Final Exam Flashcards
Strongylus vulgaris
Large strongyle
* thrombus formation, damages arterial wall, infarction
* blood feeders- anaemia, eosinophilia, elevated white cell count
* Epi- larve most abundant on pastures in spring, peak egg laying 10 months after infection
* Life cycle: L1 and L2 in faeces feed on bacteria, L3 exsheaths in SI or LI, migrates into intestinal wall- into wall of arteries and ascends to root of cranial mesenteric arteries, remains for several weeks– returns to gut in blood stream– enters lumen
PPP= 6 months.
* Treatment:
What are the important large strongyles?
Triodontophorus, Strongylus equinus, Strongylus vulgaris, Strongylus edentatus
What are the important small strongyles?
Chabertia, Oe. venulosum, Oe. dentatum, Oe. radiatum, P. rufescens, S. dentatus, Cyathostomum
What are nodule worms?
Oe. radiatum (of cattle- caecum), Oe. columbianum (of sheep- colon), Oe. venulosum (of sheep- caecum), Oe. dentatum (of pigs), Oe. quadrispinulatum (of pigs- significant pathogen)
Strongylus vulgaris
Strongylus vulgaris
Strongylus edentatus
Large strongyle
* L3 exsheaths in caecum, burrows into gut wall, enters portal veins, migrates to liver (8 weeks in the liver), migrates to the sub-peritoneal tissues, returns to gut via mesentery
* PPP= 10 months
* effect on host: found in many organs, migrating larvae cause lesions, adults cause anaemia
Strongylus equinus
Large strongyle
* L3 exsheaths in caecum, migrates into gut wall, peritoneal cavity and liver, spends 6-7 weeks in the liver, migrates via pancreas to gut
PPP= 8 months
* Effect on host: anaemia
Triodontophorus
Triodontophorus
* L3 exsheaths in caecum, L3 migrates into gland, moults to L4, L4 emerges into lumen, final moult in lumen
PPP= 9 weeks
* causes ulceration and blood loss, graze on epithelial lining of gut, occurs in groups
Cyathostomum
small strongyle (encysted)– of horses
Cyathostomum
* encysted small strongyles
* L3 exsheaths in caecum, enters caecal glands, moults to L4, L4 re-emerges into lumen, final moult in lumen
PPP= 5 weeks
* Hypobiosis is important- seasonal pattern, following removal of adults, emergence may be synchronous
* effect on host: adults feed on gut content, not pathogenic, very large numbers can cause diarrhoea, normally 115,000 encysted– can be L4 in wall and come out after treatment synchronously– can be fatal if 200,000 at once.
* Treatment: fenbendazole at 10 mg/kg BW for 5 days and then moxidectin at 0.4 mg/kg BW
* Diagnosis: find eggs in faeces, use mcmaster chamber, >300 epg pathogenic, larval culture to ID genera
Chabertia ovina
*small strongyle of ruminants
* Location: colon
* Hosts: sheep, goats, and cattle
* L3 exsheaths in SI, enters mucosal galnds, moults to L4, L4 returns to lumen, migrates to large intestine, final moult in LI
PPP= 8 weeks
* effect on host: feed on mucosa, causes haemorrhage, excess mucous production, diarrhoea, more prevalent in temperate areas, strong immunity develops, usually only a few present… > 200 pathogenic, females lay 3000 eggs/day
Oesophagostomum radiatum
* nodule worms of cattle
* L3 migrates into glands in SI and/or LI, L4 emerges and migrates to LI
PPP= 5-6 weeks
* effect on host: susceptible young host- no reaction and therefore nodule formation (second time larger nodules due to hypersensitivity)… but resistance animals intense reaction of the immune system– eosinophilia.. and less nodules formed… some will migrate into the lumen and develop into adults but not many.
