Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide







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Diagrammatic representation of the Toxoplasma gondii life cycle.
TitleLife cycle of Toxoplasma gondii
CaptionDiagrammatic representation of the Toxoplasma gondii life cycle.
Diagrammatic representation of the Toxoplasma gondii life cycle.
Life cycle of Toxoplasma gondiiDiagrammatic representation of the Toxoplasma gondii life cycle.USDA
(a) Congenital toxoplasmosis in children. Hydrocephalus with bulging forehead.  (b) Microophthalmia of the left eye.
TitleSymptoms in human
Caption(a) Congenital toxoplasmosis in children. Hydrocephalus with bulging forehead. (b) Microophthalmia of the left eye.
(a) Congenital toxoplasmosis in children. Hydrocephalus with bulging forehead.  (b) Microophthalmia of the left eye.
Symptoms in human(a) Congenital toxoplasmosis in children. Hydrocephalus with bulging forehead. (b) Microophthalmia of the left eye.USDA


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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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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.

Host Animals

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Animal nameContextLife stageSystem
Bos indicus (zebu)Domesticated host; Wild hostCattle and Buffaloes|All Stages
Bos taurus (cattle)Domesticated host; Wild hostCattle and Buffaloes|All Stages
Camelus dromedarius (dromedary camel)
Capra hircus (goats)Sheep and Goats|All Stages
Gallus gallus domesticus (chickens)Domesticated host; Wild hostPoultry|Cockerel; Poultry|Day-old chick; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry
Homo sapiens
Meleagris gallopavo (turkey)Domesticated host; Wild hostPoultry|Cockerel; Poultry|Day-old chick; Poultry|Mature female; Poultry|Mature male; Poultry|Young poultry
Ovis aries (sheep)Domesticated host; Wild hostSheep and Goats|All Stages
Sus scrofa (pigs)Domesticated host; Wild hostPigs|All Stages
Ursus americanus

Hosts/Species Affected

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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.

Systems Affected

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digestive diseases of large ruminants
digestive diseases of pigs
digestive diseases of poultry
digestive diseases of small ruminants
multisystemic diseases of large ruminants
multisystemic diseases of pigs
multisystemic diseases of poultry
multisystemic diseases of small ruminants
nervous system diseases of large ruminants
nervous system diseases of pigs
nervous system diseases of poultry
nervous system diseases of small ruminants
respiratory diseases of large ruminants
respiratory diseases of pigs
respiratory diseases of poultry
respiratory diseases of small ruminants


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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).

Distribution Table

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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 details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Last updated: 10 Jan 2020
Continent/Country/Region Distribution Last Reported Origin First Reported Invasive Reference Notes


Cabo VerdeAbsent, No presence record(s)
Côte d'IvoireAbsent, No presence record(s)
EritreaAbsent, No presence record(s)
GuineaAbsent, No presence record(s)
MadagascarAbsent, No presence record(s)
MauritiusAbsent, No presence record(s)
SudanAbsent, No presence record(s)
TunisiaAbsent, No presence record(s)
UgandaAbsent, No presence record(s)
ZimbabweAbsent, No presence record(s)


GeorgiaAbsent, No presence record(s)
IranAbsent, No presence record(s)
KazakhstanAbsent, No presence record(s)
KuwaitAbsent, No presence record(s)
-Peninsular MalaysiaAbsent, No presence record(s)
-SabahAbsent, No presence record(s)
North KoreaAbsent, No presence record(s)
OmanAbsent, No presence record(s)
PhilippinesAbsent, No presence record(s)
Saudi ArabiaPresent
South KoreaAbsent, No presence record(s)
Sri LankaAbsent, No presence record(s)
TaiwanAbsent, No presence record(s)
ThailandAbsent, No presence record(s)
TurkmenistanAbsent, No presence record(s)
United Arab EmiratesAbsent, No presence record(s)
UzbekistanAbsent, No presence record(s)


BelarusAbsent, No presence record(s)
CyprusPresentCAB Abstracts Data Mining
GermanyAbsent, No presence record(s)
Isle of ManPresent
JerseyAbsent, No presence record(s)
LatviaAbsent, No presence record(s)
LiechtensteinAbsent, No presence record(s)
LithuaniaAbsent, No presence record(s)
LuxembourgAbsent, No presence record(s)
MaltaAbsent, No presence record(s)
MoldovaAbsent, No presence record(s)
RomaniaAbsent, No presence record(s)
Serbia and MontenegroAbsent, No presence record(s)
UkraineAbsent, No presence record(s)
United KingdomPresent
-Northern IrelandPresent

North America

BarbadosAbsent, No presence record(s)
BermudaAbsent, No presence record(s)
British Virgin IslandsAbsent, No presence record(s)
Cayman IslandsAbsent, No presence record(s)
CubaAbsent, No presence record(s)
CuraçaoAbsent, No presence record(s)
DominicaAbsent, No presence record(s)
Dominican RepublicPresent
HaitiAbsent, No presence record(s)
JamaicaAbsent, No presence record(s)
Saint Kitts and NevisAbsent, No presence record(s)
Trinidad and TobagoAbsent, No presence record(s)
United StatesPresent, Serological evidence and/or isolation of the agent


French PolynesiaAbsent, No presence record(s)
New CaledoniaPresent
New ZealandPresent
VanuatuAbsent, No presence record(s)

South America

Falkland IslandsPresent
GuyanaAbsent, No presence record(s)
ParaguayPresent, Serological evidence and/or isolation of the agent


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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 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).

