Tick-Borne Diseases, Lyme
Background: Lyme disease is a systemic infection caused by the spirochete
Borrelia burgdorferi. The bacterium is inoculated into the skin by a tick bite. The
tick is almost always of the genus Ixodes.
Although various parts of the syndrome were described in Europe more than 100
years ago, the full spectrum had not begun to be identified until 1975, when a
cluster of statistically improbable cases of juvenile arthritis occurred in
Connecticut. This outbreak stimulated intensive clinical and epidemiologic
research that led to the discovery of the causative agent, the ecology, an
expanding list of clinical manifestations, and the geographic range. Furthermore,
the initial antibiotic responsiveness of the cutaneous manifestations described in
the European literature was confirmed and extended.
Pathophysiology: The pathophysiology of Lyme disease is incompletely
understood. While active infection by the spirochete causes many
manifestations, others may be caused by immunopathogenic mechanisms.
Although any body part can be involved, the organism shows a distinct tropism
for the skin, CNS, heart, joints, and eye.
The bacterium is introduced into the skin with a bite from an infected Ixodes tick.
In the northeastern and upper midwestern United States, Ixodes scapularis is the
vector. In other parts of the country and world, other Ixodes species serve that
function. Other ticks (eg, Amblyomma americanum) and insects can carry B
burgdorferi, but Ixodes tick bites are thought to cause the vast majority of cases.
In the southern and mid-central United States, a Lymelike illness has been
reported; the vector appears to be A americanum, and the causative organism or
organisms is likely to be a related spirochete. One such organism, named
Borrelia lonestarii, has been cultured in a single case.
Once in the skin, the spirochete (1) can be overwhelmed and eliminated by host
defense mechanisms; (2) remain viable and localized in the skin where it
produces the pathognomonic skin lesion, or erythema migrans (EM); or (3)
disseminate through the lymphatics or blood. Hematogenous dissemination can
occur within days to weeks of initial infection; the organism can travel to the skin,
heart, joints, CNS, and other parts of the body.
Study findings show that in roughly 10% of patients with isolated EM and no
systemic symptoms, B burgdorferi can be cultured or that its DNA can be
detected in the bloodstream. Using high volume (9 mL) of plasm for culture, one
2005 study suggests that nearly 44% of patients are spirochetemic, some of
them with a single skin lesion and no systemic symptoms. Also, early in the
course of the disease when EM is still present, the spirochete and its DNA have
been isolated from the cerebrospinal fluid (CSF), indicating early CNS
penetration. This penetration can occur even in the absence of neurologic
symptoms.
The organism can also persist in skin (and possibly in the CNS) for years without
causing symptoms. Experimentally, the spirochete can penetrate human
fibroblasts and live intracellularly, even when the extracellular medium contains
ceftriaxone well above bacteriocidal levels for the spirochete. Clinically,
organisms have been cultured from skin many years after primary infection. This
mechanism may allow the spirochete to elude the normal host defense
mechanisms directed against it.
As with syphilis, the disease classically is divided into stages: early localized,
early disseminated, and late. However, distinct cutoff points between the stages
are frequently unclear. Early localized Lyme disease refers to isolated EM and
patients with an undifferentiated febrile illness. Early disseminated disease refers
to the extracutaneous manifestations and secondary skin lesions that occur
during the first weeks to months after infection. Late Lyme disease refers to later
manifestations (usually in the nervous system and joints) that occur months to
years later. Many patients initially have EM; however, in others, neurologic or
rheumatologic complaints may be the initial symptoms, either because EM is not
present or because it was unrecognized or misdiagnosed.
Frequency:
• In the US: The Centers for Disease Control and Prevention (CDC) track
cases of Lyme disease by using strict surveillance criteria (not designed
for diagnosis of individual cases). The incidence has been increasing over
time. This is not simply a result of increased recognition, since in states
that perform active surveillance, true incidence and geographic range
have increased. The likely causes of this increase are expansion of deer
herds and the expanded range of the vector.
In 2001, the CDC reported 17,029 cases and, in 2002, that number rose to
23,763—a 40% increase. Year-to-year variation can be significant. More
than 95% of cases come from 12 states (Connecticut, Delaware, Maine,
Maryland, Massachusetts, Minnesota, New Hampshire, New Jersey, New
York, Pennsylvania, Rhode Island, and Wisconsin). Even within these
states, incidence can be quite variable from county to county and even
neighborhood to neighborhood.
