Cattle 3 Flashcards
Faecal egg count (larval culture) to diagnose nematodes how done, individual or bulk, interpretation and what need to consider, what is important to do - EXAM
○ Eggs float in saturated NaCl or ZnSO4 solutions
○ Generally NOT done as a bulk unlike sheep -> treat individually
○ FEC interpretation difficult
§ Large volume of faeces
§ Mixed populations
§ Mixed stages
§ Ostertagia low fecundity; Cooperia very high
□ Higher pathogenicity vs low
□ Cannot differentiate eggs
○ Need to do a larval culture -> hatch eggs and identify the percentage of each larvae present
Plasma pepsinogen in the diagnosis of nematodes what does it measure and therefore disease it detects, what does not detect, what is important factor to note about secretion and drench
○ A measure of Ostertagia damage to abomasum
○ In Type I Ostertagiasis only
○ Does not rise with hypobiotic larvae
○ Half-life (days), secretion does not stop immediately
§ Can’t drench and then test efficacy 10 days later with this
§ BUT can be used to determine if parasite an issue EVEN IF been drenched
Bulk milk ostertagia ELISA what is it, what does it detect, where common, how to interpret and what need to consider
○ An ELISA is available on vat milk
○ detects the level of parasitism regardless of whether cows are clinically affected or not
○ detects antibodies to Cooperia, Dictyocaulusand Ostertagia
○ Common in NZ; sporadic use in AUS
○ Difficult to interpret
○ Antibodies have a half-life measured in months!
Toxocariasis what is it, main one that is the issue, length, age an issue, what results in and treatment
(large roundworm infection)
- Toxocara vitulorum
- Up to 30cm long
- Thick pitted eggs diagnostic
- Calves 1 -6 months of age
- Can cross the placenta
- Normally self -cure
- No specific treatments usually in Australia
- Serious in buffalos!
Intestinal cestodes what are they, structures, length, what do they do to host, what drench cannot use
- Tapeworms
- Scolex and then lots of proglottids
- Several metres long
- Only one point of attachment
- Absorb nutrients directly through skin
- Don’t do much harm
- Intermediate host (pasture mites)
- Not susceptible to MLs unlike nematodes
○ Every 2-3 years rotate to drench that deal with tapeworms
What are the 4 main intestinal cestodes and the disease they cause
1) Moniezia bendeniand M. expansa
2) Cysticercosis
○ Taenia saginata(Cysticercusbovis)
3) Echinococcus granulosis
○ The most common cause of downgrades in QLD abattoirs
○ Notifiable
○ NZ is hydatidfree (? Tasmania too)
4) Coenurosis cerebralis(Taenia multiceps)
Tremadoes what is the main one, species involved in, general presentation and main time found
- Fasciola hepatica
- Parasite of all grazing ruminants
- Also kangaroos, wombats and rabbits
- Humans too (contaminated water -water cress (ingestion of plant))!
- Any time but mostly Spring
Presentation - Chronic wasting disease
- Mostly calves and yearlings
- Anaemia , weakness, death well described but uncommon
- Loss of production, weight gain, fertility etc common
- Condemnation of livers at slaughter
- Black disease (Cl novyi) & bacilliary haemoglobinuria (Cl haemolyticum
Liver fluke transmission and the 7 steps in lifecycle, how long live for
Intermediate hosts
- Lymnea tomentosa (native)
- L columella (introduced)
- Both live in bodies of water
Pathogenesis
1. Ingestion of encysted metacercariaeon forage or while drinking
2. > immature flukes in small intestine (1mm)
3. Burrow through intestinal well
4. Migrate through peritoneum to liver
5. Penetrate liver (4 -5 days)
6. Feed and migrate in parenchyma for 5 -8w
7. Move to bile ducts where they lay eggs
○ 10,000 eggs per day
- Live 6mo -2 years
Acute fluke disease and chornic fluke disease clinical signs and what occurs
Acute Fluke Disease
- Large numbers of migrating juvenile fluke common in sheep
- Blood loss associated with feeding of adult fluke more a problem in cattle
- Anorexia, weakness, reluctance to move
- Hypochromic but normocytic anaemia with eosinophilia
Chronic disease
- Can be subclinical to clinical
- Adults in bile ducts
- 5-10% drop in milk yield with low burden
- 54 fluke caused 9% growth rate decrease
- 300 -400 fluke caused anaemia and hypoproteinemia - bottle jaw