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Abnormal colour of stool in birds, white, green, yellow faeces Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
Digestive Signs / Diarrhoea Sign
General Signs / Abnormal proprioceptive positioning, knuckling Sign
General Signs / Ataxia, incoordination, staggering, falling Sign
General Signs / Ataxia, incoordination, staggering, falling Sign
General Signs / Ataxia, incoordination, staggering, falling Sign
General Signs / Cyanosis, blue skin or membranes Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Fever, pyrexia, hyperthermia Sign
General Signs / Generalized weakness, paresis, paralysis Sign
General Signs / Hemiparesis Sign
General Signs / Inability to stand, downer, prostration Sign
General Signs / Inability to stand, downer, prostration Sign
General Signs / Increased mortality in flocks of birds Sign
General Signs / Opisthotonus Sign
General Signs / Pale comb and or wattles in birds Sign
General Signs / Pale mucous membranes or skin, anemia Sign
General Signs / Paraparesis, weakness, paralysis both hind limbs Sign
General Signs / Regression of the comb, wattles in birds Sign
General Signs / Tetraparesis, weakness, paralysis all four limbs Sign
General Signs / Torticollis, twisted neck Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign
General Signs / Weight loss Sign
Nervous Signs / Circling Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sign
Nervous Signs / Tremor Sign
Nervous Signs / Tremor Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Cataract, lens opacity Sign
Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling Sign
Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature Sign
Ophthalmology Signs / Conjunctival, scleral, redness Sign
Ophthalmology Signs / Microphthalmia, small globe, cornea, phthisis bulbi Sign
Ophthalmology Signs / Nystagmus Sign
Ophthalmology Signs / Purulent discharge from eye Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Sign
Reproductive Signs / Female infertility, repeat breeder Sign
Reproductive Signs / Mummy, mummified fetus Sign
Reproductive Signs / Mummy, mummified fetus Sign
Reproductive Signs / Small litter size Sign
Respiratory Signs / Coughing, coughs Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign

Disease Course

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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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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.

Impact: Economic

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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).

Zoonoses and Food Safety

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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.

Disease Treatment

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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.

Prevention and Control

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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 animalsrequires 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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Abdo Cuza A; Suarez Savio O; Garcia Navarro ME; Castellanos Gutierrez R; Gomez Peyre F; Parellada Blazco J; Alvarez Plasencia A; Rafael Truy B; Castellanos Becerril F; Verdecia Gorrita N; Howland Alvarez I; Cruz Gomez Y, 2001. Epidemiological characteristics of a group of multi organ donors used to transplant organs in Cuba. Rev. Neurol., 33(12):1117-1119.

African Union-Interafrican Bureau for Animal Resources, 2011. Panafrican Animal Health Yearbook 2011. Pan African Animal Health Yearbook, 2011:xiii + 90 pp.

Ali CN; Harris JA; Watkins JD; Adesiyun AA, 2003. Seroepidemiology of Toxoplasma gondii in dogs in Trinidad and Tobago. Vet. Parasitol., 113(3-4):179-187.

Al-Qurashi AR; Ghandour AM; Obeid OE; Al-Mulhim A; Makki SM, 2001. Seroepidemiological study of Toxoplasma gondii infection in the human population in the Eastern Region. Saudi Med. J., 22(1):13-18.

Altintas N; Kuman HA; Akisu C; Aksoy U; Atambay M, 1997. Toxoplasmosis in last four years in Aegean region, Turkey. Journal of the Egyptian Society of Parasitology, 27(2):439-443; 9 ref.

Arias ML; Chinchilla M; Reyes L; Linder E, 1996. Seroepidemiology of toxoplasmosis in humans: possible transmission routes in Costa Rica. Revista de Biología Tropical, 44(2/A):377-381; 29 ref.

Arko-Mensah J; Bosompem KM; Canacoo EA; Wastling JM; Akanmori BD, 2000. The seroprevalence of toxoplasmosis in pigs in Ghana. Acta Tropica, 76(1):27-31; 13 ref.

Ashrafunnessa Khatun S; Islam MN; Huq T, 1998. Seroprevalence of Toxoplasma antibodies among the antenatal population in Bangladesh. J. Obstet. Gynaecol. Res., 2:115-119.

Bahia-Oliveira LM; Jones JL; Azevedo-Silva J; Alves CC; Orefice F; Addiss DG, 2003. Highly endemic, waterborne toxoplasmosis in north Rio de Janeiro state, Brazil. Emerg. Infect. Dis., 9:55-62.

Baril L; Ancelle T; Goulet V; Thulliez P; Tirard-Fleury V; Carme B, 1999. Risk factors for Toxoplasma infection in pregnancy: a case-control study in France. Scandinavian Journal of Infectious Diseases, 31(3):305-309; 23 ref.

Belbacha I; Hafid J; Tran Manh Sung R; Flori P; Raberin H; Aboufatima R; Regragui A; Dalal A; Chait A, 2004. Toxoplasma gondii: level of carriage in sheep of Marrakech region (Mnabha). Schweiz. Arch. Tierheilkd., 146(12):561-564.

Benenson MW; Takafuji ET; Lemon SM; Greenup RL; Sulzer AJ, 1982. Oocyst-transmitted toxoplasmosis associated with ingestion of contaminated water. N. Engl. J. Med., 307:666-669.

Bobic B; Jevremovic I; Marinkovic J; Sibalic D; Djurkovic-Djakovic O, 1998. Risk factors for Toxoplasma infection in a reproductive age female population in the area of Belgrade, Yugoslavia. European Journal of Epidemiology, 14(6):605-610; 29 ref.

Bobic B; Nikolic A; Djurkovic-Djakovic O, 2003. Identification of risk factors for infection with Toxoplasma gondii in Serbia as a basis of a program for prevention of congenital toxoplasmosis. Srp Arh Celok Lek., 131(3-4):162-167.

Bourée P; Dumazedier D; Magdeleine C; Sobesky G, 1997. Toxoplasma encephalitis and AIDS in Martinique. Médecine Tropicale, 57(3):259-261; 17 ref.

Bowie WR; King AS; Werker DH; Isaac-Renton JL; Bell A; Eng SB; Marion SA, 1997. Outbreak of toxoplasmosis associated with municipal drinking water. Lancet (British edition), 350(9072):173-177; 22 ref.

Burnett AJ; Shortt SG; Isaac-Renton J; King A; Werker D; Bowie WR, 1998. Multiple cases of acquired toxoplasmosis retinitis presenting in an outbreak. Ophthalmology, 105(6):1032-1037; 22 ref.

Carme B; Bissuel F; Ajzenberg D; Bouyne R; Aznar C; Demar M; Bichat S; Louvel D; Bourbigot AM; Peneau C; Neron P; Darde ML, 2002. Severe acquired toxoplasmosis in immunocompetent adult patients in French Guiana. J. Clin. Microbiol., 40(11):4037-4044.

Chan KF; Le Tran H; Kanenaka RY; Kathariou S, 2001. Survival of clinical and poultry-derived isolates of Campylobacter jejuni at a low temperature (4 degrees C). Appl. Environ. Microbiol., 67:4186-4191.

