Diseases / List of Parasitic Diseases / Disease description:

Toxoplasmosis in Waterfowl, Lagomorphs and Ferrets (with notes on Hedgehogs, Elephants, Bears and Great Apes)

INFORMATION AVAILABLE

GENERAL INFORMATION

CLINICAL CHARACTERISTICS & PATHOLOGY

INVESTIGATION & DIAGNOSIS

TREATMENT & CONTROL

SUSCEPTIBILITY & TRANSMISSION

ENVIRONMENT & GEOGRAPHY

 

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General and References

Disease Summary

Protozoal infection, for which cats are the definitive host, causing severe disease in some species (e.g. Lemuridae - Large lemurs (Family)) and abortion in sheep, but rarely causing clinical disease in many other species (e.g. waterfowl).

IN LAGOMORPHS

  • Toxoplasmosis is a rare cause of neurological disease in domestic rabbits. (B606.13.w13, B609.2.w2)
  • There are also reports of spontaneous toxoplasmosis occurring in wild rabbits and hares. (B614.10.w10)
  • Lepus europaeus - Brown hare: there is a high incidence of acute fatal toxoplasmosis in these hares in Scandinavia and they are thought to be exceptionally susceptible to primary rather than latent Toxoplasma gondii infection. (J1.30.w8)

IN FERRETS

  • Ferrets can carry this parasite without symptoms, but it can also cause clinical disease and death. (B626)
  • The deaths of one-day-old kittens have been related to the presence of Toxoplasma gondii, which suggests congenital infection. (B626)

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Alternative Names (Synonyms)

  • Toxoplasma gondii infection

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Disease Type

 Parasitic - Single-celled/Protozoa

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Infectious/Non-Infectious Agent associated with the Disease

Toxoplasma gondii is an obligate intracellular coccidian protozoan parasite. (B609.2.w2)
Life cycle
  • Intermediate hosts are infected by ingestion of sporulated oocysts (faecal-oral transmission), ingestion of infected animals or meat, or transplacentally. (B614.10.w10)
  • Through endodyogeny and several cycles, the tachyzoites and bradyzoites are formed. (B614.10.w10)
  • Tachyzoites are found in acute, disseminated infections. (B614.10.w10)
  • Bradyzoites are the resting form of Toxoplasma gondii and are found in acquired and congenital, chronic or asymptomatic infections; they are present in cysts, commonly in the central nervous system. (B614.10.w10)
  • Cats are the definitive host for this parasite. Toxoplasma gondii oocysts are formed in these species. When the oocysts sporulate, they become infective for virtually all vertebrates. (B614.10.w10)
Pathogenesis
  • Ingested infective Toxoplasma oocysts hatch in the duodenum, spread to the extraintestinal organs via lymph or blood and then can lead to focal necrosis in many organs (CNS, eye, heart). (B603.4.w4, B609.2.w2)

IN LAGOMORPHS

  • Only the sexual cycle, which consists of the proliferative and cyst stages, is seen in the rabbit. 
    • The proliferative organisms (trophozoites) occur during the acute phases of the disease and may be intra- or extra-cellular. (B614.10.w10)
    • The cyst stage (bradyzoites) becomes prominent as immunity develops or in latent disease. (B614.10.w10)
      • The cysts are often asymptomatic and will remain for the rest of the animal's life. (B603.4.w4)
  • Rabbits do not shed infective Toxoplasma gondii oocysts in their faeces. (B603.4.w4)

IN FERRETS

  • Ferrets can act as an intermediate host to Toxoplama gondii. (B627.16.w16, B626, J10.34.w1, J215.23.wl)
  • Toxoplasma are morphologically, biologically, and serologically the same as those found in rabbits. (B626)

Infective "Taxa"

Non-infective agents

--

Physical agents

-- Indirect / Secondary

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References

Disease Author

Debra Bourne MA VetMB PhD MRCVS (V.w5); Nikki Fox BVSc MRCVS (V.w103); Gracia Vila-Garcia DVM, MSc, MRCVS (V.w67), Bridget Fry BSc, RVN (V.w143)
Click image for main Reference Section

Referees

John Chitty BVetMed CertZooMed MRCVS (V.w65); Richard Saunders BVSc BSc CertZooMed MRCVS (V.w121)

Major References / Reviews

Code and Title List

Th3, J4.205.w1

Waterfowl:
B11
.X.w11, B13.46.w1, B14, B15, B16.19.w1
J5.6.w1
J6.21.w3

Hedgehogs:
B214.3.26.w11
J96.74.w1
J172.12.w1

Elephants:

J1.11.w8
J4.189.w7
J11.85.w1, J11.87.w1
J32.137.w1
P75.9.w1

Bears:
B22.32.w15, B419.14.w14
J4.175.w1, J4.189.w7
J11.81.w1, J11.84.w3
J13
.55.w1
P5.29.w5, P5.31.w2

Lagomorphs:
B208.17.w17d, B600.12.w12, B601.11.w11, B602.20.w20, B603.1.w1, B603.3.w3, B603.4.w4, B606.13.w13, B609.2.w2, B614.10.w10
J15.28.w1, J32.93.w2, J42.117.w1, J42.117.w2, J63.8.w1, J495.42.w3

Ferrets:
B626
, B627.16.w16, J64.15.w5, J213.3.w1, J10.34.w1, J215.23.wl

Great Apes:
B22.31.w31g
J258.2-5758.w1

Other References

Code and Title List

Lagomorphs:
J1.30.w8, J1.39.w8, J4.167.w5, J11.48.w1, J15.28.w1, J32.93.w2, J42.117.w1, J42.117.w2, J63.8.w1, J194.25.w2, J495.42.w3, J469.495.w1

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Clinical Characteristics and Pathology

Detailed Clinical and Pathological Characteristics

General

  • Infection may be inapparent or cause severe disease with non-specific signs, neurological signs, abortion and/or other signs, depending on the species affected. (Th3, J4.205.w1)
  • Clinical signs are variable; different tissues may be most affected. (B22.32.w15)
General WATERFOWL Infection usually subclinical in waterfowl. Systemic disease causing non-specific and nervous signs.
BEARS Usually subclinical, but clinical, fatal disease has been reported.
LAGOMORPHS
In rabbits
  • Infection is usually subclinical and latent. (B601.11.w11)
In hares
FERRETS
  • Stunted growth has been noted in neonatal ferrets that acquired Toxoplasma gondii oocysts. (B626, J10.34.w1)
GREAT APES  

Clinical Characteristics

WATERFOWL Listlessness, nervous signs (e.g. paralysis of feet, opisthotonus, nervousness, tremors), diarrhoea, ruffled feathers, pasted eyelids, emaciation, anorexia, diarrhoea (J5.6.w1, B13.46.w1, B16.19.w1)
BEARS Fatal infection in a six-day-old Ursus maritimus - Polar bear. (P5.31.w2)
LAGOMORPHS
  • Acute, chronic and latent forms of toxoplasmosis have been described in rabbits. (J63.8.w1)
  • Toxoplasma gondii infection in rabbits is usually subclinical and latent (B601.11.w11, J15.28.w1) or causes only mild signs (transient fever). (J42.117.w1)
Acute toxoplasmosis 

Clinical findings may include:

