Coughing Youngstock and Parasitic Respiratory Disease

integrated parasite management

-two or more things combined in order to become more effective

-system where multiple approaches for control are utilised, taking into consideration economic factors, epidemiology, resistance status, production system and management structure in place

3 categories for parasite management

-identifying risk (temporal (time of year) and geographical)

-treating appropriately (right animals at right time)

-avoiding resistance (maintain 'in refugia' parasite population

why are parasitic diseases temporal

parasites like certain weather, temp, humidity etc

trickle or low infectious challenge

over time allows immunity to develop without clinical signs of disease → want this

high abrupt infectious challenge

encountered over short period of time exceeds threshold and causes clinical/sub clinical disease

can be fatal

avoiding all parastic challenges

animals naive and susceptible to infection

worm contorl programme aim

reduce worm burden while allowing to generate immunity

cant eliminate→ overwintering, etc

grazing history risks

-when did species last graze pasture

-did they shed a lot of eggs

-were there any clinical signs: coughing or mortality?

what does lungworm like

little bit of wet and warm

temperature risks with parasitology

infective stages rely on stored energy to survive, cool and dry weather prolongs survival as movement reduces

-increased temp means more bacteria and parasites plus they move more

-can predict risk from prev weather

rainfall risks of parasites

-moisture required for larvae to igrate from pat to pasture where they are ingested

worst weather for parasite burdens

wet and hot

cattle lung nematode

only nematode in lung

-dictyocaulus viviparus

sheep lung nematodes

-dictyocaulus filaria (most pathogenic but mostly not fatal)

-muellerius capillaris (subcliinical)

-others but less common

lifecycle of dictyocaulus

adults in trachea/ bromchi

direct

what do dictylocaulus worms look like

little white hair thickness worms

lifecycle of muellerius capillaris

indirect

intermediate host: slugs nd snails

pre patent period of dictylocalus

ppp 3-4wk

dictylocaulus clinical signs

cough

poor weight gain

not really mortality

pathogenicicty of mullerius capillaris

non pathogenic or weak

risk factors for lung nematodes

-wetter/western area

-late summer/autumn

-high stocking density

-first season grazer/naive animals

life cycle of dictyocaulus viviparus

-L1 passed in faeces

-develops into infective L3 (takes <1 week in optimal conditions)

-rain, vectors and pilobolus fungus aid dispersion of L3 from dung

-L3 ingested, migrate to lungs, develop into adults which produce eggs

-eggs hatch and L1 larvae coughed up and swallowed

PPP for dictyocaulus viviparus

3-4 weeks

mushroom that spread dictyocaulus viviparus

pilobolus fungus

why can high infection levels of dictyocaulus develop quickly

L1→ L3 development fast

carrier animals of dictyocaulus viviparus

-inhibited L4

-L3 overwintering on forage are both source infection

pathoegenesis of dictyocaulus viviparus

-ingested L3 become more active in presence of bile

-cross small intestine into lymphatic system and mesenteric LNs then to lungs

-colonise alveoli then bronchioles, ending up as adults at base of trachea

what does dictyocaulus viviparus do to animal

-promotes inflam, eosinophil rich mucus and parasite debris

• host inflam itself can cause most of the damage

-inhibits gaseous exchange

-loss of ciliated epithelium → more prone to resp infection

carrier animals of dictyocaulus viviparus presentation

few adverse effects for individuals but shed

subclinical disease of dictyocaulus viviparus

-weight loss

-milk drop

→ economic loss

clinical disease of d.viviparus

-coughing

-dyspnoea

-tachypnoea

-squeaks and crackles over posterior lung lobes

-sudden death within 24-48 hours

will cows always cough with d. viviparus

May be mild and brought on by exercise through to persistent and present at rest

how might tachypnoea and dyspnoea be seen in cows

-abducted elbows and outstretched neck due to breathing difficulty

what decides the extent of disease from d.viviparus

parasitic burden and level of immunity

phases of d.viviparus

-penetration

-pre patent

-patent

-post patent

penetration phase of d.viviparus

-days 1-7 post infection

-larvae penetrate body of host and migrate to lungs

pre patent phase of d.viviparus

-day 8-25 post infection

-larvae develop into lungs so when alveoli damage occurs

-can see clinical signs if high burden

patent phase of d.viviparus

-day 26-60 post infection

-worms mature and produce eggs

post patent phase of d.viviparus

-day 61-90 post infection

-recovery phase once adult worms have been expelled

-post patent parasitic bronchitis can cause severe clinical signs/death

-immune system in this period kills parasite but causes massive antigenic stim that can cause signs→ 2ndary inflam reaction to the worms