Overall in the United States, incidence is 6.0-8.2 cases per 100,000
population (2001 and 2002 data). However, in Connecticut in 2001, the
rate was nearly 134 cases per 100,000 population, and, on the island of
Nantucket, Massachusetts, the rate exceeds 1000 cases per 100,000
population.
Epidemiologic data suggest that the actual incidence of Lyme disease
could be as much as 10 times higher than the CDC data indicate. This
probably is a result of a restrictive case definition from the CDC, inevitable
misdiagnosis, and the fact that physicians tend to underreport reportable
diseases of all kinds.
• Internationally: Lyme disease exists throughout the world, including
Scandinavia; central, southern, and western Europe; the former Soviet
Union; Japan; and China. While Lyme disease is far more common in the
northern hemisphere, occasional cases have been reported in more
tropical locales, and it may exist in Australia. Ecology for the disease
differs in various parts of the world. Furthermore, different strains of the
organism are present in Europe and very likely account for differences in
clinical manifestations; these have implications for diagnostic testing and
vaccination strategies.
Mortality/Morbidity: Rare fatalities are reported in patients with Lyme disease.
• Some fatal cases occur in patients who were simultaneously co-infected
with other tick-borne pathogens. In North America, these other infections
are generally babesiosis and ehrlichiosis. In Europe, in addition to these 2
organisms, fatalities have been reported with co-infecting tick-borne
encephalitis, a tick-borne flavivirus.
• Patients with neurologic disease that is not promptly diagnosed and
treated can have neurologic damage that can be difficult to treat. These
fixed neurologic deficits may not respond to antibiotics.
• Similarly, some genetically predisposed patients with arthritis may have
ongoing joint inflammation that does not respond to further antibiotic
therapy.
Race: No known differential frequency exists in patients of different races;
however, EM maybe more difficult to diagnose in dark-skinned individuals.
Sex: Developing Lyme disease is more a function of tick exposure than sex.
Likely for this reason, the disease is slightly more common in males than in
females.
Age: Lyme disease occurs in patients of all ages. However, a bimodal peak
exists: one at 5-14 years of age and a second one at 50-59 years.
• About 25% of cases occur in children younger than 14 years.
• The likelihood of contracting Lyme disease is related more to tick
exposure than to age, sex, or race per se.
History: Because only about 25-30% of patients with Lyme disease recall the
bite, history taking must be directed toward determining the epidemiologic
probability of a tick bite. Because Lyme disease can affect many body parts,
many presenting complaints can exist. Examples may include the following:
• Systemic manifestations
o Fever is generally low grade. A high-grade fever or toxic
appearance suggests co-infection, such as ehrlichiosis or
babesiosis, or an alternative diagnosis.
o Fatigue is common.
o Myalgias and arthralgias occur early. Frank arthritis (ie, joint
swelling, redness, pain) usually is a later manifestation but can
occur in the early disseminated phase.
o Flulike illness (undifferentiated febrile illness) may occur. Although
the frequency of this is unknown, the phenomenon of Lyme disease
with typical flulike symptoms of fevers, chills, myalgias, arthralgias,
and malaise (without rash) is well documented. The season of
onset, epidemiologic likelihood of a tick bite, paucity of respiratory
and GI symptoms, and prompt response to antiborrelial therapy are
diagnostic clues.
• Cutaneous symptoms
o The classic rash, erythema multiforme (EM), is present in about
75% of patients. Because it is neither pruritic nor painful (although it
can be either), some patients may have the rash but not notice it.
EM can occur in the same patient more than once.
o About 20% of patients with Lyme disease have multiple lesions
(from hematogenous dissemination). The higher figure is from
earlier studies; current information suggests that the rate of multiple
lesions is closer to 20%.
o Borrelial lymphocytoma, a nodule usually found on the ear lobe or
areola of the nipple, develops in some patients early in the course
of disease. This is more common in Europe.
o Almost exclusively observed in Europe, acrodermatitis chronicum
atrophicans is a rash that patients describe as inflammation or
thinning of the skin, usually on the distal legs and hands.
• Neurologic symptoms
o Headache can occur in early infection as a nonspecific finding and
can herald CNS penetration and lymphocytic meningitis. The
headache of Lyme disease typically is described as waxing and
waning, and the severity varies from mild to severe, even in
patients with frank meningitis.
o Patients notice facial weakness, which is similar to a typical Bell
palsy and which can be the presenting symptom of Lyme disease.
