-
Educate the public about Lyme disease, especially
regarding the mode of tick transmission and use of personal
protection. Cases of Lyme disease usually occur between April and
November in West Virginia; increased public education should be
targeted for this time frame.
-
Educate providers
and laboratories to report cases of Lyme disease to the local health
department in the patient’s county of residence within one week of
diagnosis.
-
Educate
providers about appropriate diagnosis of, and testing for Lyme disease:
-
Laboratory
confirmation of Lyme disease requires:
-
Demonstration
of diagnostic immunoglobulin M (IgM) or immunoglobulin G (IgG)
antibodies to Borrelia burgdorferi in serum or
cerebrospinal fluid (CSF) using a sensitive enzyme immunoassay (EIA)
or immunofluorescence antibody (IFA) assay, with
-
Western
immunoblot confirmation.
-
Conduct
an appropriate investigation as follows:
-
If case
presented with EM, interview patient to determine where the patient
was during the month prior to onset of EM to identify the location
of the likely exposure. If
no EM is present identify and document any late manifestations of
Lyme disease that the patient is experiencing.
-
Complete a
yellow card, a CDC Lyme Disease Case Report Form (may be filled out
by diagnosing physicians office) and attach copies of all
appropriate laboratory reports (diagnostic total antibody with
confirmatory western immunoblot) and send to IDEP.
-
Educate the
person about personal protection and potential for re-infection in
those treated with antibiotics for early disease (i.e.; persons who
do not mount an antibody response).
Prevent
cases of Lyme disease by educating public about prevention measures that
can be effective in reducing exposure to infected ticks.
-
Reduce
disease risk through public education by encouraging use of personal
protective measures.
-
Increase number of patients successfully
treated with antibiotics in the early stages of Lyme disease to reduce
number of patients with disseminated and late disease.
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To understand the demographic characteristic
of persons with Lyme disease.
-
To identify Lyme endemic areas and the tick
species involved in transmission.
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To
identify risk factors for infection with Lyme disease.
Lyme disease is transmitted to
humans by the bite of infected deer ticks and cause more than 16,000
infections in USA each year.
In the USA, endemic foci of Lyme
disease exist along the Atlantic coast and are concentrated between
Massachusetts and Maryland; in the upper midwest, an expanding focus is
currently concentrated in Wisconsin and Minnesota; and in some areas of
California and Oregon. Lyme disease continues to increase nationally as
well as in West Virginia.
Initial
infection occurs primarily during summer, with peak in June and July, but
may occur throughout the year, depending on the seasonal abundance of the
tick in different geographic areas. The distribution of the majority of
cases coincides with the distribution of Ixodes scapularis (formerly
called I. dammini) ticks in the eastern and midwestern USA. The
explosive repopulation of white-tailed deer in the eastern USA has been
linked to the spread of Lyme disease in this region.
Lyme disease spirochetes
disseminate from the site of the tick bite by cutaneous lymphatic and
blood-borne routes. If left untreated a secondary EM lesion may present as
well as neurological, muscluoskeletal and cardiac manifestations that may
last for years.
This tickborne,
spirochetal, zoonotic disease is characterized by a distinctive skin
lesion, systemic symptoms and neurologic, rheumatologic and cardiac
involvement that occur in varying combinations over a period of months to
years. The early symptoms are intermittent and changing. The illness
typically begins in the summer, and the first manifestation in about 90%
of patients appears as a red macule or papule that expands slowly in an
annular manner, often with central clearing.
This distinctive skin lesion is called “erythema migrans”. EM
may be single or multiple. To
be considered significant for case surveillance purposes, the EM lesion
must be physician diagnosed and measure at least 5 cm in diameter. With or
without EM, early systemic manifestations of Lyme disease may include
malaise, fatigue, fever, headache, stiff neck, myalgia, migratory,
arthralgias and/or lymphadenopathy, all of which may last several weeks or
more in untreated patients. Patients with acute Lyme disease almost
always have objective signs of infection (e.g., EM, facial nerve palsy,
arthritis). Nonspecific symptoms commonly accompany these specific signs
but are almost never the only evidence of Lyme disease.
Within weeks to months after onset of the EM lesion,
neurologic abnormalities such as aseptic meningitis and cranial
neuritis–incloneuritis, myeuding facial palsy, cerebellar ataxia, motor
or sensory radicullitis and encephalitis–may develop; symptoms
fluctuate, may last for months and may become chronic. Cardiac
abnormalities (including atrio-ventricular block and rarely, acute
myopericarditis or cardiomegaly) may occur within a few weeks after onset
of EM. Weeks to years after onset (mean, 6 months), intermittent episodes
of swelling and pain in large joints, especially the knees, may develop
and recur for several years; chronic arthritis may occasionally result.
