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DVM 2 - 2 > Parasitology PROTIST 2 > Flashcards

Parasitology PROTIST 2 Flashcards

1
Q

Trichomonads what type of lifecycle, transmission and what is difference

A
  • Simple direct life cycle
  • Faecal-oral (close contact, wet environment) FELINE and venereal transmission CATTLE
  • No cysts – trophozoites only - need to be ingested quickly in the environment
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2
Q

Bovine Trichomoniasis what is the major significance and when most of the issue

A 
- Infertility – Trichomonas foetus 
○ (inflammation in the uterine layer of the cow)
○ various strains
○ STDs - carrier bull to female 
○ If AI -> NO TRANSMISSION 
○ reduced pregnancy rate - economic loss
Most common in:
- Extensive cattle farms (North)
○ uncontrolled mating
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3
Q

What is the main species involved in Bovine Trichomoniasis, how transmitted, main issues and where endemic

A
  • Agent: Tritrichomonas foetus
  • Venereal disease
    ○ STD – mating / coitus
    ○ ± iatrogenic
  • Infertility and early embryonic death
  • Costs to endemic herd
    ○ Culling, replacement herd, vet fees etc.
    Endemic in the NT extensive cattle farming –uncontrolled mating
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4
Q

Bovine Trichomoniasis what is the presentation in the bull and location

A
  • Infected bull – asymptomatic
  • Organism in microscopic folds of penis and prepuce
  • Permanent carriers of disease
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5
Q

Bovine Trichomoniasis what is the presentation in teh cow

A 
- Self-limiting infection –cows become clear in 95 days
○ Mild vaginitis ± discharge, metritis, salpingitis
○ Embryonic death and absorption
§ Return to service
○ Early abortion of foetus
○ Retained foetus - pyometra
○ Or normal calving
- COW SUSCEPTIBLE TO REPEAT INFECTION
○ Poor immunity
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6
Q

Bovine Trichomoniasis what is the presentation in the herd

A
  • High rate of return to service (20-40%)
  • Abortions (2-3 months old foetuses)
  • Long, strung-out calving
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7
Q

List 5 diagnositc techniques for Bovine Trichomoniasis

A 
1) Bull sheath wash sample: (need to sedate first) 
○ once per week, 3 successive negatives at least 2 weeks after last service
-allows build-up of organisms better Se
2) Cow cervical wash following abortion
3) Direct microscopy
4) Culture (In-PouchTM)
○ Look for trophozoites 
5) Direct PCR
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8
Q

Control and treatment of Bovine Trichomoniasis

A
  • Test and cull bulls
  • Notifiable disease
  • No approved, effective treatment or vaccine in Australia
  • Therefore need to use management strategies
    ○ Replacement virgin heifers and bulls
    ○ Pre-entry test bulls
    ○ Artificial insemination - doesn’t contain trophozoites in this case
    ○ Good fencing - prevent natural breeding
  • Vaccination (TrichGuard®) only reduces severity (not Aus)
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9
Q

Feline intestinal trichomoniasis what is the species involved, transmission what are 5 characteristics of infection

A

T. blagburni nov. spp. (different to the cattle one
Transmission via faecal-oral route (cat-cat)
Typically:
- Large bowel diarrhoea
- Waxes and wanes
- Chronic diarrhoea (weeks) cats up to 2 years of age
- Cattery outbreaks
- Asymptomatic shedding common

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10
Q

Feline intestinal trichomoniasis diagnosis and treatment

A

Diagnosis
- Fresh faecal smear for motile trophozoite
○ DO NOT PRODUCE CYSTS
- Faecal culture (In Pouch TF, Biomed Diagnostics) – 12 days!
- PCR (Gribbles)
- Great way to collect rectal sample from cat!
○ Link: Colon Flush Cat
Treatment:
- Off label ronidazole 30 mg / kg once daily for 14 days + probiotic
- Variable success – relapse common
- Caution: neurotoxicity!

