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Microsoft word - 10 toxoplasma guideline web edition.rtf

Toxoplasma gondii infection
Agent properties
Toxoplasma (T.) gondii is an obligate intracellular coccidian parasite that can infect virtually all species of warm-blooded animals, including people. Domestic cats and other Felids are the definitive hosts. All non-feline hosts are intermediate hosts (Dubey, 2005; There are three infectious stages: sporozoites in oocysts, tachyzoites (the actively multiplying stage), and bradyzoites (the slowly multiplying stage) enclosed in tissue cysts. Oocysts are excreted in faeces, whereas tachyzoites and bradyzoites are found in tissues and milk (Dubey, 2005; Dubey & Lappin, 2006). Entero-epithelial Life Cycle
This cycle is found only in the definitive feline host. Most cats are infected by ingesting intermediate hosts infected with tissue cysts. Bradyzoites are released in the stomach and intestine from the tissue cysts when their wall is dissolved by digestive enzymes. Bradyzoites penetrate the epithelial cells of the small intestine and give rise to schizonts, initiate five types of predetermined asexual stages, and merozoites released from schizonts form male and female gamonts. After fertilization, a wall is formed around the fertilized macrogamont to form an oocyst. Oocysts are round to oval, 10 x 12 µm in size, and are unsporulated (uninfective) when passed in faeces. After exposure to air and moisture for one to five days, they sporulate to contain two sporocysts, each with four sporozoites (Dubey, 2005; Dubey & Lappin, 2006). The enteroepithelial (coccidian) cycle is usually completed within three to ten days after ingestion of tissue cysts and occurs in up to 97% of naive cats. However, after ingestion of oocysts or tachyzoites, the formation of oocysts is delayed and shedding can occur up to 18 days (rarely more), and only 20% of cats fed oocysts will shed (Dubey, 2005; Extraintestinal Life Cycle
The extraintestinal development of T. gondii is the same for all hosts, including cats, dogs, and people, and is not dependent on whether tissue cysts or oocysts are ingested. After the ingestion of oocysts, sporozoites hatch in the lumen of the small intestine and penetrate intestinal cells, including the cells in the lamina propria. Sporozoites divide into two by an asexual process known as endodyogeny and thus become tachyzoites. Tachyzoites are lunate in shape, approximately 6 x 2 µm, and multiply in almost any cell of the body. If the cell ruptures, they infect new cells. Otherwise, tachyzoites multiply intracellular for an undetermined period and eventually encyst. Tissue cysts vary in size from 15 to 60 µm and usually conform to the shape of the parasitized cell. Tissue cysts are formed mainly in the CNS, muscles, and visceral organs, and probably persist for the life of the host (Dubey, 2005; Dubey & Lappin, 2006). Parasitaemia during pregnancy of the host can cause placentitis followed by spread of tachyzoites to the foetus. In people and sheep, congenital transmission occurs usually when the woman or ewe becomes infected during pregnancy. Many kittens born to queens infected with T. gondii during gestation become infected transplacentally or via suckling. Clinical signs are common in these kittens, varying with the stage of gestation at the time of infection, and some newborn kittens shed oocysts (Dubey, 2005; Dubey & Epidemiology
In cats, antibody prevalence to T. gondii varies geographically; in a study in Portugal, 24% of cats had antibodies (Duarte et al., 2010) and in the USA around 30% of cats were antibody-positive, but this varies from 16% to 40% depending on the states (Dubey & Lappin, 2006). Only 3 (0.9%) samples of faeces from 326 cats in the Morro Bay area of California contained T. gondii-like oocysts and 1 among 252 in Switzerland (Berger-Schoch, 2011). On the basis of the estimated tonnage of cat faeces deposited outdoors in this area, the annual burden in the environment was estimated to be 94 to 4,671 oocysts/m2 (9 to 434 oocysts/ft2; Dabritz et al., 2007). The proportion of T. gondii- positive samples collected between January and June was