Parasitology B Flashcards

1
Q

What stage of ascaradids is passed in the faeces? How long does it take for them to become infective in the soil? How long can they survive in the soil?

A

Unembryonated eggs
2-3 weeks to become embryonated and infective
Last for years (5-10) in soil

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2
Q

What type of toxocara canis lifecycle does not involve tracheal migration?

How long is the PPP for different types of lifecycle with this species?

A

Transmammary (2-3 weeks)
Transplacentally (2 weeks)
Eggs ingested by pup (4-5 weeks)

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3
Q

What diseases are of particular public health significance with respect to ascarids?

A

Visceral larva migrans

Ocular larva migrans

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4
Q

What are some characteristic features of enoplids? What worms are included in this order?

A

Non-muscular oesophagus with stichosome.
male either has a single ensheathed spicule or none (trichinella).
1. Trichinella
2. Trichuris (whipworm)
3. Capillaria (hairworm)
4. Acanthocephalans (thorny-headed worms)

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5
Q

Briefly describe the lifecycle and significance of trichinella

A

Adult worms occur in SI. Female worms penetrate deep into mucosal glands -> lymphatics-> blood-> skeletal muscle. Ingested through meat-eating.
Significance: causes trichinellosis through ingestion of raw or undercooked infected meat, especially pigs.

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6
Q

What are the differences between the two groups of Trichinella sp.

A
  1. Encapsulated species- found in mammals only. The L1 is surrounded by a collagen capsule (“nurse cell”) within muscle.
  2. Unencapsulated species- in mammals, birds, reptiles and marsupials. L1 is freeeeeee!
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7
Q

Which trichonella species is present in Aust?

A

Trichonella pseudospiralis

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8
Q

What are some clinical signs of trichinellosis?

A

In animals there are none. in humans, the severity of clinical signs is proportional to the dose ingested.
In peracute infections- diarrhoea, abdominal pain, vomiting, fever.
in acute infections, eosinophilia, elevated CK, myalgia, fever, vasculitis, cardiac problems and death

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9
Q

How do you diagnose trichonellosis and how may it be treated? How may it be controlled?

A

Dx: serology
Tx: corticosteroids and albendazole
Control: prevent raoming/ scavenging of pigs, proper meat prep (microwave, salting and smoking are all ineffective)

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10
Q

Which trichuris species affect the following animals:

  1. Primates
  2. Dogs
  3. Pigs
A
  1. Primates- T. trichiura
  2. Dogs- T. vulpis
  3. Pigs- T. suis
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11
Q

What clinical signs might one see with trichuris infections? How might these be diagnosed and treated?

A

CS: congestion, submuc oedema, epithelial desquamation, necrosis/ fibrosis, watery/mucoid diarrhoea, tenesmus, rectal prolapse, hypoproteinaemia/ hyperkalaemia (colitis causes loss of Na and K)
Dx: Faecal float (SG>1.2)
Tx: Oxantel, MLs (not selamectin though) or BZs

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12
Q

Which capillaria are of concern in poultry and where do they occur? What do they cause?

A

C. annulata (crop)
C. contortus (crop)
C. caudinflata (SI)
C. obstignata (SI)

CS: Light infections-> poor weight gain, decreased egg prod.
Heavy infections: catarrhal thickening, infl. of oesophagus and crop and enteritis. High mortality
Tx: ivermectin, BZs, levamisole

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13
Q

Which worms have no digestive tracts?

A

Acanthocephalans (thorny-headed worms)

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14
Q

What is the IH of acanthocephalans? What are some examples of this species of worm?

A
Arthropods
Macracanthorhynchus hirudinaceus (piggies)
Onicola sp. (dogs and cats)
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15
Q

Briefly describe the general lifecycle of Ascarids.

A

DIrect lifecycle. Eggs are passed unembryonated in the faeces, they take 2-3 weeks to embryonate. Paratenic host may then ingest the L3 stage. Definitive host may ingest infected paratenic host or may ingest L3 egg. Larvae undergo hepatopulmonary migration before being coughed up and swallowed. Adults in small intestine.

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16
Q

What are the effects of ascarids in pigs?

A

HPM causes mechanical and infl. damage to organs. Milk spots. Eosinophilic pneumonia

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17
Q

What stage of ascarid is found in muscle and passed though milk?

A

L3

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18
Q

How can you tell the difference between toxocara canis and toxascaris leonina?

A

T. canis has a ventriculus and a digitiform tip on its posterior end (in males)

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19
Q

How long is the prepatent period for T. leonina

A

7-9 weeks

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20
Q

What are some important ascarids of birds? What is their predilection site? What are their effects?

A

Ascaridia galli (SI)- Usually not a big deal but can cause haemorrhagic enteritis or intestinal occlusion and nutritional deficiency.

Heterakis gallinarum (caecum)- may cause caecal thickening but of liitle pathological sig. Phoresy.

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21
Q

What is phoresy? Give an example

A

An association between two organisms. The transmission of ameboid, histomonas meleagradis, occurs through the egg of Heterakis gallinarum.

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22
Q

Why is Phoresy a problem in Heterakis gallinarum?

A

The protozoa histomonas meleagradis is not pathogenic to chickens but is extremely pathogenic to turkeys causing necrotizing typhlitis and focal liver necrosis

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23
Q

What are some treatment and management options for ascarids?

A
  • Hygiene, decontamination of property (flame gun, Na hypochlorite).
  • Disinfect? Often resistant to bleach
  • Rodent and pest control
  • Don’t feed raw meat
  • Treat and quarantine new arrivals
  • deworm regularly
  • Reduce environmental contamination (pick up poo daily)
  • Anthelmintics (MLs, morantel, benzimidazoles)
  • Rotate pastures (horses)
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24
Q

Propose a treatment regime to control ascaris suum in pigs.

