Lyme Disease


Symptoms & Characteristics
A compilation of peer-reviewed literature reports.






Borrelia burgdorferi.
Burgdorfer W. Keynote Address - The Complexity of Vector-borne Spirochetes.
12th International Conference on Lyme Disease and Other Spirochetal
and Tick-Borne Disorders. 1999.





“Initially thought to be a disorder beginning in the skin and progressing to involve the joints,
Lyme disease is now ranked as one of the great mimickers of other diseases,
in a manner similar to that once ascribed to syphilis.”
Duray PH. Clinical pathologic correlations of Lyme disease.
Reviews of Infectious Diseases, Vol 11, Suppl. 6: S1487-S1493. 1989.


June, 2006

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Contents



I.
Overview of Lyme Disease ...................................................................................................... 1


II.
Symptoms:

• General/Constitutional............................................................................................................ 4
• Head/Face/Neck....................................................................................................................... 5
• Ears/Hearing............................................................................................................................ 7
• Eyes/Vision............................................................................................................................... 8
• Gastrointestinal System ........................................................................................................ 12
• Respiratory & Circulatory Systems .................................................................................... 15
• Hepatatic System (Liver) ...................................................................................................... 17
• Musculoskeletal System ........................................................................................................ 18
• Neurologic System ................................................................................................................. 22
• Psychological Symptoms....................................................................................................... 35
• Cognitive Symptoms ............................................................................................................. 37
• Reproduction/Sexuality ........................................................................................................ 40
• Skin/Hair................................................................................................................................ 41
• Other (including cancer-like presentation)......................................................................... 45


III. Fatality Reports........................................................................................................................ 46


IV. Detection of Borrelia burgdorferi in Host Tissues & Fluids...................................... 47










by Joanne Rubel

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Lyme Disease

Overview & Cause
“Lyme disease, also called Lyme borreliosis, is a widely distributed multi-system disease caused by a tick-
transmitted spirochete, Borrelia burgdorferi. ...Although other ticks or even flies or other biting insects may
transmit the disease in some areas, the usual vectors are small, hard-bodied ticks of the genus Ixodes. Within the
United States, it is now the most commonly reported tick-transmitted infection.”
Louis Reik, Jr., M.D. Lyme Disease and the Nervous System. New York:Thieme Medical Publishers. 1993.

“Although there are regional variations, the basic outlines of this disorder are similar worldwide...”
Steere AC. Lyme disease. New England Journal of Medicine 1989;321:586-596.

“Lyme disease... shares many features with the other [human spirochetal] diseases. ...These similarities include a
skin or mucous membrane portal of entry...; spirochetemia early in the course of disease, with wide dissemination
through tissue and body fluid; and then one or more subsequent stages of disease, often with intervening latent
periods. ...chronic arthritis is unique to Lyme disease.”
Schmid GP, Centers for Disease Control. Epidemiology and clinical similarities of human spirochetal diseases.
Rev Infect Dis 1989;11(Suppl 6):S1460-9.

“Although Lyme disease was initially described as a form of juvenile arthritis following the development of erythema
chronicum migrans..., it is now known to be a multisystem disease, with prominent neurologic involvement.”
Halperin JJ; Little BW; Coyle PK; Dattwyler RJ. Lyme disease: Cause of a treatable peripheral neuropathy. Neurology 1987;37:1700-6.

Protean Clinical Manifestations
“Clinically, this borrelial infection is most like syphilis in its multisystem involvement, occurrence in stages, and
mimicry of other diseases. ...Lyme disease’s great range of presentations can make recognition difficult.”
Steere AC. Lyme disease. New England Journal of Medicine 1989;321:586-596.

“...it should be emphasized that marked variation is possible in the clinical expression of the disease. Even without
treatment, some patients have very mild disease... At the opposite end of the spectrum, an occasional patient will
have severe involvement of the skin, nerves, heart, and joints at the same time.”
Steere AC; Malawista SE; et al. The clinical spectrum and treatment of Lyme disease. Yale Journal of Biology and Medicine 1984;57(4):453-64.

“Symptoms can be surprisingly variable, so that days of near normality can alternate with days of profound debility.”
Pachner AR. Early disseminated Lyme disease. American Journal of Medicine 1995;98 (suppl):4A-30S-43S.