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11
Q

Avian trichomoniasis what are the diseases it causes in pigeons and falcons, species involved and the host

A
  • CANKER in pigeons
  • FROUNCE in falcons
    ○BOTH Cheesy abscess in upper digestive tract and nasal cavity of the bird
    § Decrease respiration and ability to feed
  • Trichomonas gallinae
  • Affects pigeons, budgerigars, backyard poultry and raptorial birds
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12
Q

Avian trichomoniasis what are the 3 mechanisms of transmission and what are risk factors

A

1) Infected parent feeding young “pigeon milk”
2) Contaminated drinking water
○ Pigeons asymptomatic carriers
○ Source for domestic birds
3) Prey meal for another bird (raptors most commonly)
Risk factors
- Young, immunocompromised birds
○ Circovirus
○ Poor hygiene, overcrowding, stress

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13
Q

What is the presentation of avian trichomoniasis and when worse

A

SQUABS’ = symptomatic
- Stops feeding, lose weight, ruffled and dull, dyspnoea, difficulty swallowing
- Circumscribed caseous plaques oro-pharynx, oesophagous, crop, proventriculus
○ Ulceration, abcessation
○ Localized and systemic (invasive) forms
Worse when
- Young and immunocompromised

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14
Q

What is the diagnosis and treatment/control of avian trichomoniasis

A

Diagnosis
- Detection of trichomonads
○ scrape / crop flush
○ Microscopy, PCR or culture (In- Pouch-TF®)*
Treatment and control
- Quarantine
- Surgical removal of caseous material
- Ronidazole (compound of choice), metronidazole
- Eliminate carriers
○ Important for aviaries with multiple birds - need to remove the carrier

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15
Q

Histomoniasis what is the main significance and what species occurs with

A
  • Enterohepatitis or Blackhead
    ○ Target lesions on the liver
    ○ Leads to hepatitis, reduction in circulation
  • Histomonas meleagridis + coinfection with E. coli
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16
Q

Histomoniasis what is the pathogensis in different species, mortality and when most vunerable

A
  • TURKEYS»> chickens»pheasants and other game birds (ducks, geese)
  • Outbreaks may lead to high morbidity and mortality (80-100%)
  • Young turkeys are the most vulnerable and severely affected
    ○ Up to 14 weeks of age
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17
Q

Histomoniasis what are the 5 steps in the lifecycle including the 3 ways of transmission

A
  1. TRANSMISSION
    - Co-transmitted with gastrointestinal worm (Heterakis)
    ○ When present and secreting eggs Histomonas can penetrate the worm and move into the eggs within (can last here for <2years)
    OR
    - Through paratenic host (worm) which is ingested (can last here for <2years)
    OR
    - Cloacal drinking -> turkeys will suck faces with their cloaca
    ○ One reason more susceptible to infection
  2. Eggs ingested by susceptible animal
  3. Proliferation trophozoites
    - Haemorrhaging into intestines
  4. Spread to liver - hepatitis, lesions -> liver failure
  5. Back into intestines and transmitted as above
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18
Q

Histomoniasis what is the presentation in chickens and turkeys

A

CHICKENS = mainly act as reservoir
○ Can get disease but not common
- Turkeys:
○ Localized form (caeca) – necrotising typhlitis
§ Mustard diarrhoea
§ Thickening and caseous exudate ceca
§ ± peritonitis
○ Systemic form – enters circulation -> liver, spleen, lung
‘target’ lesions – focal necrosis -> peripheral extension

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19
Q

What are the 3 diagnosis techniques for Histomoniasis

A
  • Necropsy: lesions pathognomonic
  • Lesion scrapings / microscopy
  • Lesion fixed sections – histopathology
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20
Q

Control/ treatment strategies for histomoniasis list 6

A

1) Anthelmintic control (Heterakis) - transport worm
2) Separate chickens / turkeys
3) Quarantine
4) Management (intensive v free-range)
○ Slatted flooring better for blocking transmission
5) Strict on-farm biosecurity
○ Prevent introduction
6) Drugs not registered
○ Nitroimidazoles such as ronidazole, ipronidazole for non-food producing birds only!

