(Lyme) Borreliose
Anhang 2
[Ronald D. Whitmont, M.D.]
Abstract: The epidemiology, and vital statistics of Lyme disease in the U.S.
are discussed along with a review of other tick borne illnesses with mention of
their conventional diagnosis and treatment. The differences between
conventional and homeopathic management of Lyme disease are explored with
respect to some of the advantages and disadvantages of these modalities. There
is a discussion of the pitfalls of antibiotic treatment and the subsequent
development of Chronic Lyme disease and Lyme related complications which may
result from this strategy. Finally, the article advocates a classical
homeopathic approach toward Lyme disease and other tick borne infectious
illnesses. Several case studies are presented which demonstrate the
effectiveness of the classical homeopathic medical approach in all three
clinical stages of Lyme disease. The article will be of interest to homeopathic
clinicians, particularly those working in regions where Lyme disease is
endemic.
Making the diagnosis of Lyme disease has become increasingly
complicated. Two extremes seem to dominate the field: many clinicians feel that
Lyme is frequently over-diagnosed and that too many cases with so-called “soft
evidence”, meaning vague complaints, such as chronic fatigue, fibromyalgia and
depression, are inappropriately diagnosed and treated as Lyme.
Conversely, many cases with physical and cognitive symptoms resembling
Lyme are difficult to differentially diagnose, despite their symptoms dating
back to a tick bite. Both the professional and popular literature contain an
ever-growing number of reports on this topic.
In addition to the difficulty of correct diagnosis, effective management
and cure are also controversial topics. Cases of recurrent Lyme disease,
chronic Lyme disease and post-Lyme disease syndrome, are steadily increasing in
number, in spite of prolonged use of antibiotic therapies, the accepted
standard of care, suggesting that this approach may not be as effective as
desired.
Microorganisms tend to evolve resistance to antibiotics in proportion to
the length of exposure to these agents. Lyme disease is no exception5,6.
Resistance does not develop to classical homeopathic treatment, however, and
its efficacy does not diminish with use over time. Therefore, homeopathy may be
the most viable alternative treatment for use in Lyme disease and other
infectious illnesses.
Demographics:
Lyme Disease is not a common illness, although it is the most common
vector-borne disease reported in the U.S. The Centers
for Disease Control (CDC) considers it to be the fastest growing vector-borne disease
in the U.S., with an overall incidence of 7.9 per 100,000 population. In
endemic tick areas, the incidence is as high as 31.6 per 100,000 population.
95% of all U.S. cases are found within 12 states: Connecticut, Massachusetts,
New York, Rhode Island, New Jersey, Pennsylvania, Delaware, Wisconsin,
Minnesota, Maine, New Hampshire and Maryland. Of all the states, only Montana
has never reported Lyme disease.
Lyme disease was first described in the mid-1970s near Old Lyme,
Connecticut. It is not known whether this finding represented a new disease
agent that had suddenly evolved in response to environmental stressors and
shifts in the balance of host populations or whether it had been in existence
for many years but was only then identified from the background population of
all zöonotic illnesses. Whatever its origins, it now
receives tremendous publicity as an ever increasing number of individuals are
exposed to and found to have signs of infection by it. In 2005, over 23,000
cases of Lyme disease were reported to the CDC in the U.S.
Many illnesses and syndromes have been misdiagnosed as Lyme disease
(false positives) including systemic lupus erythematosus,
rheumatoid arthritis, juvenile rheumatoid arthritis, ankylosing
spondylitis, osteoarthritis, amylotrophic
lateral sclerosis, multiple sclerosis, Alzheimer’s disease, syphilis, endocarditis, Epstein-Barr Virus, infectious mononucleosis,
pinta, yaws, bejel, leptospirosis, malaria and fibromyalgia.
Many cases of Lyme disease have also been mistakenly diagnosed as
rheumatologic ailments (false negatives).
Lyme disease is typically described in three clinical phases or stages
categorized as Early Localized disease (stage 1), Early Disseminated disease
(stage 2) and Late Chronic disease (stage 3).
Stage 1: early-localized disease, may appear in the first few days after
the tick bite, and up to a month later. In 50-70% of cases it is characterized
by Erythema Migrans rash
(EM) which can be accompanied by fatigue, malaise, lethargy, headache, myalgias, arthralgias, and
regional generalized lymphadenopathy. If Rash is not
present, then the symptoms at this stage may be indistinguishable from an upper
respiratory infection (URI).