significantly lower than between July and December. The age of cats shedding T. gondii oocysts was not significantly different from the age of negative control cats (Herrmann et al., 2010). The three major modes of transmission of T. gondii to all host species, including humans and cats, are congenital infection, ingestion of infected tissues, and ingestion of oocyst- contaminated food or water (Dubey & Lappin, 2006). Minor modes of transmission include blood transfusion and organ transplantation (Dubey, 2005; Dubey & Lappin, Tachyzoites of T. gondii have been found in the milk of sheep, goats, cows, and mice, and infection by ingestion of raw goat milk has been documented in humans. Lactational transmission from infected cats to their kittens is also suspected since the organism has been detected in feline milk (Powell et al., 2001). T. gondii blocks the innate aversion of rats for cat urine, instead makes them attracted by the feline pheromone, which may increase the likelihood of a cat predating a rat. This is thought to reflect adaptive, ”behavioural manipulation“ by T. gondii in that the parasite reproduces only in the feline intestines. The "behavioural manipulation" hypothesis postulates that a parasite will specifically manipulate host behaviours essential for enhancing its own transmission. However, the neural circuits implicated in innate fear, anxiety, and learned fear all overlap considerably, raising the possibility that T. gondii may disrupt all of these non-specifically (Vyas et al., 2007). Some studies looking at experimental infection of rodents (Flegr & Havlicec ,1999; Hrda et al., 2000; Havlicec et al., 2001; Webster, 2001; Flegr et al., 2002; Flegr et al., 2003) found that T. gondii may change chemical messages in the CNS that affect behaviour; the proposed mechanism is that T. gondii infection may lead to cyst formation in the CNS with production of tyrosine hydroxylase (which is needed for dopamine production), leading to a lack of dopamine. Meat contaminated with T. gondii cysts has been the primary source of infection in persons in Europe and the United States, but recent changes in animal management and husbandry practices, and improved food handling and processing have significantly reduced the prevalence of cysts in meat. Nonetheless, antibody prevalence in humans remains relatively high, suggesting that exposure from oocyst contaminated soil or water is likely. Indeed, waterborne outbreaks of toxoplasmosis have been reported worldwide and support the theory that exposure to the environmental oocyst form poses a health risk. Research on the prevalence of T. gondii oocysts in the water and environment is limited due to the lack of tools to detect oocysts in the environment (Staggs et al., Pathogenesis
Clinical signs develop due to inflammation and tissue necrosis caused by intracellular growth of tachyzoites (Dubey & Lappin, 2006). Congenital infection tends to be much more serious than infection of the adult cat (Dubey & Lappin, 2006). Clinical signs
Approximately 10 to 20% of cats experimentally inoculated with T. gondii tissue cysts develop self-limiting small bowel diarrhoea for one to two weeks; this is caused by local replication of the organism during the intestinal phase of infection. However, detection of oocysts in faeces is rarely reported in client-owned cats with diarrhoea, and T. gondii infection therefore does not seem to be a major cause of diarrhoea. In cats, toxoplasmosis can develop during dissemination and intracellular replication of tachyzoites. Usually the disease develops from reactivation of latent infections rather than after a newly acquired infection. If a cat with chronic T. gondii infection is immunosuppressed, bradyzoites in tissue cysts can replicate rapidly and disseminate again as tachyzoites. This is also common in humans with acquired immune deficiency syndrome (AIDS). Clinical toxoplasmosis has also been documented in cats infected with FIV or FeLV (Davidson et al., 1993). Commonly used doses of glucocorticoids do not appear to predispose to activated toxoplasmosis (Lappin et al, 1992). However, administration of cyclosporine to cats or dogs with renal transplantations