Kill Toxoplasmosis for good

[Karmeleon]

Identification of compounds that suppress Toxoplasma gondii tachyzoites and bradyzoites​

Identification of compounds that suppress Toxoplasma gondii tachyzoites and bradyzoites - PubMed

Drug treatment for toxoplasmosis is problematic, because current drugs cannot eradicate latent infection with Toxoplasma gondii and can cause bone marrow toxicity. Because latent infection remains after treatment, relapse of infection is a problem in both infections in immunocompromised patients...

pubmed.ncbi.nlm.nih.gov

Drug treatment for toxoplasmosis is problematic, because current drugs cannot eradicate latent infection with Toxoplasma gondii and can cause bone marrow toxicity. Because latent infection remains after treatment, relapse of infection is a problem in both infections in immunocompromised patients and in congenitally infected patients. To identify lead compounds for novel drugs against Toxoplasma gondii, we screened a chemical compound library for anti-Toxoplasma activity, host cell cytotoxicity, and effect on bradyzoites. Of 878 compounds screened, 83 demonstrated >90% parasite growth inhibition. After excluding compounds that affected host cell viability, we further characterized two compounds, tanshinone IIA and hydroxyzine, which had IC50 values for parasite growth of 2.5 μM and 1.0 μM, respectively, and had no effect on host cell viability at 25 μM. Both tanshinone IIA and hydroxyzine inhibited parasite replication after invasion and both reduced the number of in vitro-induced bradyzoites, whereas, pyrimethamine, the current therapy, had no effect on bradyzoites. Both tanshinone IIA and hydroxyzine are potent lead compounds for further medicinal chemistry. The method presented for evaluating compounds for bradyzoite efficacy represents a new approach to the development of anti-Toxoplasma drugs to eliminate latency and treat acute infection.

Two old drugs, NVP-AEW541 and GSK-J4, repurposed against the Toxoplasma gondii RH strain​

Identification of compounds that suppress Toxoplasma gondii tachyzoites and bradyzoites

Drug treatment for toxoplasmosis is problematic, because current drugs cannot eradicate latent infection with Toxoplasma gondii and can cause bone marrow toxicity. Because latent infection remains after treatment, relapse of infection is a problem in ...

www.ncbi.nlm.nih.gov

Background​

Toxoplasma gondii is a zoonotic pathogen that causes toxoplasmosis and leads to serious public health problems in developing countries. However, current clinical therapeutic drugs have some disadvantages, such as serious side effects, a long course of treatment and the emergence of drug-resistant strains. The urgent need to identify novel anti-Toxoplasma drugs has initiated the effective strategy of repurposing well-characterized drugs. As a principled screening for the identification of effective compounds against Toxoplasma gondii, in the current study, a collection of 666 compounds were screened for their ability to significantly inhibit Toxoplasma growth.

Hit compounds from 1st screening.

compound​	Parasite Inhibition (%)(a)​	Host Viability (%)(b)​
Bromocriptine​	105​	85​
Perphenazine​	104​	84​
Mefloquine​	101​	87​
Isoconazole​	104​	101​
Hydroxyzine​	97​	101​
(±)-Terfenadine​	104​	85​
Clotrimazol​	99​	94​
FLUPHENAZINE​	103​	83​
Domperidone​	93​	94​
Hycanthone​	97​	82​
Propidium Iodide​	91​	91​
PENITREM A​	105​	79​
Tanshinone IIA​	91​	83​
Niguldipine​	103​	77​
N-Hydroxy-N2-isobutyl-N2-[(4-methoxyphenyl)sulfonyl]glycinamide​	101​	98​
N-{[(2-Methyl-2-propanyl)oxy]carbonyl}glycyl-N-[(2S)-3-methyl-1-oxo-2-butanyl]-L-valinamide​	105​	106​
Butein​	96​	93​
MC-1293​	103​	85​
Entinostat​	91​	83​
TCMDC-125497​	106​	82​
Perospirone​	100​	96​
Omeprazole​	92​	97​
AM404​	103​	100​
(2Z)-2-(1,3-Benzodioxol-5-yl)-4-(4-methoxyphenyl)-4-oxo-3-(3,4,5-trimethoxybenzyl)-2-butenoic acid​	93​	85​

In vitro effects of aqueous extracts of Astragalus membranaceus and Scutellaria baicalensis GEORGI on Toxoplasma gondii​

In vitro effects of aqueous extracts of Astragalus membranaceus and Scutellaria baicalensis GEORGI on Toxoplasma gondii | Request PDF

Request PDF | In vitro effects of aqueous extracts of Astragalus membranaceus and Scutellaria baicalensis GEORGI on Toxoplasma gondii | Toxoplasma gondii is a parasite that infects animals and humans worldwide. The standard treatment for toxoplasmosis is limiting due to toxic... | Find, read and...

www.researchgate.net

Toxoplasma gondii is a parasite that infects animals and humans worldwide. The standard treatment for toxoplasmosis is limiting due to toxic adverse effects, thus there is a need to identify new drugs that are less toxic. Both Astragalus membranaceus and Scutellaria baicalensis GEORGI are popular traditional Chinese herbs widely used for the treatment of various inflammatory diseases in Asia, and we have previously demonstrated that water extracts of A. membranaceus (AmE) and S. baicalensis GEORGI (SbE) have good efficacy in controlling T. gondii replication in mouse models. This study was designed to further evaluate their effects against developing tachyzoites of the RH strain of T. gondii in HeLa cell cultures. AmE, SbE, and TMP-SMX (trimethoprim-sulfamethoxazole) were added into the wells containing both HeLa cells and replicating T. gondii of green fluorescent protein (GFP)-expressing RH tachyzoites. The proliferation and morphous of the tachyzoites were observed, the fluorescence intensity expressed as the fluorescence gray scale value was measured, and the living tachyzoites were counted at different culture times after treatment. The results showed that, compared to untreated controls, parasites treated with either AmE or SbE had significantly decreased intracellular replication at 72, 96, and 120 h after treatment (P < 0.01); while compared to either AmE- or SbE-treated groups, SMX-treated groups had even significantly decreased replication (only a few living parasites were detected) at the above times (P < 0.01). Our data demonstrated that both AmE and SbE had remarkable in vitro activities against T. gondii.

----------------------------------------------------------------------

It seems apparently the parasite infects up to 30% of the population by meaning of consuming foods - most pigs, sheep and goats meat (maybe the milk too) have the parasite cysts.
A non Antibiotic alternative and or combination therapy of Anti-Histamine with anti toxoplasma activity and anti toxoplasma herbals would be quite important.
If Hydroxyzine is highly active against the bug, i wonder if cetirizine is also potent. Also Cyproheptadine has decent inhibitory action. Hydroxyzine has the advantage of killing the bradyzoites not only the tachyzoites. A viable approach is maybe Azithromycin or Doxycycline as main Antibiotic against tachyzoites. Against the bradyzoites stage Hydroxyzine and the herbal TCM medicines Astralagus and Scutellaria Baicalensis, and a diet which incorporates a lot of lutein, which is also active. Also some Lapodin - beta lapachone would round up the kill mix.

Very interesting that some folks had success against serotonergic symptoms with Bromocriptine + Cypro, bromo is highly active and cypro decent.
The connection to schizophrenia is known and schizophrenia has excess serotonin symtoms incl. IBS, so intestinal infection is very likely too.
Toxoplasma is scavening nutrients of its host, a lot of b-vitamins ,so high dose full spectrum is in likely needed too.

I hope this helps a lot of people - i try the herbal mix + Hydroxyzine atm and my ibs is nearly gone, go figure.

