Toxoplasma Gondii Research Project

Abstract
Toxoplasmosis, caused by the protozoan parasite Toxoplasma gondii, is one of the most

common parasitic infections of men, women and other warm-blooded animals. It has been

found world-wide from Alaska to Australia. Nearly one-third of humanity has been exposed

to this parasite. In most adults it does not cause serious illness, but it can cause blindness and

mental illness in congenitally infected children and devastating disease in

immunocompromised individuals. Toxoplasma gondii infection is widespread in humans,

although its prevalence varies widely from place to place. In the United States and the United

Kingdom, it is estimated that 16–40% of the population are infected, where as in Central and

South America and continental Europe, estimates of infection range from 50 to 80%. The

socio-economic impact of toxoplasmosis in human suffering and the cost of care of sick

children, are enormous. The testing of all pregnant women for T. gondii infection is routine in

some European countries, including France and Austria. The cost-benefit of such mass

screening is being debated in many other countries. Toxoplasma gondii has emerged as an

interesting candidate as a possible cause of some cases of schizophrenia. Past infectious

research on schizophrenia has focused almost exclusively on bacteria and viruses, but

Toxoplasma gondii​ is a protozoan. Other protozoa known to chronically infect human brain

tissue and causes behavioural changes include Plasmodium and Trypanosoma. Toxoplasma

gondii has a known effect on the developing fetal central nervous system when it infects

women early in pregnancy.

 Introduction

Infection with the protozoan ​Toxoplasma gondii​ is one of the most common parasitic

infections of man and other warm-blooded animals. It has been found worldwide in nearly

one-third of the human population. In most adults it does not cause serious illness, however,

blindness and mental illness can result in congenitally infected children and severe disease in

those with depressed immunity. Toxoplasmosis, until recently, was not considered

water-borne. 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.

Toxoplasma gondii​ is recognized as a category B priority pathogen by the National Institutes

of Health, Bethesda, USA. In several of its hosts, ​Toxoplasma gondii​ is associated with

congenital infection and abortion. In addition, ​Toxoplasma gondii​ can cause encephalitis or

systemic infections in the immunocompromised, particularly individuals with human

immunodeficiency virus/acquired immunodeficiency syndrome. The present paper reviews

information on the biology of ​Toxoplasma gondii​ infections in humans and animals and

examines possible importance of transmission. The information will provide a brief overview

of the causes, symptoms, effects, immune reaction/response, and treatment of a host infected

by the parasitic infection. A basic understanding of these aspects will help appreciate how the

life cycle fits into the overall biology of the parasite and the technical aspects of studying it.

Following this introduction, the description on current understanding of ​Toxoplasma gondii,​

with the causes of the infection of ​Toxoplasma gondii​ sporozoites or tachyzoites leading to

the rapid spread throughout the whole body. How the symptoms and effects of ​Toxoplasma

gondii​ can provide early warning signals of the parasite infection, an insight to the link with
schizophrenia and how other organs of the body with abnormalities may occur if the host is

infected for a long period of time. With the Immune response. immune reaction,

pathophysiology, immunology and the antibiotics used to counter the parasite. Then finally

move on to the treatment and immunisation with patients who suffer from ​Toxoplasma gondii

along with patients who have compromised immune systems, human immunodeficiency

virus, acquired immunodeficiency syndrome or ocular disease. This entire article will provide

as much detail from gathered sources of approved research through many of the medical

scientists and practitioners who conducted these experiments and an insight of discussion and

conclusion of ​Toxoplasma gondii.

Causes:

Toxoplasmosis is an infection caused by a parasite called ​Toxoplasma gondii.​ ​Toxoplasma

gondii​ is one of the world's most common parasites infecting most animals (more than 30

species of birds and 300 species of mammals), and it is the most prevalent infection in

humans (estimated to be 30–50% of the world population). The parasite has received

considerable scientific and medical attention as it causes severe disease in

immunocompromised individuals.

Cats are important in the natural life cycle of Toxoplasma gondii because they are the only

hosts that can directly spread Toxoplasma gondii in the environment. This is because

although Toxoplasma gondii​’s​ life cycle has both sexual and asexual phases, the sexual life

cycle only occurs in cats (definitive hosts of the parasite). In the cat stomach the parasite

differentiates into male and female gametocytes allowing sexual reproduction. Infected cats

can shed millions of oocytes.