“As in other spirochetoses, such as syphilis, the symptoms may be fulminant, with a sudden onset, or may develop
insidiously over many years. The variable clinical manifestations have led to an awareness of this disorder as a
“great imitator” that must be considered in the differential diagnosis of numerous complaints, especially in those
geographic areas where the spirochete is endemic.”
Cooke WD; Dattwyler RJ. Complications of Lyme borreliosis. Annual Review of Medicine 1992;43:93-103.

“Lyme disease has now been shown to involve nearly every organ and organ system in both sexes.”
Duray PH. Clinical pathologic correlations of Lyme disease. Rev Infect Dis 1989;Vol 11(Suppl. 6):S1487-S1493.

Variable Temporal Sequence
“Early infection consists of stage 1 (localized erythema migrans), followed within days or weeks by stage 2
(disseminated infection) and within weeks or months by intermittent symptoms. Late infection, or stage 3
(persistent infection), usually begins a year or more after the onset of the disease. A patient may have one or all of
the stages, and the infection may not become symptomatic until stage 2 or 3.”
Steere AC. Lyme disease. New England Journal of Medicine 1989;321:586-596.

“In practice, however, infection forms a continuum along which early and late features may overlap.”
Coyle PK; Schutzer SE. Neurologic presentations in Lyme disease. Hospital Practice 1991; 6(11):55-66.

“Illness can begin in any one of these organ systems, the systems are not always involved sequentially,
other skin lesions can develop in later stages, and neurologic abnormalities can accompany arthritis.”
Louis Reik, Jr., M.D. Lyme Disease and the Nervous System. New York:Thieme Medical Publishers. 1993.
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Lyme Disease
“In syphilis, ...staging is particularly useful because it is likely that the pathophysiology of stage 2 and stage 3
disease differs; this is far less clear with neuroborreliosis. Considerable data suggest that the differences between
early and late neuroborreliosis are more quantitative than qualitative, with the different syndromes representing
different points on a continuum, all with the same pathophysiologic mechanism. Moreover, the clinical
phenomena in neuroborreliosis often do not follow an obligatory temporal sequence; any symptoms may develop
without an antecedent stage 1 illness. For example, arthritis (generally considered stage 3 disease) may occur
early, on occasion even preceding EM; meningitis (nominally stage 2) may develop after arthritis, and so on. All
this suggests that dividing neuroborreliosis into early versus late phenomena, while occasionally reassuring to the
physician and patient, may lack pathophysiologic validity.”
Halperin JJ. Neuroborreliosis. Am J Med 1995;Vol 98(4A):52S-56S.

Waxing & Waning Symptoms / Latent Periods
“This pattern of persistent infection, acute disease, disease remission, and intermittent bouts of exacerbation is
typical of untreated human Lyme disease.”
Barthold SW; de Souza MS; Janotka JL; Smith AL; Persing DH. Chronic Lyme borreliosis in the laboratory mouse. Am J Path 1993;143(3):959-71.

“Some of the symptoms are present only for a rather short period of time. For instance, palpitations may be noted
only for a few minutes, and patients may have only one to five attacks of palpitations.”
Weber K; Neubert U; Büchner SA. Erythema migrans and early signs and symptoms. In Aspects of Lyme Borreliosis, ed. Klaus Weber, M.D.,
Willy Burgdorfer, Ph.D., M.D. Berlin Heidelberg:Springer-Verlag:pp 105-121. 1993.

“[Lyme disease] is similar to syphilis in that, if left untreated, the disease tends to progress in stages with extended
periods where the patient may feel totally asymptomatic.” / “The 20 to 30 year period between primary and
tertiary syphilis is the classical statement regarding the chronic condition. In this regard, we already know that
certain manifestations of Lyme disease can take up to a decade to develop.”
Benach JL; Coleman JL. Overview of spirochetal infections. In Lyme Disease, ed. Coyle PK. St. Louis: Mosby-Year Book Inc., pp.61-68. 1993.

“The syphilis spirochete can live in the CNS for long periods, as evidenced by the fact that patients with general
paresis usually do not manifest neurologic symptoms until 15 years after infection. A lengthy latency within the CNS
also appears to exist in Lyme disease, with neurologic symptoms not becoming manifest for months or even years.”
Pachner AR. Neurologic manifestations of Lyme disease, the new “Great Imitator.” Rev Inf Dis 1989;Vol. 11(Suppl 6):S1482-6.

