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DVM 2 - 2 > Parasitology TREM > Flashcards

Parasitology TREM Flashcards

1
Q

Platyhelminths what are the main general features

A
  • Flattened - dorsolateral flattened - pancakes
  • No cuticle (nematodes do)
  • Bilaterally symmetrical
  • Tegument (role in diffusion of nutrients)
  • Triploblastic, acoelomate (solid mesoderm)
  • Hermaphroditic
  • “Flame cells” (protonephridium) -> excrete waste products
  • “Cephalisation” - earliest form of a nerve ring
  • Blind ended (no anus) (trematodes) or no gut (cestodes)
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2
Q

Order Digenea what is the general lifecycle, hosts and veterinary and medical significance

A
  • Life cycle – indirect
    ○ generations of sexual (adult) and asexual (larval) generations in alternate hosts
    ○ 2+ hosts
    Veterinary -> Fasciola main issue 0> acute and chronic fasicoliasis (lover flukes)
    Medical -> can lead to carcinomas with schistosmosis and clonorchiosis and opisthorchiosis
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3
Q

Digenea adult features and the two types in terms of sex

A
  • Non-segmented
  • Suckers (oral, ventral or posterior)
  • Spines (tegument) - some such as Fasciola
  • Digestive tract; usually no anus
  • Mostly hermaphrodites (monoecious); some dioecious (Schistosoma)
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4
Q

What are the 3 main layers of the Digenea (flukes) integument and features within

A 
TEGUMENT (mesodermal) 
- Cytoplasmic extension
- Microvilli –like invaginations
- May have spines
- Protection, nutrient absorption and metabolism
- Rich in mitochondria, vacuoles, ER
MUSCLE LAYER 
SUB-TEGUMENT 
- Reproductive organs 
- parenchyma (digestive tract, osmoregulatory system, nervous system)
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5
Q

Describe the nervous system of Digenea (flukes)

A

Ganglia run down the body of the worm

Longitudinal and transverse cords around them

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6
Q

What are the 4 main steps of the lifecycle and the name of the stages of Digenean (flukes)

A

1) Egg with miracidium
- Hatch from cell and either aquatic or terrestrial
2) First intermediate host - molluscs (snail)
- Asexual reproduction (Sporocyst) form cercariae which are released from snail
3) May have second intermediate host
4) INFECTIVE once develop into Metacercariae
1. Directly penetrate after free living stage
2. Secondary aquatic host - then ingested by definitive
3. Secondary terrestrial host - then ingested by definitive

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7
Q

Digenean (flukes) what are the two types and the common features

A
  • Possess a ‘cap’ or operculum ± spines
  • Aquatic or terrestrial hatching
    ○ Contains miracidium (terrestrial) or unembryonated when passed
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8
Q

Digenean (fluke) aquatic lifecycle what is the main example and the egg features

A 
Fasciola 
- Unembryonated, embryonate over weeks 
- When in water cap will open and miracidium will swim out 
○ Have cilia that allow them to swim 
- thin shelled
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9
Q

List the 4 main stages of Digenean (flukes) after hatch and before adult

A

1) Miracidium - hatch from shell
2) sporocyst - within the snail
3) cercariae - after the snail
4) metacercariae - in environment

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10
Q

Miracidium what stage in what parasite, features, important function and how achieves this

A 
Digenean (flukes) - hatch from shell 
- Aquatic - ciliated epithelium
- Highly sensory – must find snail!	
○ Light, temp., salinity, chemotaxis (secretions snail), negative geotaxis (get away from earth) 
- Retractable apical papilla
○ Sensory nerve endings
○ Apical glands – enzymes for penetration into the snail 
○ Muscular contractions
= PENETRATION SNAIL
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11
Q

Sporocyst what stage in what parasite, what is the main thing that occurs at this stage

A

Digenean (flukes) - within the snail
- Asexual reproductive stage -
○ “Sac-like” structure (with germinal cells) within snail – produce daughter sporocysts or rediae

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12
Q

Cercariae what stage in what parasite, main function how achieve and then what does it do

A

Digenean (flukes) - after the snail

  • Escape from snail
  • Actively motile (tail first swimmers)
  • May penetrate host (DH or 2nd IH) directly
  • Mechanical head movement and protease enzymes force entry into host within minutes
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13
Q

Metacercariae what stage in what parasite, what are the 3 main functions in this stage and which genus does this

