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Selected content from the Animal Health and Production Compendium (© CAB International 2013). Distributed under license by African Union – Interafrican Bureau for Animal Resources.

Whilst this information is provided by experts, we advise that users seek veterinary advice where appropriate and check OIE manuals for recent changes to regulations, diagnostic tests, vaccines and treatments.

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Identity    Pathogen/s    Overview    Distribution    Distribution Map for Africa    Distribution Table for Africa    Hosts/Species Affected    Host Animals    Pathology     Diagnosis    Disease Course    Disease Treatment Table    Vaccines    Prevention and Control    References    Links to Websites    OIE Reference Experts and Laboratories    Images

 

 Identity

Preferred Scientific Name
toxoplasmosis
International Common Names
English
sporozoan encephalomyelitis in sheep and calves, systemic toxoplasmosis in sheep and goats, toxoplasma abortion in sheep and goats, Toxoplasma gondii infection, toxoplasmosis as a zoonosis, toxoplasmosis in birds, toxoplasmosis in cattle, toxoplasmosis in pigs, toxoplasmosis in wild animals

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 Pathogen/s

Toxoplasma gondii

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Overview

Infection with the protozoan parasite Toxoplasma gondii is one of the commonest parasitic infections of man and other warm-blooded animals (Dubey and Beattie, 1988). In most adults it does not cause serious illness, but it can cause blindness and mental retardation in congenitally infected children, blindness in persons infected after birth, and devastating disease in immunocompromized individuals. Consumption of raw or undercooked meat products and other food or drink contaminated with oocysts are major risk factors associated with T. gondii infection.

Toxoplasma gondii is a coccidian parasite with cats as the definitive host, and warm-blooded animals as intermediate hosts (Frenkel et al., 1970). It is one of the most important parasites of animals. There is only one species of Toxoplasma, T. gondii. Unlike many other microorganisms, and in spite of a wide host range and worldwide distribution, T. gondii has a low genetic diversity. Toxoplasma gondii strains have been classified into two to three genetic types (I, II, III), based on antigens, isoenzymes, and restriction fragment length polymorphism (RFLP) (Howe and Sibley, 1995; Guo and Johnson, 1996; Darde et al., 1988). Type I strains are highly virulent in outbred laboratory mice whereas Types II and III are less virulent in mice (Howe and Sibley, 1995; Howe et al., 1997; Mondragon et al., 1998; Owen and Trees, 1999) but there is no correlation between virulence in mice and clinical disease in other animals or humans.

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Distribution

Toxoplasma gondii has been found worldwide, on every continent except Antarctica. Nearly one third of the human population has been exposed to this parasite (Dubey and Beattie, 1988).

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Distribution Map for Africa

 Distribution Map for AfricaDistribution Map for Africa

present, no further details = Present, no further details    widespread = Widespread    localised = Localised
confined and subject to quarantine = Confined and subject to quarantine    occasional or few reports = Occasional or few reports
evidence of pathogen = Evidence of pathogen    last reported = Last reported...    presence unconfirmed = Presence unconfirmed

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 Distribution Table for Africa

The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further information for individual references may be available in the Animal Health and Production Compendium. A table for worldwide distribution can also be found in the Animal Health and Production Compendium.