Erythema Migrans
rash (EM) is pathognomonic for Lyme disease. It
appears as a red ring in a “bulls-eye” pattern, with a central area of lighter erythema or clearing. The rash blanches when light pressure
is applied; it can be pruritic, and warm to the
touch. It is usually concentric with the site of the tick’s bite and attachment
to the host, but it can also appear at unrelated bodily sites distant
to the site of attachment or as multiple intersecting and
non-intersecting ring-like rashes. It enlarges over several days as the
spirochetes migrate centrifugally in the skin, provoking an immune inflammatory
response, visible as erythema.
Stage 2: early disseminated disease, may occur shortly after stage 1 or
be delayed by as much as 10 months after the initial tick bite. The average
latency is three weeks. Over 50% of cases develop skin rashes at this stage,
with multiple ring-like lesions. In addition, 50% of untreated patients develop
moderate to severe musculoskeletal symptoms including migratory polyarthritis and fibromyalgia-like symptoms. 10% of cases
develop neurologic manifestations, including meningitis, encephalitis, cranial
neuropathy, peripheral neuropathy, myelitis and most
commonly, Bell’s palsy. 8 – 1% of cases present with symptoms of carditis, including conduction defects with bradycardia and mild cardiomyopathy.
Other less frequent symptoms include lymphadenopathy,
conjunctivitis, liver enzyme abnormalities, hepatitis, kidney abnormalities and
proteinuria.
Stage 3: late chronic disease, may occur many months or years after the
tick bite. Fifty percent of untreated patients develop musculoskeletal
manifestations including migratory polyarthritis.
An additional 10% develop chronic monoarthritis,
most commonly in the knee. Less than 10% develop fibromyalgia. Neurologic
manifestations of the late chronic stage can include peripheral neuropathies, encephalopathies, meningoencephalitis,
Bells palsey, ataxia, dementia, and sleep disorders.
Skin problems are also frequently occurences.
While the stages share many overlapping symptoms, they are distinguished
by time of occurrence, extent and severity of symptoms and increasing
resistance to treatment.
Confirming the diagnosis of active Lyme disease requires a history of
one of the above clinical stages along with supportive findings of positive
Lyme antibody serology (ELISA). Lyme seroconversion
usually takes place 3 - 6 weeks after inoculation by tick bite. ELISA testing
is 89% sensitive and 72% specific. Positive and borderline positive ELISA tests
require confirmation with Western Blot analysis. Polymerase chain reaction
(PCR) testing may also be useful, but since it has not yet been standardized it
is not in general use.
Microbiology
The organism responsible for the complex illness known as Lyme disease
is a spirochete. Three main species have been isolated in the United States,
Asia and Europe. These include: Borrelia burgdorferi, Borrelia afzelii, and Borrelia garinii. More than 100 lesser strains of these spirochetes
have been found in the U.S. along with more than 300 others worldwide. The
diversity of these spirochetes may complicate the process of diagnosis since
they may affect the sensitivity and specificity of existing diagnostic tests.
The common Ixodes tick (the blacklegged or
deer tick) is the principal vector for the Borrelia
spirochete. Three principle subspecies of tick are found in the United States,
Europe and Asia. These include: Ixodes scapularis (formerly Dammini) in
the Eastern and North Central U.S., Ixodes pacificus in the Western U.S. and Ixodes
rincus in Europe and Asia.
The life cycle of the Ixodes tick is as follows:
1. The mature female tick lays her eggs in the fall. The eggs are
dormant over the winter and hatch into larvae in the spring or summer. After
hatching, the larvae begin to search for nourishment in
the form of a blood meal. The Ixodes larvae
are not capable of spreading Lyme disease until they actually feed on an
infected host and acquire the spirochete infection. Once aquired,
this infection resides in their digestive tracts.
2. After feeding, the larvae drop off the host, molt
over fall and winter, and emerge as nymphs the following spring. The nymphs
search for a second blood meal in the Spring or Summer. If the tick became
infected in its earlier feeding, then the spirochetes will migrate from the
tick’s digestive tract into its salivary glands where they can be released
during the next feeding process. The time of greatest risk of infection by the
nymph is from late spring to early fall, as this is when it is searching for a
blood meal, but may occur at any time of year.
3. The satiated nymph drops off the host after feeding and eventually molts into an adult which seeks yet another host and
another blood meal, usually between late fall and early the following spring.
This is the second most likely period of infection risk. Once fed, the adult
female can lay eggs and re- start the cycle, all of which spans about two
years. The eggs of the infected adult
Ixodes tick do not carry the spirochete,
which is found only in the mouth parts and gut. In some other species of tick
(see below) the female may pass on the infection to her eggs.
In one study 50% to 65% of adult Ixodes ticks
in endemic Lyme areas were found infected with the Borrelia
spirochete, while only 20 – 30% of nymphs were infected. Nymphs are not only
much smaller than adults, and more difficult to detect, but they also outnumber
adults ten to one. Not surprisingly, more than 90% of human infections develop
from nymph tick bites
It frequently takes the Ixodes tick up to 24
hours to find and make a suitable attachment on a host and an additional 36-48
hours to transmit the spirochete during the feeding process. Thus, as many as
72 hours can go by after tick exposure without developing an infection.