Similarly, sometimes following long periods of latent infection, chronic
neurologic manifestations may develop and include encephalopathy,
polyneuropathy or leukoencephalitis; the CSF often shows lymphocytic
pleocytosis and elavated protein levels, while the electromyogram is
usually abnormal.
The causative
spirochete of North American Lyme disease, Borrelia burgdorferi, was
identified in 1982.
Certain ixodid ticks
through transstadial transmission. Wild rodents, especially Peromyscus spp.
in the northeastern and midwestern USA and Neotoma spp. in the
western USA maintain the enzootic transmission cycle. Deer serve as
important maintenance mammalian hosts for vector tick species. Larval and
nymphal ticks feed on small mammals, and adult ticks feed primarily on
deer. The majority of Lyme disease cases result from bites by infected
nymphs.
Tickborne: In
experimental animals, transmission by I. scapularis and I.
pacificus usually does not occur until the tick has been attached for
24 hours or more: this may also be true in humans.
For EM, from 3 to 32 days (mean 7 to 10 days) after
tick exposure; however, the early stages of the illness may be inapparent,
and the patient may present with later manifestations.
No evidence of natural transmission from person to
person. There are rare case reports of congenital transmission, but
epidemiologic studies have not shown a link between maternal Lyme disease
and adverse outcomes of pregnancy.
In hyperendemic areas, particular attention should
be paid to identification of the tick species involved and areas infested,
and to recommendations for avoiding tick infested areas and taking
precautions if unable to avoid these areas.
Clinical Description
A systemic, tickborne disease with protean manifestations, including
dermatologic, rheumatologic, neurologic, and cardiac abnormalities. The
best clinical marker for the disease is the initial skin lesion (i.e.,
erythema migrans (EM) that occurs in 60%–80% of patients.
Laboratory Criteria for Diagnosis
-
Isolation of Borrelia burgdorferi from
a clinical specimen; or
-
Demonstration of diagnostic immunoglobulin M
(IgM) or immunoglobulin G (IgG) antibodies to B. burgdorferi in
serum or cerebrospinal fluid (CSF). Requires a two-test approach using
a sensitive enzyme immunoassay (EIA) or immunofluorescence antibody (IFA)
test followed by Western immunoblot confirmation.
Case classification
Confirmed:
-
A case with physician diagnosed EM measuring
at least 5 cm; or
-
A case with at least one late manifestation
(as defined below in comments section) that is laboratory confirmed
(diagnostic total antibody with confirmatory Western immunoblot).
Comment:
This surveillance case definition was developed for national reporting
of Lyme disease; it is not intended to be used in clinical diagnosis.
Definition of terms used in the clinical description and case
definition:
-
Erythema migrans: For
purposes of surveillance, EM is defined as a skin lesion that
typically begins as a red macule or papule and expands over a period
of days to weeks to form a large round lesion, often with partial
clearing. A single primary lesion must reach >5 cm in size.
Secondary lesions also may occur. (Annular erythematous lesions
occurring within several hours of a tick bite represent
hypersensitivity reactions and do not qualify as EM). For most
patients, the expanding EM lesion is accompanied by other acute
symptoms, particularly fatigue, headache, mildly stiff neck,
arthralgia, or myalgia. These symptoms are typically intermittent. A
physician must make the diagnosis of EM. Laboratory confirmation
is recommended for person with no known exposure.
-
Late manifestations: Late
manifestations include any of the following when an alternate
explanation is not found:
-
Musculoskeletal system: Recurrent,
brief attacks (weeks or months) of objective joint swelling in one
or a few joints, sometimes followed by chronic arthritis in one or a
few joints. Manifestations not considered as criteria for diagnosis
include chronic progressive arthritis not preceded by brief attacks
and chronic symmetrical polyarthritis. Additionally, arthralgia,
myalgia, or fibromyalgia syndromes alone are not criteria for
musculoskeletal involvement.
-
Nervous system: Any of
the following, alone or in combination: lymphocytic meningitis;
cranial neuritis, particularly facial palsy (may be bilateral);
radiculoneuropathy, or, rarely, encephalomyelitis. Encephalomyelitis
must be confirmed by demonstration of antibody production against B.burgdorferi
in the CSF, evidenced by a higher titer of antibody in
CSF than in serum. Headache, fatigue, paresthesia, or mildly stiff
neck alone are not criteria for neurologic involvement.
-
Cardiovascular system: Acute
onset of high-grade (2o or 3o)
atrioventricular conduction defects that resolve in days to weeks
and are sometimes associated with myocarditis. Palpitations,
bradycardia, bundle branch block, or myocarditis alone are not
criteria for cardiovascular involvement.
-
Exposure:
Exposure is defined as having been in wooded, brushy, or grassy areas
(i.e., potential tick habitats) in a county in which Lyme disease is
endemic within the 30 days prior to onset of EM. A history of tick
bite is not required.