CountryDistributionLast ReportedOriginFirst ReportedInvasiveReferencesNotes
AFRICA
AlgeriaNo information available    OIE Handistatus, 2005 
AngolaNo information available    OIE Handistatus, 2005 
BeninNo information available    OIE Handistatus, 2005 
BotswanaReported present or known to be present    OIE Handistatus, 2005 
Burkina FasoNo information available    OIE Handistatus, 2005 
BurundiNo information available    OIE Handistatus, 2005 
CameroonNo information available    OIE Handistatus, 2005 
Cape VerdeDisease not reported    OIE Handistatus, 2005 
Central African RepublicNo information available    OIE Handistatus, 2005 
ChadNo information available    OIE Handistatus, 2005 
Congo Democratic RepublicNo information available    OIE Handistatus, 2005 
Côte d'IvoireDisease not reported    OIE Handistatus, 2005 
DjiboutiReported present or known to be present    OIE Handistatus, 2005 
 No information available    OIE Handistatus, 2005 
EritreaDisease not reported    OIE Handistatus, 2005 
EthiopiaLast reported2002   OIE Handistatus, 2005 
GhanaNo information available    OIE Handistatus, 2005 
GuineaDisease never reported    OIE Handistatus, 2005 
Guinea-BissauNo information available    OIE Handistatus, 2005 
KenyaNo information available    OIE Handistatus, 2005 
LibyaNo information available    OIE Handistatus, 2005 
MadagascarDisease not reported    OIE Handistatus, 2005 
MalawiNo information available    OIE Handistatus, 2005 
MaliNo information available    OIE Handistatus, 2005 
MauritiusDisease not reported    OIE Handistatus, 2005 
MoroccoReported present or known to be present    OIE Handistatus, 2005 
MozambiqueNo information available    OIE Handistatus, 2005 
NamibiaLast reported2000   OIE Handistatus, 2005 
NigeriaNo information available    OIE Handistatus, 2005 
RéunionNo information available    OIE Handistatus, 2005 
RwandaNo information available    OIE Handistatus, 2005 
Sao Tome and PrincipeLast reported2003   OIE Handistatus, 2005 
SenegalNo information available    OIE Handistatus, 2005 
SeychellesNo information available    OIE Handistatus, 2005 
SomaliaNo information available    OIE Handistatus, 2005 
South AfricaNo information available    OIE Handistatus, 2005 
SudanDisease not reported    OIE Handistatus, 2005 
SwazilandNo information available    OIE Handistatus, 2005 
TanzaniaNo information available    OIE Handistatus, 2005 
TogoNo information available    OIE Handistatus, 2005 
TunisiaDisease not reported    OIE Handistatus, 2005 
UgandaDisease not reported    OIE Handistatus, 2005 
ZambiaNo information available    OIE Handistatus, 2005 
ZimbabweDisease not reported    OIE Handistatus, 2005 

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 Hosts/Species Affected

All warm blooded animals that have access to the outdoors or access to wildlife in areas where cats or their faeces are present are potentially susceptible to Toxoplasma infection. Toxoplasmosis may be acquired by ingestion of oocysts or by ingestion of stages of the parasite living in tissue. Contamination of the environment by oocysts is widespread because oocysts are shed by domestic cats and other felids (Dubey and Beattie, 1988; Frenkel et al., 1970). Domestic cats are probably the major source of contamination because oocyst formation is greatest in domestic cats, and cats are very common. Widespread natural infection of the environment is possible since a cat may excrete millions of oocysts after ingesting as few as a single bradyzoite or tissue cyst, and many tissue cysts may be present in one infected mouse (Frenkel et al., 1970; Dubey, 2001). Sporulated oocysts survive for a long time under most ordinary environmental conditions and even in harsh environments for months. They can survive in moist soil, for example, for months and even years (Dubey and Beattie, 1988; Dubey, 2004). Oocysts in soil can be mechanically transmitted by invertebrates such as flies, cockroaches, dung beetles, and earthworms, which can spread oocysts onto human food and animal feeds.

Infection rates in cats are determined by the rate of infection in local avian and rodent populations because cats are thought to become infected by eating these animals. The more oocysts in the environment, the more likely it is that prey animals would be infected, and this in turn would increase the infection rate in cats.

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Host Animals

Animal name Context 
Bos indicus (zebu) Domesticated host, Wild host 
Bos taurus (cattle) Domesticated host, Wild host 
Camelus dromedarius (dromedary camel)  
Capra hircus (goats)  
Felis  
Gallus gallus domesticus (chickens) Domesticated host, Wild host 
Homo sapiens  
Meleagris gallopavo (turkey) Domesticated host, Wild host 
Ovis aries (sheep) Domesticated host, Wild host 
Procyonidae  
Sus scrofa (pigs) Domesticated host, Wild host 
Ursus americanus  

