Tick Borne Diseases

Lyme Disease


Lyme disease is an infection transmitted by the bite of ticks carrying the spiral-shaped bacterium Borrelia burgdorferi. The disease was named for Lyme, Connecticut, the town where it was first diagnosed in 1975 after a puzzling outbreak of arthritis. The organism was named for its discoverer, Willy Burgdorfer. The effects of this disease can be long-term and disabling unless it is recognized and treated properly with antibiotics.


Lyme disease, which is also called Lyme borreliosis, is a vector-borne disease. This term means that it is delivered from one host to another. It is also classified as a zoonosis, which means that it is a disease of animals that can be transmitted to humans under natural conditions. In this case, a tick bearing the Borrelia burgdorferi organism literally inserts it into a host's bloodstream when it bites the host to feed on its blood. It is important to note that neither Borrelia burgdorferi nor Lyme disease can be transmitted directly from one person to another, or from pets to humans.

Controversy clouds the true incidence of Lyme disease because no test is definitively diagnostic for the disease, and many of its symptoms mimic those of so many other diseases. Cases of Lyme disease have been reported in 49 of the 50 states; however, 92% of the 17,730 cases reported to the Centers for Disease Control and Prevention (CDC) in 2000 were from only nine states (Connecticut, Rhode Island, New York, Pennsylvania, Delaware, New Jersey, Maryland, Massachusetts, and Wisconsin). The disease is also found in Scandinavia, continental Europe, the countries of the former Soviet Union, Japan, and China; in addition, it is possible that it has spread to Australia.

In the United States, Lyme disease accounts for more than 90% of all reported vector-borne illnesses. It is a significant public health problem and continues to be diagnosed in increasing numbers. The Centers for Disease Control and Prevention (CDC) attributes this increase to the growing size of the deer herd and the geographical spread of infected ticks rather than to improved diagnosis. In addition, some epidemiologists believe that the actual incidence of Lyme disease in the United States may be 5-10 times greater than that reported by the CDC. The reasons for this difference include the narrowness of the CDC's case definition as well as frequent misdiagnoses of the disease.

The risk for acquiring Lyme disease varies, depending on what stage in its life cycle a tick has reached. A tick passes through three stages of development-larva, nymph, and adult-each of which is dependent on a live host for food. In the United States, Borrelia burgdorferi is borne by ticks of several species in the genus Ixodes, which usually feed on the white-footed mouse and deer (and are often called deer ticks). In the summer, the larval ticks hatch from eggs laid in the ground and feed by attaching themselves to small animals and birds. At this stage they are not a problem for humans. It is the next stage-the nymph-that causes most cases of Lyme disease. Nymphs are very active from spring through early summer, at the height of outdoor activity for most people. Because they are still quite small (less than 2 mm), they are difficult to spot, giving them ample opportunity to transmit Borrelia burgdorferi while feeding. Although far more adult ticks than nymphs carry Borrelia burgdorferi, the adult ticks are much larger, more easily noticed, and more likely to be removed before the 24 hours or more of continuous feeding needed to transmit Borrelia burgdorferi.


See Rickettsia and RMSF.

What is Rocky Mountain spotted fever?

Rocky Mountain spotted fever is a serious, generalized infection that is usually spread to people by the bite of infected ticks. The disease gets its name from the Rocky Mountain area where it was first identified.

What is the infectious agent that causes Rocky Mountain spotted fever?

Rocky Mountain spotted fever is caused by Rickettsia rickettsii, a specialized bacteria. Ticks infected with the organism transmit the disease to humans.

Where is Rocky Mountain spotted fever found?

Rocky Mountain spotted fever is found throughout the United States, except in Maine, Alaska, and Hawaii. Despite the name, few cases are reported from the Rocky Mountain region. Most cases occur in the southeastern United State with North Carolina being the state reporting the highest number of cases.

Rocky Mountain spotted fever is spread by the American dog tick, the lone-star tick, and the wood tick, all of which like to live in wooded areas and tall, grassy fields. The disease is most common in the spring and summer when these ticks are active, but it can occur anytime during the year when the weather is warm.

How do people get Rocky Mountain spotted fever?

People get Rocky Mountain spotted fever from the bite of an infected tick or by contamination of the skin with the contents of an attached tick when it is removed from the skin. Rocky Mountain spotted fever is not spread from person to person, except rarely by blood transfusion.

What are the signs and symptoms of Rocky Mountain spotted fever?

