- What is Toxoplasmosis?
- Statistics on Toxoplasmosis
- Risk Factors for Toxoplasmosis
- Progression of Toxoplasmosis
- Symptoms of Toxoplasmosis
- Clinical Examination of Toxoplasmosis
- How is Toxoplasmosis Diagnosed?
- Prognosis of Toxoplasmosis
- Toxoplasmosis Prevention
- How is Toxoplasmosis Treated?
- Toxoplasmosis References
- Drugs/Products Associated with Toxoplasmosis
What is Toxoplasmosis?
- Tachyzoite (active);
- Bradyzoite (inactive but capable of being reactivated); and
- Sporozoite (past the sexual stage of the life cycle).
Toxoplasmosis is characterised by acute infection that is, infection with T. gondii tachyzoites.
Life cycle of T. gondii
Tachyzoites are active T. gondii organisms, meaning that they can invade and replicate themselves within cells. They can invade all organs of the body, but are most likely to infect muscles (including the heart), the liver, spleen and central nervous system. It is in the tachyzoite stage that T. gondii causes toxoplasmosis.
In the bradyzoite phase of the life cycle, T. gondii parasites are dormant and live in tissue cysts. T gondii parasites cannot invade cells and replicate within them when they are in the bradyzoite phase of their life cycle. Following infection with T. gondii, bradyzoites remain in the body indefinitely. They may be re-activated (converted to tachyzoites, which can cause acute infection) if a person's immune system becomes weak.
Sporozoites are T. gondii organisms that have passed the sexual stage of the life cycle and can no longer replicate. They cannot therefore infect humans or other animals.
Primary hosts of T. gondii
Felines, including domestic cats, are the primary host for T. gondii. Unlike other hosts, they can excrete infectious T. gondii oocysts in their faeces. Following acute infection with T. gondii tachyzoites, felines excrete non-infectious T. gondii oocysts for several weeks. Under appropriate environmental conditions, the oocysts can sporulate (develop spores which allow them to reproduce). This occurs within several weeks of the T. gondii oocysts being excreted in cat faeces. T. gondii oocysts may remain infectious for up to a year after they sporulate, if environmental conditions are favourable (e.g. in warm, moist soil).
Intermediate hosts of T. gondii
Species other than felines (including humans and animals consumed by humans) are intermediate hosts. Intermediate hosts can carry the active (tachyzoite) or inactive (bradyzoite) T. gondii parasites in their cells or tissues. However, they do not excrete infectious oocysts in their faeces. The parasite resides within their body tissues.
Human infection with T. gondii
Infection in humans from a primary host (cat) can occur through direct contamination by cat faeces, for example, when a person's hands are contaminated cleaning a cat litter tray or gardening in soil containing contaminated cat faeces.
The risk of T. gondii infection from an intermediate host arises if flesh from an infected animal is consumed (e.g. pork from a pig with latent T. gondii infection). Following consumption of the contaminated meat, the bradyzoites enter the digestive tract. From there they spread to the bloodstream and spread throughout the body. They tend to invade mostly nerve and muscle tissues.
Bradyzoites enter the tissues and form cysts within days of ingestion, but cannot replicate or leave the tissues unless they are activated (converted to tachyzoites). If activated, the T. gondii parasites can spread further by invading new cells and replicating within them.
Statistics on Toxoplasmosis
Globally, the prevalence of T. gondii infection varies. It is higher in tropical areas, where environmental conditions are more favourable for T. gondii organisms. In Australia, some 30–40% of the population hosts the disease, although in most people the parasites reflect previous rather than current infection. These individuals have T. gondii bradyzoites (inactive) in their cells.
Most individuals (90%) who are infected with T. gondii are unaware they host the parasite as they never experienced severe symptoms of infection. They are therefore not diagnosed in the acute phase of their illness. However, the T. gondii parasites hosted by these individuals can be reactivated if their immune system is compromised. The immune system may become compromised for numerous reasons, including as a result of:
- Acute illness (e.g. the flu);
- Chronic illness (e.g. AIDS);
- Taking medications that suppress the immune system;
- Ageing: Immune functions decline gradually as a person ages; and
- Pregnancy, during which there is a risk that the infection will be passed on to the foetus.