Liver fluke diagnosis what are the 3 main ones
1) faecal egg count
2) antibody ELISA
3) post-mortem - find flukes, scarring
Faecal egg count for diagnosis of liver fluke how to perform, what is high, main issues
○ Do not float well in normal solutions
○ Many labs use sedimentation techniques
○ Very dense solutions can cause osmotic collapse of eggs
○ Most cattle <10 epg; >100 is very high
Main issues
○ False negatives due to pooling in gall bladder
○ Low sensitivity of bulk egg counts
Only detects adult fluke infection (12w after infection)
Antibody ELISA for diagnosis of liver fluke sensitivity, what detects, in what samples and what useful for
○ Sensitivity of 97.5% reported (cf~70% for FEC)
○ Detects non-patent infections (from 14d)
○ Blood, milk or bulk milk
○ Useful as a screening test for a group of animals
§ Ostertagia not good, fluke one is
Treatment/prognosis for liver fluke
- Prognosis good if diagnosed and treated early
- Liver damage can be permanent though
- Various anthelmintics - depends what they are using locally that works
- Effectiveness varies with life cycle stage
Control of liver fluke
- Difficult to control intermediate host
- Common program:
○ Fasinexin autumn
§ Control immature and mature fluke
○ Then again in late winter/early spring
§ Reduce contamination - Fasinex highly effective against many stages
○ But it has a milk withholding period - Drench lactating cows at drying off
Lungworm what is the parasite called, general presentation, results in, diagnosis, how common and how controlled
- Dictyocaulis viviparus
- Wide distribution
○ Mostly young stock (classically <10 mo)
○ “Coughing calves that are not sick” - Severe infections can result in death
○ Secondary infections are bad too - Severity related to infective larvae on grass
○ Larvae are excreted in the faeces
§ Can’t do a fecal float! -> L1 not egg
§ Baermann technique - Used to be a common diagnosis
○ Less so now because MLs are very effective treatment
○ BZ’s “aid in control” - every day for 3 days - NOT DONE - Nowadays, normally controlled by routine drenching as MLs commonly used and pre-patent period greater than ostertagiaet al.
What are the 3 main treatment of parasites in general
- Anthelmintic drugs
- selective drenching to reduce resistance - Grazing/Management strategies
- Management of resistance
In terms of anthelmintics for parasite treatment what are the 3 main groups and types within
1) “White Drenches” ○ Benzimidazolesand pro-benzimidazoles 2) “Clear Drenches” ○ Levamizole ○ (Morantel) 3) “MLs” or “ Mectins” ○ Macrocyclic Lactones
White drenches for parasite treatment, types, characteristics, how act, main issues and does it get larval and hypobiotic stages
- First modern broad -spectrum drenches - all oral
- Oxfendezole , fenbendezole, albenazole
- Febantel
- Low level of toxicity; possibly teratogenic
- Poorly soluble –mostly oral administration
- Absorption is slow –which is important
- Act by starving the worms –takes time
- Resistance
Acts against hypobiotic and larval stages
Clear drenches and MLs main examples, mechansim of action, how given, what need to be cautious of
- Acts against hypobiotic and larval stages
2. Clear Drenches - Levamisole
- Reversible cholinergic agonist -> paralysis
○ Paralysing hyopbiotic larvae transiently not very useful! - NOT FOR HYPOBIOTIC - Limited use where worms are a problem …
3. Macrocyclic Lactones - Act on all stages of life cycle
- Pour -on or injection
- Prolonged action
- Dangerous to fish and aquatic life - need to be careful about where they are used
When choosing a drench what things need to consider and what is the best drench for calves but considerations
- Target nematodes and resistance
- Price
- Withholding periods
- Duration of action
- Application method
- Resistance
The best drench for dairy calves - dectomax injectable - But would you find a return on investment????
- Cooperia -> advantage over the others for this but this isn’t that pathongenic
Withholding periods what present on anthelmintics and what important about them
- Anthelmintics have
○ Meat withholding periods
○ Milk withholding periods
○ ESIs (Export Slaughter Intervals) - often different to withholding period - These vary between brands and formulations
- They can be quite long (42 days!)