About 25% of patients with borrelial facial palsy have bilateral
involvement, which may be sequential and is a point of differential
diagnostic significance. Other than Lyme disease and Guillain-
Barré syndrome, bilateral seventh nerve palsy is rare.
o Radicular pain can occur and present as acute disk disease. More
common in European patients, radicular pain may be associated
with lymphocytic pleocytosis (Bannwarth syndrome).
o Late Lyme disease can cause paresthesias or pain due to
peripheral neuropathy and personality, cognitive, and sleep
disturbances from chronic encephalopathy. All sorts of neurologic
syndromes caused by Lyme disease involving nearly every part of
the CNS and peripheral nervous system have been reported in
numerous case reports; therefore, Lyme disease may produce
numerous symptoms. Although the likelihood that these other
symptoms result from Lyme disease in any particular patient may
be small, the clinician must remain open minded to this possibility.
• Cardiovascular involvement
o Cardiovascular involvement occurs in fewer than 10% of patients
with untreated Lyme disease and is more common in male patients
than in female patients.
o Palpitations, lightheadedness, and syncope may be a manifestation
of varying degrees of heart block, including complete heart block,
which occurs in 50% of patients with cardiac involvement. Lyme
disease is an important reversible cause of heart block.
o Chest pain and dyspnea can occur in the setting of Lyme
pericarditis, myocarditis, and myopericarditis. Tamponade has been
reported.
• Migratory pains in and around the joints and muscles
o Migratory pain may occur from myositis, tendonitis, and bursitis.
o These symptoms classically wax and wane over hours or days.
o Later, arthritis occurs generally with swelling, redness, and pain in
one or a few large joints, typically the knees.
o Synovitis occasionally occurs in the early-disseminated phase of
Lyme disease.
• Red, itchy eyes from conjunctivitis
o Red, itchy eyes are the most common ocular symptom.
o Blurred vision and eye pain can occur from keratitis and iritis.
Unilateral blindness from panophthalmitis has been reported as
well.
• Nausea and vomiting
Physical: The physical examination in patients with Lyme disease can reveal
numerous findings, depending on the target organs involved and the phase of the
disease at presentation. In addition to fever, findings may include the following:
• Dermatologic findings
o Classic EM is an erythematous papule or macule that occurs at the
site of the tick bite (1-33 d later; average, 7-10 d). Often, a central
punctum is found at the site. The size varies enormously (as large
as 70 cm; average, 16 cm) and depends on disease duration.
Central clearing, a phenomenon emphasized in earlier literature,
occurs in only a minority of cases in North America (about 40% in
one study of culture-proven EM). Central clearing is more common
in European patients than in North American patients.
o EM usually is flat, round, or oval and monocyclic. Generally, neither
itching nor pain is present. The rash enlarges a few centimeters per
day and fades, even if untreated, after a few weeks. The rash can
be triangular or linear and is sometimes fleeting in duration. Rash
location is another important diagnostic clue.
o The clinician must be able to recognize atypical manifestations of
EM, such as necrotic and vesicular lesions. The lesion may have
central darkening or be uniform in color, and the edges may be
raised. Scaling is unusual.
o EM rarely is found on the hands and feet (unlike spider and other
arthropod bites). Ticks tend to bite where natural barriers impede
their forward motion (eg, axillary or gluteal folds, hairline, areas
near elastic bands in bra straps or underwear). In children, the
scalp, face, and hairline are more common locations.
o Approximately 20% of patients with EM have secondary lesions.
These lesions generally are smaller than the primary one, lack the
central punctum, and are not necrotic or vesicular.
o Borrelial lymphocytoma most frequently is observed in European
patients. This finding can be early or late and can follow or occur
concurrently with EM. It is a reddish purple nodule on the ear lobe
or the nipple (other locations are possible).
o Acrodermatitis chronicum atrophicans is nearly exclusively
observed in European patients. The two phases are an
inflammatory phase with edema and erythema in the distal
extremities and a scarring phase with atrophy and skin as thin as
cigarette paper. B burgdorferi has been cultured from lesions in
which the primary infection occurred over 10 years prior.
• Neurologic signs
o Neck stiffness can occur early, with or without frank meningitis.
o Facial nerve palsy is a lower motor neuron lesion that causes facial
weakness of both the lower face and forehead. It can be bilateral.