  • Anorexia, central nervous system signs, raised temperature, death within 2 - 8 days. (J63.8.w1, J495.42.w3)
  • Sudden anorexia (B603.4.w4, B614.10.w10)
  • Fever (>104 °F) (B601.11.w11, B603.4.w4, B614.10.w10, J15.28.w1)
  • Lethargy (B601.11.w11, B614.10.w10, B603.4.w4)
  • Hepatosplenomegaly may occur; the spleen can become ten times its normal size (B603.4.w4)
  • Increased respiratory rate (tachypnoea) (B614.10.w10, J42.117.w1)
  • Serous or seropurulent nasal and ocular discharge (B614.10.w10, J42.117.w1, J63.8.w1)
  • Head tremors (B601.11.w11, B602.20.w20, B609.2.w2, B614.10.w10, J15.28.w1)
  • Head tilt (B600.12.w12, B606.13.w13, B609.2.w2)
    • Note: toxoplasmosis is a rare cause of head tilt. (B603.1.w1)
  • Ataxia (B601.11.w11, B602.20.w20, B603.3.w3, B606.13.w13, B609.2.w2, B614.10.w10, J15.28.w1)
  • Dysuria (B603.1.w1)
  • Muscle tremors (B603.4.w4, B606.13.w13)
  • Convulsions may occur within a few days of the onset of the clinical signs listed above. (B603.4.w4, B609.2.w2, B614.10.w10, J63.8.w1)
  • Posterior paresis (B602.20.w20, B603.3.w3, B609.2.w2, J15.28.w1)
  • Paralysis in some cases, particularly in the hindquarters. (B601.11.w11, B602.20.w20, B603.4.w4, B606.13.w13, B609.2.w2, B614.10.w10, J63.8.w1)
  • Tetraplegia (B602.20.w20, B603.1.w1, B609.2.w2)
  • Death will usually occur after two to eight days of illness. (B603.4.w4, B614.10.w10, J15.28.w1, J63.8.w1)
  • In three pet French lop rabbits: (J495.42.w3)
    • Anorexia, dehydration, tetraplegia and temperature 41.6 °C (J495.42.w3)
    • Anorexia, ataxia, developing to muscle tremors, posterior paresis, temperature 41.1 °C (J495.42.w3)
    • Sudden death. (J495.42.w3)
  • In experimentally infected Lepus europaeus - Brown hare. (J32.93.w2)
    • Lassitude, sitting in a corner, loss of shyness, ruffled fur and reduced food consumption. (J32.93.w2)
    • No behavioural changes in some hares before death. (J32.93.w2)
Chronic toxoplasmosis

This form of the disease is usually seen in older rabbits. (B614.10.w10)

  • The course of the disease is protracted and the rabbit becomes anorexic and emaciated. This commonly results in anaemia. Central nervous signs may occur as the disease progresses, usually as posterior paralysis. Sudden death may occur but many animals recover. (B614.10.w10, J63.8.w1)
Clinical pathology
  • Haematology, biochemistry and urinalysis are usually normal unless the Toxoplasma organisms have affected non-neural tissue. (B609.2.w2)
FERRETS Clinical signs in ferrets that carry Toxoplasma gondii are uncommon, but are usually seen when immunosuppressed. (J10.34.w1)

Clinical signs that may occur include:

Systemic signs;

  • Anorexia. (B626, J10.34.w1)
  • Lethargy. (B626)
  • Hepatitis with clinical jaundice. (B626)
  • Respiratory distress, dyspnoeic. (B626)
  • Diarrhoea. (B626)
  • Pyrexia; individuals are known to reach 105.3°F. (B626, J10.34.w1)
  • Depressed.(B626)
  • Dehydration. (B626)
  • Tachycardia. (B626)
  • Orthopnoea: difficulty breathing when lying down. (B626)
  • In congenitally infected ferret kits, some died without obvious clinical signs, while survivors showed stunted growth. (J10.34.w1)

Neuromuscular signs

  • Posterior weakness and ataxia. (B626, J10.34.w1)

Ocular signs

  • Ocular lesions, such as retinitis or iritis can be present. (B626)
  • Blindness has also been reported. (B626)
  • Corneal oedema and ataxia.(B626)
GREAT APES In a Pan troglodytes - Chimpanzee experimentally infected orally with about 2.5 million oocyts divided over two days: (J258.2-5758.w1)
  • Listlessness and anorexia for about a week. (J258.2-5758.w1)
  • Superficial lymph nodes enlarged for about six weeks. (J258.2-5758.w1)
  • No clinical signs in a similarly-infected chimpanzee which was already seropositive. (J258.2-5758.w1)

Incubation

WATERFOWL --
BEARS --
LAGOMORPHS In experimental infection in Lepus timidus- Mountain hare, clinical signs were seen in one hare seven days after oral inoculation (J42.117.w1)
FERRETS --
GREAT APES In a Pan troglodytes - Chimpanzee experimentally infected orally with about 2.5 million oocyts divided over two days, less than a week. (J258.2-5758.w1)

Mortality / Morbidity

WATERFOWL Infection may be common, but clinical disease is rare in waterfowl (J4.205.w1, B15).
BEARS Infection is relatively common (seroprevalence rates as high as 80% detected in Pennsylvania black bears Ursus americanus - American black bear) (J1.29.w14), but clinical disease is rare: one, fatal case reported. (P5.31.w2)
LAGOMORPHS
  • In Oryctolagus cuniculus domesticus - Domestic European rabbit:
    • Exposure to this infection is reported as widely prevalent in the domestic rabbit. However, infection is usually subclinical and latent; clinical disease is rare. (B601.11.w11, B603.4.w4, J15.28.w1) Fatal disease occurs occasionally. (J495.42.w3)
    • Occurs in outbreaks with many deaths, particularly in young rabbits. (J63.8.w1)
    • High mortality with acute toxoplasmosis (50% mortality in two weeks in one outbreak in 600 young rabbits. (J63.8.w1)
  • In Lepus europaeus - Brown hare:
    • A high incidence of acute fatal toxoplasmosis has been reported in these hares in Scandinavia. (B208.17.w17d, J1.30.w8)
    • In experimentally infected Lepus europaeus - Brown hare, all individuals given 10 oocysts or more died. (J32.93.w2)
FERRETS Death can occur without clinical signs. (B626, J10.34.w1)
GREAT APES In Pan troglodytes - Chimpanzees experimentally infected orally with about 2.5 million oocyts divided over two days, no clinical signs in an individual already seropositive, and mild clinical illness in an individual previously seronegative. (J258.2-5758.w1)

Pathology

WATERFOWL Miliary white, necrotic foci in the liver, congestion of the lungs, splenomegaly with areas of necrosis, clear to sanguineous exudate in body cavity. Crescent-shaped Toxoplasma gondii organisms visible on Giemsa-stained smears of liver and peritoneal fluid (J5.6.w1)
BEARS In a six-day-old Ursus maritimus - Polar bear. (P5.31.w2)
  • Generalised infection; lesions were most severe in the liver, skeletal muscles and brain. There was necrosis of the liver and pancreas. (B22.32.w15, P5.31.w2)

Gross pathology

  • Liver: Pinpoint necrotic foci, petechial haemorrhages.
  • GIT: Mucosal haemorrhage.
  • Skeletal muscles: Very pale and marbled.
  • Lungs: Acute oedema
  • Cardiac: Right ventricle dilated. 

(P5.31.w2)

Histopathology

  • Liver: localised areas of necrotising inflammation; at the margins of such lesions, Toxoplasma tachyzoites and in cells, pseudocysts containing Toxoplasma.
  • Pancreas: Necrotising inflammation.
  • Lung: Slight interstitial inflammatory reaction.
  • Heart: Slight cellular proliferation.
  • Skeletal muscles and diaphragm: Significant necrosis, with pseudocycts in the area around the necrotic lesions. 
  • Thymus: Significant necrosis, with pseudocycts in the area around the necrotic lesions.
  • Retina: Slight accumulation of lymphoblastic cells in foci in the retina, with Toxoplasma cysts present. 
  • CNS: Purulent meningitis, mainly per-ventricular lesions, with oedema and Toxoplasma cysts. (P5.31.w2)

In four- to seven-month old Kodiak bears (Ursus arctos - Brown bear) at Rostock Zoo. (P5.29.w5)

  • CNS: Encephalitis, toxoplasma cysts present.
  • Pulmonary: Interstitial pneumonia with Toxoplasma present.
  • Cardiac: Myocarditis.