 

[ursidae]

interesting to see inhibition by bromocriptine. I've been told by an alternative medical practitioner that toxoplasma causes pituitary adenomas and found some studies showing increased prolactin in toxoplasmosis, presumably PRL was exerting a protective effect by modulating humoral and cellular immune responses in infection by protozoa. Inhibiting toxoplasma might be another mechanism by which bromocriptine lowers prolactin and shrinks pituitary tumours

 

[Ben.]

hope this helps a lot of people - i try the herbal mix + Hydroxyzine atm and my ibs is nearly gone, go figure.

Cool.

Do you have diagnosed toxoplasma gondi?
What herbal mix? Only AmE and SbE?

 

[Karmeleon]

I've got antibodies IGM & IGG could be latent infection.
Yeah only AmE and SbE + 200mcg Selenium and Hydroxyzine, if that doesn't do it 2 weeks of doxy as add on.

Symtoms are severe headaches and weak immune system with ibs intestinal problems - rectal mucosa inflammation, liver enzymes ALT raised
and hepato-spleno megaly, raised Prolactin. All are on the list of Toxoplasmosis infection, big red flag are the headaches 5-7 times a week and
severe migraine at the slightest pufa intake - little bit of pork fat or dürüm-kebap chicken. -->there's a post about PUFA is a signal for Toxo to replicate...

That got me into searching of a cause, after being on a strictly peaty diet AND Haidut's finest metabolic aids.
Azithromycin and a round of Doxycycline got me completely well but only for 3 weeks.

I think a lot of people who cant get well on a good diet + thyroid-metabolic aids have some hidden nasties bugging arround....
This ones completely ignored by western medicine, only in aids, cancer chemo and pregnancy. But immune deficiency seems to be widespread due to pufa.
Mercury from Amalgams is also inhibitory to Toxoplasmosis, maybe a clue why it so heavily used. Toxoplasmosis also raises Serotonin several fold in infected tissue,
secondary is prolactin rise.

Ben you're also from Austria i've read?

 

[Ben.]

I've got antibodies IGM & IGG could be latent infection.
Yeah only AmE and SbE + 200mcg Selenium and Hydroxyzine, if that doesn't do it 2 weeks of doxy as add on.

Symtoms are severe headaches and weak immune system with ibs intestinal problems - rectal mucosa inflammation, liver enzymes ALT raised
and hepato-spleno megaly, raised Prolactin. All are on the list of Toxoplasmosis infection, big red flag are the headaches 5-7 times a week and
severe migraine at the slightest pufa intake - little bit of pork fat or dürüm-kebap chicken. -->there's a post about PUFA is a signal for Toxo to replicate...

That got me into searching of a cause, after being on a strictly peaty diet AND Haidut's finest metabolic aids.
Azithromycin and a round of Doxycycline got me completely well but only for 3 weeks.

I think a lot of people who cant get well on a good diet + thyroid-metabolic aids have some hidden nasties bugging arround....
This ones completely ignored by western medicine, only in aids, cancer chemo and pregnancy. But immune deficiency seems to be widespread due to pufa.
Mercury from Amalgams is also inhibitory to Toxoplasmosis, maybe a clue why it so heavily used. Toxoplasmosis also raises Serotonin several fold in infected tissue,
secondary is prolactin rise.

Ben you're also from Austria i've read?

Interesting, thanks for sharing.

Yes i am. You aswell? I wonder how you get your hands on hydroxyzine and doxy. Anyhow, i wish you good luck on your endevaour, keep us updated.

 

[Karmeleon]

There is also a connection to Chlamydia trachomatis, both are scavenging for nutrients in the host tissue concurrently.
Higher Dose Aspirin inhibts Chlamydia, and retinol does too. Riboflavin, Thiamine are scavenged heavily so metabolism is impaired.
Both are implicated in cancer induction and growth, so better to get rid of them as good as possible.
So retinol 25k - 100k, retinol metabolic co-factors - B2, B3, B6, Folate and Zinc are needed too.

Interesting that both are inhibited by Doxycycline & the Macrolides -Azithromycin, Doxy is also Anti Cancer....

A novel co-infection model with Toxoplasma and Chlamydia trachomatis highlights the importance of host cell manipulation for nutrient scavenging​

A novel co-infection model with Toxoplasma and Chlamydia trachomatis highlights the importance of host cell manipulation for nutrient scavenging

Toxoplasmaand Chlamydia trachomatis are obligate intracellular pathogens that have evolved analogous strategies to replicate within mammalian cells. Both pathogens are known to extensively remodel the cytoskeleton, and to recruit endocytic and exocytic ...

www.ncbi.nlm.nih.gov

Summary​

Toxoplasmaand Chlamydia trachomatis are obligate intracellular pathogens that have evolved analogous strategies to replicate within mammalian cells. Both pathogens are known to extensively remodel the cytoskeleton, and to recruit endocytic and exocytic organelles to their respective vacuoles. However, how important these activities are for infectivity by either pathogen remains elusive. Here, we have developed a novel co-infection system to gain insights into the developmental cycles of Toxoplasma and C. trachomatis by infecting human cells with both pathogens, and examining their respective ability to replicate and scavenge nutrients. We hypothesize that the common strategies used by Toxoplasma and Chlamydia to achieve development results in direct competition of the two pathogens for the same pool of nutrients. We show that a single human cell can harbor Chlamydia and Toxoplasma. In co-infected cells, Toxoplasma is able to divert the content of host organelles, such as cholesterol. Consequently, the infectious cycle of Toxoplasma progresses unimpeded. In contrast, Chlamydia’s ability to scavenge selected nutrients is diminished, and the bacterium shifts to a stress-induced persistent growth. Parasite killing engenders an ordered return to normal chlamydial development. We demonstrate that C. trachomatis enters a stress-induced persistence phenotype as a direct result from being barred from its normal nutrient supplies as addition of excess nutrients, e.g., amino acids, leads to substantial recovery of Chlamydia growth and infectivity. Co-infection of C. trachomatis with slow growing strains of Toxoplasma or a mutant impaired in nutrient acquisition does not restrict chlamydial development. Conversely, Toxoplasma growth is halted in cells infected with the highly virulent Chlamydia psittaci. This study illustrates the key role that cellular remodeling plays in the exploitation of host intracellular resources by Toxoplasma and Chlamydia. It further highlights the delicate balance between success and failure of infection by intracellular pathogens in a co-infection system at the cellular level.

#########################################

Aspirin inhibits Chlamydia pneumoniae-induced NF-kappa B activation, cyclo-oxygenase-2 expression and prostaglandin E2 synthesis and attenuates chlamydial growth​

Aspirin inhibits Chlamydia pneumoniae-induced NF-kappa B activation, cyclo-oxygenase-2 expression and prostaglandin E2 synthesis and attenuates chlamydial growth - PubMed

Infection with Chlamydia pneumoniae has been implicated as a potential risk factor for atherosclerosis. This study was designed to investigate the mechanisms of the anti-chlamydial activity of aspirin. A reporter gene assay for NF-kappa B activity, immunoblot analysis for cyclo-oxygenase (COX)-2...

pubmed.ncbi.nlm.nih.gov

Infection with Chlamydia pneumoniae has been implicated as a potential risk factor for atherosclerosis. This study was designed to investigate the mechanisms of the anti-chlamydial activity of aspirin. A reporter gene assay for NF-kappa B activity, immunoblot analysis for cyclo-oxygenase (COX)-2 and radioimmunoassay for prostaglandin E(2) (PGE(2)) were performed. Following infection of HEp-2 cells with C. pneumoniae, NF-kappa B was activated, COX-2 was induced and PGE(2) was elevated. Aspirin inhibited NF-kappa B activation at a concentration of 0.1 mM, partially inhibited COX-2 induction and blocked PGE(2) synthesis completely. In addition, high doses of aspirin (1 and 2 mM) inhibited chlamydial growth in HEp-2 cells, decreasing the number and size of inclusion bodies; this effect could be overcome by adding tryptophan to the culture. Indomethacin also blocked the synthesis of PGE(2), but had no effect on COX-2 expression or chlamydial growth. These results indicate that aspirin not only has an anti-inflammatory activity through prevention of NF-kappa B activation but also has anti-chlamydial activity at high doses, possibly through depletion of tryptophan in HEp-2 cells.