As in idiopathic Bell palsy, sometimes a polycranial neuropathy
exists with any nerve involved; this more commonly is reported in
the European literature. Nearly every cranial nerve has been
reported to be involved, although this is uncommon.
o Weakness and abnormal sensation can occur because of
meningoradiculitis and more commonly is reported in European
patients. Diminished reflexes can occur with this syndrome. CSF
frequently reflects pleocytosis.
o Neuropsychiatric testing and mini-mental status testing may
uncover cognitive, memory, and personality changes that occur in
late Lyme encephalopathy.
o Peripheral axonal neuropathy can lead to patchy, generally distal
abnormalities in sensation. Sensory findings are more pronounced
than motor findings.
• Cardiovascular findings
o In patients with complete heart block, Canon A waves may be
observed in the neck. A slow or irregular pulse may be palpated.
o A cardiac rub, S3 and/or S4, may be auscultated in patients with
myocarditis or pericarditis. Signs of tamponade very rarely can
occur. In patients with chronic cardiac involvement with congestive
heart failure, typical signs of congestive heart failure may be
present.
• Musculoskeletal findings
o Muscle tenderness can result from myositis; tenderness of tendons
and periarticular structures may be present.
o Frank arthritis can occur after weeks, months, or years and may
lead to erythema, edema, synovial effusion, and tenderness of the
affected joints. Usually, this is a monoarthritis or oligoarthritis
involving large joints, especially the knee. Swelling often is
disproportional to the tenderness.
• Ocular signs
o Conjunctival erythema and injection or retinal hemorrhages and
exudates may be present.
o On slitlamp examination, signs of keratitis and cells in the anterior
chamber from iritis may be seen.
o In children (especially in North America), papilledema may be
present in a pseudotumor cerebri–like syndrome.
• Other signs – Splenomegaly, hepatomegaly, regional lymphadenopathy
Causes: Lyme disease is caused by infection with the spirochete, B burgdorferi,
the complete genome of which has been described recently.
• The species Borrelia burgdorferi sensu lato has several well-characterized
groups that may lead to different clinical manifestations. These 3 groups
are B burgdorferi sensu stricto, Borrelia garinii, and Borrelia afzelii. Other
strains, which may be sufficiently different in their genetic structure to be
considered separate strains, exist; however, most of these are
nonpathogenic to humans. This is an area of active research.
o B burgdorferi sensu stricto is present in most North American
isolates.
o B afzelii is common in Europe and is frequently isolated in patients
with acrodermatitis chronicum atrophicans.
o B garinii, more common in Europe, is commonly isolated in patients
with lymphocytic meningoradiculitis (Bannwarth syndrome) and
white matter encephalitis.
• Occupational or recreational activities that place an individual in contact
with ticks are the major risk factors.
• Arthritis that is nonresponsive to antibiotics may develop in some
genetically predisposed individuals (ie, those who have the HLA-DR4
antigen).
• Some patients will have persistent or recurrent symptoms after what is
considered adequate antibiotic therapy for Lyme disease. This
phenomenon has been termed chronic Lyme disease, or post-Lyme
syndrome. The cause for this is controversial.
Differential:
Babesosis
Bell’s palsy
Bites, insects
Meningitis
Myocarditis
Pericarditis
Tick borne diseases (babesosis, erhlichiosis, Q-fever, relapsing fever, Rocky Mtn spotted
fever, tularemia)
Workup:
Lab Studies:
• Laboratory testing depends entirely on the presenting problem of the
patients. Evaluation of the CBC, erythrocyte sedimentation rate, and liver
function generally is unnecessary, and serologic tests can be misleading if
performed in the wrong setting.
o The patient with solitary, typical EM requires no laboratory testing
whatsoever. Expected results for the CBC and erythrocyte
sedimentation rate are likely normal. At this stage of illness,
serologic testing is unnecessary because the pretest probability of
Lyme disease is high, and the sensitivity of the serologic test is low
(during the first several weeks).
o Leukopenia or thrombocytopenia suggests co-infection with
Ehrlichia or Babesia species.
o Elevation of at least one liver function test result is reported to
occur in 40% of patients with Lyme disease. This finding also is
common in ehrlichiosis.
• Culture of B burgdorferi
o Because of the organism’s fastidious growth requirements, culture
has not been a useful test in the past; however, this situation is
improving. Its usefulness depends on the specimen being cultured.
Nevertheless, in routine practice, borrelial cultures are often
unavailable.
o In the skin, where findings are most likely to be positive, culturing is
least likely to be clinically useful, except in cases of atypical rash.
o In other body fluids (eg, blood, synovial fluid, CSF), the yield is
lower. However, recent data suggests that if a high volume (9 mL)
of plasma is used, approximately 44% of patients with EM are
determined to be spirochetemic at presentation.