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21
Q

List and describe the 4 Kinetoplastids morphology

A

1) Trypomastigote – motile, extracellular, flagellum attached via undulating membrane. Kinetoplast posterior to nucleus.
2) Amastogote – intracellular, no flagella, asexual binary fission. Kinetoplast anterior to nucleus.
3) Epimastigote – extracellular, motile. Kinetoplast centrally located just anterior to nucleus, flagellum.
4) Promastigote – extracellular motile. Kinetoplast anterior to nucleus,

22
Q

Trypanosoma what disease does it cause, where present in the world, hosts and list the 3 different types

A
  • trypanosomiasis
  • NOT IN AUSTRALIA
    -> subtropical/tropical regions - New and Old world species
  • HOST: humans and animals
    3 groups
    1) Salivaria trypanosomiasis
    2) Stercoraria trypanosomiasis
    3) Mechanical trypanosomiasis
23
Q

Salivaria Trypanosomiasis what is the disease called in animals and humans, what transmitted by and main clinical signs

A 
§ Nagana (cows, goats, pigs, horses, etc)
§ African sleeping sickness (humans)
- Tsetse fly 
§ systemic disease, fever, lethargy
§ wasting / organ failure
24
Q

Salivaria Trypanosomiasis what are the 6 general steps in the lifecycle and where/what disease process occurs

A
  1. Tsetse fly bites and injects into bloodstream
  2. Extracellular form (Trypomastigote) within the blood stream
  3. Replicate via binary fission -> causes disease
    - Take up plasma -> mainly glucose
    ○ Leads to hypoglycaemia -> starvation of organ tissues, lethargy
    - Can spread to the lymph and other organs in high infections
  4. Trypomastigotes are taken up by bite of the Tsetse fly
  5. Asexual replication in Tsetse fly forming Epimastigote
  6. Epimastigote replicated in salivary gland of the Tsetse fly forming trypomastigotes
25
Q

Stercoraria trypanosomiasis what is the disease called, vector how transmitted, where replicate, main clinical signs and intra or extracellular

A 
Chagas disease; 
VECTOR - Triatoma (kissing bug)
§ Spread through faeces and replicates in muscles 
§ Chagoma (inflammation)
§ Systemic disease / organ failure
§ Intracellular (pseuodcysts)
26
Q

Mechanical trypansomiasis what is the disease called, how transmitted, main host, and clinical signs

A 
Dourine 
§ Mainly sexually transmitted 
§ Affects equids
§ Genital swelling / mucoid discharge
§ chronic infection (wasting / fever / death)
27
Q

What is the other name for African tyrpanosomiasis and how effective is control

A
  • Sleeping Sickness in humans
  • Targeted for elimination by 2020, WHO
  • Incidence decreased 70% since 2000 – present
28
Q

Saliva trypanosomiasis what is the main effect and list 7 clinical signs

A

Robbed of nutrients leads to the main clinical signs

  1. Fever (cyclical)
  2. Lymph node enlargement
  3. Splenomegaly
    - Filtering out the trypanosomes -> leading to enlargement
  4. Anaemia, lethargy
  5. Oedema
  6. Wasting
  7. Neurological (cf. rabies), cardiac, digestive signs, death
    - Look like rabies due to replication within the brain - uncommon
29
Q

List 5 diagnosis techniques for salivary trypanosomiasis

A
  1. Detection of parasite in chancre, blood or CSF (chronic forms may be aparasitaemic)
  2. Thin and thick blood smears
  3. Concentration tests
  4. Detection of antibody in ELISA, card agglutination test (IgM)
  5. Molecular
30
Q

List 4 treatment and control options for salivary trypanosomiasis

A
  1. Release of sterile male flies
  2. Trypano-tolerant cattle (N’Dana)
    - Breed for these cattle
  3. Test and treat (early before BBB crossed)
  4. Drugs – arsenicals, anti-neoplastics
    ○ Nasty -> 1 n 10 people treated by these drugs will die from the drug itself
31
Q

List 1 and 3 drugs for animals and humans respectively to control trypanosomiasis

A 
Animals:
- Diminazine
Humans:
- Pentamidine
- Nifurtimox and eflornithine
- Melarsoprol (late stages – 10% die drug)
32
Q

