Bacterial and Protozoal Intestinal Disease in Commercial Poultry Flashcards Preview

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1
Q

What is poultry metabolism like compared to mammals?

A

Metabolism is high compared to mammalian species due to energy demands of flight and the GI tract is relatively short with a low volume to keep weight low

2
Q

What are some considerations when thinking about poultry litter management?

A
  • What type of litter is typically used in a broiler house?
  • Amount of litter-how deep is his litter spread?
  • Ventilation-what control do producers have over ventilation?
  • Leaks from house / drinkers
  • Temperatures-what temperature would you run a house for 25 day old broilers?
3
Q

What are some desirable traits for litter for poultry?

A
  • Absorbant
  • Biodegradable
  • Minimal dust
  • Bio-secure source
  • Pure source
  • Comfortable
  • Affordable
  • Concrete floors underneath for more effective biosecurity and litter management
4
Q

When is enteritis seen most commonly in chicks?

A

Enteritis is seen around 24-25 days old, when chicks are just over 1kg in BW

5
Q

What type of litter is typically used in a broiler house?

What about commercial turkey and duck?

A

Majority are on wood shavings – good absorbent substrate but varies in price

Chopped paper, rice husks, grass, chopped straw can also be used

Commercial turkeys and ducks – hopped straw as high requirement for bedding, so wood shavings is too expensive

6
Q

How much litter should there be in a broiler house?

How does this change?

A

When they first go in – only a couple of centimetres, houses are heated

Want droppings to hit the litter – want composting of the faecal material mixing in with the shavings to produce a deep litter so by the time they are caught up at 40 days – there should be a deep litter, composting.

Can top up shavings if need to – but extra cost, try to get it running efficiently

7
Q

Why does litter become wet?

A

In simplest terms moisture / water in the litter

  • Water from drinkers
  • Water from environment
  • Water from birds-possibly exacerbated by disease
8
Q

Once depopulated, what happens to the litter?

A
  • Colossal amount of it!
  • Can be sold as compost in garden centers – small amount of it though
  • Most of it is tumped up on arable land that will carry on composting process prior to being used as fertilizer
  • Other half is sold to power plants – powers them. Another reason why it has to be kept relatively dry as the powerplant will only pay for littler that is relatively dry, need to burn it to make electricity
9
Q

Why is poultry litter only used for arable land?

A

Due to risk of botulism! High risk of carcasses in litter

10
Q

What are some important points about drinker management in a poultry house - why does litter become wet because of the drinkers?

E.g. heigh, leakage, pressure, temperature?

A
  • water spillage may be an important part of litter deterioration, A key area for workers is how they manage the drinkers
    • possible breed effect?
  • drinker heights – spillage – want them to reach it and it be able to flow down their neck easily, they cannot lap water – if its at ground level they have to flick it up and swallow it – often has to be changed in height as they grow!
  • nipple leakage – damage / limescale – if they have the cups under the nipples, some birds will come along and drink this and it will be warm and contaminated
  • water pressure – leakage – birds will under perform if it isn’t high enough pressure as they wont get the right amount of water
  • condensation from manifolds/high water flow – insulation important
  • Pulling cold water into warm house on a cold day – so water hits the litter
11
Q

Why does the litter become wet because of the environment - why is early litter maintenance critical?

A
  • Early litter maintenance is critical
    • Dry warm concrete prior to applying shavings
      • Else direct moistening / condensation
    • Litter may be damp before 7 days
    • Will lead to pododermatitis / increased coccidial development / increased environmental bacterial and viral challenge
12
Q

Why does the litter become wet because of the environment - why should we consider the heat source?

A

Consider heat source

  • Most sites used to employ gas brooders or warm air convectors
    • Heat not located close to litter
    • Produce water
  • Now biomass is the most common heat source – huge number of existing broiler sheds have been fitted with these. Can use biomass to make energy. A radiating source of heat – so no moisture produced
  • Some sites have underfloor heating – relative inefficient as have underfloor heating, then layer of shavings
13
Q

What do most broiler sites use now to keep it warm?