Between 2 and 5 of every 1,000 pregnant Australian women who host inactive T. gondii organisms will experience reactivation during pregnancy (i.e. the latent bradyzoites in their cells will convert to active tachyzoites). For these women, there is a risk that the infection will be passed onto their foetus, which is known as congenital transmission.
The risk of reactivation is higher in women who have other health conditions that compromise their immune system, including AIDS. When T. gondii parasites become active during pregnancy, they almost always invade organs in the central nervous system, such as the brain. T. gondii infections involving the central nervous system (as opposed to other body systems and organs) are more likely to result in severe symptoms, including meningitis (an inflammatory condition affecting the membranes surrounding the brain).
Amongst newborn babies whose mothers had toxoplasmosis or active T. gondii infection during pregnancy, 20–50% are also infected at birth. The risk of infection is reduced if the mother receives antibiotic therapy while she is pregnant; 44% of infants born to untreated mothers with acute T. gondii infection are infected at birth, compared to 29% of those born to women with acute infection who were treated with antibiotics during pregnancy.
Some 10% of infants born to infected mothers are severely infected and show symptoms of the infection at birth. The remainder have sub-acute infection, meaning that they host active T. gondii parasites (tachyzoites) but do not display symptoms of the infection when they are born. In these babies, symptoms may develop later in life, although some babies born infected with T. gondii never develop symptoms of the infection.
Australian statistics regarding the number of babies born with T. gondii infection are limited. Studies from the United States have reported an overall incidence of congenital toxoplasmosis (toxoplasmosis in a newborn) of 1.1 infections per 1,000 live births. Up to 4,000 cases of congenital toxoplasmosis are estimated to occur in the United States each year.
Risk Factors for Toxoplasmosis
Immunosuppression (reduced function of the immune system) is a key risk factor for reactivation of latent (inactive) T. gondii infection or acute primary infection. Immunosuppressed patients include those who:
- Are human immunodeficiency virus (HIV) positive, particularly if their CD4+ T lymphocyte count < 100 cells/microlitre;
- Hve other conditions that compromise their immune system; and
- Are taking immunosuppressing medication.
The immune system of a foetus is underdeveloped. Therefore the risk of infection with active T. gondii is high for the foetus. The degree of risk differs depending on the stage of the pregnancy.
The risk of foetal infection from an acutely infected mother is relatively low (10%) in the first trimester. However, infection at this stage presents the greatest danger of severe symptomatic infection in the newborn. Some 70% of foetuses infected with T. gondii in the first trimester experience severe consequences as a result of their infection, compared to < 1% infected in the final trimester. The risk of infection is much greater in the third trimester (60%).
Exposure to T. gondii
Toxoplasmosis only occurs in individuals who have been exposed to T. gondii parasites. Risk factors for exposure to T. gondii include owning a cat or cleaning a cat litter box. It should be noted that only infected cats pose a risk of toxoplasmosis, and indoor cats that do not hunt or eat raw meat are unlikely to become infected. As T. gondii is only present in faeces and has not been found in the fur of infected cats, there is no risk of infection from touching a cat if there is no contact with the faeces.
Other risk factors for new T. gondii exposure include:
- Eating raw or undercooked meat (if the animals have inactive T. gondii infection);
- Eating raw or unwashed vegetables (if the vegetables have been exposed to infected cat faeces);
- Gardening or undertaking other activities involving contact with soil, which may contain contaminated cat faeces;
- Poor hygiene practices, including infrequent hand washing and not washing knives often enough;
- Exposure at work, including working with meat or in a toxoplasma laboratory; and
- Travelling to developing countries.