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Systems Affected

Digestive - Large Ruminants
Digestive - Pigs
Digestive - Poultry
Digestive - Small Ruminants
Multisystem - Large Ruminants
Multisystem - Pigs
Multisystem - Poultry
Multisystem - Small Ruminants
Nervous - Large Ruminants
Nervous - Pigs
Nervous - Poultry
Nervous - Small Ruminants
Respiratory - Large Ruminants
Respiratory - Pigs
Respiratory - Poultry
Respiratory - Small Ruminants

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Epidemiology

Coccidia in general have complicated life cycles. Most coccidia are host-specific, and are transmitted via a faecal-oral route. Transmission of Toxoplasma gondii occurs via the faecal oral route, as well as through consumption of infected meat, and by placental transfer from mother to fetus (Dubey and Beattie, 1988; Frenkel et al., 1970).

The tachyzoite enters the host cell by active penetration of the host cell membrane and can tilt, extend, and retract as it searches for a host cell. After entering the host cell, the tachyzoite becomes ovoid in shape and becomes surrounded by a parasitophorous vacuole. The parasitophorous vacuole protects Toxoplasma gondii from host defense mechanisms. The tachyzoite multiplies asexually within the host cell by repeated divisions in which two progeny form within the parent parasite, which they then consume. Tachyzoites continue to divide until the host cell is filled with parasites. Cells rupture, and free tachyzoites infect neighbouring cells and the cycle is repeated. After an unknown number of cycles, T. gondii forms tissue cysts. Although tissue cysts containing bradyzoites may develop in visceral organs, including lungs, liver, and kidneys, they are more prevalent in muscular and neural tissues, including the brain, eye, skeletal, and cardiac muscle. Intact tissue cysts probably do not cause any harm and can persist for the life of the host.

All coccidian parasites have an environmentally resistant stage in their life cycle, called the oocyst. Oocysts of T. gondii are formed in cats, and probably in all members of the Felidae. Cats shed oocysts after ingesting any of the three infectious stages of T. gondii; tachyzoites, bradyzoites, or sporozoites (Dubey et al., 1998; Dubey and Frenkel, 1972; Dubey and Fenkel, 1976; Dubey, 1996). Prepatent periods (time to the shedding of oocysts after initial infection) and frequency of oocyst shedding vary according to the stage of T. gondii ingested. Prepatent periods are 3 to 10 days after ingesting tissue cysts and 18 days or more after ingesting tachyzoites or oocysts (Dubey and Frenkel, 1972; Dubey and Frenkel, 1976; Dubey, 2002). Less than 50% of cats shed oocysts after ingesting tachyzoites or oocysts, whereas nearly all cats shed oocysts after ingesting tissue cysts (Dubey and Frenkel, 1976).

After the ingestion of tissue cysts by cats, the tissue cyst wall is dissolved by proteolytic enzymes in the stomach and small intestine. The released bradyzoites penetrate the epithelial cells of the small intestine and initiate development of numerous generations of asexual and sexual cycles of T. gondii (Dubey and Frenkel, 1972). Toxoplasma gondii multiplies profusely in intestinal epithelial cells of cats (entero-epithelial cycle) and these stages are known as schizonts. Organisms (merozoites) released from schizonts form male and female gametes. The male gamete has two flagella and it swims to and enters the female gamete. After the female gamete is fertilized by the male gamete, the oocyst wall formation begins around the fertilized gamete. When oocysts are mature, they are discharged into the intestinal lumen by the rupture of intestinal epithelial cells.

As the entero-epithelial cycle progresses, bradyzoites penetrate the lamina propria of the feline intestine and multiply as tachyzoites. Within a few hours after infection of cats, T. gondii may disseminate to extra-intestinal tissues via the lymphatics and the bloodstream. Toxoplasma gondii persists in intestinal and extra-intestinal tissues of cats for at least several months, and possibly for the life of the cat.