A
  • Most sites used to employ gas brooders or warm air convectors:
    • Heat not located close to litter
    • Produce water
  • Now biomass is the most common

heat source – huge number of existing broiler sheds have been fitted with these. Can use biomass to make energy. A radiating source of heat – so no moisture produced

14
Q

Why does little become wet because of the ventilation?

A
  • Humid air cooled will release moisture
    • Difficult in temperate climate
    • If humid air is allowed to fall onto cold litter, it will condense
  • Air distribution affects bird distribution
  • Using a smoke machine allows air movement to be visualised - smoke should be forced in and starts to roll, drop as its cold, picks up heat and moisture, rolls up and is ventilated out of the house
  • Relative humidity - want to draw air from outside and create turbulence so cold air drops to floor, then as it heats, it gains moisture and then it ends up getting it out of the house
15
Q

What is chick paper and what is it used for?

A

Place on litter and shavings, has feed on it – so they are standing on a floor of food so they cant help but eat it. Also very absorptive to help stop litter from being wet. If too much of it, affects absorptive capacity of it

16
Q

Why does the litter become wet because of the birds?

A
  • Breed and genetic progression
    • Some negative traits developed with regards to leg health – want to stop this
  • Nutrition
    • Always trying to keep up with genetics and evolving diets to allow them to get as close as possible to genetic potential – but has to be done on a budget! We import cereals and soil – might change and be very difficult with Brexit!
  • Gut health / disease
    • A lot of endemic viruses and bacteria that can ause gut disease
17
Q

What is the maximal stocking density for broilers in the UK?

A

If you have 500 or more conventionally reared meat chickens on your holding you can stock birds at up to 33kg per square metre. You can increase this up to 39kg birds per square metre but there are extra requirements

18
Q

When stocking above 33kg per square metre you must keep documents in the housing with technical details and information on equipment, including what?

A
  • a plan that shows the dimensions of the surfaces the chickens occupy
  • a ventilation plan and target air quality levels (including airflow, air speed and temperature) and details of cooling and heating systems and their location.
  • the location and nature of feeding and watering systems (eg automatic or manual, how many feeders, how each is operated)
  • alarm and backup systems if any equipment essential for the chickens’ health and wellbeing fails
  • floor type and litter normally used
  • records of technical inspections of the ventilation and alarm systems
19
Q

What is the nutrition like for broilers?

A
  • Mineral density
    • Be wary of wheat dilution
    • Avian anatomy:
      • Urinary system as well as gastrointestinal system contributes to dropping consistency
  • High levels of vegetable protein
  • High wheat dependency in UK
  • Be aware that different feeds vary in quality! Which will affect muscle development
20
Q

How do the colour of chickens vary between the UK and USA and why?

A

In USA – the colour of chickens is yellow, genetically the same as UK, but yellow because fed corn diet, but in UK they are fed wheat diet.

21
Q

How does breed and genetic progression play a role in litter quality?

A
  • Different breeds housed in different sheds on same site give consistently different litter quality
  • Stocking rate is important but not necessarily a critical feature
    • Slow growing breeds used in freedom foods stocking densities vs. use of standard bird at same stocking density
22
Q

What is the role on enteric disease in broiler house?

A
  • Probably overstated, but can be important
    • We commonly see similar gross enteric signs in routine health checks of birds on very good litter, that are attributed to the cause of poor litter in other houses, especially where different breeds are involved
23
Q

A broiler client reports ‘wet litter’….

What questions do you ask initially?

A

Have you checked your drinkers? Are they leaking? Does this explain it? What is the ventilation like – is he ventilating the house as best as he can? What vaccinations have they had? Any other signs of disease?

24
Q

A broiler client reports ‘wet litter’

What recorded information so you want from him?

A

What vaccinations have they had?

Any other signs of disease?

25
Q

A broiler client reports ‘wet litter’

What sample do you want from him?

A

A representative sample for PM

Fresh euthanised birds – not the best ones! The ones you think are the cause of the wet litter

26
Q

Label the following

What is your diagnosis?