You can largely prevent exposure to T. gondii and in doing so prevent toxoplasmosis, even if you have a higher risk of infection. Prevention measures include:
- Avoiding certain foods (including undercooked meats, contaminated water and food prepared in unhygienic environments);
- Good personal hygiene;
- Hygienic food storage; and
- Hygienic food preparation measures.
Being aware of the ways in which T. gondii parasites are transmitted and strategies to avoid infection is a key way in which the infection can be controlled. Pregnant women and others whose immune systems are compromised should pay particular attention to informing themselves of the risks and implementing prevention strategies.
Progression of Toxoplasmosis
Infection through tachyzoites in cat faeces
Humans and other animals can become infected if they come into contact with infectious oocysts (tachyzoites). This may occur through accidental ingestion of cat faeces, for example by forgetting to wash your hands after gardening in contaminated soil or changing a cat litter box. Eating unwashed fruit or vegetables that have been in contact with cat faeces may also lead to active infection with T. gondii oocysts.
When a human body is infected through direct contamination with cat faeces, tachyzoites enter the body and cause toxoplasmosis after a dormancy period of 5–20 days. For a period of several weeks, the parasites invade and replicate within cells. This is the stage at which symptoms of acute infection might appear. Following the active phase, tachyzoites convert to their inactive form (bradyzoites).
In adult humans, acute infection with tachyzoites is usually asymptomatic or results in only mild, flu-like symptoms. Hence toxoplasmosis typically goes undiagnosed in adults.
Infection through bradyzoite-contaminated meat
Humans can become infected by eating meat contaminated with inactive T. gondii bradyzoites. Cooking meat thoroughly kills T. gondii, but consuming raw or undercooked meat increases the risk of infection.
The limited available evidence from the United States suggests that some 50% of T. gondii infections arise from eating contaminated meat. In these cases, there is not necessarily a period of acute infection; toxoplasmosis only occurs if the meat consumed was infected with tachyzoites (from an animal with acute infection), or the ingested bradyzoites convert to tachyzoites. Conversion typically only occurs in immunosuppressed people. In cases of tachyzoite ingestion or weakened immune function, bradyzoites may convert to tachyzoites and cause acute infection 10–23 days after eating undercooked meat.
Foetal infection during pregnancy
When active parasites infect the body of a pregnant woman, they can be transmitted to the foetus. This can have serious health consequences. In these cases, tachyzoites are transferred via the placenta, infect the foetus and replicate within the cells of the foetus. Transmission to the foetus can only occur at times when the mother has acute infection, and does not occur if she has latent or inactive infection. The risk of transmission is reduced if the acutely infected pregnant woman receives antibiotic therapy throughout her pregnancy.
Infection during organ transplant
In rare cases, infection has occurred following organ transplantation or blood transfusion with an infected organ or blood. These infections may occur as a result of reactivation of bradyzoites in the transplanted organ. They may also occur if the person receiving the transplant had bradyzoite infection and their immune system is suppressed following transplantation.
Symptoms of Toxoplasmosis
Non-pregnant healthy adults
Infection is asymptomatic in 90% of healthy adults with well functioning immune systems. The remaining 10% may present with symptoms of chorioretinitis (inflammation of the eye).
If you are a woman and have had active infection you should not conceive for at least six months. Be sure to talk to the doctor about contraception if you are sexually active and not currently using a contraceptive method.
Non-pregnant immunocompromised adults
People who are immunocompromised have immune systems that do not to work as effectively as they should. Such people include those with HIV-related immunosuppression and those who have recently had an organ transplant.
In immunocompromised individuals, toxoplasmosis typically causes symptoms of encephalitis (inflammation of the brain) or chorioretinitis (inflammation of the eyes). Retinitis is common and may cause blurred vision, which is one of the key symptoms that can alert a doctor to the possibility of toxoplasmosis.
If toxoplasmosis leads to encephalitis, focal neurological deficit (a problem with the nervous system that affects the function of a specific body system, such as preventing movement on the left side of the body) is a common symptom. Other commonly seen symptoms in people with encephalitis include:
Less common symptoms of toxoplasmosis involving the brain or eye include:
- Lymphadenopathy (disorder of the lymph nodes);
- Hepatitis (inflammation of the liver);
- Pneumonitis (inflammation of the lung); and
- Myocarditis (inflammation of the heart muscle).
