Lyme Disease ( Borrelia burgdorferi)

This page will provide links and data related to Lyme Disease and Borrelia burgdorferi in Wisconsin. Lyme Disease is a “reportable” infectious disease. In 2012, there were nearly 2000 cases of Lyme Disease reported to state and federal public health agencies.  Case rreports were lower in 2012 because of a change in surveillance policy.  Since many Wisconsin cases go unreported, this is an underestimate of the actual incidence of this illness.  A recent evaluation of surveillance reports and disease incidence by CDC implies that there may actually be 20-30,000+ cases of Lyme Disease in Wisconsin each year.

Lyme cases 2012

Figure 1.  Graph showing increase in reported confirmed (and probable) cases of Lyme Disease in Wisconsin since 1990.  Figure courtesy of the Wisconsin State Department of Health Services.  Additional maps and the most recent data can be found at http://www.dhs.wisconsin.gov/communicable/tickborne/Lyme/dataandstatistics.htm

Nymph rates by county

Figure 2.  Infection rates in questing nymphal blacklegged (=deer) ticks in Wisconsin.  Statewide, an average of 22% of nymphs are infected.  The numbers represent the number of ticks testing positive over the total number of ticks tested for each site. There is significant variation from year to year at the same site which may reflect environmental conditions or relatively small samples of nymphs.  Approximately twice as many adults will be infected (roughly 44% of adults in Wisconsin).

Data from Northern Wisconsin is based upon work supported by the National Science Foundation under grant NSF 1216200.

Any opinions, findings or conclusions and recommendations expressed in this material are those of the author and do not reflect the views of the National Science Foundation.

What is Lyme disease and how is it transmitted?

Lyme disease or Lyme borreliosis is caused by the bacteria Borrelia burgdorferi  (CDC, 2011).   Transmission of Lyme disease is known to occur via two species of blacklegged ticks, Ixodes scapularis in the northeastern and upper midwestern states, and Ixodes pacificus in the western United States (CDC, 2011). These two tick species are considered competent vectors of Lyme disease. A “competent vector” refers to the ability of a tick to acquire a disease organism such as a bacteria or virus from an infected vertebrate host and then transmit it to a susceptible vertebrate animal (e.g. a human or domestic dog) during a subsequent blood meal. Some species of ticks can acquire the pathogens during feeding but cannot transmit them as the pathogens are unable to survive within or invade the salivary glands of the tick.  As far as scientists know, the wood tick Dermacentor variabilis, is unable to transmit Borrelia burgdorferi, although it can pick up the pathogen during feeding.

In general, a blacklegged (deer) tick must be attached for 36-48 hours before Borrelia burgdorferi can be transmitted  (Piesman et al. 1987; des Vignes et al. 2001). [PLEASE NOTE:  this is not the case for other pathogens transmitted by blacklegged (deer) ticks including Powassan or deer tick virus,  Anaplasma phagocytophilum and Borrelia miyamotoi. These pathogens may be transmitted earlier.]  Why does it take so long?  The answer lies in the biology of the interaction between tick and bacteria.  A tick first picks up the spirochete during a feeding in a prior stage.  The  bacteria stays in the tick’s gut, even while the tick molts to the next stage (nymph or adult).  When that nymph or adult attaches to a new host, B. burgforferi bacterial organisms have to multiply, then cross the wall of the tick’s gut and gain entry  into the circulatory system, and finally move from the circulatory system into the tick’s salivary glands.  From there, they can infect the host when transported along with the tick’s saliva (de Silva and Fikrig 1995).   The whole process takes quite a bit of time, which means that early removal of ticks is a good defensive move.

Currently there is no evidence to support natural person-to-person transmission of Lyme disease (such as by touching, kissing or sexual transmission) (CDC, 2011; Porcella and Schwam, 2001; Woodram and Oliver, 1999; Schmid 1989). No cases of Lyme disease have been associated with receiving  blood products, although B. burgdorferi bacterial organisms have been shown to survive in blood stored for donation purposes (CDC, 2011).

Although domestic animals such as dogs and horses can acquire Lyme disease, there is no evidence they are able to spread the disease directly to humans (Appel et al. 1993). However,  domestic animals may carry infected ticks into the home or yard which may then move to humans.  This may increase the risk of infection with Lyme disease or other tick-borne diseases (CDC, 2011).