Imaging Studies:
• Imaging studies are almost never indicated in patients with Lyme disease
who present with early syndromes. Patients with some clinical syndromes
may require imaging studies, depending on the specifics of the case. For
example, a patient with fever and severe back pain, with signs of
radiculopathy, might require spine imaging.
Other Tests:
• Serologic testing for Lyme disease is complex. Rational ordering and
interpretation of these tests requires some understanding of the basic
underlying principles and performance characteristics of the test.
• Most importantly, the most commonly performed test measures antibodies
to various proteins of the spirochete, some of which are very specific for
the organism and others of which are nonspecific. The test results do not
rule in or rule out Lyme disease; however, the results make a clinical
diagnosis of Lyme disease more (or less) likely.
• The CDC recommends a 2-step procedure consisting of a screening
enzyme-linked immunoassay (ELISA) (or immunofluorescent assay [IFA])
and a confirmatory Western blot for specimens that have positive or
equivocal results with the ELISA. Furthermore, in patients with a high
likelihood of having Lyme disease (eg, classic EM in an endemic area), no
serologic test should be ordered. Conversely, in a patient with a low
pretest likelihood of having Lyme disease (eg, someone with vague
symptoms where the test is being used as a screening test), testing is also
not recommended because in such a population, the number of falsepositive
results greatly outnumbers the true positive results.
• Numerous conditions (eg, viral and bacterial infections, inflammatory
diseases, neoplasms) can cause false-positive ELISA results. Also, a
small percentage of the healthy population has positive test results with
ELISA testing. For these reasons, confirmatory Western blot testing is
recommended.
• Timing is extremely important. Seroconversion may take several weeks in
patients infected with the spirochete, so early seronegativity is to be
expected.
• Even occasional patients with facial nerve palsy or carditis (ie, early
disseminated disease) may be seronegative on presentation. However,
testing is recommended in these individuals. Furthermore, early or partial
treatment with antibiotics may blunt or abrogate the subsequent serologic
response. Some patients with late disease are seronegative, but
significant controversy exists regarding the frequency of late
seronegativity. Most authorities suggest that this phenomenon is rare.
• On the other hand, patients with prior Lyme disease may have persistently
positive results. Also, vaccinated patients will have a positive ELISA result
(although Western blot results should be negative). Lack of attention to the
details of the test result and the reliability of the laboratory performing the
test might lead the physician to an erroneous conclusion about the cause
for a given patient’s symptoms.
• Patients may remain seropositive for long periods; therefore, serologic test
results cannot be used as a proof or test of cure. Also, if a patient with
past Lyme disease who remains seropositive comes in with new
symptoms, care should be taken to not necessarily ascribe these new
symptoms to Lyme disease.
• The emergency physician must remember 2 important concepts. First, a
negative Lyme test result does not indicate the absence of disease, nor
does a positive result indicate the presence of disease. Second, a positive
result is not required for someone with clear-cut EM; these earlypresenting
patients frequently have negative results, and they should be
treated for EM empirically.
• In the last few years, research on newer serologic tests—specifically the
C6 peptide and the VslE—is promising. These test results may well turn
positive earlier and revert to negative after successful treatment. As of mid
2005, these tests have not been incorporated into routine clinical practice
and the CDC recommendations above still stand.
Procedures:
• Because the spirochete can enter the CSF early in the course of infection
and because the finding of meningitis (defined here as abnormal CSF in
the setting of active Lyme disease) changes the treatment, many
physicians have a low threshold for performing a lumbar puncture in
patients with EM and any CNS symptoms or in patients with isolated
seventh nerve palsy due to Lyme disease. The finding of elevated protein
levels or pleocytosis mandates parenteral therapy. Definitive data to either
support or refute this practice are lacking.
• In addition, a lumbar puncture ought to be performed if Lyme meningitis is
in the differential diagnosis.
• Occasional patients with Lyme disease–related heart block will require
temporary cardiac pacing. The indications for cardiac pacing are the same
as for any other patient with varying degrees of heart block. Permanent
wires are very rarely needed.
Treatment:
Emergency Department Care: ED care of patients with Lyme disease depends
on the presenting complaint. In general, Lyme disease is not fatal, and the
emergency physician may be able to consult specialists and refer the patient to a
primary care physician.
