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Parasitology > Protozoa - Flagellates > Flashcards

Protozoa - Flagellates Flashcards

1
Q

Flagellate cyst

A

Transmissive stage

Comes from asexual reproduction

Is a vegetative form resistant to unfavourable environment conditions outside of the host

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2
Q

Flagellate trophozoite

A

Parasitic stage

  • active, feeding and motile
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3
Q

Flagellate Promastigote

A

Has a single anterior flagellum

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4
Q

Flagellate Amastigote

A

non-flagellated intracellular stage

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5
Q

Where does replication of Giardia occur?

A

In the intestine -> diarrhoea

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6
Q

How Giardia causes diarrhoea?

A

Disrupts absorption of nutrients -> malabsorption

  • causes immune response
  • extracellular parasite - sits on top of the hosts cells and absorbs glucose from the host
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7
Q

Significance of Giardia

A

Malabsorption and diarrhoea -> reduced growth and reduced cognitive development

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8
Q

Wheres vets come across Giardia?

A

In high populations desities - kennels

Day care centre

Farms (intensive)

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9
Q

Giardia zoonosis?

A

In waterborne outbreaks - Giardia cysts more susceptible to chlorination than Cryptosporidium oocysts

particularly from cattle

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10
Q

Lifecycle of Giardia

A

Cyst shed in faeces -> 24-48 hr for trophozoite to mature -> ingested -> into stomach -> pH changes, CO2 stimulates hatching -> trophozoite ready to go with flagella (suction cup to hold onto intestinal wall) -> asexual replication -> pushed further down GI tract OR immune system attacks it -> encystation process -> forms a cyst -> passed in faeces

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11
Q

Pathogenesis of Giardia

A

Villous atrophy and malabsorption via sheer bulk of numbers

immune response is to completely flush out GI tract -> Gi tract also loses mucous layer

-> IBS post Giardia

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12
Q

Clinical presentation with Giardia

A

Acute/chronic diarrhoea

flatulence

vomiting

Bali belly

OR asymptomatic

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13
Q

Diagnosis of Giardia

A

Faecal smear -> look for cysts

In acute stage may see trophozoite with 2 nuclei and a central spine

  • Zinc sulphate floatation of cysts
  • Giardia SNAP (cysts shedding is intermittent so may need to take a few samples over time)
  • ELISA
  • PCR
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14
Q

What is this?

A

Giardia cyst

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15
Q

Treatment of Giardia

A

Supportive care

Metronidazole (resistance) needs multiple doses for 5-7 days (can cause encephalopathy)

  • Febantel for 3 days
  • Fenbendazole for 5 days
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16
Q

Control of Giradia

A

Hygiene, reduce overcrowding and stress

  • wash diarrhoea with ammonia
  • wash bedding in hot soapy water - dry in sunlight
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17
Q

Trichomonads features

A

Faecal-oral transmission (fresh faeces)

Can be transmitted during sex

No cysts! Trophozoites only

Single nucleus

3-6 anterior fagella with one that forms undulating membrane

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18
Q

Bovine - Tritrichomonas foetus significance

Transmission?

Epidemiology?

A

Infertility and reduced pregnancy

  • sexually transmitted through preseminal fluid (no transmission by AI)
  • Bulls are asymptomatic carriers - survives in folds of penis
  • extensive cattle farms (North QLD) with uncontrolled mating
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19
Q

Tritrichomonas blagurni infects what species?

A

Feline

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20
Q

Significance of Tritrichonomas blagburni

A
  • Large bowl disease with chronic diarrhoea
  • outbreaks in catteries
  • asymptomatic carriers with chronnic shedding
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21
Q
A
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22
Q

Diagnosis of felin tritrichonomas

A

Fresh faecal smear and look for motile trophozoite

Faecal culture - grow trophozoites in anaerobic bag

PCR

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23
Q

Treatment of feline tritrichomoniasis

A
  • off label use of ronidazole (30mg/kg) once daily for 14 days
  • borad spectrum antibiotic -> use probiotic after treatment
  • beware of neurotoxicity
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24
Q

Bovine tritrichomonas replication?

