Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
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Post by Yvonne » Fri 19 Dec 2008 11:24
Abstract: The 53-year-old woman was initially diagnosed with multiple sclerosis,
despite the fact that she did not really meet the clinical criteria. Her only symptoms
were clumsiness and weakness of the right extremities. Being a veterinary research
worker she had been exposed to infectious material. In 1995, she was diagnosed with
ELISA as having toxoplasmosis and treated as such. In 2002, after the infectious, flu-
like disease, she revealed arthritis and drowsiness, also with memory and language
impairment. The patient continued to have symptoms consistent with previously
examined clumsiness. She was diagnosed with Lyme via ELISA and PCR, and treated.
She made a full recovery from acute symptoms. After a few months, neurological and
neuropsychological examinations were performed. On the background of mild cognitive
decline apraxia and difficulties of attention were noted as the main problems. A apraxia
of the right hand complicated the patient’s life and depreciated her quality of life. The
patient underwent MRI examination. FSE, FAST and FLAIR sequences were made.
The MRI demonstrated the appearance of several small hyperintense lesions in the
white matter of the left and right frontal and left parietal lobe. These lesions were
typical of the post-inflammatory leucoencephalopathy. Additionally, a ring-shaped,
low-intensity lesion in the posterior part of the left parietal lobe was noticed. The lesion
was 8 mm in diameter and described to be an old toxoplasmosis lesion. The patient had
been treated and the symptoms consistent with Lyme disease resolved. Patient continues
to have symptoms consistent with focal destruction of the parietal lobe. Over the past
six months, she has not progressed and relapsed in a manner that is consistent with MS.


M.K., a 53-year-old woman and highly educated, was
examined. She was right-handed, but when she noticed
problems with that hand she began to use her left hand.
She now claims to be left-handed.
She was examined with a 7-year history of clumsiness,
weakness of the right extremities, and memory and
language impairment. Being a veterinary research worker,
she had been exposed to infectious material.
In 1995, the patient suffered from lymph nodes
enlargement and fever.
She was diagnosed with ELISA as toxoplasmosis. After
a routine treatment (Rovamycine and Fansidar) she was
expected to make a full recovery. Her only complaint was
clumsiness of the left extremities without any clear-cut
picture of paresis (according to the history).
At the beginning of the year 2002, she suffered from an
infectious flu-like disease. She revealed arthritis and
drowsiness, with memory and language impairment. That
patient continued to have symptoms consistent with
previously examined clumsiness. She was initially
suspected of and diagnosed with multiple sclerosis.
According to the history, however, she did not really meet
the clinical criteria for MS. Symptoms did not disappear
after the treatment for MS. After a few weeks (2002), she
was admitted to the Department of Occupational
Biohazards Institute of Agricultural Medicine in Lublin.
She underwent careful neurological examination as well
as a careful history inquiry. She did not remember a tick-
bite episode, but was being exposed to infectious material.
Finally, she was diagnosed with Lyme neuroborreliosis
by ELISA and PCR. After 4-weeks treatment with
cefalosporines intravenously, she recovered from arthritis,
drowsiness and language impairment.
The patient, however, continues to have symptoms
consistent with focal destruction of the parietal lobe.
It is important to note is that over the past 6 months she
has not progressed or relapsed in a manner consistent with
Multiple Sclerosis.
Thus, a careful neuropsychological examination was
performed and neuroimaging (MRI) repeated.


The patient underwent a standard magnetic resonance
maging examination. FSE, FAST and FLAIR sequences
were made to acquire T1 and T2-weighted images in
axial, saggital, and transverse planes of the head (Fig. 1).
The MRI examination in the T2-weighted and FLAIR
mages demonstrated the appearance of several small
hyperintense lesions in the white matter of the left frontal
and left parietal lobe. A similar lesion was seen in the
ight frontal lobe. These lesions could have been consi-
dered rather typical for the post-inflammatory leucoence-
phalopathy. Additionally, the ring-shaped low-intensity
esion in the posterior part of the left parietal lobe, a little
below the level of the lateral ventricles was observed. The
esion was 8 mm in diameter and did not enhanced after
.v. paramagnetic contrast medium administration. Based
on this picture, an old toxoplasmosis lesion with calcifica-
ions was suspected. The cerebral ventricular system was
ymmetrical and not enlarged. The infratentorial structu-
es were within normal limits.
It was concluded that the ring-shaped lesion could be a
oxoplasmosis lesion, while the small hyperintense lesions
could be the consequences of neuroborreliosis.