Chen Y; Qian X; Tang Z; Banta HD; Hu F; Cao J; Huang J; Wang Q; Lv J; Ying X; Chen J, 2004. Situation analysis of prenatal diagnosis technology utilization in China: current situation, main issues, policy implications. Int. J. Technol. Assess. Health Care, 20(4):524-530.

Chirgwin K; Hafner R; Leport C; Remington J; Andersen J; Bosler EM; Roque C; Rajicic N; McAuliffe V; Morlat P; Jayaweera DT; Vilde JL; Luft BJ, 2002. Randomized phase II trial of atovaquone with pyrimethamine or sulfadiazine for treatment of toxoplasmic encephalitis in patients with acquired immunodeficiency syndrome: ACTG 237/ANRS 039 Study. Clin. Infect. Dis., 34:1243-1250.

Choi WY; Nam HW; Kwak NH; Huh W; Kim YR; Kang MW; Cho SY; Dubey JP, 1997. Foodborne outbreaks of human toxoplasmosis. J. Infect. Dis., 175:1280-1282.

Contreras M; Schenone H; Salinas P; Sandoval L; Rojas A; Villarroel F; Solis F, 1996. Seroepidemiology of human toxoplasmosis in Chile. Rev. Inst. Med. Trop. Sao Paulo, 38(6):431-435.

Cook AJC; Gilbert RE; Buffolano W; Zufferey J; Petersen E; Jenum PA; Foulon W; Semprini AE; Dunn DT, 2000. Sources of Toxoplasma infection in pregnant women:European multicentre case control study. Br. Med. J., 321:142-147.

Crucerescu E, 1998. Epidemiological data on toxoplasmosis. The aspects of congenital toxoplasmosis. Bacteriol. Virusol. Parazitol. Epidemiol., 43(3):147-155.

Darde ML; Bouteille B; Pestre-Alexandre M, 1988. Isoenzymic characterization of seven strains of Toxoplasma gondii by isoelectrofocusing in polyacrylamide gels. American Journal of Tropical Medicine and Hygiene, 39(6):551-558; 28 ref.

de Amorim Garcia CA; Orefice F; de Oliveira Lyra C; Gomes AB; Franca M; de Amorim Garcia Filho CA, 2004. Socioeconomic conditions as determining factors in the prevalence of systemic and ocular toxoplasmosis in Northeastern Brazil. Ophthalmic Epidemiol., 11(4):301-317.

Derouin F; Gérard L; Farinotti R; Maslo C; Leport C, 1998. Determination of the inhibitory effect on Toxoplasma growth in the serum of AIDS patients during acute therapy for toxoplasmic encephalitis. Journal of Acquired Immune Deficiency Syndromes and Human Retrovirology, 19(1):50-54; 14 ref.

Desmonts G; Couvreur J, 1974. Congenital toxoplasmosis. A prospective study of 378 pregnancies. N. Engl. J. Med., 290:1110-1116.

Devada K; Anandan R; Dubey JP, 1998. Serologic prevalence of Toxoplasma gondii in chickens in Madras, India. Journal of Parasitology, 84(3):621-622; 6 ref.

Diallo S; Ndir O; Dieng Y; Leye A; Dieng T; Bah IB; Diop BM; Gaye O; Faye O, 1996. Seroprevalence of toxoplasmosis in Dakar (Senegal) in 1993: a study carried out in women of child-bearing age. Cahiers d'Etudes et de Recherches Francophones/Sante, 6(2):102-106; 15 ref.

Diaz-Suarez O; Estevez J; Garcia M; Cheng-Ng R; Araujo J; Garcia M, 2003. Seroepidemiology of toxoplasmosis in a Yucpa Amerindian community of Sierra de Perija, Zulia State, Venezuela. Rev. Med. Chil., 131(9):1003-1010.

Dubey JP, 1986. A review of toxoplasmosis in pigs. Veterinary Parasitology, 19(3/4):181-223; 25 ref.

Dubey JP, 1988. Long-term persistence of Toxoplasma gondii in tissues of pigs inoculated with T. gondii oocysts and effect of freezing on viability of tissue cysts in pork. American Journal of Veterinary Research, 49(6):910-913; 13 ref.

Dubey JP, 1996. Infectivity and pathogenicity of Toxoplasma gondii oocysts for cats. Journal of Parasitology, 82(6):957-961; 30 ref.

Dubey JP, 1997. Toxoplasmosis. In: Microbiology & Microbial Infections, Vol. V: Parasitology. London, UK: Arnold, 1997.

Dubey JP, 1998. Toxoplasma gondii oocyst survival under defined temperatures. Journal of Parasitology, 84(4):862-865; 17 ref.

Dubey JP, 2001. Oocyst shedding by cats fed isolated bradyzoites and comparison of infectivity of bradyzoites of the VEG strain Toxoplasma gondii to cats and mice. J. Parasitol., 87:215-219.

Dubey JP, 2002. Tachyzoite-induced life cycle of Toxoplasma gondii in cats. J. Parasitol., 88:713-717.

Dubey JP, 2004. Toxoplasmosis - a waterborne zoonosis. Vet. Parasitol., 126(1-2):57-72.

Dubey JP; Beattie CP, 1988. Toxoplasmosis of animals and man. Boca Raton, Florida, USA: CRC Press.

Dubey JP; Frenkel JK, 1972. Cyst-induced toxoplasmosis in cats. J. Protozool., 19:155-177.

Dubey JP; Frenkel JK, 1976. Feline toxoplasmosis from acutely infected mice and the development of Toxoplasma cysts. J. Protozool., 23:537-546.

Dubey JP; Gamble HR; Hill D; Sreekumar C; Romand S; Thuilliez P, 2002. High prevalence of viable Toxoplasma gondii infection in market weight pigs from a farm in Massachusetts. J. Parasitol., 88:1234-1238.

Dubey JP; Garner MW; Willette MM; Batey KL; Gardiner CH, 2001. Disseminated toxoplasmosis in magpie geese (Anseranas semipalmata) with large numbers of tissue cysts in livers. Journal of Parasitology, 87(1):219-223.

