protozoan parasites with indirect life cycles Flashcards

1
Q

what is a sarcicystidae?

A

○ Phylum apicomplexa
○ Similar to eimeria but have indirect life cycles
○ Asexual stages occur in intermediate hosts
○ Asexual and sexual stages occur in definitive hosts
-Examples- toxoplasma, neospora, sarcocystitis

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2
Q

what is toxoplasma gondii?

A

-Apicomplexan protozoan parasite that infects most species of warm blooded animals, including humans, causing the disease toxoplasmosis
-Cat family (felidae) are the only known definitive hosts for the sexual stages to T.gondii and thus are the main reservoirs of infection
-toxoplasmosis in an important cause of abortion and foetal abnormality in humans, sheep and goats
-Also causes significant infections in immunocompromised humans e.g. In HIV/AIDs
-Important zoonosis

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3
Q

what is the definitive and Intermediate hosts of toxoplasma gondii life cycle?

A

Definitive hosts
-domestic cat
-other felids

Intermediate Hosts
-rodents
-birds

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4
Q

what happens in the life cycle of toxoplasma gondii?

A

-The parasite multiplies within the intestine of difinitive host cats and following the sexual cycle of gametology, oocysts are shed in the cats faeces
-Oocysts sporelate in and contaminate the environment and infect intermediate hosts which inadvertantly consumed them
-Within these intermediate hosts, the parasites migrate widely and form tissue cysts which are infective for cats which predate the intermediate hosts

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5
Q

what are the accidental hosts of toxoplasma gondii?

A

-sheep
-pigs
-other mammals
-humans

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6
Q

how can humans be accidental hosts?

A

-inadvertently consume oocysts contaminating food or drinking water or by handling litter trays with insufficient hand hygiene
-may be infected by consuming cysts in tissues of raw or undercooked meat of sheep and pigs

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7
Q

what is the life cycle of cats, the definitive hosts of toxoplasma gondii?

A

-generally become infected by ingesting infected mammals or birds
-shed oocysts which become infectious to most mammals or birds
-most commonly infected as kittens
-shed large numbers of oocysts
-but only for 1-2 weeks
-develop immunity

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8
Q

immediate and accidental hosts are infected by?

A

-sporulated oocysts- sporulate in 1-5 days
-carnivorism/omnivorism or
-transplacentally- most important in humans, sheep and goats

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9
Q

what are tachyzoites?

A

-rapidly multiplying crescent shaped in the development of an acute tissue phase of infection

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10
Q

what are bradyzoites?

A

-slow-growing, comma-shaped forms
-found in clusters with cysts in the tissues
-chiefly muscles and th brain, in chronic (latent) toxoplasmosis

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11
Q

how do tachyzoites move?

A

-Gliding, flexing, undulating and rotating
-no externally visible means of locomotion such as cilia, flagella or pseudopodia
-motion affected by apical complex

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12
Q

what is the lytic cycle of tachyzoites?

A

-enter host cells by actively penetrating cell membrane, or by phagocytosis
-multiply asexually repeatedly within host cells
-two progeny form within and consume the parent parasite: endodyogeny
-host cell ruptures when it can no longer support the growth of tachyzoites

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13
Q

What is the endodyogeny cycle??

A
  1. two inner membrane complexes develop in middle of cell from rudimentary conoid and microtubule organising centre
  2. nucleus and mitochondria divide into membranous outlines
  3. nascent apical organelles divide and inner membrane complex from mother dissociated
  4. cleavage furrow
  5. division continues to posterior end
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14
Q

what occurs in the development of bradyzoites?

A

-multiply asexually within host cells by repeated endodyogeny
-tissue cysts appear 7-10 days post-infection
-contain hundreds of brazyzoites
-within host cell cytoplasm
-cyst wall
-quiescence

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15
Q

what is the cyst (pseudocyst) wall?

A

-composed of host cell and parasite materials
-resistance to digestion by gastric juice
–> protection from host immune response

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16
Q

what does the immune response normally prevent?

A

dissemination of tachyzoites

17
Q

how do cats acquire toxoplasma by ingesting infected intermediate hosts?

A

-ingest quiescent bradyzoites occupying tissue cysts
-ingest rapidly multiplying tachyzoites in recently infected intermediate hosts

18
Q

what happens to oocysts once ingested by the feline definitive host?

A

-excreted unsporulated in the faeces
-sporulates to become infectious 1-5 days after excretion

19
Q

what is toxoplasmosis like in sheep and goats?