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Impact: Economic

The socio-economic impact of toxoplasmosis in human morbidity and the cost of care of sick children, especially those with mental retardation and blindness, are enormous (Burnett et al., 1998; Luft and Remington, 1992). The testing of all pregnant women for T. gondii infection is compulsory in some European countries including France and Austria. The cost benefits of such mass screening are being debated in many other countries (Gilbert et al., 2001). A number of recent studies have raised questions about the effectiveness of treating acutely infected pregnant women to prevent transmission to the fetus and or prevent sequelae in infants (Jones et al., 2002; Montoya, 2002; Montoya et al., 2002). Newborn screening is another option for identifying infected infants and has been used in two states in the USA (Petersen and Schmidt, 2003), but infected newborns that are identified by screening require a year of follow-up and treatment with potentially toxic drugs and the efficacy of treating infants with congenital toxoplasmosis has not been documented in well controlled studies (Wilson et al., 2003).

Postnatally acquired infection may be localized or generalized. Oocyst-transmitted infections may be more severe than tissue cyst-induced infections (Leport et al., 1996; Morlat and Leport, 1997; Dubey and Beattie, 1988; Derouin et al., 1998). Enlarged lymph nodes are the most frequently observed clinical form of toxoplasmosis in humans. Lymphadenopathy may be associated with fever, fatigue, muscle pain, sore throat, and headache. Although the condition may be benign, diagnosis of T. gondii-associated lymphadenopathy is important in pregnant women because of the risk to the fetus. In a British Columbia (Canada) outbreak, of 100 people who were diagnosed with acute infection, 51 had lymphadenopathy and 20 had retinitis (Leport and Duval, 1999; Kapperud et al., 1996). Encephalitis is an important manifestation of toxoplasmosis in immunosuppressed patients because it causes the most severe damage to the patient (Dubey and Beattie, 1988; Gilbert and Stanford, 2000). Infection may occur in any organ. Patients may have headache, disorientation, drowsiness, hemiparesis, reflex changes, and convulsions, and many become comatose.

Toxoplasmosis is ranked high on the list of diseases which lead to death of patients with acquired immunodeficiency syndrome (AIDS) in the USA; approximately 10% of AIDS patients in the USA and up to 30% in Europe were estimated to die from toxoplasmosis (Gilbert and Stanford, 2000) before prophylactic medications such as trimethoprim-sulfamethoxazole and treatment of HIV infection with highly active antiretroviral therapy were widely available. However, since use of prophylactic therapy and highly active antiretroviral therapy (HAART) became common in the mid 1990's, the number of persons with AIDS dying of toxoplasmosis has greatly declined (Stanford et al., 2003). Although in AIDS patients any organ may be involved, including the testis, dermis, and the spinal cord, infection of the brain is most frequently reported. Most AIDS patients with toxoplasmosis have bilateral, severe, and persistent headache, which responds poorly to analgesics. As the disease progresses, the headache may give way to a condition characterized by confusion, lethargy, ataxia, and coma. The predominant lesion in the brain is necrosis, especially of the thalamus (Gilbert and Gras, 2003).