Neuropsychological diagnosis was performed twice
within 6 months.
Standard battery of tests (Wechsler Inteligence Scale
WAIS) - R, Benton Test, Rey’a Figure Test, ADAS,
MMSE were used. Standard battery of test does not
provide qualitative analyses of the structure of disorders,
so experimental methods were also used.
tests and consists of: oral praxis, ideomotor praxis,
ideational praxis and dynamic praxis (synchronization of
hand movements).


The results indicated that the level of intellectual skills
of the patient was lower than average (II = 88, manifests
lower than an average level of intellectual progress). The
lowest results were assessed in arithmetic’s. This
suggested that she had problems with operations on the
figural material. This lower then average score could have
affected her thinking. The score on knowledge
(knowledge, vocabulary) was also lower than average.
The patient, however was aware of her problems, and was
critical of the effects of her work on items.
Both transmission and reception activities of the speech
were correct. Story speech was preserved. The dominant
problem was a limited vocabulary. Patient’s speech was
hesitant and the patient had difficulty in finding the word
in spontaneous speech, despite the fact that she was
looking for very difficult words. The patient additionally
had problems with attention. She could be distracted very
easily. The patient correctly constructed items which
needed generalization and abstractions (ex. classification).
Modest difficulties in calculation were noticed. Patient
complained of writing difficulties; she could not write a
sentence correctly or copy correctly. Despite problems
with motor skill, she could write correctly with her left
hand. Her drawing, however, was tremulous and
Praxis seemed to be the most impaired function. The
affected hand could not move on command. Patient’s
hand attempted unsuccessfully to perform movement, or
was undertaken very slowly.
There was also disorder in ideational praxis. The
patient was not able to demonstrate how to pray, how to
brush teeth or how to salute. There were no disorders
noticed, however, in oral praxis.
In the second investigation (after 6 months), improve-
ment, especially within memory skills, was noticed. The
patient made significant progress in developing strategies
for remembering (from the interview and the observa-


There is substantial data in the literature which
illustrate that months to years after initial infection,
patients with borreliosis develop a subtle encelopathy
characterized primarily by memory difficulty [12]. The
same phenomenon following long periods of latent
infection was described [12]. In addition, some of these
patients exhibit peripheral sensory symptoms. For
example, distal paresthesias or spinal radicullar pain were
described [13]. These neurological abnormalities may
occur in association with Lyme arthritis, or occur long
after joint involvement has been resolved [13].
A few data have been published to characterize the
memory disturbances of borreliosis encephalopathy.
Steere et al., [12] compared patients with this disorder to
fibromyalgia and depressed patients using neuropsycholo-
gical tests. Patients with borreliosis encephalopathy
showed mild but statistically significant memory deficits
in California Verbal Learning Tests and Wechsler
Memory Scale. In contrast, the other 2 groups had normal
test scores on memory, but abnormal on the tests that are
more sensitive to somatic concerns, including anxiety and
depression. In another study, the researchers compared
the patients with Lyme disease to those with CSF
abnormalities and those without. The patients with
abnormal CSF analyses had significantly lower memory
tests scores that the patients in the 2 control groups. Thus,
it is possible to document the memory deficit in most
patients with neuroborreliosis. These data are the
evidence to prove the existence of borreliosis
encephalopathy. These findings confirm that patients with
neuroborreliosis can have active spirochetal infection in
the white matter areas of the brain.
The other problem which occurred in the case of
patients to be discussed is the growing body of evidence
describing difficulties in diagnosis between neuro–
borreliosis and multiple sclerosis.
There were data suggesting that Borrelia might have
been involved in the etiology of MS [4].
This suggests the consideration of MS in the
differential diagnosis of neuroborreliosis.
Because of age (41) and sex (female), 2 facts
corresponding with multiple sclerosis, this diagnose was
considered as well in the case of our patient.
After extensive differential diagnosis it was concluded,
however, that she did not meet the clinical criteria for MS.
Multiple sclerosis is an autoimmune disease involving
predominantly the white matter of the brain and spinal
cord, and is one of the most common neurological
disorders of younger adults and a substantial cause of
lasting neurological disability [7].
Clinical pattern of multiple sclerosis have been defined
by international consensus [6]. About 85% of patients
initially experienced one or more relapses followed by
complete or incomplete recovery. This clinical pattern is
referred to as the relapsing-remitting phase. Over 10
years, roughly 50% of these patients will experience a
transition to the secondary progressive phase,
characterized by a gradually worsening disability, with or
without superimposed relapses. About 10% of patients
experienced a clinical course that is progressive from
onset, primary progressive multiple sclerosis. The
remaining 5% of patients experienced progressive
disability from onset, later accompanied by one or more
superimposed relapses; this pattern is referred to as
progressive relapsing multiple sclerosis [6].
None of the above mentioned clinical patterns can be
applied to the patient’s experiences.