A

Drugs: levamisole, ivermectin, morantel, piperazine or fenbendazole (in feed)
Treat growers at 8 weeeks old (bc that the PPP of A. suum)
Treat sows and boars every three months (to reduce pasture cont)
Treat sows 7-14 days prior to farrowing
Test herd every 6 months

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25
Q

Propose a treatment regime to control parascaris equorum in horses.

A

Deworm foals every 2 months for the first year of its life with rotations of MLs, BZs and pyrantel. Start this at 2 months of age.
Rotate pastires for mares and foals annually
Do a FEC prior to deworming adults in spring and autumn (want to test before you treat in adults to reduce resistance)

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26
Q

Propose a treatment regime to control Toxocara canis in dogs.

A

Deworm puppies first at 2wo (3wo for kittens) then fortnightly until 10wo (8 wo for kittens), then monthly until 6 months old.
Deworm the bitch at the same time

During pregnancy: fenbendazole 50mg/kg daily from day 40 to 14 days post whelping (larvacidal) OR selamectin topically at day 40 and day 55 PLUS monthly moxidectin (This is for bitches not queens. For queens apply selamectin topically at the end of gestation)

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27
Q

What is anasakiasis?

A

Illness caused by ingestion of L3 anisakidae in raw or uncooked fish.

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28
Q

Where do oxyurids (“pinworms”) occur?

A

Caecum, colon and rectum

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29
Q

What are some features of spirurids?

A
  • Two lateral lips (or none)
  • Unequal spicules
  • Arthropod IH
  • Oesophagus with anterior muscular and posterior glandular secretions
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30
Q

What is the difference between Draschia sp. and Habronema sp?

A

Habronema causes ulcers/ gastritis and draschia causes nodules in stomach wall

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31
Q

What is the IH for Draschia? What about Habronema? how can you tell the difference between these worms?

A

Draschia megastoma= Musca spp.
Habronema microstoma= stomoxys calcitrans

Draschia has a cephalic constriction and a big funnel shaped buccal capsule (cff cylindrical)

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32
Q

What is important to remember if you want to do a faecal floatation of equine spirurids?

A

Floatation solution needs to have a SG>1.2

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33
Q

How can spirurids of horses be treated/controlled?

A
  • Adults can be targeted with OXFENDAZOLE or MOXIDECTIN.
  • For cutaneous lesions: MLs (eg. Ivermectin) +/- surgical debridement, cryotherapy, CSs
  • Fly control (get rid of manure, insect growth regulators)
  • Face and eye masks, fans etc.
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34
Q

Where is spirocerca lupi common? How might it be diagnosed?

A

Tropical/ subtropical regions globally

Eggs may not be present in faeces. Therefore, endoscopy or radiography

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35
Q

How might spirocerca lupi be managed/ treated?

A

Difficult because adults are protected in granulomas

  • Moxi (prophylactically)
  • Surgical removal where feasible
  • Aid feeding (upright position)
  • Prevent free-roaming/ scavenging
  • Tx= off label use of doramectin, moxi and milbemycin for up to 6 months
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36
Q

Which parasite has a characteristic uni-plugged eggs on faecal floatation>

A

Gnathostoma spp

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37
Q

How does gnathostomiasis occur in humans?

A

Fish borne zoonosis

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38
Q

What is the IH for Ascarops strongylina/ physocephalus sexalatus in pigs?

A

Dung beetle

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39
Q

What does thelezia cause?

A

Keratitis, ulceration and opacity of eye

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40
Q

What are some spirurids in birds and where do they occur?

A

Gongylonema spp. - crop, IH= cockroach
Acuaria spp. and Tetrameres spp. - proventriculus/ ventriculus. IH=grasshoppers and beetles
Oxyspirura mansoni- conjunctival sac. IH= cockroach

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41
Q

Where are adult filaroids located?

A

Blood and lymph (NOT GIT)

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42
Q

Where is Onchocerca cervicalis found (what animal and where in animal)? What does it cause?
What about Onchocerca reticulata?

A

Horses nuchal ligament-> oedema, chronic granulomatous nodules and fibrosis

Horse flexor tendons

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43
Q

What is Queensland itch?

A

Onchocerciasis in horses. Mff dying in dermal tissue causes pruritic dermatitis on the ventral midline, face, neck, chest, withers, forelegs and abdomen. Can also cause scales, crusts, ulcerations, alopecia and depigmentation. Treat with Ivermectin or moxi. Permethrin pour on can be used by way of prevention.

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44
Q

What are the filaroidea of cattle and where do they occur?

A

O. gutturosa (Nuchal ligament)
O gibsoni (dermal tissue of brisket)
O. lienalis (gastrosplenic ligament)
Stephanofilaria stilesi (ventral thorax and abdomen)

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45
Q

What is the vector for Stefanofilaria stilesi? How may this be controlled?

A

Haematobia irritans
Control is difficult. No anthelmintic is effective against adults.
-Walk through fly traps
-Dung beetle
-Synthetic pyrethroids or OPs (pour-on, ear tags, dips)

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46
Q

What is the pathogenesis of heartworm?

A

Presence of worm and its endosymbyont (wolbachia) -> proliferative endarteritis of pulmonary arteries.
This leads to decreased arterial compliance plus thrombosis and thromboembolism (esp. from dead parasites) -> pulmonary hypertension -> increased afterload for RV -> RV hypertrophy and dilation -> RSCHF +/- caval syndrome

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47
Q

How may heartworm be diagnosed?

A

Hx, CSs, detection of mff in blood (Knotts test and filtration method), SNAP ELISA antigen test (need at least 3 females though)

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48
Q

Up to 30% of heartworm infections may be occult. Why is that?

A

All worms may be same sex
May have a single worm infection
May have a pre-patent infection or geriatric worms
May have ectopic infections
May have drug induced/ immunologically mediated elimination

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49
Q

What is the “soft kill” regimen for heartworm treatment?