Dubey JP; Graham DH; de Young RW; Dahl E; Eberhard ML; Nace EK; Won K; Bishop H; Punkosdy G; Sreekumar C; Vianna MC; Shen SK; Kwok OC; Sumners JA; Demarais S; Humphreys JG; Lehmann T, 2004. Molecular and biologic characteristics of Toxoplasma gondii isolates from wildlife in the United States. J. Parasitol., 90:67-71.

Dubey JP; Humphreys JG; Thulliez P, 1995. Prevalence of viable Toxoplasma gondii tissue cysts and antibodies to T. gondii by various serologic tests in black bears (Ursus americanus) from Pennsylvania. Journal of Parasitology, 81(1):109-112; 9 ref.

Dubey JP; Kotula AW; Sharar A; Andrews CD; Lindsay DS, 1990. Effect of high temperature on infectivity of Toxoplasma gondii tissue cysts in pork. Journal of Parasitology, 76(2):201-204; 13 ref.

Dubey JP; Levy MZ; Sreekumar C; Kwok OC; Shen SK; Dahl E; Thulliez P; Lehmann T, 2004. Tissue distribution and molecular characterization of chicken isolates of Toxoplasma gondii from Peru. J. Parasitol., 90(5):1015-1018.

Dubey JP; Lindsay DS; Speer CA, 1998. Structures of Toxoplasma gondii tachyzoites, bradyzoites, and sporozoites and biology and development of tissue cysts. Clinical Microbiology Reviews, 11(2):267-299; 183 ref.

Dubey JP; Morales ES; Lehmann T, 2004. Isolation and genotyping of Toxoplasma gondii from free-ranging chickens from Mexico. J. Parasitol., 90(2):411-413.

Dubey JP; Odening K, 2001. Parasitic Diseases of Wild Mammals. Ames, USA: Iowa State University Press.

Dubey JP; Parnell PG; Sreekumar C; Vianna MC; de Young RW; Dahl E; Lehmann T, 2004. Biologic and molecular characteristics of Toxoplasma gondii isolates from striped skunk Mephitis mephitis, Canada goose Branta canadensis, black-winged lory Eos cyanogenia, cats Felis catus. J. Parasitol., 90(5):1171-1174.

Dubey JP; Thayer DW, 1994. Killing of different strains of Toxoplasma gondii tissue cysts by irradiation under defined conditions. Journal of Parasitology, 80(5):764-767; 20 ref.

Dubey JP; Thulliez P; Powell EC, 1995. Toxoplasma gondii in Iowa sows: comparison of antibody titers to isolation of T. gondii by bioassays in mice and cats. Journal of Parasitology, 81(1):48-53; 19 ref.

Dubey JP; Weigel RM; Siegel AM; Thulliez P; Kitron UD; Mitchell MA; Mannelli A; Mateus-Pinilla NE; Shen SK; Kwok OCH; Todd KS, 1995. Sources and reservoirs of Toxoplasma gondii infection on 47 swine farms in Illinois. Journal of Parasitology, 81(5):723-729; 29 ref.

Duncanson P; Terry RS; Smith JE; Hide G, 2001. High levels of congenital transmission of Toxoplasma gondii in a commercial sheep flock. International Journal for Parasitology, 31(14):1699-1703.

El-Metenawy TM, 2000. Seroprevalence of Toxoplasma gondii antibodies among domesticated ruminants at Al-Qassim region, Saudi Arabia. Deutsche Tierärztliche Wochenschrift, 107(1):32-33; 11 ref.

El-Moukdad AR, 2002. Serological studies on prevalence of Toxoplasma gondii in Awassi sheeps in Syria. Berliner und Münchener Tierärztliche Wochenschrift, 115(5/6):186-188; 8 ref.

Elnahas A; Gerais AS; Elbashir MI; Eldien ES; Adam I, 2003. Toxoplasmosis in pregnant Sudanese women. Saudi Med. J., 24(8):868-870.

Etheredge GD; Michael G; Muehlenbein MP; Frenkel JK, 2004. The roles of cats and dogs in the transmission of Toxoplasma infection in Kuna and Embera children in eastern Panama. Rev. Panam. Salud. Publica., 16(3):176-186.

Fan CK; Su KE; Tsai YJ, 2004. Serological survey of Toxoplasma gondii infection among slaughtered pigs in northwestern Taiwan. J. Parasitol., 90(3):653-654.

Fertig A; Selwyn S; Tibble MJ, 1977. Tetracycline treatment in a food-borne outbreak of toxoplasmosis. Br. Med. J., 1:1064.

Foulon W; Naessens A; Ho-Yen D, 2000. Prevention of congenital toxoplasmosis. J. Perinat. Med., 28:337-345.

Foulon W; Naessens A; Derde MP, 1994. Evaluation of the possibilities for preventing congenital toxoplasmosis. American Journal of Perinatology, 11(1):57-62; 13 ref.

Frenkel JK; Dubey JP; Miller NL, 1970. Toxoplasma gondii in cats: fecal stages identified as coccidian oocysts. Science, 167:893-896.

Freyre A; Bonino J; Falcón J; Castells D; Correa O; Casaretto A, 1999. The incidence and economic significance of ovine toxoplasmosis in Uruguay. Veterinary Parasitology, 81(1):85-88; 15 ref.

Froen JF; Vege A; Ormerod E; Stray-Pedersen B, 2001. Finding the cause of death in intrauterine death - which examination should be done? Tidsskr. Nor. Laegeforen., 121(3):326-330.

Frolich K; Wisser J; Schmuser H; Fehlberg U; Neubauer H; Grunow R; Nikolaou K; Priemer J; Thiede S; Streich WJ; Speck S, 2003. Epizootiologic and ecologic investigations of European brown hares Lepus europaeus in selected populations from Schleswig-Holstein, Germany. J. Wildl. Dis., 39(4):751-761.

Gamble HR; Brady RC; Dubey JP, 1999. Prevalence of Toxoplasma gondii infection in domestic pigs in the New England states. Veterinary Parasitology, 82(2):129-136; 15 ref.

Gauss CB; Almeria S; Ortuno A; Garcia F; Dubey JP, 2003. Seroprevalence of Toxoplasma gondii antibodies in domestic cats from Barcelona, Spain. J. Parasitol., 89(5):1067-1068.

