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GI2 > Farm 5 - Pigs and poultry > Flashcards

Farm 5 - Pigs and poultry Flashcards

1
Q

What are the direct and indirect economic effects of GI disease on the pig industry?

A

Direct – death, treatment

Indirect – slow growth, poor performance

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2
Q

What are the most common clinical signs of GI disease in pigs?

A

DIARRHOEA, sudden death, vomiting, perineal staining, poor growth

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3
Q

Pre-weaning (0-4wks) GI differentials?

A 
Rotavirus 
Colibacillosis 
Coccidiosis 
Clostridial enteritis 
Corona virus
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4
Q

Post weaning (>4wks) GI differentials?

A 
Post-weaning colibacillosis
Proliferative Enteropathy – ileitis
Spirochaetal diarrhoea (Colitis)
Salmonellosis
Brachyspira – swine dysentery
Yersiniosis
GI torsions
Gastric ulcers
Parasites – Trichuris, Ascaris, Eimeria (rare)
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5
Q

What are the clinical signs of post weaning colibacillosis?

A

Within 10 days post weaning
Pigs alert and eating
Watery yellow diarrhoea
PM – loops of intestine will be dilated with watery yellow fluid

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6
Q

What is the aetiology of post weaning colibacillosis?

A

E. coli with specific attachment factors and verotoxins
(Note: if shiga toxins are present there will be oedema disease not diarrhoea – swelling above eye, oedema in guts, neuro signs)

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7
Q

How is post weaning colibacillosis controlled and treated?

A

Sow and piglet vaccines available
Zinc oxide in feed (soon to be banned)
Acidification of water
Diets with lower crude protein (but lower growth in pigs)
Treatment: apramycin, paramomycin, florfenicol

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8
Q

How is post weaning colibacilosis diagnosed?

A

Lab diagnosis – C+S and toxins

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9
Q

What are the 4 clinical presentations of porcine proliferative enteropathy complex (ileitis)?

A

1-Porcine Intestinal 1-Adenopathy (PIA) chronic disease in growers
2-Necrotic Enteritis (NE) chronic disease in young growing pigs
3-Regional Ileitis (RI) chronic watery diarrhoea
4-Proliferative haemaorrhagic enteropathy (PHE) - Acute haemorrhagic disease in finishers and breeders

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10
Q

What is the aetiology of porcine proliferative enteropathy complex (ileitis)?

A

Lawsonia intracellularis
Shed by other pigs
Is an endemic disease that is triggered by changes in diet/environment
Severity of disease depends on dose

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11
Q

How can Porcine Intestinal Adenopathy (PIA) be diagnosed?

A

Faeces: PCR (unvalidated) - Not diagnostic as the bacteria is so wide spread
Post Mortem: ‘Hosepipe’ ileum
Histopathology: pathognomonic (needed for definitive diagnosis – gut degradation can impact diagnosis

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12
Q

What are the clinical signs of chronic ileitis?

A 
6 to 20 week-old pigs
Mild to severe diarrhoea 
Brown-grey-green diarrhoea 
Not mucoid
Non-haemorrhagic in the chronic and sub-clinical forms
Pigs with weight loss
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13
Q

What are the clinical signs of proliferative haemorrhagic enteropathy (PHE)?

A 
Usually young adults – 4-12 months
Sudden deaths
Blood in faeces
Anaemic
Rare
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14
Q

How is ileitis treated?

A

Vaccine – effective but challenging to use (oral live) and expensive
Antibiotics – Tiamulin, Tylosin, lincomycin – in feed (chronic outbreak) and soluble (acute outbreak)

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15
Q

What is the aetiology and epidemiology of swine dysentery?

A

Microaerophilic spirochaete Brachyspira hyodysenteriae
Faeco-oral infection
Incubation period 7-60 days
Carriers may remain sub clinically affected for up to 90 days
40-60d survival in faeces

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16
Q

What are the clinical signs of swine dysentery?

A

Severe muco-haemorrhagic colitis usually in growing pigs (6-14 weeks), but can also see disease in sows.
Drop in live weight gain
Significant mortality
Can be transmitted by other animals and insects

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17
Q

How is swine dysentery diagnosed?

A

Clinical signs and gross post mortem findings +/- histopathology
Faecal sample - PCR (16s RNA), Culture
NO USEFUL SEROLOGICAL TEST

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18
Q

How is swine dysentery treated?