A

ML + Doxycycline (10 mg/kg, 1 month on, 2 months off) over 9-12 months

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50
Q

How does heartworm differ in cats from dogs? WHat are some clinical signs of it in cats? How is it treated? How is it diagnosed?

A
Prevalence is 5-20% of that in dogs
Most worms don't mature
PPP=8 months (cff. 3)
Often no mff
Shortened adult survival time
Aberrant migration

CS: Heartworm associated resp disease (HARD)
Tx: Prednisolone or surgery. NO MELARSAMINE
Dx is challenging. Can do Ab test (at 8 weeks post infection), Ag test if more than 1 female, radiographic changes (bronchioalveolar pattern, enlargement of caudal lobar arteries, adults on ultrasound)

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51
Q

What are some radiographic signs of HARD?

A

bronchialveolar patter
slight enlargement of caudal lobar arteries
adult worm on ultrasound

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52
Q

How might heartworm in dogs be treated?

A
  • Day 0: start pred (0.5 mg/kg) every altenate day before and up to 1 month starting adulticide treatment.
  • MLs from day 0 to prevent new infections. Monthly.
  • Doxy (10mg/kg) from day 0 to target walbachia (1 month)
  • Melarsamine from day 60. 1 injection followed by 2 injections one month later given 24hrs apart
  • Retest 6 month
  • Restrict exercise
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53
Q

Which three classes of platyhelminths are trematodes?

A

Monogenea (marine and freshwater)
Digenea (vertebrates)
Aspidogastrea (marine or freshwater)

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54
Q

What are some distinguishing features of platyhelminths?

A
  • flattened
  • tegument instead of cuticle
  • tribloblastic and acoelomate
  • hermaphroditic
  • flame cells
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55
Q

What are flame cells?

A

Cells in trematodes responsible for osmoregulation (primitive kidneys)

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56
Q

What is the mechanism of reproduction in hermaphroditic trematodes?

A

Sperm stored in testes travels to seminal receptacle. The oocyteis released from the ovary and travels up oviduct to be fertilised. Fertilised egg is nurtured in ootype where shell formation takes place as a result of vitelline material and Mehlis gland. Egg shrinks in size as it passes down the uterus and is released from genital pore.

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57
Q

What is the general lifecycle of digenean trematodes?

A

eggs-> miracidium-> rediae-> cercariae-> metacercariae-> ingested (note, with schistosomes, the cercariae are ingested directly after being released form the snail).

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58
Q

What is a miracidium?

A

The first larval stage of trematodes with an aquatic lifecycle. They have a ciliated epithelium and respond to 5 factors:

  1. negative geotaxis
  2. water salinity
  3. light intensity
  4. temperature
  5. chemotaxis
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59
Q

What is a sporocyst?

A

The asexual reproductive stage of trematodes that occurs in the snail. Stage is between miracidium and rediae.

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60
Q

What is a cercariae?

A

Actively motile larvae of flukes which escape from the snail. They swim tail first

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61
Q

What are metacercariae?

A

Final stage larvae of flukes which encyst on vegetation and modify host behaviour when eaten.

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62
Q

What snail is the intermediate host of Fasciola flukes? What are some characteristics of this snail?

A

Lymnae snails

Clockwise spiral, flat/ triangular tentacles

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63
Q

What is the difference between the acute and chronic forms of fascioliasis. Include things in your comparison such as timeframe, animal affected etc.

A

ACUTE: 4-6 weeks. Large numbers of 5-6 week old juvenile flukes. Flukes go through intestinal wall to peritoneal cavity and liver. Seen in sheep more than cattle. Can lead to black disease and acute toxaemia.

CHRONIC; more than 6 weeks. Involves adult flukes which establish in bile ducts and cause fibrosis and hypertrophy. May see calcification of parasite. Seen in Cattle more than sheep. May cause bottle jaw.

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64
Q

When and how does acute fascioliasis occur? What are some DDx?

A

Massive intake of metacercariae over short time. Usually in spring-> clostridium novyi
DDx: other clostridials, toxins (pasture), anthrax

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65
Q

What are some DDx for chronic fascioliasis?

A
Hypoproteinaemia
Protein-losing enteropathy
Haemonchus
Johne's 
Strongyles
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66
Q

What diagnostic technique would you use for fascioliasis?

A

Necropsy or Serology.

Not faecal float because it has a long PPP (unless its a chronic infection)

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67
Q

What are the effects of fascioliasis that lead to production losses?

A
Reduced production
Decreased wool and milk quantity/quality
Low lambing rates
Poor growth and feed conversion
Sudden death
10 million in drenching
Total of 60-80 million loss
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68
Q

Liver flukes are found in all australian states except…?

A

WA and NT

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69
Q

When are different stages of the lifecycle of Fasciola hepatica seen in Victoria? With this in mind, when would you treat and with what?

A

Eggs hatch mid-sept.
2 months later- cercariae
5-6 weeks later- acute infection in sheep
Chronic fluke disease seen in winter

Tx:

  1. Late Dec/Jan- triclabendazole (kills juvs)
  2. Going into Autumn (April/ May)- adulticide (eg. Closnatel + oxfendazole)
  3. Aug/Sept- adulticide to reduce pasture contamination and remove fluke carrying over from late autumn and winter
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70
Q

How might Fasciola hepatica be controlled within a herd/mob?

A
  1. Keep sheep away from water source
    - fence off snail-prone areas
    - drain marshy pastures
    - build dams
  2. Strategic flukicide treatment
  3. 5-in-1 vaccines
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71
Q

What s fasciola buski?

A

Giant intestinal fluke. Pigs act as reservoirs for human infection

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72
Q

Are fasciola eggs passed embryonated or not?