A

Digenean (flukes) - in the environment
1. Free – encyst on vegetation e.g. Fasciola
2. Second aquatic IH – encyst in tissue of second intermediate host e.g. Clonorchis
3. Second terrestrial IH – ingested by ant to form metacercariae e.g. Dicrocoelium
○ Modify host behaviour!
§ Ant climb to leaf and stay there all night -> eaten by livestock

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14
Q

Fasciola first and second intermediate host and definitive hosts

A

Intermediate host - lymnaea snail
Second intermediate - DOESN’T EXIST
Definitive host - ruminants (humans)

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15
Q

What are the 9 steps in the fasciola lifecycle and the time it takes

A

1) Adult live in bile duct of ruminants and humans
2) Eggs unembryonated when pass -> 2-3 weeks to embryonate
3) When conditions are right
Swim out and penetrate the foot of the snail
4) Asexual multiple stage within the snail -> produce daughter sporocyte
○ 2 - 2.5 months
○ One Miracidium can produce 1000-2000 cercariae (successful asexual reproduction)
5) Once cercariae release form metacercaria
6) Encyst and stick to blades of grass
7) Definitive host ingest and get infected
8) Immature flukes migrate from intestinal tract into liver for 4-6 week - main pathology
9) Mature adult within the bile ducts

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16
Q

Fasciola lifecycle what are the “right” conditions for the miracidium to swim out and how long is PPP and the overall lifecycle

A
  • need aquatic environment
  • Rainfall (nothing under 400ml of rainfall average per year -> aquatic)
  • and temperature (average >10 degrees) - SPRING IN VIC
    Important with timing - 6 MONTHS LIFECYCLE
    PPP = 3 months
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17
Q

Fasciola hepatica morphological features and the 2 main features that help differentiate species

A
  • Large (1-3 cm), leaf-like, broad
  • Anterior end broader that posterior
  • Spines on tegument - in immature flukes -> leads to damage while in the liver
  • “Conical projection” anterior end
  • Caeca highly branched
    BOTTOM 2 -> differentiate between species
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18
Q

Acute/sub-acute fascioliasis which species most effected, how occurs and what leads to

A

SHEEP > cattle
- Massive intake of metacercariae over short time (500-2000)
○ Usually seasonal
- Traumatic hepatitis, haemorrhage
- Clostridium novyi toxaemia, resulting in “black disease” (Necrotic Hepatitis)
Anaemia, abdominal pain, sudden death

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19
Q

Chronic fascioliasis which species most effected, what leads to and the 1 disease it looks like in the sheep and cattle

A 
CATTLE > sheep 
- Cirrhosis of the liver
- Biliary calcification
○ Anaemia
○ Bottle jaw, ascites -> hypalbuminaemia 
○ Diarrhoea
○ Wasting
○ Autumn, early winter
- Looks like Haemonchus in sheep 
- Looks like Johne's disease in cattle
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20
Q

What are the 5 diagnosis techniques for Fasciola

A
  1. History and Clinical Signs
  2. Faecal egg counts
    ○ Thin shelled, large, tan, operculum
    ○ SEDIMENTATION TECHNIQUE
  3. Serology (IgG ELISA) - antibodies
    ○ 4-6 weeks sheep
    ○ 6-8 weeks cattle
  4. Post-mortem -> focus on the liver
  5. CBC/biochemistry
    ○ Anaemia
    ○ Elevated liver enzymes
    ○ Hypoporoteinaemia
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21
Q

What are the 3 main economic significance of Fasciola

A

1) Production losses – 60-80 million p.a.
○ Reduced production and quality wool / milk
○ Low lambing rates
○ Poor growth and feed conversion
○ Sudden death
2) Drenching – 10 million
3) Condemnation of livers

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22
Q

Epidemiology of Fasciola what are the 4 things needed where in australia present and what occurs in VIC in terms of acute and chronic disease and perfect growth months

A
  • Parasite + Snail + Rainfall (>400 mm average per year) + Temp >10ºC
  • Freshwater, shallow, stagnant, pond
  • Present in all States except WA and NT
    VICTORIA - Winter rainfall
  • Sept - perfect weather -> hatch -> takes 2 month to be ingested by definitive host
  • Within 5-6 weeks within definitive host -> ACUTE DISEASE - SUMMER - JANURARY (sudden death)
  • CHRONIC DISEASE after PPP -> 3 months after mid-November -> March/April
    May be reversed in summer rainfall areas where sheep graze infected areas in dryer seasons (winter) e.g. SE Qld, Northern NSW
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23
Q