(P5.29.w5)

LAGOMORPHS
Acute toxoplasmosis

Generalised lesions are seen characterised by extensive necrosis of heart, lungs, liver, spleen and lymph nodes. (B614.10.w10)

Gross pathology: Histopathology:
  • The vascular connective tissue and the reticuloendothelial elements are most often affected. There is pronounced cellular necrosis with or without inflammatory cell infiltration. (B614.10.w10)
  • Toxoplasma gondii trophozoites may be seen intra- and extracellularly. (B614.10.w10)
  • In experimentally infected Oryctolagus cuniculus domesticus - Domestic rabbit killed at eight days post inoculation, lesions were minor, mainly focal mononuclear cell accumulations in the liver, (J42.117.w1)
  • Brain: 
    • Focal necrotic areas. (B609.2.w2)
    • Non-suppurative meningoencephalitis. (B609.2.w2)
  • Hepatic:
    • Focal interstitial granulomatous hepatitis. (B603.3.w3)
    • In Lepus timidus - Mountain hare, areas of necrotic hepatocytes, small amount of macrophage infiltration, Toxoplasma gondii organisms found in groups or singly in association with lesions. (J42.117.w1)
    • In three French Lop rabbits, multifocal necrosis and granulomatous reaction, with both tachyzoites and tissue cysts. (J495.42.w3)
    • In experimentally infected Lepus europaeus - Brown hare, irregular foci of coagulative necrosis. (J32.93.w2)
  • Lymph nodes:
  • Splenic:
    • In Lepus timidus - Mountain hare, focal necrosis. (J42.117.w1)
    • In three French Lop rabbits, multifocal necrosis and granulomatous reaction, with both tachyzoites and tissue cysts. (J495.42.w3)
    • In experimentally infected Lepus europaeus - Brown hare, irregular foci of coagulative necrosis, slight peripheral inflammatory reaction, and slight follicular lymphocyte depletion. (J32.93.w2)
  • Pulmonary:
    • In Lepus timidus - Mountain hare, focal necrosis. (J42.117.w1)
    • In three French Lop rabbits, multifocal necrosis and granulomatous reaction, with both tachyzoites and tissue cysts. (J495.42.w3)
  • Bone marrow:
  • Cardiac:
  • GIT:
    • In Lepus timidus - Mountain hare, foci of necrosis in the mucosa. (J42.117.w1)
    • In experimentally infected Lepus europaeus - Brown hare, in the small intestines, epithelial cell necrosis and desquamation, in the lamina propria hyperaemia and haemorrhages, and in the submucosa a mixed inflamatory exutdate. Toxoplasma gondii tachyzoites were present in the epithelial lining. (J32.93.w2)
  • Skeletal muscles:
  • Diaphragm:
  • Immunohistochemistry: 
    • In Lepus timidus - Mountain hare, Toxoplasma gondii demonstrable in multiple organs, particularly liver, mesenteric (and popliteal) lymph nodes, small intestine, spleen, lung and bone marrow. (J42.117.w1)
    • In Oryctolagus cuniculus domesticus - Domestic rabbit, organisms rarely detected at eight days post-inoculation. (J42.117.w1)
    • In three French Lop rabbits, positive reaction to anti-Toxoplasma gondii serum but not to anti-Neospora caninum serum. (J495.42.w3)
Chronic toxoplasmosis
  • Gross pathology: the gross lesions are more variable in this form of the disease. Various organs may have oedematous enlargement and scattered necrotic foci. (B614.10.w10, J63.8.w1)
  • Histopathology: marked reticuloendothelial hyperplasia especially in the lymph nodes, liver, spleen, and central nervous system. Toxoplasma gondii organisms are more difficult to isolate than in the acute disease. (B614.10.w10, J63.8.w1)
Latent disease
  • Lesions are primarily in the central nervous system in the form of cysts with or without reaction. Gliosis and granulomatous encephalitis with perivascular cuffing and nonsuppurative meningitis. These lesions may be confused with Encephalitozoonosis. (B614.10.w10)
FERRETS
Gross pathology:
  • Pulmonary: Multiple white foci (necrotic areas) in lung tissue. (B626, B627.16.w16,J10.34.w1)
  • Cardiac: multiple necrotic areas may be present. (B626, B627.16.w16)
  • Hepatic: multiple necrotic areas may be present. B626, B627.16.w16)
Histopathology:
  • Hepatic: Multiple foci of coagulated necrosis, lightly infiltrated by macrophages. (J10.34.w1)
  • Myocardium: Multiple foci of coagulated necrosis were present, with diffuse interstitial infiltration with moderate numbers of lymphocytes. A small number of protozoa were found and intrascarcoplasmic Toxoplasma-like colonies. (J10.34.w1)
  • Lung: Diffuse pneumonia with macrophages within the alveoli. Also foci of coagulative necrosis and protozoal colonies within the macrophages. (J10.34.w1)
  • CNS: 
    • Cysts have been found in the brains of ferrets that are serologically positive for Toxoplasma gondii. (J10.34.w1)
    • Mengingoencephalitis or meningoencephalomyelitis has been found in ferrets that showed posterior weakness and ataxia. (B626)
  • Immunohistochemistry: Immunohistochemistry confirmed that the protozoan detected associated with lesions in various organs in ferret kits in New Zealand was Toxoplasma gondii. (J10.38.w1)
GREAT APES  

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Human Health Considerations

Zoonosis; risk of infection if an infected animal is eaten under-cooked (J4.205.w1).
  • The two main sources of infection for humans are oocysts shed by cats (the definitive host), which may be picked up for example while cleaning the cat litter tray or while gardening, and raw or undercooked meat products, particularly lamb and pork. (Th3, J4.205.w1)
  • Humans are at risk of infection with Toxoplasma gondii if they eat undercooked meat from an infected animal. This includes a risk from bear meat. (J1.36.w7)

RISK FROM LAGOMORPHS

  • Rabbits: Infected rabbits may act as a source of toxoplasmosis for humans if undercooked rabbit meat is eaten, and in people slaughtering rabbits. (B603.4.w4, B609.2.w2, B614.10.w10, J495.42.w3)
  • Brown hare: A high incidence of acute fatal toxoplasmosis has been reported in Lepus europaeus - Brown hare in Scandinavia but there is a low prevalence of latent Toxoplasma gondii infection, therefore meat from clinically healthy hares may be unimportant as a potential source of human toxoplasmosis. (J1.30.w8)

RISK FROM FERRETS

  • Ferret faeces are not a source of Toxoplasma gondii for human infection because Toxoplasma gondii does not complete its life cycle within the ferret and therefore no infectious cysts are shed. (J215.23.wl)

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Susceptibility / Transmission

General information on Susceptibility / Transmission

Transmission of toxoplasmosis usually occurs following ingestion of sporulated oocysts (oocysts are shed by cats and become sporulated in one to five days and are then infective), which may be present in soil or on fodder or animal feedstuffs, or by ingestion of tissue cysts containing Toxoplasma gondii bradyzoites in meat which is eaten either raw or undercooked. The active form of the parasite in tissues, tachyzoites, is less infective. Transplacental transmission also occurs and is important in sheep and humans. Transmission can also occur by, for example, organ transplantation. (Th3, J4.205.w1)

Susceptibility: 

  • It is probable that all mammals and birds can become infected with Toxoplasma gondii however species vary greatly in their susceptibility to the development of clinical disease. Cattle and horses are relatively resistant, sheep often abort if infected during pregnancy, Australian marsupials are quite susceptible and small New World primates (Callitrichidae - Marmosets and Tamarins (Family)) and lemurs (e.g. Lemuridae - Large lemurs (Family)) are very susceptible. (Th3, J4.205.w1)
  • Susceptibility to clinical disease is increased in the very old, very young, fetus, and individuals which are immunocompromised. (Th3, J4.205.w1)
  • Susceptibility to clinical disease may be increased by the presence of concurrent disease (e.g. in carnivores, infection concurrent with distemper (Canine Distemper). (Th3, J4.205.w1)
  • More than 200 species of mammals and birds are known to act as intermediate hosts. (B22.32.w15)
WATERFOWL
  • Transmission: Ingestion of sporulated oocysts (shed by cats) in contaminated feed, water or invertebrates.
  • Susceptibility: All bird and mammal species may be infected. Waterfowl do not appear to be particularly susceptible to clinical disease.

