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Toxoplasmosis |
Definition
Toxoplasmosis is an infectious disease caused by the one-celled parasitic organism Toxoplasma gondii. Although most individuals do not experience any symptoms, the disease can be very serious and even fatal in fetuses, newborns, and individuals with weakened immune systems.
Description
Toxoplasmosis is caused by a one-celled parasite Toxoplasma gondii. This parasite is found worldwide. It causes infections that can be either acute or chronic. In about 60 percent of healthy adults who become infected, the organism causes no symptoms (asymptomatic). Most of the remaining 40 percent experience mild, flu-like symptoms, low-grade fever, and fatigue that resolve without intervention in a few weeks. Once exposed, reinfection does not occur in healthy individuals. However, in immunocompromised individuals, such as those with HIV/AIDS, symptoms can be severe, life threatening, and recurring. T. gondii infection of a fetus or newborn can also cause severe neurological impairment, blindness, mental retardation, and death. When a fetus acquires the infection through its mother, this is called congenital toxoplasmosis.
Transmission
The organism that causes toxoplasmosis can be transmitted in four ways. The most common way is through contact with feces of an infected cat. Cats, the primary carriers of the organism, become infected by eating rodents and birds infected with T. gondii. Once ingested, the organism reproduces in the intestines of the cat, producing millions of eggs known as oocysts. These oocysts are excreted in cat feces daily for approximately two weeks. In the United States, approximately 50 percent of cats have been infected with T. gondii.
Oocysts are not capable of producing infection until approximately 24 hours after being excreted in warm climates and longer in cold climates. However, they remain infective in water or moist soil for about one year. Humans become infected when they come in contact with and accidentally ingest oocysts when changing cat litter, playing in contaminated sand, working in the garden or similar activities, or by eating unwashed vegetables and fruit irrigated with untreated water that has been contaminated with cat feces.
The second way humans become infected with T. gondii is through eating raw or undercooked meat. When cattle, sheep, or other livestock forage through areas contaminated with cat feces, these animals become carriers of the disease. The organism forms cysts in the muscle and brain of the livestock. When humans eat raw or undercooked infected meat, the walls of the cysts are broken down in the human digestive tract, and the individual becomes actively infected. The encysted organism can be killed by freezing or cooking the meat well.
The only form of direct person-to-person transmission occurs from mother to fetus during pregnancy. This transmission occurs only if the mother is in the acute, or active, stage of infection when the organism is circulating in the mother's blood. It is estimated that about one third of women with active infections pass the infection along to their fetus. Women who have become infected six months or more before conception do not pass the infection on to their fetus, because the organism has become dormant (inactive) and formed thick-walled cysts in muscle and other tissues of the body. Reactivation of the infection in healthy individuals is extremely rare. Women who give birth to one infected child do not pass the infection to their fetus during subsequent pregnancies unless they are immunocompromised (for example, with AIDS) and the infection recurs.
Finally, individuals can also become infected through blood and organ transplant from an infected person.
Demographics
Men and women of all races are equally affected by T. gondii, however, except for immunocompromised individuals, the implications are more serious for women, as they can pass the infection on to their offspring. The rate of infection in the United States varies considerably with location. Studies have found that the infection rate in women of childbearing age ranges from 30 percent in Los Angeles to 3.3 percent in Denver. Varying sanitary conditions and culinary habits, such as eating raw meat, account for some of this variation. The rate of infection increases with the age of the individual. About 3,500 to 4,000 children are born in the United States each year with congenital toxoplasmosis. Outside the United States, fetal infection rates tend to be higher, although the number of babies born with congenital toxoplasmosis was as of 2004 declining worldwide.
Causes and Symptoms
In fetuses, the severity of infection is dependent on the time of transmission. Fetuses who acquire the infection during the first trimester of pregnancy often are still-born or die shortly after birth. Fetuses who acquire the infection late in pregnancy often show no symptoms when born.
Severe infections lead to seizure disorders, neurological disorders, abnormal muscle tone, deafness, partial or complete blindness caused by a condition called chorioretinitis, and mental retardation. These conditions may not be present at birth, especially if the infection occurred late in pregnancy. Vision deficits, especially, tend to show up later in life.