Infection pressure with Fasciola what are the 2 main things

A

Season and grazing habits
- Winter rainfall areas (VIC/TAS):
○ Snails breed and egg hatching in spring and early summer in cooler climates (>10ºC)
○ Metacercariae available ~ early to mid-December
- Grazing habits (sheep)
○ Summer rainfall, sheep graze near water in winter
○ Winter rainfall (graze near water in summer)

24
Q

Treatment of Flukes what is the drug that kills them from 2 weeks other disease that is used for older flukes and adulticide in lactating cows

A

Only one drug that kills all stages of fluke from 2 weeks
1. Triclabendazole - acute diease
- Resistance is developing -> rotation
Others
1. Closantel plus oxfendazole
Adulticide in lactating cows
- Oxyclozanide -> good for chronic which cattle are more susceptible to

25
Q

List 5 control methods for Fasciola

A
  1. Fencing off snail-prone areas from sheep/cattle
  2. Draining marshy pastures
  3. Building dams - don’t like deep water
  4. Strategic flukicidal treatment
  5. 5-in-1 vaccines
26
Q

Strategic anthelminitic treatment for Fasciola what occurs in august/september, Jan/feb and April/May

A
  • August/September – late winter
    ○ Reduce pasture contamination with eggs as snails emerge in late winter/spring
    ○ Adulticide -> 10+ weeks such as Closantel plus oxfendazole
  • Jan/Feb – mid summer
    ○ To kill immature flukes acquired over early summer - prevent acute fascioliasis
    ○ If worried go to triclabendazole
  • ± April/ May
    ○ To kill flukes if Jan/Feb dose was not effective against immature flukes
    ○ OPTIONAL
27
Q

Fasciolopsis buski what is it, host and where found

A

Giant intestinal fluke
humans and pigs
Adult in the intestines not bile duct

28
Q

Family Paramphistomatidae where belong and features including location and effects of host of adults

A

Class: Trematodes
- Fleshy, pear-shaped body, 5–12 mm long by 2–4 mm in diameter
- Juvenile fluke are small (1–2 mm long)
○ Highest pathogenicity - cause the damage
- Large ventral sucker posterior end
- Ovaries behind testes
Rumen fluke - adults live in rumen/reticulum but cause no issues

29
Q

What is the general lifecycle of Paramphistomatidae, what similar to and PPP

A
  • Epidemiology and LC similar to Fasciola - treatment similar
  • PPP ~2-3 months
    1. Hatch when embryonate -> 10 days
    2. Miracidium swim in water and penetrate the planorbid (aquatic snail)
    3. Asexual reproduction - 2-3 months -> radiae
    4. Emerge as Cercariae
    5. Into the plants -> ingestion of plants -> infection
    6. Encyst in duodenum and then excyst and remain in the duodenum for 3–6 wk
    7. Migrate to reticulum and rumen
30
Q

Paramphistomatidae pathgenesis of larvae and adults and what occurs with light and moderate infections

A
  • First 4-8 weeks juveniles move from s.i. to rumen and reticulum
    ○ Can go up to 4 months
  • Adults cause no harm
  • Light infections – asymptomatic
  • Moderate infection – ill thrift, reduced weight gain, loss milk production
31
Q

What are some clinical signs and reasons for heavy infections of Paramphistomatidae and when most susceptible

A
  • Heavy infection (up to 72,000 worms!) – juvenile migration delayed: in s.i. for up to 4 months
    ○ watery diarrhoea or haemorrhagic diarrhoea, dehydration and death -> signs of enteritis
  • Exposure increased immunity - wouldn’t normally see in adult animals
    ○ Weaners or immuno-naïve animals (introduced animals) most susceptible
    § Drought, movement, stressed
32
Q

List the 4 ways to diagnose Paramphistomatidae, are they effective and what need to differentiate between

A

1) History
○ Temperature, rainfall, grazing conditions, age groups affected, drench hx
2) Clinical signs
3) Post-mortem
4) Eggs in faeces?
○ Not a good way to diagnosis as the larvae are causing the damage and could be up to 5 months before see the eggs in faeces
- Differentiate between strongyles and Haemonchus and Fasciola (doesn’t matter as much because treatment is the same)

33
Q

What are the 2 main treatment and control methods for Paramphistomatidae,and what to do with adult and juvenile flukes - when treat

A

1) Fence / drain affected areas
2) Anthelmintics
○ extra-label use only
§ Closantel and oxyclozanide -> Fasciola treatment and off label for Paramphistomes
- Adult flukes in rumen - only things that can be killed, cannot kill larvae
○ Reduce contamination of pasture for next cycle
○ Late Winter
- Juvenile flukes
○ Treat / prevent clinical disease -> decrease stress, weaners most susceptible so ensure don’t go onto contaminated pasture
○ Summer – early winter