Moreover, the neuroimaging pictures did not meet MRI
criteria for multiple sclerosis.
Although brain MR is abnormal in 95% of patients
with clinically definite multiple sclerosis, the MRI alone
cannot be a key factor in diagnostic procedures. For
example MS plaque can mimic even neoplasm. On the
other hand, lesion burden on T1 weighted images
correlates well with clinical disability.
Key imaging findings, such as multiple perpendicular
calloseptal hyperintensities and incomplete rim
enhancement in MRI, are the best diagnostic clues to
support clinical diagnosis of multiple sclerosis. Although
iso- to hypodense changes with mild to moderate
enhancement can be seen in CT, magnetic resonance
imaging is crucial.
Acute multiple sclerosis demyelinating plaques are to
mildly hypointense and hypointensity increases in
initially demyelinated plaques while decreases in
remyelinating lesions in T1 weighted images. Chronic
lesions, however, in T1 weighted images usually have
hypointense centres and with a mild hyperintense rim so-
called lesion within a lesion appearance. In T2 weighted
and FLAIR (saggital images are crucial) bilateral,
asymmetric linear ovoid hyperintense lesions in corpus
callosum, periventricular region (perpendicular to
ventricles at calloseptal interface) are observed. Mostly,
subcortical lesions are seen . In 10–20% of chronic MS
cases, however, hypointense basal ganglia or (in 5%)

cortical lesions are seen in T2WI and FLAIR. Perilesional
edema can also be seen. There are characteristic changes
in contrast-enhanced T1 weighted images. The other
modality (MRS, DWI) findings differ with clinical type.
The best recommendation for MS therefore is routine MR
(sagittal FLAIR, coronal contrast enhanced T1WI).
In our patient no such a picture was observed, however.
The MRI examination in the T2-weighted and FLAIR
images demonstrated the appearance of several small
hyperintense lesions in the white matter of the left frontal
and left parietal lobe. A similar lesion was seen in the
right frontal lobe.
These lesions could have been rather typical for the
post-inflammatory leucoencephalopathy. The character of
the changes observed in MRI corresponded well with the
clinical picture of neuroborreliosis.
Moreover, unspecific Borrelia antibodies can be present
in patients with demyeliniating processes. Not only
Borrelia specific antibodies, however, can be seen in MS.
CSF antibodies against other pathogens such as measles,
rubella, VZV, mumps, HSV are present in MS [4].
Rehse-Kupper et al.[9] investigated unclassified MS
patients with definite diagnosis for serum antibodies
against Ixodes ricinus Borrelia, followed by CSF
analysis, both by ELISA.
Their results did not support the hypothesis of a
frequent etiologic role of Borrelia in MS.
Obviously, latent neuroborreliosis can be combined
with MS serendipitously.
Thus, in order to differentiate neuroborreliosis from
MS, the existence of a significant level of CSF antibodie
n the beginning of the process, and normalization of th
iter after specific therapy is needed.
Moreover regardless of the clinical picture, MS patient
eropositive to Borrelia should be treated specifically
with respect to latent Borrelia infection, especially when
he patient has undergone immunosuppressive therapy.


To the best of our knowledge, this is the first case in
he literature describing the coexistence of
neurotoxoplasmosis and neuroborreliosis.
Chronic Lyme neuroinfection can cause mild cognitive
decline of the patient. Chronic infection with
oxoplasmosis can lead to immunodeficiency. It may be
suggested that toxoplasmosis can facilitate Lyme
nfection, while any kind of focal neurological sign in an
mmunodeficient patient can suggest neurotoxoplasmosis.