A
27
Q

What is the problem with gut health and disease in broiler houses?

A
  • Is always multifactorial and is poorly understood
    • protozoal / bacterial / viral mix
    • Bacteria / viruses often non-pathogenic, but driven to overgrowth by environmental conditions
      • We commonly monitor “enteritis” developing as a result of poor environment, not the cause
  • Good chance other things going on also, and with coccidia, likely there is also bacterial infection also
28
Q

What is Dysbacteriosis?

A

An upset in the balance of the bacteria in the bird’s gut that results in diarrhoea leading to wet litter and poor performance

All lagging as when manifested it’s too late to take corrective actions

29
Q

What kind or organism is clostridium perfringens?

Where is it present?

A

•Ubiquitous organism

  • Present in the intestines & environment
  • Where there are chickens, there will be Cp
30
Q

What does uncontrolled growth of clostridium perfringens lead to?

A
  • Uncontrolled growth leads to intestinal integrity disruption. Cp await an opportunity to flourish
    • e.g. coccidial challenge, immunological stress (vaccine)
  • Fast proliferating organism:
    • In 1 hour it can multiply from 1million to 64 million organisms under ideal conditions
31
Q

When is likely the only time we see clostridial enteritis in broiler chickens in the EU?

A

Growth promoters removed from poultry feeds in EU. Only time we see Clostridial Enteritis in broiler chickens is when new season wheat starts to be blended into feed – quite different in consistency to previous season. If CE very severe, will also get liver damage as well – turns into VPH issue here – as then get Cholangiohepatitis as then there are liver and whole bird rejects

32
Q

What antibiotic is used to treat bacterial enteritis?

What is the mode of administration?

What is the dose rate?

What are the withdrawal times?

A
  • Which antibiotics used?
    • Class used to kill clostridium – amoxicillin
  • Mode of administration?
    • Justified to put in drinking water for all of those birds as likely to all be at risk
  • Dose rate?
    • 20mg/kg for 3 days
    • Relatively cheap – especially compared to the economic losses!
  • Withdrawal times?
    • Short – if you start 24, and treat until day 26 – most have 24h withdrawal
33
Q

What are the 2 types of drugs used to treat bacterial enteritis?

Which one is better?

A
  • Amoxicillin 20mg/Kg/day orally (for 3 days)
  • Anther one that might be used is: Tylosin 20mg/Kg/day orally – but older school now as it is a macrolide (for 3 days)
    • Nil withdrawal
  • Amoxicillin is treatment of choice though
  • Both relatively cheap, short withdrawal times, easily administered through the water, though tylosin is a macrolide!
34
Q

What are some methods of control for bacterial enteritis?

A
  • Prophylactic antibiotics?
    • Trying to prevent it happening in the first place
    • If there is signs of it developing – better to try and push the pathogen out before it takes hold.
    • Avigard and broilervac (?)– freeze dried chicken gut commensals – can be sprayed on environment, top dress the feed or put in water – scientific evidence that they squeeze out pathogens
  • Probiotics
  • Competitive exclusion products
  • Prebiotics (Nondigestible compounds)
    • Affect binding sites for some pathogens
  • Supplementary enzymes & acids
    • Organic acids – drop pH of water, squeezes out clostridial
  • Husbandry
  • Feed manipulation
  • No clostridial vaccines available at the moment for enteritis in chickens
35
Q

What vaccines are available for clostridial disease in chickens?

A

No clostridial vaccines available at the moment for enteritis in chickens

36
Q

Name some viruses that affect broiler chickens commonly?

What is the route of diagnosis sometimes?

A
  • Infectious Bronchitis – coronoavirus
    • Kidney damage – water loss through urinary tract
  • Gumboro Virus (IBD)
    • Direct GIT damage and immunosuppression
  • Adenovirus
    • Gizzard erosion and severe scouring
  • Others…….
  • Have to go down the route of PCR for diagnosis and would be suspicious on histology
37
Q

What are alflatoxins in poultry produced by?

