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Summer of the tick.

Summer is upon us. The shining sun, singing birds, blue skies, and warm weather are luring people outside; however, in certain parts of the country, predominantly the Mid Atlantic to the Northeast and upper Midwest, ticks are also part of that beautiful outdoors. Of particular concern is the deer tick (Ixodes scapularis), which is host to at least five potentially dangerous pathogens including Borrelia burgdorferi, Babesia microti, Anaplasma phagocytophilium, Borrelia miyamotoi, and Deer Tick Virus.

The deer tick has a multi-year life cycle. Larvae hatch from eggs every August and may be infected with Deer Tick Virus and Borrelia miyamotoi. They then seek out a blood meal, most often from a white-footed mouse, through which they may acquire the organisms of Babesia microti, Anaplasma phagocytophilia, Borrelia burgdorferei, or Deer Tick Virus. The larvae molt and emerge as nymphs in the spring. The nymph is the main vector of these diseases in humans. After a blood meal, the nymphs then molt to adults. The adult female deer tick needs yet another blood meal, from a white-tailed deer, to successfully produce eggs. And so the cycle continues.

Surge in Disease

The reason why we are seeing a growing incidence of tick-borne diseases is complex while at the same time simply a reflection of the changes in our land use, along with the reemergence of the deer tick and return of the white-tailed deer. Deer ticks have always been around, albeit in fewer numbers due to the lack of adequate habitat and smaller population of white-tailed deer (critical hosts for female deer tick reproduction).

During the 20th century, the previously deforested landscape was allowed to regrow, with pastures disappearing and brush giving way to forests. These changes enabled the white-tailed deer population to rebound as they found more food sources and adequate cover. In the Northeast, deer populations went from the hundreds to the hundreds of thousands, paving the way for exponential expansion of the tick population as the flora and fauna proved to be a sustaining habitat for these arachnids. Consequently, the stage was set to see the increased diagnosis of tick-borne diseases. From the late 1960s through 2011, these diseases were recognized, pathogens identified, and treatment protocols developed.


The Pathogens

Borrelia burgdorferi is the bacterium which causes the most common of the tickborne diseases, Lyme borreliosis or Lyme disease. This has often been portrayed by the media as the "Fifth Horseman of the Apocalypse" but when recognized and treated early, Lyme disease is easily cured. Long-term untreated patients may experience complications but the spirochete can be eradicated.

Lyme disease most often presents as an expanding rash, the infamous "bull's-eye," which can appear within several days to weeks at the site of the bite. In my experience, the rash is often not typical. It can be oval with no central clearing and, when appearing in the popliteal space, may be present as cellulitis. The rash is most often on the back, axilla, or flanks-places not easily checked. Rarely, with blood stream dissemination, multiple rashes may appear. I've seen up to 40 of these scattered over the patient. And, in some cases, rashes may not appear at all. In fact, in 20 percent of Lyme patients there are no rashes.

The first stage of Lyme disease is often accompanied by flu-like symptoms. Fever, headache, chills, and myalgia are common. A patient with cough, coryza, or gastrointestinal symptoms does not have Lyme disease. The second stage may present with cardiac arrhythmias, heart block, facial palsy, and occasionally, meningitis. Late stage disease may present as arthritis, with migratory joint swelling and pain. Most often this involves large joints, particularly the knee, and is usually unilateral. In about five percent of patients, chronic neurological symptoms may appear with polyneuropathy and rarely an encephalopathy with subtle cognitive disturbances in concentration and memory.

The testing for Lyme disease has been the source of much confusion and misunderstanding. The most common testing is antibody based. The problem is the window needed to develop antibodies may be as long as four to six weeks. Therefore, testing too soon may give a false negative result. A positive test may also remain positive for months to years after appropriate and successful treatment. This is the main issue with Lyme testing and it is often difficult to convey these nuances to patients. Polymerase chain reaction (PCR) tests can be used but are only useful in the brief bacteremia phase of the infection. Current testing is accurate when used in the appropriate clinical situation, but research is underway to develop alternative tests.

The treatment of Lyme disease in all stages is straightforward. The effective medications are oral Amoxicillin, Doxycycline, Ceftin, and intravenous Ceftriaxone. The length of treatment is usually three to four weeks. This may be repeated but there is no evidence that prolonged treatment is beneficial. Also, long-term treatment often obscures the true nature of the patient's complaints and delays effective therapy for non-Lyme disease conditions. For example, an alternative explanation for a patient's symptoms is a malfunction of the immune system perhaps triggered by Lyme disease.