Aspirin inhibits Chlamydia pneumoniae-induced nuclear factor-kappa B activation, cytokine expression, and bacterial development in human endothelial cells​

Aspirin inhibits Chlamydia pneumoniae-induced nuclear factor-kappa B activation, cytokine expression, and bacterial development in human endothelial cells - PubMed

These data provide evidence that NF-kappaB-mediated gene activation represents a crucial step in the developmental cycle of C pneumoniae. Aspirin exerts an anti-chlamydial effect that is due to the inhibition of C pneumoniae-induced NF-kappaB activation, which might account for some of the...

pubmed.ncbi.nlm.nih.gov

Objective: Chlamydia pneumoniae has been associated with atherosclerosis. Infection of vascular endothelial cells with C pneumoniae increases the expression of proatherogenic cytokines mediated by nuclear factor (NF)-kappaB, a transcription factor. The present study was designed to test the effect of aspirin on C pneumoniae-induced NF-kappaB activation, interleukin expression, and bacterial development in cultured human endothelial cells.

Methods and results: Aspirin, its metabolite salicylic acid, and 2 other unrelated NF-kappaB inhibitors showed a strong concentration-dependent inhibitory effect on chlamydial growth, indicated by the reduction of bacterial inclusions and the titer of infectious progeny. Involvement of the transcription factor NF-kappaB was confirmed by electrophoretic mobility shift assay and by transfection experiments with appropriate decoy oligodeoxynucleotides. Attenuation of the C pneumoniae-induced activation of NF-kappaB by aspirin also reduced the secretion of interleukin-6 and interleukin-8, indicating efficient inhibition of NF-kappaB gene expression. Reduction of chlamydial growth was not caused by apoptosis of the host cell, as determined by monitoring characteristic chromatin condensation.

Conclusions: These data provide evidence that NF-kappaB-mediated gene activation represents a crucial step in the developmental cycle of C pneumoniae. Aspirin exerts an anti-chlamydial effect that is due to the inhibition of C pneumoniae-induced NF-kappaB activation, which might account for some of the cardioprotective activity of aspirin.

Retinoic acid inhibits the infectivity and growth of Chlamydia pneumoniae in epithelial and endothelial cells through different receptors​

Retinoic acid inhibits the infectivity and growth of Chlamydia pneumoniae in epithelial and endothelial cells through different receptors - PubMed

Chlamydia pneumoniae is a human respiratory pathogen that has also been associated with cardiovascular disease. C. pneumoniae infection accelerates atherosclerotic plaque development in hyperlipidemic animals and promotes oxidation of low density lipoprotein in vitro. All-trans-retinoic acid...

pubmed.ncbi.nlm.nih.gov

Chlamydia pneumoniae is a human respiratory pathogen that has also been associated with cardiovascular disease. C. pneumoniae infection accelerates atherosclerotic plaque development in hyperlipidemic animals and promotes oxidation of low density lipoprotein in vitro. All-trans-retinoic acid (ATRA), an antioxidant, has been shown to inhibit C. pneumoniae infectivity for endothelial cells by preventing binding of the organism to the M6P/IGF2 receptor on the cell surface. This current study investigates whether ATRA similarly affects C. pneumoniae infectivity of epithelial cells, which are the primary site of infection in the respiratory tract, and the effects on intracellular growth in both endothelial and epithelial cells. Because ATRA binds to both the nuclear retinoid acid receptor (RAR) and the M6P/IGF2 receptor, 4-[(E)-2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthalenyl)-1-propenyl]benzoic acid (TTNPB), an ATRA analog, which binds to the RAR but not the M6P/IGF2 receptor was used to differentiate the receptor mediating the effects of ATRA. The results of this study showed two separate effects of ATRA. The first effect is through interaction with the M6P/IGF2 receptor on the cell surface preventing attachment of the organism (inhibition by ATRA but not TTNPB) in endothelial cells and the second is through the nuclear receptor (inhibition by both ATRA and TTNPB) which inhibits growth in both epithelial and endothelial cells.

#########################################

ТокÑоплазмоз

ТокÑоплазмоз. СимпÑомÑ. ÐиагноÑÑика. ЧÑо делаÑÑ Ð¿Ñи диагнозе ÑокÑоплазмоз. ÐонÑеÑваÑивное леÑение и опеÑаÑии. ÐлаÑнÑе и беÑплаÑнÑе клиники, в коÑоÑÑÑ Ð»ÐµÑиÑÑÑ ÑокÑоплазмоз.

www.krasotaimedicina.ru

Pathogenesis​

Once in the human body through the gastrointestinal tract, oocysts are introduced into the enterocytes of the lower parts of the small intestine, from where they penetrate into the mesenteric lymph nodes, causing their inflammation (mesadenitis), necrosis, calcification and the formation of specific granulomas. From the primary lymphatic focus, Toxoplasma enters the bloodstream and is hematogenously carried throughout the body, where they are fixed in target organs: liver, spleen, myocardium, central nervous system, eye membranes, skeletal muscles, causing the formation of necrosis, granulomas, impaired function of the affected organs.
The vital activity of Toxoplasma is accompanied by the release of allergens and toxins, which is expressed in the development of general infectious and allergic syndromes. As specific antibodies are produced, the vegetative forms of Toxoplasma are incysted, which is marked by the transition of toxoplasmosis to a chronic form. With a decrease in the activity of the immune system (in AIDS patients, hematological and oncological patients), reactivation of infection with a generalized course is possible.​

Symptoms of acquired toxoplasmosis​

Taking into account the nature of infection, congenital and acquired toxoplasmosis are distinguished. Acquired infection can occur in acute, chronic and latent form; in this case, the latent form is divided into primary and secondary, developing after acute or relapse of chronic toxoplasmosis.​

Latent form​

In about 95-99% of people, toxoplasmosis occurs as a latent infection. In the acute manifest form of toxoplasmosis, the incubation period is 2-3 weeks. The mild and subclinical course of toxoplasmosis is usually diagnosed retrospectively by the positive results of skin tests with toxoplasmin, serological reactions, calcified lymph nodes and other signs.​

Generalized uniform​

Clinical manifestations of severe generalized toxoplasmosis develop acutely with sudden fever (t - up to 38-39 ° C) and phenomena of general intoxication (cognition, decreased appetite, myalgia, arthralgia). Characterized by an increase in the liver and spleen (hepatosplenomegaly), the development of lymphadenopathy, the appearance of maculopapulous rashes on the skin. Most often, the reaction is expressed from the cervical, axillary, inguinal, mesenteric lymph nodes, as well as the lymph nodes of the mediastinum. Skin rashes with toxoplasmosis are located throughout the body (except for the scalp, palms and soles), can merge into spots with uneven wavy edges. At the height of the severity of the process, acute myocarditis, encephalitis, meningoencephalitis, encephalomyelitis can develop. Severe forms of acute toxoplasmosis can be fatal.​

Chronic form​

Chronic toxoplasmosis is characterized by a long torpid course. Common symptoms include subfebrile condition, malaise, weight loss, generalized arthralgia, lymphadenopathy. Manifestations of mesadenitis are dyspeptic disorders: nausea, flatulence, abdominal pain, constipation. Specific signs of chronic toxoplasmosis are muscle tissue damage, manifested by myositis. Heart damage causes the development of focal or diffuse changes in the myocardium or pericarditis, manifested by fatigue, palpitations, shortness of breath, cardialgia.
On the part of the nervous system, the phenomena of asthenia and vegetative-vascular dystonia, neurasthenic reactions and phobias are noted. The long-term chronic course of toxoplasmosis leads to the development of epilepsy, mental disorders, and a decrease in intelligence. Endocrine disorders may include impotence, menstrual irregularities, and secondary adrenal insufficiency. Eye damage in toxoplasmosis occurs in the form of progressive myopia, uveitis, retinitis and chorioretinitis with atrophy of the optic nerve.​