A

Not. takes 2-3 weeks to embryonate

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73
Q

What is the intermediate host for paramphistomatidae flukes?

A

Planorbid snail (Gyraulus sp. or Helicorbis sp.)

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74
Q

What are some characteristics features of paramphistomatidae?

A

Pear shaped
oral and ventral sucker
Juveniles are small (1-2mm)
Ovaries are behind testes

75
Q

What are some paramphistomes of Australia and what is their IH?

A
Calicophoron calicophorum  (Gyraulus scottianus)
Orthocoelium streptocoelium (gyraulus gilberti)
Paramphistomum (helicorbis australiensis)
76
Q

What are some clinical sigs of a heavy infestation of paramphistomes?

A

Watery diarrhoea, dehydration and death. Mainly affects weaners because strong immunity develops.

(Mod infection may cause ill thrift, reduced weight gain, decreased milk production)

77
Q

How might paramphistomiasis be diagnosed? How might it be treated?

A

Post-mortem
Sediment
Clinical signs
History (temp, rainfall, age groups affected, drenching hx etc)

Drugs: Closantel/oxyclozanide (off-label)
Fence/ drain affected areas

78
Q

What is the lancet fluke? What are some of its features?

A

Dicrocoelium dendriticum.

Small, genital pore in front of ventral sucker.
Unbranched caeca
Not in Aust

79
Q

What do lancet flukes cause?

A

Juveniles migrate up bile ducts and may cause calcification of the bile ducts leading to liver condemnation

80
Q

How might lancet flukes be treated or controlled?

A

Difficult to control bc we can’t control the ants
Benzimidazoles may be effective at high doses
Praziquantel

81
Q

WHat are some examples of fish-borne liver flukes? What might these cause?

A

Opisthorchidae (Opisthorchis and Clonorchis)
Heterophyidae
Echinostomatidae

May be asymptomatic
gall bladder stones
cholangitis, jaundice
cholangiocarcinoma

82
Q

What are some risk factors for fish-borne liver flukes? How might it be controlled/ prevented?

A

Eating raw/ undercooked fish
Poor sanitation (animal or human effluent as fish food)
uncontrolled reservoir host population

Control:

  • alter traditional eating practices
  • cook fish
  • freeze for more than 24hrs
  • indoor defecation
  • dont feed raw fish to dogs/cats
83
Q

What is paragonimiasis? Where is it endemic? What are the reservoir hosts? What does it cause and how may it be treated?

A

A food-borne parasitic disease caused by ingestion of metacercaria of paragonimus spp. (lung fluke). It is endemic in SE Asia, the americas and Africa.

Reservoirs include dogs and cats.
Cough, haemoptysis (“non-responsive TB”) or neurological disease if juvenile forms “wander”

Treat with praziquantel.

84
Q

What causes schistosomiosis? Is it in Australia?

A
Blood flukes (dioecious)
Not in Australia
85
Q

What is the intermediate host for schistosomes?

A

Snails!
S. japonicum - Oncomelania quadrasi
S. haematobium- Bulinus truncatus
S. mansoni- B. alexandrina

86
Q

Where is asian schistosomiasis common? WHat is the main problematic species?

A

S. japonicum

Phillipines, Indonesia, SE china

87
Q

What does acute schistosomiasis look like?

How does it differ to chronic?

A

Self limiting cercarial dermatitis
Delayed HS response (with fever, arthralgia, bronchopneumonia, urticaria, angio-oedema)

Chronic:

  • portal and pulmonary hypertension
  • nephrotic syndrome
  • Ab-mediated glomerulonephritis
  • anaemia
88
Q

Explain how the chronic signs of schistosomiasis occur?

A

Eggs are laid within venules of bladder, distal colon and rectum. Eggs penetrates wall using their spine and proteolytic enzymes to enter lumen and be passed. However, many get drained to lover via portal vein. They cause portal and pulmonary hypertension leading to ascites

89
Q

What are some treatment options for schistosomiasis?

A
  • mass Tx with praziquantel
  • improving household sanitation and access to clean water
  • education
  • molluscicidal Tx ($$$)
  • vaccines
90
Q

What is Swimmers itch?

A

Cercarial dermatitis. Self-limiting HS reaction due to fluke cercaria burrowing into skin

91
Q

Match the following schistosome species to their host :)

a) S. bovis
b) S. matthei
c) S. spindale
d) S. indicum
e) S. incognitum
f) S. nasale

  1. Cattle
  2. Pigs
  3. Cattle and buffalo
  4. Cattle. goats and sheep
  5. Cattle, goats and sheep
A

a) S. bovis- Cattle, goats and sheep
b) S. matthei- Cattle and buffalo
c) S. spindale- Cattle. goats and sheep
d) S. indicum- Cattle
e) S. incognitum- Pigs
f) S. nasale- Cattle

92
Q

What clinical signs are associated with visceral schistosomiasis?

A

Low to moderate burdens are usually subclinical but may cause production losses.
High burdens in younger animals may lead to
-diarrhoea
-haematuria
- ascites
-wasting
-death within a few months of infection

93
Q

What is a parasitophorus vacuole?

A

Membrane in apicomplexans that is partly parasite derived and partly host derived. Gives the parasite some level of masking from the hosts immune system.

94
Q

What are some husbandry risk factors which may contribute to eimeria infections?

A

Overcrowding
Stress (climate)
Poor hygiene
Poor nutrition

95
Q

How can you diagnose different eimeria species?

A

Based on oocyte morphology and where haemorrhage is in GIT (need to do a shallow scrape)

96
Q

What solution is needed for sporulation of eimeria?

A

2% potassium dichromate

97
Q

How might you control coccidiosis in poultry?