Screening and prophylaxis for HIV-positive people
There is a higher risk of bradyzoites activating in individuals who are HIV positive and have become immunocompromised. As a person's immune system deteriorates some years following HIV infection, your doctor may give prophylactic medicines to help prevent latent infection becoming active.
If you are HIV positive, it is important to tell your doctor so you can be screened for T. gondii infection. A blood test that screens for an antibody called toxoplasma IgG is usually used.
A positive test result for toxoplasma IgG indicates past exposure to T. gondii. If you host T. gondii and are HIV positive with a CD4+ T lymphocyte count < 100 cells/microlitre, your doctor will give you prophylactic medication. You will need to continue taking the prophylactic medicine until your doctor determines your immune function has improved.
A negative test indicates your blood does not contain antibodies for toxoplasma IgG and that you have not been previously exposed to T. gondii. In this case, it is important to try to avoid future exposure to the organism which might cause infection. Your doctor will give you advice about how to avoid becoming infected, but you do not need to take prophylactic medicines.
Screening and prophylaxis for organ transplant patients
The risk of T. gondii reactivation is also much greater if you have just had an organ transplant, particularly if the organ transplanted was a heart. Before the transplant, a blood test will be performed to check for toxoplasma IgG antibodies, the presence of which indicates you host inactive T. gondii bradyzoites. The organ being transplanted may also be tested for toxoplasma IgG antibodies.
If either you or the organ test positive, your doctor will start prophylactic treatment to reduce the risk of the infection becoming active.
Toxoplasmosis or active T. gondii infection is difficult to detect in pregnant women, as the infection usually only causes mild symptoms, which are similar to symptoms of the flu. As a result, toxoplasmosis is often not diagnosed in pregnant women.
However, if active infection occurs during pregnancy, T. gondii can be transmitted to the foetus. Taking antibiotics during pregnancy can reduce the risk of transmission to the foetus, but if active infection is not detected, antibiotic prophylaxis will not be given. Tests that can be used to detect active infection can also harm the foetus, so doctors do not usually screen for toxoplasmosis in pregnant women in Australia.
Women who are HIV positive should be screened, as they have an increased risk of reactivation during pregnancy. Toxoplasmosis is also more likely to induce severe symptoms such as encephalitis (inflammation of the brain) in HIV-positive women.
Pregnant women who show symptoms of acute toxoplasmosis, which typically include malaise, fever and lymphadenopathy (disorders of the lymph nodes) are often also screened.
At birth, infected babies may show symptoms including:
Newborn babies with symptomatic toxoplasmosis typically have a group of symptoms, which include:
- Eye infections, including chorioretinitis;
- Hydrocephalus (fluid accumulation in the skull which, when it affects a baby, often causes the soft spot at the top of the head to bulge);
- Intracranial calcifications (calcium deposits in the skull); and
Other possible symptoms include:
- Blueberry muffin appearance (blue-grey nodules under the skin);
- Symptoms of anaemia;
- Hepatosplenomegaly (enlarged liver or spleen);
- Lymphadenopathy (disorders of the lymph nodes);
- Lethargy or malaise;
- Vomiting or diarrhoea;
- Poor feeding; and
- Fluctuating temperature.
Premature babies with toxoplasmosis often develop severe symptoms affecting their central nervous system or eyes within three months of birth. Those born at full term are more likely to display mild symptoms in the first two months.
Newborn babies often also display a range of non-specific symptoms. In these cases, toxoplasmosis symptoms are similar to the symptoms of a number of viral infections, including cytomegalovirus, herpes simplex virus and rubella virus. This makes it difficult to diagnose toxoplasmosis and means the doctor may do blood tests for toxoplasmosis, as this is the only way to differentiate it from other possible conditions.