immunity to d viviparus 2 main components

1. reduction in number of larvae reachings lungs (approx 4 months)→ short term immunity from git

2. destruction of adult worms that have reached lungs (approx 2 years)

reinfection syndrome

-immunity can wane during housing

-if cattle turned out onto heavily contam pasture large numbers reach lungs, as short duration immunity waned (so bypasses it)

-longer duration immunity in lungs kills large numbers of mature worms causing acute illness

-can be reinfected if dont see parasite again

diagnosis of d viviparus

-clin signs and grazing history

-detect L1 in faeces with baermann technique

-exam sputum for eggs/larvae

-bulk molk or blood ELISA

-post mortem

issue with baermann technique

if negative could cattle be in pre or post patent phase or could it be re infection syndrome

d. viviparus

why is sputum exam for eggs/larvae good

detects patent infection slightly earlier than faecal samples

earliest form of detection

bulk milk or blood ELISA

-sens of ELISA for patent infections low

-serconversion can take 4-6 weeks

-bulk milk useful for routine monitoring of dairy herds

-better for monitoring than diag

post mortem

adult worms seen in bronchi and bronchioles

what cells are involved in the lungs when infected with d.viviparus

alveolar macrophages

inflam cells

these take up more space than the actual worms

which lung lobe is more affeced in muellerius capillaris

caudodorsal

risk of oral administration of wormers

oral drenches may cause more stress to administer than injectable/pour-on which is important to note for animals in respiratory distress.

group 1 wormers

benzimidazoles

-no persistent action

-oral

group 2 wormers

levamisole

-no persistent action

-oral

group 3 wormers

macrocyclic lactones

-persistent action

-can be poured on back

what needs to be discussed with farmers with womrers

Farmers should be advised that treatment may worsen clinical signs.

which wormer to use on d viviparus

macrocyclic lactones e.g. ivermectin

what needs to be considered when chosing a wormer

• duration of action is an important consideration

• if going back into a potentially ‘dirty’ field – MLs have persistent activity (4-6 weeks), neither levamisole or benzimidazoles do (last about 24hrs).

issue with worming too much

cant generate immunity

what to consider with treatment of d viviparus

-route of admin

-advise farmers that treatment may worsen clin signs

-effect on parasitic gastroenteritis

-timing of treatment

-housing

best timing for treatment of d vivparus

-early season dose to reduce pasture contam/rumen boluses.

-need to allow enough exposure to promote immune response

supportive treatment for d viviparus

NSAIDs

-antibiotics if pyrexic

grazing strategies

-delay turnout

-rotational grazing

why delay turnout

keep stock in until laye april/may to reduce larval levels that have overwintered

why rotational grazing

outbreaks less predictable than parasitic gastroenteritis so harder to utilise

what does the vacc do

low level exposure

some immunity generated

so why do it a few weeks before turnout

vaccination for calves

calves more than 8 weeks old get 2 doses 4 weeks apart at least 2 weeks pre turnout

older sheep vacciantion

can give booster doses in follpwing years but if low level natural infection then will naturally boost immunity

naive and vaccinated animals

must be kept apart as the vaccine contains lungworm so if no history of lungworm do not vaccinate as would be introducing

length of time between vacciantion

not within 2 weeks of eachother

vacc for lung worm

huskvac

issues with huskvac

expensive

situational

prevention of lungworm (not vacc)

• closely monitoring stock,

• identifying low-risk grazing

• trying to achieve ‘trickle infection’ (sufficient exposure to promote immune response but not disease).

chnages to bronchioles of worms

-folding in with hyperplasia

-reaction to parasite