A
  1. Vaccination (inoculate chick or hatchery, live or live attenuated available with species specific immunity induced)
  2. Hygiene (clean with ammonia based disinfectants; quarantine; on farm biosecurity)
98
Q

What causes hepatic coccidiosis in rabbits? What are some signs of this disease?

A

Eimeria stiedae.

Clinical signs: jaundice, diarrhoea, sudden death
PM signs: focal white-yellow nodules or cords in liver along path of bile ducts, cholangitis

(Merogony occurs in bile duct/ gall bladder epithelium)

99
Q

Which eimeria species are found in cattle? What age cattle do they affect and what do they cause?

A

E. zuernii and E. bovis

1-2 month old calves

Calf diarrhoea/ bloody scours and secondary colibacillosis. Subclinical coccidiosis May lead to production losses

100
Q

What are some treatment/ control options for coccidiosis in cattle?

A

Have coccidiostats in milk replacer (monensin, lasalocid)

Single drench before weaning (toltazuril)

101
Q

Coccidiosis affects what age lambs? What species are involved? How might it be prevented?

A

1-5 month old
E. crandallis and E. ovinoidalis
Prevention: coccidiostats in feed, drench ewes 21 days prior to lambing, prior to weaning in lambs

102
Q

What is the PPP for cystisospora? How is it diagnosed? How may it be treated?

A

4-11 days
Dx: faecal float
Tx: supportive care, sulphonamides (1-2 weeks) or toltrazuril for 1-3 days
Prevent with mass treatment of all animals, drench before whelping and during lactation

103
Q

How might you control cystisospora in piglets?

A
All in all out system 
Hygiene
Biosecurity
Medicare sow feed with coccidiostats
Piglets: single dose of toltazuril (3-5 days) or long acting sulphonamide at 6 days old
104
Q

What are the reproductive stages of the protozoa Apicomplexa?

A

Schizogony (asexual): schizont -> merozoite (shattering pathogenic stage)

Gametogeny (sexual): gamont-> zygote -> unsporulated cyst

Sporogony (asexual): sporocyst -> sporozoite (infective unit)

105
Q

What is the difference in sporulated morphology between eimeria, isospora and sarcocystic apicomplexans?

A

Eimeria 1:4:2 (1 oocyte, 4 sporocysts, 2 sporozoites)
Isospora 1:2:4
Sarcocystis 0:2:4

(Crypto is 1:0:4)

106
Q

What is the prepatent period for eimeria? How long does sporulation take?

A

3-21 days

1-3 days (21-30 degrees, humid)

107
Q

How do you diagnose coccidiosis due to eimeria? How do you treat it?

A

PM- gross observation (site of GIT haemorrhage)
Histo- schizonts with merozoites

Antemortem techniques include:
Faecal float (look at oocyte morphology/size)
Sporulation in 2% potassium dichromate. McMaster method for oocyte counts and Id

Tx:
supportive (fluids and electrolytes)
prevention!! (None registered for layers, so in chickens give regular doses of anti-coccidials)

108
Q

What are some common anti-coccidial agents? (State in what animals they can be used and briefly how they act)

A

Ionophore antibiotics such as monensin (chickens, turkeys, cattle, sheep, goats; affect cell membranes; coccidiostatic). Only effective for extracellular stages!

Toltrazuril (poultry, dogs, cattle, sheep, pigs; coccidiocidal- affect plastid-like organelles). Single dose for prophylaxis, multiple for treatment. Long withdrawal

Sulfonamides- (birds, dogs, cats, pigs; coccidiocidal; interfere w/ folate and DNA prduction)

Vaccines (live and live attenuated, species specific)

109
Q

What eimeria species affect chickens and have high pathogenicity effects? How about cattle? In lambs?

A

Chickens: E. tenella, E. necatrix, E. acervulina and E. brunetti

Cattle: E. bovis and E. zuernii (1-2 month old calves)

Lambs: E. crandallis and E. ovinoidalis (1-5 month old lambs)

110
Q

Briefly illustrate the life cycle of eimeria.

A

Oocysts shed in faeces ➡️ sporulates ➡️ swallowed by IH ➡️ excystation and release of sporocysts ➡️ sporocysts release sporozoites ➡️ invade gut cells ➡️ trophozoite ➡️ schizont ➡️ merozoites released from schizont ➡️ male and female gametes ➡️developing oocyst

111
Q

What eimeria species affects rabbits?

A

Eimeria stiedae. Undergoes merogony in bile duct and gall bladder epithelium.

Caused jaundice, diarrhoea, sudden death, focal white yellow nodules or cords in liver and cholangitis

112
Q

How can you prevent coccidiosis in lambs?

A

Coccidiostats in feed. 21 days prior to lambing (ewe) and prior to weaning in lambs

113
Q

What are some host specific species of cystisospora for the following animals
Dog
Cat
Pig

A

Dog: C. canis, C. ohioensis complex
Cat: C. felis, C. rivolta
Pig: C. suis

114
Q

How common is disease caused by cystisospora in adult dogs?

A

Not very common. Strong acquired immunity develops following infection therefore more likely to see in puppies (manifests as diarrhoea)

115
Q

Propose a treatment for a dog infected with cystisospora.

A
Supportive care (fluids/electrolytes) 
Give sulphonamides for 1-2 weeks, OR toltrazuril for 1-3 days

Prevent with good hygiene practices, ammonia based disinfectants, prophylactic treatment before whelping and during lactation. Also prevent predation and feeding of raw meat

116
Q

What are the three forms of cryptosporidiosis? What do they cause?

A
  1. Intestinal: diarrhoea, steatorrhea
  2. Gastric: Postprandial regurgitation
  3. Respiratory problems mainly in birds (C. baileyi)
117
Q

What is the pathogenesis of cryptosporidiosis?

A

Sit in epicellular position of microvillous borders. Cause villous atrophy and T-cell induced apoptosis.
Also cause cytokines release leading to increased water and chloride ➡️ watery diarrhoea and malabsorption

118
Q

What parasite should you be aware of in swimming pools? Why? Where else should you be particularly aware of it?