Listen to all,
plucking a feather from every passing goose,
but follow no one absolutely

Posts: 2768
Joined: Thu 1 Jul 2010 8:33


Post by RitaA » Wed 18 Jul 2012 8:22

Yvonne has also posted about the potential for ticks to carry toxoplasmosis gondii here:

Ixodes Ricinus as a potential vector of toxoplasma gondhi ... sis#p19606

I don't recall coming across any articles where Ixodes scapularis or Ixodes pacificus (found in North America) have been tested for t. gondii , however it has been found in many animals worldwide -- including rodents.

My question at this time is whether some individuals with tick-borne illnesses might also be suffering from toxoplasmosis or whether the case study above is an isolated instance. A related question is whether or not non-pregnant individuals are routinely tested for toxoplasmosis.

One thing I've noticed lately is that people seem to be getting shingles in record numbers. Shingles is caused by reactivation of a dormant virus called varicella-zoster (which causes chickenpox). Is this simply because baby boomers are now aging and our immune systems are less robust or is there some other explanation for this? There is even a shingles vaccine available to those over 50 or 60 (depending on where you live) -- which leads me to believe the incidence of shingles is on the rise. I haven't looked into this at all, but shingles just came to mind as I was writing this.

Okay, enough questions and speculating.

To demonstrate just how widespread toxoplasmosis really is, and how even the CDC now considers it to be worthy of attention, I'm posting a few links. I'm using mostly North American examples for this post just for the sake of simplicity:
Clin Infect Dis. 2009 Sep 15;49(6):878-84.

Risk factors for Toxoplasma gondii infection in the United States.

Jones JL, Dargelas V, Roberts J, Press C, Remington JS, Montoya JG.
Division of Parasitic Diseases, National Center for Zoonotic, Vectorborne, and Enteric Diseases, Coordinating Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30341, USA.

Toxoplasmosis can cause severe ocular and neurological disease. We sought to determine risk factors for Toxoplasma gondii infection in the United States.

We conducted a case-control study of adults recently infected with T. gondii. Case patients were selected from the Palo Alto Medical Foundation Toxoplasma Serology Laboratory from August 2002 through May 2007; control patients were randomly selected from among T. gondii-seronegative persons. Data were obtained from serological testing and patient questionnaires.

We evaluated 148 case patients with recent T. gondii infection and 413 control patients. In multivariate analysis, an elevated risk of recent T. gondii infection was associated with the following factors: eating raw ground beef (adjusted odds ratio [aOR], 6.67; 95% confidence limits [CLs], 2.09, 21.24; attributable risk [AR], 7%); eating rare lamb (aOR, 8.39; 95% CLs, 3.68, 19.16; AR, 20%); eating locally produced cured, dried, or smoked meat (aOR, 1.97; 95% CLs, 1.18, 3.28; AR, 22%); working with meat (aOR, 3.15; 95% CLs, 1.09, 9.10; AR, 5%); drinking unpasteurized goat's milk (aOR, 5.09; 95% CLs, 1.45, 17.80; AR, 4%); and having 3 or more kittens (aOR, 27.89; 95% CLs, 5.72, 135.86; AR, 10%). Eating raw oysters, clams, or mussels (aOR, 2.22; 95% CLs, 1.07, 4.61; AR, 16%) was significant in a separate model among persons asked this question. Subgroup results are also provided for women and for pregnant women.

In the United States, exposure to certain raw or undercooked foods and exposure to kittens are risk factors for T. gondii infection. Knowledge of these risk factors will help to target prevention efforts.

[PubMed - indexed for MEDLINE]
Free full text ... id=6821480
Parasitology (2009), 136 : pp 1877-1885
Copyright © Cambridge University Press 2009
DOI: (About DOI)
Published online: 21 September 2009