or dermatologic disease has been associated with clinically manifest disease (Beatty & Barrs, 2003; Last Commonly, pulmonary and CNS tissues are involved; hepatic and pancreatic involvement is less likely. Clinical signs in cats with toxoplasmosis include depression, anorexia, fever followed by hypothermia, peritoneal effusion, icterus, and dyspnoea. T. gondii infection also can cause anterior or posterior uveitis, fever, muscle hyperesthesia, weight loss, anorexia, seizures, ataxia, diarrhoea, or pancreatitis. T. gondii is also a common cause of uveitis in cats (Dubey & Lappin, 2006). Transplacentally or lactationally infected kittens develop more severe signs and frequently die of pulmonary or hepatic disease (Dubey et al., 1995). Chronic toxoplasmosis is rare and appears with vague and recurrent clinical signs. Immune complex formation (Lappin et al., 1993) and deposition in tissues and delayed hypersensitivity reactions may be involved in chronic clinical toxoplasmosis. Since T. gondii is never cleared from the body, neither naturally, nor with drugs, recurrence of the Immunity
Immunity to T. gondii in the cat is poorly understood. More work has been done in the mouse than in the cat. In the mouse and in people, immunity is highly dependent on cell- mediated effector responses (Sanchez et al., 2010). Only 80% of infected cats develop IgM antibodies, all develop IgG and IgA. IgG can take four to six weeks to appear, and maximal antibody titres are achieved within two to three weeks after antibody first appeared (Dubey & Lappin, 2006). Diagnosis
Antibody testing
Several antibody tests have been used in the diagnosis of toxoplasmosis. The indirect fluorescence test can be adapted to detect IgM, IgG, or IgA antibodies, using whole or immunoblotted antigens. For assessing human health risks, antibody test results from healthy cats can be interpreted. An antibody-negative cat is potentially shedding oocysts (early infection before antibodies have developed) and will likely shed oocysts if exposed for the first time; this cat poses the greatest public health risk. An antibody-positive cat is unlikely to currently shed oocysts (antibodies need two to three weeks to develop, and by that time cats usually do not shed any more - and a cat is only shedding once in its lifetime) and is also unlikely to shed oocysts if re-exposed or Because antibodies occur in both healthy and sick cats, results of these tests do not prove clinical toxoplasmosis. Also antibodies of the IgM class are commonly detected in healthy cats, and thus are not diagnostically useful. T. gondii-specific IgM is detected in cats with latent or reactivated infection and does not always correlate with clinical signs. Thus, antemortem diagnosis of clinical toxoplasmosis ideally is based on the detection of the organism in muscle biopsies or bronchoalveolar lavage, or by PCR in CSF or aqueous humour. Tachyzoites may be detected in various tissues and body fluids by cytology during acute illness. They are rarely found in blood, but occasionally in CSF, fine-needle aspirates of organs (e.g., lymph nodes), transtracheal or bronchoalveolar washings, and are common in the peritoneal and thoracic fluids of animals developing thoracic effusions or ascites. Detection of tachyzoites leads to a definitive diagnosis. If appropriate samples cannot be taken, a tentative diagnosis is sometimes based on the presence of high or increasing IgM titers, exclusion of other causes for the clinical signs, and beneficial clinical response to an anti-Toxoplasma drug (Dubey, 2005; Dubey & Gross and microscopic changes may be found in any organ but are most common in lungs, CNS, eyes, and mesenteric lymph nodes. Granulomas may be present in intestines and mesenteric lymph nodes (Dubey, 2005). Cholangiohepatitis, found in cats infected with T. gondii, has not been reported in any other host. The bile ducts are hyperplastic and plugged with desquamated bile duct epithelium and exudate. T. gondii schizonts (not tachyzoites) were seen in the biliary epithelium in both naturally occurring and experimentally induced disease. (Dubey, 2005). Detecting oocysts in faeces