Geographic Distribution & Spread
“Lyme disease has been reported from five continents—Africa, Asia, Australia, Europe, and North America.
...In North America, Lyme disease occurs in both the United States and Canada. Within the United States, it is
now the most commonly reported tick-transmitted infection...The disease is endemic along the East Coast from
Maryland to Massachusetts, in the upper Midwest in Minnesota and Wisconsin, and on the Pacific coast in
California and Oregon. Increasing numbers of cases have also been reported from mid-Atlantic, southeastern,
midwestern, and southcentral states. But the illness remains most common in the states from which it was
originally reported...New York, New Jersey, Pennsylvania, Connecticut, Massachusetts, Rhode Island, Wisconsin,
and Minnesota. ...Lyme disease is both widespread and common in Europe where thousands of cases are
estimated to occur each year. The disease is most common in Austria, Germany, France, Sweden, and
Switzerland. But is also occurs in the three other Scandinavian countries, Belgium, Czechoslovakia, Hungary,
Italy, the Netherlands, Romania, Spain, the United Kingdom, the USSR, and Yugoslavia.”
Louis Reik, Jr., M.D. Lyme Disease and the Nervous System. New York:Thieme Medical Publishers. 1993.

“Patients with the disease have also been found in China, Japan, and Australia.”
Steere AC. Lyme disease. New England Journal of Medicine 1989;321:586-596.

“B. burgdoferi-infected ticks may be transported from Lyme-endemic areas into nonendemic areas, which may
establish new Lyme-endemic foci. Infected I. ricinus complex ticks (including I. scapularis) and infected I. uriae
have been found on migratory birds and along migratory “flyways”; they may be transported into new areas by these
birds as they travel between endemic and nonendemic areas, including counties, states, countries, continents, and
even hemispheres.”
Gardner T. Lyme disease. In Infectious Diseases of the Fetus and Newborn Infant, ed. Remington JS; Klein JO.
Philadelphia:W.B. Saunders Co. pp. 519-641. 2001.
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Lyme Disease

Co-Infections & Disease Severity
“In medicine, general emphasis has been to explain most of the manifestations with a single diagnosis;
however, in vector borne diseases, multiple infections can occur in the same patient.”
Jacobi C; Schwark C; Kress B; Hug A; et al. Subarachnoid hemorrhage due to Borrelia burgdorferi-associated vasculitis.
Eur J Neurol 2006;13(5):536-8.

“Any disease developing as a result of tick bite should be regarded as a potentially mixed infection. Clinically,
tick-borne mixed infections proceed more severely than the corresponding diseases caused by a single agent.”
Korenberg EI. Problems in the study and prophylaxis of mixed infections transmitted by ixodid ticks.
Int J Med Microbiol 2004;293 Suppl 37:80-5.

“…human coinfections involving various combinations of these pathogens [Lyme disease, babesiosis, and
ehrlichiosis] are common, and some tend to be particularly severe.”
Thompson C; Spielman A; Krause PJ. Coinfecting deer-associated zoonoses: Lyme disease, babesiosis, and ehrlichiosis.
Clinical Infectious Diseases 2001;33(5):676-85.

“…symptoms and duration of illness in patients with concurrent infections can be greater than in those with
either infection alone.”
Sweeney CJ; Ghassemi M; Agger WA; Persing DH. Coinfection with Babesia microti and Borrelia burgdorferi in a western Wisconsin
resident. Mayo Clinic Proceedings 1998;73(4):338-341.

“In tick-dominated areas, patients should always be tested for coinfection with Ehrlichia, Babesia, and Borrelia
burgdorferi.”
Javed MZ; Srivastava M; Zhang S; Kandathil M. Concurrent babesiosis and ehrlichiosis in an elderly host.
Mayo Clinic Proceeding 2001;76(5):563-5.

“Our data implicate B henselae as a potential human tick-borne pathogen. Patients with a history of
neuroborreliosis who have incomplete resolution of symptoms should be evaluated for B henselae infection.”
Eskow E; Rao RV; Mordechai E. Concurrent infection of the central nervous system by Borrelia burgdorferi and Bartonella henselae:
evidence for a novel tick-borne disease complex. Archives of Neurology 2001;58(9):1357-1363.

Infection Rates: I. Scapularis Ticks in Northeastern United States

Connecticut:
Woodbridge, CT:
32.9% of nymphal ticks / 52.6% of adult ticks positive for Lyme disease
Bridgeport, CT:
32.7% of nymphal ticks / 55.0% of adult ticks positive for Lyme disease
Findings reported in: Levin ML; des Vignes F; Fish D. Disparity in the natural cycles of Borrelia burgdorferi and the agent of Human
Granulocytic Ehrlichiosis. Emerg Infect Dis 1999;Vol 5(2):204-8.