** nodules will interfere with gut motility, anorexia, reduced weight gains, and diarrhoea in adults
* strong immunity by 12 months of age
Stephanurus dentatus
* eggs passed in urine, L3 ingested or can penetrate skin, migrate to liver via portal system (3 days) or aorta (8-40 days), migrate in liver for 2-3 months, migrate to perirenal area…. may migrate anywhere in the body
PPP= 9 months
* effect on host- fibrosis in liver, abscesses in carcass, organs condemned at slaughter, weight loss
* Diagnosis- eggs in urine, elevated liver enzymes
Syngamus trachea
* Eggs coughed up, swallowed, L1-L3 within egg, molluscs, oligochaetes are the paratenic hosts, L3 ingested, migrates to trachea via liver than lungs (in circulation)
PPP= 2 weeks
* effects on host: excess mucus production, block airways, respiratory distress- birds gape, blood feeders
* Diagnosis- eggs in feaces (ellipsoidal thin shelled eggs with a thick operculum at both sides)
Ancylostoma caninum
* encysted strongyles
* treatment: fenbendazole and moxidectin (day 40 pregnancy treatment regime everyday until whelping will kill greater than 90% of larvae)
* skin penetration and transmammary infection important
* adult can be dormant in muscles–> SI (via circulation)
* Effect on host: females 0.1 ml/day, black tarry faeces, microcytic, hypochromic anaemia, heavy infestations (pups) cause death, strong immunity following exposure
* epi: common in warm climates, less common in southern Australia, sandy or loam areas ideal for larva
* Diagnosis: eggs in faeces, egg counts high > 5000 epg, eggs small < 65 micrometers
* older dogs- chronic
* zoonosis (eosinophilic enteritis in man)
Ancylostoma braziliense
* common in tropical and sub-tropical regions
* less pathogenic- can cause hypoproteinaemia and diarrhoea
* primary cause of cutaneous larva migrans or creeping eruption in man
* tortuous erythmatous inflammatory tracts within dermis associated with severe pruritis
Bunostomum phlebotomum- cattle- SI
* found mainly in warm areas, skin penetration, transcolostral infection
* cause anaemia, hypoproteinaemia and 1000 fatal burden!!!
PPP= 7 weeks
Bunostomum trigonocephalum- sheep- SI
* found mainly in warm areas, skin penetration, transcolostral infection
* cause anaemia, hypoproteinaemia and 1000 fatal burden!!!
PPP= 7 weeks
Globocephalus- hookworms of pigs
* found mainly in warm areas, skin penetration, transcolostral infection
* cause anaemia, hypoproteinaemia and 1000 fatal burden!!! Weight loss too
PPP= 7 weeks
General characteristics
Dictyocaulus spp.
* long slender worms
* up to 10 cm long
* location- trachea and bronchi
Main hookworm of dogs
Uncinaria stenocephala
* common in cooler areas
* L3 are ingested
* no extra- intenstinal migration
* less pathogenic
* eggs > 65 micrometers
Strongylus equinus
What are the three that affect sheep in the small intestine in Australia?
Trichostrongylus
* Trichostrongylus vitrinus, T. rugatus, T. colubriformis
What are the three from the SI of a sheep?
Nematodirus
* N. spathiger, N. filicollis, N. abnormalis
What is this one?
What are the other two found in goats and sheep?
Cattle?
Ostertagia circumcincta
* goats and sheep: O. trifurcata, Teladorsagia davtiani
* Ostertagia ostertagi
Strongylus vulgaris
Bunostomum phlebotomum
Triodontophorus (caecum of a horse)
Cyathostomum (caecum of a horse)
Oesophagostomum venulosum (caecum of a sheep)
From a pig. Name the genus
Oesophagostomum (could be either Oe. quadrispinulatum or Oe. dentatum)
Ancylostoma caninum
Chabertia ovina
What is the genus.
Name the four species found in cattle and one found in sheep.
Cooperia
Cattle: C. oncophora, C. surnabada, C. pectinata, C. punctata
Sheep: C. curticei
Oesophagostomum radiatum (little hat!)
Uncinaria stephocephala (cutting plates)
Aelurostrongylus abstrusus
Aerulostrongylus abstrusus
Strongylus edentatus
Ostertagia ostertagi (arrested larvae- L4)
Histopathological changes caused by intestinal parasites
* hypoproteinaemia because of increased permeability of capillaries and therefore leakage of plasma proteins into gut, globulin levels increasing in blood to mount immune response (therefore reduced wool production and reduced growth rate)
* villous atrophy
* Reduced bone growth because cannot take in calcium (absorption occurs in the duodenum)
* Anorexia- feed intake reduced
* Diarrhoea- parasites secrete analogues of parasympathetic transmitters, increased frequency and strength of peristaltic waves, together with poor absorption leads to diarrhoea (dag score)
Ostertagia
Trichostrongyloid eggs (which are trichostrongylus, nematodirus, haemonchus, ostertagia, cooperia)
ID of L3 trichostrongyloid nematodes
a. Teladorsagia circumcinta
b. Trichostrongylus
c. Haemonchus contortus
ID of L3 trichostrongyloid nematodes
a- larva and sheath
b- tail
c- sheath
d- length of filament
Argas persicus life cycle
Egg- Larva- 2 nymphs- Adult
Morphological identification of lungworms L1 stage- why is this important in sheep?
ID of lungworms in live animals. e.g. Sheep can be infected by 3 types of lungworms
Muelleris capillaris
Protostrongylus rufescens
Dictyocaulus filaria
What are the three lungworms of pigs?
Metastrongylus apri, M. pudendotectus, M. salmi
Lungworms of dogs
Angiostrongylus vasorum (pulmonary artery)
Lungworms of cats
Aelurostrongylus abstrusus
Angiostrongylus vasorum and Aelurostrongylus abstrusus
Fresh faeces of a dog- what could you find if infected?