A

Antimicrobials: tylosin (resistance), lincomycin tylvalosin (intermediate), pleuromutilin (important)
Total or partial depopulation eradication programs
- Medicated Eradication
- Partial depopulation: Remove the susceptible (growing - ‘growers’ ) population and medicate sows
- Total Depopulation: a last resort option
Organism killed by disinfectants if used appropriately

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19
Q

What is the causative agent of porcine intestinal spirochaetosis (colitis)?

A

Non-hyodysenteriae spriochaetes

Brachyspira pilosicoli

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20
Q

What is the epidemiology of porcine intestinal spirochaetosis (colitis)?

A 
Same as swine dysentery 
Faeco-oral infection 
Incubation period 7-60 days 
Carriers may remain sub clinically affected for up to 90 days 
40-60d survival in faeces
Can be transmitted by dogs and rodents
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21
Q

What are the clinical signs of porcine intestinal spirochaetosis (colitis)?

A

Diarrhoea (mucoid and sloppy), colitis, rarely fatal, reduced daily live weight gain

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22
Q

How is porcine intestinal spirochaetosis (colitis) diagnosed?

A

Clinical signs and culture/PCR to rule out SD

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23
Q

How is porcine intestinal spirochaetosis (colitis) managed?

A

Same as swine dysentery
Antibiotics
Total or partial depopulation eradication programs

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24
Q

What are the most common salmonella organisms in pigs in the UK?

A

S. typhimurium
S. Dublin
S. choleraesuis (now very rare in UK)

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25
Q

What are the pathological findings of salmonellosis in pigs?

A

Diptheritic typhlocolitis (inflammation of the caecum and colon)
Septicaemia
Later: rectal strictures

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26
Q

What are the clinical signs of salmonellosis in pigs?

A

Mucin casts and blood in diarrhoea (need to rule out SD)
+/-Pyrexia
Scouring (can be only mild)
Purple skin discolouration (septicaemia)

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27
Q

What is the epidemiology of salmonellosis in pigs?

A

Infectious dose important in determining if clinical disease occurs
Concurrent infections predispose
S. typhimurium is often multidrug resistant so AB treatment can be a risk factor

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28
Q

How is salmonellosis treated in pigs?

A

Antibiotics (in water) – C+S important due to multi drug resistance

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29
Q

How is salmonellosis controlled in pigs?

A

Identify and remove source e.g. rodents
Organic acids in feed/water
Cleaning and disinfection between batches
All in all out systems
Vaccines are of little effect and not licenced in UK

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30
Q

What is the causative agent to yersinosis in pigs?

A

Y. pseudotuberculosis

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31
Q

What are the clinical signs of yersinosis in pigs?

A

Watery, dark, mucoid diarrhoea

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32
Q

What is the most important consideration in a yersinosis outbreak?

A

Zoonosis - personal hygiene, important to talk to staff

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33
Q

How is yersinosis controlled?

A

Hygiene and AIAO measures

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34
Q

How common is GI torsion in pigs?

A

Very common

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35
Q

Where do GI torsions occur in pigs?

A
  • Long length SI volvulus at the mesenteric root

- Gastric dilatation/volvulus in older pigs

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36
Q

When are pigs most likely to get SI volvulus at the mesenteric root?

A

Growers 8-12wks
Tend to eat a lot and jump, fight and roll
Usually single cases of sudden death

37
Q

When are pigs most likely to get a GDV?

A

Older pigs

Usually when there has been a change in feed or they eat a lot and fight

38
Q

How common are stomach ulcers in pigs?

A

Very common >60% of growers at slaughter

39
Q

What are the 3 main factors that cause stomach ulcers in pigs?

A

Finely ground feed components
Cessation of feed intake for one day
Wet fed with whey
(can also be secondary to lung infections)

40
Q

What are the clinical signs of stomach ulcers in pigs?

A

Subacute – pale skin, weak, breathless, vomiting, teeth grinding (pain), passing dark faeces (digested blood)
Acute – sudden death, very pale carcase
PM- ulceration and damage to the upper part of the pigs stomach

41
Q

How are stomach ulcers treated?

A

Move the affected animals to a loose bedded peaceful environment
Feed a weaner type diet containing highly digestible material
Inject multivitamins esp vit E and iron weekly
Cull affected pigs

42
Q

What are the important gut parasites of pigs?

