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PARASITOLOGY - 2 > 3b – Cattle and Sheep Protozoa II > Flashcards

3b – Cattle and Sheep Protozoa II Flashcards

1
Q

What is the distribution of Cryptosporidium sp.?

A
  • World wide
  • *zoonotic potential
  • Many hosts susceptible including livestock and people
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2
Q

What is the big difference in morphology and life cycle of Cryptosporidium compared to coccidia?

A
  • Intracellular, but INFECTS MICROVILLI BRUSH BORDER
  • OOCYSTS are IMMEDIATELY infective and very resistant to environmental conditions
    o Sporogony happens INSIDE the host
  • Infections can be subclinical or cause diarrhea varying in severity
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3
Q

What is the most common cause of human cryptosporidiosis?

A
  • Ingestion of contaminated water and food
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4
Q

Which animals does C. parvum usually affect?

A
  • Calves as early as 2 days of age
  • *zoonotic
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5
Q

Which animals does C. andersoni usually affect?

A
  • Post-weaned calves
  • Adults
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6
Q

How do animals acquire Cryptosporidiosis?

A
  • Ingestion of contaminated feed
  • Water
  • Grooming
  • *auto infection is possible
    o Can be serious in immunocompromised individuals
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7
Q

Cryptosporidium life cycle

A
  • Parasitic development within the microvilli of luminal surface of enterocytes
  • 2 cycles of asexual reproduction (merogony) followed by sexual reproduction (gametogony)
  • **Oocyst are sporulated and infective when passed in feces of host
    o Thick walled=leave host and infect other animals following ingestion
    o Thin-walled=hatch within intestine and establish autoinfection
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8
Q

What is cryptosporidiosis cause in neonates? What is the infective dose?

A
  • Neonatal diarrhea
    o Almost 100% prevalence: million of oocysts/gram of feces
  • *LOW infectious dose (1 oocyst)
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9
Q

What are the clinical signs of Cryptosporidiosis?

A
  • Malabsorptive diarrhea
    o Yellow, pasty, profuse
  • Depression
  • Anorexia
  • Abdominal pain
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10
Q

Malabsorptive diarrhea

A
  • Yellow pasty and profuse
  • Usually self-limited
    o May have high mortality in NAÏVE herds
  • Epithelial cell damage affects nutrient absorption and fluid transport in gut
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11
Q

What are the clinical signs of C. andersoni?

A
  • Gastroenteritis
  • Production losses (reduced milk production)
  • Present in ~10% of adult cattle ABOMASAL GLANDS
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12
Q

How do you diagnosis cryptosporidium?

A
  • Detection of oocysts in feces
    o Multiple fecal samples over 2-3 interval days
    o Centrifugal flotations (Sheather’s sugar solution)
    o Fecal smears (acid-fast stain)
  • *Immunoflurescent staining: cyst antigen
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13
Q

What is the size of cryptosporidium oocysts?

A
  • Small! (4-8 micrometres)
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14
Q

How do you treat cryptosporidium?

A
  • NONE labelled
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15
Q

How can do sanitation for cryptosporidium?

A
  • Steam clean
  • Disinfectants
  • *resistance to chlorine
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16
Q

What is supportive care for cryptosporidium?

A
  • Hydration
  • Ensure colostrum
17
Q

What are the examples of apicomplex with a tissue cyst forming, indirect life cycle?

A
  • Sarcocystis
  • Neospora: cattle
  • Toxoplasma: sheep
18
Q

Sarcocystis: 2 stages

A
  • Sporulated sporocysts: in feces of DH=immediately infective
  • Sarcocysts with bradyzoites in tissues=infective stage for carnivores
19
Q

What is the life cycle of Sarcocystis?

A
  • Carnivore DH: sexual reproduction (gametogony) in SI with SPOROGONY
  • Sporocysts with 4 sporozoites=immediately infective
  • Ingested by herbivore IH (will NOT shed eggs)
    o Asexual reproduction (merogony) in vascular endothelium, enter striated muscle/nervous cells
  • Sarcocysts with bradyzoites in IH can be ingested by DH carnivore
20
Q

Where are the 2 areas you can INTERUPT the Sarcocystis life cycle?