-
Disease endemic to
county: A county in which Lyme disease is endemic is one in
which at least two confirmed cases have been previously acquired or in
which established populations of a known tick vector are infected with
B. burgdorferi.
Diagnosis is made clinically during the early stages
of Lyme disease if EM is present. While cultures of a biopsy specimen of
the perimeter of this lesion frequently yield the organism, Borrelia cultures
(which require special media) are not available commercially. In patients
without rash who manifest signs of a later stage of Lyme disease,
diagnosis also should be based on clinical findings, using serologic tests
as an adjunct.
The diagnosis of Lyme disease can be difficult, in part because of poor
standardization and inappropriate use of serologic diagnostic tests. The
IgM–specific antibody titer usually peaks between weeks 3 and 6 after
the onset of infection; specific IgG antibody titers usually rise slowly
and generally are highest weeks to months later. Localized EM typically
occurs from 3 to 32 days (mean 7 to 10 days)
after the tick bite; therefore, antibodies
against B. burgdorferi will not be detectable in most patients
presenting with EM. Some patients who are treated early with antimicrobial
agents never develop antibodies against B. burgdorferi. However,
most patients with early-disseminated disease and virtually all patients
with late disease will have antibodies against B burgdorferi. As
with other infections, once such antibodies develop, they may persist for
many years despite cure of the disease. Consequently, tests for antibodies
should not be used to assess the success of treatment.
The enzyme immunoassay (EIA) is the most commonly used test for
detection of antibodies against B. burgdorferi. This test and the
immunofluorescense assay (IFA) may give false-positive results because of
cross-reactive antibodies in patients with other spirochetal infections
(e.g., syphillis, leptospirosis, relapsing fever), certain viral
infections (e.g., varicella), and certain autoimmune diseases (e.g.,
systemic lupus erythematosus). While antibodies to B. burgdorferi
cross-react with other spirochetes, including Treponema pallidum (syphillis),
patients with Lyme disease do not have positive non-treponemal syphilis
test results, such as VDRL or RPR (rapid plasma reagin). In addition,
antibodies directed against bacteria in the normal oral flora may
cross-react with antigens of B. burgdorferi and produce a
false-positive test result.
Currently, the Western immunoblot assay is the most useful test for
corroborating positive or equivocal EIA or IFA results and, as a result, a
2-test approach is required for the serologic diagnosis of B.
burgdorferi infection. Serum specimens that give positive or equivocal
results by EIA or IFA must be confirmed by a Western immunoblot assay.
Serum specimens that give negative results by EIA of IFA do not require
immunoblot confirmation. If a patient with suspected early disease has a
negative serologic test result, evidence of infection is best obtained by
testing of paired acute- and convalescent-phase serum samples. Persons
with early disseminate or late-stage Lyme disease almost always have a
robust antibody response to B burgdorferi antigens.
The widespread practice of ordering serologic tests for patients with
nonspecific symptoms (such as fatigue or arthralgia) who have a low
probability of having Lyme disease is not recommended. Almost all positive
serologic test results in these patients are false-positive results.
Prevention measures can be effective in reducing
exposure to infected ticks.
Share these prevention methods with the public:
-
Avoid potential tick habitat (such as woody,
brushy, or grassy areas) when possible.
-
Minimize exposure by wearing light colored
clothing that covers legs and arms so that ticks are more easily seen;
tuck pants into socks and apply tick repellent such as
diethyltoluamide (DEET, Autan) to the skin (according to label
directions) or permethrin (a repellent and contact acaricide) to pant
legs and sleeves.
-
If working or playing in an infected area,
search the total body area daily, do not neglect haired areas, and
remove ticks promptly; these ticks may be very small.
-
Remove any attached ticks by using gentle,
steady traction with tweezers applied close to the skin to avoid
leaving mouth parts in the skin; protect hands with gloves, cloth or
tissue when removing ticks from humans or animals. Following removal,
cleanse the attachment site with soap and water.
Doxycylcline (age >8 years) and
amoxycillin are the preferred drugs for early disease. Intravenous
ceftriaxone or penicillin G are given for patients with late
manifestations.
-
Proportion of cases with
complete demographic information.
-
Proportion of cases with complete clinical
information (i.e., presence of physician diagnosed EM or late
manifestations).
-
Proportion of cases with complete tick
exposure history.
-
Proportion of cases with complete
laboratory work-up (i.e., diagnostic total antibody with
confirmatory Western blot).
-
Proportion of case investigations that are
totally complete: complete WV BPH Confidential Reportable Disease
Case report (yellow card), complete CDC Lyme disease case report
form, and copies of supporting laboratory results are sent to WVBPH
with complete information and within a week of disease being
diagnosed.
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