L1 of strongyloides stercoralis and eggs of A. caninum.. You could also find Uncinaria stenocephala eggs.
Treatment of inhibited ostertagia
Broad spectrum anthelmintics will kill most hypobiosed larvae of ostertagia
Direct Life cycle of lungworms- which ones of dogs? What is the odd one out?
Oslerus osleri (trachea) and Filaroides hirithri (alveoli) have direct lifecycles with no intermediate host.
Angiostrongylus vasorum howevere has a snail as an intermediate host. Common in Europe though, not in AUS.
Simple direct life cycle of lung worms- which ones? which hosts?
Dictyocaulus. Ruminants and horses.
* L1-L3 in faeces, L3 ingested, migrates to lungs via lymphatic system.
PPP= 21 days.
Which lungworms have an intermediate host?
Protostrongylus rufescens, Muellerius capillaris, Metastrongylus, Aelurostrongylus
What do both Haemonchus and Trichostrongylus have in common in regards to host immunity? (Ostertagia too)
Self cure- basically most animals have some immunity by 12 months of age.
How do you control trichostrongyles?
* Smart grazing- overgrazing with wethers, treat with anthelmintics to overgraze and expose the worms killing them with UV rays– therefore wethers drop less eggs to keep contamination low and ready for weaners who have no immune system– do this three times with a rest of about a month in between (this is preparing for the weaner lambs)
* Paddock spelling- effective over summer
* Crops- sowing reduced contamination
* alternate grazing (except for T. axei)- horses and kangaroo. (goats and sheep have the same parasites though)
*Anthelmintic drugs- timing of treatments– treat in the SUMMER!!! winter treatments have limited effects (in southern Australia) because L3 pasture count is low, so larva picked up is low
Type I Ostertagiasis vs. Type II Ostertagiasis
Type 1: in spring and winter occurring in the animals which are exposed to L3 of Ostertagia during their first grazing season. Young animals with no immunity. Diagnose with egg counts and plasma pepsinogen
Type II: Occurs in autumn in pregnant 2-4 year old animals due to autumn calving and stress– larvae emerge synchronously… Diagnose with plasma pepsinogen. This occurs in the autumn because they are undergoing hypobiosis in the summer and therefore emerge when conditions are more favorable.
Life cycle of Strongyloides
* L1- L3 develops in the soil free living feeding on bacteria– can either penetrate skin, ingested (less imp. route of infection), or develop on soil to adult.
* female is parthenogenetic.
* HETEROGONIC- free living– WHICH WILL HAVE RHABDITIFORM
* HOMOGONIC- parasitic life cycle– WHICH WILL HAVE STRONGYLIFORM (infective and parasitic stages)
** Auto-infection can occur
** S. ransomi important in pigs– because they travel through the lungs and can cause pneumonia, dermatitis, diarrhoea, and reduced growth rate
* S. ransomi, S. papillosus, S. westeri– all transcolostral
Treatment of hookworms for domestic species (A. caninum and U. stenocephala)?
Febantel (BZ), pyrantel (tetrahydropyrimidines), selamectin (ML)
What is Ostertagia resistant to?
What is Haemonchus resistant to?
What should you use to treat?
How do you control the parasites and prevent re-infection?
Ostertagia resistant to BZs.
Haemonchus resistant to Levamisole.
So use a combo. Or you can use Montepatel or Salicylanilides for Haemonchus.
* Vaccinate (against haemonchus at least), switch classes every two years, treat only affected animals, do regular FEC (1-2 times per year), strategic deworming, rotational grazing
How would you treat Dictyocaulus?
Tertiary BZs, Levamisole, MLs will do the job.
NSAIDs often as well to deal with inflammation.
Faecal flotation
* mix infected host faeces with water- sieving out debris using forced water flow- then use NaCl (due to specific gravity but not too high because faecal/ debris matter will then rise to the top). (1.2 specific gravity).
Critical test for efficacy of anthelmintics
Comparing the number of worms expelled by the animal to the number remaining at necropsy.
Each animal is maintained singly and dosed with the test compound. Faeces are collected daily from one day before treatment and usually 7 days post treatment, when the animal is killed and necropsied. Worms recovered from the faeces and at necropsy are identified and counted.
The efficacy is calculated using the following formula
% efficacy= (Ex100)/(E+N)
E= number of parasites expelled in faeces
N= number of parasites remaining at necropsy
** disadvantage is that parasites normally found in the stomach may be partially digested when passed in the faeces and therefore difficult to ID.
Will topical macrocyclic lactone (selamectin) kill Felicolus subrostratus?
Yes
Can Damalinia ovis persist away from host? What are D. ovis resistant to?