Consequently, it is estimated that only about 1% of Ixodes
tick bites will result in actual human infection.
STANDARD TREATMENT
Conventional protocols for treatment and prophylaxis of Lyme disease
recommend antibiotics when one or more of the following criteria are met.
1. Presence of EM rash alone. This is sufficient when the patient is in a
Lyme disease endemic region. No serologic confirmation is required before
initiation of treatment. EM is considered pathognomonic
for Lyme disease.
2. Diagnosis of active Lyme disease via serologic testing with
confirmation by Western Blot analysis in a symptomatic patient. Positive tests
without active symptoms are not considered cause to treat since there is a 7%
false-positive rate in the serologic (ELISA) test.
Other illnesses which produce false positive serology results, include
syphilis, endocarditis, Epstein Barr Virus,
Infectious Mononucleosis, rheumatoid arthritis, juvenile rheumatoid arthritis,
systemic lupus erythematosis, pinta,
yaws, bejel, leptospirosis,
and malaria. Western Blot analysis helps separate the false positives from true
positives.
3. Recent history of an Ixodes tick bite with
attachment lasting more than than 24 hours, with or
without confirmatory symptoms, when the patient is in a Lyme endemic area. The
prophylaxis protocol for adults who meet this criteria is a single oral dose of
doxycycline (200mg), unless allergy exists. When
administered within 72 hours, this treatment has been found to decrease the
risk of infection by about 20%.
The full course of antibiotic treatment recommended for active Lyme
disease in adults is oral doxycycline, 100mg 2x daily
for 2 - 3 weeks. Treatment typically extends for three to four weeks, even
though the American College of Physicians advises that a ten day course is
sufficient.
In pregnant or lactating women and in children less than 9 years old,
oral amoxicillin is generally considered the first line of treatment.
CO-MORBITITY
Diagnosis and treatment of Lyme disease is frequently complicated by
co-infection with Ehrlichiosis, Babesiosis
and other disease agents which are easily confused with Lyme. Knowledge of the
signs and symptoms of these other infections is important in making a thorough
evaluation and differential diagnosis of tick-borne illnesses.
Co-infection should be considered in cases of Lyme disease that appear
particularly severe, or if there is evidence of atypical signs and symptoms
(including severe anemia, enlarged spleen,
thrombocytopenia, or elevated liver function tests). Co-infection with either Babesiosis or Ehrlichiosis takes
place in as many as 23% of cases.
Ehrlichiosis:
Human Monocytic Ehrlichiosis
(HME) is caused by the organism Ehrlichia chaffeensis. It is transmitted primarily by the Lone Star
tick, Amblyomma americanum.
It can also be transmitted by the American dog tick, Dermacentor
variabilis. The white tailed deer is the principle
animal reservoir for HME.
Early infection with HME may be non-specific and signs may resemble
various other illnesses. Many who are infected never even become ill, and some
only develop mild symptoms of illness that
are frequently overlooked.
The incubation period for HME is between 5 - 10 days. Initial symptoms
may include fever, headache, malaise and muscle aches. Rash is uncommon in
adults, but frequent (up to 60%) in children. Laboratory findings may include leucopenia, thrombocytopenia and elevated liver function
tests.
Illness may also be severe, especially in the immunocompromised
host. It may progress to renal failure, disseminated intravascular coagulation,
meningoencephalitis, Acute Respiratory Distress
Syndrome, seizures, and coma. Mortality rate may reach 3 - 5%.
HME is most commonly reported in the Southeast and Midwestern U.S. (Arkensas/Florida/Georgia/Missouri/North
Carolina/Oklahoma/Tennessee/Texas/Virginia).
Most cases of HME have been reported in states that also have a high
incidence of Lyme disease (Connecticut/Minnesota/New York/Wisconsin).
Human Granulocytic Ehrlichiosis (HGE) is
caused by the organism Ehrlichia phagocytophilia.
HGE is carried by the same tick that carries Lyme disease and Babesiosis, the black legged tick (Ixodes
scapularis on the East Coast and Ixodes
pacificus, the Western black-legged tick on the West
Coast). The white-tailed deer and white-footed mouse are the principal animal
reservoirs for HGE.
Symptoms of HGE are similar to HME, and include an acute febrile illness
accompanied by headache, malaise, myalgias, fatigue,
vomiting, anemia and rigors. Symptoms may mimic
common viral illnesses like the a URI, the flu, viral hepatitis, aseptic
meningitis, pneumonia and cholecystitis. Less
frequent symptoms include cough, sore throat, diarrhea,
lymphadenopathy, rash, seizures, abdominal pain and
confusion. Untreated, mortality rate may reach about 7 - 10% for HGE.