Young children can acquire toxoplasmosis in the same ways as adults. However, symptoms and complications when the disease is acquired after birth tend to be much milder than with congenital toxoplasmosis.
Children and adults with weakened immune systems have a high risk of developing serious symptoms, including cerebral toxoplasmosis, an inflammation of the brain (encephalitis), one-sided weakness or numbness, mood and personality changes, vision disturbances, muscle spasms, and severe headaches. If untreated, cerebral toxoplasmosis can lead to coma and death.
When to Call the Doctor
Women who believe they may have become infected shortly before conception or during pregnancy should call their doctor immediately. Treatment is possible during pregnancy. Symptoms in the newborn may be obvious during the newborn examination. If they are not, parents should consult their doctor if they feel their child has any neurological or vision complications or is not meeting appropriate developmental milestones.
Diagnosis
A diagnosis of toxoplasmosis is made based on clinical signs and supporting laboratory results, including visualization of the organism in body tissue or isolation in animals. Blood tests for toxoplasmosis are designed to detect increased amounts of a protein or antibody produced in response to infection with T. gondii. Antibody levels can be elevated for years, however, even when the disease is in a dormant state. Amniocentesis (sampling amniotic fluid) between 20 and 24 weeks of gestation can detect toxoplasmosis in the fetus.
Treatment
Most healthy individuals who contract toxoplasmosis do not require treatment, because the healthy immune system is able to control the disease. Symptoms are not usually present. Mild symptoms may be relieved by taking over-the-counter medications, such as acetaminophen (Tylenol) and ibuprofen (Motrin, Advil). Sore throat lozenges and rest may also ease the symptoms.
The benefits of treating women who contract toxoplasmosis during pregnancy almost always outweigh any risks involved. Treatment is with antibiotic and antimicrobial drugs. Transmission of toxoplasmosis from the mother to the fetus may be prevented or reduced if the mother takes the antibiotic spiramycin. Later in a pregnancy, if the fetus has contracted the disease, treatment with the antibiotic pyrimethamine (Daraprim, Fansidar) and folinic acid (an active form of folic acid) may be effective. Babies born with toxoplasmosis who show symptoms of the disease may be treated with pyrimethamine, the sulfa drug sulfadiazine (Microsulfon), and folinic acid. Healthy children over the age of five usually do not require treatment. Infected individuals with weakened immune systems may require lifetime drug treatment to keep the infection from recurring.
Prognosis
The prognosis is poor when congenital toxoplasmosis is acquired during the first three months of pregnancy. Afflicted children die in infancy or suffer damage to their central nervous systems that can result in physical and mental retardation. Infection later in pregnancy often results in only mild symptoms, if any. The prognosis for acquired toxoplasmosis in adults with strong immune systems is excellent. The disease often disappears by itself after several weeks. However, the prognosis for immunodeficient patients is not as positive. These patients often relapse when treatment is stopped. The disease can be fatal to all immunocompromised patients, especially individuals with AIDS, and particularly if not treated.
Prevention
There are no drugs that can eliminate T. gondii cysts in animal or human tissues. Humans can reduce their risks of developing toxoplasmosis by practicing the following measures:
Parental Concerns
Fear of infection during pregnancy is the most common parental concern. When a fetus is found early in pregnancy to be infected, parents are faced with the decision of whether to continue the pregnancy given the likelihood of serious complications to the fetus.
Resources
Books
Ambrose-Thomas, P., et al. Congenital Toxoplasmosis: Scientific Background, Clinical Management, and Control. New York: Springer, 2000.
Joynson, David H. M., et al. Toxoplasmosis: A Comprehensive Clinical Guide. Cambridge, UK: Cambridge University Press, 2001.
Periodicals
Jones, J. "Congenital Toxoplasmosis." American Family Physician 67 (May 15, 2003): 2131–8.
Web Sites
Leblebicioglu, Hakan, and Murat Hökelek. "Toxoplasmosis." eMedicine.com August 10, 2004. Available online at www.emedicine.com/ped/topic2271.htm (accessed October 15, 2004).
The Merck Manual of Diagnosis and Therapy, 17th ed. Edited by Mark Beers and Robert Berkow. Available online at www.merck.com/mrkshared/mmanual/home.jsp (accessed October 15, 2004).