Gilbert R; Dunn D; Wallon M; Hayde M; Prusa A; Lebech M; Kortbeek T; Peyron F; Pollak A; Petersen E, 2001. Ecological comparison of the risks of mother-to-child transmission and clinical manifestations of congenital toxoplasmosis according to prenatal treatment protocol. Epidemiol. Infect., 127:113-120.

Gilbert R; Gras L, 2003. Effect of timing and type of treatment on the risk of mother to child transmission of Toxoplasma gondii. European Multicentre Study on Congenital Toxoplasmosis. Brit. J. Obstet. Gyn., 110:112-120.

Gilbert RE; Stanford MR, 2000. Is ocular toxoplasmosis caused by prenatal or postnatal infection? Br. J. Ophthalmol., 84:224-226.

Gómez-Marín JE; Montoya-de-Londono MT; Castano-Osorio JC, 1997. A maternal screening program for congenital toxoplasmosis in Quindio, Colombia and application of mathematical models to estimate incidences using age-stratified data. American Journal of Tropical Medicine and Hygiene, 57(2):180-186; 30 ref.

Guebre-Xabier M; Nurilign A; Gebre-Hiwot A; Hailu A; Sissay Y; Getachew E; Frommel D, 1993. Sero-epidemiological survey of Toxoplasma gondii infection in Ethiopia. Ethiopian Medical Journal, 31(3):201-208; 21 ref.

Guerina NG; Hsu HW; Meissner HC; Maguire JH; Lynfield R; Stechenberg B; Abroms I; Pasternack MS; Hoff R; Eaton RB; Grady GF; New England Regional Toxoplasma Working Group, 1994. Neonatal serologic screening and early treatment for congenital Toxoplasma gondii infection. New England Journal of Medicine, 330(26):1858-1863; 19 ref.

Guo ZG; Johnson AM, 1996. DNA polymorphisms associated with murine virulence of Toxoplasma gondii identified by RAPD-PCR. Current Topics in Microbiology and Immunology, No. 219:17-26; 32 ref.

Harries A, 1991. Some clinical aspects of HIV infection in Africa. Afr. Health, 13(5):25-26.

Holland GN, 2003. Ocular toxoplasmosis: a global reassessment. Part 1: epidemiology and course of disease. Am. J. Ophthalmol., 136:973-988.

Hove T; Dubey JP, 1999. Prevalence of Toxoplasma gondii antibodies in sera of domestic pigs and some wild game species from Zimbabwe. Journal of Parasitology, 85(2):372-373; 10 ref.

Howe DK; Honoré S; Derouin F; Sibley LD, 1997. Determination of genotypes of Toxoplasma gondii strains isolated from patients with toxoplasmosis. Journal of Clinical Microbiology, 35(6):1411-1414; 19 ref.

Howe DK; Sibley LD, 1995. Toxoplasma gondii comprises three clonal lineages: correlation of parasite genotype with human disease. Journal of Infectious Diseases, 172(6):1561-1566; 38 ref.

Humphreys JG; Stewart RL; Dubey JP, 1995. Prevalence of Toxoplasma gondii antibodies in sera of hunter-killed white-tailed deer in Pennsylvania. American Journal of Veterinary Research, 56(2):172-173; 10 ref.

Ibrahim BB; Salama MMI; Gawish NI; Haridy FM, 1997. Serological and histopathological studies on Toxoplasma gondii among the workers and the slaughtered animals in Tanta Abattoir, Gharbia Governorate. Journal of the Egyptian Society of Parasitology, 27(1):273-278; 15 ref.

Jeannel D; Niel G; Costagliola D; Danis M; Traore BM; Gentilini M, 1988. Epidemiology of toxoplasmosis among pregnant women in the Paris area. International Journal of Epidemiology, 17(3):595-602; 43 ref.

Jenum PA; Kapperud G; Stray-Pedersen B; Melby KK; Eskild A; Eng J, 1998. Prevalence of Toxoplasma gondii specific immunoglobulin G antibodies among pregnant women in Norway. Epidemiology and Infection, 120(1):87-92; 32 ref.

Jittapalapong S; Sangvaranond A; Pinyopanuwat N; Chimnoi W; Khachaeram W; Koizumi S; Maruyama S, 2005. Seroprevalence of Toxoplasma gondii infection in domestic goats in Satun Province, Thailand. Vet. Parasitol., 127(1):17-22.

Jones JL; Kruszon-Moran D; Wilson M; McQuillan G; Navin T; McAuley JB, 2001. Toxoplasma gondii infection in the United States: seroprevalence and risk factors. Am. J. Epidemiol., 154:357-365.

Jones JL; Sehgal M; Maguire JH, 2002. Toxoplasmosis-associated deaths among human immunodeficiency virus-infected persons in the United States, 1992-1998. Clin. Infect. Dis., 34:1161.

Kaplan JE; Masur H; Holmes KK, 2002. Guidelines for preventing opportunistic infections among HIV-infected persons - 2002. Recommendations of the US Public Health Service and the Infectious Diseases Society of America. Morbidity and Mortality Weekly Report, 51(RR-08):1-46.

Kapperud G; Jenum PA; Stray-Pedersen B; Melby KK; Eskild A; Eng J, 1996. Risk factors for Toxoplasma gondii infection in pregnancy. Results of a prospective case-control study in Norway. American Journal of Epidemiology, 144(4):405-412; 22 ref.

Karunajeewa H; Siebert D; Hammond R; Garland S; Kelly H, 2001. Seroprevalence of varicella zoster virus, parvovirus B19 and Toxoplasma gondii in a Melbourne obstetric population: implications for management. Aust. N. Z. J. Obstet. Gynaecol., 41(1):23-28.

Kawashima T; Khin-Sane-Win; Kawabata M; Barzaga N; Matsuda H; Konishi E, 2000. Prevalence of antibodies to Toxoplasma gondii among urban and rural residents in the Philippines. Southeast Asian J. Trop. Med. Public Health, 31(4):742-746.

Kean BH; Kimball AC; Christenson WN, 1969. An epidemic of acute toxoplasmosis. J. Am. Med. Assoc., 208:1002-1004.

Konishi Houki Y; Harano K; Mibawani RS; Marsudi D; Alibasah S; Dachlan YP, 2000. High prevalence of antibody to Toxoplasma gondii among humans in Surabaya, Indonesia. Jpn. J. Infect. Dis., 53(6):238-241.