New Jersey:
“Using polymerase chain reaction, we analyzed 529 Ixodes scapularis Say adults collected from 16 of New
Jersey's 21 counties for the presence of Borrelia burgdorferi, the etiological agent of Lyme disease.
Overall, 261 (49.3%) were positive.”
Schulze TL;Jordan RA;Hung RW;Puelle RS;Markowski D;Chomsky MS. Prevalence of Borrelia burgdorferi in Ixodes scapularis adults in
New Jersey, 2000-2001. J Med Entomol 2003;40(4):555-8.

“PCR analysis of Ixodes scapularis ticks collected in New Jersey identified infections with Borrelia burgdorferi
(33.6%), Babesia microti (8.4%), Anaplasma phagocytophila [Ehrlichiosis] (1.9%),
and Bartonella spp. (34.5%).”
Adelson ME; Rao RV; Tilton RC; Cabets K; Eskow E; Fein L; Occi JL; Mordechai E. Prevalence of Borrelia burgdorferi, Bartonella spp.,
Babesia microti, and Anaplasma phagocytophila in Ixodes scapularis ticks collected in Northern New Jersey.
J Clin Microbiol 2004;42(6):2799-2801.

Pennsylvania:
Northwestern PA:
61.6% positive for Lyme disease; 1.9% positive for Ehrlichiosis
Southeastern PA:
13.1% positive for Lyme disease; 39.8% positive for Ehrlichiosis
Findings reported in: Courtney JW; Dryden RL; Montgomery J; et al. Molecular characterization of Anaplasma phagocytophilum and
Borrelia burgdorferi in Ixodes scapularis ticks from Pennsylvania. Journal of Clinical Microbiology 2003;41(4):1569-1573.
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Lyme Disease

Symptoms
Citations
General/Constitutional “These symptoms are typically intermittent and changing, with the

exception of fatigue, which is often persistent and may be debilitating.”

Clinical manifestations of Lyme disease in the United States.
Trock DH; Craft JE; Rahn DW.
Connecticut Medicine, 53(6). 1989.
Achiness (generalized)
(1) The early clinical manifestations of Lyme disease.
Steere AC; Bartenhagen NH; Craft JE; Hutchinson GJ; Newman JH; Rahn DW; Sigal LH;
Spieler PN; Stenn KS; Malawista SE.
Annals of Internal Medicine, 99(1):76-82. 1983.
Chills
(1) The early clinical manifestations of Lyme disease.
“Chills were common, but not
Steere AC; Bartenhagen NH; Craft JE; Hutchinson GJ; Newman JH; Rahn DW; Sigal LH;
rigors.” (1)
Spieler PN; Stenn KS; Malawista SE.
Annals of Internal Medicine, 99(1):76-82. 1983.
Fatigue/Malaise/Lethargy
(1) The early clinical manifestations of Lyme disease.
Most common symptom. “some
Steere AC; Bartenhagen NH; Craft JE; Hutchinson GJ; Newman JH; Rahn DW; Sigal LH;
patients felt profoundly weak” (1)
Spieler PN; Stenn KS; Malawista SE.

Annals of Internal Medicine, 99(1):76-82. 1983.
“often constant and may be

incapacitating” (2)
(2) The clinical spectrum and treatment of Lyme disease.

Steere AC; Malawista SE; Bartenhagen NH; Spieler PN; Newman JH; Rahn DW; et al.
“Fatigue is common in all stages of
Yale Journal of Biology and Medicine, 57(4):453-64. 1984.
symptomatic infection.” (3)


(3) Neurologic presentations in Lyme disease.

Coyle PK; Schutzer SE.
Hospital Practice, 26(11):55-66; discussion 66, 69-70. 1991.
Fever
(1) Clinical manifestations of Lyme disease.
“Fever is usually absent.” (1)
Sigal L.

