Protozoa- Apicomplexa 3: Toxoplasma & Neospora

Question 1

What are the only definitive hosts of Toxoplasma gondii?

Answer 1

Wild and domestic cats.

Question 2

What are the paratenic/intermediate hosts of T. gondii?

Answer 2

Many mammalian species and birds.

Question 3

T. gondii have _________________ pathogenic importance in cats.

Answer 3

Little, if any.

Question 4

T. gondii have ______________ veterinary and public health importance in their intermediate stage.

Answer 4

Considerable.

Question 5

What does paratenic mean?

Answer 5

Similar to an intermediate host except it is not required for the parasite’s life cycle.

Question 6

Describe the life cycle of T. gondii.

Answer 6

Fecal oocysts are taken in by birds or small mammals and form tissue cysts that infect felines when they feed on their prey.

Can be transmitted to humans in the same way by sheep/pigs and from contaminated food.

Question 7

The spread of T. gondii to humans by sheep/pigs or contaminated food is referred to as what?

Answer 7

Horizontal transmission.

Question 8

The transmission of T. gondii from mother to fetus is referred to as what?

Answer 8

Vertical transmission.

Question 9

What are the characteristics of T. gondii?

Answer 9

• Oocysts have 2 sporocysts with 4 sporozoites each.
• 10-12 mm in diameter.
• Unsopulated when shed.

Question 10

What are the two types of sporozoites in T. gondii?

Answer 10

• Tachyzoites: fast growing; seen in acute infections.
• Brachyzoites: slow growing; cyst forms; seen in chronic infections and remains viable as tissue cysts longer.

Question 11

Most kittens become infected with T. gondii when?

Answer 11

In the first few weeks of life.

Question 12

What happens to the T. gondii once it is ingested by the cat?

Answer 12

Schizogony followed by gametogony in the SI.

Question 13

What is the PPP of T. gondii in the cat?

Answer 13

5-7 days.

Question 14

What aspect of the feline gut promotes gametogony of T. gondii?

Answer 14

Linoleic acid.

Question 15

What is endodyogony?

Answer 15

Proliferation of the tachyzoites within blood cells such as monocytes to produce bradyzoites in the life cycle of T. gondii.

Question 16

What is the major clinical significance of T. gondii?

Answer 16

• Tachyzoites can cross the placenta and infect fetus.
• Causes disruption of pregnancy, congenital infections, or neurological effects.
• Reactivation of infection from bradyzoites to tachyzoites during immunosuppression.

Question 17

Toxoplasmosis in small ruminants is a major cause of what?

Answer 17

Ovine abortion when ewes acquire primary infection during gestation.

Question 18

Describe how the effects of toxoplasmosis in ewes depend on the timing of infection vs the gestational stage.

Answer 18

• Early: resorption of fetus.
• Mid: abortion with obvious placentitis and fetal infection.
• Late: weak lambs with congenital infections.

Question 19

What are the control methods for toxoplasmosis in small ruminants?

Answer 19

Keep environment free of cat feces and carcasses of rodents.

Question 20

How do you diagnose toxoplasmosis in small ruminants?

Answer 20

• Gross and histopathological appearance of the placenta and fetal tissues.
• Molecular detection of T. gondii DNA via PCR.

Question 21

The toxoplasmosis vaccine for small ruminants is based on what?

Answer 21

Parasite strain that does not form tissue cysts called Toxovax; gives acute phase, immune-system reacts and limits infection.

Question 22

When is the Toxoplasmosis vaccine for small ruminants given and why?

Answer 22

Must be before pregnancy because it is a live vaccine.

Question 23

Where is the Toxoplasmosis vaccine for small ruminants not licensed?

Answer 23

Not licensed in the USA.

Question 24

What are the sources of zoonotic toxoplasmosis?

Answer 24

• Undercooked animal products.
• Direct contact with oocysts from cat feces.
• Vegetable matter contaminated with oocysts from cat feces.

Question 25

Describe the prevalence of T. gondii in humans.

Answer 25

- 11% in USA. - 30-50% worldwide. - Higher in vets, animal handlers, and those who consume rare meat.