(J4.205.w1).

BEARS
  • Infection in a six-day-old Ursus maritimus - Polar bear was considered to be intra-uterine (trans-placental). (P5.31.w2)
    • It was considered possible that the mother of the bear might have been infected by eating infected meat or by eating food which had become contaminated with oocysts. (P5.31.w2)
LAGOMORPHS Susceptibility
  • Immunosuppressed animals:
    • In most species including lagomorphs, clinical disease is frequently associated with immunosuppression. (B602.20.w20, B603.4.w4, B609.2.w2)
    • Toxoplasma gondii is often not clinically apparent unless concurrent illness or immunosuppression allows the organism to proliferate which results in an acute inflammatory response in the affected animal. (B609.2.w2)
  • Young animals: acute disease is primarily found in young animals. (B603.4.w4, B614.10.w10)
  • Pregnant and nursing does in colonies:
    • These animals are particularly affected by toxoplasmosis. (B603.4.w4)
  • Lepus europaeus - Brown hare: this species is thought to be exceptionally susceptible to primary Toxoplasma gondii infection because in Scandinavia there are reports of a high incidence of acute fatal toxoplasmosis in brown hares but a low prevalence of latent Toxoplasma gondii infection (no seropositive hares detected in a serosurvey of 176 individuals). (B208.17.w17d, J1.30.w8)
  • Lepus timidus - Mountain hare is also susceptible to acute fatal toxoplasmosis. (J42.117.w1)
  • High susceptibility of hares is probably associated with a lack of cellular response to Toxoplasma gondii infection. (J42.117.w2)
  • Chronic disease is usually seen in older rabbits. (B614.10.w10)

Transmission

  • Faecal-oral transmission of infectious oocysts occurs from the definitive host of the cat to the intermediate host, the rabbit. (B614.10.w10)
    • Infection occurs following the ingestion of food or water that has been contaminated with infected cat faeces. (B601.11.w11, B603.4.w4, B606.13.w13, B609.2.w2, J15.28.w1)
    • Most likely sources of infection are contaminated bedding, hay, grazing areas, and vegetables. (B603.3.w3)
    • "infection comes from ingesting the organism, in cat faeces, which must be more than 2 days old for the organism to be infectious". (B603.3.w3)
  • Transplacental transmission also occurs in the rabbit. (B601.11.w11, B609.2.w2, B614.10.w10, J15.28.w1)
  • Infected wild hares and rabbits may act as a source of infection for cats. (B603.4.w4, B614.10.w10)
  • Experimentally, transmission can occur via numerous routes. ((J63.8.w1)0
FERRETS Note: Oocysts in cat faeces can survive in the external environment for years, which means there is a long-term risk to ferrets. (B626. B627.16.w16)

Susceptibility

  • Young animals: can be transmitted congenitally, infecting ferrets and causing death as neonates. (B626)

Transmission

  • Faecal-oral transmission: Possible routes of infection include sporulated oocytes ingested by the intermediate host (e.g. rats) and sporulate oocysts in cat faeces. (B626)
  • Uncooked infected meat containing encysted Toxoplasma gondii, given to or caught by the ferret. (B626, B627.16.w16)
  • Congenital acute disease: the organism can be passed to neonates during pregnancy. (B626, B627.16.w16)
GREAT APES Can become infected. In two Pan troglodytes - Chimpanzee experimentally infected orally with about 1.5 or 2.5 million oocyts, infection was successful (as indicated by seroconversion and detection of the organism) in the chimpanzee which was previously seropositive). The other individual was already seropositive, indicating previous infection. (J258.2-5758.w1)

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Disease / Agent has been reported in either the wild or in captivity in:

Disease has been reported in:

Infection has also been reported in:

IN HEDGEHOGS:

IN ELEPHANTS:

  • Antibodies against Toxoplasma gondii have been documented in captive Elephas maximus - Asian Elephants and free-living Loxodonta africana - African Elephants. (J1.11.w8, J4.189.w7, J11.85.w1, J11.87.w1)
    • In the USA, one of three tested Elephas maximus - Asian Elephants , a three-year-old female, was seropositive using the indirect haemagglutination test (IHA) (titre 524,288) and the complement-staining fluorescent antibody test (titre at least 4,096). (J4.189.w7)
    • In Thailand, 45.5% of captive Elephas maximus - Asian Elephants sampled from four locations during 1994 - 1999 were positive (titre > 1: 50) with the modified agglutination test (MAT) and 25.6% were positive (> 1:64) with the latex agglutination test (commercial kit, Eiken, Japan). (J11.87.w1)
    • A seroprevalence study of Toxoplasma gondii in East African free-living mammals detected antibodies in four of 63 Loxodonta africana - African Elephants tested, using the indirect haemagglutination test (titre of >1: 64 considered positive). Positive titres varied: 1:128, 1:4,096 (two elephants) and 1:8192. (J1.11.w8)
    • Antibodies against Toxoplasma gondii were found in two of 19 Loxodonta africana - African Elephants ( 10.5%) from game Parks in Zimbabwe. (J11.85.w1)
    • In Sri Lanka, antibodies to Toxoplasma gondii were detected in the sera of 14 of 45 privately owned elephants (32%) at titres of 1:25 to 1: 400 using the modified agglutination test (MAT); the elephants were all older than 20 years of age. All of eight elephants tested from the Pinnawala Elephant Orphanage were seronegative. (J32.137.w1, P75.9.w1)

IN BEARS:

  • A survey of wildlife in Ontario, Canada, using the Sabin-Feldman dye test, detected antibodies to Toxoplasma gondii in one of three (33%) Ursus americanus - American black bear tested. (J1.12.w10)
  • A survey of wildlife in Central Ontario, Canada, using the Sabin-Feldman dye test, detected antibodies to Toxoplasma gondii in seven of 16 (43.8%) Ursus americanus - American black bears tested. (J1.12.w11)
  • Antibodies to Toxoplasma gondii were detected by indirect haemagglutination test (IHA) using RH strain in 23/303 sera (8%) from 265 Ursus americanus - American black bear from northcentral Idaho, 1971-1975. (J1.16.w12)
  • A serological survey of Pennsylvania black bears Ursus americanus - American black bear detected Toxoplasma gondii antibodies in 80% of bears (535/665 bears) using the agglutination test at dilutions of 1:25 (10%), 1:50 (37%) and 1:500 (33%). Seroprevalence did not vary significantly between males and females but was significantly higher in adults (83%) than in juveniles (65%). (J1.29.w14)
  • A survey using a commercially available latex agglutination test detected antibodies to Toxoplasma gondii at a titre of > 64 in 87 of 480 grizzly bears Ursus arctos - Brown bear) (18%), ranging from 9% on Kodiak Island to 28% in northern Alaska, and in six of 40 (16%) Ursus americanus - American black bear from Interior Alaska (where the prevalence in grizzly bears was 13%, five of 40. No grizzly bears under two years of age were seropositive. (J1.31.w12)
  • A survey of blood samples from 892 grizzly bears (Ursus arctos - Brown bear), collected 1973-1987 from Alaska, using the modified agglutination test, detected titres >25 (the minimum threshold titre) in 25% of 220 sera. In different areas, prevalence varied: from 9% in southern areas (18 of 196 sera positive) to 37% in northern areas (162 of 433 sera). (J1.33.w13)
  • Antibodies to Toxoplasma gondii were detected in 13/34 bears Ursus americanus - American black bears in Florida, 1980-1987: in one of three from Calhoun county, 4/6 bears from Columbia/Baker counties, 3/13 bears from Putnam county, 4/8 bears from Marion county, 1/1 bear from Orange county, none of three bears from Lake county. (B419.14.w14)
  • A survey of wild animals in Florida, USA found all four Ursus americanus - American black bear tested from Columbia/Baker counties to be seropositive for Toxoplasma gondii. (J4.175.w1)
  • Antibodies to Toxoplasma gondii were detected by microtitre latex agglutination test in 37/66 sera (56%) from free-ranging Ursus americanus - American black bear from Florida, USA, 1994-1995. (J1.34.w11)
  • A serological survey in wildlife in Alaska, using a modified agglutination test (MAT), detected antibodies in 62/143 (43%) Ursus americanus - American black bear tested. (J1.36.w7)
  • Antibodies to Toxoplasma gondii were detected in 13% of 38 Ursus americanus - American black bears, 0% of 36 grizzly bears (Ursus arctos - Brown bear) and 0% of 60 Ursus maritimus - Polar bear in Canada, from 1994-2001. (J3.155.w2)
  • Antibodies to Toxoplasma gondii were detected, using a commercially available latex agglutination test (Eiken Chemical Co.), in 6% of Ursus maritimus - Polar bear from the Beauford and Chukchi seas, from samples collected 1982-1999. (J3.156.w2)
  • A survey of blood samples from wildlife from Alaska, collected 1976-1996, using the modified agglutination test, detected Toxoplasma antibodies in 62 of 1443 (43%) Ursus americanus - American black bear; prevalence was highest in bears from the southeastern area of Alaska. (J1.36.w7)
  • Using an indirect haemaglutination test (IHA), antibodies to Toxoplasma gondii were detected in 40 of 149 sera (40%) from Ursus americanus - American black bears trapped during a population study in California, USA. [1982](J4.181.w4)
  • Antibodies to Toxoplasma gondii were detected in one of two tested polar bears (Ursus maritimus - Polar bear), but not in a single tested Asiatic black bear Selenarctos thibetanus (Ursus thibetanus - Asiatic black bear) in the USA. (J4.189.w7)
  • Fatal toxoplasmosis was diagnosed in a six-day-old Ursus maritimus - Polar bear. (P5.31.w2)
  • Fatal acute to subacute toxoplasmosis was diagnosed as the main cause of death in nine of 20 juvenile (four- to seven-month-old) Kodiak bears (Ursus arctos - Brown bear) at Rostock Zoo, and was an additional finding in a further seven cubs. (P5.29.w5)
  • Toxoplasma infection is common in bears in Pennsylvania. Serum (from heart blood) of 28 Ursus americanus - American black bears from Pennsylvania was tested by several serological tests: Sabin-Feldman dye test (DT), modified agglutination test (MAT), latex agglutination test (LAT) and indirect haemagglutination test (IHA). Antibodies were detected in the MAT at titres >1:40 in 22 bears; the DT detected antibodies (>1:10) in 21 bears, the LAT (>1:32) detected antibodies in nine bears and the IHA (>1:64) in 6 bears. All bears negative by MAT were also negative by other serological tests. Bioassay of heart muscle in mice detected viable Toxoplasma gondii in samples from three of 11 bears, while bioassay in cats detected viable Toxoplasma gondii in eight bears (including one which was also detected by mouse bioassay), giving a total of 10 bears in which viable Toxoplasma gondii were detected. All these bears were seropositive with the MAT and the DT but only six were LAT positive and five IHA positive. (J11.81.w1)
  • A serological survey of mammals in Czech and Slovak zoos detected antibodies to Toxoplasma gondii, using a commercially available indirect fluorescent antibody test (Sevatest toxoplasma NIFR, Sevapharma, Prague, Czech Republic) in the single tested Ursus maritimus - Polar bear and in all three tested Ursus americanus - American black bears. (J32.136.w1)
  • Serological testing of Ursus americanus - American black bears from Florida detected antibodies to Toxoplasma gondii by the indirect haemaglutination test in 17/38 bears (45%). (B419.14.w14)
  • Serological testing of samples from hunter-killed Ursus americanus - American black bears from North Carolina, 1996-1997, detected antibodies to Toxoplasma gondii in 120/143 individuals (83%). Titres were significantly higher in females than in males, and increased with age. (J11.84.w3)

IN LAGOMORPHS:

There have been many reports of spontaneous toxoplasmosis in the domestic rabbit from many parts of the world as well as in wild rabbits and hares. (B614.10.w10)
  • In Oryctolagus cuniculus - European rabbit in New Zealand. (J194.25.w2)
  • In Oryctolagus cuniculus domesticus - Domestic European rabbit:
    • Toxoplasmosis was first reported in the domestic rabbit in 1908. (B614.10.w10)
    • Exposure to this infection is reported as widely prevalent in the domestic rabbit. However, infection is usually subclinical and latent. Clinical disease is rare. (B601.11.w11, B603.4.w4)
    • Antibody prevalence figures in clinically normal rabbits have been reported as up to 50 %. (B614.10.w10)
    • Fatal toxoplasmosis was reported in a domestic rabbit in the USA (1992). (B614.10.w10)
  • In Lepus europaeus - Brown hare:
    • Toxoplasmosis has been diagnosed in hares in the wild in Europe. (J63.8.w1)
    • Acute fatal toxoplasmosis is common in this species in Scandinavia. (J1.30.w8)
      • In Sweden the incidence of acute disease among free-living hares that were examined at post mortem has been reported at 12 % (1961) and 10 % (1988). (J1.30.w8)
    • Subclinical toxoplasmosis
      • The prevalence of subclinical infection in this species is reportedly low in Sweden. No toxoplasma antibodies were found in serum samples from 176 brown hares ("Lepus europaeus P.") that were shot in three different areas of south and central Sweden (1984 - 1985). (J1.30.w8)
      • Studies have also indicated a very low prevalence in Australia, Austria, and the Netherlands. (J1.30.w8)
    • In a study of Lepus europaeus - Brown hares in Schleswig-Holstein, Germany, 1997-1999, antibodies to Toxoplasma gondii were detected in 46% (147/318 hares). (J1.39.w8)
  • Lepus timidus - Mountain hare (J1.30.w8)
  • Sylvilagus floridanus - Eastern Cottontail
    • A study in Maryland found 21/95 (22.1%) seropositive, with dye test titres ranging from 16 - 256. (J11.48.w1)
  • In a study of Lepus europaeus - Brown hares in Schleswig-Holstein, Germany, 1997-1999, antibodies to Toxoplasma gondii were detected in 46% (147/318). (J1.39.w8)
  • A survey in California found antibodies in 1/16 Sylvilagus bachmani - Brush rabbit and 3/39 Lepus californicus - Black-tailed jackrabbit. (J4.167.w5)

IN FERRETS:

  • 30% of 750 neonatal ferrets that were raised for fur died without clinical signs due to Toxoplasma gondii infection. (B627.16.w16, J10.34.w1, J10.38.w1)
  • Chronic Toxoplasma gondii infection has been found in both free-living and captive mustelids (Mustelidae - Weasels (Family)). (J10.34.w1)

IN GREAT APES

  • Rarely reported. (B22.31.w31g)
  • Experimental infection reported in a Pan troglodytes - Chimpanzee; another chimpanzee was already seropositive, indicating previous (natural) infection. (J258.2-5758.w1)

Further information on Host species has only been incorporated for species groups for which a full Wildpro "Health and Management" module has been completed (i.e. for which a comprehensive literature review has been undertaken). Host species with further information available are listed below:

Host Species List

BIRDS:

MAMMALS:

(List does not contain all other species groups affected by this disease)

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Disease / Agent has been specifically reported in Free-ranging populations of:

Clinical disease not reported in wild waterfowl (B15).