A third organism, Ehrlichia ewingii, has recently been recognized and reported in
Missouri, Oklahoma and Tennessee, mostly in immunocompromised
hosts.
All Ehrlichial organisms are obligate
intracellular parasites. Diagnosis of Ehrlichiosis
can be made by examination of the blood from a peripheral smear. Serologic
testing is not helpful in making the diagnosis in acute cases (but it can be
confirmatory) since a rise in titer, or seroconversion, usually only occurs during convalescence. Coinfection with Lyme disease and Ehrlichiosis
occurs in 20% of cases. The conventional medical treatment of Ehrlichiosis is doxycycline or chloramphenicol.
Babesiosis:
In the Northeast U.S., Babesiosis is caused by
the intraerythrocytic protozoan Babesia
Microti and several related species. In Europe, Babesia is caused by Babesia divergens. Like Lyme disease and HGE, it is also
transmitted by the Ixodes tick17.
Babesiosis is usually an asymptomatic
infection, but in immunocompromised hosts it may
cause a febrile hemolytic anemia
with thrombocytopenia, atypical lymphocytes, potential for liver damage and
renal failure. Symptoms may resemble malaria, including intermittent fever,
chills, fatigue, headache, muscle pain, hepatosplenomegaly,
jaundice, anemia, nausea, and shaking night sweats.
Aproximately 25% of patients with Babesiosis are co-infected with Lyme disease. These
patients typically experience more severe symptoms and longer duration of
illness18.
The white tailed deer is the principle animal reservoir for Babesiosis.
The diagnosis of Babesiosis relies upon a high
clinical index of suspicion and may be confirmed by serologic analysis, PCR, or
direct examination of the peripheral blood smear. Conventional treatment for Babesiosis includes clindamycin
and quinine. Asymptomatic patients do not require treatment.
Rocky Mountain Spotted Fever (RMSF)
Rocky Mountain Spotted Fever is misnamed since 97% of cases occur in
states unconnected to the Rocky Mountains. It is caused by the organism Rickettsia rickettsii which
infects endothelial cells. It has been reported in all of the United States except
Maine, Vermont, Hawaii and Alaska. The highest incidence has been reported in
North Carolina and Oklahoma. RMSF is carried by the American dog tick, Dermacentor variabilis in the
Eastern U.S. and by the wood tick, Dermacentor andersoni in the Western U.S. Rocky Mountain Spotted Fever
has a 3% mortality rate.
Unlike Lyme disease, the Rickettsia parasite
may be transmitted between ticks in body fluids during the process of mating,
and female ticks may transmit the parasite to their eggs through a process
called transovarial transmission.
RMSF is difficult to diagnose in the early stages. Symptoms include
fever, malaise, myalgias, nausea, frontal headache,
vomiting, cough, pleuritic chest pain and abdominal
pain. Only 80% of cases develop a measles-like petechial
rash that initially affects only the palms and soles of the feet, but spreads
centrally over the entire body. Other signs may include thrombocytopenia, hyponatremia and elevated liver function tests. Advanced
stages include seizures and pulmonary edema.
Long term sequellae of RMSF may include
partial paralysis of the lower extremities, gangrene, hearing loss, loss of
bowel and bladder control, movement disorders and language disorders. The
disease is particularly virulent and fulminant in
those with Glucose-6phosphate dehydrogenase (G6PD)
deficiency.
Since the Rickettsial organism is an obligate
intracellular parasite it is detectable by visual microscopic examination of
the peripheral blood smear. Immunoflorescent staining
is about 60% sensitive. Conversion of ELISA titers
are generally unhelpful because they are usually delayed until convalescence19.
Conventional medical treatment includes use of doxycycline
or chloramphenicol.
Colorado Tick Fever:
Colorado Tick Fever is a viral illness caused by the Colorado Tick Fever
virus, a member of the Coltivirus genera. It is
transmitted by the Rocky Mountain Wood tick, Dermacentor
andersoni. The illness occurs in the Rocky Mountain
states at altitudes ranging from 4,000 – 10,000 feet. The highest number of
cases were reported from Colorado. Acute illness lasts up to 10 days and is
typically more severe in children younger than 10 years of age.
Colorado Tick Fever is characterized by a biphasic or “saddleback” fever
with two distinct stages. The incubation period ranges between 1-19 days. Early
signs are nonspecific, but may include sudden onset of fever, chills, headache
and retro-orbital pain, photosensitivity, myalgias,
malaise, fatigue, abdominal pain, conjunctivitis, nausea and vomiting.