[Article by: Tish Davidson, A.M.]
Gale Encyclopedia of Public Health:
Toxoplasmosis |
Toxoplasmosis is an infection caused by a single-celled protozoan parasite named Toxoplasma gondii found throughout the world in humans, mammals, and birds. Cats, the definitive host for T. gondii, usually become infected by eating infected prey, and are the only animal that sheds the organism (as oocysts) in their feces. Animals other than cats are usually infected by ingesting oocysts in the soil or by eating infected animals.
Humans can become infected with T. gondii by one of three main routes: (1) by eating raw or inadequately cooked meat that contains T. gondii cysts (bradyzoites) or by eating uncooked foods that have come in contact with infected meat via, for example, cutting boards or cooking utensils;(2) by inadvertently ingesting oocysts that cats have passed in their feces either from a cat litter box or from soil (for example, from gardening) or by eating unwashed fruits and vegetables; (3) a newly infected woman can transmit the infection to her fetus.
Toxoplasmosis in adults usually does not cause symptoms, or causes only mild, nonspecific symptoms such as fever and swelling of the lymph glands. Therefore, the diagnosis is usually made by testing for antibodies that are produced in reaction to T. gondii infection. However, serious illness can occur when a newly infected woman passes the infection to her unborn fetus. Such an infection can lead to an infant with mental retardation, blindness, or other neurologic disorders. An estimated 400 to 4,000 congenital infections with T. gondii occur in the United States each year. Serious illnesses, including infection of the brain, can also occur in persons who have either old (latent) or new T. gondii infections when they do not have normal immune system function. Such persons include those with human immunodeficiency virus (HIV) infection or congenital immune illnesses, persons taking drugs that decrease immune system function, and persons with some types of cancer.
Effective means of preventing toxoplasmosis are as follows: (1) cook meat fully (internal temperature of 160° F) before eating it; (2) peel or wash fruits and vegetables before eating them; (3) wash hands, kitchen tools, counters, and sinks with soap and water after they have touched raw meat or unwashed fruits or vegetables; (4) clean the cat litter box every day so T. gondii oocysts do not have time to become infectious (one to five days); (5) wear gloves and wash hands after changing cat litter (pregnant women should not change cat litter if at all possible); (6) keep cats indoors so they do not become infected by eating prey; (7) feed cats only commercially prepared cat food, never undercooked or raw meat; and (8) wear gloves when gardening and wash hands after contact with soil and sand with which cats may have had contact.
(SEE ALSO: Communicable Disease Control)
Bibliography
Centers for Disease Control and Prevention (1999). "1999 USPHS/IDSA Guidelines for the Prevention of Opportunistic Infections in Persons Infected with Human Immunodeficiency Virus: U.S. Public Health Service (USPHS) and Infectious Disease Society of America (IDSA)." Morbidity and Mortality Weekly Report 48(RR-10):7–9.
—— (2000). "CDC Recommendations Regarding Selected Conditions Affecting Women's Health: Preventing Congenital Toxoplasmosis." Morbidity and Mortality Weekly Report 49(RR-2):57–76.
Dubey, J. P. (1994). "Toxoplasmosis." Journal of the American Veterinary Medical Association 205:1593–1598.
Frenkel, J. K., and Fishback, J. L. (2000). "Toxoplasmosis." In Hunter's Tropical Medicine and Emerging Infectious Diseases, 8th edition, ed. G. T. Strickland. Philadelphia, PA: W. B. Saunders Company.
— JEFFREY L. JONES
Saunders Veterinary Dictionary:
toxoplasmosis |
A contagious disease of all species caused by the sporozoan parasite Toxoplasma gondii. The principal manifestation in animals is as abortion in ewes. It is also a cause of sporadic cases of pneumonia, central nervous system disease, and less often retinochoroiditis, and hepatitis in dogs and cats. Clinical signs include fever, malaise, lymphadenitis, abortion, fetal malformation. Major importance as a zoonosis from bradyzoites in meat.
Mosby's Dental Dictionary:
toxoplasmosis |
A disease caused by protozoa in the bloodstream and body tissues.