Where is Lyme Disease found in Wisconsin? 

The geographic distribution of Lyme Disease has been spreading along with the increase in case numbers.

Lyme map resizedFigure 2.  Map of incidence of Lyme Disease.  This map reflects the county of residence of each sick person, rather than the county where exposure to the infected tick occurred. The map reflects case reports from each county to the State Department of Health Services.  Figure courtesy of the Wisconsin State Department of Health Services. Additional data and maps can be found at http://www.dhs.wisconsin.gov/communicable/tickborne

General information about the incidence of Lyme disease in the United States and Wisconsin. 

In the United States, Lyme disease has been a nationally notifiable condition to the Centers for Disease Control and Prevention (CDC) since 1991 and was the 5th most common nationally notifiable disease in 2009 (CDC, 2011). Nationally notifiable or reportable diseases are considered to be of great public health importance. Local, state, and national agencies (for example, county and state health departments and the U.S. Centers for Disease Control and Prevention) require that these diseases be reported when they are diagnosed by doctors or laboratories. Reporting allows for the collection of statistics that show how often the disease occurs and this helps researchers identify disease trends and track disease outbreaks as well as  help control future outbreaks.

 In Wisconsin, the number of confirmed cases has increased from 329 in 1991, to 2376 confirmed cases in 2011 since the disease became nationally reportable (Hoang Johnson, 2010).   According to the CDC, in 2010, 94% of human Lyme disease cases were reported from 12 states (CT, DE, ME, MD, MA, MN, NJ, NH, NY, PA, VA, WI).  In Wisconsin, the statewide average incidence of Lyme disease has more than tripled in the past 19 years from an average of 8.0 confirmed cases per 100,000 population from 1991-1995 to 41.8 confirmed cases per 100,000 in 2011 (WI DHS, 2012). The rate for both confirmed and probable cases in 2011 was 61.8 cases per 100,000 population. (WI-DHS 2012).

The five Wisconsin counties with the highest incidence of confirmed cases (per 100,000 population) of Lyme disease in 2011 were: Marquette (396.0), Menominee (236.3), Price (211.9), Barron (207.1) and Sawyer (199.3). 

To see your specific county please follow the link provided to the  Wisconsin Department of Health Services webpage with more detailed statistics on Lyme Disease 2011 Cases by County. http://www.dhs.wisconsin.gov/communicable/Tickborne/Lyme/2011WICoCount.htm

Are some groups at higher risk? Yes, Lyme disease is most commonly reported in boys 5-9 years of age (8.6 cases per 100,000 population) and adults 55-69 years of age (7.8 cases per 100,000 population)  (see graph below) (CDC, 2011; Bacon et al., 2008). The lowest rates are generally seen among young adults 20–24 years of age (3.0 cases per 100,000 population). Male patients typically account for slightly over half of reported cases nationally (53.1%) (Bacon et al., 2008).  Incidence rates with regards to age and sex in Wisconsin also follow the national trends (WI-DHS, 2012). 

Figure 3.  Rate of Confirmed Lyme disease reported by Age Group in Wisconsin, 2010
Source: Wisconsin Department of Health Services

What are the Clinical Signs and Symptoms of Lyme disease? 

In humans, Lyme disease is considered to occur in three possible stages or scenarios depending on when it is diagnosed and treatment is initiated. 

The first stage is called the early or localized stage which occurs anywhere from around 3-30 days after the tick-bite. Common clinical signs and symptoms which may be noted during this early stage may include:

-The red, expanding “bulls-eye” or erythema migrans (EM) rash at the site of the tick bite. The rash may appear on any area of the body and does not always take on the typical bulls-eye form.

- Fever, chills, muscle and joint aches, tiredness, headache and swollen lymph nodes.

The second stage is called the early, disseminated stage which occurs anywhere from days to weeks after the tick-bite. If the infection with Lyme disease is left untreated or unnoticed, the Lyme bacteria may spread from the site of the bite to other parts of the body. Clinical signs and symptoms which may be noted during the early, disseminated stage may include:

- Additional bulls-eye or EM rashes in other areas of the body

- Loss of muscle tone on one or both sides of the face (Facial or Bell’s Palsy)

- Severe headaches or stiffness of the neck due to inflammation of the spinal cord (meningitis)

- Pain and swelling of large joints (such as knees or elbows)

- Dizziness or heart palpitations (due to changes in heartbeat)

Many of these symptoms may lessen or go away after several weeks to months, even without antibiotic treatment (Steere et al. 2004). Lack of a proper diagnosis and treatment may lead to additional complications described in the third stage, also known as, the late, disseminated stage, described below. 