Symptoms of congenital toxoplasmosis​

The course and outcomes of congenital toxoplasmosis depend on the gestational age of the fetus. Infection in the I and II trimester leads to intrauterine fetal death or the formation of intrauterine defects - blastopathies, embryo- and fetopathies. In the case of later intrauterine infection (in the third trimester), the child is born with a chronic, subacute or acute form of toxoplasmosis; however, the later the infection occurs, the more severe the symptoms at the time of birth.
The condition of newborns with an acute form of toxoplasmosis is severe from the first days. There is febrile body temperature, severe intoxication, abundant polymorphic rashes on the skin, generalized lymphadenopathy, hemorrhages in the mucous membranes and sclera. The liver and spleen are usually enlarged, often develop jaundice, dyspeptic disorders. Acute toxoplasmosis in newborns can lead to the development of pneumonia, myocarditis, encephalitis, meningoencephalitis and death. The subacute and chronic course of toxoplasmosis is characterized by hydrocephalus, convulsive syndrome, prolonged jaundice, subfebrile, chorioretinitis.
In the long term, persistent irreversible changes due to intrauterine infection are detected. Such consequences can serve as a lag in physical development, delayed mental and speech development (ZPR and ZRD), microcephaly, oligophrenia, epilepsy, microphthalmia, blindness, hearing loss, deafness. These and other disorders are regarded as residual toxoplasmosis. Congenital toxoplasmosis can have a long latent course with a clinical manifestation at 2-7 years of the child's life.​

Diagnosis of toxoplasmosis​

In the diagnosis of intrauterine infection, an important role is given to obstetric history, the results of the analysis for TORCH infection in the mother and serological reactions in the newborn, the study of amniotic fluid and placenta by PCR. Children need the supervision of a pediatrician, pediatric ophthalmologist, otolaryngologist, neurologist; lumbar puncture, CT scan of the brain, neurosonography. Congenital toxoplasmosis should be differentiated from congenital rubella, herpes, listeriosis, cytomegaly, chlamydial infection, intracranial birth trauma.
Among the clinical manifestations, the greatest diagnostic value in acquired toxoplasmosis is a combination of lymphadenopathy, hepatosplenomegaly, eye and CNS lesions. Be sure to consult the patient with a neurologist, ophthalmologist, therapist or cardiologist. The main list of instrumental studies includes EEG, Echo-EG, radiography or CT of the skull, ophthalmoscopy, ECG.
Parasitological and immunological methods are used for laboratory confirmation of toxoplasmosis. The first involve microscopic detection of the pathogen in smears-imprints of the affected organs, a biopsy of lymph nodes, blood or cerebrospinal fluid. It is possible to conduct a biological test with infection of laboratory rodents. Immunological diagnosis of toxoplasmosis includes serological methods (RSK, RNIF, ELISA, RNGA), as well as an intradermal allergic test with toxoplasmin. In the case of acquired infection, tuberculosis, lymphogranulomatosis, rheumatism, cat scratch disease, infectious mononucleosis, herpes virus infection are primarily excluded..​

Treatment of toxoplasmosis​

Depending on the predominant organ lesions, the treatment of patients with toxoplasmosis is carried out in specialized departments: neurological, therapeutic, cardiological, ophthalmological, etc. Etiotropic therapy for manifest toxoplasmosis is carried out with antiparasitic drugs: more often chloridine in combination with sulfa drugs or antibitetracycline edema; with contraindications - metronidazole, chloroquine, aminoquinol. Usually, the course of treatment of toxoplasmosis consists of 3 5-10-day cycles, repeated at intervals of 7-10 days. Additionally, antihistamines and fortifying agents, multivitamins are prescribed. In chronic toxoplasmosis, the drug course of treatment is supplemented by immunotherapy - intradermal administration of toxoplasmin. The tactics of managing pregnant women with primary-chronic or primary-latent toxoplasmosis involves chemoprophylaxis with spiramycin. In the acute form of toxoplasmosis in a pregnant woman, medical abortion is recommended.​

#########################################

Toxoplasmosis as a cause of mental disorders​

2a06:98c0:3600:0000:0000:0000:0000:0103 26.03.2024 09:36:29

Transmission of the parasite during pregnancy and children born with toxoplasmosis

The ability of almost all IgG subclasses – with the notable exception of IgG2 – to cross the placenta provides some form of fetal protection. The period of pregnancy in which the expectant mother becomes infected strongly affects the frequency and severity of the disease. Infection in the first trimester of pregnancy carries approximately 6% of the risk of transmission to the fetus, whereas in the second and third trimesters the risk of congenital transmission is approximately 33–47% and 60–81%, respectively. Unlike the gestational risk of transmission, the risk of developing clinical symptoms of the disease (congenital toxoplasmosis) is highest when maternal infection occurs during the first trimester, and gradually decreases in the second and third trimesters.

Congenital transmission of T. gondii carries a risk of miscarriage or stillbirth, and babies born with toxoplasmosis may suffer from severe symptoms, such as hydrocephalus, brain calcifications, or retinochoriiditis, later in life if not treated for toxoplasmosis.

RhD blood type protects against toxoplasmosis

Finally, five independent studies involving blood donors, pregnant women, and military personnel have shown that RhD blood type positive, especially in RhD heterozygotes, protects infected subjects from various effects of latent toxoplasmosis, such as increased reaction time, increased risk of traffic accidents, and excessive weight gain during pregnancy.

Toxoplasmosis as a cause of road accidents

Toxoplasmosis increases the reaction time of infected subjects, which may explain the increased likelihood of road traffic accidents in infected people, which was reported in three retrospective and one very large prospective case-control study.

Laboratory diagnosis of toxoplasmosis

During acute primary T. gondii infection, immunoglobulin M (IgM) against T. gondii is first produced. However, IgM titers decline over the next few months and become undetectable throughout the year. The immune system also produces IgG to T. gondii a few weeks after the initial infection. Levels of IgG antibodies usually peak within one or two months of infection, but are detected throughout the life of an infected person.

Neuroimmunological effects of the parasite

The effects of Toxoplasma (parasite) are not related to manipulation in the evolutionary sense, but simply to the neurological or more precisely neuroimmunological effects of the presence of the parasite. Tachyzoites can invade various types of nerve cells, such as neurons, astrocytes, and microglial cells in the brain, as well as Purkinje cells in the cerebellum. Intracellular tachyzoites manipulate several signs of transduction mechanisms involved in apoptosis, the functions of antimicrobial effectors, and the maturation of immune cells.

Latent toxoplasmosis is associated with immunosuppression, which may explain the increased likelihood of having a boy in Toxoplasma-infected women, as well as the extremely high prevalence of toxoplasmosis in mothers of children with Down syndrome.

It is assumed that the presence of parasite cysts in the brain causes an increase in the concentration of dopamine.

Epidemiological studies

The prevalence of antibodies against T. gondii. is reported worldwide and ranges from 51% to 72% in several countries in Latin America and the Caribbean, including Argentina, Brazil, Cuba, Jamaica and Venezuela. It is reported that in Scandinavia, the seropositivity of antibodies specific to T. gondii ranges from 11% to 28%, while in Southeast Asia, China and Korea, seropositivity to the effects of T. gondii is estimated in the range from 4% to 39%. women of reproductive age. In addition, both active and latent T. gondii infections have been reported in many African countries, especially in people suffering from HIV/AIDS. For example, 88.2% of HIV-infected people seeking medical care at Arba Minch Hospital in Ethiopia also had seropositive T. gondium infection, and a study conducted in Burkina Faso among pregnant women showed an overall seropreparation of 31.1%.