A

Cryptosporidium parvum. It’s the only zoonotic crypto and it is resistant to chlorine. It is a major water-borne pathogen that causes self-limiting diarrhoea (2-4 weeks)

Calves <4 weeks old. Shed for 4-5 weeks. They have a high intensity of oocyte excretion if infected with a very low infectious dose (5-10 oocysts)

119
Q

How might crypto be diagnosed? How might it be treated in calves?

A
Zinc or sucrose floats (SG: 1.12-1.18)
Immunofluorescence (oocyst wall protein)
MZN stain (acid fast)
ELISA or immunochromatography
PCR

Tx:
Supportive care
Hyper-immune bovine colostrum
Halofuginone (reduces oocyte output)

120
Q

What is the IH for toxoplasma gondii? How long is is shed from the DH?

A

Any warm blooded animal (DH is felids). Cats will shed oocysts in faeces for 10-21 days.

121
Q

Which Toxoplasma developmental stage is capable of crossing the placenta?

A

Tachyzoites

122
Q

Toxoplasmosis acute, subacute or chronic symptoms in susceptible hosts. What is the difference?

A

Acute: caused by proliferating tachyzoites ➡️ flu-like symptoms. Immunity may develop (and symptoms subside) or may persist and form subacute disease characterised by lesions in the liver, lungs, heart, brain and/or eyes (chorioretinitis).

Chronic infections are caused by encysted bradyzoites usually cause no clinical signs

123
Q

How might T. gondii be diagnosed? How might it be treated?

A

Dx:
Faecal float (only sheds for 10-21 days)
Ab detection (IgM or IgG)
Detection of tachyzoites via biopsy, CSF, PCR
CBC and biochem (to look for organ specific disease)
Other ancillary tests (eg. X-ray)

Tx:
Pyrimethamine plus clindamycin, sulfonamides or azithromycin (to suppress tachyzoite replication)

Prevention:
Hygiene, cooking or deep freezing of meat, washing vegetables (vaccine available in sheep)

124
Q

What is the significance of neospora infections?

A
  1. Causes abortion on cattle at 5-7 months
  2. Can cause congenital malformations in cattle
  3. Can have asymptomatic carrier calves
  4. Causes paralysis in pups
  5. Can cause multisystemic disease in older or immunocompromised dogs
125
Q

What are some pathognomonic signs of neospora in dogs?

A

Progressive Polyradiculoneuritis

Myositis

126
Q

What is the significance of sarcocystis?

A

Condemnation of carcasses (sheep and cattle)
Vasculitis ➡️ abortions, still-births, multisystemic disease, equine protozoal myeloencephalitis, myositis, fever
Zoonotic (S. hominis, S. suihominis)

127
Q

How does sarcocystis differ to toxoplasma?

A

No schizogony in DH (occurs in cyst). Shed in sporulated form

128
Q

How can sarcocystis be diagnosed?

A

Histopath
PM inspection
PCR
Sporocysts in faeces of DHs

129
Q

How is babesia transmitted? What does it cause?

A

Tick vector

High fever, shaking, chills, haemolytic anaemia, organ failure

130
Q

Which species are responsible for babesiosis in dogs? What do they cause?

A

B. vogeli (rhipicephalus sanguineus) ➡️ Pyrexia, icterus, splenomegaly, haemaglobinuria. Affects pups 3-4 months old or naive adults.

B. gibsoni (haemophysalis longicornis-blush tick) ➡️ as above but more severe in adults. Also has direct and vertical transmission.

131
Q

Tell me about babesiosis in cattle.

A

▪️Caused by B. bovis and B. bigemina.
▪️Transmitted by rhipicephalus australis tick. Therefore disease distribution follows tick distribution
▪️Subclinically, it causes weight-loss and decreased mild prod’n
▪️Acutely, it causes fever, abortion, ill-thrift, pale mm, jaundice, coagulopathy, haemoglobinuria, neurological signs, death

132
Q

With regards to babesia, where does schizogony occur?

A

In RBCs

133
Q

What makes immunity to babesia inversely proportional to age?

A

Strong spleen dependent innate response to initial infection in young cattle

134
Q

How might babesia be diagnosed?

A

Dx:
History
Blood smears (with romanovsky stain)-look for piroplasm size, morphology
Serology
PCR
PM signs (semi-translucent blood that does not clot, haemoglobinuria, distended capillaries, enlarged spleen etc. )

135
Q

How can babesiosis be treated?

A
  1. Supportive care (blood transfusion, Fe and vitB12 supp)
  2. Anti-protozoal agents (eg. Imidocarb dipropionate, diminazine aceturate)

In dogs it is difficult as relapses are common. Can give macrolid antibiotic plus antiprotozoal drug (eg. Clindamycin and imidocarb)

136
Q

What are some theileria species of significance?where are they important?
What is their vector?

A

T. orientalis buffali
T. orientalis ikeda
T. orientalis chitose

America, Southern Europe, Africa

Ixodid ticks

137
Q

Theileria parva causes what? What about theileria annulata?

A

East coast fever (hyalomma spp. of ticks)

Mediterranean or tropical theileriosis (R. appendiculatus)

138
Q

Where do the two major schizogony phases of theileria occur?

A
  1. Leukocytes, lymphoid tissue
  2. RBCs

(Gametogony occurs in tick gut)

139
Q

How might you diagnose theileria?how might you treat it?

A

Dx: similar to babesia
Fever, lymphadenopathy, blood smears (infected leukocytes, Maltese cross, bayonet cells)

Tx:
Buparvaquone or primaquine (not registered in Aust)
Imidocarb, erythromycin in calves, halofuginone at high dose

140
Q

What is plasmodium responsible for and where is it endemic?