Toxoplasma gondii​ can infect a wide range of mammals and birds, in addition to its definitive

host. They are called intermediate hosts and it’s where the asexual phase of the parasite’s life

cycle occurs. The parasite divides into two daughter cells through the endodyogeny process,

where two daughter cells form within the mother cell, which will dissolve when the daughter

cells are fully formed and separated.

There are three major ways of acquiring ​Toxoplasma gondii​ infection for both definitive and

intermediate hosts;​ transmission by ingestion of contaminated food​, animal to human

(zoonotic) transmission and mother to child (congenital) transmission.

Food-borne infection is most commonly caused by the ingestion of undercooked meat but it

can also occur by accidental ingestion of soil that contains ​T. gondii​ oocysts as a result of

unwashed fruit and vegetables or by drinking water that is contaminated with oocysts. Eating

raw, undercooked or cured meat (beef, lamb or other meats) contributes to between 30 per

cent and 63 per cent of infections, and soil contact contributes up to 17 per cent of infections.

(Cook A et al, British Medical Journal, 2000).

The zoonotic transmission occurs when humans have contact with the ​Toxoplasma gondii

oocytes that are shed from the faeces of infected cats into the environment or a litter box. For

this reason contaminated litter boxes are a concern for pregnant women, as an infection

during pregnancy can result in the transmission of the parasite to the fetus. This condition is

called congenital toxoplasmosis and can cause severe neurological and ocular diseases in

children. In Europe, congenital toxoplasmosis affects between one and 10 in 10,000 newborn

babies, of whom one to two per cent develop learning difficulties or die and four to 27 per

cent develop permanent vision impairment.(Cook A et al, British Medical Journal, 2000).

Although rare, there are other ways the transmission of the parasite can occur. Exposure of

children playing in sandpits, transmission during organ transplants or blood transfusion are a
few of them. Poor hygiene, lower socioeconomic status and less education may also

contribute to a higher rate of infection.

Symptoms/Effects:

Effects of Toxoplasma?

A strange thing happens to a part of the Brain Called ​Amygdala​ which is a part of

the brain which is linked to fear and anxiety, turns fear into desire!

How Does It Affect the Brain?

The parasite Toxoplasma gondii (T. gondii) may invade the brain and might induce

behavioral changes, Toxoplasma gondii, an intracellular protozoan parasite, can infect

humans in 3 different ways: ingestion of tissue cysts, ingestion of oocysts, or

congenital infection with tachyzoites. After proliferation of tachyzoites in various

organs during the acute stage, the parasite forms cysts preferentially in the brain and

establishes a chronic infection, which is a balance between host immunity and the

parasite’s evasion of the immune response. A variety of brain cells, including

astrocytes and neurons, can be infected. In vitro studies using non-brain cells have

demonstrated profound effects of the infection on gene expression of host cells,

including molecules that promote the immune response and those involved in signal

transduction pathways, suggesting that similar effects could occur in infected brain

cells. Interferon-c is the essential mediator of the immune response to control T.

gondii in the brain and to maintain the latency of chronic infection.

Infection also induces the production of a variety of cytokines by microglia, astrocytes, and

neurons, which promote or suppress inflammatory responses. The strain (genotype) of T.

gondii, genetic factors of the host, and probably the route of infection and the stage

(tachyzoite, cyst, or oocyst) of the parasite initiating infection all contribute to the

establishment of a balance between the host and the parasite and affect the outcome of the

infection.

Twenty-four hours post infection, by which time the parasite has replicated 2–4 times,

a variety of host glycolytic and mevalonate metabolic transcripts are upregulated,

presumably, in response to the nutritional drain imparted by the infection.