Toxoplasmosis. (Neville/Damm/Allen/Bouquot, 2002)
Random House Word Menu:
categories related to 'toxoplasmosis' |
Rhymes:
toxoplasmosis |
Wikipedia on Answers.com:
Toxoplasmosis |
| Toxoplasmosis | |
|---|---|
| Classification and external resources | |
 T. gondii tachyzoites |
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| ICD-10 | B58 |
| ICD-9 | 130 |
| DiseasesDB | 13208 |
| MedlinePlus | 000637 |
| eMedicine | med/2294 |
| MeSH | D014123 |
Toxoplasmosis is a parasitic disease caused by the protozoan Toxoplasma gondii.[1] The parasite infects most genera of warm-blooded animals, including humans, but the primary host is the felid (cat) family. Animals are infected by eating infected meat, by ingestion of feces of a cat that has itself recently been infected, or by transmission from mother to fetus. Cats are the primary source of infection to human hosts, although contact with raw meat, especially pork, is a more significant source of human infections in some countries. Fecal contamination of hands is a significant risk factor.[2]
Over half of the world's human population is estimated to carry a Toxoplasma infection.[3][4] The Centers for Disease Control and Prevention notes that overall seroprevalence in the United States as determined with specimens collected by the National Health and Nutritional Examination Survey (NHANES) between 1999 and 2004 was found to be 10.8%, with seroprevalence among women of childbearing age (15 to 44 years) 11%.[5]
During the first few weeks post-exposure, the infection typically causes a mild flu-like illness or no illness. Thereafter, the parasite rarely causes any symptoms in otherwise healthy adults. However, those with a weakened immune system, such as AIDS patients or pregnant women, may become seriously ill, and it can occasionally be fatal. The parasite can cause encephalitis (inflammation of the brain) and neurologic diseases, and can affect the heart, liver, inner ears, and eyes (chorioretinitis). Recent research has also linked toxoplasmosis with brain cancer, Attention Deficit Hyperactivity Disorder, Obsessive Compulsive Disorder, and Schizophrenia.[6][7]
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Contents
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Infection has two stages:
During acute toxoplasmosis, symptoms are often influenza-like: swollen lymph nodes, or muscle aches and pains that last for a month or more. Rarely, a patient with a fully functioning immune system may develop eye damage from toxoplasmosis. Young children and immunocompromised patients, such as those with HIV/AIDS, those taking certain types of chemotherapy, or those who have recently received an organ transplant, may develop severe toxoplasmosis. This can cause damage to the brain (encephalitis) or the eyes (necrotizing retinochoroiditis). Infants infected via placental transmission may be born with either of these problems, or with nasal malformations, although these complications are rare in newborns.
Swollen lymph nodes are commonly found in the neck or under the chin, followed by the axillae (armpits) and the groin. Swelling may occur at different times after the initial infection, persist, and/or recur for various times independently of antiparasitic treatment.[8] It is usually found at single sites in adults, but in children multiple sites may be more common. Enlarged lymph nodes will resolve within one to two months in 60% of patients. However, a quarter of patients take 2–4 months to return to normal and 8% take 4–6 months. A substantial number of patients (6%) do not return to normal until much later.[9]
It is easy for a host to become infected with Toxoplasma gondii and develop toxoplasmosis without knowing it. In most immunocompetent patients, the infection enters a latent phase, during which only bradyzoites are present, forming cysts in nervous and muscle tissue. Most infants who are infected while in the womb have no symptoms at birth but may develop symptoms later in life.[10]
While rare, skin lesions may occur in the acquired form of the disease, including roseola and erythema multiforme-like eruptions, prurigo-like nodules, urticaria, and maculopapular lesions. Newborns may have punctate macules, ecchymoses, or “blueberry muffin” lesions. Diagnosis of cutaneous toxoplasmosis is based on the tachyzoite form of T. gondii being found in the epidermis. It is found in all levels of the epidermis, is about 6 μm by 2 μm , bow-shaped, the nucleus being one-third of its size. It can be identified by electron microscopy or by Giemsa staining tissue where the cytoplasm shows blue, the nucleus red.[11]
Studies have been conducted that show the toxoplasmosis parasite may affect behavior and may present as or be a causative or contributory factor in various psychiatric disorders such as depression, anxiety and schizophrenia.[12][13][14] In 11 of 19 scientific studies, T. gondii antibody levels were found to be significantly higher in individuals affected by first-incidence schizophrenia than in unaffected persons. Individuals with schizophrenia are also more likely to report a clinical history of toxoplasmosis than those in the general population.[15] Recent work at the University of Leeds has found that the parasite produces an enzyme with tyrosine hydroxylase and phenylalanine hydroxylase activity. This enzyme may contribute to the behavioral changes observed in toxoplasmosis by altering the production of dopamine, a neurotransmitter involved in mood, sociability, attention, motivation and sleep patterns. Schizophrenia has long been linked to dopamine dysregulation.[16]
Toxoplasmosis can be difficult to distinguish from that of primary central nervous system lymphoma, and as a result, the diagnosis is made by a trial of therapy (pyrimethamine, sulfadiazine + leucovorin), followed by a brain biopsy if the drugs produce no effect clinically and no improvement on repeat imaging.