Research Article

Evidence for high levels of vertical transmission in Toxoplasma gondii


a1 Centre for Parasitology and Disease Research, School of Environment and Life Sciences, University of Salford, Salford, M5 4WT, UK

a2 Misurata Central Hospital, PO Box 65 Misurata, Libya

a3 Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK


Toxoplasma gondii is a highly ubiquitous and prevalent parasite. Despite the cat being the only definitive host, it is found in almost all geographical areas and warm blooded animals. Three routes of transmission are recognised: ingestion of oocysts shed by the cat, carnivory and congenital transmission. In natural populations, it is difficult to establish the relative importance of these routes. This paper reviews recent work in our laboratory which suggests that congenital transmission may be much more important than previously thought. Using PCR detection of the parasite, studies in sheep show that congenital transmission may occur in as many as 66% of pregnancies. Furthermore, in families of sheep on the same farm, exposed to the same sources of oocysts, significant divergent prevalences of Toxoplasma infection and abortion are found between different families. The data suggest that breeding from infected ewes increases the risk of subsequent abortion and infection in lambs. Congenital transmission rates in a natural population of mice were found to be 75%. Interestingly, congenital transmission rates in humans were measured at 19·8%. The results presented in these studies differ from those of other published studies and suggest that vertical transmission may be much more important than previously thought.

(Received June 12 2009)
(Reviewed July 19 2009)
(Accepted July 22 2009)
(Online publication September 21 2009)
Exp Parasitol. 2010 Jan;124(1):10-25. Epub 2009 Mar 24.

Waterborne toxoplasmosis--recent developments.

Jones JL, Dubey JP.
Division of Parasitic Diseases, National Center for Zoonotic, Vectorborne and Enteric Diseases, Coordinating Center for Infectious Diseases, Centers for Disease Control and Prevention, 4770 Buford Highway, MS: F22, Chamblee, GA 30341, USA. JLJ1@CDC.GOV

Humans become infected with Toxoplasma gondii mainly by ingesting uncooked meat containing viable tissue cysts or by ingesting food or water contaminated with oocysts from the feces of infected cats. Circumstantial evidence suggests that oocyst-induced infections in humans are clinically more severe than tissue cyst-acquired infections. Until recently, waterborne transmission of T. gondii was considered uncommon, but a large human outbreak linked to contamination of a municipal water reservoir in Canada by wild felids and the widespread infection of marine mammals in the USA provided reasons to question this view. The present paper examines the possible importance of T. gondii transmission by water.

Published by Elsevier Inc.

[PubMed - indexed for MEDLINE]

Healthy people (nonpregnant)

Healthy people who become infected with Toxoplasma gondii often do not have symptoms because their immune system usually keeps the parasite from causing illness. When illness occurs, it is usually mild with "flu-like" symptoms (e.g., tender lymph nodes, muscle aches, etc.) that last for several weeks and then go away. However, the parasite remains in their body in an inactive state. It can become reactivated if the person becomes immunosuppressed.

Page last reviewed: November 2, 2010
Page last updated: November 2, 2010
Foodborne Pathog Dis. 2011 Jul;8(7):751-62. Epub 2011 Apr 12.

Toxoplasma in animals, food, and humans: an old parasite of new concern.

Cenci-Goga BT, Rossitto PV, Sechi P, McCrindle CM, Cullor JS.
Sezione di Ispezione degli Alimenti di Origine Animale, Facoltà di Medicina Veterinaria, Università degli Studi di Perugia, Perugia, Italy.

All hosts, including humans, can be infected by any one of the three forms of the parasite Toxoplasma gondii that correspond to three morphological stages: tachyzoite, bradyzoite, and sporozoite form. Felids are definitive hosts for T. gondii, which is an intracellular pathogen that infects a wide range of warm-blooded intermediate hosts. Toxoplasmosis is a disease where the interest of the diverse medical and veterinary specialties converge. Awareness needs to be increased that toxoplasmosis can induce clinical disease not only in immunocompromised patients or through congenital infections, but also in healthy patients. This is a review article that aims at illustrating why toxoplasmosis should be regarded a veterinary public health issue and how veterinary practitioners can contribute in controlling the infection.

[PubMed - indexed for MEDLINE]
Foodborne Pathog Dis. 2011 Sep;8(9):961-73. Epub 2011 May 11.

The occurrence and prevention of foodborne disease in vulnerable people.

Lund BM, O'Brien SJ.
Institute of Food Research, Norwich, UK.