T. gondii oocysts are 10 µm in size and are best demonstrated by centrifugation using Sheather’s sugar solution during the shedding period. T. gondii oocysts are morphologically indistinguishable from oocysts of Hammondia hammondi, Besnoitia orcytofelisi and Besnoitia darlingi (Dubey & Lappin, 2006). A modified CsCl method that easily purifies T. gondii oocysts from faeces of infected cats has also been described Treatment
Clindamycin is the treatment of choice (Davidson, 2000) and should be administered at 10 to 12 mg/kg orally q 12 h for four weeks (Table 1). Cats with systemic disease combined with uveitis should be treated with clindamycin in combination with topical, oral, or parenteral corticosteroids to avoid secondary glaucoma and lens luxations (Lappin et al., 1998). Prednisolone acetate (1% solution) applied topically to the eye three to four times daily is generally sufficient. Clinical signs not involving the eyes or the CNS usually begin to resolve within the first two to three days of clindamycin administration. Ocular and CNS toxoplasmosis respond more slowly. In cases of pulmonary toxoplasmosis, total resolution of radiographic abnormalities may not occur for several weeks. The prognosis is usually poor in pulmonary or hepatic disease, particularly in immunocompromised animals (Dubey et al., Prevention
Prevention of Cat Infections
The best way to avoid T. gondii infection in cats is not to feed any raw meat. It is currently discussed whether there is benefit of testing cats for T. gondii infection and of treating antibody-positive animals before administering cyclosporine therapy for other Public Health Considerations
Because of pet ownership issues, it is important for all small animal practitioners to familiarize themselves with the T. gondii infection. Discussions have come in focus, partially because of the increasing number of immunocompromised persons (e.g., people infected with the human immunodeficiency virus), and because of recent research linking psychological and cognitive disorders (reduced IQ evidenced by psychomotor and verbal intelligence tests) to T. gondii infection. Unfortunately, a recent survey on US obstetrician-gynaecologists to determine their knowledge and practices about toxoplasmosis prevention and testing found that most overestimated the risk of having pets in a household, versus environmental risk factors (Jones at al., 2010). A systematic review of risk factors for T. gondii infection in pregnant women is available (Leroy, 2005); it reports a relatively low risk of cat ownership. In addition to questions that arise concerning risk for human health, veterinarians will be confronted with cases in which T. gondii has caused illness in cats and dogs. These are possible routes in infection for humans: Ingestion of meat containing tissue cysts is the most common route. Thorough cooking or freezing for several days will kill tissue cysts (Lunden & Uggla., 1992; Dubey, 1988; Dubey et al., 1990; Dubey, 1998). Ingestion of sporulated oocysts, either from the environment, e.g., through contact with soil containing sporulated oocysts (indirectly) or from contact with faeces of cats that are shedding oocysts, is the second most common route. This can also occur indirectly through eating unwashed fruit or vegetables. Contamination via the environment is more common than via cats. Other routes of human infection are less common: Ingestion of sporulated oocysts through contact with contaminated water Ingestion of raw (unpasteurised) goat milk Inhalation of sporulated oocysts on dust particles is possible but extremely rare. The Feline Advisory Bureau has collected research data, indicating that cats are a minor risk for people to acquire toxoplasmosis (http://www.fabcats.org/owners/toxoplasmosis/info.html). Contact with cats does not increase the risk of T. gondii infection (Elmore et al., 2010). Studies have shown that: Cats shedding oocysts in faeces are rarely identified. While 24% of 206 cats had antibodies to T. gondii indicating prior infection, oocysts were not found in the faeces of any of them (Hill et al., 2000). (Berger–Schoch, 2011: 1 cat among 252 - mainly domestic cats - sheds oocysts in a Swiss