No. D. ovis are resistant to synthetic pyrethroids but they can be successfully treated with ivermectin.
This parasite was found in a scraping taken from scabs on the scrotum of a sheep.
Chorioptes bovis. Can also be found on horses and cattle. found on the ventral midline, axilla, legs
* can be treated with a variety of things!! oral or topical
What mite and louse can cause pulled wool of sheep?
Psorergates ovis and Damalinia ovis
Linguatula serrata
Indirect.
Tx: Flood nasal cavity with ivermectin
Nematocera (midges, mosquitoes)
Brachycera (march or horse flies)
Cyclorrhapha (true flies)
Where do Cuilicoides brevitarsis breed? Why are they important?
Cattle dung. Transmit Blue Tongue.
Midges only feed at night, so stable horses, use repellents.
Chorioptes bovis.
Scrotal mange in rams. Legs and belly affected too.
Psoroptes ovis- lives under scabs, jabs hyperstome in and feeds on tissue fluids. Causes serous exudate. Irritation and scabs and hypersensitivity. Starts on shoulders and back and spread all over body.
Can have emaciation and high mortality as sheep stop eating.
** most abundant when fleece long= cool weather, life- cycle 9-10 days.
ERADICATED FROM AUS
Ornithonyssus spp. (O. bursa or O. sylviarun)
Severe anaemia and reduced egg production (not host specific)
Dermanyssus gallinae (Mesostigmata)
7 days LC
Feeds nocturnally
Anaemia, irritation, Borrelia anserina (blood infection and fever)
Haemaphysalis longicornis: bush tick
Cattle, dogs and others
3 host tick
Eastern AUS/ SE Asia
Anaemia, hide damage, vector Babesia gibsoni of dogs
Rhipicephalus sanguineus: brown dog tick
* tropical countries, northern AUS, present in melb but uncommon
* dog
* Anaemima and irritation, vector Babesia canis
Aponomma and Ambylomma
* Long mouthparts, ornate
* Important in cattle in Africa and USA… in AUS on repitles.
Haemaphysalis longicornis
Haemaphysalis longicornis
Haemaphysalis longicornis
Boophilus microplus
Boophilus microplus
Boophilus microplus
Wet tropics grazing cattle (QLD). Lost appetite.
Boophilus microplus
Horses, sheep, dogs, and pigs
eggs hatch–> seed ticks climb up grass and attach to passing cattle, larvae, and nymph remain on cattle and moult quickly to form adults. Female ticks drop off (early morning 18-37, mostly day 22) and lay eggs
** can’t travel far <1 m or blown 30 m
* controlled by temp and humidity. Winters suppress tick development.
* Control by spelling paddocks: 4 weeks in summer, 10% will survive. 11 weeks in cooler weather. High level of resistance… currently using MLs with growth regulators. 4 x pour on treatments at 35 day intervals…. vaccine against tick gut protein.
Ixodes holocyclus
* 1 larval, 1 nymph, 1 adult stage
* LC 19 months- spends 6 months in environment between moults (larvae and adults in spring, nymphs in autumn)
* Females engorge up to 21 days
* find and remove tick, acaricidal wash (pyrethroids or OPs), hyperimmune serum neutralizes toxin, some animals can develop immunity when exposed at low doses (nymph and larva)
Ixodes holocyclus
Ixodes holocyclus
Rhipicephalus sanguineus
Rhipicephalus sanguineus
Argas persicus- what is the LC? Which life stage causes paralysis? Which do you see on chickens? What are problems? Control?
Eggs laid in cracks–> hatch in 3 weeks–> larvae feed for 5-10 days–> moult in crevices in the shed–> 4 nymph stages feed 1-2 hours–> moult to adults and they feed in minutes
* larval stag they feed the longest and cause the paralysis- need 6 on a chicken to cause paralysis
* Other problems: Anaemia and irritation leads to loss in egg production, transmits Borrelia anserina (tick fever) and Aegyptianella pullorum
* Control: OP spray, kerosene emulsion
General life cycle of a flea
Eggs fall to ground–> larva hatches (anal struts and hairy)–> 3 larval stages in the environment, feed on detritus (broken down organic matter and skin cells)–> pupal stage (can last long time inside >1 year, outdoors less)–> adult flea emerges–> jumps on host–> female needs blood meal to produce lots of eggs
What are some blow flies that might cause secondary strike?
*Green and native: Chrysomya rufifacies (larvae feeds on maggots, Chrysomya varipes
* Brown and native: Calliphora stygia, Calliphora augur
Control of blow fly strike
Most common form of blow fly strike? Predisposing characteristics? When?
Lucilia cuprina’s life cycle? How does it strike? Clinical signs?
Haematobia exigua
Gasterophilus