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Zoonoses and Food Safety

Increased risk for Toxoplasma gondii infection has been associated with many food-related factors, including eating raw or undercooked pork, mutton, lamb, beef, or mincemeat products (Roghmann et al., 1999; Kean et al., 1969; Masur et al., 1978), eating raw or unwashed vegetables, raw vegetables outside the home, or fruits (Roghmann et al., 1999), washing kitchen knives infrequently (Lord et al., 1975), and having poor hand hygiene (Roghmann et al., 1999). Decreased risk for T. gondii infection has been found to be associated with eating a meat-free diet (Fertig et al., 1997). Outbreaks of toxoplasmosis have been attributed to ingestion of raw or undercooked beef, lamb, pork, or venison (Choi et al., 1997; Sacks et al., 1983; Ross et al., 2001; Lopez et al., 2000; Dubey, 1986; Nogami et al., 1999), and consumption of raw goat's milk (Dubey et al., 1995a). In the USA, infection in humans is probably most often the result of ingestion of tissue cysts contained in undercooked meat (Dubey and Beattie, 1988; Weigel et al., 1995; Fertig et al., 1977), though the exact contribution to human infection of foodborne toxoplasmosis compared with oocyst-induced toxoplasmosis is unknown. T. gondii infection is common in many animals used for food, including sheep, pigs, goats, and rabbits. Birds and other domesticated and wild animals can also become infected (Dubey and Beattie, 1988). Animals that survive infection carry tissue cysts, and can therefore transmit T. gondii infection to human consumers. (Gamble et al., 1999; Dubey et al., 2002). In one study, viable T. gondii tissue cysts were isolated from 17% of 1000 adult pigs (sows) from an abattoir in Iowa, USA (Wyss et al., 2000). Serological surveys of pigs from Illinois (USA) pig farms indicate an infection rate of about 3% in market weight animals and 20% for breeding pigs, suggesting that age is a factor for pigs acquiring Toxoplasma infection (Tenter et al., 2000). Serological surveys of pigs on New England (USA) farms revealed an overall infection rate of 47% (Sroka, 2001), and from one farm, T. gondii was isolated from 51 of 55 market-age (feeder) pigs (Chan et al., 2001). In the USA, infection in cattle is less prevalent than it is in sheep or pigs, however, recent surveys in several European countries using serology and PCR to detect parasite DNA have shown that infection rates in pigs and horses are negligible, while prevalence in sheep and cattle ranges from 1 to 6% (Kotula et al., 1991; Lindsay et al., 1991). Serological surveys in eastern Poland revealed that 53% of cattle, 15% of pigs, and 0-6% of chickens, ducks, and turkeys were positive for T. gondii infection, and nearly 50% of the people in the region were also serologically positive for T. gondii infection (Humphreys et al., 1995). The prevalence of T. gondii infection in commercially produced chickens in the USA and elsewhere has not been investigated; however, most chicken meat in the USA is cooled to near freezing or is completely frozen at the packing plant (Vanek et al., 1996), which would kill organisms in tissue cysts (see Dubey , 1988; Dubey, 1998). The relative contributions of undercooked pork, beef and chicken to T. gondii infection in humans is unknown. A nationwide retail meat survey is being conducted to determine the risk to USA consumers of purchasing pork, beef, and chicken containing viable T. gondii tissue cysts at the retail level (Dubey et al., unpublished). From published information, it appears that there is relatively little risk of acquiring T. gondii after ingestion of beef and chicken.

Toxoplasma gondii infection is also prevalent in game animals. Among wild game, T. gondii infection is most prevalent in black bears and in white-tailed deer. Serological surveys of white-tailed deer in the USA have found seropositivity in 30 to 60% (Dubey et al., 1995b; Dubey et al., 1995c; Dubey and Odening, 2001), and viable T. gondii is demonstratable in 50% of seropositive deer (Jones et al., 2001). A recent study reported the occurrence of clinical toxoplasmosis and necrotizing retinitis in deer hunters with a history of consuming undercooked or raw venison (Nogami et al., 1999). Approximately 80% of black bears are infected in the USA (Renold et al., 1992), and about 60% of raccoons have antibodies to T. gondii (Desmonts and Couvreur, 1974). Because raccoons and bears scavenge for their food, infection in these animals is a good indicator of the prevalence of T. gondii in the environment.

Virtually all edible parts of animals can carry viable T. gondii tissue cysts, and tissue cysts can survive in food animals for many years.

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Pathology

Pathogenicity of Toxoplasma gondii infection is determined by the virulence of the strain and the susceptibility of the host species. T. gondii strains may vary in their pathogenicity in a given host. Certain strains of mice are more susceptible than others and the severity of infection in individual mice within the same strain may vary. Certain species are genetically resistant to clinical toxoplasmosis. For example, adult rats do not become have clinical signs, while young rats can die of toxoplasmosis. Mice of any age are susceptible to clinical T. gondii infection. Adult dogs, like adult rats, are resistant, whereas puppies are fully susceptible to clinical toxoplasmosis. Cattle and horses are among the hosts that are more resistant to clinical toxoplasmosis, whereas certain marsupials and New World monkeys are highly susceptible to T. gondii infection (Dubey and Beattie, 1988). Little is known of the relationship between genetics and susceptibility in other mammals, including humans.