The third stage is called the late, disseminated stage and may occur anywhere from months to years after the initial tick-bite. 

Patients with untreated Lyme disease in the late, disseminated stage may have intermittent or waxing and waning bouts of arthritis with severe swelling and joint pain, especially in the large joints such as the knees or elbows. With late stage Lyme disease, up to 60% of untreated patients may experience intermittent attacks of arthritis (Stafford, 2004) and up to 5% of untreated patients may develop chronic neurological complaints months to years after infection (CDC, 2011). Approximately 10-20% of patients experience symptoms that last months to years after antibiotic treatment often called post-treatment Lyme disease syndrome (PTLDS) or chronic Lyme disease. Symptoms include chronic fatigue, arthralgias, myalgias, neurological and cognitive defects and sleep disturbances (Marques, 2008).

How is Lyme Disease Diagnosed?

If you think you may have Lyme disease or may have been exposed to the tick vector please contact your physician or medical provider. Diagnosis of Lyme disease is based on a thorough medical history, possible exposure to established high-risk areas for Lyme disease where you live or spend time outdoors, tick-infested habitat and/or the tick vector and physician observed clinical signs and symptoms as well as accompanying diagnostic laboratory methods to support the diagnosis. 

Laboratory Detection: 

Laboratory methods for the detection of B. burgdorferi infection or past exposure to the bacteria include methods which have been adequately validated and published in peer-reviewed literature (CDC, 2011). Current recommendations for testing blood for evidence of antibodies against Lyme disease include a two-step or “two-tier” process. Both of these steps can be done using the same blood sample.

Caution regarding testing for Lyme disease: Some commercial laboratories that conduct testing for Lyme disease use assays whose accuracy and clinical usefulness have not been adequately established. In the United States, the Food & Drug Administration has authorized 70 serologic assays (to detect antibodies produced against the Lyme disease bacteria) to aid in the diagnosis of Lyme disease. 

http://www.cdc.gov/lyme/diagnosistreatment/LabTest/OtherLab/

A list of unvalidated tests available as of 2011 include:

  • Capture assays for antigens in urine
  • Culture, immunofluorescence staining, or cell sorting of cell wall-deficient or cystic forms of B. burgdorferi
  • Lymphocyte transformation tests
  • Quantitative CD57 lymphocyte assays
  • “Reverse Western blots”
  • In-house criteria for interpretation of immunoblots
  • Measurements of antibodies in joint fluid (synovial fluid)
  • IgM or IgG tests without a previous ELISA/EIA/IFA 

Methods for laboratory detection of B. burgdorferi include the direct detection of the organism including polymerase chain reaction (PCR), microscope-based assays or culturing of the Lyme disease bacterial organism and indirect methods for detection of a host immune response to the organisms or production of antibodies (Aguero-Rosenfeld et al., 2005). 

Direct detection (looking for the Lyme disease bacteria) is only reliable during early stages of the disease before antibiotic treatment has been initiated and therefore it may be more difficult to confirm illness in unusual clinical presentations–such as those without the “bulls-eye” rash (Aguero-Rosenfeld et al., 2005). Due to current limitations in direct detection of B. burgdorferi in clinical specimens, antibody detection methods have been the main laboratory method used to support a clinical diagnosis of human Lyme disease (Aguero-Rosenfeld et al., 2005). Positive results of recommended two-tiered serologic testing (EIA followed by Western blot) help provide confirmation of infection in patients with musculoskeletal, neurologic or cardiac symptoms (CDC, 1995).  Laboratory methods are not required to confirm diagnosis for Lyme disease case reporting and surveillance purposes in patients with a recent onset of the characteristic bulls-eye or erythema migrans (EM) rash (Bacon et al., 2008).