People with Rocky Mountain spotted fever get a sudden fever (which can last for 2 or 3 weeks), severe headache, tiredness, deep muscle pain, chills, nausea, vomiting, diarrhea and a characteristic rash (not in all cases). The rash might begin on the legs or arms, can include the soles of the feet or palms of the hands, and can spread rapidly to the trunk or the rest of the body.

How soon after exposure do symptoms appear?

Symptoms usually begin 3 to 12 days after a tick bite.

How is Rocky Mountain spotted fever diagnosed?

The disease is diagnosed by special blood tests.

Who is at risk for Rocky Mountain spotted fever?

Anyone who is exposed to tick-infested areas or to tick-infested pets is at risk for Rocky Mountain spotted fever.

What complications can result from Rocky Mountain spotted fever?

Without prompt medical care, kidney failure and shock can lead to death.

What is the treatment for Rocky Mountain spotted fever?

Rocky Mountain spotted fever must be treated with antibiotics. Many persons with the disease need to be hospitalized.

How common is Rocky Mountain spotted fever?

Rocky Mountain spotted fever CDC case reports for 2007 where 665 in North Carolina and 56 in South Carolina

How can Rocky Mountain spotted fever be prevented?

No vaccine is available to protect humans against Rocky Mountain spotted fever. The best way to avoid getting the disease is to avoid areas such as the woods or fields where ticks are found. If this is not possible, you can reduce your risk by taking these precautions:

CO-INFECTIONS IN LYME - Babesiosis, Ehrlichiosis, Bartonella.

BABESIOSIS (Piroplasmosis)


Piroplasms are not bacteria, they are protozoans. Therefore, they will not be eradicated by any of the currently used Lyme treatment regimens. Therein lies the significance of co-infections - if a Lyme patient has been extensively treated yet is still ill, suspect a co-infection.

Babesia infection is becoming more commonly recognized, especially in patients who already have Lyme Disease. It has been published that as many as 66% of Lyme patients show evidence of co-infection with Babesia. It has also been reported that Babesial infections can range in severity from mild, subclinical infection, to fulminant, potentially life-threatening illness. The more severe presentations are more likely to be seen in immunocompromised and elderly patients. Milder infections are often missed because the symptoms are incorrectly ascribed to Lyme. Babesial infections, even mild ones, may recrudesce and cause severe illness. This phenomenon has been reported to occur at any time, even up to several years after the initial infection. Furthermore, asymptomatic carriers pose risks: to the blood supply as this infection has been reported to be passed on by blood transfusion, and to the unborn child from an infected mother as it can be transmitted in utero.

"Subjects with evidence of both infections reported a greater array of symptoms than those infected by the spirochete or piroplasm alone." "Co-infection generally results in more intense acute illness and a more prolonged convalescence than accompany either infection alone." "Spirochete DNA was evident more often and remained in the circulation longer in co-infected subjects than in those experiencing either infection alone." "Co-infection might also synergize spirochete-induced lesions in human joints, heart and nerves." "Babesial infections may impair human host defense mechanisms" "The possibility of concomitant Babesial infection should be considered when moderate to severe Lyme Disease has been diagnosed."


In milder forms, symptoms may include a vague sense of imbalance without true vertigo, headache, mild encephalopathy, fatigue, sweats, air hunger and occasionally cough. When present as a co-infection with Lyme, initial symptoms of the illness are often more acute and severe. Suggestions of co-infection include the above symptoms, but the headaches are more severe, and encephalopathy is out of proportion to the other Borrelia symptoms. The fulminant presentations include high fevers, shaking chills and hemolysis, and can be fatal.


Diagnostic tests are insensitive and problematic. There are at least thirteen Babesial forms found in ticks, yet we can currently only test for B. microti and WA-1 with our serologic and nuclear tests. Standard blood smears reportedly are reliable for only the first two weeks of infection, thus are not useful for diagnosing later infections and milder ones including carrier states where the germ load is too low to be detected. Krause, PJ, Telford, SR, Spielman, A, et.al. Concurrent Lyme disease and Babesiosis. JAMA 1996. 275 (21):1660 "As is common in the case of Babesial infections, parasites frequently cannot be seen in blood films." Therefore, multiple diagnostic test methods are available and each have their own benefits and limitations and often several tests must be done. Be prepared to treat based on clinical presentation, even with negative tests.


Unlike Lyme, Babesia titers can reflect infection status. Thus, persistently positive titers or western blots suggest persistent infection.


This is more sensitive than smears for B. microti, but will not detect other species.