A

-acute phase rarely observed
-affects non immune pregnant females
-clinical signs are dependent on the stage of pregnancy

20
Q

what are the signs of toxoplasmosis in sheeps and goats in the early, mid and late stage of gestation
abortion- barren ewe
abortion, lesions in cotyledons of placenta and foetus or mummification of dead foetus
still born or weak lambs

A

Early - abortion- barren ewe
Mid - abortion, lesions in cotyledons of placenta and foetus or mummification of dead foetus
Late - still born or weak lambs

21
Q

what are the appearances of toxoplasmosis in sheep and goats?

A

-grossly the placental cotyledons have characteristic 1-2mm white or yellow focal lesions

22
Q

what is infection of toxoplasmosis in humans acquired by?

A

-Eating raw or undercooked meat
-Unpateruased dairy products
-ingestion of occysts

23
Q

what does infection of toxoplasmosis in humans result in?

A

-Acute phase–>flu-like illness
-Congeintal infection–> risk of abortion, foetal abnormality
-Reactivation of cysts possible in highly immunosuppressed individuals

24
Q

what are the signs of severe toxoplasmosis?

A

-Acute or reactivated toxoplasma infection
-Damage to brain, eyes or other organs
-More likely in immunocompromised individuals
-Very young, very old, HIV/AIDS, immunosuppressive therapy

25
Q

what is neospora canium?

A

○ An emerging and now widepread cause of abortion in cattle, that has many similarities to toxoplasmosis, but with a canine definitive host
Identifies in 1984 as a cause of bovine abortion and neonatal death in cattle which acts as intermediate hosts

26
Q

what are the definitive hosts of neospora canium?

A

dogs, producing oocysts

27
Q

how does neosporosis present in the dog?

A

-Puppies and dogs <1 year old
-Myositis
-Encephalomyelitis- Paralysis

28
Q

how does neosporosis cause abortions in cattle?

A

Repeat abortions
Returns to service

29
Q

what are congenitally infected claves with neosporosis like?

A

-Still born, weak or apparently normal
-Vertical transmission: heifers may abort during first pregnancy

30
Q

what is the life cycle of neospora cranium in cows?

A

-Canines infected by consuming tissues from cattle especially placenta
-After asexual and sexual development cycles, dogs pass oocysts in faeces which sporulate and contaminate environment, exposing cattle to risk of ingesting
-Other animals may also act as intermediate hosts
-Cattle may abort hteir calves and release placentas that may be eaten by dogs, completing the life cycle

31
Q

what is the exogenous transplacental transmission of neospora in cattle?

A

-infections resulting from ingestion of sporulated oocysts
-involved dog defintive host
-new infection of naive herds

32
Q

what is the endogenous transplacental transmission of neospora in cattle?

A

-infections resulting frmo reactivation of bradyzoites during pregnancy
-principle route of infection of cattle
-does not involve dog definitive host
-maintenance of infection in endemic herds

33
Q

what is sarcocystitis?

A

-A genus of protozoa with indirect life-cycles, infecting mammals, birds and reptiles
-The carnivore definitive hosts have asymptomatic gut infections while their herbivore prey, the intermediate hosts, have cysts in muscle and other tissues that may lead to clinical signs

34
Q

what is the sarcocystis life cycle?

A
  1. Definitive host carnivores are infected by ingestion of bradyzoites within sarcoses, which penetrate lamina propria of small intestine
  2. Immediately undergo gametogeny to produce oocysts which sporulate before being passed in faeces
  3. Sporulated oocysts are more fragile than those of eimeria, toxoplasma or neospora
  4. Sporocysts released into environment where may be ingested by intermediate hosts
  5. Initial asexual multiplication takes place within endothelial cells of intermediate hosts followed by development of tissue cysts in striated muscle cells which contain bradyzoites surrounded by thick outer wall known as sarcocysts
  6. These are consumed by definitive host carnivores
35
Q

what is equine protozoal myeloencephalitis?

A

-First recognised in 1995
-Neurological problem in horses in USA
-Caudal ataxia and weakness
-Sarcocystitis neurona
-Sarcocysts develop in equine CNS
Natural cycle= Opossum<–>birds/racoon/skunk/armadillo
-Horse is accidental or ‘dead end’ host

36
Q

What is Besnoitia besnoiti features

A
  • Widespread in africa but spreading into europe
  • Clinically affects cattle, goats
37
Q

What is Besnoitia bennetti features

A

Affects IH horses, donkeys, mules and zebras
- reported in UK donkeys

38
Q

What are clinical signs of Besnoitia

A

causes subcutaneous oedema with tachyzite replication in vascular endothelial cells
Brasyzoites form firm nodules - sclera of eye can dx

39
Q

What are clinical signs of Besnoitia in cattle

A

Skin and hoof lesions
Vulvitis, vaginitis, orchitis causing infertility