New Jersey Medicine, 87(7):549-555. 1990.
[In early stage disease:] “Fever was

reported in 30% of patients but was
(2) Clinical characteristics and treatment outcome of early Lyme disease in patients with
documented at office evaluation in
microbiologically confirmed erythema migrans
only 6%.” (2)
Smith RP; Schoen RT; Rahn D; Sikand VK; Nowakowski J; Parenti DL; Holman M;

Persing, DH; Steere AC.
[In early stage disease:] “typically
Annals of Internal Medicine, 136(6):421-428. 2002.
low-grade and intermittent. However,
children in particular sometimes had
(3) The early clinical manifestations of Lyme disease.
high (up to 40ºC) or persistent
Steere AC; Bartenhagen NH; Craft JE; Hutchinson GJ; Newman JH; Rahn DW; Sigal LH;
temperature elevations.” (3)
Spieler PN; Stenn KS; Malawista SE.
Annals of Internal Medicine, 99(1):76-82. 1983.
Swollen glands
(1) The early clinical manifestations of Lyme disease.
(lymphadenopathy)
Steere AC; Bartenhagen NH; Craft JE; Hutchinson GJ; Newman JH; Rahn DW; Sigal LH;
“lymph node swelling of the neck
Spieler PN; Stenn KS; Malawista SE.
and groin” (2)
Annals of Internal Medicine, 99(1):76-82. 1983.


“Regional (and occasionally
(2) Clinical pathologic correlations of Lyme disease by stage.
systemic) lymphadenopathy may
Duray PH; Steere AC.
occur.” (3)
Annals NY Academy of Sciences, 539:65-79. 1988.

(3) Clinical manifestations of Lyme disease.
Sigal L.
New Jersey Medicine, 87(7):549-555. 1990.
Stiffness
(1) The early clinical manifestations of Lyme disease.
generalized or hand (1)
Steere AC; Bartenhagen NH; Craft JE; Hutchinson GJ; Newman JH; Rahn DW; Sigal LH;
Spieler PN; Stenn KS; Malawista SE.
Annals of Internal Medicine, 99(1):76-82. 1983.
Sweating
(1) Clinical features of early erythema migrans disease and related disorders.
profuse sweating (1)
Weber K; Neubert U.
Zentralbl Bakteriol Mikrobiol Hyg (A), 263:209-228. 1986.
Thirst
(1) Lyme meningoencephalitis -- report of a severe, penicillin resistant case.
“increased thirst”
Diringer MN; Halperin JJ; Dattwyler RJ.
Arthritis & Rheumatism, 30:705-708. 1987.
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Lyme Disease
Symptoms
Citations
Head/Face/Neck
“We review our institutional experience with 266 patients with Lyme

disease, 75% of whom experienced head and neck symptoms.”
Otolaryngologic aspects of Lyme disease.
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
Laryngoscope, 101(6 Pt 1):592-5. 1991.
Bell’s palsy (uni or bilateral)
“Bell’s palsy—is among those

telltale diagnostic signs, particularly
(1) Lyme borreliosis in Bell’s palsy. Long Island neuroborreliosis collaborative study group.
when it is bilateral. It is associated
Halperin JJ; Golightly M.
with the early disseminated phase of
Neurology, 42(7):1268-70. 1992.
the infection. ...About a third of the

time, the palsy in Lyme disease is
(2) Neurologic presentations in Lyme disease.
bilateral, but both sides of the face
Coyle PK; Schutzer SE.
may not be equally affected and
Hospital Practice, 26(11):55-66; discussion 66, 69-70. 1991.
involvement can be subtle.” (2)


(3) Clinical pathologic correlations of Lyme disease by stage.
“Bilateral Bell’s palsy...almost
Duray PH; Steere AC.
constitutes a firm clinical sign that a
Annals NY Academy of Sciences, 539:65-79. 1988.
given patient in an endemic area with

bi-lateral Bell’s palsy has Lyme
(4) Acute onset of facial nerve palsy associated with Lyme disease in a 6 year-old child.
disease until proven otherwise.” (3)
Siwula JM; Mathieu G.

Pediatr Dent, 24(6):572-4. 2002.
“Lyme disease has been implicated
as the cause of over 50% of the FNPs
[facial nerve palsies] in children.” (4)
Facial/Oralfacial/Dental
(1) Otolaryngologic aspects of Lyme disease.
pain
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
“clinical manifestations may include
Laryngoscope, 101(6 Pt 1):592-5. 1991.
facial and dental pain, facial nerve

palsy, headache, temporomandibular
(2) Lyme disease: considerations for dentistry.
joint pain, and masticatory muscle
Heir GM; Fein LA.
pain.” (1)
J Orofacial Pain, 10:74-86. 1996.
Headache

“typically intermittent (hours)... but
(1) The triad of neurologic manifestations of Lyme disease: meningitis, cranial neuritis, and
could be generalized or persistent.”
radiculoneuritis.
[some] “had excruciating headache”
Pachner AR; Steere AC.
(1)
Neurology, 35(1):47-53. 1985.