Epidemiological studies point to the role of toxoplasmosis in the etiology of schizophrenia, probably during pregnancy and in early life. This association is consistent with animal studies indicating that exposure of the developing brain of animals to infectious agents or immunomodulatory agents may be associated with behavior changes (psychopathological symptoms) that do not manifest until the animal reaches full maturity.

Toxoplasma gondii and mental disorders

Patients with psychiatric disorders have elevated levels of toxoplasmic antibodies, with the difference between cases and the control group greatest in individuals examined shortly before the onset of psychopathological symptoms.

Toxoplasmosis and schizophrenia

Increased dopamine levels in the brains of infected subjects may represent the missing link between toxoplasmosis and schizophrenia. Toxoplasma also appears to be involved in the occurrence of more severe forms of schizophrenia. At least 40 studies have confirmed an increased prevalence of toxoplasmosis among patients with schizophrenia. Patients with schizophrenia infected with Toxoplasma differ from patients with schizophrenia who do not suffer from Toxoplasma, brain anatomy and a greater intensity of delusions and hallucinations.

Toxoplasmosis and obsessive-compulsive disorder

Toxoplasmosis and obsessive-compulsive disorder (OCD): Seropositivity level for anti-T. Gondii IgG antibodies in patients with OCD are significantly higher than in healthy volunteers. Infection of the basal ganglia may be involved in the pathogenesis of OCD in seropositive subjects on Toxoplasma.

Toxoplasmosis and personality

Men infected with the parasite seem more dogmatic, less confident, more jealous, more cautious, less impulsive, and more orderly than others. Conversely, infected women become warmer, more conscientious, insecure, more sanctimonious and persistent than other women of this sex. People infected with Toxoplasma differ from uninfected control groups in a personality profile assessed using two variants of the Cattell 16PF questionnaires, Cloninger's TCI and the Big Five. Most of these differences increase over time since the onset of infection, suggesting that Toxoplasma affects a person's personality, rather than a person's personality, affects the likelihood of infection. Recently, a negative association between Toxoplasma infection and the desire for novelty has been reported in the literature.

People with a positive reaction to Toxoplasma had lower finding novelty scores (NS) (P = 0.035) and lower scores for three of the four subscales, namely impulsivity, extravagance, and disorder, than subjects with a negative reaction to Toxoplasma.

Toxoplasmosis and cytomegalovirus

A decrease in the desire for novelty is also associated with cytomegalovirus infection. Because cytomegalovirus is spread in the population through direct contact (rather than by predation, as with Toxoplasma), the observed changes are a byproduct of brain infections, not the result of the parasite's manipulative activity.

Toxoplasmosis and hormones

Male students infected with Toxoplasma are about 3 cm taller than toxoplasma-free subjects, and their faces are rated by women as more masculine and dominant. These differences may be caused by an increased concentration of testosterone.

Treatment of toxoplasmosis

Patients with toxoplasmosis can be treated with a combination of drugs such as pyrimethamine and sulfadiazine (an antibiotic), as well as folic acid. Drugs such as "Fancidar", "Rovamycin" and "Biseptol" are also used.

Effect of antipsychotics and normotimics on the parasite

Haloperidol and the mood stabilizer valproic acid most effectively inhibit the growth of toxoplasma in vitro with synergistic activity.

Research conducted in our clinic ( LLC "Mental Health" )

In our clinic, we compared elevated IgG titers to Toxoplasma with the peculiarities of psychopathological symptoms and a particular mental disorder, and also analyzed the general blood test of patients with toxoplasmosis and a number of mental disorders.

It turned out that chronic toxoplasmosis is characterized by: a decrease in such indicators of a general blood test as MCV and MCH, that is, signs of microcytic anemia are recorded; also reduced, the total number of leukocytes, and in particular, neutrophils and at the same time increased MPV (platelet volume, indicating their large size and increased activity). It is interesting to note that according to experimental observations by Biswas et al., (2017), neutrophil depletion leads to a decrease in IFN-γ production, which leads to an increase in the parasitic load on the central nervous system. Although the exact molecular processes driving these differences are still unclear, there is growing evidence that latent toxoplasmosis can cause chronic, low-severity inflammation, which in turn can lead to anemia.

Schizophrenia is characterized by similar changes (a decrease in leukocytes and neutrophils, an increase in MPV, but there are no signs of microcytic anemia (MCV and MCH are usually elevated). The blood of a patient with recurrent depression is somewhat similar to the blood of a patient with chronic toxoplasmosis (microcytic anemia, increased MPV), however, the number of leukocytes and neutrophils in recurrent depression is increased, on the contrary, in contrast to the blood of patients with elevated IgG titers to toxoplasma. According to For most indicators, the general blood count of a patient with chronic toxoplasmosis resembled the blood parameters of a patient with obsessive-compulsive disorder.

Based on the above, it can be assumed that drugs such as Pyrimethamine and Sulfadiazine, as well as "Fancidar", "Rovamycin" and "Biseptol". may be useful for patients with OCD with high IgG to Toxoplasma titers.

 

[Karmeleon]

Interesting, thanks for sharing.

Yes i am. You aswell? I wonder how you get your hands on hydroxyzine and doxy. Anyhow, i wish you good luck on your endevaour, keep us updated.

Ya greetings from Linz nice to know that there are more people from Austria arround here
I think I'll start a log about my endeavor, hopefully very successful.

 

[Karmeleon]

Interesting, thanks for sharing.

Yes i am. You aswell? I wonder how you get your hands on hydroxyzine and doxy. Anyhow, i wish you good luck on your endevaour, keep us updated.

In Covid times... go to your favourite urologist or hospital and say you got unprotected sex and some leaking afterwards... chance is really high
to get doxy right away for a week atleast, maybe after said week go to GP and say it ain't good yet.
Hydroxyzine is likely prescribed for sleep and anxiety issues, so pick your story line. Hope that guides you.
Here you dont even have to try convince the docs with studies, they only think of you as "schwurbler" and hypochondriac.
I've got my IGG and IGM testing at a appoinment for tropical disease testing of "being sick" after visiting a foreign country....

 

[Peater]

No benefit from ivermectin for this beastie?

 

[Karmeleon]

I don't know if ivermectin has activity against it, but hydroxy-chloroquine and methylene blue are mentioned in literature.
The interesting thing is about Hydroxyzine, that it kills the other form, the bradyzoites. The oocytes there is no cure it seems atm.
Also Quinine is on the list.