Intracellular tachyzoites are manipulating a change of signal transduction pathways

related to apoptosis, antimicrobial effector system, and immune cell maturation. The

recent finding of delivery of protein

phosphatase 2C released from rhoptries of tachyzoites into the host nucleus will likely

be a key step forward toward understanding the molecular basis of such

transcriptional manipulation. Similar studies on brain cells have not been reported, T.

gondii infection may also influence the brain

Congenital Toxoplasmosis

Congenital Toxoplasmosis is a zoonotic infection caused by the Parasite ​Toxoplasma gondii,​

when contracted just before or during pregnancy it can lead to miscarriage, still births and

disabilities. Primary infection in an immunocompetent woman is asymptomatic in 60% of

cases. Symptoms, if any during pregnancy are often mild and non-specific such as fatigue,

malaise, low-grade pyrexia, and myalgias. (Wolf and Cowen (1937). Around 1,000 to 10,000

new-borns are infected each year across Europe. The risk of having an infant with symptoms

at birth or later in childhood is 60% with maternal seroconversion at 12 weeks gestation and

decreases to 5% or less with seroconversion after 36 weeks gestation ​(R.E Gilbert, 2000).​ 1%

-2% of fetus die or develop learning disabilities and a further 4%-17% develop impaired

vision. The controlled study shows the risk factors with undercooked meat products being the

main contributor and cats, kittens and litter boxes not being a risk factor. Transmitting

through breastfeeding has not been reported. (Guerina NG, Hsu HW, Meissner HC, Maguire

JH, Lynfield R, Stechenberg B, Med 1994).

Cases Controls

Exposure Expose Not Expose Not

d expose d expose
d d
Cat
Kitten in home 14 233 28 793

Adult cat in home 36 210 110 703

Cat and kitten in home 8 238 14 807

Any cat in home 42 206 124 697

Cleaning litter tray 26 214 65 748

Cat that hunts 23 230 47 752

Cat fed raw meat 14 225 43 763

Cat fed tinned food 37 208 113 705

Meat
Cooked meat 27 7 79 18
†
<1/week​

† 212 725
Cooked meat ≥1/week​

† 22 210 60 745
Raw sausage <1/week​

† 9 8
Raw sausage ≥1/week​

Dry to cured meat 64 136 202 518

†
<1/week​

Dry to cured meat 42 90

†
≥1/week​

† 76 47 297 187
Salami <1/week​

† 125 335
Salami ≥1/week​

Raw/undercooked beef 103 140 181 636

Raw/undercooked 19 220 17 795

lamb
Raw/undercooked pork 21 219 33 779

Other raw/undercooked 15 225 11 801

meat
Frozen meat 207 39 715 103

Taste meat cooking 52 182 88 717

†
<1/week​

Taste meat cooking 14 13

†
≥1/week​

Other “food related” exposures

Unpasteurised milk 36 210 75 746

Untreated water 53 194 123 697

 Use of microwave 41 206 101 718
cooker
Other “lifestyle” exposures
Contact with soil 109 139 267 553

Working with animals 30 218 54 767

Travel outside 29 220 49 759

Europe/US or Canada
Living on farm 23 229 47 811

Table 1
Risk factors for ​Toxoplasma gondii​ infection adjusted for age, location, and period between
diagnosis of infection and interview in 252 infected women and 852 control women*
·​ ​ ​↵​* Numbers do not always add up to total as some women did not answer all questions.
·​ ​ ​↵​† Compared with no exposure in past four months.
·​ ​χ2​​ test for trend across all five levels of exposure (never, exposed but not in past four
months, monthly, weekly, or daily):
·​ ​ ​↵​‡P<0.01;
·​ ​ ​↵​§ P<0.001.

Screening

New-borns with congenital Toxoplasmosis in Europe are asymptomatic and usually go

undetected. If postnatal screening is carried out, then an early diagnosis can help with

intervention to improve the neurodevelopmental outcome. (​ Jacquemard F, Mirlesse V,

Daffos F 2000)​ According to (Esklid, Oxman, Mangus, 1996) Screening for the antibodies

has been a debate by clinician for the past 30 years, screening depend on the magnitude of

infected new-born’s per country. France introduced screening after 55% of babies were tested

positive for the infection. Toxoplasmosis is generally a rare disease in Ireland when

compared to most of continental Europe. Population seropositivity to Toxoplasmosis was

reported to be as high as 70% in some regions of France but it is only around 19% (Dublin) to
40% (midlands) in Ireland. This is the main reason why routine screening is worthwhile in

France and not in Ireland​. (​ Katherine Elliott, Maeve O’Connor, Julie Whealen 2009).