It should be noted that many newborns are born with no obvious signs of toxoplasmosis. Nevertheless, if the mother experienced toxoplasmosis during pregnancy, the doctor may conduct tests to determine whether or not the baby is infected.
Newborn babies who display no or only mild symptoms are at risk of experiencing complications later in life because of their toxoplasmosis infection. 80% of infants infected at birth are asymptomatic but will develop complications at some point in the future, sometimes decades after birth. The complications may not occur until the baby reaches their 20s or 30s. Late complications that may occur in infected newborns include:
- Chorioretinitis (eye inflammation);
- Hepatosplenomegaly (enlarged spleen or liver);
- Mental retardation;
- Psychomotor retardation (characterised by reduces physical and mental activity);
- Sensorineural hearing loss/deafness (deafness due to dysfunction of the ear's nerve) ;
- Epilepsy; and
- Learning difficulties.
Late complications and severe disease in the newborn are more likely if the mother became infected during the first trimester of pregnancy. The risk of late complications is reduced by half if the condition is diagnosed promptly and antibiotic therapy is given for the first year of the newborn's life.
Clinical Examination of Toxoplasmosis
When an adult presents to a doctor with toxoplasmosis, the most common symptom is chorioretinitis or inflammation of the eye. In these cases, the doctor will examine the eye for retinal lesions (tears, ulcers or other discontinuities in the tissues of the eye's retina), which are an indicator that toxoplasmosis is a likely cause of the eye problems. If retinal lesions are found in the eye examination, the doctor will conduct blood tests for toxoplasma antibodies.
If a mother experienced toxoplasmosis during pregnancy, a paediatricianwill usually attend the birth in order to perform a full physical examination of the baby when it is born. The examination will probably include an eye examination. Blood tests are also likely to be performed if the eye examination reveals retinal lesions.
How is Toxoplasmosis Diagnosed?
Toxoplasmosis can be diagnosed with a blood test for anti-toxoplasma IgM. A positive test indicates toxoplasmosis. A blood test for anti-toxoplasma IgG indicates past infection which is currently latent.
T. gondii infection in pregnant women can also be detected using blood tests for anti-toxoplasma IgM and anti-toxoplasma IgG. Positive results indicate acute and latent infection respectively.
Women who test positive for toxoplasma antibodies may have further blood taken for specialist testing to determine when the active infection occurred.
If you experience toxoplasmosis while you are pregnant, tests may also be conducted to determine whether or not the infection has been transmitted to your foetus. The tests are conducted using a sample of amniotic fluid (fluid from the amniotic sac which protects the foetus and placenta. This is the sac that breaks when a woman's 'water breaks' just before she is about to give birth).
If the foetus is found to be infected with toxoplasmosis, an ultrasound may be performed to assess for deformities in the foetus, although most foetuses with toxoplasmosis appear normal on ultrasound.
A newborn baby's blood may also be tested for anti-toxoplasma IgG and IgM if they are born to a mother who had toxoplasmosis during pregnancy. Ultrasound and other tests may also be used to diagnose toxoplasmosis in a newborn baby.
Tests may also be performed using tissues from the placenta (often referred to as the afterbirth) to diagnose infection in a newborn baby whose mother experienced acute infection while pregnant. The baby may also have its skull and brain examined using ultrasound or CT scan.
A CT scan may be conducted to evaluate the brain of immunocompromised people who have focal deficits or reduced consciousness. Tests may also be performed using blood, bone marrow or other tissues. Individuals who fail to improve after two weeks of antibiotic therapy may have a brain biopsy to check for other diseases which might be causing the symptoms.
Prognosis of Toxoplasmosis
Toxoplasmosis does not usually result in symptoms and does not usually affect the health of adults. In immunocompromised and a limited number of apparently healthy adults, acute infection (following either primary infection or reactivation of a dormant infection) may lead to chorioretinitis (eye inflammation) and/or encephalitis (brain inflammation).