Babesia microti is a plasmodium that infects red blood cells, leading to hemolysis. It typically presents as high fevers with bed shaking chills and night sweats. In the laboratory, there is typically anemia, mild leukopenia, and thrombocytopenia. In addition, the intraerythrocytic ring forms may be seen on a thick blood smear. PCR and antibody testing is available when the smear is negative for organisms.

Primary treatment is Atovaquone and Zithromax given for seven days. Occasionally, exchange transfusions have been used when there is a high parasitemia and hemolysis. Patients with certain malignancies such as B-cell lymphomas and chronic lymphocytic leukemia may require prolonged treatment to clear the organisms.

Anaplasmosis, a disease caused by the bacterium Anaplasma phagocytophilium, presents one to two weeks after the bite of an infected tick. There is no rash and patients usually complain of fever, headache, myalgia, chills, and malaise. A blood smear may show morulae in white blood cells. A low platelet count and leukopenia with elevated liver enzymes are suggestive of the diagnosis. Early PCR testing can be helpful, and later antibody testing will help confirm the diagnosis. (A positive antibody test may remain positive for months to years after successful treatment.) Anaplasmosis is treated with Doxycycline and rapid improvement in fever and symptoms occur within 24 to 72 hours. If a patient does not improve, the diagnosis should be questioned.

Borrelia miyamotoi is a bacterium initially described in a 2011 Russian report as a human pathogen. It has subsequently been recognized in many countries including the U.S. In contrast to the other mentioned diseases, the larval deer tick as well as the nymph can transmit Miyamotoi. This probably accounts for the later peak of cases in the summer. It occurs as frequently as Anaplasmosis, with which it has been confused.

The presentation is with fever, muscle aches, and severe headache. In fact, the headache is a prominent complaint compared to Anaplasmosis and Lyme, and the patients appear sicker. There is no rash associated with this disease. Laboratory results show leukopenia thrombocytopenia and transaminase elevations similar to Anaplasmosis. PCR testing and serology can confirm infection.

The treatment of a Borrelia miyamotoi infection is the same as Lyme disease using Amoxicillin, Doxycycline, or Ceftriaxone; however, symptomatic improvement of the patient is slower compared to the response in Anaplasma infection.

The final agent is Deer Tick Virus. This virus is very closely related to the agent of Powassan encephalitis. This virus may be transmitted within 15 minutes of the bite of an infected tick. There is no treatment at this time for this disease and there have been relatively few cases. Patients typically present with fever, headache, weakness, and lethargy. The reported mortality rate has been between 20 to 40 percent.

Prevention is the Key

Although prevention should be a major weapon in controlling these diseases, surveys reveal that people attempt protective measure less than

50 percent of the time. Simple tick checks can significantly reduce the likelihood of transmission. The deer tick requires 24 to 30 hours of attachment to the host to transmit the mentioned diseases (except for the Deer Tick Virus which transmits within minutes). Doing thorough body checks to remove ticks after being outdoors is cheap and effective. Other preventive measures include avoiding high-risk areas, using tick sprays, tucking pants into socks, wearing light-colored clothes so you can easily spot ticks, and using repellants and permethrin-impregnated clothing. Also, removing leaf Utter and cutting back brushy areas will help control tick populations. Deer ticks desiccate easily and require areas that are shaded and moist to survive.

Finally, control of the white-tailed deer population is crucial to reducing tick numbers. Each deer may play host to several hundred ticks, with each female tick laying up to 2,000 eggs.

The treatments of these diseases are generally successful but the final answer to this problem is a comprehensive approach to prevention involving public education, land use, and deer control.

By Timothy J. Lepore, MD, FACS

Dr. Lepore spoke on tick-borne diseases at the AMAA's 44th Annual Sports Medicine Symposium at the Boston Marathon. He is Medical Director and Chief of Surgery for the Nantucket Cottage Hospital, Nantucket, Massachusetts, and is regularly referred to as Nantucket's surgeon, medical examiner, school physician, Lyme disease expert, and occasionally "Dr. Doolittle."
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Title Annotation:deer tick
Author:Lepore, Timothy J.
Publication:AMAA Journal
Date:Jun 22, 2015
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