In developed countries, such as the United Kingdom and the United States, between 15% and 20% of the population show greater susceptibility than the general population to foodborne disease. This proportion includes people with primary immunodeficiency, patients treated with radiation or with immunosuppressive drugs for cancer and diseases of the immune system, those with acquired immune-deficiency syndrome and diabetics, people suffering from liver or kidney disease or with excessive iron in the blood, pregnant women, infants, and the elderly. Malnutrition and use of antacids, particularly proton-pump inhibitors, also increase susceptibility. We review the occurrence of infection by foodborne pathogens in these groups of people and measures to prevent infection. The nature and use of low microbial diets to reduce the risk of foodborne disease in immunocompromised patients are very variable. Diets for vulnerable people in care should exclude higher-risk foods, and vulnerable people in the community should receive clear advice about food safety, in particular avoidance of higher-risk foods and substitution of safer, nutritious foods.

[PubMed - indexed for MEDLINE]
Free PMC Article
Parasites - Toxoplasmosis (Toxoplasma infection)

Toxoplasmosis is considered to be a leading cause of death attributed to foodborne illness in the United States. More than 60 million men, women, and children in the U.S. carry the Toxoplasma parasite, but very few have symptoms because the immune system usually keeps the parasite from causing illness. Toxoplasmosis is considered one of the Neglected Parasitic Infections, a group of five parasitic diseases that have been targeted by CDC for public health action.

However, women newly infected with Toxoplasma during pregnancy and anyone with a compromised immune system should be aware that toxoplasmosis can have severe consequences.

Page last reviewed: February 1, 2012
Page last updated: February 1, 2012 ... 8.abstract
Clin Infect Dis. (2012) doi: 10.1093/cid/cis508 First published online: May 22, 2012

Foodborne Toxoplasmosis

Patricia M. Griffin, Section Editor
Jeffrey L. Jones1 and
J. P. Dubey2
Author Affiliations

1Parasitic Diseases Branch, Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Atlanta, Georgia
2Animal Parasitic Diseases Laboratory, Agricultural Research Institute, Animal and Natural Resources Institute, Agricultural Research Service, United States Department of Agriculture, Beltsville, Maryland

Correspondence: Jeffrey L. Jones, MD, MPH, Parasitic Diseases Branch, Division of Parasitic Diseases and Malaria, Center for Global Health, Centers for Disease Control and Prevention, Bld. 24, 1600 Clifton Rd, NE, Mailstop A-06, Atlanta, GA

Toxoplasmosis can be due to congenital infection or acquired infection after birth and is one of the leading illnesses associated with foodborne hospitalizations and deaths. Undercooked meat, especially pork, lamb, and wild game meat, and soil contaminated with cat feces on raw fruits and vegetables are the major sources of foodborne transmission for humans. The new trend in the production of free-range organically raised meat could increase the risk of Toxoplasma gondii contamination of meat.

Foodborne transmission can be prevented by production practices that reduce T. gondii in meat, adequate cooking of meat, washing of raw fruits and vegetables, prevention of cross contamination in the kitchen, and measures that decrease spread of viable oocysts into the environment.

Received December 27, 2011.
Accepted May 15, 2012.
Last, but not least – and to finally get to my real point: ... oplasmosis
Ocular Toxoplasmosis


Toxoplasma gondii is a protozoan (single cell organism) that lives within other cells (parasite). The definitive host (where organism can reporduce) is a cat, but other organisms, including humans, can contract the disease. In humans, there are two types of disease that affect the eyes, congenital and acquired toxoplasmosis. Toxoplasmosis is the most common cause of posterior uveitis, which is inflammation in the back part of the eye. Twenty to seventy percent of US adults are seropositive, indicating past exposure to the organism.



Treatment is not always indicated and does not result in the elimination of the organism from the eye. It is felt that the cyst form of the organism persists for life and can reactivate later. Certain lesions, such as macular threatening lesions, or lesions between the macula and nerve have a high chance of causing visual loss and are almost always treated. Those associated with severe inflammation (vitritis) and any lesion in patients with AIDS or other immune deficient state are treated as well. Small, peripheral lesions that do not threaten central vision may often be observed.


While there is no consensus on the best treatment, there is agreement that treatment should last a minimum of six weeks. The classic treatment is a triple drug regimen consisting of sulfadiazine, pyramethamine (Daraprim), and folinic acid. However, side effects are common and blood tests have to be performed to monitor for toxicity. Common side effects of some of these medicines are listed below

Sulfadiazine - Stevens-Johnson syndrome, kidney stones and bone marrow suppression
Pyramethamine - Bone marrow depression, especially platelets
Clindamycin - Pseudomembranous colitis (Treatment: vancomycin)

Because of this, newer alternatives include clindamycin, minocycline, atovaquone (Mepron), Bactrim DS, and azithromycin. We often use Bactrim DS twice a day because of its easy dosing and good safety profile.