Infectious sequellae include meningitis,
encephalitis and hemorrhagic fever. Severe headache, muscle aches and flat or
“pimply” rashes are present in up to 12% of cases. Laboratory findings may
include leucopenia, thrombocytopenia and elevated
liver function tests.
This illness is self-limiting, it may recur, and is not alleviated by
antibiotic therapy. Supportive care may be helpful. Lifelong immunity appears
to follow recovery.
Relapsing Fever:
Relapsing Fever is caused by the Borrelia
spirochetes hermsii, turicatae,
parker and recurrentis. The first three are
transmitted by soft ticks of genus Ornithodorus,
mostly in the Western U.S. and the last is spread by the human body louse, Pediculus humanus. Reservoir
hosts for the tick-borne infections include rabbits and rodents. There are no
animal reservoirs for the louse-spread illness except humans.
Unlike Lyme disease, this infection can be transmitted from tick to host
within a matter of minutes after tick attachment. Once inoculated the
spirochetes invade the endothelial cells producing a low-grade disseminated
intravascular coagulation and thrombocytopenia. Relapses occur due to
genetically “programmed” shifts in the outer surface proteins of the
spirochete.
Relapsing fever is characterized by repeated episodes of fever, chills,
headaches, weakness, anorexia, cough, muscle and joint pains that spontaneously
abate and then recur. Duration of illness is approximately one week with an
average of three recurrences.
Frequent complications include epistaxis, hemoptysis, iridocyclitis,
jaundice, hypotension, tachycardia, cranial nerve palsies, meningitis,
seizures, lymphadenopathy, pneumonitis,
myocarditis, meningial
signs, splenomegally and splenic
rupture. There may be a petechial or maculopapular rash.
Diagnosis is made by direct microscopic visualization of the spirochete
in blood or cerebrospinal fluid during a febrile episode. Spirochetes are
typically not found between relapses.
Mortality is less than 1% in the tick borne variety of Relapsing fever.
Conventional medical treatment includes doxycycline.
Tick Paralysis:
Tick Paralysis (tick toxicosis) is one of the
eight most common tickborne diseases in the U.S. It
is a potentially fatal reaction (in up to 10% of cases) to a neurotoxin secreted
by a female feeding tick. The neurotoxin appears to act by diminishing the
release of the neurotransmitter acetylcholine in the host.
Several species of tick carry the neurotoxin, including the American dog
tick (Dermacentor variabilis)
the Rocky Mountain wood tick (Dermacentor andersoni) the Lone Star tick (Amblyomma
americanum), the black legged tick (Ixodes scapularis), and the
Western black legged tick (Ixodes pacificus).
The illness occurs worldwide and is reported most frequently in girls less than
10 years old.
Symptoms include headache, vomiting and malaise, followed by an
ascending flaccid motor paralysis (resembling Guillain-Barre
syndrome, botulism, and myasthenia gravis) that may progress to respiratory
failure and death, if untreated.
Ticks usually feed for several days before symptoms develop. Treatment
includes removal of the tick from its site of attachment followed by supportive
care. Resolution usually follows within several hours after detachment of the
tick.
Tularemia:
Tularemia, or Rabbit Fever, is caused by the
facultative intracellular bacterium Francisella tularensis that multiplies within macrophages. It can be
transmitted by the American dog tick, the Lone Star tick, the Rocky Mountain
tick and the Pacific Coast tick. It can also be transmitted by horseflies,
deerflies and direct contact with infected animals, including rabbits. Tularemia is considered one of the most infectious
pathogenic bacteria known to man, since as few as 10 micro-organisms are enough
to cause disease. The case fatality rate is 1.4%.
Tularemia has been reported throughout North
America and Eurasia. The majority of cases have been reported in South-central
and the Western U.S. No cases have been reported in Hawaii.
Symptoms depend upon the route and site of inoculation and can include ulceroglandular, oculoglandular, oropharyngeal, gastrointestinal, pulmonary and typhoidal manifestations. Illness usually begins 5 - 7 days
after inoculation and includes recurrent fevers, generalized lymphadenopathy leading to ulceration, conjunctivitis and
pneumonia. It is usually characterized by a primary pustular
lesion on an extremity. Chest X-Ray may present with a triad of oval opacities,
hilar adenopathy and
pleural effusion.
Diagnosis should be based on history of direct exposure to animals or
ticks. Contact with lesions for diagnostic examination is not recommended and
is considered hazardous due to high risk of infectivity. Conventional medical
treatment includes streptomycin, doxycyline or
ciprofloxacin.