Infection has been reported in:

IN ELEPHANTS:

IN BEARS:

  • A survey of wildlife in Ontario, Canada, using the Sabin-Feldman dye test, detected antibodies to Toxoplasma gondii in one of three (33%) Ursus americanus - American black bear tested. (J1.12.w10)
  • A survey of wildlife in Central Ontario, Canada, using the Sabin-Feldman dye test, detected antibodies to Toxoplasma gondii in seven of 16 (43.8%) Ursus americanus - American black bears tested. (J1.12.w11)
  • Antibodies to Toxoplasma gondii were detected by indirect haemagglutination test (IHA) using RH strain in 23/303 sera (8%) from 265 Ursus americanus - American black bear from northcentral Idaho, 1971-1975. (J1.16.w12)
  • A serological survey of Pennsylvania black bears Ursus americanus - American black bear detected Toxoplasma gondii antibodies in 80% of bears (535/665 bears) using the agglutination test at dilutions of 1:25 (10%), 1:50 (37%) and 1:500 (33%). Seroprevalence did not vary significantly between males and females but was significantly higher in adults (83%) than in juveniles (65%). (J1.29.w14)
  • A survey using a commercially available latex agglutination test detected antibodies to Toxoplasma gondii at a titre of > 64 in 87 of 480 grizzly bears Ursus arctos - Brown bear) (18%), ranging from 9% on Kodiak Island to 28% in northern Alaska, and in six of 40 (16%) Ursus americanus - American black bear from Interior Alaska (where the prevalence in grizzly bears was 13%, five of 40. No grizzly bears under two years of age were seropositive. (J1.31.w12)
  • A survey of blood samples from 892 grizzly bears (Ursus arctos - Brown bear), collected 1973-1987 from Alaska, using the modified agglutination test, detected titres >25 (the minimum threshold titre) in 25% of 220 sera. In different areas, prevalence varied: from 9% in southern areas (18 of 196 sera positive) to 37% in northern areas (162 of 433 sera). (J1.33.w13)
  • Antibodies to Toxoplasma gondii were detected by microtitre latex agglutination test in 37/66 sera (56%) from free-ranging Ursus americanus - American black bear from Florida, USA, 1994-1995. (J1.34.w11)
  • A serological survey in wildlife in Alaska, using a modified agglutination test (MAT), detected antibodies in 62/143 (43%) Ursus americanus - American black bear tested. (J1.36.w7)
  • Antibodies to Toxoplasma gondii were detected in 13% of 38 Ursus americanus - American black bears, 0% of 36 grizzly bears (Ursus arctos - Brown bear) and 0% of 60 Ursus maritimus - Polar bear in Canada, from 1994-2001. (J3.155.w2)
  • Antibodies to Toxoplasma gondii were detected, using a commercially available latex agglutination test (Eiken Chemical Co.), in 6% of Ursus maritimus - Polar bear from the Beauford and Chukchi seas, from samples collected 1982-1999. (J3.156.w2)
  • A survey of wild animals in Florida, USA found all four Ursus americanus - American black bear tested to be seropositive for Toxoplasma gondii. (J4.175.w1)
  • A survey of blood samples from wildlife from Alaska, collected 1976-1996, using the modified agglutination test, detected Toxoplasma antibodies in 62 of 1443 (43%) Ursus americanus - American black bear; prevalence was highest in bears from the southeastern area of Alaska. (J1.36.w7)
  • Using an indirect haemaglutination test (IHA), antibodies to Toxoplasma gondii were detected in 40 of 149 sera (40%) from Ursus americanus - American black bears trapped during a population study in California. (J4.181.w4)
  • Toxoplasma infection is common in bears in Pennsylvania. Serum (from heart blood) of 28 Ursus americanus - American black bears from Pennsylvania was tested by several serological tests: Sabin-Feldman dye test (DT), modified agglutination test (MAT), latex agglutination test (LAT) and indirect haemagglutination test (IHA). Antibodies were detected in the MAT at titres >1:40 in 22 bears; the DT detected antibodies (>1:10) in 21 bears, the LAT (>1:32) detected antibodies in nine bears and the IHA (>1:64) in 6 bears. All bears negative by MAT were also negative by other serological tests. Bioassay of heart muscle in mice detected viable Toxoplasma gondii in samples from three of 11 bears, while bioassay in cats detected viable Toxoplasma gondii in eight bears (including one which was also detected by mouse bioassay), giving a total of 10 bears in which viable Toxoplasma gondii were detected. All these bears were seropositive with the MAT and the DT but only six were LAT positive and five IHA positive. (J11.81.w1)
  •  in all three tested Ursus americanus - American black bears. (J32.136.w1)
  • Serological testing of Ursus americanus - American black bears from Florida detected antibodies to Toxoplasma gondii by the indirect haemaglutination test in 17/38 bears (45%). (B419.14.w14)
  • Serological testing of samples from hunter-killed Ursus americanus - American black bears from North Carolina, 1996-1997, detected antibodies to Toxoplasma gondii in 120/143 individuals (83%). Titres were significantly higher in females than in males, and increased with age. (J11.84.w3)

IN LAGOMORPHS:

  • There have been many reports of spontaneous toxoplasmosis in wild rabbits and hares [species not specified]. (B614.10.w10)
  • In Oryctolagus cuniculus - European rabbit in New Zealand. (J194.25.w2)
  • In Lepus europaeus - Brown hare:
    • Acute fatal toxoplasmosis is common in this species in Scandinavia. (J1.30.w8)
      • In Sweden the incidence of acute disease among free-living hares that were examined at post mortem has been reported at 12 % (1961) and 10 % (1988). (J1.30.w8)
    • Subclinical toxoplasmosis
      • The prevalence of subclinical infection in this species is reportedly low in Sweden. No toxoplasma antibodies were found in serum samples from 176 brown hares that were shot in three different areas of south and central Sweden (1984 - 1985). (J1.30.w8)
      • Studies have also indicated a very low prevalence in Australia, Austria, and the Netherlands. (J1.30.w8)
    • In a study of Lepus europaeus - Brown hares in Schleswig-Holstein, Germany, 1997-1999, antibodies to Toxoplasma gondii were detected in 46% (147/318 hares). (J1.39.w8)
  • Lepus timidus (J1.30.w8)
  • In a study of Lepus europaeus - Brown hares in Schleswig-Holstein, Germany, 1997-1999, antibodies to Toxoplasma gondii were detected in 46% (147/318). (J1.39.w8)
  • A survey in California found antibodies in 1/16 Sylvilagus bachmani - Brush rabbit and 3/39 Lepus californicus - Black-tailed jackrabbit. (J4.167.w5)

IN FERRETS:

Further information on Host species has only been incorporated for species groups for which a full Wildpro "Health and Management" module has been completed (i.e. for which a comprehensive literature review has been undertaken). Host species with further information available are listed below:

Host Species List

BIRDS:

MAMMALS:

(List does not contain all other species groups affected by this disease)

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Environment/Geography

General Information on Environmental Factors/Events and Seasonality

  • The presence of Toxoplasma gondii depends on the presence of the definitive host – the domestic cat and other Felidae. 
  • Survival of oocysts in the environment is affected by temperature, humidity and sunlight. 

(J4.205.w1)

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Regions / Countries where the Infectious Agent or Disease has been recorded

  • Disease in waterfowl: Argentina (J5.6.w1). 
  • Toxoplasma gondii infection may occur worldwide wherever cats (the definitive host) are present (J4.205.w1).
  • 30% of cats and humans have been exposed to Toxoplama gondii within the USA. (B626)

IN LAGOMORPHS

  • Worldwide (B614.10.w10)

IN FERRETS

  • Between 1992 and 1999 there was an epizootic of Toxoplama gondii in the USA; this occurred in captive Mustela nigripes. The source was thought to be frozen uncooked rabbits. This outbreak highlighted several points of the disease and of captive maintenance of endangered species: inbreeding and increased stresses of captivity can cause increased susceptibility to diseases. (B626, J64.15.w5)
  • Chronic toxoplasmosis in a ferret was diagnosed in South Africa. (B627.16.w16)
  • In New Zealand, congenital infection in ferret kits. (J10.34.w1, J10.38.w1)

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Regions / Countries where the Infectious Agent or Disease has been recorded in Free-ranging populations

  • In waterfowl: in Czechoslovakia (J6.21.w3). 
  • Toxoplasma gondii infection may occur worldwide wherever cats (the definitive host) are present (J4.205.w1).