What are the DH and IHs?

A

Malaria!
PNG and SE Asia
DH- female mosquito (anopheles), IH- vertebrate

141
Q

Where do the different schizogony phases occur for plasmodium?

A

1st: hepatocytes
2nd: intra-erythrocytic

142
Q

What are hypnozoites?

A

Dormant stage of plasmodium

143
Q

How can malaria be diagnosed and controlled?

A

Dx: blood smears (giemsa, romanovsky stain), pcr
Control: mosquito control (bed nets, repellants, biological- wolbachia), drugs (eg. Quinone, chloroquinone)

144
Q

How might neospora caninum be transmitted?

A

Transplacental transmission can occur in dogs. Significant knowledge gaps otherwise

145
Q

What are some characteristic features of giardia?

A

Half pear shaped trophozoites

8 flagella

146
Q

What is the common name for Diphyllobothrium latum?what does it cause and how might you treat it?

A

=broad fish tapeworm

➡️ nausea, abdominal discomfort, diarrhoea, vit B12 def, anaemia

Tx: praziquantel and niclosamide

147
Q

What causes sparganosis? What are the definitive hosts? How might it be treated?

A

Spirometra erinacei (zipper worm)
Dogs and cats
Praziquantel (x5) or surgery

*can lead to blindness

148
Q

What is the common name for dipylidium caninum? What are the intermediate and definitive hosts? How is it treated?

What is a defining characteristic of this worm?

A

Double-pored tapeworm
DH= dogs, cats and humans
IH= fleas (ctenocephalides canis/felis, trichodectus canis)
Can cause anal irritation and is zoonotic

Cucumber seed-shaped segments and a retractable scolex

149
Q

What are some characteristic features of anoplpcephalan tapeworms? What is their IH?

What do they cause?
How can they be diagnosed and treated?

A

Large lappets and thin leaf-like proglottids

Transmitted via oribatid mites

➡️ ulceration, diptheretic membrane/ thickening, diarrhoea, ileo-caecal intussusception
Dx: serology, coprology
Tx: praziquantel, pyrantel

150
Q

What is a characteristic feature of moniezia spp. of tapeworm?
What is the DH?

A

Inter-proglottid glands and 2x genitalia per segment

M. benedini = mainly cattle
M. expansa = mainly sheep

151
Q

Which are the non-taeniid cyclophyllidea pathogenic to birds. What are their IH? (What are the non-path genera?)

A

Raillietina (large)- arthropod IH
Davainea (sml)- slugs

(Choanotaenia (lge) and Amoebotaenia (sml))

152
Q

Which taenia species are zoonotic?

A

T. solium and T. multiceps

153
Q

What is the pork measles worm? What does it cause?

What causes sheep measles?

A

Taenia solium
cysticerci nodules on the muscles, heart, tongue, diaphragm etc. in humans (which are accidental hosts), it can cause neurocysticercosis or ocular cysticercosis

Taenia ovis

154
Q

What are beef measles? What tapeworm is associated with black disease?

A

Cysticerci nodules caused by T.saginata in cattle

Taenia hydatigena

155
Q

What causes gid or sturdy? What is it?

What are some Ddx?

A

Progressive disease affecting sheep, goats, cattle, humans.
Over 6-8 months the animal develops in coordination, head pushing, blindness.
Caused by taenia multiceps.

Ddx: listeriosis, scrapie, mad cow disease, parelaphostrongylosis

156
Q

What is the intermediate host of taenia serialis? What is the Dh?

A
IH= rabbits
DH= canids
157
Q

What is the common name for echinococcus granulosus? What are it’s effects?

A

Hydatid tapeworm
In dogs -> “furred intestine”. No real pathological effects
In sheep and other IH -> cystic hydatidosis which can cause pressure atrophy, collateral circulation, and, if ruptured, anaphylactic shock.

158
Q

What is the drug of choice against adult cestodes? What else is important in treating cestodes?

A

Praziquantel!

(Except in D. caninum need to test the fleas as well!)

Other: education campaigns, regular treatment of dogs with praziquantel, and abattoir surveillance (and vaccines in future)

159
Q

How might you treat cystic hydatidosis?

A

Drain fluid to prevent spread of hydatids (from rupture)
Add fixative
+/- surgical removal

With drugs (try fenbendazole because it is lipid soluble and can penetrate tissues)

160
Q

What are some measures of control for echinococcosis?

A
  1. Epidemiological surveillance
    - dx in canids (coproantigen, PCR tests)
    - abattoir surveillance
    - dx in humans
    - immunological, x-ray and US
  2. Control measures
    - education, legislation and implementation
    - prevent access of dogs to infected offal
    - correct disposal of offal
    - regular treatment of dogs
    - exclude dogs from pastures
    - prevent contact between dogs and humans where endemic
    - *vaccination of IH
161
Q

What does eimeria cause?

A

Coocidiosis
Involves scours/ diarrhoea (that may be haemorrhagic). Immunity is species specific. Therefore naive animals (esp weaners) mostly affected

162
Q

What are some clinical signs of giardiosis?

A

Chronic subclinical infection leads to stunted growth and reduced cognitive development.
Causes acute or chronic diarrhoea (watery/steatorrhea) in humans and animals and is common in waterborne outbreaks. Also causes flatulence and vomiting. May be asymptomatic

163
Q

How does giardia cause disease?

A

It’s an extracellular pathogen. It attaches via ventral adhesive or sucking disk to intestinal mucosa. It causes villous atrophy and malabsorption and an increase in intestinal permeability . There is strong exposure related immunity developed

164
Q

What diagnostic tools can be used for the diagnosis of giardia?