A

Uterine mucosa and causes infertility by disrupting the uterine membrane

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25
Q

Tritrichomonas foetus presentation in a cow

A

mild vaginitis +- discharge, metritis, salpingitis

  • embryonic death and absorption -> return to service
  • early foetus abortion
  • retained foetus -> pyometra
  • abnormal calving
  • cow susceptible to repeat infection with poor immunity
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26
Q

Diagnosis of bovine tritrichomonas

A

Bull sheath wash sample - once a week (3 neg in succession after last service

  • Cow cervical wash following abortion
  • direct microscopy
  • Culture
  • PCR
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27
Q

Control of Bovine Tritrichomoniasis

A
  • Test and cull bulls
  • Replacement virgin heifers and bulls
  • test bulls before coming in
  • good fencing
  • Vaccine reduces severity of infection in cows
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28
Q

Avian Trichomonas causes

A

Canker in pigeons

Frounce in falcons

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29
Q

Causes of trichomoniasis in birds

A

Trichomonas gallinae

30
Q

Site of Trichomonas gallinae

A

Upper digestive tract

nasal cavity -> resp tract

31
Q

Transmission of Trichomonas gallinae

Epidemiology

A
  • through feeding of young
  • contaminated drinking water

Pigeons are asymptomatic carriers

Young, immuncompromised birds susceptible

(poor hygiene, overcrowding and stress all factors)

32
Q

Presentation of trichomonas is birds

A

SQUABS

Stop feeding and lose weight, ruffled and dull, dyspnoea, difficulty swallowing

  • circumscribed caseous plaques on oro-pharynx, oesophagus, crop, proventriculus. Ca form ulcers and abcesses
  • can be localised or systemic
33
Q

Diagnosis of trichomonas in birds

A
  • detect trichomonads
  • scrape/crop fluch
  • Microscopy
  • PCR
  • culture
34
Q

Treatment of trichomonas in birds

A
  • Surgical removal of caseous material
  • Quarantine
  • Ronidazole, metronidazole
  • eliminate carries
35
Q

Cause of enterohepatitis or Blackhead

A

Histomonas melaegridis + E. coli

36
Q

Histomonas melaegridis is most pathogenic in which species?

A

TURKEYS>>>> chickens >> pheasants, ducks and geese

37
Q

Outbreaks of M. melaegridis mortality and morbidity rate

A

80-100%

38
Q

Difference of H. meleagridis to Eimeria in birds

A
  • this spreads out of the GI system and up the bile duct and into the liver -> target lesions
39
Q

Lifecycle of H. meleagridis

A

no cyst stage

Have amastigote that go into the Heterakis worm and passed in the Heterakis egg in the faeces -> egg ingested by paretenic hosts (earthworm) -> bird eats the worm -> infected with Heterakis and Histomonas trophozoites-> replicates in caecum and intestine -> up bile duct -> goes between the liver cells and replicates here to-> causing destruction

40
Q

Presentation of Histomonas is Turkeys

A
  • yellow diarrhoea
  • Necrotising typhlitis
  • thinkening and caseous exudate on caeca

+- peritonitis

Target lesions in liver - maybe also spleen and lungs

41
Q

Diagnosis of Histomonas

A
  • Necropsy - lesions on liver and caecal infection
  • lesion scraping / microscopy Look for trophozoites feeding outside of the cells (to differentiate from Eimeria where you look for intracellular replicating stages)
  • Lesions on histopath
42
Q

Control of Histomonas

A

Control the Nematodes (Heterakis)

Separate chickens and turkeys

Turkeys do cloacal drinking where they squat over another birds faeces and and suck it up their cloaca. Spread the disease.

  • quarantine
  • Management (high stocking density they pass to each other via cloacal sucking (so clean up faeces) but in extensive system have worms -> control worms)
  • strict biosecurity
  • No registered drug. Only use Nitroimidazoles eg ronidazole if not being used for food production
43
Q

What is a Trypomastigote?

A
  • motile, extracellular, flagellum attached via undulating membrane. Kinetoplast posterior to nucleus
44
Q

What is the Amastogote?

A

Kinetoplastid stage that is intracellular, has no flagella, has asexual binary fission. Kinetoplast anterior to nucleus

45
Q

What is the Epimastigote

A

extracellular, motile. Kinetoplast centrally located just anterior to nucleus, flagellum

46
Q

What is a promastigote?