Sterocoraria trypanosomiasis what are the 8 steps in the lifecycle

A
  1. Triatoma bug bites a human (corner of eye), sucks blood and poos (transmit trypomastigotes)
  2. Trypomastigotes penetrate cells at bite site -> inflammation and enlargement
  3. Trypomastigotes replicate into amastigotes which multiply via binary fission
  4. Amastigotes transform into trypomastigotes burst from the cells and invade other cells
  5. They also move through the blood stream and undergo the same cycle with other cells
    ○ Mainly muscles cells - especially the heart
  6. Replicate within cells as amastigotes resulting in destruction of heart tissues
    ○ Enlarged heart -> congestive heart failure -> terminal
  7. Trypomastigote within blood taken up by bug
  8. Replication within the gut of the bug forming epimastigotes then trypomastigotes before transmitted back into human
33
Q

Trypanosoma cruzi what disease does it cause, what transmitted by and clinical signs

A

Chagas Disease - Sterocoraria typanosomiasis

  • Transmitted by a chinch that feeds on blood
  • Fever, shivering, tiredness, mild cases are asymptomatic
  • Swollen eyes and possible lesions on the skin called chagoma
34
Q

Leishmania what disease does it cause, where found in the world and why significant

A 
Leishmaniasis
- NOT ENDEMIC IN AUSTRALIA* (but is found in kangaroos) 
○ tropical / subtropical
○ Mediterranean region
○ New v Old World species
Significance ->Affects humans and animals
○ zoonotic
○ 100s of millions infected
35
Q

What are the 3 main types of Leishmaniasis and give an example of one species and disease it causes

A 
Some species can move between the types and cause more than 1 type
1. Cutaneous]
○ Weepy crusty lesions on the skin 
2. Muco-cutaneous
3. Visceral (e.g. L. donovani -> Kala-azar
○ hepato-splenomegaly
○ anaemia
○ oedema
36
Q

What are the 5 steps in the general lifecycle of Leishmania, what leads to disease and transmitted by

A

Transmitted by blood-sucking sandflies (Phlebotomus - old world, Lutzomyia - new world)
1. Amastigotes (within macrophages) ingested by vector during feeding transform in mid or hindgut to promastigotes which undergo binary fission
2. Sandfly takes blood meal results in promastigote stage injected into host blood stream
3. Promastigotes are phagocytised by macrophages
4. Replicates within macrophages as amastigotes
○ Becomes paralysed cells -> macrophages can no longer function
§ Immunosuppressive organism
5. Will rupture where can replicate within more macrophages
- OR taken up by sandfly

37
Q

What are 3 types of Leishamaniasis, species involved and distrubution

A

1) Old world cutaneous Leishmaniasis (Zoonotic) -> L. major -> Africa
2) New world Cutaneous Leishmaniasis -> L. mexicana -> Mexico
3) Visceral Leishmaniasis -> L. chagasl -> mexico

38
Q

Visceral leishmaniasis what occurs in healthy vs young/old/immuno-suppressed population, what stage main issue and clinical signs from this

A
  • In healthy populations:
    ○ Asymptomatic or mild infection
  • Young, old, immuno- suppressed
    ○ 85% fatality rate without treatment (esp. HIV / AIDs)
    ○ 0-50% fatality rate with treatment
  • Amastigotes multiply in RES
    ○ Fever, hepato-splenomegaly and pancytopenia
    ○ Liver failure, bleeding, anaemia, secondary infections
39
Q

Cutaneous leishmaniasis what is teh main clinical sign, what age groups affected, what occurs if untreated and how transmit

A
  • Localised nodulo-ulcerative lesion
    ○ Continues to grow and manifest, very hard to get rid of
  • Affects all age groups
  • If left untreated may become diffuse with invasion of mucosa and cartilages
    ○ Can then form visceral leishmaniasis depending on the species
  • Can transmit directly through the open sore on the skin - ZOONOTIC
40
Q

Infantile leishmaniasis what is the main species involved, primary reservoir species, prevalence, and clinical signs

A

Leishmania infantum

  • Dogs are primary reservoirs
  • Prevalence up to 15% in Mediterranean/ Middle East/ South America
  • Only 10-15 % display overt disease
  • Non-specific dermatitis
  • Signs of visceral disease
  • anaemia, wasting, bleeding disorders, protein losing nephropathy
41
Q

List the 6 ways to diagnose Leshmania

A
  1. Detection of amastigotes in RES (macrophages) cells
  2. Blood smear – buffy coat
  3. Lymph node aspirate
  4. Impression smear of lesion
  5. PCR
  6. Serology
42
Q