For Lyme disease case definition and surveillance purposes an algorithm or “map” was created by the Wisconsin Division of Public Health in order to help medical providers and public health officials in the clinical diagnosis and Lyme disease surveillance case definition criteria (WI-DHS, 2011). http://www.dhs.wisconsin.gov/communicable/Tickborne/Lyme/PDFfiles/Algorithm2011.pdf

How is Lyme Disease Treated? 

People who are diagnosed with Lyme disease by a physician or medical professional and treated with appropriate antibiotic therapy during the early stages of Lyme disease will most often recover completely (CDC, 2011). Effective oral antibiotics often used during the early stages of infection include doxycycline and amoxicillin for adult patients (Steere et al., 2004). Doxycycline is not recommended for children under 8 years of age or women who are pregnant or breastfeeding (CDC, 2011). Intravenous (IV) antibiotic treatment with drugs such as penicillin or ceftriaxone is recommended for patients with neurologic or cardiac clinical signs or symptoms to prevent development of late, disseminated or persistent Lyme disease (Marques, 2008).

Prophylactic or preventive treatment of tick bites may be used in some cases to prevent the development of EM rash or infection with Lyme disease. This method does not prevent Lyme disease in people who do not recognize they were bitten by a tick (e.g. if the bite occurred in an area on the body not readily visible such as the scalp). As many as 75% of patients with a “bulls-eye” (EM) rash do not notice the tick bite before the rash develops (Hayes & Piesman, 2003).

Prophylactic antibiotic treatment is only recommended when the following circumstances are present (Wormser et al. 2006):

  • The attached tick can be reliably identified as an adult or nymphal I scapularis tick that is estimated to have been attached for longer than 36 hours. This may be determined by the degree of engorgement of the tick with blood or if the individual can reliably recall the time of exposure to the tick or tick-infested areas.
  • Prophylaxis antibiotic treatment can begin 72 hours or earlier from the time that the tick was removed
  • Research and investigative information have reliably shown that the local rate of infection of ticks within the area of exposure with B. burgdorferi is more 20%.  NOTE that this requirement has been met for most areas in Wisconsin.
  • Doxycycline treatment is not contraindicated

 

References:

Aguero-Rosenfeld, ME., Wang, G., Schwartz, I., Wormser, GP. (2005). Diagnosis of Lyme Borreliosis. Clinical Microbiology Reviews, 18, 484-509.

Anderson JF, Magnarelli LA, Stafford KC 3rd. (1990). Bird-feeding ticks transstadially transmit Borrelia burgdorferi that infect Syrian hamsters. J Wildl Dis; 26(1): 1-10. http://www.jwildlifedis.org/content/26/1/1.full.pdf

Appel MJG, Allen S, Jacobson RH, Lauderdale TL, Chang YF, Shin SJ, Thomford JW, Todhunter RJ, Summers BA. (1993). Experimental Lyme disease in dogs produces arthritis and persistent infection. J Infect Dis; 167:651-664.

Bacon, R.M., Kugeler, KJ. Mead,PS. (2008). Surveillance for Lyme disease–United States, 1992-2006. MMWR Surveillance Summary, 57:1–9.

Burgdorfer, W., Barbour, A.G., Hayes, S.F., Benach, J.L., Grunwaldt, E., Davis, J.P. (1982). Lyme disease a tick-borne spirochetosis? Science, 216: (1317-1319).

Caporale DA, Johnson CM, Millard BJ. (2005). Presence of Borrelia burgdorferi(Spirochaetales: Spirochaetaceae) in southern Kettle Moraine State Forest, Wisconsin, and characterization of strain W97F51. J Med Entomol; 42(3): 457-72.http://www.bioone.org/doi/pdf/10.1603/00222585%282005%29042%5B0457%3APOBBSS%5D2.0.CO%3B2
Centers for Disease Control and Prevention (CDC). Lyme disease website. 1600 Clifton Rd. Atlanta, GA 30333, USA http://www.cdc.gov/lyme/ 

CDC. (2007). Lyme disease in the United States 2003-2005. MMWR, 56 (23), 573-596. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5623a1.htm 

CDC. (2004). Lyme disease—United States, 2001–2002. MMWR, 53:365–9. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/ mm5317a4.htm 

CDC. (1995). Recommendations for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR, 44:590–1.

de Silva AM and Fikrig E. Growth and migration of Borrelia burgdorferi in Ixodes ticks during blood feeding. Amer J Trop Med Hyg 1995; 53:397-404.

des Vignes F, Piesman J, Heffernan R, et al. Effect of tick removal on transmission of Borrelia burgdorferi and Ehrlichia phagocytophila by Ixodes scapularis nymphs. J Infect Dis 2001;183(5):773-778.