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General Investigation / Diagnosis

General Information on Investigation / Diagnosis

  • In the definitive host (domestic cats and other felines) examination of faeces for three weeks post infection may reveal the presence of oocysts. (B22.32.w15)
  • In other species, paired serum samples can show a rising antibody titre. (B22.32.w15)
  • Goats and other laboratory animals have been found to transmit toxoplasmosis congenitally to their offspring. (B627.16.w16)
WATERFOWL
  • Romanowski-stained impression smears of peritoneal fluid, liver, other tissues (J5.6.w1, J4.205.w1).
  • Mouse inoculation (B15).
  • Serological tests indicate infection but not necessarily disease, unless a rising titre is demonstrated (J4.205.w1, B13.46.w1).
BEARS
  • Serological tests. A study in which serum (from heart blood) of 28 Ursus americanus - American black bears from Pennsylvania was tested by several serological tests: Sabin-Feldman dye test (DT), modified agglutination test (MAT), latex agglutination test (LAT) and indirect haemagglutination test (IHA) found that the modified agglutination test is the most sensitive serological test for detection of T. gondii in bears. (J11.81.w1)
    • Antibodies were detected in the MAT at tites >1:40 in 22 bears; the DT detected antibodies (>1:10) in 21 bears, the LAT (>1:32) detected antibodies in nine bears and the IHA (>1:64) in 6 bears. All bears negative by MAT were also negative by other serological tests. Bioassay of heart muscle in mice detected viable Toxoplasma gondii in samples from three of 11 bears, while bioassay in cats detected viable Toxoplasma gondii in eight bears (including one which was also detected by mouse bioassay), giving a total of 10 bears in which viable Toxoplasma gondii were detected. All these bears were seropositive with the MAT and the DT but only six were LAT positive and five IHA positive. The study indicated (J11.81.w1)
  • The presence of viable Toxoplasma gondii can be detected by bioassay in mice or cats. (J11.81.w1)
  • In four- to seven-month old Kodiak bears (Ursus arctos - Brown bear) at Rostock Zoo, diagnosis was made on the basis of the pathological findings, and histological findings of toxoplasma tachyzoites in the parenchyma of organs, the brain and lymph nodes, and in one case also by electron microscopy. (P5.29.w5)
LAGOMORPHS Diagnosis can be difficult; definitive diagnosis is usually made at post mortem. (B603.4.w4)
  • Cytology of impression smears or histopathology. (B603.4.w4, B614.10.w10)
  • Identification of Toxoplasma organisms by light and electron microscopy.
    • Samples must be taken from a fresh carcass (less than a few hours) or the organism becomes unidentifiable. (B603.4.w4)
    • Wright-Giemsa stained smears of mesentery, omentum, or peritoneal exudate can be examined for the organisms in the acute form of the disease. (B614.10.w10)
    • Toxoplasma organisms have a strong uptake of haematoxylin stain and this is a useful feature to differentiate this organism from Encephalitozoon cuniculi. (B603.3.w3, B609.2.w2)
    • Toxoplasma gondii organisms can also be differentiated from Encephalitozoon cuniculi by the following characterisitics: gram negative, non birefringent when viewed with polarised light, and they do not stain with Goodpasture's carbol fuchsin. (B602.20.w20)
    • Toxoplasma sporozoites ultrastructurally resemble Plasmodium and coccidia. (B614.10.w10)
    • Peroxidase techniques can be used to identify Toxoplasma organisms in tissue sections using antiserum specific to this protozoa. (B614.10.w10)
  • Serological methods
    • Serological testing is available. (B601.11.w11, B603.3.w3)
    • "anecdotal reports of using serum antibody titres available for testing in dogs and cats to support diagnosis in rabbits exist; however, no data exist to direct proper interpretation of results". (B609.2.w2)
  • "Sabin-Feldman dye, indirect immunofluorescence antibody, carbon immunoassay, and agglutination tests are currently the most widely used for toxoplasmosis in rabbits". (B614.10.w10)
FERRETS
  • Faecal examinations are necessary to positively identify toxoplasma. (B602.2.w2)
  • Antibody titers to Toxoplasma gondii can be found in carrier ferrets. (B626)
  • Usually diagnosed by possible exposure. (B626)
  • Antibody ELISAs can detect Toxoplasma gondii specific immunoglobulin G (IgG) and immunoglobulin M (IgM) and antigen ELISA can detect specific antigens in the serum. (B626, B627.16.w16)
  • Histological examination or inoculation is used for diagnosis. (B627.16.w16)
  • In ferret kits in New Zealand, immunohistochemistry confirmed that the protozoan detected associated with lesions in various organs was indeed Toxoplasma gondii. (J10.38.w1)
  • Blood results: Neutrophilia, leukocytosis, microcytic, non-regenerative anaemia, and decreased serum albumin. (B626)
GREAT APES
  • Consider in an individual with hepatosplenomegally, atypical pulmonary infection, chorioretinitis, myocardial inflammation or CNS signs. (B22.31.w31g)
  • Detection of tachyzoites in blood of a previously seronegative Pan troglodytes - Chimpanzee one week after experimental infection. (J258.2-5758.w1)
  • Detection of antibodies using the Sabin Feldman dye test, complement fixation test and indirect fluorescent anitibody test in naturally and experimentally infected Pan troglodytes - Chimpanzee. (J258.2-5758.w1)
  • Detection of the organism by mouse inoculation of biopsy specimens from inguinal lymph node and from thigh muscle, 11 weeks post infection in a previously seronegative Pan troglodytes - Chimpanzee. (J258.2-5758.w1)
Related Techniques
WaterfowlINDEXDisInvTrCntr.gif (2325 bytes)

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Similar Diseases (Differential Diagnosis)

WATERFOWL Other causes of nervous signs e.g. lead poisoning, botulism, Newcastle disease, (B14).
LAGOMORPHS Other, more common causes of encephalopathy in rabbits:
  • Bacterial:
    • Brain abscess (B609.2.w2)
    • Meningoencephalitis (B609.2.w2)
    • Extension of infection from otitis interna / media. (B609.2.w2)
    • Pasteurellosis (B603.4.w4)
      • Differentiate toxoplasmosis from pasteurellosis by serological testing which can be useful in ruling out pasteurellosis:
        • a paired rising titre will indicate an active Pasteurella infection. (B609.2.w2)
        • a single titre will only indicate exposure to Pasteurella spp.. (B609.2.w2)
  • Encephalitozoonosis (B603.4.w4, B609.2.w2, J495.42.w3): 
    • Central nervous system lesions that are seen in the latent form of toxoplasmosis may be confused with lesions seen in this disease. (B614.10.w10)
    • Differentiate toxoplasmosis from encephalitozoonosis by:
      • Serologic testing (B602.20.w20, B609.2.w2)
        • only useful in ruling out encephalitozoonosis because a positive titre just indicates exposure to Encephalitozoon cuniculi and does not confirm the organism as the cause of the clinical signs. (B609.2.w2)
      • Demonstrating gram-negative spores in brain tissue on histopathology (Encephalitozoon cuniculi spores stain gram-positive). (B602.20.w20, J495.42.w3)
  • Fungal or viral diseases are rare in the rabbit. (B609.2.w2)
  • Brain tumour (B609.2.w2)
  • Ischaemic encephalopathy is rare in the rabbit. (B609.2.w2)
  • Note: Neospora caninum infection is a differential diagnosis in other species, however, it has not yet been reported in the rabbit. (B603.3.w3)

Various causes of acute lethargy or pyrexia such as:

FERRETS
  • Sarcocystosis: Sarcocystis muris is related to Toxoplasma gondii. This parasite can produce cysts in ferrets' muscle tissue. (B626)
  • Neosporosis: caused by Neospora caninum. This disease causes similar symptoms to toxoxplasmosis. (B626)
  • Other coccidians: Hammondia, Besnoitia and Frenkelia all are possible differential diagnoses. (J10.34.w1)
GREAT APES --