Southern Tick-Associated Rash Illness (STARI)
STARI is a condition associated with bites from the Lone Star tick (Amblyomma americanum). Symptoms
include an EM type rash with associated fatigue, fever, headache, muscle and
joint pains. Symptoms develop within one week of a tick bite and resolve
promptly with treatment.
The Lone Star tick is found from central Texas and Oklahoma eastward
across the southern states and along the Atlantic coast as far north as Maine.
The infectious agent has not been identified23.
Homeopathic Treatment
The cornerstone of homeopathic medical treatment is understanding the
way in which the illness manifests itself through changes in a particular
individual’s health. The history provides the foundation with which to
understand the individual patient, making it possible to comprehend how the
disease manifesting in each given case constitutes a change from that person’s
pre-morbid state.
The classical homeopathic prescription is based, not on the diagnosis of
Lyme disease per se, but on this personalized understanding of the
characteristic form of disease expression in that individual host; the
particular way this individual has departed from his or her own pre-morbid
normalcy.
Understanding this point is critical, since it marks the divergence of
homeopathy from conventional allopathic treatment. One cannot practice
homeopathy effectively or be true to homeopathic principles if one fails to
utilize this methodology.
Classical homeopathic treatment of Lyme disease can only be undertaken
after a thorough analysis of an individual who is affected by a disturbance in
their health. Since illness manifests uniquely in each individual, effective
treatment must follow the same guidelines.
CASES
Case One: Stage 1, early-localized disease.
A fourteen year-old female was evaluated in early September 1996. Her
symptoms included a single ring-like lesion on the right thigh for one week. An
“insect bite” had been noted about 10 days earlier. No insect had been seen.
Complaints included pain in the thigh, but no systemic symptoms, fever, chills
or viral-like illnesses.
Physical exam revealed mild facial acne, normal pulmonary and cardiac
exam, a clear bull’s-eye rash with central clearing on the left posterior thigh
reaching around to the mid-anterior inguinal area, measuring 20+ cm in
diameter. Neurologic and lymphatic examinations were normal. Vital signs were
normal and she was afebrile.
Impression: Stage of 1 Lyme disease with EM rash.
Treatment: A Stat dose of the homeopathic medicine, Lyme Tick Nosode 30C, repeated at 24 and 48 hours for a total of
three doses.
First follow up occurred five weeks later in Mid October 1996. The EM
rash had faded rapidly and disappeared after one week. She was symptom-free at
this appointment and at three subsequent follow up visits over the next twelve
months. There was no further evidence of infection or recurrence.
Lyme Tick Nosode was used as an isopathic nosode, since it is
prepared from the macerated body of an Ixodes tick.
Homeopathic and isopathic nosodes
are frequently useful in cases that fail to demonstrate characteristic
individualizing symptoms due to either to the early stage of illness, or when
too much suppressive treatment has eradicated important symptoms of a later
stage. The homeopathic medicine, Ledum palustre, prepared from wild rosemary, has also been
advocated by numerous homeopathic physicians for use in stage 1 Lyme
prophylaxis.
Cases of stage 1 prophylaxis are considered controversial precisely
because guiding individual symptoms may be absent or minimal at presentation.
Some homeopaths have argued in favor of the routine
use of antibiotics in these cases.24 However, due to the considerations
discussed below, I do not recommend this approach.
Case Two: Stage 2, early disseminated disease.
A 9 year-old female was seen in June 1996. She had been diagnosed with
juvenile rheumatoid arthritis (JRA) seven months earlier; a month after an
engorged deer tick was removed from her scalp.
Symptoms included three separate episodes of bilateral knee swelling, leg
swelling, a “target” rash on her leg and pains in the left elbow and left
ankle. The skin of her legs was described as “tingly” and her knees felt “hot”
and occasionally looked red. She reported feeling tired in the afternoons after
about 1:00 p.m. Pain was present throughout both the legs for the previous
three weeks. Knee pain forced her to limp while walking. Her joint pains were
relieved from external heat and better from continual movement.
Additional symptoms included poor appetite and constipation. She
preferred fresh, open air.
Physical exam revealed temperature was 97.6 with a pulse of 80.
Examination of head and neck was remarkable for a mildly tender cervical adenopathy. The extremities were remarkable for a grossly
deformed left knee with positive ballotment sign of
the patella, and marked effusion. The left knee was warmer than the right, but
it was not erythematous. Range of motion was limited
due to pain on flexion. There were no rashes and no further lymphadenopathy
was noted.
Impression: Stage 2, early disseminated Lyme disease with intermittent monoarticular arthritis of the knee and recurrent episodes
of polyarticular arthritis over seven months.
Treatment: Lyme titer with a complete blood
count (CBC) and erythrocyte sedimentation rate (ESR) were ordered. She was
treated with the homeopathic medication Veratrum viride 200C, which was given stat and then “plussed” in water every 24 hours, for three days.