Question 26

When will you see clinical signs of T. gondii in humans?

Answer 26

- Mild or inapparent in immunocompetent individuals. - Potentially life-threatening in immunocompromised individuals such as transplant recipients. - Primary infection during pregnancy causes fetal death and congenital infection.

Question 27

What are the veterinary public health measures for toxoplasmosis?

Answer 27

- Education and understanding. - Risk during pregnancy; avoid contact with lambing ewes and avoid consumption of undercooked meats. - Wear gloves when gardening. - Keep litter trays clean.

Question 28

In what country do they have antibody titers and serological screening for toxoplasmosis?

Answer 28

France.

Question 29

Toxoplasmosis is thought to be responsible for what behavioral changes?

Answer 29

- Anxiety and predator aversion. - Less likely for humans to avoid extreme sports or dangerous activities.

Question 30

What are the characteristics of N. caninum?

Answer 30

- Canids definitive hosts. - Reproductive impact cows & deer. - No evidence of zoonosis. - Neurotropic tissue cysts.

Question 31

Describe the life cycle of N. caninum.

Answer 31

- Oocysts shed only by canids. - Taken in by intermediate hosts and tissue cysts are formed. - Cysts consumed by canids when they feed on intermediate hosts.

Question 32

Describe the shedding period of N. caninum in dogs.

Answer 32

Brief: oocysts are seldom seen.

Question 33

True or false: only horizontal transmission of N. caninum is seen.

Answer 33

False: vertical and horizontal transmission occur. ## Footnote - Horizontal: puppy to bitch. - Vertical: transplacental.

Question 34

In what types of dogs will you see a higher seroprevalence of N. caninum?

Answer 34

In farm dogs/rural dogs who are more likely to be around cattle, or those housed in large groups.

Question 35

When is infection by N. caninum most commonly seen in dogs?

Answer 35

Young dogs (less than 6 months); infection is commonly not clinically apparent.

Question 36

What are the clinical signs of Neosporosis in dogs?

Answer 36

- Limb paralysis and rigidity. - Progression to paralysis, dysphagia, and mortality. - Cutaneous neosporosis seen in older, immunocompromised dogs that result in nodular lesions with tachyzoites.

Question 37

Why is fecal examination not useful in the diagnosis of neosporosis?

Answer 37

Oocyst shedding precedes clinical signs and the shedding period is very short.

Question 38

How is Neosporosis diagnosed?

Answer 38

Serology for the presence of Ab's and rising use of titers.

Question 39

What is the treatment for neosporosis?

Answer 39

- Clindamycin for 4-8 weeks (7.5-15 mg/kg). - Surveillance and treatment of littermates.

Question 40

What is the prevention for neosporosis?

Answer 40

Reduce feces in environment and access to bovine carcasses or placental material.

Question 41

When do you see endogenous vs exogenous transplacental transmission of neosporosis in cattle?

Answer 41

Endogenous: after recrudescence during pregnancy. Exogenous: after primary infection.

Question 42

Can cows transmit neosporosis in successive pregnancies?

Answer 42

Yes, but they are more likely to the first one after primary infection.

Question 43

Describe the epidemiology of neosporosis in cattle.

Answer 43

Outbreaks, called abortion storms, are followed by endemic steady-state transmission.

Question 44

What are the risk factors for neosporosis in cattle?

Answer 44

- Previous abortions or seropositivity rates in herd. - Farm dogs/wild canids in vicinity. - Placental remains not removed. - Stocking density. - Feed store hygiene (rodents).

Question 45

What are the prevention and control methods for neosporosis in cattle?

Answer 45

- Establish diagnosis by detecting parasites in aborted fetus. - Study herd health epidemiological trends. - Cull seropositive cows and test replacements. - Biosecurity measures via feed and general hygiene.

Question 46

What are the two common 'imposters' of Neoplasma?

Answer 46

- N. hughesi in horses: occasional cause of equine protozoal myeloenchephalomyelitis. - Hammondia heydorni/H. hammondi: tissue-cyst forming apicomplexans that are usually pathogenic in dogs and cats.