34
Q

Dicrocoelium dentriticum what are they commonly called, size, features and are they present in australia

A

The ‘lancet fluke’

  • Small, elongate (~0.5 cm)
  • Genital pore in front of ventral sucker - see ventral sucker not genital pore
  • Unbranched caeca
  • Not in Australia
35
Q

Dicrocoelium dentriticum common name and 10 steps in the lifecycle

A

Lancet fluke
1) Embryonated eggs
2) Penetrate terrestrial snails
3) Egg gets crushed and larvae released within snail gut
4) Asexual multiplication
5) Cercariae are released in the slime of the snail trail
6) Ants ingest slime
7) Goes to the brain - change behaviour by going to the top of the grass
8) Ingested by cows, pigs and rarely humans
9) Excyst in the small intestine
10) Migrate to the bile duct -> adults reside here
○ Not large migration so not high pathogenicity

36
Q

Dicrocoelium dentriticum common name pathogenic effects and the major significance

A

Lancet fluke
- Not in Australia
- Juveniles migrate up bile ducts to become adults
- Mildly pathogenic except heavy infections (50,000 +)
- Calcification of bile ducts
○ Liver condemnation at the abattoir

37
Q

Treatment and control of Dicrocoelium dentriticum

A
  • Control v. difficult!
    ○ Difficult to control the intermediate host -> snail and ants
  • Benzimidazoles (e.g. albendazole) at high dose (e.g. 20 mg/kg)
  • Praziquantel
38
Q

Opisthorchidae what are they, where mainly located in the world, why significant and 4 main results for infection and the most important

A 
Fish-borne liver flukes (bile duct)
- 20 million people infected in Asia - ZOONOTIC - one health significance 
- Signs
○ Asymptomatic - mild 
○ Gall bladder stones
○ Cholangitis, jaundice - moderate 
○ Cholagiocarcinoma - most important
39
Q

Heterophyidae and Echinostomatidae what are they, what effects on host and where located in the world

A

Fish-borne intestinal flukes
- Asymptomatic or enteritis/ gastritis, ulceration
○ diarrhoea, upper gastric pain (dff. peptic ulcers)
- SE Asia and China

40
Q

What is the general lifecycle for fish-borne intestinal/liver flukes

A

1) Adult flukes live in the bile duct or intestines
- Variety of fish eating mammals and birds
2) Eggs passed in faeces - embryonated when passed
3) Eggs are ingested by the first intermediate host snail - terrestrial
4) Second intermediate is the fish from free swimming cercariae
5) Fish ingested without proper cooking by definitive host

41
Q

Fish-borne intestinal/liver flukes what are the risk factors and best way to diagnose

A

Risk Factors
- Traditional dietary practices of eating raw, fermented or pickled fish
- Poor sanitation:
○ Use of animal or human effluent as fish food
- Uncontrolled reservoir host population -> cats and dogs
Diagnosis
Eggs - cannot differentiate
- adult morphology a little easier
- PCR good to differentiate

42
Q

What are the 3 main families of fish-borne flukes and some distinguishing features

A 
Opisthorchiadae 
- glands (yolk sacs) on the ventral surface 
- Large worms 
- Lateral and condensed 
Heterophyidae
- Tiny - how to differentiate 
- 3rd sucker - genital sucker -> ontop of ventral sucker 
○ Hard to see
Echinostomatidae
- 1-1.5cm 
- Double row of spines on the head
43
Q

What are the 2 control and prevention strategies and things within

A 
1) Monitor and Chemotherapy:
○ Mass praziquantel for humans
§ Doesn't help reservoir host and fish 
2) Education:
○ Alter traditional eating practices - doesn't work 
○ Cook fish - doesn't work
○ Freeze @ -20C for >24 hours
○ Indoor defaecation
○ Do not feed raw fish to dogs/ cats
44
Q

Paragonimus what is it and the 7 steps in the lifecycle

A

A fluke (trematode)
1) Adults form granuloma around the lung parenchyma
- Dogs, cat, humans
- Cough - can be misdiagnosed as TB
2) Eggs in faces
3) Miracidium penetrate snail
4) Asexual reproduction
5) Free swimming cercaria go into crabs - 2nd intermediate host
6) Can use pigs as paratenic host or just straight into definitive host via ingestion
7) Excyst in small intestines and penetrate peritoneal cavity -> diaphragm -> pleura -> lungs
○ May get lost and go to other tissues and organs