Kotula AW; Dubey JP; Sharar AK; Andrews CD; Shen SK; Lindsay DS, 1991. Effect of freezing on infectivity of Toxoplasma gondii tissue cysts in pork. Journal of Food Protection, 54(9):687-690.

Kuticic V; Wikerhauser T, 2000. A survey of chickens for viable toxoplasms in Croatia. Acta Veterinaria Hungarica, 48(2):183-185; 11 ref.

Laing RB; Flegg PJ; Brettle RP; Leen CL; Burns SM, 1996. Clinical features, outcome and survival from cerebral toxoplasmosis in Edinburgh AIDS patients. Int. J. STD AIDS, 7(4):258-264.

Lebech M; Larsen SO; Petersen E, 1993. Prevalence, incidence and geographical distribution of Toxoplasma gondii antibodies in pregnant women in Denmark. Scandinavian Journal of Infectious Diseases, 25(6):751-756; 30 ref.

Lee YH; Noh HJ; Hwang OS; Lee SK; Shin DW, 2000. Seroepidemiological study of Toxoplasma gondii infection in the rural area Okcheon-gun, Korea. Korean J. Parasitol., 38(4):251-256.

Leport C; Chêne G; Morlat P; Luft BJ; Rousseau F; Pueyo S; Hafner R; Miro J; Aubertin J; Salamon R; Vildé JL, 1996. Pyrimethamine for primary prophylaxis of toxoplasmic encephalitis in patients with human immunodeficiency virus infection: a double-blind, randomized trial. Journal of Infectious Diseases, 173(1):91-97; 36 ref.

Leport C; Duval X, 1999. Cerebral toxoplasmosis in an HIV-infected patient. Diagnosis, development, treatment and prevention. Rev. Prat., 49:2271-2274.

Lindsay DS; Blagburn BL; Dubey JP; Mason WH, 1991. Prevalence and isolation of Toxoplasma gondii from white-tailed deer in Alabama. Journal of Parasitology, 77(1):62-64; 9 ref.

Lopez A; Dietz VJ; Wilson M; Navin TR; Jones JL, 2000. Preventing congenital toxoplasmosis. Morbidity and Mortality Weekly Report, 49:59-75.

Lord WG; Boni F; Bodek A; Hilberg RW; Rosini R; Clack FB, 1975. Toxoplasmosis - Pennsylvania. Morbidity and Mortality Weekly Report, 24:285-286.

Luft BJ; Remington JS, 1992. Toxoplasmic encephalitis in AIDS. Clinical Infectious Diseases, 15(2):211-222; 138 ref.

Lunden A; Lind P; Engvall EO; Gustavsson K; Uggla A; Vagsholm I, 2002. Serological survey of Toxoplasma gondii infection in pigs slaughtered in Sweden. Scand. J. Infect. Dis., 34(5):362-365.

Masur H; Jones TC; Lempert JA; Cherubini TD, 1978. Outbreak of toxoplasmosis in a family and documentation of acquired retinochoroiditis. Am. J. Med., 64:396-402.

McQuillan GM; Kruszon-Moran D; Kottiri BJ; Curtin LR; Lucas JW; Kington RS, 2004. Racial and ethnic differences in the seroprevalence of 6 infectious diseases in the United States:data from NHANES III, 1988-1994. Am. J. Public Health, 94(11):1952-1958.

Measures LN; Dubey JP; Labelle P; Martineau D, 2004. Seroprevalence of Toxoplasma gondii in Canadian pinnipeds. J. Wildl. Dis., 40(2):294-300.

Mondragon R; Howe DK; Dubey JP; Sibley LD, 1998. Genotypic analysis of Toxoplasma gondii isolates from pigs. Journal of Parasitology, 84(3):639-641; 14 ref.

Montoya JG, 2002. Laboratory diagnosis of Toxoplasma gondii infection and toxoplasmosis. J. Infect. Dis., 185(Suppl 1):S73-82.

Montoya JG; Liesenfeld O; Kinney S; Press C; Remington JS, 2002. VIDAS test for avidity of Toxoplasma-specific immunoglobulin G for confirmatory testing of pregnant women. J. Clin. Microbiol., 40:2504-2508.

Morlat P; Leport C, 1997. Prophylaxis for toxoplasmosis in immunosuppressed patients. Annales de Médecine Interne, 148(3):235-239; 32 ref.

Moschen ME; Stroffolini T; Arista S; Pistoia D; Giammanco A; Azara A; Mattia Dde; Chiaramonte M; Rigo G; Scarpa B, 1991. Prevalence of Toxoplasma gondii antibodies among children and teenagers in Italy. Microbiologica, 14(3):229-234; 22 ref.

Navidpour S; Hoghooghi-rad N, 1998. Seroprevalence of anti-Toxoplasma gondii antibodies in buffaloes in Khoozestan province, Iran. Veterinary Parasitology, 77(2/3):191-194; 8 ref.

Nissapatorn V; Abdullah KA, 2004. Review on human toxoplasmosis in Malaysia: the past, present and prospective future. Southeast Asian J. Trop. Med. Public Health, 35(1):24-30.

Nissapatorn V; Lee CK; Khairul AA, 2003. Seroprevalence of toxoplasmosis among AIDS patients in Hospital Kuala Lumpur, 2001. Singapore Med. J., 44(4):194-196.

Nogami S; Tabata A; Moritomo T; Hayashi Y, 1999. Prevalence of anti-Toxoplasma gondii antibody in wild boar, Sus scrofa riukiuanus, on Iriomote Island, Japan. Veterinary Research Communications, 23(4):211-214; 14 ref.

OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.

OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.

OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.

OIE, 2012. World Animal Health Information Database. Version 2. World Animal Health Information Database. Paris, France: World Organisation for Animal Health.

Onadeko MO; Joynson DH; Payne RA; Francis J, 1996. The prevalence of Toxoplasma antibodies in pregnant Nigerian women and the occurrence of stillbirth and congenital malformation. Afr. J. Med. Med. Sci., 25(4):331-334.

Owen MR; Trees AJ, 1999. Genotyping of Toxoplasma gondii associated with abortion in sheep. Journal of Parasitology, 85(2):382-384; 23 ref.