Immune Reaction/Response:

Immune Response

The immune response to the pathogenic disease known as ​Toxoplasma gondii​ has an

immediate effect upon entering the body of a host, where the immune system goes into active

alert when our white blood cells, primarily T helper cells alert B-lymphocytes which is

another type of mature white blood cell. (Wyler, D. J. 2004) These two cells are memory

cells and plasma cells. Once the disease enters the body, it travels within the blood which

induces high levels of Gamma Interferon. Gamma Interferon is a dimerized soluble cytokine

which is part of a group of signalling proteins such as hormones made and released by​ ​host

cells in response to the presence of several viruses. Cytokines are primarily secreted by

certain cells of the immune system and have an effect on other cells. (Wyler, D. J. 2004)

The effect of an IFN-gamma mAb which is an interferon monoclonal antibody on the

protective activity of immune T Cells against Toxoplasma infection was examined in a

murine model of toxoplasmosis. Mice that received anti-IFN-gamma antibody and immune

spleen cells all died to toxoplasmosis after the challenge with Toxoplasma tachyzoites, in

contrast, mice that receive normal IgG which is an antibody called “Gamma” and the immune

spleen cells all survive the infection. The protective activity of immune T cells, previously

shown to be the principal mediators of resistance against toxoplasma in mice was completely

ablated by the anti-IFN-gamma mAb. These results suggest that IFN-gamma is the major

mediator of the resistance against Toxoplasma infection. To understand what a tachyzoite is

and what anti-IFN-gamma antibodies are, IFN Gamma are immune regulator in normal

immunity. When IFN gamma production is disturbed, various autoimmune diseases can

develop, in which we suggest that anti-IFN gamma could have a beneficial effect.

Tachyzoites are rapidly multiplying stage in the development of the tissue phase of certain

coccidial infections, as in Toxoplasma gondii development in acute infections of

toxoplasmosis. (Y Suzuki and J S Remington 1954)

Immune Reaction

Toxoplasmosis is capable of triggering nonspecific activations of macrophages and natural

killer cells this activation is to inhibit parasite proliferation due to its cytotoxic action to

trigger a specific immune response due to the antigens which are part of the disease. The job

of macrophages is detecting, engulfing and destroying pathogens while natural killer cells

play a major role in the host rejection of both tumours and virally infected cells. (Denis

Filisette and Ermmano Candolfi, 2004) Since antigens are a toxin or other foreign substance

which induces an immune response the word cytotoxin explains itself as a cell with toxin.

CD4+ (T-helper Cells) and CD8+ (Natural Killer Cells) are the main cells involved with

​ ature CD4+ TL are divided into two sub

resistance of the host to ​Toxoplasma gondii. M

populations; Th1 and Th2 meaning T-helper cells 1 and 2 this distinction is based on the list

of cytokines secreted following stimulation.

 Pathophysiology

The pathophysiology of ​Toxoplasma gondii p​ roduces toxoplasma cysts which produce

lesions when they disintegrate, due to the delayed type of hypersensitivity accompanying

infections. In the presence of immunity, the released bradyzoites which are a slowly

multiplying encysted form of sporozoan parasite typical of chronic infection with

​ hey become destroyed, but when the protective immunity fails, the
Toxoplasma gondii. T

bradyzoites can develop again into actively multiplying tachyzoites which are enclosed

within a pseudocyst of parasite and host origin. (J.K Frenkel, 1988) They can parasitize and

destroy cells in expanding foci meaning foci is one of the most frequent findings in cerebral

magnetic resonance imaging when it comes to brain scanning in an MRI machine. (U.

Dietrich, M. Maschke, A. Dörfler, M. Prumbaum, M. Forsting, 2000)

Immunology

While increasing numbers of patients suffering from immune deficiencies the varying

radiological appearances of infectious brain lesions is becoming more important. The true

prevalence of cerebral toxoplasmosis seems to be higher. Diagnosis is possible by direct

detection of toxoplasma cysts or tachyzoites, histological demonstration of necrotising

encephalitis, positive or increasing IgG or IgM antibodies in serum or cerebrospinal fluid.