45
Q

What is the main disease caused by Paragonimus, where found in the world, 2 forms and treatment

A

Paragonimiasis
- Endemic in SE Asia, the Americas and Africa
- 20 million people infected
- Canids and felids reservoirs
1) Pulmonary form:
○ Cough, haemoptysis
○ “non-responsive tuberculosis”
2) 30% extra-pulmonary (brain, abdominal – juvenile forms ‘wander’)
Treatment with praziquantel will kill them -> multiple doses

46
Q

Schistosomiosis what also called, where found in host, what leads to pathogenicity, significance and is it present in australia

A

Schistosomiosis = Bilharziosis

  • “Blood flukes” (vessels - portal, mesenteric, bladder and other)
  • Eggs that cause the pathology
  • Human pathogens; not in Australia
  • Affecting 200-300 million people
47
Q

What are the main adult morphology of the Schistosomatiidae and size

A
  • Schisto= split soma=body
  • 0.5-2 cm long
  • Two suckers
  • Dioecius
  • In-copula (female in gynecophoric groove of male)
48
Q

Schistosoma what are the 4 steps in the lifecycle

A

1) Mostly infect mesenteric or bladder vessels
○ Bladder
§ Coming out through the urine
○ Mesenteric
§ Into the lumen of the gut -> out of the faeces
2) Hatch when hit water
3) Miracidium enter intermediate host - snail
4) Release cercaria that penetrate the skin of the definitive host - human

49
Q

Oriental (Asian) schistosomiasis what species caused by, risks, source of zoonosis and countries

A
  • Schistosoma japonicum
  • Risks:
    ○ Rice farming
    ○ Fishing
    ○ swimming
  • Zoonosis!!
    ○ water buffalo - highest risk source due to large amount of faeces and eggs, cattle, pigs, dogs, cats etc.
  • Philippines, Indonesia, SE China
50
Q

Acute schistosomiosis what is it caused by and the resulting effets

A
  • Self-limiting cercarial dermatitis (24 hr) - acute hypersensitivity reaction
  • Delayed hypersensitivity response (3-4 wk)
  • TH1 pro-inflammatory response
  • Hypereosinophilia
  • Fever, arthralgia, bronchiopneumonia, and urticaria or angio-oedema
51
Q

Chronic schistosomiosis what are the steps that lead to this and the 4 main effects

A
  1. Eggs laid within venules of urinary bladder / distal colon and rectum
  2. Eggs penetrate venule and intestinal / bladder wall using spine and proteolytic enzymes to enter lumen and be passed
    - Some eggs lodge in organs causing granulomas esp. intestines, liver, bladder
    ○ Ectopic sites e.g. brain
    1) Portal and pulmonary hypertension, ascites
    2) Worm/egg antigens in circulation
    ○ antibody-mediated glomerulonephritis
    ○ nephrotic syndrome
    3) Anaemia, stunting children
    4) HIV/AIDS co-infection complications
52
Q

Diagnosis of schistosomiosis what are the 3 main ways

A

1) History/ clinical signs
2) Eggs in faeces / urine**
- spines on the eggs
3) Serology

53
Q

What are the 4 main ways to control schistosomiosis

A

1) Mass Treatment with praziquantel
2) One Health approach?
○ Improving household sanitation and access to clean water
○ Educating fishermen and boatmen about the dangers of infested water.
3) Molluscicidal treatment
4) Vaccines - Humans? Animals?
○ Phase 1-3 development
○ ≥ 40% decrease in worm burden

54
Q

Cercarial dermatitis what is it commonly called, is it in australia, what parasite result from and how occurs

A
  • ‘Swimmers itch’
  • Common in Australia
  • Austrobilharzia or Trichobilharzia (aquatic birds)
  • Skin penetration of the “wrong host”
  • Self-limiting hypersensitivity reaction (multiple exposures)
55
Q

Visceral schistosomiasis in animals, what results from low and high burdens

A
  • Pathophysiology, treatment, control similar to humans
  • Low to mod. burden – subclinical, production losses
  • High burdens, younger animals
    ○ Diarrhoea, heamaturia, ascites, wasting
    ○ Severely affected animals deteriorate rapidly and usually die within a few months of infection
56
Q

Selecmectin and moxidectin in dogs what dosage

A

SELAMECTIN - NOT DOGS

MOXIDECTIN - once a month, pups over age of 7 weeks

DVM 2 - 2 (27 decks)

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