Is it just possible that some doctors who treat their Lyme disease patients with antibiotics like minocycline, azithromycin, Bactrim DS, etc. may unknowingly be addressing toxoplasmosis or other yet-to-be-identified infections? As one example, Mepron/Azithromycin and Clindamycin/Quinine are used to treat Babesiosis -- a co-infection sometimes verified by blood smear (or other testing) in Lyme disease patients -- and other times clinically diagnosed by LLMDs.

While I don't believe any of the medications listed above are recommended for use by the IDSA for the treatment of Lyme disease, it seems they just might have a place in the treatment of toxoplasmosis and possibly other common infections that may be reactivated when a person's immune system is challenged when fighting off other infections. Could the cocktails of antibiotics prescribed by some doctors be successful in part because they are treating much more than Lyme disease?

Has anyone else wondered about this?

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Post by RitaA » Wed 18 Jul 2012 15:34 ... ne.0023866

Prandovszky E, Gaskell E, Martin H, Dubey JP, Webster JP, et al. (2011) The Neurotropic Parasite Toxoplasma Gondii Increases Dopamine Metabolism. PLoS ONE 6(9): e23866. doi:10.1371/journal.pone.0023866
The Neurotropic Parasite Toxoplasma Gondii Increases Dopamine Metabolism

Emese Prandovszky1, Elizabeth Gaskell1, Heather Martin1, J. P. Dubey2, Joanne P. Webster3, Glenn A. McConkey1*

1 Institute of Integrative and Comparative Biology, Faculty of Biological Sciences, University of Leeds, Leeds, United Kingdom, 2 Animal Parasitic Diseases Laboratory, USDA, ARS, ANRI, BARC-East, Beltsville, Maryland, United States of America, 3 Department of Infectious Disease Epidemiology, Faculty of Medicine, Imperial College, London, United Kingdom


The highly prevalent parasite Toxoplasma gondii manipulates its host's behavior. In infected rodents, the behavioral changes increase the likelihood that the parasite will be transmitted back to its definitive cat host, an essential step in completion of the parasite's life cycle. The mechanism(s) responsible for behavioral changes in the host is unknown but two lines of published evidence suggest that the parasite alters neurotransmitter signal transduction: the disruption of the parasite-induced behavioral changes with medications used to treat psychiatric disease (specifically dopamine antagonists) and identification of a tyrosine hydroxylase encoded in the parasite genome. In this study, infection of mammalian dopaminergic cells with T. gondii enhanced the levels of K+-induced release of dopamine several-fold, with a direct correlation between the number of infected cells and the quantity of dopamine released. Immunostaining brain sections of infected mice with dopamine antibody showed intense staining of encysted parasites. Based on these analyses, T. gondii orchestrates a significant increase in dopamine metabolism in neural cells. Tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, was also found in intracellular tissue cysts in brain tissue with antibodies specific for the parasite-encoded tyrosine hydroxylase. These observations provide a mechanism for parasite-induced behavioral changes. The observed effects on dopamine metabolism could also be relevant in interpreting reports of psychobehavioral changes in toxoplasmosis-infected humans.
The link above contains the full article. Here’s a snippet from the “Discussion” portion:
Malfunctions of dopamine metabolism have a serious impact on human behavior. Dopamine dysfunction has been associated with a variety of neurological disorders including schizophrenia, attention deficit hyperactivity disorder, tic disorders, Tourette's syndrome, and dyskinesias. The novel findings of this study, that demonstrate T. gondii's ability to directly alter dopamine levels will not only help to better understand the relationship between schizophrenia and T. gondii seroprevalence, but these findings may be critical for understanding the mechanism(s) involved in a variety of pathogen-associated neurological disorders [10], [13]. Thus, it is crucial to determine if other pathogens associated with neurological disorders also have the ability to directly alter dopamine levels. It is also critical to determine the possible contributions of T. gondii infection to other dopamine-related diseases [33], [34].

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