study) Veterinarians working with cats are not more likely to be infected than the general population, including people without cat contacts (Behymer et al., 1973; Sengbusch & Sengbusch, 1976; DiGiacomo et al., 1990). Contact with cats has no influence on the probability of people having antibodies to T. gondii, whereas consuming raw meat significantly increases the risk of acquiring Stroking a cat will not spread infection from cats to people. Even when cats are shedding oocysts in their faeces, oocysts cannot be found on their coat (Dubey 1995). Studies performed in dogs have shown that oocysts do not sporulate on their fur and the same is probably true for cats (Lindsay et al., 1997). Cat ownership does not increase the risk of toxoplasmosis in people suffering from AIDS. Although they are generally at an increased health risk, this results from reactivation of a previous infection rather than from acquiring a new infection. The risk of infection from cats is low, except for young children playing in soil contaminated with sporulated oocysts. Most people are infected through ingestion of undercooked meat, especially goat, mutton, and pork (Wallace et al., 1993). Infection is not transmitted by bites or scratches from an infected cat. Infected cats under treatment with immunosuppressive drugs at standard doses do not start shedding oocysts in their faeces (Lappin et al., 1992). Infected cats do not re-shed oocysts in their faeces if they become immunosuppressed due to infection with FIV or FeLV (Lappin 2001). Cats infected with FIV or FeLV that are subsequently infected with T. gondii do not shed oocysts for any longer or in any greater numbers than other cats (Lappin et Newly identified strains of T. gondii are highly infectious for species other than cats; some scientists think that cats are becoming less important in the spread of Although the risk of parasite transmission from a cat to its owner is low, it can be further reduced and its consequences minimised by adopting the following recommendations: Litter trays should be emptied daily so that oocysts do not have sufficient time (24 Gloves should be used when handling cat litter, and hands should be washed thoroughly after cleaning the litter tray. Litter tray liners should be used if possible, and the litter tray should be cleaned regularly with detergent and scalding water. Cat litter should be disposed in sealed plastic bags. Children's sandpits should be covered when not in use to prevent cats using them Only properly cooked food or commercial cat food should be fed to cats. Hands should be washed after contact with a cat (especially before eating). Veterinary surgeons may get questions from clients whether or not to remove their cat. If the above hygiene recommendations are followed, the risk of transmission is minimal, and the ABCD does not recommend removing the cat. Toxoplasmosis is particularly severe in immunosuppressed people, and infection is problematic in pregnant women. In households with immunosuppressed people or pregnant women the following additional advice can be given: Immunosuppressed persons and pregnant women should avoid contact with cat Cats should be kept indoors to prevent hunting and access to intermediate hosts Cats should not be fed raw or partially cooked meat. If avoidable, cats should not eat insects (e.g., cockroaches). Cats should be tested for T. gondii antibodies; their presence indicates an infection in the past. These cats will not be a source of infection as they have completed their period of oocyst shedding. Cats without antibody have not been infected with T. gondii in the past and are likely to shed oocysts in their faeces for a short time if they become infected in the future. These cats should stay indoors during the phase of immunosuppression or pregnancy of the owner. Disease control in specific situations