Infection with Toxoplasma gondii leads to progressive encephalitis in immunocompromised

patients. During the period of profound leukopenia the patients are at high risk of

opportunistic infection and do not show typical signs of cerebral infection clinically or

radiologically.
Acute acquired toxoplasma infection in a pregnant woman may result in a tragic outcome for

her offspring transmission to the fetus has been limited almost solely to those women who

acquire the infection during gestation. The dictum has been that women infected before

conception are at virtually no risk unless they are severely immunocompromised by drugs

they receive during pregnancy. Recently increasing numbers of pregnant women who are

coinfected with HIV which is a sexual transmitted disease and also toxoplasma gondii and

whose immune deficiencies cause reactivation of T.gondii infection leading to dual infections

of the offspring have been recognised. All of these events occur in the setting of a

preventable infection and disease. (Sin-Yew Wong and Jack S. Remington, 1994)

Antibiotics and Immunity

Antibiotics may be used in pregnant women, Immunocompromised patients with organ

involvement, congenitally infection infants or individuals with ocular disease. Antibiotics

cannot destroy the tissue cysts and may not be able to eradicate actively dividing parasites if

the presence of acute T.gondii infection in pregnant woman is confirmed. Antibiotics are

used to treat clinical disease/ Antibiotics do not destroy the bradyzoites and do not eliminate

infections. Pyrimethamine with triple sulpha drugs has given good results. It has been

reported that oocyst shedding in toxoplasma infected cats was reduced with combination of

pyrimethamine and Sulphadiazine. Antibiotics are used to treat clinical disease also

antibiotics do not destroy the bradyzoites and do not eliminate infections. Pyrimethamine

with triple sulpha drugs has given good results. It has been reported that oocyst shedding in

toxoplasma infected cats was reduced with combination of pyrimethamine and

Sulphadiazine. Oocyst shedding was much reduced following administration of

2-sulphamolyl -1-4,4-diaminodiphenysulphone (Sonar S. S. and Brahmbhatt M.N, 2010)

Treatment/Immunisation:

TREATMENT

Most healthy people recover from Toxoplasmosis without treatment because Toxoplasmosis

does not always require treatment, especially in healthy individuals. In certain situations,

however, such as with pregnant women or those who are immunocompromised,

medications may be recommended to decrease the severity of the toxoplasmosis infection.

Healthy individuals with symptoms​:

The doctor may recommend treatment with medications such as pyrimethamine (Daraprim)

and sulfadiazine. However, symptoms will often clear up without the need for treatment.

It may also be recommended that you take folic acid during treatment, as pyrimethamine may

interrupt absorption of the mineral folate. Side effects of the medication include

suppression of bone marrow activity and toxicity in the liver.

People with HIV or AIDS:

If you have HIV/AIDS, the treatment of choice for toxoplasmosis is also pyrimethamine and

sulfadiazine, with folinic acid (leucovorin). An alternative is pyrimethamine taken with

clindamycin (Cleocin). Therapy may be lifelong in certain situations.

Pregnant women and infants:

If you're pregnant and infected with toxoplasmosis, treatment may vary depending on where

you receive medical care.

If infection occurred before the 16th week of pregnancy, you may receive the antibiotic

spiramycin. Use of this drug may reduce your baby's risk of neurological problems from

congenital toxoplasmosis. Spiramycin is routinely used to treat toxoplasmosis in Europe

but is still considered experimental in the United States.

If infection occurred after the 16th week of pregnancy, or if tests show that your unborn child

has toxoplasmosis, you may be given pyrimethamine and sulfadiazine and folinic acid

(leucovorin). Your doctor will help you determine the optimal treatment.

Persons with ocular disease

Persons with ocular toxoplasmosis are sometimes prescribed medicine to treat active disease

by their ophthalmologist. Whether or not medication is recommended depends on the size

of the eye lesion, the location, and the characteristics of the lesion (acute active, versus

chronic not progressing).

Persons with compromised immune systems

Persons with compromised immune systems need to be treated until they have improvement

in their condition. For AIDS patients, it may be necessary to continue medication for the

rest of their lives, or for as long as they are immunosuppressed.

If a woman transmits toxoplasmosis to the fetus during pregnancy, doctors typically

recommend treatment with pyrimethamine and sulfadiazine. This does not eliminate the

T. gondii cells but forces them to remain dormant in certain tissues.

This treatment is reserved for extreme cases of the infection that occur after week 16 of

pregnancy, due to the potential for serious side effects in the mother and fetus. Once born,

infants can be treated with a regimen including pyrimethamine, sulfadiazine, and folic

acid.

What to expect from your doctor?

Your doctor is likely to ask you several questions, such as:

· When did your symptoms start?

· How severe are your symptoms?

· Have you recently consumed raw or undercooked meat?

