Scour in poultry Flashcards
what are the litter and management factors that affect scour in poultry?
why does litter become wet?
- Litter substrate (should be absorbent, biodegradable, comfortable, affordable, from a bio-secure source)
- Depth of litter
- Ventilation-controlled environment versus naturally ventilated
- Leaks from house / drinkers
- Temperature control
wet litter due to:
* Poor drinker management
* Condensation from the concrete floor
* Moisture from burning gas (though more houses have a radiating heat source from biomass)
* Sub-optimal ventilation
what genetic and nutritional factors have a role in litter management?
- breed seems to play a major role in litter quality
- Slow growing breeds used in freedom foods lower stocked production systems have a lower prevalence of intestinal disease
- Stocking rate is important but not necessarily a critical feature
- UK birds on a predominantly wheat based diet (compared with a corn based diet in the USA)
- Soya beans are a major protein source. Ever more expensive and unsustainable
- High sodium (in salt), magnesium (in limestone) or potassium (in soya) can result in increased water consumption
- Poor quality protein is not digested => increased pH => increased chance of bacterial scour
- In broilers every 1% increase in protein results in 3% extra water consumption
what are the components of poultry droppings?
urates and urine from the renal system as well as faecal material
how do you investigate wet litter issues in commercial poultry?
- A good history from the client. Ask about water consumption changes, daily liveweight gain (DLWG), food conversion rate (FCR), egg production (in layers & breeders), mortality & cull levels, other clinical signs
- Decide whether a site visit or birds being submitted for post-mortem examination is appropriate
what clostridium affects poultry?
what type of pathogen is this?
when does it affect chickens?
what are the clinicla and PM signs?
Clostridium perfringens (Cp)
Ubiquitous organism
- Present in the intestines & environment
- Where there are chickens, there will be Cp
- oportunistic pathogen
- G+ve, spore forming bacillus
Uncontrolled growth leads to intestinal integrity disruption. and Cp can then infect
e.g. coccidial challenge, immunological stress (vaccine)
Clinical signs:
- Peracute necrotic enteritis:- sudden death, after a short spell of huddling, depression and dullness
- Thinned walled guts, necrosis and gassy intestinal contents
- Subclinical necrotic enteritis:-No discomfort or mortality
- However, the birds are scouring and have intestinal gross pathology
what are the predisposing factors for clostridium in poultry?
Cp is ubiquitous so there needs to be contributory factors for disease
* Concurrent infections e.g. coccidiosis
* Excessive protein in the ration
* Protein/energy imbalance in the ration
* High levels of non-starch polysaccharides in the ration
* Sub-optimal husbandry
what is the pathogenesis of clostridium in birds?
Cp bacteria releases toxin that accumulates and damages enterocytes
what is the prevention and control of clostidium in poultry?
Amoxicillin 20mg/Kg/day orally (for 3 days)
Tylosin 20mg/Kg/day orally (for 3 days)
- Relatively cheap, short withdrawal times, easily administered through the water, though tylosin is a macrolide!
prevention:
* Better coccidiosis control and site hygiene
* Enzymes (e.g. beta-mannanases) supplementation to enhance protein digestion
* Competitive exclusion products
* Prebiotics (e.g. mannooligosaccharides [MOS]) to selectively encourage commensal bacterial growth
* Ongoing research into optimising the microbiota
* No vaccine commercially available
*
what is brachyspira?
what birds does it affect?
what are the clinical signs?
how is it diagnosed?
what is the treatment?
what is the prevention?
- G-ve spirochetes, colonising birds’ large intestine
- B. alvinipulli, B. intermedia & B. pilosicoli cause avian intestinal spirochaetosis (AIS)
- Concurrent bacterial infections e.g.Sarcina
- Disease affects layer hens and broiler breeders causing a yellow frothy diarrhoea, and egg drop and typhlitis
- Spread by the faecal oral route
- The bacteria can cause end-on attachment to intestinal cells, thus creating an pseudo-brush border. They also invade enterocytes and disturb tight junctions
- Diagnosis on PCR of affected faeces
- Treatment with tylosin or tilmicosin
- Autogenous vaccines have been used
what two salmonella species affect birds and cause intestinal disease?
what are the signs on post morten for each of these?
what are the clinical signs?
How are they diagnosed?
Fowl Typhoid (Salmonella Gallinarum)
- results in high mortality, anaemia, green diarrhoea, hepatomegaly (the liver may also be bronze in colour).
- Persistent carriers in the flock need identifying by ELISA or slide agglutination tests. This allows an eradication programme
Pullorum Disease (Salmonella Pullorum)
- results in acute mortality and diarrhoea (with white caked vents), predominantly in young birds.
- Again, if the carriers can be identified by ELISA or slide agglutination tests the chain of vertical transmission can be easily broken
what is the lifecycle of eimeria?
what disease does it cause in birds?
what is the manifestaion in birds?
how is it diagnosed?
4 – 8 day life cycle - Depending on species prepatent period and environment
results in lots of sporulated oocysts very quickly
causes coccidiosis in poultry
manifestation:
* Poor FCRs
* Poor/variable weights
* Poor bone mineralization
* Dehydration
* Decreased pigmentation?
* Increased mortality
* Assists onset of enteritis
diagnosis:
- microscopy
- gross pathological lesions
- molecular biological methods (PCR)
what 7 emeria species affect chickens?
what are the main three species?
where do the three main species infect within the bird?
main:
E. acervulina - upper intestine
E. maxima - upper and middle intestine
E. tenella - caeca
others
E. brunetti
E. mitis
E. necatrix
E. praecox
why is 24 days of age the time where there is a peak challange with emeria in poultry?
Several life cycles of coccidiosis are required to stimulate immunity.
- This is believed to be three
By the third passage (8x3 = 24 days of age) the cell mediated immunity component has had the required exposure to antigens and is able to control lesions
After the 3rd life cycle, lesions are controlled by the immune system of the broiler
what is the treatment of coccidosis?
vaccination (live attenuated):
* for broilers in the EU
* expensive so not commonly used
* used in commercial egg laying chickens
- species specific
coccidiostats:
Two types: chemicals and ionophores
Active against all Eimeria-species
outbreaks of coccidiosis:
- Toltrazuril (baycox), amprolium
what causes turkey haemorrhagic enteritis?
what is the mortality rate?
what are the clinical signs?
how is it diagnosed?
how is it controlled?
- Caused by Turkey siadenovirus A
- Average mortality rate 10-15% but can be up to 60%
- Depressed turkeys passing blood stained droppings
- Anaemic carcases with diffuse haemorrhagic enteritis & mottled (marbled) spleen
- Large lightly basophilic intranuclear inclusion bodies are found in the cells in the spleen and the lamina propria of the intestine
- Diagnosis on PCR testing
- Control by vaccinating with an attenuated live vaccine through the drinking water at 18-28 days (used off licence to vaccinate earlier)
what is the pathogenesis if infectious bursal (gumboro) disease?
what clinical signs does it cause?
how is it diagnosed?
how is it controled?
- Member of the Birnaviridae family
- The virus has a tropism for B-lymphocytes within the Bursa of Fabricius; hence bursitis as a gross lesion
- Hunched, pale, depressed birds with diarrhoea
- IBD is an immunosuppressive virus so exacerbates secondary infections
- Diagnosis; lesions are almost pathognomic but require PCR testing to be definitive
- Control with live attenuated vaccines in the drinking water (14 to 19 days of age) or vector vaccines in the hatchery