First follow up took place four weeks later in July 1996. Lyme titer was reported as strongly positive. The ESR was
elevated at 44 (normal 10-20), and her CBC was normal. At that time she felt
“much better”. She reported that there was no further pain and only a slight
swelling remained in the left knee. All her symptoms were steadily improving.
Treatment: She was given a single dose of the homeopathic medicine Syphilinum Nosode 1M.
The third follow up occurred in September 1996. At that appointment, she
was completely symptom-free without any recurrences. Her physical exam was
completely normal. Her cervical adenopathy had
resolved, and her knees were now unremarkable.
She continued to follow up over two more years, but there were no
further recurrences.
Verat-v.: the homeopathic medicine prepared from the
root of the American Hellebore plant. The plant contains Veratrine
and other alkaloids and is known for its affinity for producing symptoms in
muscular tissue as well as acute rheumatism. This remedy was chosen on the
basis of the patient’s total symptom picture.
Syph.: the nosode of
syphilis, another illness transmitted by spirochete. It was selected as a
homeopathic nosode to finish the case.
Case Three: Stage 3, late chronic disease.
A twenty-six year old female was evaluated in July 2006. She complained
of complications resulting from chronic, recurring Lyme disease diagnosed 8
years before. Previously, she had tested positive for Lyme disease, Ehrlichiosis and Babesiosis and
had undergone extensive treatment for each of these conditions including
extended courses of oral, intravenous and intramuscular antibiotic therapy. Her
symptoms now included two “major relapses” annually that included symptoms of
hot flashes, gastralgia, arthralgias,
anorexia, nuchal rigidity, confusion of sensorium and cognition, difficulty concentrating, and
complete exhaustion. Each major relapses typically lasted several months, and
were only mitigated by extended courses of oral or intravenous antibiotics.
She also suffered from chronic daily symptoms of severe fatigue and
gastrointestinal ill health that included bloating, fullness, easy satiety,
post-prandial abdominal distension, frequent
belching, nausea, vomiting, muscle cramps, watery diarrhea
with mucus, alternating with dry stools and constipation. Her symptoms of early
satiety and gastroparesis prevented any weight gain.
She had been chronically underweight and malnourished since initiating
conventional antibiotic treatment for Lyme.
She had been amenorrheic for 3 years.
The list of medications that had been treated with included Rocephin, Zithromax, mepron, bicillin, Larium, Malarone, doxycycline, flagyl, and various cephalosporins. She had also received treatment reglan and zelnorm. Her current
medications included armor thyroid, Claritin and tinidazole.
Over the course of her treatment she had developed a panoply of
complications including hypothyroidism, candidiasis, cholelithiasis (leading to cholecystectomy),
gastroparesis, intestinal disbiosis,
an occular thrombosis with retinal vein occlusion and
constipation.
Impression: stage 3 Lyme disease with multi-system involvement and
treatment failure using antibiotics.
Treatment: She was treated with the homeopathic medicine Abrotanum artemesia in the Q1
formulation, administered once daily.
First follow up took place one month later in August 2006. At that time,
she noted general improvement in all areas. She did note the development of an
initial aggravation of her gastrointestinal symptoms that was rapidly followed
by increase in her appetite and some modest weight gain.
The next series of follow ups occurred between October and May 2007. She
noted continued improvement and stability in all areas. Although this case only
has follow up over one year, it is still important since severity and periodicity
of her symptoms (which she had experienced for eight years) was immediately
altered following homeopathic intervention.
Abrot.; known to be associated with malnutrition,
emaciation and marasmus. It was selected on the basis
of all of her her symptoms at the time of
presentation. Treatment in this case followed the patient’s individual
manifestations of illness without particular emphasis on the suppressive nature
of her previous treatments or the actual diagnosis of Lyme disease. I
anticipate that she may need
a disease nosode at some point in the future,
but the timing of this medicine will be determined by her clinical progress,
not by formulae.
These cases illustrate how the specific symptoms of an individual
patient may guide the practitioner in the selection of a homeopathic medicine
capable of curing Lyme disease without the need for antibiotic treatment.
All three of the cases demonstrate the effectiveness of homeopathic
medicines in the prevention and treatment of Lyme disease and related syndromes.
Treatment is based upon repertorization of symptoms
and analysis of the individual case at hand whenever possible.
DISCUSSION
It is important to recognize both the clinical manifestations of Lyme
disease and other tick-borne illnesses, and to understand the treatment options
available for these conditions including both the conventional allopathic
approach and the homeopathic approach.
Using antibiotics in accordance with the standard of conventional care
does not guarantee cure of these illnesses. For this reason, some authorities
advise treatment protocols that extend antibiotic
use indefinitely25. The outcome of this approach appears to be an
increasing number of recurrent and chronic cases difficult to manage or even to
fit into clear diagnostic categories.