This utilizes buffy coat, prolonged scanning (up to three hours per sample!) and digital photography through custom-made microscopes. Although more sensitive than standard smears, infections can still be missed. The big advantage is that it will display multiple species, not just B. microti.


This technique is also a form of blood smear. It is said to be 100-fold more sensitive than standard smears for B. microti, because instead of utilizing standard, ink-based stains, it uses a fluorescent-linked RNA probe and ultraviolet light. The Babesial organisms are then much easier to spot when the slides are scanned. The disadvantage is that currently only B. microti is detected.


Treating Babesia infections had always been difficult, because the therapy that had been recommended until 1998 consisted of a combination of clindamycin plus quinine. Reports suggest that a more successful regimen is available to treat this infection. See http://aafp.org/afp/20010601/tips/3.html

Krause, PJ. Spielman, A, Telford, SR et.al.. Persistent parasitemia after acute Babesiosis N Engl J Med 1998. 339:162

"Of the treated subjects, almost half had symptoms that were consistent with reactions to quinine, including hearing loss, tinnitus, hypotension, and such gastrointestinal symptoms as anorexia, vomiting, and diarrhea." "Although treatment with clindamycin and quinine reduces the duration of parasitemia, infection may persist and recrudesce and side effects are common."

Because of these dismal statistics, the current regimen of choice for Babesiosis is the combination of atovaquone plus azithromycin. This combination was initially studied in animals, and then applied to Humans with good success, because when atovaquone was used alone, resistance developed in 20% of cases, but reportedly did not occur when azithromycin was added. Fewer than 5% of patients have to halt treatment due to side effects, and the success rate is clearly better than that of clindamycin plus quinine. The duration of treatment with atovaquone plus azithromycin for Babesiosis varies depending on the degree of infection, duration of illness before diagnosis, the health and immune status of the patient, and whether the patient is co-infected with Borrelia burgdorferi. Typically, a three-week course is prescribed for acute cases, while chronic, longstanding infections with significant morbidity and co-infection will require several months of therapy. Relapses have occurred, and retreatment is occasionally needed. Problems during therapy include diarrhea, mild nausea, the expense of atovaquone (over $600.00 per bottle - enough for three weeks of treatment), and rarely, a temporary yellowish discoloration of the vision. Regular blood counts, liver panels and amylase levels are recommended during any prolonged course of therapy. Patients who are not cured with this regimen can be retreated but with higher doses, as this has proven effective in many of my patients. Artemesia (a non-prescription herb) may be added, but is not effective when used alone. Metronidazole can also be added to increase efficacy, but there is minimal clinical data on how much more effective this regimen is.

EHRLICHIOSIS (Anaplasma phagocytophila, Human Granulocytic Ehrlichiosis HGE, Human Monocytic Ehrlichiosis HME )

Three emerging tick-borne diseases caused by the obligate intracellular bacteria of the genus Ehrlichia have been recognized. Human monocytic ehrlichiosis (HME) was first described in 1986 and is caused by Ehrlichia chaffeensis. Human granulocytotropic anaplasmosis (HGA), formerly known as human granulocytic ehrlichiosis (HGE), was described in 1993 and is caused by Anaplasma phagocytophilia. Both types have been referred to as spotless Rocky Mountain spotted fever. Ehrlichia ewingii was described in 1999 as an agent of human ehrlichiosis.

Anaplasma phagocytophila is a recently described tick-borne pathogen that causes Human Granulocytic Ehrlichiosis. Anaplasma infects the neutrophils (immune system cells) of host organisms. Infection can lead to fever, chills, myalgia (muscle ache), headache, nausea, confusion, cough, and arthralgias (joint aches). Antibiotic treatment is usually sufficient to clear up infection, but if left untreated, infection can lead to fatality.


While it is true that this illness can have a fulminant presentation, and may even become fatal if not treated, milder forms do exist, as does chronic low-grade infection, especially when other tick-borne organisms are present. The potential transmission of Ehrlichia during tick bites is the main reason why doxycycline is now the first choice in treating tick bites and early Lyme, before serologies can become positive. When present alone or co-infecting with B. burgdorferi, persistent leukopenia is an important clue. Thrombocytopenia and elevated liver enzymes are less common, but likewise should not be ignored. Headaches, myalgias, and ongoing fatigue seem to relate to this illness, but are extremely difficult to separate from symptoms caused by Bb.