A

Produced by Aspergillus flavus +/- Aspergillus parasiticus

38
Q

What is the source of alflatoxins in poultry?

A
  • grains, maize, soyabeans, peanuts, millet
  • warm and humid conditions in storage
39
Q

Which alflatoxin is the most toxic?

A

Aflatoxin B1 is the most toxic

40
Q

Which order of birds are most at risk for alflatoxins?

A
  • Ducklings > turkeys > goslings >chickens
    • adult hens are the least susceptible
41
Q

How do the consequences of contaminated feed with alflatoxins vary?

A

•Consequences of contaminated feed vary with

  • species
  • age and sex (M>F)
  • nutritional status
  • level of intake/concentration in feed
42
Q

What are some clinical signs of alflatoxicosis?

A
  • reduced appetite
  • weakness
  • decreased efficiency of food conversion
  • decreased growth rate
  • decreased egg production and hatchability
  • immune suppression
    • coccidiosis, Marek’s disease, salmonella
  • abnormal pigmentation +/- bruising
43
Q

What is the worst case scenario of a bird with alflatoxicosis?

A

Worst case scenario –> severe liver necrosis –> death

Sub acute/chronic situation –> decreased productivity

44
Q

How can you treat and control alfaltoxicosis?

A

Treatment:

  • none
  • aflatoxins don’t accumulate or persist
    • recovery possible if moderate intoxication
    • remove contaminated feed

Prevention/control:

  • hygiene
  • ensure litter is not mouldy and/or move mobile systems onto fresh ground
  • store food appropriately (dry place)
  • buy smaller quantities of food in winter
  • protective role of some food additives?
45
Q

What are the common manifestations of coccidiosis?

A
  • Poor FCRs
  • Poor/variable weights
  • Poor bone mineralization
  • Dehydration
  • Decreased pigmentation?
  • Increased mortality
  • Assists onset of enteritis
46
Q

What kind of parasite is coccidiosis?

What is its life cycle and replication like?

A
  • Ubiquitous and successful parasite
  • 4 – 8 day life cycle
    • Depending on species prepatent period and environment
  • Explosive nature of replication:
  • 1 sporulated oocyst can result in 2.5 MILLION 2nd generation merozoites!!
47
Q

What are the 2 main types of immunity?

Which is most important in the control of coccidiosis?

A
  • There are two main types of immunity:
    • CMI which involves heterophils and heterophages
    • Humoral which is antibody production and NK cells
  • Both play a role in coccidiosis control, however, CMI is the most important.
  • Immunity requires stimulation and time to build up.
48
Q

Why is there a peak time challenge for coccidia are 24 days of age?

A
  • 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 CMI 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.
49
Q

What do the internal phases of replication of coccidiosis within the bird consist of?

What is the external phase?

A

•Internal phases of replication within the bird comprising:

  • Schizogony (2 phases)
  • Gametogony (1 phase)
  • Release of unsporulated oocysts
  • The internal phase is where anticoccidials /
    vaccines act

•External phase where the oocysts become sporulated

  • This is where litter management and terminal
    hygiene are critical
50
Q

For each sporulated oocyst of coccidia - how many sporozoites does it contain?

A

Each sporulated oocyst contains 8 sporozoites

51
Q

Name some Eimeria species from the chicken

A
52
Q

Where does Eimeria Acervulina infect?

A

Upper intestine

53
Q

Where does Eimeria maxima infect?

A

Upper intestine and middle intestine

54
Q

What is a blood filled caecae pathognomic of?

A

E - tenella

Coccidia

55
Q

If you have the mucosal layer of duodenum and if white dots through mucosal lining - what is this pathognomic of?

A

pathognomic of Eimeria Acervulina

56
Q

What is petechial haemorrhage pathognomic of?

A

Eimeria Maxima

57
Q

How do we diagnose coccidiosis?

A

1.On a dead bird?

•See gross lesions

2.On faecal samples?

•Coccidia oocyst count

3.To determine emergence of drug resistant strains?

58
Q

What is OPG with regards to diagnosing coccidia and why is interpretation difficult?