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Diagnosis

Diagnosis is made by biological, serological, histological, or combined methods. Clinical signs of toxoplasmosis are nonspecific and are not sufficiently characteristic for a definite diagnosis. Detection of T. gondii antibody in patients may help diagnosis. There are numerous serological procedures available for detection of humoral antibodies; these include the Sabin-Feldman dye test, the indirect haemagglutination assay, the indirect fluorescent antibody assay (IFA), the direct agglutination test, the latex agglutination test, the enzyme-linked immunoabsorbent assay (ELISA), and the immunoabsorbent agglutination assay test (IAAT). The IFA, IAAT and ELISA tests have been modified to detect IgM antibodies (Gilbert et al., 2001). IgM antibodies appear sooner after infection than IgG antibodies and IgM antibodies disappear faster than IgG antibodies after recovery (Gilbert et al., 2001). Detection of IgM and IgG antibodies, along with a panel of other serological tests, including the avidity test, have been found to be very helpful in diagnosing acute infection in pregnant women when conducted at a reference laboratory (Chirgwin et al., 2002; Kaplan et al., 2002).

Clinical signs

Toxoplasma gondii infection is widespread in humans though, geographically, its prevalence varies widely. In the USA and the UK, it is estimated that 16 to 40% of people are infected (Holland, 2003), whereas in Central and South America and continental Europe, estimates of prevalence rates range from 50 to 80% (Dubey and Beattie, 1988; Bahia-Oliveira et al., 2003). Most infections in humans are asymptomatic but at times the parasite can produce devastating disease. Infection may be congenitally or postnatally acquired. Congenital infection occurs only when a woman becomes infected during pregnancy. Congenital infections acquired during the first trimester are more severe than those acquired in the second and third trimester (Wallon et al., 1999; Gilbert et al., 2001). While the mother rarely has symptoms of infection, she does have a temporary parasitaemia. Focal lesions develop in the placenta and the fetus may become infected. At first there is generalized infection in the fetus. Later, infection is cleared from the visceral tissues and may localize in the central nervous system. Although most children are asymptomatic at birth (Petersen and Schmidt, 2003), a wide spectrum of clinical diseases can occur in congenitally infected children (Wallon et al., 1999; Teutsch et al., 1979) or develop later in life (Benenson et al., 1982). Mild disease may consist of slightly diminished vision, whereas severely diseased children may have many signs; retinochoroiditis (inflammation of the inner layers of the eye), hydrocephalus (big head), convulsions and intracerebral calcification. Of these, hydrocephalus is the least common but most dramatic result of toxoplasmosis. By far the most common sequela of congenital toxoplasmosis is ocular disease (Wallon et al., 1999; Gilbert et al., 2001). In addition to ocular infection that occurs with congenital disease, up to 2% of adults newly infected with T. gondii develop ocular lesions. Some authorities now believe that the majority of ocular disease is a result of infection with T. gondii after birth (Smith, 1993).

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Disease Course

Toxoplasma gondii can multiply in virtually any cell in the body. How T. gondii is destroyed in immune cells is not completely known (Gilbert and Gras, 2003). All extracellular forms of the parasite are directly affected by antibody but intracellular forms are not. It is believed that cellular factors, including lymphocytes and lymphokines, are more important than humoral factors in immune mediated destruction of T. gondii (Gilbert and Gras, 2003).

Immunity does not eradicate infection. Toxoplasma gondii tissue cysts persist several years after acute infection. The fate of tissue cysts is not fully known. Whether bradyzoites can form new tissue cysts directly without transforming into tachyzoites is not known. It has been proposed that tissue cysts may at times rupture during the life of the host. The released bradyzoites may be destroyed by the host's immune responses, or there may be formation of new tissue cysts.

In immunosuppressed patients, such as those given large doses of immunosuppressive agents in preparation for organ transplants and in those with AIDS, rupture of a tissue cyst may result in transformation of bradyzoites into tachyzoites and renewed multiplication. The immunosuppressed host may die from toxoplasmosis unless treated. It is not known how corticosteroids cause relapse, but it is unlikely that they directly cause rupture of the tissue cysts.