- ALWAYS READ THE LABELS !
When to drench dairy cows and beef cattle
Dairy ○ Calves § from 3 weeks after exposure to pasture § every 4 to 8 weeks until 1yo (can do fecal egg count and larval culture if eggs are present) § at joining ○ Heifers § A couple of summer drenches ○ Cows § depends who you ask !! □ standard recommendation “drench at calving” □ drying off - due to the meat withholding period □ Calving ? Beef - first summer before calving
Drench resistance which parasites an issue, what is the main way to reduce, 3 sources arise and how to apply on dairy farms
○ Especially Cooperia
○ But increasingly in Ostertagia
- REFUGIA
○ If have a subpopulation of parasites that have not been exposed to anthelmintic then average level of resistance on the farm with reduce
○ Arise from 3 sources
§ Free living stages on pasture
§ Untreated animals -> don’t treat the entire mob
§ Inhibited/encysted larvae -> depending on the drench used
○ How to apply on dairy farms
i. Move to clean pasture let there be contamination then drench
□ Next set of warm eggs ingested will not be selected for resistance
□ OTHERWISE -> if drench then move, the paddock contaminated will have all resistant worms to the drench
ii. AND/OR Selective treatment of individuals - don’t treat the healthy looking animals
□ Saves money so more appetising
Pour-ons and combination anthelmintics what are the current issues/recommendations
A note on pour-ons
- High proportion (>60%) absorbed via licking
- High between animal variability (sub -therapeutic levels?)
- RESIDUES!!!!
Combination anthelmintics
- Useful from an anthelmintic resistance perspective:
○ Effective in the face of drench resistance
○ Slow the development of resistance
○ Eclipse (pour-on) -abamectin + levamisole
○ Trifecta (oral) –abamectin + levamisole + oxfendazole
Quarantine drenching how should be performed properly
- Administer a combination (as many actives as possible) upon arrival
- Quarantine animals for 3-4days (as eggs in the intestines not affected) on quarantine paddock where no other animals going to go on
- By 10-14 days should be no more eggs coming out - do faecal egg reduction test - ensure drench working no resistance
Management of anthlemintic resistance how done
- Ensure your farmers get the basics right
○ Accuracy of the drenching gun - needs to be calibrated
○ Weighing the animal to determine dose rate -> reasonable guess of weight and dose based on the HEAVIEST - Implement key concepts:
○ Refugia -to be done when HAVE resistance
○ Stay away from pour-ons
○ Combination drenches
○ Quarantine
What are the 4 main effects of diarrhoea
- Dehydration
- Electrolyte imbalance
○ loss of bicarbonate
○ acidosis -> hyperkalaemia (compensate for loss of bicarbonate) - heart will stop - Hypoglycaemia
- Hypoproteinaemia
Bovine virus diarrhoea what type of virus and the 2 main types and what worried about
- Bovine pestivirus - bovine viral diarrhoeal virus
○ Noncytopathic (NCP)
○ Cytopathic (CP)
§ Note: The distinction between NCP and CP is laboratory based (what it does to cells in cell culture) and is not correlated with clinical pathogenicity
Worried about naive infection in pregnant dam -> different effects <100, 100-150d, >150d
List 4 main causes of non-parasitic diarrhoea
1) bovine virus diarrhoea virus (PI)
2) salmonella
3) yersinosis
4) Johne’s disease
Bovine virus diarrhoea acute disease in naive animals, mortality, clinical disease type, what occurs afterwards and how transmitted
- High morbidity. Low mortality.