A
  1. Visualisation of motile binucleated trophozoites in fresh faecal smear- need three consecutive faecal samples
  2. Visualisation if cysts (zinc sulfate solution of sg 1.18)-faecal float
  3. In house ELISA snap tests (detects Ag of cyst wall)
  4. Pcr
165
Q

What are some treatment and control options for giardia?

A
  1. Supportive care (fluids and anti-emetics)
  2. Metronidazole for 5-7 days
  3. Fenbendazole for 5 days
  4. Hygiene, reduce overcrowding/stress (note: ammonia based cleaning is needed)
166
Q

What protozoan might cause infertility in cattle? What else might it cause?

A

Tritrichomonas foetus

Can also cause early embryonic death and causes economical losses (affected animals need to be culled)

167
Q

What agent is responsible for feline intestinal trichomoniasis? What are characteristics of this disease? How can it be diagnosed and treated?

A

Tritrichomonas blagburni
Large bowel disease, waxing and waning (chronic diarrhoea, asymptomatic shedding)
Dx: fresh faecal smear (motile trophozoite), faecal culture (takes 12 days), pcr

Tx: off label RONIDAZOLE (30mg/kg once daily for 14 days with probiotic)- be careful, can cause neurotoxicity!

168
Q

How does bovine tritrichomonas present in a cow?

A

It’s a self limiting infection. Cows are clear in 95 days. Causes mild vaginitis and discharge, metritis and salpingitis. Return to service (due to EEM). Might get pyometra due to retained foetuses. Abortions

169
Q

How can you diagnose and treat bovine tritrichomonas?

A

Dx: bull sheath wash sample (1x per week. Need to get three successive negatives at least 2 weeks after last service)
Can also do cervical wash of cow following abortion, direct microscopy, culture or PCR

Tx: test and cull, replacement virgin heifers and bulls, AI, good fencing. No approved effective treatment or vaccine in Australia. Overseas vaccination only reduces severity

170
Q

What causes canker in pigeons and trounce in falcons?

A

Trichomonas Galliano ( in upper resp tract, nasal cavity and digestive tract)

171
Q

What is the typical presentation of avian trichomoniasis?

A

Seen in squabs (young and immunocompromised)
They stop feeding, lose weight, become ruffled and dull, dyspnoeic and have difficulty swallowing

They have circumscribed caseous plaques in their oropharynx, oesophagus, crop and proventriculus (plus ulceration and abscessation).

It can be localised or systemic

172
Q

How can you diagnose and treat avian trichomoniasis?

A

Dx: scrape/ crop flush, microscopy/ pcr/ culture
Tx: quarantine, surgical removal, ronidazole, metronidazole, eliminate carriers

173
Q

How does histomoniasis present in turkeys?

How can it be diagnosed and treated?

A

CS: necrotising typhlitis, mustard diarrhoea, thickening and caseous exudate in caeca ( maybe peritonitis as well). In systemic form, see target lesions of focal necrosis in organs (liver spleen lung)

Dx: necropsy (target lesions), lesion scrapings (microscopy), histopath of lesions

Tx: anthelmintic control (for heterakis), separate chickens and turkeys, quarantine, on farm biosecurity, no registered drugs for commercial poultry. If it is a pet can use off label ronidazole or ipronidazole

174
Q

What are the three forms of trypanosomiasis? What do they each cause?

A
  1. Salivaria (sleeping sickness, Tsetse fly)
    - sleeping sickness. Systemic disease, fever, lethargy, wasting, organ failure
  2. Stercoraria (Chagas disease, triatoma)
    - systemic disease and organ failure
  3. Mechanica (via coitus)
    - genital swelling/mucous discharge, wasting, fever death
175
Q

What is nagana and how does it present?

A

African trypanasomiasis (T. evansi)

Cyclical fever, LN enlargement, splenomegaly, anaemia, lethargy, oedema, wasting, neurological, cardiac, digestive signs and death

176
Q

How can you diagnose and treat African trypanosomiasis?

A

Dx: detection of parasite of chancre, blood or CSF, thin and thick blood smears, concentration tests, detection of Ab in elisa, molecular techniques

Tx: release of sterile male flies, trypano-tolerant cattle, early test and treat, drugs (arsenicals, anti-neoplastics, diminazine, homidium bromide)

177
Q

What are the three forms of leishmania?

A
  1. Cutaneous
  2. Mucocutaneous
  3. Visceral (hepatosplenomegaly, anaemia, oedema)
178
Q

What is infantile leishmaniasis?

A

Caused by L. infantum. Dogs are primary reservoirs. Often starts as visceral disease but then goes cutaneous and forms non-specific dermatitis. Often see signs of visceral disease (eg. anaemia, wasting, protein losing nephropathy, bleeding disorders)

179
Q

How do you diagnose and treat leishmania?

A

Detection of amastigotes in RES cells. Can do blood smear, lymph node aspirate, impression smear of lesion, PCR or serology

Cx: vector and reservoir control, insecticide sprays, repellants. Treatment in dogs is controversial (meglumine + allopurinol) It suppresses clinical disease but doesn’t eliminate parasite.

180
Q

What is the significance of Balantidium coli?

A

Can be asymptomatic or cause diarrhoea in weaners.

Is zoonotic but mostly affects immunocompromised people. Can treat with nitroimidazoles

181
Q

Where is entaemoeba histolytica found (geographically)? What does it cause?

A

Tropics and subtropics
Mild diarrhoea, colitis, cramps, moderate dysentery . Severe cases may invade liver and form necrotic abscesses (in other organs too). These may rupture and cause fistulas.

182
Q

How might you treat amoebic dysentery?

A

Drain abscesses
Drugs (nitroimidazoles + paromomycin)
Basic sanitation and hygiene (indoor defecation, ban use of night soli, water treatment, wash fruit and veggies)

183
Q

What causes amoebic meningoencephalitis?

A

Naegleria
Acanthamoeba
Balamuthia

(Free-living amoeba)