· Do you own or care for a cat? Who changes the litter box?

· Do you wear gloves when gardening or working with soil?

· Do you have conditions or take medications that affect your immune system?

Prevention

· Exclusion from childcare, preschool, school or work is not necessary.

· Avoid eating and minimise handling raw meat.

· ​ ​Cooking all meat thoroughly and washing hands and utensils after handling raw meat .

All meat eaten by pregnant women should be cooked 'well done'.

· wash all vegetables thoroughly before eating, especially salad vegetables.

· Use gloves when emptying cat litter trays. Trays can be disinfected with boiling water.

Eggs need over 24 hours to become infectious after being passed in the faeces, so clean

litter trays daily

· Cats should be fed dry, canned or cooked food. Discourage pet cats from hunting. Since

eating rodents and birds infects cats, pet cats that do not hunt will not be exposed and do

not pose a risk to their owners. Even if a cat does become exposed, it only sheds infective

eggs in its faeces for about 10 days.

Conclusion

Toxoplasmosis is a risk factor for many neurological disorders, and thus this infection has to

be taken into consideration when developing strategies for preventing or delaying the onset

of various brain diseases. There is a number of simple strategies to decrease the risk of

infection among healthy people. They include avoiding the consumption of raw or
undercooked meat (among humans, this is the most common way of getting infected), as

well as general basic food handling safety practices. It is important to mention here that not

all researchers believe that ​T. gondii​ infection really affects human behavior or the risk of

diseases to any significant degree. Some recently published studies indicate that these risks

are very small, and the previously published correlations with various behavioral changes

are not as significant as we might think.

Discussion

​ nters the host body

It is actively shown that when the parasite known as ​Toxoplasma gondii e

it triggers an immediate immune response from that where the white blood cells known as

leukocytes engage in targeting the antigen of the parasite with the help of an administration

of normal IgG antibodies rather than IFN-gamma mAb antibodies to prevent fatal death due

to the tachyzoites of the infectious stages of ​Toxoplasma gondii​. The protective activity of

immune T cells, previously shown to be the principal mediators of resistance against

Toxoplasma gondii.​ Since IFN-gamma mAb antibodies caused death upon test mice who

were infected by ​Toxoplasma gondii,​ it was due to the IFN gamma production being

disturbed which can triggered various autoimmune diseases to develop. Since

"Toxoplasmosis is capable of triggering nonspecific activations of macrophages and natural

killer cells this activation is to inhibit parasite proliferation” due to its cytotoxic action to trigger

a specific immune response. If that can be suppressed it will disrupt the proliferation of

Toxoplasma gondii​ and can be easier to treat patients with the proper medication and

primary care. Targeting the parasites antigens and cytokine release can stop the rapid

reproduction of ​Toxoplasma gondii ​within the host.

References

Karen Sugden
* E-mail: karen.sugden@duke.edu
Affiliations Department of Psychology & Neuroscience, Duke University, Durham, North
Carolina, United States of America, Duke Center for Genomic & Computational Biology,
Duke University, Durham, North Carolina, United States of America
Terrie E. Moffitt
Affiliations Department of Psychology & Neuroscience, Duke University, Durham, North
Carolina, United States of America, Duke Center for Genomic & Computational Biology,
Duke University, Durham, North Carolina, United States of America, Department of
Psychiatry and Behavioral Sciences, School of Medicine, Duke University, Durham, North
Carolina, United States of America, Social, Genetic, and Developmental Psychiatry Centre,
Institute of Psychiatry, King’s College London, London, United Kingdom
Lauriane Pinto
Affiliation Duke Center for Genomic & Computational Biology, Duke University, Durham,
North Carolina, United States of America
Richie Poulton
Affiliation Department of Psychology, University of Otago, Dunedin, New Zealand
Benjamin S. Williams
Affiliations Department of Psychology & Neuroscience, Duke University, Durham, North
Carolina, United States of America, Duke Center for Genomic & Computational Biology,
Duke University, Durham, North Carolina, United States of America
Avshalom Caspi

Affiliations Department of Psychology & Neuroscience, Duke University, Durham,

North Carolina, United States of America, Duke Center for Genomic & Computational
Biology, Duke University, Durham, North Carolina, United States of America,
Department of Psychiatry and Behavioral Sciences, School of Medicine, Duke
University, Durham, North

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