually treeless when vas tracts of land were cleared for agriculture. Tremendous quantities of wood were needed for domestic fuel. It was typical for a New England homestead to exhaust 20 cords of wood for heating and cooking; additional wood was needed for charcoal for iron smelting and glass manufacturing.

The forests disappeared, taking with them deer and their natural predators. Grand tall trees such as oaks and larches were replaced by an ecosystem that was as artificial as a concrete parking lot, patchy new woodlands comprised of scrub brush, non-shade trees, thick underbrush, and emerging rodents and deer populations unchecked by natural predators.

As agriculture moved West, the reforestation of the East became ideal for the resurgence of wildlife, a perfect environment for rodents and ticks to thrive. During this time (the post World War II economic boom), urbanites became suburbanites. Housing tracts were cut right into the new growth forests, bringing humans into this new ecosystem. The new outdoor-oriented life-styles of the 1970s moved individual homes right into the forest edge where deer, rodents, and ticks were flourishing, creating the perfect environment for Lyme disease to emerge.

In 1975, in Old Lyme, Conn., a group of mothers noticed a strange pattern of illness: Many of their children were suffering from long bouts of recurrent fever and aching joints. While these patients were originally diagnosed as having juvenile rheumatoid arthritis, this illness came to be known as Lyme disease, which increased twentyfold from 1982 to 1992. From 1993 to 1994, reported cases have increased by 58%.

RELATED ARTICLE: Tips for avoiding tick infection

Avoid tick-infested areas whenever possible. Precautions to prevent tick bites include, but are not limited to, wearing light-colored clothing that covers legs and arms to allow for greater visibility of crawling ticks and tucking pants into socks to minimize exposure. Repellents containing compounds such as permethrin, a repellent and contact acaricide, can be applied to clothing.

After partaking in outdoor activity in an infested area, search your entire body, particularly along your hairline, under your arms, and behind your knees. While protecting your hands with gloves, cloth, or tissue, remove ticks promptly and carefully without crushing them using tweezers or forceps applied close to the skin. Using a steady, gentle traction to pull backward without twisting will decrease your chances of leaving parts of the tick's mouth in your skin.

Immediately clean the site of possible infection with a disinfectant. Tick repellent such as diethyltoluamide can be applied to the skin.

Cynthia R. Bartlett is serology program coordinator and James W. Brown assistant commissioner, New Jersey State Department of Health, Division of Public Health and Environmental Laboratories, in Trenton, N.J.
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Author:Bartlett, Cynthia R.; Brown, James W.
Publication:Medical Laboratory Observer
Date:Mar 1, 1996
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