Preventing toxoplasmosis in dogs and cats involves measures intended to reduce the incidence of infections and subsequent shedding of oocysts into the environment. Kittens raised outdoors usually become infected shortly after they are weaned and begin to hunt. Cats should preferably be fed only dry or canned, commercially processed cat food. The prevalence of canine and feline T. gondii infection has been higher in countries where raw meat products are fed to pets. Freezing or X-ray irradiation can kill tissue cysts without affecting meat quality. Household pets should be prevented from hunting and eating potential intermediate hosts or mechanical vectors, such as cockroaches, earthworms, and rodents. If meat is provided, it should always be thoroughly cooked before feeding, even if frozen. Cats should be prevented from entering buildings where food-producing animals are housed or where feed storage areas are located (Dubey, 2005). References
Barrs VR, Martin P, Beatty JA (2006). Antemortem diagnosis and treatment of toxoplasmosis in two cats on cyclosporin therapy. Aust Vet J; 84(1-2):30-5. Beatty JA, Barrs VR (2003). Acute toxoplasmosis in two cats on cyclosporin therapy. Aust Vet J.; 81(6): 339. Behymer RD , Harlow DR , Behymer DE , Franti CE (1973) Serologic diagnosis of toxoplasmosis and prevalence of Toxoplasma gondii antibodies in selected feline, canine, and human populations. Journal of the American Veterinary Medical Association 162, 959-963 Berger-Schoch AE, Herrmann DC, Schares G, Müller N, Bernet D, Gottstein B, Frey CF (2011). Prevalence and genotypes of Toxoplasma gondii in feline faeces (oocysts) and meat from sheep, cattle and pigs in Switzerland. Vet Parasitol. 2011 May 11;177(3-4):290-7. Conrad PA, Patton S, Lindsay DS, Dubey JP. (2010). Toxoplasma gondii: epidemiology, feline clinical aspects, and prevention. Trends Parasitol.;26(4):190-6. Dabritz HA, Miller MA, Atwill ER, Gardner IA, Leutenegger CM, Melli AC, Conrad PA (2007). Detection of Toxoplasma gondii-like oocysts in cat faeces and estimates of the environmental oocyst burden. J Am Vet Med Assoc.;231(11):1676-84. Davidson MG. (2000). Toxoplasmosis. Vet Clin North Am Small Anim Pract. 30(5):1051-62. Davidson MG, Rottman JB, English RV, Lappin MR, Tompkins MB (1993). Feline immunodeficiency virus predisposes cats to acute generalized toxoplasmosis. A J Pathol.; 143(5):1486-97. DiGiacomo RF, Harris NV, Huber NL, Cooney MK (1990). Animal exposures and antibodies to Toxoplasma gondii in a university population. American Journal of Epidemiology 131, 729-733 Duarte A, Castro I, Pereira da Fonseca IM, Almeida V, Madeira de Carvalho LM, Meireles J, Fazendeiro MI, Tavares L, Vaz Y. (2010). Survey of infectious and parasitic diseases in stray cats at the Lisbon Metropolitan Area, Portugal. J Feline Med Surg. 2010 May 11. 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, 910-913. Dubey JP (1995) Duration of immunity to shedding of Toxoplasma gondii oocysts by cats. Journal of Parasitology 81, 410-415. Dubey JP (1998). Toxoplasma gondii oocyst survival under defined temperatures. Journal of Parasitology 84, 862-865. Dubey JP. (2005). Toxoplasma update. WSAVA Proceedings. Available at http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2005&PID=10951&O=Generic Dubey JP, Ferreira L, Martins J, Jones J (2011). Sporulation and survival of Toxoplasma gondii oocysts in different types of commercial cat litters. J Parasitol. 2011 May 3. Dubey JP, Lappin MR (2006). Toxoplasmosis and Neosporosis. In Infectious Diseases of the Dog and Cat (2nd) C. E. Greene (ed.),WB Saunders, Philadelphia . 754-775 Dubey JP, Lappin MR, Thulliez P. (1995). Diagnosis of induced toxoplasmosis in neonatal cats. J Am Vet Med Assoc.;207(2):179-85. Elmore SA, Jones JL, 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, 201-204. Flegr J, Havlicek J (1999). Changes in the personality profile of young women with latent toxoplasmosis. Folia Parasitologica (Praha)46, 22-8. Flegr J, Havlicek J, Kodym P, Maly M, Smahel Z (2002). Increased risk of traffic accidents in subjects with latent toxoplasmosis: a retrospective case-control study. BMC Infectious Diseases 2, 11. Flegr J, Hrda S, Tachezy J (1998). The role of psychological factors in questionnaire-based studies on routes of human toxoplasmosis transmission. Central European Journal of Public Health 6, 45-50. Flegr J, Preiss M, Klose J, Havlicek J, Vitakova M, Kodym P (2003). Decreased level of psychobiological factor novelty seeking and lower intelligence in men latently infected with the protozoan parasite Toxoplasma gondii. Dopamine, a missing link between schizophrenia and toxoplasmosis? Biological Psychology 63, 253-68. Havlicek J, Gasova ZG, Smith AP, Zvara K, Flegr J (2001). Decrease of psychomotor performance in subjects with latent 'asymptomatic' toxoplasmosis. Parasitology 122, 515-20. Herrmann DC, Pantchev N, Vrhovec MG, Barutzki D, Wilking H, Fröhlich A, Lüder CG, Conraths FJ, Schares G (2010). Atypical Toxoplasma gondii genotypes identified in oocysts shed by cats in Germany. Int J Parasitol. 