A

Ascaris suum- large roundworm
Trichuris suis- large intestine whipworm
Oesophagostomum sp - nodule worm
Hyostrongylus rubidus- red stomach worm
Strongyloides ransomi- intestinal threadworm

43
Q

What are the clinical signs of Trichuris suis?

A

Weight loss, bloody diarrhoea, anaemia, worms or autopsy

44
Q

What are the clinical signs of oesophagostomum?

A

Not pathogenic, nodules in the small and large intestines at slaughter, not a problem

45
Q

How can GI parasites in pigs be controlled?

A

Indoor - Fenbendazole (top-dressed) for 2 days on entry to farrowing accommodation
Outdoor – ivermectin in feed for 7 days 2-34 times per year
Good hygiene of the weaner accommodation

46
Q

How can an outbreak of GI disease in pigs be managed?

A

History – age, duration, treatment, mortality
First aid – TLC, biosecurity, oral rehydration
Visit farm – general appraisal
Clinical examination
Samples – faecal samples
PME – cull, fresh and fixed samples of gut
Treatment of surviving pigs

47
Q

What are the common vaccinations in pigs?

A

Clostridia perfringens a, b or c

E. coli (vaccines for both toxins and bacteria)

48
Q

What samples do you need to submit for a definitive diagnosis to distinguish between commensal and virulent E.coli?

A

Necropsy samples – samples from ilium and jejunum for histo and culture
Euthanised piglet – samples are taken and processed rapidly after death

49
Q

What diagnostic tests need to be performed to identify virulent enterotoxigenic E coli likely to cause disease in neonatal piglets?

A

Agglutination or PCR for fimbriae

PRC for e.coli toxin genes

50
Q

Which quick tests would allow you to distinguish between diarrhoea likely caused by rotavirus from that likely caused by E. coli?

A

PCR to identify E. coli or rotavirus DNA
Rotavirus snaptest
Litmus paper – E. coli diarrhoea is alkaline (blue) malabsorptive diarrhoea caused by viral infections is more acidic (red colour change)

51
Q

How is coccidiosis controlled in pigs?

A

Hygiene - oocysts are very resistant to conventional disinfectants, limewashing is effective, burning/removal of any bedding
Coccidiostats e.g. toltrazuril

52
Q

What traits should poultry litter have?

A

Absorbent, biodegradable, minimal dust, bio-secure source, pure source, comfortable, affordable, concrete floors underneath for better biosecurity and litter management

53
Q

Why does poultry litter become wet?

A

Water from drinkers – drinker height, damage, water pressure, condensation
Water from environment – concrete should be dry and warm before applying litter, some heat sources will produce water, ventilation (humid air will release water)
Water from birds – breed, stocking density, nutrition, gut health/disease

54
Q

Why is it important for birds to have dry litter?

A

Can lead to pododermatitis, increased coccidial development, increased bacterial and viral damage

55
Q

If you have 500 or more meat chickens, what is the maximum stocking density?

A

33kg per square metre

Can increase up to 39kg per square metre but there are additional requirements

56
Q

What additional requirements are needed when stocking birds above 33kg per square metre?

A

Plan showing dimensions of surfaces the chickens occupy
Ventilation plan and target air quality levels
Location and nature of feeding and watering systems
Alarm and back up systems for if essential equipment fails
Floor type and litter normally used
Records of technical inspections of ventilation and alarm systems

57
Q

What is dysbacteriosis in the context of chicken GI health?

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

58
Q

How common is clostridium perfringens in poultry?

A

Ubiquitous – present in the intestines and environment

59
Q

When will C. perfringens affect poultry?

A

Cp waits for an opportunity e.g. coccidial challenge or immunological stress
Uncontrolled growth will lead to disruption of intestinal integrity

60
Q

What is the pathogenesis of Clostridium perfringens in poultry?

A

Disruption of intestinal integrity by Cp toxins  dysbacteriosis  clostridial enteritis (NE) or cholangiohepatitis

61
Q

How is bacterial enteritis treated in poultry?

A

Oral antibiotics in the water e.g. amoxicillin, tylosin

62
Q

How is bacterial enteritis controlled in poultry?

A 
Prophylactic antibiotics?
Probiotics
Competitive exclusion products
Prebiotics (Nondigestible compounds)
Supplementary enzymes & acids
Husbandry
Feed manipulation
No vaccines available
63
Q

What are the common GI viruses in poultry?