Treatments for tick bites, EM, early disseminated disease, and arthritis are as
follows:
• Tick bite without other symptoms or signs: Several factors influence the
decision to treat tick bites with therapy to prevent Lyme disease.
o Animal studies have shown that transmission of infection is unlikely
if the duration of tick attachment is less than 24 hours, and
transmission is very likely for ticks attached for longer than 72
hours. This finding presumes that the tick is infected in the first
place and the percentage of Ixodes ticks that are infected varies
with geography. It also depends on the species of tick. Non-Ixodes
ticks and other insects, although they can contain the organism, are
highly unlikely to cause disease. The one clinically relevant
exception may be bites by A americanum in the central and
southern midwestern United States, but data exist on treating these
tick bites prophylactically at the present time.
o Several randomized placebo-controlled studies have been
conducted to investigate prophylactic treatment of tick bites. All
revealed that the rate of symptomatic infection and asymptomatic
seroconversion is about 2% in placebo groups. This study occurred
in areas in which about 15-30% of ticks were infected; this finding
indicates that many bites from infected ticks do not result in
transmission of the spirochete. These studies form the basis of the
often-cited recommendation to withhold tick bite prophylaxis.
o In 2001, a study was published showing that only female nymphal
ticks transmitted Lyme disease. It also corroborated the finding that
duration of attachment is an important marker for transmission.
o However, findings of other studies of culture-proven EM in the
United States and Europe suggest that a non-trivial minority of
patients had tick attachments of less than 24 hours, some less than
6 hours. Therefore, one cannot be dogmatic with the criterion of
duration of tick attachment. Poor technique in tick removal also may
facilitate infection. For further information, see Tick-borne Diseases,
Introduction.
o Although most patients do not require treatment, consider tick bite
prophylaxis on a case-by-case basis. Base the decision on the
species of the tick, duration of attachment (degree of engorgement
of the tick is a surrogate marker), geography (percentage of ticks
infected where the bite took place), method of tick removal, anxiety
level of patient, and pregnancy (lower threshold to treat pregnant
women).
o After performing this exercise in clinical decision-making, one may
decide to treat a given patient with prophylactic antibiotics. In the
studies mentioned previously, no patient in the treatment group
(which received 10 d of antibiotic treatment) had the disease.
Historically, if one were to choose to treat, 10 days of oral
amoxicillin, doxycycline, or cefuroxime axetil would seem prudent,
depending on patient factors such as age, allergy, and pregnancy.
o In one of the most recent studies (2001), a single 200-mg dose of
doxycycline was used for prophylaxis with excellent results.
o Serologic testing plays no role in the care of patients with tick bites.
• Solitary EM: Oral antibiotics (eg, amoxicillin, doxycycline, cefuroxime
axetil, erythromycin, azithromycin, amoxicillin-clavulanate) should be
administered for 10-30 days. The author recommends therapy of 3 weeks
duration. Given recent findings that early disseminated Lyme disease
responds very well with 21 days of oral therapy, not exceeding that
duration for localized disease seems logical. That said, one recent study
suggests that 10 days of antibiotic treatment is just as effective as 20
days.
• Early disseminated disease findings such as isolated facial palsy or
secondary skin lesions (not meningitis) or disease with first-degree heart
block (not a high-degree heart block) may be treated with oral antibiotics
for 21-30 days. Recent data show that 21 days of oral doxycycline is as
effective as 14 days of intravenous ceftriaxone for disease in this stage.
• Early disseminated disease with meningitis or a high-degree heart block
may be treated with intravenous ceftriaxone for 2-4 weeks. In the case of
heart block, a permanent pacemaker rarely is necessary, but close
monitoring in a telemetry unit is warranted. Once patients are no longer
dependent on the pacemaker dependent, their intravenous antibiotics may
be switched to oral antibiotics. Occasionally, prednisone may hasten
resolution of the conduction defect.
• Arthritis may be treated with oral antibiotics for 30-60 days, and
intravenous ceftriaxone may be administered for coexistent neurologic
disease.
Consultations: The need for consultation depends on the emergency
physician’s confidence in the clinical diagnosis.
• At times, input from a dermatologist, neurologist, infectious diseases
specialist, or cardiologist assists in making a firm diagnosis, particularly in
the setting of chronic disease.
• Always refer patients to primary care physicians to monitor for later
manifestations of the disease.
Adapted from eMedicine.com. Author Jonathan Edlow MD et al. 2005