- Short clinical disease
○ Mild, subclinical or not observed - Seroconvert and are subsequently immune
- More severe form exists
○ Genotypic difference… BVDV II - but rare - Transmitted
○ Horizontally (oronasal)
○ Vertically (intra-uterine)
○ Iatrogenic (vaccines and other biologicals - contaminated with Pestivirus)
Bovine virus diarrhoea virus in utero infection (naive dam) at < 100 days what occurs
(no foetal immune system)
○ Embryonic or foetal death in ~30%
§ Return to service and absorption, if later than possible signs of abortion
○ Surviving calves
§ immuno-tolerant (thinks that virus is self) and
§ persistently infected (PI) - IMPORTANT CARRIER
Bovine virus diarrhoea in utero infection (naive dam) at 100-150 days what occurs
○ Could be born normal ○ Viral damage to developing organs § especially CNS ○ May be PI (persistently infected) or have high Ab levels Congenital Defects § CNS defects: □ Cerebellar hypoplasia □ Hydranencephaly □ Spinal hypomyelinogenesis § Ocular defects: □ Microphthalmia □ Cataracts - if have cloudy calf eye - THINK THIS □ Optic neuritis
Bovine virus diarrhoea virus in utero infection (naive dam) at >150 days what occurs
○ Usually no clinical effect on foetus
○ Transitory, mild effect on dam
○ Virus free
○ Seroconverted to pestivirus
Persistently infected calves with pestivirus what is the disease called, what occurs
Mucosal disease
- ALWAYS FATAL -generally younger animals
generally low numbers affected
- progressive diarrhoea
- Disease occurs with simultaneous CP and NCP infection
○ Persistency infected with one strain and then infected with the other OR mutation of that strain - why they become clinical - not 100% sure
- acute or chronic forms
Persistently infected calves with pestivirus what is the main presentation and results
- skinny, poor coat, oil scours
- ill-thrifty calves
- erosions in the mouth, gums, teeth and hard palate,
- sharp pointy feet - infected coronary band
- Thrombocytopaenia with bleeding in immuno-competent animals - petechiae bleeding
- Increased susceptibility to other pathogens - immunocompromised - issue for feedlots
- Reduced conception rates
- Embryonic loss
What are the 4 main laboratory diagnostic techniques for pestivirus and what 2 main ones use and how
1. Virus isolation ○ Buffy coat of whole blood ○ Lymphoid organs 2. Antigen detection ○ Capture ELISA ○ Ear notch test ○ Positive -> PI or infected 3. Serology ○ Antibody detection using ELISA or SN ○ Antibody negative -> PI OR in early stages of BVB (need two pair samples) 4. PCR ○ Scope for use as screening of herds dt -> sensitivity DO antigen and serological testing -> distinguish between PI and infected
Control/prevention of pestivirus on a farm what are the 3 main ways
1) Elimination of PI animals
○ Do serology antibody test (cheaper than antigen) first -> if positive then NOT PI if negative then could not be exposed or PI so then do antigen testing on these (more expensive so lower population) if positive then PI -> cull
2) Controlled exposure
○ Ensure exposure prior to pregnancy - how to control?
§ Vaccination OR use PI as natural vaccinator -> just expose to a herd -> not that effective
3) Vaccination
§ “Pestigard” inactivated vaccine (poorer protection but immunosuppressed), 2 strains, 2 shots prior to joining then annual boosters.
□ NEED TO KEEP DOING OTHERWISE VULNERABLE POPULATION (as ubiquitous in environment cannot eradicate from the environment)
§ Label claim to ↓ repro losses
Salmonellosis what are the main species involved and transmisssion
- S. enterica subsp enterica
○ Lots of serotypes - S. Typhimurium and S. Dublin (abortion) most common
○ Also S. Bovismorbificans, S. Newport, S. Zanzibar, S. Montevideo… - Transmission primarily via faecally contaminated water
What is the transmission and carries for S. dublin and S. typhimurium
Epidemiology of S. Dublin - Host-adapted to cattle - Many cattle are subclinical carriers ○ Excretion increases during times of stress - calving, drought - Endemic in herds ○ outbreak then sporadic cases - More common in irrigation areas Epidemiology of S. Typhimurium - Shed by many species ○ (eg rodents and birds - if they get into silos and faecal contamination of feed) - Infections do not persist in cattle - Not endemic, but outbreaks may be prolonged ○ Spikes of infection
What are the 3 main clinical presentations of salmonella infection and the clinical signs within
1) Acute/Peracute Septicaemia ○ Often found dead ○ More common in calves ○ Peripheral gangrene § ears, tail and hooves 2) Acute enteritis ○ Anorexia, reduced milk production, pyrexia, depression ○ Profuse, putrid diarrhoea ± dysentery ○ Abdominal pain ○ Dehydration, recumbency, death 3) Abortion may occur subsequently