Detection of Toxoplasma gondii in human blood samples may also be achieved by using the polymerase chain reaction (PCR).[17] Inactive cysts may exist in a host which would evade detection.
Toxoplasmosis cannot be detected with immunostaining. Lymph nodes affected by toxoplasma have characteristic changes, including poorly demarcated reactive germinal centers, clusters of monocytoid B cells and scattered epithelioid histiocytes.
Transmission may occur through:
Cats excrete the pathogen in their feces for a number of weeks after contracting the disease, generally by eating an infected rodent. Even then, cat faeces are not generally contagious for the first day or two after excretion, after which the cyst 'ripens' and becomes potentially pathogenic.[20]
Congenital toxoplasmosis is a special form in which an unborn child is infected via the placenta. A positive antibody titer indicates previous exposure and immunity and largely ensures the unborn baby's safety. A simple blood draw at the first pre-natal doctor visit can determine whether or not the woman has had previous exposure and therefore whether or not she is at risk. If a woman receives her first exposure to toxoplasmosis while pregnant, the baby is at particular risk. A woman with no previous exposure should avoid handling raw meat, exposure to cat feces, and gardening (cat feces are common in garden soil). Most cats are not actively shedding oocysts and so are not a danger, but the risk may be reduced further by having the litterbox emptied daily (oocysts require longer than a single day to become infective), and by having someone else empty the litterbox. However, while risks can be minimized, they cannot be eliminated. For pregnant women with negative antibody titer, indicating no previous exposure to T. gondii, as frequent as monthly serology testing is advisable as treatment during pregnancy for those women exposed to T. gondii for the first time decreases dramatically the risk of passing the parasite to the fetus.
Despite these risks, pregnant women are not routinely screened for toxoplasmosis in most countries (Portugal,[21] France,[22] Austria,[22] Uruguay,[23] and Italy[24] being the exceptions) for reasons of cost-effectiveness and the high number of false positives generated. As invasive prenatal testing incurs some risk to the fetus (18.5 pregnancy losses per toxoplasmosis case prevented),[22] postnatal or neonatal screening is preferred. The exceptions are cases where fetal abnormalities are noted, and thus screening can be targeted.[22]
Some regional screening programmes operate in Germany, Switzerland and Belgium.[24]
Treatment is very important for recently infected pregnant women, to prevent infection of the fetus. Since a baby's immune system does not develop fully for the first year of life, and the resilient cysts that form throughout the body are very difficult to eradicate with anti-protozoans, an infection can be very serious in the young.
Treatment is often only recommended for people with serious health problems or with HIV with CD4 count under 200, because the disease is most serious when one's immune system is weak. Trimethoprim/sulfamethoxazole is the drug of choice to prevent Toxoplasma, but is not the drug to treat.
Medications that are prescribed for acute toxoplasmosis are:
(Other antibiotics such as minocycline have seen some use as a salvage therapy).
In people with latent toxoplasmosis, the cysts are immune to these treatments, as the antibiotics do not reach the bradyzoites in sufficient concentration.
Medications that are prescribed for latent toxoplasmosis are:
The parasite itself can cause various effects on the host body, some of which are not fully understood.