Paul M; Petersen E; Szczapa J, 2001. Prevalence of congenital Toxoplasma gondii infection among newborns from the Poznan region of Poland: validation of a new combined enzyme immunoassay for Toxoplasma gondii-specific immunoglobulin A and immunoglobulin M antibodies. J. Clin. Microbiol., 39(5):1912-1916.

Petersen E; Schmidt DR, 2003. Sulfadiazine and pyrimethamine in the postnatal treatment of congenital toxoplasmosis: what are the options. Expert Rev. Anti-Infect. Ther., 1:175-182.

Plant JW; Freeman P; Saunders E, 1982. Serological survey of the prevalence of Toxoplasma gondii antibodies in rams in sheep flocks in New South Wales. Aust. Vet. J., 59(3):87-89.

Punda-Polic V; Tonkic M; Capkun V, 2000. Prevalence of antibodies to Toxoplasma gondii in the female population of the County of Split Dalmatia, Croatia. Eur. J. Epidemiol., 16(9):875-877.

Rah H; Chomel BB; Follmann EH; Kasten RW; Hew CH; Farver TB; Garner GW; Amstrup SC, 2005. Serosurvey of selected zoonotic agents in polar bears Ursus maritimus. Vet. Rec., 156(1):7-13.

Rai SK; Kubo T; Yano K; Shibata H; Sumi K; Matsuoka A; Uga S; Matsumura T; Hirai K; Upadhyay MP; Basnet SR; Shrestha HG; Mahajan RC, 1996. Seroepidemiological study of Toxoplasma infection in central and western regions in Nepal. Southeast Asian J. Trop. Med. Public Health, 27(3):548-553.

Remington JS; McLeod R; Thulliez P; Desmonts G, 2001. Toxoplasmosis, In: Remington JS, Klein JO, eds. Infectious Disease of the Fetus and Newborn, edition 5. Philadelphia, USA: W.B. Saunders Company, 205-346.

Renold C; Sugar A; Chave JP; Perrin L; Delavelle J; Pizzolato G; Burkhard P; Gabriel V; Hirschel B, 1992. Toxoplasma encephalitis in patients with the acquired immunodeficiency syndrome. Medicine (Baltimore), 71(4):224-239; 70 ref.

Robben SR; le Nobel WE; Dopfer D; Hendrikx WM; Boersema JH; Fransen F; Eysker ME, 2004. Infections with helminths and/or protozoa in cats in animal shelters in the Netherlands. Tijdschr. Diergeneeskd., 129(1):2-6.

Roberts T; Frenkel JK, 1990. Estimating income losses and other preventable costs caused by congenital toxoplasmosis in people in the United States. Journal of the American Veterinary Medical Association, 196(2):249-256; 42 ref.

Roberts T; Murrell KD; Marks S, 1994. Economic losses caused by foodborne parasitic diseases. Parasitology Today 10: 419-423.

Rodger SM; Maley SW; Wright SE; Mackellar A; Wesley F; Sales J; Buxton D, 2006. Role of endogenous transplacental transmission in toxoplasmosis in sheep. Veterinary Record, 159(23):768-772.

Roghmann MC; Faulkner CT; Lefkowitz A; Patton S; Zimmerman J; Morris JGJr, 1999. Decreased seroprevalence for Toxoplasma gondii in Seventh Day Adventists in Maryland. American Journal of Tropical Medicine and Hygiene, 60(5):790-792; 17 ref.

Ronday MJ; Stilma JS; Barbe RF; McElroy WJ; Luyendijk L; Kolk AH; Bakker M; Kijlstra A; Rothova A, 1996. Aetiology of uveitis in Sierra Leone, West Africa. Br. J. Ophthalmol., 80(11):956-961.

Ross RD; Stec LA; Werner JC; Blumenkranz MS; Glazer L; Williams GA, 2001. Presumed acquired ocular toxoplasmosis in deer hunters. Retina., 21:226-229.

Sacks JJ; Delgado DG; Lobel HO; Parker RL, 1983. Toxoplasmosis infection associated with eating undercooked venison. American Journal of Epidemiology, 118(6):832-838; 25 ref.

Sacks JJ; Roberto RR; Brooks NF, 1982. Toxoplasmosis infection associated with raw goat’s milk. JAMA, 248:1728-1732.

Sarciron ME; Gherardi A; Delorme C; Peyramond D; Petavy AF, 2004. Prevalence of Toxoplasma encephalitis in AIDS patients treated with Didanosine hospitalised in a French infectious service. Curr. HIV Res., 2(4):301-307.

Singh S; Pandit AJ, 2004. Incidence and prevalence of toxoplasmosis in Indian pregnant women: a prospective study. Am. J. Reprod. Immunol., 52(4):276-283.

Smith GC; Gangadharan B; Taylor Z; Laurenson MK; Bradshaw H; Hide G; Hughes JM; Dinkel A; Romig T; Craig PS, 2003. Prevalence of zoonotic important parasites in the red fox Vulpes vulpes in Great Britain. Vet. Parasitol., 118(1-2):133-142.

Smith JL, 1993. Documented outbreaks of toxoplasmosis: transmission of Toxoplasma gondii to humans. Journal of Food Protection, 56(7):630-639; 116 ref.

Sroka J, 2001. Seroepidemiology of toxoplasmosis in the Lublin region. Ann. Agric. Environ. Med., 8:25-31.

Stanford M; See SE; Jones LV; Gilbert RE, 2003. Antibiotics for toxoplasmic retinochoroiditis, an evidence-based systematic review. Ophthalmology, 110:926-931.

Sukthana Y, 1999. Difference of Toxoplasma gondii antibodies between Thai and Austrian pregnant women. Southeast Asian J. Trop. Med. Public Health, 30(1):38-41.

Svobodová V; Literák I, 1998. Prevalence of IgM and IgG antibodies to Toxoplasma gondii in blood donors in the Czech Republic. European Journal of Epidemiology, 14(8):803-805; 13 ref.

Szénási Z; Ozsvár Z; Nagy E; Jeszenszky M; Szabó J; Gellén J; Végh M; Verhofstede C, 1997. Prevention of congenital toxoplasmosis in Szeged, Hungary. International Journal of Epidemiology, 26(2):428-435; 37 ref.