This situation has created a number of different dilemmas among
conventional allopathic physicians, not only in diagnosis, but also in
management and appropriate use of antibiotics.
Since the allopathic system of management is diagnosis-driven, the first
stumbling block preventing appropriate treatment may occur if diagnosis is not
clearly defined. Once diagnosis is determined, there are still more issues
regarding appropriate length of antibiotic therapy and management of treatment
failures.
By contrast, the classical homeopathic paradigm is not based on
diagnosis, but on the particular idiosyncratic symptoms and history pattern of
each individual patient. The homeopath accepts that each case represents a
unique blend of symptoms that can be treated safely regardless of diagnosis.
Verifying laboratory confirmation is helpful in determining the name of the
illness, but not in selecting treatment.
Homeopathic medicine selection is driven by the subjective symptom
pattern, not by the diagnostic disease label. This approach takes aim at the
specific pattern of disturbance in an individual. It appears to do this without
provoking disease resistance, and may in fact promote host resistance. Further
study needs to evaluate exactly what systems are involved in this process and
to what degree.
The homeopathic methodology is not rigid. The pharmacopea
provides an extremely wide range of treatment options. There are a number of
different style, including classical homeopathy, which make the application of
homeopathic principles extremely flexible.
In comparison with conventional antibiotics, homeopathy offers far more
advantages than disadvantages.
Antibiotics may have definite curative effects, but on the whole they
are not as effective in treating Lyme disease as would be ideally desired.
Their effectiveness also varies at different stages of Lyme disease. Grasping
this understanding will help determine when their use will be more or less
useful and when homeopathy would be the preferred intervention modality.
Prolonged use of antibiotic therapy is associated with greater risk and
likelihood of developing drug resistance. This phenomenon is a huge global
concern, and is mostly the result of a history of indiscriminate overuse of
these agents in both medicine and agriculture.
The issue of resistance, with the subsequent development of recurrent
infections, chronic infections and the proliferation of progressively stronger
strains of micro-organisms has been the focus of extensive investigation and
concern.
Antibiotics do play a pivotal role in the treatment of severe
infections, but in those infections that are less severe these drugs may
actually work against disease resolution. There is definite evidence (often
ignored) that these agents actually delay the development of host immunity
while promoting a state of perpetual illness due multiple factors associated
with their use.
[Goodman & Gilman state in The Pharmacological Basis of
Therapeutics]
Another interesting twist that may influence the efficacy of antimicrobial
therapy is that these agents have been shown to affect various host immune
responses adversely; these include leukocyte chemotaxis,
lymphocyte and monocyte transformation, antibody
production, phagocytosis, and the microbicidal
action of polymorphonuclear leukocytes. While the
clinical significance of this immunosuppression is
not known, these observations should help discourage the indiscriminate use of
antibiotics.
These phenomena are suppressive in nature and will directly contribute
to the disease resistance and chronic illness. Samuel Hahnemann foresaw this
dilemma when he wrote, in par. 60 of The Organon:
When these ill consequences arise from the antipathic
employment of medicines (as may very naturally be expected) the ordinary
physician believes he can aid his cause by giving, with each renewed
aggravation, a stronger dose of the medicine. This results, likewise, in only a
short-lasting pacification. Since this necessitates an ever higher
intensification of the palliative, there ensures either another greater malady
or frequently even incurability, danger to life or death itself, but never cure
of a malady that is old or very old.
The sad result of this conventional antibiotic approach is that these
agents become overused, and over time individuals become more dependent upon
their periodic reapplication to palliate their care. With these practices comes
the development of a chronic state of illness and drug dependency.
These outcomes are frequently misinterpreted by conventional physicians and
the blame is laid either on the disease or the patient, thereby providing
justification for the means. In this manner, allopathic practices have always
proceeded to advocate for their own existence in the very face of empiric proof
that other, perhaps less “logical” (homeopathic) therapies, provide curative
treatments with far less morbidity and mortality.
CONCLUSION
Homeopathic treatment has demonstrated worldwide effectiveness in the treatment
of a wide variety of infectious illnesses. The mechanism through which these
agents work remains unknown, but they appear to support the function of the
immune system rather than suppress it.
The judicious use of the classical homeopathic method has proven itself
clinically effective in preventing and treating illnesses like Lyme disease in
all its clinical stages.
Homeopathy is a viable and effective method of treatment of Lyme disease
and other infectious illness. Clinical experience demonstrates that the
judicious use of homeopathic medicines applied through the classical
homeopathic approach is an excellent method of treating and curing Lyme
disease. It is an approach worthy of further study and application.