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Disease Treatment

In general, physicians are most likely to consider treatment for T. gondii infection in four circumstances; pregnant women with acute infection to prevent fetal infection, congenitally infected infants, immunosuppressed persons, usually with reactivated disease, and acute and recurrent ocular disease (Dubey et al., 1990). Although well designed clinical trials have demonstrated the effectiveness of treatment in immunosuppressed persons for reactivated disease (Dubey and Thayer, 1994; Foulon et al., 2000; Contreras et al., 1996), there is less evidence for the effectiveness of treatment in the other circumstances listed above (Jones et al., 2002; Montoya, 2002; Montoya et al., 2002; Wilson et al., 2003; Ibrahim et al., 1997; Rai et al., 1996).

Sulfadiazine and pyrimethamine (Daraprim) are 2 drugs widely used for treatment of toxoplasmosis (Petersen and Schmidt, 2003; Guebre-Xabier et al., 1993). While these drugs have a beneficial action when given in the acute stage of the disease process when there is active multiplication of the parasite, they will not usually eradicate infection. It is believed that these drugs have little effect on subclinical infections, but the growth of tissue cysts in mice has been restrained with sulfonamides. Certain other drugs, such as diaminodiphenylsulfone, atovaquone, azithromycin, clarithromycin, dapson, spiramycin, and clindamycin are also used to treat toxoplasmosis in difficult cases, often in combination with pyrimethamine. Medications are also prescribed for preventive or suppressive treatment in HIV-infected persons and have been quite effective when used for this purpose (Yamaoka and Konishi, 1993). Treatment of infected animals is rarely warranted.

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Prevention and Control

To prevent infection of humans by Toxoplasma gondii, people handling meat should wash their hands thoroughly with soap and water before they go to other tasks (Dubey and Beattie, 1988; Weigel et al., 1995). All cutting boards, sink tops, knives, and other materials coming in contact with uncooked meat should also be washed with soap and water. Washing is effective because of physical removal of material from the hands and because the stages of T. gondii in meat are killed by contact with soap and water (Dubey and Beattie, 1988).

T. gondii organisms in meat can be killed by exposure to extreme cold or heat. Tissue cysts in meat are killed by heating the meat throughout to 67°C (Lebech et al., 1993). T. gondii oocyst survival was studied by Dubey (1998). Toxoplasma in tissue cysts are also killed by exposure to 0.5 kilorads of gamma irradiation (Moschen et al., 1991). Meat should be cooked to 63°C (beef), 71°C (pork, ground meat, and wild game) or 82°C (poultry), before consumption. Tasting meat while cooking or seasoning should be avoided. Pregnant women should avoid contact with cats, soil, and raw meat. Pet cats should be fed only dry, canned, or cooked food. The cat litter box should be emptied every day, and should not be emptied by a pregnant woman or an immunesuppressed person. Pregnant women and immunesuppressed people should wear gloves while gardening or changing cat litter (if no one else can change the litter) and wash their hands thoroughly afterwards. Fruits and vegetables should be washed thoroughly before eating because they may have been contaminated with cat faeces or soil containing oocysts from cat faeces. Untreated water should not be consumed, particularly in developing countries. Women of childbearing age and expectant mothers should be aware of the dangers of toxoplasmosis (Jeannel et al., 1988; Plant et al., 1982; Weigel et al, 1995). At present there is no vaccine to prevent toxoplasmosis in humans.

Infection in food animals requires strict management in confinement and elimination of exposure to cats and their excrement, rodents, and other forms of wildlife. Prevention of footwear that has been worn outside from entering animal confinement barns is another important measure.

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 Diagrammatic representation of the Toxoplasma gondii life cycle. © USDADiagrammatic representation of the Toxoplasma gondii life cycle. © USDA

 (a) Congenital toxoplasmosis in children. Hydrocephalus with bulging forehead. (b) Microophthalmia of the left eye. © USDA(a) Congenital toxoplasmosis in children. Hydrocephalus with bulging forehead. (b) Microophthalmia of the left eye. © USDA

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Date of report: 03/06/2013

© CAB International 2013. Distributed under license by African Union – Interafrican Bureau for Animal Resources.

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