A
  • OPG = Oocysts Per Gram = oocyst count in faeces or litter.
  • (Basic) laboratory is needed
    • Microscope
    • McMaster counting chamber
  • Can also look at size – Eimeria Maxima is the largest
  • Interpretation difficult!
    • The 7 chicken Eimeria have a different reproductive potential
    • Birds 3-6 weeks of age – cannot help but find oocyts!
59
Q

What is AST with regards to testing for coccidia?

What does it tell us?

A
  • AST = Anticoccidial Sensitivity Testing
  • Vast majority is controlled with coccidiostats – some more efficacious than others. Determined by harvesting oocysts and determining their sensitivities
  • To monitor efficacy of anticoccidial products
  • Products are compared regarding their efficacy against a specific field-isolate (compare with antibiogram)
  • Very complicated, thus very expensive
  • Only monitoring-tool that can make predictions
60
Q

What is the procedure of anticoccidial sensitivity testing?

A
61
Q

What are the requirements for a good necropsy session?

A
  • LIVE birds !!! (no dead animals or guts of a few hours or days old)
  • Autolysis of intestinal tract if been dead for any length of time – needs to be done on very fresh killed birds to make it accurate
  • Minimum of 5 birds / house
  • Age of birds: 18 – 42 days
  • Microscopy !!! (2-3 persons)
  • Take enough time: max. 5 houses per hour !
62
Q

What can we do against coccidiosis?

A
  • Vaccines
  • Alternative products – most of it doesn’t work really! Oregano or garlic based products to control coccidiosis – just not efficacious!
  • Anticoccidial Drugs
63
Q

What is the live attenuated vaccine for chickens for coccidia in the EU?

What is the cheapter version?

A

•Chickens: live attenuated (or live unattenuated (not in EU)) – paracox 8

  • In Europe not frequently used in broilers
  • Expensive
  • Can see problems with NE, bacterial enteritis
  • Possible issue: species present in field but not in vaccine e.g. Paracox 5 (cheaper vaccine than 8) only contains Eimeria acervulina, E. maxima, E. mitis and E. tenella.
  • As an addition to the anti-coccidial arsenal, usually problem solver
  • This method of prevention is very common in commercial egg laying chickens
64
Q

What are some anti-coccidial tools for broilers?

A

•Vaccines

  • Not frequently used
  • Expensive
  • Problems with NE, bacterial enteritis
  • Alternative products (herbal products)
  • No product has yet been proven to work

•Anticoccidial Drugs

  • According to Chapman, 2005
  • Anticoccidial products (ACP) in feed: 95% of broilers
  • Vaccination and other: 5%
65
Q

What are some anticoccidials/coccidiostats?

What birds are they available for and what species are they effective against?

A

•Applicable for different animal-species

  • chickens, turkeys, rabbits, game birds, …
  • ‹−› vaccines: species-specific

•Active against all Eimeria-species

  • E. acervulina, E. tenella, E. maxima, E. brunetti, E. mitis,…
  • Where as vaccines are species specific
66
Q

What is the classification are anticoccidials?

A

•Synthetic anticoccidials = ‘Chemicals’: DON’T NEED TO REMEMBER THESE NAMES! JUST LOOK AT MOST COMMON ONE USED IN UK – NICARBISIN AS THEIR CHEMICAL

  • robenidine (Cycostat®) / diclazuril (Clinacox®) / nicarbazin
    (+narasin) (Maxiban®) / decoquinate (Deccox®) / (halofuginon)
  • Once you have more control, drop down from the chemical to the ionophore – so at some point you can use a finished ration – lower efficacy. Slowly reduce it
  • Polyether ionophore anticoccidials = ‘Ionophores’:
    • Monovalent:
  • Salinomycin (Salinomax®/Bio-Cox®, Sacox®, Kokcisan®)
  • Monensin (Elancoban®, Coxidin®)
  • Narasin (Monteban®, Maxiban®)
  • Monovalent glycoside:
  • Maduramicin (Cygro®)
  • Semduramicin (Aviax®)
  • Divalent:

•Lasalocid (Avatec®)

67
Q

What is the cross resistance between ionophores (used to treat coccidiosis)?