Duncan AW, Correa MT, Levine JF, Breitschwerdt EB. (2004).The dog as a sentinel for human infection: prevalence of Borrelia burgdorferi C6 antibodies in dogs from southeastern and mid-Atlantic states. Vector Borne Zoonotic Dis; 4:221–9.

Falco RC, Smith HA, Fish D, Mojica BA, Bellinger MA, Harris HL, et al. (1993). The distribution of canine exposure to Borrelia burgdorferi in a Lyme-disease endemic area. Am J Public Health; 83:1305–10. doi:10.2105/AJPH.83.9.1305

Guerra MA, Walker ED, Kitron U. (2001). Canine surveillance system for Lyme borreliosis in Wisconsin and northern Illinois: geographic distribution and risk factor analysis. Am J Trop Med Hyg; 65:546–52.

Hayes, EB. & Piesman, J. (2003). How can we prevent Lyme disease? New England Journal of Medicine, 348:2424-30.

Hoang-Johnson, D. (2010). Tickborne Illness in Wisconsin – Lyme Disease , Tickborne Surveillance in WI. Wisconsin Division of Public Health. http://www.dhs.wisconsin.gov/communicable/resources/pdffiles/Lyme_training071210.pdf

Keirans JE, Hutcheson HJ, Durden LA, Klompen JS. (1996). Ixodes (Ixodes) scapularis (Acari:Ixodidae): redescription of all active stages, distribution, hosts, geographical variation and medical and veterinary importance. J Med Entomol; 33(3): 297-318.

Marques, A. (2008). Chronic Lyme disease: a review. Infect Dis Clin North Am, 22: 341-60.

Mead P, Goel R, Kugeler K. (2011). Canine serology as adjunct to human Lyme disease surveillance. Emerging Infectious Diseases; 17(9): 1710-1712. http://wwwnc.cdc.gov/eid/article/17/9/pdfs/11-0210.pdf

Piesman J, Mather TN, Sinsky RJ, et al. (1987). Duration of tick attachment and Borrelia burgdorferi transmission. J Clin Microbiol; 25:557-558.

Piesman J, Maupin GO, Campos EG, et al. Duration of adult female Ixodes dammini attachment and transmission of Borrelia burgdorferi, with description of a needle aspiration isolation method. J Infect Dis 1991;163(4):895-897.

Porcella SF, Schwan TG, 2001. Borrelia burgdorferi and Treponema pallidum: a comparison of functional genomics, environmental adaptations, and pathogenic mechanisms. J Clin Invest 107: 651-6.

Schmid GP, 1989. Epidemiology and clinical similarities of human spirochetal diseases. Rev Infect Dis 11 Suppl 6: S1460-9.

Stafford, K.C. III. (2004). Tick management handbook: an integrated guide for homeowners, pest control operators, and public health officials for the prevention of tick-associated disease. The Connecticut Agricultural Experiment Station, pp. 1- 60.

Steere AC, Coburn J, Glickstein L. (2004). The emergence of Lyme disease. J. Clin. Invest; 113(8):1093.

Steere, AC., Malawista, SE., Snydman, DR., et al. (1977). Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three Connecticut communities. Arthritis & Rheumatism, 20, 7-17.

Wisconsin Department of Health Services. Lyme disease website. D. Hoang Johnson, Vectorborne Epidemiologist, Wisconsin Division of Public Health. Accessed June 13, 2012. http://www.dhs.wisconsin.gov/communicable/tickborne/lymedisease/index.htm

Woodrum JE, Oliver JH, Jr., 1999. Investigation of venereal, transplacental, and contact transmission of the Lyme disease spirochete, Borrelia burgdorferi, in Syrian hamsters. J Parasitol 85: 426-30.

Wormser GP, Dattwyler RJ, Shapiro ED, Halperin JJ, Steere AC, Klempner MS, et al. (2006). The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis.;43(9):1089-134. 

Webpage content prepared by D. Murphy, June 2012.