----
Correction, I looked it up and:

EFFECT OF SOME SELECTED DRUGS (PYREMETHAMIN,CLARITHROMYCIN, SPIRAMYCIN AND IVERMECTIN )ON EXPERIMENTAL TREATMENT OF TOXOPLASMOSIS CREATED IN MICE​

ABEER A.ALI, SHEHAB A.MOHHAMED, HUSSAIN S. ASWED
Journal of university of Anbar for Pure science
2011, Volume 5, Issue 3, Pages 25-34

Abstract​

In the present study, Toxoplasma gondiiwas isolated and diagnosed from human as first attempt, andthen the infection was created in laboratory mice as an essential step for growing the parasite. Thesecond step was studying the effect of some selected drugs on the experimental treatment for disease oftoxoplasmosis created in the mice. The drugs are: Pyrimethamin ,Clarithromycin , Spiramycin,Ivermectin .The results of the study showed the effects of these drugs on the tissue cyst formed in thebrain and lungs. The number of tissue cysts in the brain of the mouse treated with pyrimethamin was14.8 ±1.067 after 28 days. Significant differences appeared when this result compared with the controlgroup in which it was 27.4±1.029.The number of tissue cysts formed in lung, tissue in the mousetreated with the same drug after the same period of the time was 6.2±0.583.This showed a significantdifferences as compared with the control group in which it was 10.2±0.583.No significant differencesappeared between both groups as for the treatment by Clarithromycin antibiotic as far as the number ofthe tissue cysts formed in the brain after 28 days is concerned. The number was 23.8 ±0.86 ascompared with the control group 38.6±1.029.The same compared is true of the lungs, tissue. Thenumber of the tissue cysts was 23.8±0.86 as compared with the control group 28.4±1.805.Concerningthe antibiotic Spiramycin ,the results showed the effectiveness of it in decreasing the tissue cystsformed in the brain .The significant differences were (p<0.05),the rate of the cysts was 9.6±0.6 ascompared with the control group in which it was 22.8±1.067.The same effectiveness appeared on thelungs, tissue as the rate of tissue cysts after 28 days of treatment was 4.6±0.509 as compared with thecontrol group in which was 17±1.14 and the significant differences were (p=0.000).The Ivermectindrug showed a great effectiveness in minimizing the number of the tissue cysts formed in the brain andthe lungs. The numbers of the tissue cysts formed after 28 days were 3.2±0.374 and 1±0.316respectively; significant differences are observed when these numbers are compared with the numbersof the control group which were 22±1.843 and 19.4±1.435. Thus, the use of Ivermectin drug isconsidered as a pioneer and fruitful study since this drug has not been used for the treatment ofToxoplasmosis.

Iraqi Academic Scientific Journals - IASJ

www.iasj.net

##################################################

there is also a google Patent on methylene blue for toxoplasmosis

Methylene blue therapy of parasitic infections​

Abstract​

A method for using thiazine dyes, especially methylene blue, alone or in combination with low levels of light, to treat parasitic diseases is described. Examples of useful thiazine dyes are methylene blue, azure A, azure C, toluidine, and thionine. The preferred dye is methylene blue, administered orally twice a day. Since methylene blue absorbs in the red wavelengths, i.e., approximately 670 nm, which penetrates tissue much better than other lower wavelengths, light penetrating the skin to the capillaries at the surface can be used to enhance the activity of the dye. The thiazine dye can be provided in combination with other known antibiotics, anti-inflammatories, anti-parasitics, antifungals, and antivirals.

https://patents.google.com/patent/WO2007038201A1/en

##################################################

Quinine Inhibition of Host Cell Penetration by Toxoplasma gondii, Besnoitia jellisoni, and Sarcocystis sp. In vitro

The penetration of Toxoplasma gondii, Sarcocystis sp., and Besnoitia jellisoni into cultured cells was significantly inhibited by 0.1 mg quinine sulfate/ml in the inoculation medium. The former 2 organisms were inhibited from penetration by as little as 0.01 mg of this drug. Incubation of either organisms or cells in medium containing quinine prior to inoculation of organisms in quinine-free medium did not significantly reduce penetration. Organisms remained motile in the presence of quinine and the few that entered cells remained intracellular. Results of this study parallel those with Eimeria and indicate that quinine interferes with a mechanism of host cell penetration common to all 4 genera.

Quinine Inhibition of Host Cell Penetration by Toxoplasma gondii, Besnoitia jellisoni, and Sarcocystis sp. In vitro on JSTOR

Ronald Fayer, Marjorie L. Melton, Harley G. Sheffield, Quinine Inhibition of Host Cell Penetration by Toxoplasma gondii, Besnoitia jellisoni, and Sarcocystis sp. In vitro, The Journal of Parasitology, Vol. 58, No. 3 (Jun., 1972), pp. 595-599

www.jstor.org

 

[Karmeleon]

But Quinine is out - > no killing of tachyzoites

Pentamidine and quinine had no inhibitory effect over tachyzoites.​

And the Quinones are in -> Our results suggest that the naphthoquinones may be important therapeutic agents for the treatment of toxoplasmosis.
So are Artemisinin and artsunate.

In vitro action of antiparasitic drugs, especially artesunate, against Toxoplasma gondii​

NTRODUCTION: Toxoplasmosis is usually a benign infection, except in the event of ocular, central nervous system (CNS), or congenital disease and particularly when the patient is immunocompromised. Treatment consists of drugs that frequently cause adverse effects; thus, newer, more effective drugs are needed. In this study, the possible activity of artesunate, a drug successfully being used for the treatment of malaria, on Toxoplasma gondii growth in cell culture is evaluated and compared with the action of drugs that are already being used against this parasite. METHODS: LLC-MK2 cells were cultivated in RPMI medium, kept in disposable plastic bottles, and incubated at 36ºC with 5% CO2. Tachyzoites of the RH strain were used. The following drugs were tested: artesunate, cotrimoxazole, pentamidine, pyrimethamine, quinine, and trimethoprim. The effects of these drugs on tachyzoites and LLC-MK2 cells were analyzed using nonlinear regression analysis with Prism 3.0 software. RESULTS: Artesunate showed a mean tachyzoite inhibitory concentration (IC50) of 0.075µM and an LLC MK2 toxicity of 2.003µM. Pyrimethamine was effective at an IC50 of 0.482µM and a toxicity of 11.178µM. Trimethoprim alone was effective against the in vitro parasite. Cotrimoxazole also was effective against the parasite but at higher concentrations than those observed for artesunate and pyrimethamine. Pentamidine and quinine had no inhibitory effect over tachyzoites. CONCLUSIONS: Artesunate is proven in vitro to be a useful alternative for the treatment of toxoplasmosis, implying a subsequent in vivo effect and suggesting the mechanism of this drug against the parasite.

In vitro action of antiparasitic drugs, especially artesunate, against Toxoplasma gondii

INTRODUCTION: Toxoplasmosis is usually a benign infection, except in the event of ocular,...

www.scielo.br

######################################################

Activity of natural and synthetic naphthoquinones against Toxoplasma gondii, in vitro and in murine models of infection​

The effect of 14 natural and synthetic naphthoquinones in the replication of Toxoplasma gondii was evaluated. In vitro studies were accomplished in cultures of 2C4 fibroblasts infected with RH- strain. Enzyme-linked immunosorbent assay was used to quantify parasite growth. For the studies in vivo, mice were infected with tachyzoites of the RH strain or cysts of the T. gondii EGS strain. In vitro, seven naphthoquinones demonstrated significant inhibition of intracellular T. gondii growth at concentrations of 1 and 5 μg/ml. Only three compounds were significantly protective when tested in animals: 2-hydroxy-3'-(3'-pentenyl)-l ,4-naphthoquinone (PHNQ4), 2-hydroxy-3-(l'-vinylphenyl)-l,4-naphthoquinone (PHNQ5) and 2- hydroxy-3-(l'-propen-3'-phenyl)-1,4- naphthoquinone (PHNQ6). In animals infected with the EGS strain and treated with PHNQ4 (50 mg/kg/day orally), a 7-day prolongation of the time to death was observed. Treatment with 100 mg/kg/day orally or 50 mg/kg/day i.p. of PHNQ5 resulted in a 5-day and 16-day prolongation of the time to death, respectively. Treatment with 50 mg/kg/day orally or 50 mg/kg/day i.p. of PHNQ6 resulted in a 4-day prolongation of the time to death or up to 30 days after treatment, respectively. Our results suggest that the naphthoquinones may be important therapeutic agents for the treatment of toxoplasmosis.

Activity of natural and synthetic naphthoquinones against Toxoplasma gondii, in vitro and in murine models of infection | Parasite

Parasite international open-access, peer-reviewed, online journal publishing high quality papers on all aspects of human and animal parasitology

www.parasite-journal.org

 

[ursidae]

@Karmeleon what are your IGM IGG levels? Have you tested avidity? I had a parasitologist ask me to test avidity but they never gave me useful interpretation of my results.