Once infected, adults will carry the dormant form of the parasite (bradyzoite) indefinitely. Bradyzoites may become reactivated (convert to tachyzoites) at some point in the future, typically in periods of immunosuppression or during pregnancy. Reactivation rarely occurs in healthy, non-pregnant individuals.
Reactivation of dormant bradyzoites occurs in 25 per 1,000 pregnant women who are T. gondii hosts. Activation during pregnancy following either primary infection or reactivation of dormant infection is associated with a range of health complications for babies who contract the disease from their mothers during pregnancy. The vast majority of congenital infections occur following primary infection, rather than following a reactivated infection.
Congenital infection has severe implications for the health of the foetus. If a pregnant woman with acute infection takes antibiotics during pregnancy, there is a reduced risk of congenital infection.
The risk of congenital infection also varies depending on the stage of pregnancy when a woman becomes infected or an existing infection is reactivated. In the first trimester of pregnancy, new infection carries a 1–25% risk of congenital transmission, compared to a 60–90% risk in the third trimester.
However, the health outcomes for the baby after birth are more severe when infection occurs in the first trimester of pregnancy. There is a 60–80% chance the baby will be born with abnormalities caused by retarded foetal growth if acute infection occurred in the first trimester of pregnancy. The risk of abnormalities and severe complications is reduced to 15–25% if the mother experienced toxoplasmosis in the second trimester, and to < 1% if acute infection occurred in the third trimester. There is no risk of transmission from a mother to her baby while she is breastfeeding.
Amongst babies born to infected mothers, some 10% are severely infected at birth (called neonatal toxoplasmosis). In severe cases of neonatal toxoplasmosis (about 10% of all neonatal cases), symptoms occur at birth and include eye infection, jaundice and pneumonia.
Babies who are severely infected at birth are also at risk of brain damage, blindness, deafness, and fits or seizures. In some cases, the infection is fatal, but death and severe complications such as brain damage typically only occur if the mother had toxoplasmosis in the first trimester of pregnancy.
Toxoplasmosis can be prevented by avoiding exposure to the pathogen T. gondii, which is found in cat faeces and products contaminated with it. These include raw and uncooked meats, fruits and vegetables, and other foods prepared in unhygienic environments. People can also be exposed if their hands come into contact with cat faeces (e.g. changing the litter tray or in the garden) and they then put their hands to their mouth.
Good personal and food preparation hygiene are the key preventative measures. Avoid raw and undercooked meats (especially if pregnant or immunocompromised) and observe good food hygiene practices (e.g. washing hands before touching foods, keeping food preparation surfaces clean). Wash fruit and vegetables thoroughly before consuming them, and wash your hands thoroughly after touching a cat, changing a cat litter tray or gardening.
Immunocompromised people who have experienced an incident of acute infection can use medicine to prevent reactivation of the latent infection. Prophylactic (preventative) medications are usually prescribed for the rest of the person's life, or until their immune function improves.
How is Toxoplasmosis Treated?
Prophylactic treatment is preventative treatment. In the case of toxoplasmosis, prophylactic treatment is given with the aim of preventing acute infection in someone who hosts inactive bradyzoites or has just been exposed to T. gondii parasites.
If an individual knows they have been exposed to T. gondii, prophylactic treatment can be given to reduce the risk of acute infection. In most cases, people are unaware that they have been exposed to the parasite. However, if they work in toxoplasma laboratories, they may be aware of exposure, for example if they prick themselves with a needle that had been exposed to contaminated blood.
Individuals who are HIV positive and immunocompromised should receive prophylactic treatment if they host inactive T. gondii bradyzoites. Prophylactic treatment reduces the risk that the bradyzoites will convert to tachyzoites and cause acute infection.
People who do not host T. gondii will be given prophylactic treatment if they have a heart transplant.
People who host inactive bradyzoites and are about to undergo stem cell transplants also require prophylactic treatment if they have active graft-versus-host disease (in which the immune system rejects a transplanted organ) or have previously experienced chorioretinitis as a symptom of toxoplasmosis.