A

Infectious bronchitis – also causes kidney damage
Gumbo virus (infectious bursal disease IBD) – GIT damage and immunosuppression
Adenovirus – gizzard erosion and scour

64
Q

What is the most economically important mycotoxin in poultry?

A

Aflatoxins produced by Aspergillus flavus +/- Aspergillus parasiticus
Aflatoxin B1 is the most toxic

65
Q

What is the source of aflatoxins in poultry?

A

grains, maize, soyabeans, peanuts, millet

warm and humid conditions in storage

66
Q

Which birds are most at risk from aflatoxins?

A

Ducklings > turkeys > goslings >chickens

67
Q

What are the clinical signs of aflatoxicosis in poultry?

A

reduced appetite, weakness, decreased efficiency of food conversion, decreased growth rate, decreased egg production and hatchability, immune suppression leading to coccidiosis, Marek’s disease, salmonella, abnormal pigmentation +/- bruising
Worst case scenario -> severe liver necrosis -> death
Sub acute/chronic situation -> decreased productivity

68
Q

How can aflatoxicosis be treated in poultry?

A

No treatment
Recovery is possible after moderate intoxication
Need to remove contaminated feed

69
Q

How can aflatoxicosis be prevented/controlled in poultry?

A 
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?
70
Q

What are the common manifestations of coccidiosis in poultry?

A 
Poor FCRs
Poor/variable weights
Poor bone mineralization
Dehydration
Decreased pigmentation?
Increased mortality
Assists onset of enteritis
71
Q

Which types of immunity play a part in coccidiosis control?

A

Cell mediated immunity – involves heterophils and heterophages (most important)
Humoral – antibody production and NK cells

72
Q

Why is the peak challenge of coccidiosis in chickens at around 24 days of age?

A

3 life cycles are required to stimulate immunity
There have been 3 X 8 day coccidia life cycles by 24 days
After this time the immune system can deal with the lesions

73
Q

What are the internal stages of coccidia replication in the bird?

A

Schizogony (2 phases)
Gametogony (1 phase)
Release of unsporulated oocysts

The internal phase is where anticoccidials / vaccines act

74
Q

What is the external stage of coccidia replication in the bird?

A

External phase where the oocysts become sporulated

This is where litter management and terminal hygiene are critical

75
Q

Where does Eimeria acervuline infect?

A

The upper intestine

76
Q

Where does Eimeria maxima infect?

A

The upper and middle intestine

77
Q

Where does Eimeria tenella infect?

A

The caeca

78
Q

How is coccidiosis diagnosed?

A

PM, faecal samples (OPG or AST)

79
Q

What is OPG and how is it done?

A

Oocysts per gram – oocyst count in the faeces or litter

Done using a microscope and mcmaster counting chamber

80
Q

What is AST and how is it done?

A

Anticoccidial sensitivity testing – used to monitor the efficacy of anticoccidial products
Products are compared for efficacy against field isolates

81
Q

What is total mean lesion scoring?

A

A way of scoring the effect of coccidiosis on chickens to inform treatment and management decisions
TMLS < 1 : ok
1 < TMLS < 2 : re-examination 5 to 7 days
TMLS > 2 : treatment

82
Q

How many birds are need for post mortem in a coccidiosis case?

A

Live birds needed! Minimum 5 birds (18-24days old) needed per house.

83
Q

How can coccidial disease be treated in poultry?

A

Vaccines – not commonly used
Alternative products – no evidence they work
Anticoccidial drugs – most common

84
Q

What different anticoccidial drugs are available?

A

Synthetic anticoccidials ‘chemicals’

Polyether ionophore anticoccidials ‘ionophores’ – monovalent, monovalent glycoside, divalent

85
Q

Why are anticoccidial drugs rotated?

A

Changing the anticoccidial drugs to another class after a few cycles allows recovery of anticoccidial activity and limits the build up of resistance.

86
Q

What are the possible reasons for coccidial outbreaking poultry?

A 
Drug resistance 
High infection pressure 
Reduced feed intake 
Too low a drug dose 
Overcome vaccine reaction 
Immunity breaks in birds e.g. stress and infection
87
Q

Sulphonamides have been used in the past for control of coccidiosis. Why is their use being limited?

A

Toxicity issues and 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
88
Q

What is Amprolium and how does it work?

A

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.

89
Q

What is Toltrazuril?

A

Broad spec anticoccidial
Expensive but standard treatment for severe cases
Rapid resistance to toltrazuril
Long withdrawal times (mainly used in breeders)

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