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Treatment and Control

Specific Medical Treatment

  • Sulfamerazine, 30 mg/kg every six hours, plus pyrimethamine, 1 mg/kg orally every 24 hours, for 14 days. (B22.32.w15)
WATERFOWL
  • 30 days course pyrimethamine, 0.25-0.5 mg/kg orally, twice daily (B11.X.w11).
  • Sulfamethazine 0.2-0.25% in drinking water or feed (B13.46.w1).
LAGOMORPHS
Prognosis
  • The prognosis is guarded because there is often a varied response to treatment. Residual deficits are likely (particularly neurological); however it is not possible to predict the severity of the deficits until after the course of treatment. (B609.2.w2)
Treatment options
  • Trimethoprim-sulfonamide (B601.11.w11, B602.20.w20, B603.4.w4, J15.28.w1)
    • This is the drug of choice. (B609.2.w2)
    • Use at 15 to 30 mg/kg orally every twelve hours. (B609.2.w2)
  • Sulfadiazine in combination with pyrimethamine (B601.11.w11, B602.20.w20)
    • This is another recommended option for treatment of toxoplasmosis. (B609.2.w2)
    • Use for two weeks at feline doses. (B609.2.w2)
    • Precautions: this combination can cause depression, leucopaenia, thrombocytopaenia and anaemia in cats; toxicity in rabbits has not been described. (B609.2.w2)
  • Doxycycline (B601.11.w11, B602.20.w20, J15.28.w1)
    • This has also been used in rabbits to treat toxoplasmosis; efficacy uncertain. (B609.2.w2)
    • 2.5 mg/kg orally every 12 hours. (B609.2.w2)
  • Sulfadiazine, sulfones, pyrimethamine, tetracyclines,1,2-dihydrotriazones, and spiramycin have been reportedly used to inhibit trophozoites and cysts of toxoplasmosis. (B614.10.w10)
Contraindications
  • Clindamycin
    • Oral administration of this drug has been reported as a treatment option of toxoplasmosis in other species, e.g. cats. However, it should not be used in the rabbit because it can cause a fatal enteric dysbiosis and enterotoxaemia. This also applies to other oral antibiotics that select primarily against Gram-positive bacteria (penicillins, cephalosporins, macrolides and lincosamides). (B603.3.w3, B609.2.w2)
FERRETS Note: Suphaquinoxaline is toxic to ferrets. (B626)
  • Treatment is with sulphonamides, for at least two weeks four times daily until clinical signs have stopped. (B626)
  • Pyrimethamine (0.5-0.1 mg/kg per day) plus sulfadiazine (60 mg/100 mL drinking water or 60 mg/100 g in food). These drugs will destroy the tachyzoites, but not the cyst stage. (B626)
  • Suphadiazine at 60 mg/kg per day for four times daily, given for one to two weeks and given a few days after improvement. (B627.16.w16)
  • If treatment is prolonged, folinic acid or folic Acid and bakers yeast should be given as supplements to promote haematopoiesis. (B626, B627.16.w16)
    • Monitoring of bone marrow activity is essential. Haemograms (complete blood cell counts) should be performed before and during treatment. (B627.16.w16)
  • Clindamycin hydrochloride has been used in cats at 25-50 mg/kg per day. This may not kill Toxoplasma gondii, but it stops their replication. (B626)
GREAT APES Recommended treatments based on human dosages: (B22.31.w31g)
  • Sulfadiazine (Sulphonamides) 25-50 mg/kg four times daily, orally, up to 6 g plus Pyrimethamine 2 mg/kg per day orally, up to 100 mg, for three days, then reducing to 1 mg/kg per day, up to 25 mg daily, for four weeks. (B22.31.w31g)
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General Nursing and Surgical Techniques

WATERFOWL --
LAGOMORPHS
Fluids
  • Subcutaneous or intravenous fluids may be necessary in animals where nausea or disorientation preclude oral intake. (B609.2.w2)
Activity
  • Restrict according to the severity of disequilibrium (e.g. avoid slippery surfaces) but encouraging return to activity when it is safely possible, may enhance the recovery of the vestibular function. (B609.2.w2)
Diet
  • It is vital that the rabbit continues to eat during and after the treatment period because otherwise continued anorexia will lead to an exacerbation of gastrointestinal motility disorders leading to further derangement of microflora and overgrowth of the intestinal bacterial pathogens. 
  • Offer the rabbit good quality grass hay and a decent selection of fresh greens. Note: in some rabbits, the addition of leafy greens can result in an exacerbation of the diarrhoea so for these animals only good quality hay should be offered. (B609.2.w2) See: 
  • To encourage oral fluid intake, offer fresh water, wet leafy vegetables or flavour the water with vegetable juice.
  • Syringe feeding is necessary if the rabbit is refusing to eat. 
  • Nasogastric intubation is indicated if the rabbit refuses sufficient volumes of food. 
  • Contraindications:
    • Avoid high carbohydrate or high fat nutritional supplements. (B609.2.w2)

(B609.2.w2)

FERRETS --
GREAT APES --
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Preventative Measures

Vaccination WATERFOWL --
LAGOMORPHS --
FERRETS --
Prophylactic Treatment

WATERFOWL

--
BEARS Pyrimethamine, 5 x 240 mg tablets, given to females for five days. (P5.31.w2)
LAGOMORPHS --
FERRETS --
GREAT APES --
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Environmental and Population Control Measures

General Environment Changes, Cleaning and Disinfection

WATERFOWL

Keep cats away from enclosures and stored feed (J4.205.w1).
BEARS
  • Stray cats were removed from the premises. (P5.31.w2)
  • Meat fed to pregnant females was changed to boiled beef. (P5.31.w2)
  • Fruit and vegetables were stored in a manner ensuring they would not become contaminated. (P5.31.w2)
LAGOMORPHS
  • Keep rabbits separated from cats. (B614.10.w10)
  • Ensure water, food or bedding for lagomorphs are not contaminated with cat faeces. (B602.20.w20, B603.4.w4, B606.13.w13, B609.2.w2, B614.10.w10)
    • Cover feed containers. (B601.11.w11, J15.28.w1)
    • Wash fresh vegetables before feeding. (B603.4.w4, B606.13.w13)
    • Prevent cats from accessing hay stores. (B601.11.w11)
  • Heating and drying will inactivate the oocysts, however most disinfectants will not result in inactivation. (B614.10.w10)
  • Feed rabbits on food which has been processed to at least 66 °C (to kill oocysts). (J495.42.w3)
  • Ensure rabbits are not given access to an environment where cat faeces may have been deposited. (J495.42.w3)
FERRETS
  • If ferrets are housed away from cats, this should reduce the chance of infection via faecal-oral cross-contamination. (B626)
  • Ferrets could be fed indoors or in an outdoor cage, to prevent contamination of their food. (B626)
  • Cat litter trays should be placed high up, this is to prevent ferrets from using the same tray and cross-contamination. (B626)
  • Boarding kennels/catteries should have a separate area for boarding ferrets. (B626)
  • In zoos, ferrets should be housed away from other animals, to reduce the risk of infection. (B627.16.w16)
GREAT APES
  • Good hygiene to prevent access of cats to stored food and bedding, and rodent control to prevent potentially infected rodents being eaten by apes. (V.w5)
Population Control Measures WATERFOWL --

 

LAGOMORPHS --
FERRETS Ideally cat wards should be separate from a ferret ward, to stop cross contamination of Toxoplasma gondii. (B626)
GREAT APES --
Isolation, Quarantine and Screening WATERFOWL --
LAGOMORPHS If toxoplasmosis is present in a rabbit colony then only the seronegative rabbits should be bred from because toxoplasmosis can be transmitted transplacentally. (B614.10.w10)
FERRETS --
GREAT APES --
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