Toward the end of the 19th century, scientists began to understand the important potential for ticks to act as transmitters of disease. In the last decades of the 20th century, several tick-borne diseases have been recognized in the United States, including babesiosis, Lyme disease, and ehrlichiosis.

Ehrlichiosis is caused by several bacterial species in the genus Ehrlichia (pronounced err-lick-ee-uh) which have been recognized since 1935. Over several decades, veterinary pathogens that caused disease in dogs, cattle, sheep, goats, and horses were identified. Currently, three species of Ehrlichia in the United States and one in Japan are known to cause disease in humans; others could be recognized in the future as methods of detection improve.

In 1953, the first ehrlichial pathogen of humans was identified in Japan. Sennetsu fever, caused by Ehrlichia sennetsu, is characterized by fever and swollen lymph nodes. The disease is very rare outside the Far East and Southeast Asia, and most cases have been reported from western Japan.

In the United States, human diseases caused by Ehrlichia species have been recognized since the mid-1980s. The ehrlichioses represent a group of clinically similar, yet epidemiologically and etiologically distinct, diseases caused by Ehrlichia chaffeensis, E. ewingii, and a bacterium extremely similar or identical to E. phagocytophila. The remainder of the information on this web page will focus on the types of ehrlichiosis that occur in the United States.

Human ehrlichiosis due to Ehrlichia chaffeensis was first described in 1987. The disease occurs primarily in the southeastern and south central regions of the country and is primarily transmitted by the lone star tick, Amblyomma americanum.

Human granulocytic ehrlichiosis (HGE) represents the second recognized ehrlichial infection of humans in the United States, and was first described in 1994. The name for the species that causes HGE has not been formally proposed, but this species is closely related or identical to the veterinary pathogens Ehrlichia equi and Ehrlichia phagocytophila. HGE is transmitted by the blacklegged tick (Ixodes scapularis) and the western blacklegged tick (Ixodes pacificus) in the United States.

Ehrlichia ewingii is the most recently recognized human pathogen. Disease caused by E. ewingii has been limited to a few patients in Missouri, Oklahoma, and Tennessee, most of whom have had underlying immunosuppression. The full extent of the geographic range of this species, its vectors, and its role in human disease is currently under investigation.


Testing is problematic with Ehrlichia, similar to the situation with Babesiosis. More species are known to be present in ticks than can be tested for with clinically available serologies and PCRs. In addition, serologies and PCRs are of unknown sensitivity and specificity. Standard blood smears for direct visualization of organisms in leukocytes are of low yield. Enhanced smears using buffy coats significantly raises sensitivity and will indicate a wider variety of species. Despite this, infection can be missed, so clinical diagnosis remains the primary diagnostic tool. Again, consider this diagnosis in a Lyme Borreliosis (LB) patient not responding well to therapy.


Standard treatment consists of Doxycycline, 200 mg daily for two to four weeks. Higher doses, parenteral therapy, and longer treatment durations may be needed based on the duration and severity of illness, and whether immune defects or extreme age is present. However, there are reports of treatment failure even when higher doses and long duration treatment with doxycycline is given. In such cases, consideration may be given for adding rifampin, 600 mg daily, to the regimen.


Bartonella henselae, the agent of cat scratch disease, has been found in Ixodid ticks and as a co-infection in patients with Lyme Disease. Symptoms of Bartonella are almost impossible to distinguish from Lyme, but may include lymphadenopathy, splenomegaly, hepatomegaly, headache, encephalopathy, somnolence, flu-like malaise, weight loss, sore throat, osteolysis, osteomyelitis, bacillary angiomatosis, and a papular or angiomatous rash. In acute cases, there can be hemolysis with anemia, high fever, weakened immune response, jaundice, abnormal liver enzymes, and myalgias. Endocarditis and myocarditis have been reported. More severe infections are associated with immune deficiency and possibly occurrence of opportunistic infections. As in Lyme Disease and Babesiosis, Bartonella may be transmitted to the fetus in the infected pregnant patient.

Diagnostic tests include serology, blood and CSF PCR, and biopsy of skin lesions and lymph nodes.

In the co-infected Lyme patient, eradication may be difficult. Many antibiotic agents have been reported to be effective, including cephalosporins, fluoroquinolones, erythromycins, gentamicin, rifampin and streptomycin. In practice, these patients seem to do best with a combination regimen that utilizes agents that can penetrate cells. Typical combinations include an erythromycin, plus a fluoroquinolone or rifampin.

Treatment progress is most commonly assessed by PCR post treatment and serial titers.