“Our patients show that headache can (2) Headache resembling tension-type headache as the single manifestation of Lyme
be the first, and for a long time the
neuroborreliosis.
only, prominent sign of Lyme
Brinck T; Hansen K; Olesen J.
neuroborreliosis” (2)
Cephalalgia, 13(3):207-9. 1993.


“headaches resembling migraine,...
(3) Headache characteristics in hospitalized patients with Lyme disease.
tension-type headache... we conclude
Scelsa SN; Lipton RB; Sander H; Herskovitz S.
that recent-onset headaches are
Headache, 35(3):125-30. 1995.
common in patients hospitalized with
Lyme disease.” (3)
Hoarseness
(1) Otolaryngologic aspects of Lyme disease.

Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
[Hoarseness was reported in 4.9% of
Laryngoscope, 101(6 Pt 1):592-5. 1991.
266 patients studied.] (1)

(2) Clinical features of early erythema migrans disease and related disorders.
Weber K; Neubert U.
Zentralbl Bakteriol Mikrobiol Hyg (A), 263:209-228. 1986.
Jaw pain, stiffness, or
(1) Otolaryngologic aspects of Lyme disease.
temporomandibular joint
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
disorder (TMJ)
Laryngoscope, 101(6 Pt 1):592-5. 1991.

“Fourteen patients demonstrated
(2) Lyme disease misdiagnosed as a temporomandibular joint disorder.
temporomandibular joint pain. Of
Lader E.
these, 10 patients exhibited other
J Prosthet Dent, 63(1):82-5. 1990.
coexisting arthralgias.” (1)
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Lyme Disease
Symptoms
Citations
Muscle spasm - facial
(1) Otolaryngologic aspects of Lyme disease.
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
Laryngoscope, 101(6 Pt 1):592-5. 1991.
Neck pain, stiffness, or
(1) The early clinical manifestations of Lyme disease.
pressure
Steere AC; Bartenhagen NH; Craft JE; Hutchinson GJ; Newman JH; Rahn DW; Sigal LH;
“sometimes marked” (1)
Spieler PN; Stenn KS; Malawista SE.

Annals of Internal Medicine, 99(1):76-82. 1983.
“The most common associated

symptoms [in early Lyme disease]
(2) Clinical characteristics and treatment outcome of early lyme disease in patients with
were low-grade fever, headache, neck microbiologically confirmed erythema migrans.
stiffness, arthralgia, myalgia, or
Smith RP; Schoen RT; Rahn DW; Sikand VK; Nowakowski J; Parenti DL; Holman MS;
fatigue.” (2) [italics added]
Persing DH; Steere AC.

Ann Intern Med, 136(6):421-8. 2002.
“Headache and mild neck stiffness,

which fluctuated in intensity... were
(3) Neurological findings of Lyme disease.
the common findings.” (3)
Pachner AR; Steere AC.
Yale Journal of Biology & Medicine, 57(4):481-3. 1984.
Numbness/tingling – facial
(1) Otolaryngologic aspects of Lyme disease.
“facial paresthesia”
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
”facial hypesthesia” (1)
Laryngoscope, 101(6 Pt 1):592-5. 1991.


“he developed paresthesia in his
(2) [A patient with neuroborreliosis presenting gadolinium-enhanced MRI lesions in bilateral
tongue” (2)
facial nerves.]
Tokunaga H; Ohyagi Y; Furuya H; Araki T; Yamada T; Isogai E; Kira J.
Rinsho Shinkeigaku, 41(9):632-4. 2001.
Sore throat
(1) The early clinical manifestations of Lyme disease.
“nonexudative” (1)
Steere AC; Bartenhagen NH; Craft JE; Hutchinson GJ; Newman JH; Rahn DW; Sigal LH;
“pharyngitis” (2)
Spieler PN; Stenn KS; Malawista SE.