A
  • Prevent fecal contamination of cattle feed
  • Cook meat feed to dogs or do not feed them it
21
Q

What are the acute clinical syndromes with S. cruzi=bovicannis?

A
  • *Dalmeny disease
  • Caused by merogony in vascular endothelium
  • Fever
  • Emaciation
  • Anemia
  • ABORTION
  • Rarely CNS signs
  • *high morbidity and mortality
22
Q

What are the chronic clinical syndromes with S. bovis=eosiophilc myositis?

A
  • Post-mortem diagnosis, incidental finding
  • Greenish focal stripes in skeletal muscle
  • Breakdown of Sarcocystis inducing immune response
23
Q

How do you diagnosis Sarcocystis?

A
  • Post-mortem: incidental finding
  • Abortus: histology and IHC, PCR
24
Q

How do you control Sarcocystis?

A
  • Prevent dog from eating abortuses, dead stock or raw meat
  • Keep feed away from wild and domestic canids and felids
  • NO treatment
  • NO need to cull aborting cows
    o No problem with future pregnancies
25
Q

What is the most important cause of bovine apportion in Canadian cattle?

A
  • Neospora caninum
26
Q

What is the lifecycle of Neospora canium?

A
  • Canid DH: intestinal merogony and gametogony
  • Unsporulated oocysts in environment
  • Sporogony in environment to sporulated oocysts
  • Cattle IH: extraintestinal merogony (asexual reproduction)
    o Tissue cyst with bradyzoites
    o Tachyzoites in abortus
    o Tachyzoites in congenitally infected calf=problem for own offspring
27
Q

What happens if pregnant cattle is infected with Neospora in various stages of pregnancy?

A
  • Early: death
  • Mid: abortion
  • Late: infected, but clinically normal=infect their own offspring
  • *infected cattle MAY have problems with subsequent pregnancies
28
Q

Endemic abortion (endogenous): Neospora in cattle

A
  • Recrudescence (recurrence) of chronic infection
29
Q

Epidemic abortion (exogenous): Neospora in cattle

A
  • Acute infection following ingestion of sporulated oocysts
  • *abortion storms
30
Q

How do you diagnosis neospora in cattle?

A
  • Clinical and epidemiological
  • Serology: ELISA titres
  • Abortus: CNS/muscle histology and IHC, PCR
31
Q

How do you control neospora in cattle?

A
  • Prevent dogs from eating abortuses, dead cattle, raw
  • Keep cattle feed and water from wild canids and dogs
  • Do NOT breed seropositive cattle (CULL)
32
Q

What is Toxoplasma gondii relevant in?

A
  • Sheep and goats
  • *abortions STORMS in naïve animals
33
Q

The outcome of Toxoplasma gondii depends on time of infection

A
  • Early: fetal death and resorption
  • Mid: abortion or stillborn
  • Late: weak or normal lambs
34
Q

What is the life cycle of Toxoplasma gondii

A
  • DH: cat (merogony and gametogony)
  • Environment oocysts undergoes sporulation
  • IH: tachyzoites
    o Prenatal infection and abortion can occur
    o Tissue cysts with bradyzoites
  • *humans can eat sporulated oocysts or eat tissue cysts with bradyzoites
35
Q

What are the indirect methods for diagnosing Toxoplasma?

A
  • Serolgoy
    o IgG: chronic
    o IgM: acute
36
Q

What are the direct methods for diagnosing Toxoplasma?

A
  • Gross pathology
  • Histology
  • Microscopy
  • Isolation from blood or body fluids
  • Histology/IHC
  • PCR
37
Q

How do you control Toxoplasma gondii?

A
  • *regional variation in seroprevalence in sheep (20-100%)
  • Prevent access of cats to sheep feed
  • Vaccines have been developed, but not widespread
38
Q

How can you prevent zoonotic transmission of Toxoplasma gondii?

A
  • Hand washing after handling aborted or stillborn fetuses
  • *cook lamb and mutton to 70 degree C or freeze at -20 degree C for at least 3 days

PARASITOLOGY - 2 (13 decks)

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