Tularemia is an infectious disease caused by a hardy bacterium, Francisella tularensis, found in animals (especially rodents, rabbits, and hares).

People can get tularemia many different ways, such as through the bite of an infected insect or other arthropod (usually a tick or deerfly), handling infected animal carcasses, eating or drinking contaminated food or water, or breathing in F. tularensis.

Symptoms of tularemia could include sudden fever, chills, headaches, muscle aches, joint pain, dry cough, progressive weakness, and pneumonia. Persons with pneumonia can develop chest pain and bloody spit and can have trouble breathing or can sometimes stop breathing. Other symptoms of tularemia depend on how a person was exposed to the tularemia bacteria. These symptoms can include ulcers on the skin or mouth, swollen and painful lymph glands, swollen and painful eyes, and a sore throat. Symptoms usually appear 3 to 5 days after exposure to the bacteria, but can take as long as 14 days.

Tularemia is not known to be spread from person to person, so people who have tularemia do not need to be isolated. People who have been exposed to F. tularensis should be treated as soon as possible. The disease can be fatal if it is not treated with the appropriate antibiotics.


Tick paralysis (tick toxicosis) -- one of the eight most common tickborne diseases in the United States (1) -- is an acute, ascending, flaccid motor paralysis that can be confused with Guillain-Barre syndrome, botulism, and myasthenia gravis. This report summarizes the results of the investigation of a case of tick paralysis in Washington.

On April 10, 1995, a 2-year-old girl who resided in Asotin County, Washington, was taken to the emergency department of a regional hospital because of a 2-day history of unsteady gait, difficulty standing, and reluctance to walk. Other than a recent history of cough, she had been healthy and had not been injured. On physical examination, she was afebrile, alert, and active but could stand only briefly before requiring assistance. Cranial nerve function was intact. However, she exhibited marked extremity and mild truncal ataxia, and deep tendon reflexes were absent. She was admitted with a tentative diagnosis of either Guillain-Barre syndrome or postinfectious polyradiculopathy.

Within several hours of hospitalization, she had onset of drooling and tachypnea. A nurse incidentally detected an engorged tick on the girl's hairline by an ear and removed the tick. Within 7 hours after tick removal, tachypnea subsided and reflexes were present but diminished. The patient recovered fully and was discharged on April 11. The tick species was not identified.

Editorial Note: Tick paralysis occurs worldwide and is caused by the introduction of a neurotoxin elaborated into humans during attachment of and feeding by the female of several tick species. In North America, tick paralysis occurs most commonly in the Rocky Mountain and northwestern regions of the United States and in western Canada. Most cases have been reported among girls aged less than 10 years during April-June, when nymphs and mature wood ticks are most prevalent (2). Although tick paralysis is a reportable disease in Washington, surveillance is passive, and only 10 cases were reported during 1987-1995.

In the United States, this disease is associated with Dermacentor andersoni (Rocky Mountain wood tick), D. variabilis (American dog tick), Amblyomma americanum (Lone Star tick), A. maculatum, Ixodes scapularis (black-legged tick), and I. pacificus (western black-legged tick) (3,4). Onset of symptoms usually occurs after a tick has fed for several days. The pathogenesis of tick paralysis has not been fully elucidated, and pathologic and clinical effects vary depending on the tick species (4). However, motor neurons probably are affected by the toxin, which diminishes release of acetylcholine (5). In addition, experimental studies indicate that the toxin may produce a substantial decrease in maximal motor-nerve conduction velocities while simultaneously increasing the stimulating current potential necessary to elicit a response (5).

If unrecognized, tick paralysis can progress to respiratory failure and may be fatal in approximately 10% of cases (6). Prompt removal of the feeding tick usually is followed by complete recovery. Ticks can be attached to the scalp or neck and concealed by hair and can be removed using forceps or tweezers to grasp the tick as closely as possible to the point of attachment (7). Removal requires the application of even pressure to avoid breaking off the body and leaving the mouth parts imbedded in the host. Gloves should be worn if a tick must be removed by hand; hands should be promptly washed with soap and hot water after removal of a tick.

The risk for tick paralysis may be greatest for children in rural areas, especially in the Northwest, during the spring and may be reduced by the use of repellants on skin and permethrin-containing acaricides on clothing. Paralysis can be prevented by careful examination of potentially exposed persons for ticks and prompt removal of ticks. Health-care providers should consider tick paralysis in persons who reside or have recently visited tick-endemic areas during the spring or early summer and who present with symmetrical paralysis.

This page was last updated on July 3, 2012