Annals of Internal Medicine, 99(1):76-82. 1983.
“These [neurological] symptoms

were preceded by an uncharacteristic
(2) Clinical pathologic correlations of Lyme disease by stage.
syndrome with fever, myalgia and
Duray PH; Steere AC.
pharyngitis in two cases.” (3)
Annals NY Academy of Sciences, 539:65-79. 1988.
[italics added]

(3) Chronic progressive neurological involvement in Borrelia burgdorferi infection.
Weder B; Wiedersheim P; Matter L; Steck A; Otto F.
Journal of Neurology, 234(1):40-3. 1987.
Swelling – facial
(1) Otolaryngologic aspects of Lyme disease.
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
Laryngoscope, 101(6 Pt 1):592-5. 1991.
Swallowing difficulty
(1) Otolaryngologic aspects of Lyme disease.
“Dysphagia” (1)
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
Laryngoscope, 101(6 Pt 1):592-5. 1991.

(2) Dermatomyositis associated with Lyme disease: case report and review of Lyme myositis.
Horowitz HW; Sanghera K; Goldberg N; Pechman D; Kamer R; Duray P; Weinstein A.
Clin Infect Dis, 18(2):166-71. 1994.
Twitching of facial or

other muscles
(1) Isolation of Borrelia burgdorferi from the blood of seven patients with Lyme disease.
“the other [patient] has had
Nadelman RB; Pavia CS; Magnarelle LA; Wormser GP.
intermittent facial twitches for eight
American Journal of Medicine, 88:21-6. 1990.
months. [post treatment]” (1)
Vocal paralysis

“We have seen a case where
(1) Paralysis of recurrent laryngeal nerve in Lyme disease.
serologically confirmed
Schroeter V; Belz GG; Blenk H.
B burgdorferi infection was
Lancet, 2(8622):1245. 1988.
associated with paralysis of the

recurrent laryngeal nerve.” (1)
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Lyme Disease
Symptoms
Citations
Ears/Hearing
“Otolaryngologic manifestations have been reported in all stages of the
disease.”
Otolaryngologic aspects of Lyme disease.
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
Laryngoscope, 101(6 Pt 1):592-5. 1991.
Deafness/Hearing loss

“Bilateral hearing loss was noted in 4
(1) Otolaryngologic aspects of Lyme disease.
patients” (1)
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.

Laryngoscope, 101(6 Pt 1):592-5. 1991.
“bilateral deafness and multiple other

neurological complaints some six
(2) Reversible sensorineural hearing loss in Lyme disease.
months after developing a 'target'
Quinn SJ; Boucher BJ; Booth JB.
lesion on the lower leg” (2)
J Laryngol Otol, 111(6):562-4. 1997.


“[Lyme disease] has been shown to
(3) Should we routinely screen for Lyme disease in patients with asymmetrical hearing loss?
cause asymmetrical sensorineural
Richardson H; Birchall JP; Hill J; McMaster T.
hearing loss” (3)
Br J Audiol, 28(2):59-61. 1994.


“Among the 27 patients, associated
(4) Chronic neurologic manifestations of Lyme disease.
symptoms included fatigue (74
Logigian EL; Kaplan RF; Steere AC.
percent), headache (48 percent),
New England Journal of Medicine, 323(21):1438-44. 1990.
arthritis (37 percent), and hearing

loss (15 percent).” (4)
Hypersensitivity to sound,

hyperacusis
(1) Neurologic presentations in Lyme disease.
“increased sensitivity to noise” (1)
Coyle PK; Schutzer SE.

Hospital Practice, 26(11):55-66; discussion 66, 69-70. 1991.
“Lyme disease-induced hyperacusis

can be an intensely disabling,
(2) Carbamazepine in the treatment of Lyme disease-induced hyperacusis.
chronic condition that is
Nields JA; Fallon BA; Jastreboff PJ.
accompanied by posttraumatic stress
J Neuropsychiatry Clin Neurosci, 11(1):97-9. 1999.
disorder-like psychobehavioral
sequelae.: (2)
Meniere's disease
(1) Use of electrocochleography for assessing endolymphatic hydrops in patients with Lyme
“Lyme disease can manifest itself as
disease and Meniere's disease.
Meniere's disease both clinically and
Selmani Z; Pyykko I; Ishizaki H; Ashammakhi N.
electrophysiologically” (1)
Acta Otolaryngol, 122(2):173-8. 2002.
Pain in ears
(1) The early clinical manifestations of Lyme disease.

Steere AC; Bartenhagen NH; Craft JE; Hutchinson GJ; Newman JH; Rahn DW; Sigal LH;
“Otalgia” (2)
Spieler PN; Stenn KS; Malawista SE.
Annals of Internal Medicine, 99(1):76-82. 1983.

(2) Otolaryngologic aspects of Lyme disease.
Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
Laryngoscope, 101(6 Pt 1):592-5. 1991.
Ringing in ears (tinnitus)
(1) Otolaryngologic aspects of Lyme disease.