I have the same issues as you, IBS, very high prolactin, a small adenoma and severe headaches. Melatonin, inadequate sleep and niacin and possibly calcium have been triggers for the headaches. I have some azitromycin on hand could give this a try. I like the idea of using herbs for this

 

[Peater]

@Karmeleon Very interesting thanks! Does that suggest a 28 day regime of IVM?

 

[Karmeleon]

And there is more, acording to this study Toxoplasama is implicated in Liver disease, cancer and abdominal hernia.​

Toxoplasma gondii infection in humans in China​

Toxoplasmosis is a zoonotic infection of humans and animals, caused by the opportunistic protozoan Toxoplasma gondii, a parasite belonging to the phylum Apicomplexa. Infection in pregnant women may lead to abortion, stillbirth or other serious consequences in newborns. Infection in immunocompromised patients can be fatal if not treated. On average, one third of people are chronically infected worldwide. Although very limited information from China has been published in the English journals, T. gondii infection is actually a significant human health problem in China. In the present article, we reviewed the clinical features, transmission, prevalence of T. gondii infection in humans in China, and summarized genetic characterizations of reported T. gondii isolates. Educating the public about the risks associated with unhealthy food and life style habits, tracking serological examinations to special populations, and measures to strengthen food and occupational safety are discussed.

Toxoplasmosis and schizophrenia​

Evidence is mounting to link toxoplasmosis with schizophrenia or similar psychiatric disorders. Recent studies revealed that levels of antibodies to T. gondii have been found to be increased in individuals with schizophrenia compared to controls with an odds ratio for Toxoplasma seropositivity between 2 and 4.4 [44–47]. In prospective studies, an increase in IgG antibodies to T. gondii has been found in mothers of infants who later develop schizophrenia [48].

Many reports revealed that Toxoplasma might represent a major pathogen in some cases of psychosis. It has been proven that the parasite infection could increase the dopamine level in mice brains [49]. Dopamine plays a key role in psychosis cases such as schizophrenia, and bipolar disorder [50–52]. The seroprevalence of T. gondii infection in schizophrenic patients ranged from 1% to 28.7% in China [11, 53]. A report of 67 cases of childhood schizophrenia between 6~17 years old revealed a Toxoplasma-IgG positive rate of 85.7% [54]. Another survey on Toxoplasma infection in 600 cases of the first episode of schizophrenia revealed that the Toxoplasma-IgG positive rate was 13.7% [55]. The prevalence of Toxoplasma IgG in mothers of 252 was 34.8% [55]. The alterations of behavior and psychomotor skills in schizophrenia patients have also been found to be associated with the T. gondii infection [56]. Compared with the seronegative ones, clinical manifestations of excitation, hostility, mannerisms and posturing, disturbance of volition, poor impulse control and anger, difficult to delay fulfilling request and suspiciousness in the seropositive patients were statistically different [56]. The schizophrenic patients living in rural area have a higher infection rate than these lived in cities, with prevalence of 28.6% and 6%, respectively [57].

Immunocompromised patients with toxoplasmosis​

Toxoplasmosis can be life-threatening in immunocompromised patients as a result of reactivation of chronic infection. High seroprevalence of latent T. gondii infection has been found among immunocompromised patients. Prevalence of T. gondii infection in cancer patients ranged from 24% [18] to 79% [19]. Prevalence of T. gondii infection varied with different cancers. Rectal cancer and nasopharyngeal carcinoma sufferers in Changchun city had the highest infection, with prevalence of 63.6% and 46.2%, respectively [18]. However, T. gondii infections in patients with breast cancer, hepatocellular carcinoma and gastric carcinoma in Henan Province were much higher than with other cancers, with a prevalence of 78.9%, 77.8% and 61.1%, respectively [19]. The average prevalence of T. gondii infection was 15.1% in leukemia patients. Moreover, T. gondii prevalence in refractory cases of leukemia patients was up to 35% [20].

Surveys of T. gondii infection in the individuals with tuberculosis and hepatitis B showed that the prevalence were 35.3% [21] and 19.3% [22], respectively. Most of the cases belonged to chronic infections. 70% of individuals infected with T. gondii and tuberculosis had the experience of intimate contact with animals [21]. Similarly, high prevalence of T. gondii infection have been detected among immunocompromised patients especially suffering from malignancy in Egypt and Korea [23, 24]. Although there is no direct association between the susceptibility of toxoplasmosis and the immunocompromised state, the high seroprevalence in immunocompromised patients indicates considerable risks, because toxoplasmosis is a consequence of recrudescence of a previously latent infection in most immunocompromised patients, with the chronic parasite infection activation after the immune system was damaged [25].

The first case of AIDS patient died in China was reported in 1991, and T. gondii was found in the cerebellum of this patient [26]. In a more recent report, 26% of HIV infected patients in Xinjiang were seropositive with T. gondii infection [27].

The CNS is the site most typically affected by T. gondii infection. A series of clinical manifestations including mental status changes, seizures, focal motor deficits, cranial nerve disturbances, sensory abnormalities, cerebellar signs, movement disorders, and neuropsychiatric findings have often been found among toxoplasmic encephalitis (TE) cases. The incidence of TE was from 0.6% [28] to 10.5% [9] among the HIV infected patients in Henan and Yunnan Provinces, with all the CD4+ T-lymphocyte count below 100 cells per microliter. Toxoplasmic lymphadenitis and retinitis were also found in HIV-infected patients, with the incidence of 6% (2/33) [29] and 5.3% (2/38) [9], respectively.

Toxoplasma gondii infection in humans in China - Parasites & Vectors

Toxoplasmosis is a zoonotic infection of humans and animals, caused by the opportunistic protozoan Toxoplasma gondii, a parasite belonging to the phylum Apicomplexa. Infection in pregnant women may lead to abortion, stillbirth or other serious consequences in newborns. Infection in...

parasitesandvectors.biomedcentral.com

############

Toxoplasma gondii infection and abdominal hernia: evidence of a new association​

Background​

We performed a retrospective, observational study in 1156 adult subjects from the general population of Durango City, Mexico, Fifty five subjects with a history of abdominal hernia repair and 1101 subjects without hernia were examined with enzyme-linked immunoassays for the presence of anti-Toxoplasma IgG and IgM antibodies.

Results​

The seroprevalence of anti-Toxoplasma IgG antibodies and IgG titers was significantly higher in subjects with abdominal hernia repair than those without hernia. There was a tendency for subjects with hernia repair to have a higher seroprevalence of anti-Toxoplasma IgM antibodies than subjects without hernia. The seroprevalence of anti-Toxoplasma IgG antibodies in subjects with hernia repair was significantly higher in subjects ≥ 50 years old than those < 50 years old. Further analysis in subjects aged ≥ 50 years showed that the seroprevalence of anti-Toxoplasma IgG antibodies was also significantly higher in individuals with hernia repair than those without hernia (OR = 2.72; 95% CI: 1.10-6.57). Matching by age and sex further showed that the seroprevalence of Toxoplasma infection was significantly higher in patients with hernia repair than those without hernia (OR: 4.50; 95% CI: 1.22-17.33).