It has been found that the parasite has the ability to change the behaviour of its host: infected rats and mice are less fearful of cats—in fact, some of the infected rats seek out cat-urine-marked areas. This effect is advantageous to the parasite, which is able to proliferate if a cat eats the infected rat and thereby becomes a carrier.[27] The mechanism for this change is not completely understood, but there is evidence that toxoplasmosis infection raises dopamine levels and concentrates in the amygdala in infected mice.[28]
The findings of behavioural alteration in rats and mice have led some scientists to speculate that Toxoplasma may have similar effects in humans. Toxoplasma is one of a number of parasites that may alter their host's behaviour as a part of their life cycle.[29] Some studies have linked latent toxoplasmosis to an increased incidence of traffic accidents.[30]
The evidence for behavioral effects on humans is controversial.[31] No prospective research has been done on the topic, e.g., testing people before and after infection to ensure that the proposed behavior arises only afterwards. Although some researchers have found potentially important associations with Toxoplasma, the causal relationship, if any, is unknown, i.e., it is possible that these associations merely reflect factors that predispose certain types of people to infection. However, many of the neurobehavioral symptoms that are postulated to be due to toxoplasmosis correlate to the general function of dopamine in the human brain, and the fact that toxoplasma encodes the dopamine synthesizing enzyme tyrosine hydroxylase makes it likely that neurobehavioral symptoms can result from infection.[32]
These types of studies are suggestive but cannot confirm a causal relationship (because of the possibility, for example, that schizophrenia increases the likelihood of Toxoplasma infection rather than the other way around).[33]
The U.S. NHANES (1999–2004) national probability sample found that 10.8% of U.S. persons 6–49 years of age, and 11.0% of women 15–44 years of age, had Toxoplasma-specific IgG antibodies, indicating that they were infected with the organism.[5] This prevalence has significantly decreased from the NHANES III (1988–1994).[34][35]
Two risk factors for contracting toxoplasmosis are:
A University of California, Davis study of dead sea otters collected from 1998 to 2004 found that toxoplasmosis was the cause of death for 13% of the animals.[36] Proximity to freshwater outflows into the ocean was a major risk factor. Ingestion of oocysts from cat faeces is considered to be the most likely ultimate source.[37] Runoff containing wild cat faeces and litter from domestic cats flushed down toilets are possible sources of oocysts.[38] According to an article in New Scientist[39] the parasites have been found in dolphins and whales. Researchers Black and Massie believe that anchovies, which travel from estuaries into the open ocean, may be helping to spread the disease.
The protozoan was first discovered by Nicolle & Manceaux, who in 1908 isolated it from the African rodent Ctenodactylus gundi, then in 1909 differentiated the disease from Leishmania and named it Toxoplasma gondii.[22] The first recorded congenital case was not until 1923, and the first adult case not until 1940.[22] In 1948, a serological dye test was created by Sabin & Feldman, which is now the standard basis for diagnostic tests.[40]
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 | American Heritage Dictionary. The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2007, 2000 by Houghton Mifflin Company. Updated in 2009. Published by Houghton Mifflin Company. All rights reserved. Read more |
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| Gale Encyclopedia of Children's Health. © 2006 by The Gale Group, Inc. All rights reserved. Read more |
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| Gale Encyclopedia of Public Health. Encyclopedia of Public Health. Copyright © 2002 by The Gale Group, Inc. All rights reserved. Read more |
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| Saunders Veterinary Dictionary. Saunders Comprehensive Veterinary Dictionary 3rd Edition. Copyright © 2007 by D.C. Blood, V.P. Studdert and C.C. Gay, Elsevier. All rights reserved. Read more |
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| Mosby's Dental Dictionary. Mosby's Dental Dictionary. Copyright © 2004 by Elsevier, Inc. All rights reserved. Read more |
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| Random House Word Menu. © 2010 Write Brothers Inc. Word Menu is a registered trademark of the Estate of Stephen Glazier. Write Brothers Inc. All rights reserved. Read more |
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| Wikipedia on Answers.com. This article is licensed under the Creative Commons Attribution/Share-Alike License. It uses material from the Wikipedia article Toxoplasmosis. Read more |