Moscatello AL; Worden DL; Nadelman RB; Wormser G; Lucente F.
“Six patients had sensorineural
Laryngoscope, 101(6 Pt 1):592-5. 1991.
hearing loss and five had

concomitant tinnitus, two bilateral
(2) Latent Lyme neuroborreliosis: presence of Borrelia burgdorferi in the cerebrospinal fluid
and three unilateral.” (3)
without concurrent inflammatory signs.
Pfister HW; Preac-Mursic V; Wilske B; Einhäupl KM; Weinberger K.
Neurology, 39(8):1118-20. 1989.

(3) Lyme borreliosis -- an unusual cause of vertigo.
Peltomaa M; Pyykkö I; Seppälä I; Viljanen M.
Auris Nasus Larynx, 25:233-242. 1998.
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Lyme Disease
Symptoms
Citations
Eyes/Vision
“Ophthalmologic manifestations of Lyme borreliosis may occur alone or

in combination with other manifestations of Lyme borreliosis.”
Lyme disease.
Gardner T. In Infectious Diseases of the Fetus and Newborn Infant,
Ed. Remington JS; Klein JO.
Philadelphia:W.B. Saunders Company. pp. 519-641. 2001.

“Erlichiosis, babesiosis, and Lyme disease may occur together and affect
the eye or orbit.”
The ticking time bomb.
Pendse S; Bilyk JR; Lee MS.
Survey of Ophthalmology, 51(3):274-9. 2006.

“Late-phase ocular Lyme borreliosis is probably underdiagnosed because
of weak seropositivity or seronegativity in ELISA assays. Ocular borrelial
manifestations show characteristics resembling those seen in syphilis.”
Diagnosis and clinical characteristics of ocular Lyme borreliosis.
Karma A; Seppala I; Mikkila H; Kaakkola S; Viljanen M; Tarkkanen A.
Am J Ophthalmol, 119(2):127-35. 1995.

“...as in other spirochetal infections, high-dose systemic antibiotics are
required when B. burgdorferi causes ocular symptoms.”
Clinical manifestations of Lyme disease in the United States.
Trock DH; Craft JE; Rahn DW. Connecticut Medicine, 53(6):327-330. 1989.
Blindness
(1) Unilateral blindness caused by infection with the Lyme disease spirochete,

Borrelia burgdorferi.
“The fourth child had headache and
Steere AC; Duray PH; Kauffmann DJ; Wormser GP.
visual loss attributable to increased
Annals of Internal Medicine, 103(3):382-4. 1985.
intracranial pressure and perhaps also
to optic neuritis. Despite treatment
(2) Ocular Lyme disease: case report and review of the literature.
with ceftriaxone and steroids, he had
Kauffmann DJ; Wormser GP.
persistent increased intracranial
British Journal of Ophthalmology, 74(6):325-7. 1990.
pressure leading to permanent

bilateral blindness.” (3)
(3) Optic neuropathy in children with Lyme disease.

Rothermel H; Hedges TR 3rd; Steere AC.
“Long-standing intraocular
Pediatrics, 108(2):477-81. 2001.
inflammation results in loss of

vision.” (4)
(4) Schönherr U; Strle F.
In Aspects of Lyme Borreliosis,
Ed. Klaus Weber, M.D., Willy Burgdorfer, Ph.D., M.D.
Berlin Heidelberg:Springer-Verlag:pp 248-258. 1993.
Choroiditis

“Choroiditis was the first recognized
(1) Persistence of Borrelia burgdorferi in ligamentous tissue from a patient with chronic Lyme
manifestation of Lyme disease in this
borreliosis.
patient. ... Ophthalmoscopy
Haupl T; Hahn G; Rittig M; Krause A; Schoerner C; Schonherr U; et al.
demonstrated multifocal choroiditis,
Arthritis Rheum, 36(11):1621-6. 1993.
with 1 focus involving the macula
lutea.” (1)
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Document Outline

• General/Constitutional
• Head/Face/Neck
• Ears/Hearing
• Eyes/Vision
• Gastrointestinal System
• Respiratory & Circulatory Systems
• Hepatatic System (Liver)
• Musculoskeletal System
• Neurologic System
• Psychological Symptoms
• Cognitive Symptoms
• Reproduction/Sexuality
• Skin/Hair
• Other (including cancer-like presentation)

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