A
  • Cross-resistance between the monovalent ionophores narasin, monensin and salinomycin is common in the field
  • Illustration: resistance against narasin in the USA was observed prior to its approval and use due to cross resistance with monensin and salinomycin!
  • Strains of coccidia resistant to monovalent ionophores are usually sensitive to lasalocid (= divalent)
68
Q

What is a rotaton prgram with regards to the treatment of coccidiosis?

A

What ?

  • Changing the anticoccidial drug to one of another class after a few cycles (can be in shuttle or full program)

Why ?

  • Allows to restore anticoccidial efficacy
  • Limits the build-up of resistance
69
Q

What are the four golden rules for anticoccidial programs?

A
  • Give product a sufficiently long rest period after each period of use
  • Rotate between products of different classes
  • Be wary of just using ionophore programme, likely to need a chemical programme in there at some point too!
  • Use a chemical clean up once a year
  • Do not to use same anticoccidial for too long
  • Very good reduction infection pressure !!!
70
Q

What are some possible reasons for coccidia outbreaks?

A
  • Resistance to preventive drugs (anticoccidials)
  • High infection pressures or pathogenicity field strains (overpowering the efficacy of the drugs)
  • Reduced feed intake (hot weather, management errors, disease) leading to suboptimal doses of anticoccidials (therefore usually water treatments are preferred!)
  • Too low dosage of anticoccidial in feed (mixing errors)
  • Overcome vaccine reaction (both attenuated and non-
    attenuated vaccines) or poor coccidiosis vaccination
  • Immunity breaks of birds (breeders, layers, broilers over
    42 days) presumed to be immune
  • Stress (peak of lay)
  • Immunity compromised after infection with certain viruses
  • Lack of cross protection between Eimeria strains for instance between layer rearing and production sites
71
Q

What are sulfonamides and what are they used to treat?

What is the problem with them?

A
  • First drugs used for control of coccidiosis, coccidiostatic
  • Toxicity issue in poultry, rather narrow safety margins
  • Bone marrow suppression, immuno-suppression, anti-Vit K effect
    (suppression caecal flora providing Vit K)
  • Pale, yellow-coloured bone marrow
  • Haemorrhages breast, thigh, leg muscles
  • Laying hens: drop in egg production, loss of brown pigment
  • Safety margin different for different sulfonamides

•Limit use of sulfa drugs due to toxic effects in time (reason for programs such as ‘3 – 2 -3’)

72
Q

What is Amprolium?

What does it treat and how is it given?

A
  • Drinking water formulations available next to in-feed (dose in feed = 125 ppm to 250 ppm)
  • Dose in drinking water:
  • 20 mg/kg of bodyweight per day for 5-7 days
  • Amprolium is an anticoccidial agent that acts as competitive inhibitor of thiamine in the parasite metabolism, and interferes with the metabolism of glucides necessaries for coccidian multiplication and survival.
73
Q

What is Toltrazuril (baycox) and what does it treat?

What is an issue with it?

A
  • Coccidiocidal, broad spectrum, active against all intracellular stages of parasite
  • Very rapid action at 7 mg AI / kg BW per day for two days
  • Expensive but standard treatment for severe cases
  • Rather rapid resistance to toltrazuril
  • Long withdrawal times (mainly used in breeders…)
74
Q

In conclusion - what is the therapy for coccidiosis?

A
  • It is good to have therapeutics available
  • But keep as short-term emergency tool, safeguarding performance of farms facing problems
  • First work on prevention of coccidiosis
75
Q

What is criteria for disease investigation for farm health planning?

A

ÿAddress:

ÿCriteria for disease investigation

ÿVaccination strategies

  • Medicine regimes
  • Used litter management (where does it go?)
    • Terminal clean out & disinfection
    • Water supply hygiene management
    • Biosecurity (what measures should be in place to stop intestinal disease arriving on farm or spreading between houses?)

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