List 6 control/treatment options for Leshmaniasis

A
  • Vector control and reservoir control
  • Treatment in dogs controversial
    ○ suppresses clinical disease in dogs but does not eliminate parasite
    ○ Carrier state with re-lapses common
    ○ e.g. Antimonials - Meglumine + Allopurinol
  • Insecticide sprays
  • Repellents
    ○ impregnated collars or spot-on tx (synthetic pyrethroids)
    ○ Bed nets
  • Commercial canine vaccines (80% efficacious)
  • Quarantine -> dogs from overseas
43
Q

Balantidium what is it, the disease caused and the general 4 steps in the lifecycle

A 
Ciliates 
Balantindiasis 
1. Cysts within environment 
2. Faecal-oral route 
3. Replicate via binary fission in the colon - trophozoites
4. Forms cyst and leaves through faeces 
Very similar to Giardia
44
Q

Balantidium coli hosts, clinical signs, zoonoses and treatment

A
  • Pigs, human, primates in colon (zoonosis)
  • Asymptomatic or diarrhoea (weaners)
    ZOONOSIS:
  • Immuno-compromised humans
    ○ may be invasive
    ○ dysenteric syndrome cf. Entamoeba histolytica
    Treatment -> nitroimidazoles - like giardia
45
Q

Entamoeba histolytica what conditions present, human deaths per year, disease caused by what two species, lifecycle and where located within host

A 
○ tropics / subtropics/ poverty
○ 50-100,000 deaths p.a.
- “Amoebic dystentry" - caused by:
	○ E. histolytica (pathogenic)
	○ E. dispar (not pathogenic)
§ Morphologically indistinguishable
- Faecal-oral, simple direct LC, cysts infective
- Colonic pathogen
46
Q

What are the 5 steps in the lifecycle of Entamoeba

A
  1. Cyst in faeces
  2. Ingest with contaminated water or food
  3. Replication in the gut as trophozoite
    ○ Can lead to colitis and mild diarrhoea
  4. Systemic movement into bloodstream possible
  5. Cyst forms and out through faeces
47
Q

Amoebae what is the disease, different stages of infection an clinical signs associated

A 
Amoebiasis 
- Asymptomatic
- mild – diarrhoea, colitis, cramps
- moderate - dysentery
- severe - extra-intestinal
○ invades the liver and forms necrotic abscess, other tissues (CNS, lungs)
○ Significant disease -> can be fatal 
- May rupture, fistulas
48
Q

List 2 diagnosis techniques for intestinal amoebiasis and 2 invasive forms

A 
Intestinal amoebiasis
1. • faecal smear / float (cf. E. dispar)
2. • Antigen detection
3. • copro-ELISA
4. • PCR
Invasive forms
1. • Antibody ELISA
2. • Ancillary tests (ultrasound)
49
Q

List and describe 3 main treatment/control options for Amoebiasis

A 
- Basic sanitation and hygiene!
○ Indoor defaecation
○ Ban use of night soil
○ Wash fresh fruit and vegetables
○ Water treatment
- Drain abscesses - not common 
- nitroimidazoles (e.g. metronidazole) ± paromomycin
50
Q

Amoebic meningoencephalitis what are the 3 general steps in the lifecycle and 4 sources of infection

A
  1. Free living mainly within the water
  2. Move in mucosa of the nose
  3. Move to the brain -> meningoencephalitis -> fatal
    Source of infection
    - Naegleria, Acanthamoeba Balamuthia
    - Free-living amoeba
    - Neti pots
    - Diving / swimming in ponds, lakes, ‘natural springs
51
Q

Amoebic meningoencephalitis what are the main clinical signs and treatment options

A 
Clinical signs and pathology
- Neurological / Multisystemic
○ nasal / ocular discharge
○ neurological signs
○ ± multi-systemic spread
○ Individual may be immunosuppressed, but not always!
- necrosis and haemorrhage
- Almost ALWAYS FATAL
Treatment
- >90% fatality rate
- Miltefosine recently approved for ameobic ME (registered for visceral leishmaniosis)
○ Analogue of eukaryotic membrane phospholipid – antineoplastic drug

DVM 2 - 2 (27 decks)

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