PID 3 Flashcards
life cycle for all of these
direct life cycle –> male and female live somewhere –> infective stage L3 –> ingested again …
morphological feature of Nematodirus
cephalic end –> bubble
epidemiology: hypobiosis
arrested development, facultative, involves only part of the parasite population, mechanism of defense (parasite waits for
arrested development in sheep
in ewes following grazing season –> don’t let parasite develop in the mucosa of the abomasum
peri-parturient rise in feacal count in sheep
increase in feacal egg count in adults –> increase in egge output in the feces on the mothers –> something to do with the immunological status during pregnanacy –> progesterone –> parasites resume development during pregnancy
function of progesterone
suppresses immunity
important thing about PPR
main source of infection in lambs
Teladorsagia circumcincta: morphology
adults 1cm length, brownish, long and thin spicules, well-developed bursa
epidemiology in clean pasture
source of contamination for lambs = PPr –> increase around April May –> 3 weeks later –> autoinfection peak/infection peak (eggs released by ewes) –>
epidemiology stages in contaminated pasture: sources of contamination
overwintered larvae
epidemiology stages in contaminated pasture: sources of contamination
overwintered larvae + PPR
epidemiology period in contaminated pasture
earlier peak of infection + peak of number of eggs per gram of feces in the lambs
epidemiology period in contaminated pasture
earlier peak of infection + peak of number of eggs per gram of feces in the lambs
epidemiology period in contaminated pasture
earlier peak of infection + peak of number of eggs per gram of feces in the lambs –> 2 peaks of infection in lambs
EPG proxi for what
parasite count burden –> BUT no accurate measure –> some species don’t lay + eggs of parasites all look identical –> can’t determine species unless look at the epidemiology
pathogenesis type 1/type 2
type 1 disease –> late summer, type 2 disease the spring of the following year
pathology in abomsaum
rise ph –> abomasum doesn’t function properly, failure to activate pepsinogen into pepsin, increases permeability of gut –> pepsinogen leaks into blood stream –> plasma proteins into abomasum ==> reduced feed consumption and diarrhoea
Haemonchus contortus morphological feature
adults 2-3cm, ovary of female coils around intestine, females have barber’s pole barbed spicules,
where is haemonchus?
temperate areas, single annual cycle –> eggs deposited by ewes in spring, ingested by lambs in summer, majority arrested
haemonchus in sub-tropical areas
several cycles of infection annually, disease outbreaks linked to local rainfall, development resumes just before rainy season
pathogenesis of haemonchus
significant loss of blood –> increased RBC turnover, loss of Hb, anf Fe, depleted Fe reserves
hyperacute haemonchus disease
death by haemorrhagic gastritis
acute disease of haemonchus
1-6 weeks, anaemia, oedema, loss of condition, lethargy
chronic disease haemonchus
2 months + –> loss of weight
Nematodirus morphological features
adults 2cm, small cephalic vesicle, male fused spicules, eggs larger than strongyles, L3s develop inside egg
Nematodirus morphological features
adults 2cm, small cephalic vesicle, male fused spicules, eggs larger than strongyles, EGGS IDENTIFIABLE –> gigantic
development of Nematodirsu
L3s develop inside eggshell, PPP ~3 weeks
epidemiology of Nematodirus –> periods in the year
L3s develop inside egg –> can survive up to 2 years on pasture (important to implement control strategies) –> hatching when prolonged period of chill + mean day temperature of at least 10°C (late spring)
when is disease of Nematodirus present
when large quantities of larvae ingested by lambs
when do you see disease of Nematodirus in the year?
three weeks after the conditions have been favourable
when is secondary peak of Nematodirus seen?
depending on weather –> ‘Indian’ summer otherwise –> overwintering until spring
pathogenesis of Nematodirus
diarrhoea –> lethargy, high mortality, 2-3 months set-back to growth
DIAGNOSIS FOR ALL PARASITES
clinical signs, history, management of flock, PM
faecal examination
floatation: parasite eggs float, either qualitative or quantitative, –> McMaster chamber = double slide –> count number of eggs in grade and multiply by dilution factor –> get eggs per gram –> BUT really inaccurate
larval culture
requires expertise
treatment and control of sheep PGE: what parasite in what order
nematodirus (April) –> Teladorsagia (June) –> Haemonchus (August)
problems with all parasites
anthelminthic resistance
practices to avoid anthelmintic resistance
new arrivals, sub-therapeutic dosing, high frequency of dosing, insufficient worms in refugia (=worm populations not exposed to drugs)
what are refugia?
leave proportion of parasite population untreated –> won’t develop resistance –> breed with resistant drug –> dilute genetic pool of resistance
how to prevent rise of anthelmintic resistance
test for it, effective quarantine procedures, use anthelmintics sparingly, dose correclty, avoid broad-spectrum anthelmintics, keep worms in refugia to ‘dilute’ resistant populations = keep 10% of the flock untreated, don’t move sheep on clean pasture directly after drenching
best drugs for haemonchus
blood feeder –> best drug that has long residual activity and stay in blood
prophylaxis by anthelmintics in ewes
management of PPR –> worm ewes around lambing and again 4-5 weeks later,
prophylaxis by anthelmintics in lambs
treat at weaning, move to clean pasture, if no alternative grazing available,dose at weaning and repeat at monthly intervals,
drug specific for haemonchus
closantel
prophylaxis by grazing management plus anthelmintics
one annual anthelmintic treatment of ewes prior to leaving the lambing field –> 3 year rotation with cattle