Treatment of active disease
Otherwise healthy, non-pregnant adults
The most common symptom in non-pregnant adults is chorioretinitis. In these cases, the goal of treatment is to limit damage to the eye and reduce symptoms. When the macula (section of the eye which is responsible for focus) or optic nerve (nerve which transmits light signals into the eye) are affected by severe or persistent lesions, antibiotic treatment is usually started, though it is not always necessary if the symptoms are less severe.
Individuals typically require three weeks off work and other activities if they experience symptomatic toxoplasmosis.
The goal of treatment in pregnant women is to prevent congenital transmission, that is, to prevent infection of the foetus. Prompt antibiotic therapy reduces the risk of transmission from a pregnant woman to her foetus, although the risk of congenital infection is not completely eliminated. If laboratory tests conducted during pregnancy show the foetus is not infected, the pregnant woman should be treated with antibiotics for the entire pregnancy. However, antibiotic treatment is not effective if the foetus has already been infected.
If you are pregnant and your foetus becomes infected, your doctor is likely to refer you to a specialist who will determine which medicines you should take to reduce the risk of active infection and complications for the baby after birth. You will probably be given antibiotics to take for the remainder of your pregnancy, and will also need to take a folate supplement.
Being diagnosed with toxoplasmosis may be distressing and raise concerns about the health of the foetus. If you are diagnosed with toxoplasmosis during pregnancy, be sure to take the time to discuss the risks involved and the likely outcomes for the baby. A doctor or other health professional can also give you information about tests that can be performed to check whether or not the foetus has contracted toxoplasmosis. You might benefit from seeing a counselor so you can talk about your concerns. You may consider terminating your pregnancy, and a counselor can also help you think about whether or not this is the best option for you, and provide a referral to a pregnancy termination service if needed.
Foetal damage causing the baby to be born with a defect or abnormality is highly likely if toxoplasmosis infection occurred in the first trimester of pregnancy. You may consider terminating your pregnancy if toxoplasmosis occurred in the first trimester, or if tests show that the baby is likely to be born with an abnormality. Your doctor will be able to provide you with appropriate referrals for counseling and pregnancy termination if you are considering terminating the pregnancy.
Newborn babies with toxoplasmosis will require treatment with antibiotics and a calcium folinate supplement for the first year of life. Available evidence suggests that infants treated with antibiotics for a year have better outcomes than those who are not treated.
Immunosuppressed HIV-positive patients who develop active infection are usually treated with antibiotics for six weeks. Further treatment may be necessary if symptoms do not resolve in that time. Following resolution of active disease, these people will continue to host T. gondii bradyzoites which may or may not become reactivated in the future. To reduce the risk of reactivation (which is very high when the immune system is compromised), prophylactic medication will be given while the immune system remains suppressed.
When a person received an organ transplant, medications are usually given to prevent their body rejecting the organ that has just been transplanted. The body's immune system recognises the transplanted organ as a foreign body and tries to develop an immune response to prevent the foreign body (in this case the transplanted organ) from establishing itself within the body. It is similar to the immune response that occurs when a foreign disease enters the body.
Medications given to reduce the likelihood of transplant rejection work by suppressing the immune system, and are called immunosuppressant therapies. However, they also hinder the immune system's ability from fighting diseases like toxoplasmosis. Your doctor may need to reduce the dose of immunosuppressant therapy if you host inactive T. gondii. Your doctor is also likely to prescribe prophylactic antibiotic therapy to reduce the likelihood of reactivation of an inactive infection.
Acute disease can persist for up to 12 weeks. In serious cases, including brain and eye involvement, time away from work and other activities averages more than 4 weeks.
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Symptoms of This Disease:
Drugs/Products Used in the Treatment of This Disease:
- Cleocin (Clindamycin hydrochloride)
- Daraprim (Pyrimethamine)
- Dexamethasone Sodium Phosphate Injection USP (DBL) (Dexamethasone sodium phosphate)
|Modified: 25/11/2010||Reviewed: 19/11/2010||Created: 11/10/2006|
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