Conclusions​

Results indicate that infection with Toxoplasma is associated with abdominal hernia. The contributing role of infection with Toxoplasma in abdominal hernia was observed mainly in subjects aged ≥ 50 years old. Our results might have clinical, prevention and treatment implications and warrant for further investigation.
Go to:

Findings​

The protozoan parasite Toxoplasma gondii (T. gondii) is widely distributed around the world [1,2]. Human infections with T. gondii occur by ingesting food or water that is contaminated with oocysts shed by cats or by eating undercooked or raw meat containing tissue cysts [2-4]. Infections with T. gondii may result in an asymptomatic state or lead to disease. The parasite disseminates within the host's body and may affect lymph nodes, eyes, central nervous system, and other tissues [3,5-9]. In addition, primary infection during pregnancy may lead to severe damage to the fetus [2,3]. We have explored the seroprevalence of and risk factors for T. gondii infection in some healthy [10-12] and ill [13-16] populations in Durango, Mexico. In a recent study in liver disease patients, we reported that subjects with abdominal hernia repair showed a significantly higher seroprevalence of T. gondii infection than individuals without hernia [16]. Therefore, we sought to determine whether the seroprevalence of T. gondii infection and anti-T. gondii IgG levels are associated with a history of abdominal hernia repair in subjects of the general population in Durango, Mexico. Furthermore, we investigated socio-demographic, clinical, and behavioral characteristics associated with T. gondii seropositivity in subjects with abdominal hernia repair.

Toxoplasma gondii infection and abdominal hernia: evidence of a new association

We performed a retrospective, observational study in 1156 adult subjects from the general population of Durango City, Mexico, Fifty five subjects with a history of abdominal hernia repair and 1101 subjects without hernia were examined with enzyme-linked ...

www.ncbi.nlm.nih.gov

 

[Karmeleon]

@Karmeleon what are your IGM IGG levels? Have you tested avidity? I had a parasitologist ask me to test avidity but they never gave me useful interpretation of my results.

View attachment 34798
I have the same issues as you, IBS, very high prolactin, a small adenoma and severe headaches. Melatonin, inadequate sleep and niacin and possibly calcium have been triggers for the headaches. I have some azitromycin on hand could give this a try. I like the idea of using herbs for this

I did the testing in context of a tick bite and got extended test range by being in a foreign country (asia).
Its a while back, IGM and IGG were not that high to be concerned, but by now i know i was quite immune compromised back then (cortisol, pufa).

I would start by the least harmful approach, my Azithromycin intake was unrelated to suspected Toxo (sinus infection, tooth infection) and it did not cure me.
In a treatment approach it was a week on abx, a week pause and repeat 3 times. So prolonged intake is required.
If the above substances help suppress and Hydroxyzine kills both stage (no treatmen is known for cysts) I would take the anti-histamine and
a suppressor substance of choice. If that eliminates symptoms, then I would reconsider the approach of more toxic intervention.
Also Azithromycin blocks Thiamine function, supplementation required.

Toxo also scavenges folate from tissue, supplementing folate is a good idea but is kind of frowned here due to methylation.
In deficiency immune response is impaired, so I personally take the UL of non-folic acid (quatrefolic) @1mg and 1mg B12 Hydroxy-form on top of my b-vitamins.
Folate is also required in processing of Thiamine, and Thiamine deficiency is BIG in IBS. And Vitamin A in phosphorylation of B-Vitamins, also hefty required.

Here is the study:

Toxoplasma Gondii Moderates the Association between Multiple Folate-Cycle Factors and Cognitive Function in U.S. Adults​

Toxoplasma gondii (T. gondii) is a microscopic, apicomplexan parasite that can infect muscle or neural tissue, including the brain, in humans. While T. gondii infection has been associated with changes in mood, behavior, and cognition, the mechanism remains unclear. Recent evidence suggests that T. gondii may harvest folate from host neural cells. Reduced folate availability is associated with an increased risk of neurodevelopmental disorders, neurodegenerative diseases, and cognitive decline. We hypothesized that impairment in cognitive functioning in subjects seropositive for T. gondii might be associated with a reduction of folate availability in neural cells. We analyzed data from the third National Health and Nutrition Examination Survey to determine the associations between T. gondii infection, multiple folate-cycle factors, and three tests of cognitive functioning in U.S. adults aged 20 to 59 years. In these analyses, T. gondii moderated the associations of folate, vitamin B-12, and homocysteine with performance on the Serial Digit Learning task, a measure of learning and memory, as well as the association of folate with reaction time. The results of this study suggest that T. gondii might affect brain levels of folate and/or vitamin B-12 enough to affect cognitive functioning.

Toxoplasma Gondii Moderates the Association between Multiple Folate-Cycle Factors and Cognitive Function in U.S. Adults

Toxoplasma gondii (T. gondii) is a microscopic, apicomplexan parasite that can infect muscle or neural tissue, including the brain, in humans. While T. gondii infection has been associated with changes in mood, behavior, and cognition, the mechanism remains ...

www.ncbi.nlm.nih.gov

 

[Karmeleon]

@Karmeleon Very interesting thanks! Does that suggest a 28 day regime of IVM?

Ya it seems prolonged treatment is required.

 

[Karmeleon]

@Karmeleon what are your IGM IGG levels? Have you tested avidity? I had a parasitologist ask me to test avidity but they never gave me useful interpretation of my results.

View attachment 34798
I have the same issues as you, IBS, very high prolactin, a small adenoma and severe headaches. Melatonin, inadequate sleep and niacin and possibly calcium have been triggers for the headaches. I have some azitromycin on hand could give this a try. I like the idea of using herbs for this

pituitary adenoma is also on the toxoplasmosis side effects list. I too tried to lower prolactin with B6, B6 P5P and lisuride. I got the headaches under control with add-in of 300 mg Aspirin daily, but prolactin induced gyno in the meantime... i didn't retest Prolactin lately, but start thyroid NDT + thyromix for increasing hypo symptoms,
and discovering by accident the connection of headaches, prolactin, abominal hernia! - which i suddenly got by not so hefty weight lifting and TOXO.

Two case reports of pituitary adenoma associated with Toxoplasma gondii infection​

Two case reports of pituitary adenoma associated with Toxoplasma gondii infection

The involvement of the pituitary in cases of toxoplasmosis has been described in the literature only rarely. This is the first report to describe pituitary adenoma in association with Toxoplasma gondii infection. The two patients were 43 and 19 year old ...

www.ncbi.nlm.nih.gov

and cancer again:

Possible role of Toxoplasma gondii in brain cancer through modulation of host microRNAs​

Possible role of Toxoplasma gondii in brain cancer through modulation of host microRNAs - Infectious Agents and Cancer

Background The obligate intracellular protozoan parasite Toxoplasma gondii infects humans and other warm-blooded animals and establishes a chronic infection in the central nervous system after invasion. Studies showing a positive correlation between anti-Toxoplasma antibodies and incidences of...

infectagentscancer.biomedcentral.com

 

[FoodForeal]

There's been a lot of good discussion on colloidal silver on this forum. It doesn't cause animal cell toxicity above that of selenium so it may be better than some of the harsher treatments mentioned here. Nanosilver Colloid Inhibits Toxoplasma gondii Tachyzoites and Bradyzoites in Vitro

 

[Karmeleon]

There's been a lot of good discussion on colloidal silver on this forum. It doesn't cause animal cell toxicity above that of selenium so it may be better than some of the harsher treatments mentioned here. Nanosilver Colloid Inhibits Toxoplasma gondii Tachyzoites and Bradyzoites in Vitro
View attachment 34882

Cool good to know another weapon on top, so to speak a "silver bullet" against it.
Is there data about brain tissue penetration of colloidal silver?

And is there knowledge about silver accumulation in tissue, peat warned in the past about Silver is a toxic heavy metal nearly as toxic as mercury?
Besides one point for Silver Amalgam fillings, they do contain some too, alongside mercury and other metals.
Mercury is also known to inhibit growth of Toxoplasma and other bugs, but personally I'm still happy to don't have that poison anymore in my teeth.
Maybe more bugs use teeth, teeth root as hiding grounds, to reinfect after antibiotic assault. Reminds of Weston Price and toxic root canals...
Were there not cases of cancer which could be cured after root canals were pulled?

 

[Cloudhands]

anyone have any clue where to get bromocryptine?