40(3):285-92 Hill SL, Cheney JM, Taton-Allen GF, Reif JS, Bruns C, Lappin MR (2000). Prevalence of enteric zoonotic organisms in cats. Journal of American Veterinary Medicine Association 216, 687-92. Hrda S, Votypka J, Kodym P, Flegr J (2000). Transient nature of Toxoplasma gondii-induced behavioural changes in mice. Journal of Parasitology 86, 657-63. Jones JL, Krueger A, Schulkin J, Schantz PM (2010). Toxoplasmosis prevention and testing in pregnancy, survey of obstetrician-gynaecologists. Zoonoses Public Health;57:27-33. Lappin MR (2001). Cat ownership by immunosuppressed people. In Consultations in Feline Medicine (4) J. R. August (ed.),W. B. Saunders Company, Philadelphia . pp. 18-27 Lappin MR, Cayatte S, Powell CC, Gigliotti A, Cooper C, Roberts SM (1993). Detection of Toxoplasma gondii antigen-containing immune complexes in the serum of cats. Am J Vet Res.;54(3):415-9. Lappin MR, Dawe DL, Windl PA, Greene CE, Prestwood AK (1992). The effect of glucocorticoid administration on oocyst shedding, serology, and cell mediated immune responses of cats with recent or chronic toxoplasmosis. Journal of the American Animal Hospital Association 27, 625-632 Lappin MR, George JW, Pedersen NC , Barlough JE, Murphy CJ, Morse LS (1996). Primary and secondary Toxoplasma gondii infection in normal and feline immunodeficiency virus-infected cats. Journal of Parasitology 82, 733-42. Lappin MR, Greene CE, Winston S, Toll SL, Epstein ME (1998). Clinical feline toxoplasmosis. Serologic diagnosis and therapeutic management of 15 cases. J Vet Intern Med.;3(3):139-43. Last RD, Suzuki Y, Manning T, Lindsay D, Galipeau L, Whitbread TJ (2004). A case of fatal systemic toxoplasmosis in a cat being treated with cyclosporin A for feline atopy. Vet Dermatol.;15(3):194-8. Leroy V, Hadjichristodoulou for the Eurotoxo Group (panel 3) (2005). Systematic review of risk factors for Toxoplasma gondii infection in pregnant women (unpublished report). Bordeaux (France): The Eurotoxo Group;. Lindsay DS, Dubey JP, Butler JM, Blagburn BL (1997). Mechanical transmission of Toxoplasma gondii oocysts by dogs. Veterinary Parasitology 73, 27-33. Lunden A, Uggla A (1992). Infectivity of Toxoplasma gondii in mutton following curing, smoking, freezing or microwave cooking. International Journal of Food Microbiology 15, 357-363. Powell CC, Brewer M, Lappin MR (2001). Detection of Toxoplasma gondii in the milk of experimentally infected lactating cats. Vet Parasitol. 102(1-2):29-33. Sanchez Y, Rosado Jde D, Vega L, Elizondo G, Estrada-Muñiz E, Saavedra R, Juárez I, Rodríguez-Sosa M (2010). The unexpected role for the aryl hydrocarbon receptor on susceptibility to experimental toxoplasmosis. J Biomed Biotechnol.;2010:505694. Sengbusch HG, Sengbusch LA (1976). Toxoplasma antibody prevalence in veterinary personnel and a selected population not exposed to cats. American Journal of Epidemiology 103, 595-597 Staggs SE, See MJ, Dubey JP, Villegas EN (2009). Obtaining highly purified Toxoplasma gondii oocysts by a discontinuous cesium chloride gradient. J Vis Exp. 3;(33). pii: 1420. doi: 10.3791/1420. Vyas A, Kim SK, Giacomini N, Boothroyd JC, Sapolsky RM (2007). Behavioural changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proc Natl Acad Sci U S A.;104(15):6442-7. Wallace MR, Rossetti RJ, Olson PE (1993). Cats and toxoplasmosis risk in HIV-infected adults. Journal of the American Medical Association 269, 76-77 Webster JP (2001) Rats, cats, people and parasites: the impact of latent toxoplasmosis on behaviour. Microbes and Infection 3, 1037-45.

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