A

Extracellular motile. Kinetoplast anterior to nucleus, flagellum

47
Q

Trypanosoma Features

A

Not in Aus

Old world - African sleeping sickness (anaemia->chronic fatigue)

New world - Chagas disease

100s of millions of people infected

48
Q

Trypanosomiasis 3 Groups

disease caused and vector/transmission

A

Salivaria (sleeping sickness: Tsetse fly)

Stercoraria (chagas disease: Triatoma)

Mechanica (Dourine via coitus)

49
Q

Salivaria pathogenesis

A

Replicate in blood -> anaemia feeding intercellularly on the serum

Taking glucose from the bloodstream

Systemic disease, fever, lethargy

  • wasting and organ failure
50
Q

Pathogenesis of Stercoraria

A

Transmitted in the faeces of the vector. Tratoma come out at night and bite the corners of peoples eyes and feed on blood and are also daefecating into to eye -> inflammation (intracellular)

51
Q

Mechanica pathogenesis

A

Sexually transmited

52
Q

Important Trypanosomes

A

T. brucei brucei (domestic animals)

T. brucei rhodesiense (humans)

T. b gambiense (humans + pigs)

T. evansi (bovine, equine, camels, dogs)

53
Q
A
54
Q

Salivary tryanosomiasis life cycle

A
55
Q

African trypanosomiasia features

A

Sleeping sickness in humans

Tse tse fly

increased decreased 70%

causes Nagana in animals

56
Q

Presentation of Salivarian trypanosomiasis in animals

A
  • fever
  • can evade immune system by changing its surface antigens
  • lymph node enlargement
  • splenomegaly
  • anaemia and lethargy
  • oedema
  • wasting - starvation of glucose

Neurological due to sugar starvation

57
Q

Diagnosis of African trypanosomiasis

A

Blood smear - see spindly flagella tail and wavy curtain with dark staining nucleus

smear of CSF

  • agglutination tests
  • ELISA
  • PCR
58
Q

Treatment of salivarian trypanosomiasis

A

Humans:

Pentamidine

Nifurtimox and eflornithine

Melarsoprol (arsenic - 10% die from the drug)

Animals:

Diminazine, Homidium bromide

59
Q

Control of salivary trypanosomiasis

A

Release of sterile males

Trypano-tolarant cattle

Test and treat

Drugs

60
Q

Stercoraria trypanosomiases life cycle

A

In blood and into muscles as amastogote still - replicating (in heart muscle)

61
Q

Trypanosoma cruzi (chagas disease) problems

A

Have affinity for cardiac muscle -> heart failure

Hard to get to to treat

62
Q

Leishmania epidemiology

A
  • not endemic in Aus
  • Mediterranean region

affects humans and animals

100s of millions infected

63
Q

Three main forms of leishmaniasis

A

Cutaneous

Muci-cutaneous

Visceral (hepato-splenomegaly, anaemia, oedema)

64
Q

Lifecycle of Leishmania

A

Replicate in white blood cells. Which cause WBCs to rupture -> massive inflammation.

65
Q

Leishmania species

A

Many many species

Old and new world species

L. infantum (dogs)

L. donovani

L. major

66
Q

Features of visceral leishmaniasis

A

Healthy person: asymptomatic or mild infections

Young, old or immunocompromised: 85% fatality rate withour treatment

0-50% with treatment

Replication in and around the viscera. Mostly white blood cells.

  • > fever, hepato-splenomegaly and pancytopenia
  • liver failure, bleeding, anaemia, secondary infections
67
Q

Cutaneous leishmaniasis

A

Localised nodulo-ulcerative lesion

  • 1.5 mill new cases annually
  • if left untreated may become diffuse with invasion of mucosa and cartilages
68
Q

Infantile leishmaniasis

A

Leishmania infantum

Visceral and cutaneous leishmaniosis.

Dogs are primary reservoir but it is zoonotic

  • non specific dermatitis
  • signs of visceraldisease
69
Q

Leishmania diagnosis

A

Blood smear-amastigotes in WBCs

lymph node aspiration

impression smear of lesion

PCR

Serology

70
Q

Control of leishmania

A

Vector and reservoir control

  • repellents
  • Commercial canine vaccines (80% efficacious)

Hard to treat dogs - Drugs need lots of doses. Drugs are nasty Antimonials.

all you are doing in decreasing the clinical signs

Parasitology (30 decks)

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