Tenter AM; Heckeroth AR; Weiss LM, 2000. Toxoplasma gondii: from animals to humans. International Journal for Parasitology, 30(12/13):1217-1258. [Thematic issue: Emerging parasitic zoonoses.]

Terry RS; Smith JE; Duncanson P; Hide G, 2001. MGE-PCR: a novel approach to the analysis of Toxoplasma gondii strain differentiation using mobile genetic elements. International Journal for Parasitology, 31(2):155-161; 35 ref.

Teutsch SM; Juranek DD; Sulzer A; Dubey JP; Sikes RK, 1979. Epidemic toxoplasmosis associated with infected cats. N. Engl. J. Med., 300:695-699.

Tonkic M; Punda-Polic V; Sardelic S; Capkun V, 2002. Occurrence of Toxoplasma gondii antibodies in the population of Split-Dalmatia County. Lijec. Vjesn., 124(1-2):19-22.

Uduman SA; Mohamed HNM; Bener A; Dar FK, 1998. The prevalence of Toxoplasma gondii specific IgG and IgM antibodies in blood donors in Al Ain, United Arab Emirates indicates a potential risk to recipients. Journal of Communicable Diseases, 30(4):237-239; 5 ref.

Vanek JA; Dubey JP; Thulliez P; Riggs MR; Stromberg BE, 1996. Prevalence of Toxoplasma gondii antibodies in hunter-killed white-tailed deer (Odocoileus virginianus) in four regions of Minnesota. Journal of Parasitology, 82(1):41-44; 19 ref.

Ventura MT; Munno G; Giannoccaro F; Accettura F; Chironna M; Lama R; Hoxha M; Panetta V; Ferrigno L; Rosmini F; Matricardi PM; Barbuti S; Priftanji A; Bonini S; Tursi A, 2004. Allergy, asthma and markers of infections among Albanian migrants to Southern Italy. Allergy, 59(6):632-636.

Venturini MC; Bacigalupe D; Venturini L; Rambeaud M; Basso W; Unzaga JM; Perfumo CJ, 2004. Seroprevalence of Toxoplasma gondii in sows from slaughterhouses and in pigs from an indoor and an outdoor farm in Argentina. Vet. Parasitol., 124(3-4):161-165.

Wallon M; Liou C; Garner P; Peyron F, 1999. Congenital toxoplasmosis: systematic review of evidence of efficacy of treatment in pregnancy. British Medical Journal (Clinical Research edition), 318(7197):1511-1514; 26 ref.

Weigel RM; Dubey JP; Dyer D; Siegel AM, 1999. Risk factors for infection with Toxoplasma gondii for residents and workers on swine farms in Illinois. American Journal of Tropical Medicine and Hygiene, 60(5):793-798; 48 ref.

Weigel RM; Dubey JP; Siegel AM; Hoefling D; Reynolds D; Herr L; Kitron UD; Shen SK; Thulliez P; Fayer R; Todd KS, 1995. Prevalence of antibodies to Toxoplasma gondii in swine in Illinois in 1992. Journal of the American Veterinary Medical Association, 206(11):1747-1751; 20 ref.

Williams JF; Zajac (eds) A, 1980. Diagnosis of gastrointestinal parasitism in dogs and cats, 54 pp. Louis, Missouri, USA: Ralston Purina Company.

Williams RH; Morley EK; Hughes JM; Duncanson P; Terry RS; Smith JE; Hide G, 2005. High levels of congenital transmission of Toxoplasma gondii in longitudinal and cross-sectional studies on sheep farms provides evidence of vertical transmission in ovine hosts. Parasitology, 130(3):301-307.

Wilson CB; Remington JS; Stagno S; Reynolds DW, 1980. Development of adverse sequelae in children born with subclinical congenital Toxoplasma infection. Pediatrics, 66:767-774.

Wilson M; Jones JL; McAuley JB, 2003. Toxoplasma. In: Murray PR, Baron EJ, Jorgensen JH, Pfaller MA, Yolken RH, eds. Manual of Clinical Microbiology, edition 8. Washington DC, USA: ASM Press, 1970-1980.

Wyss R; Sager H; Müller N; Inderbitzin F; König M; Audigé L; Gottstein B, 2000. Distribution of Toxoplasma gondii and Neospora caninum under aspects of meat hygiene. Schweizer Archiv für Tierheilkunde, 142(3):95-108; 41 ref.

Yamaoka M; Konishi E, 1993. Prevalence of antibody to Toxoplasma gondii among inhabitants under different geographical and climatic conditions in Hyogo Prefecture, Japan. Japanese Journal of Medical Science & Biology, 46(3):121-129; 23 ref.

Zamorano CG; Contreras Mdel C; Villalobos S; Sandoval L; Salinas P, 1999. Seroepidemiological survey of human toxoplasmosis in Osorno, X Region, Chile, 1998. Boletín Chileno de Parasitología, 54(1/2):33-36; 13 ref.

Zemlianskii OA; Evdokimov VV, 2004. Use of a helminthic indicator of soil to determine the frequency of toxoplasmosis among pregnant women. Med. Parazitol. (Mosk)., 1:57-59.

Distribution References

OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.

Links to Websites

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CFSPH: Animal Disease Information"Animal Disease Information" provides links to various information sources, including fact sheets and images, on over 150 animal diseases of international significance.
OIE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals Manual of Diagnostic Tests and Vaccines for Terrestrial Animals (Terrestrial Manual) aims to facilitate international trade in animals and animal products and to contribute to the improvement of animal health services world-wide. The principal target readership is laboratories carrying out veterinary diagnostic tests and surveillance, plus vaccine manufacturers and regulatory authorities in Member Countries. The objective is to provide internationally agreed diagnostic laboratory methods and requirements for the production and control of vaccines and other biological products.
ToxoDB - Toxoplasma gondii genome database contains draft sequence for the genome of T. gondii ME49 clone B7 (a type II strain), as well as additional T. gondii data from various sources. Sequences are available for browsing, querying, and datamining, subject to the Data Release Policy.
Toxoplasmosis - CDC Parasitic Disease Information on toxoplasmosis from the Centers for Disease Control (USA).
Toxoplasmosis - FAO technical paper 'HIV Infections and Zoonoses' by P. Pasquali

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