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Farm 5 - Pigs and poultry Flashcards

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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
What are the pathological findings of salmonellosis in pigs?
Diptheritic typhlocolitis (inflammation of the caecum and colon) Septicaemia Later: rectal strictures
26
What are the clinical signs of salmonellosis in pigs?
Mucin casts and blood in diarrhoea (need to rule out SD) +/-Pyrexia Scouring (can be only mild) Purple skin discolouration (septicaemia)
27
What is the epidemiology of salmonellosis in pigs?
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
28
How is salmonellosis treated in pigs?
Antibiotics (in water) – C+S important due to multi drug resistance
29
How is salmonellosis controlled in pigs?
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
30
What is the causative agent to yersinosis in pigs?
Y. pseudotuberculosis
31
What are the clinical signs of yersinosis in pigs?
Watery, dark, mucoid diarrhoea
32
What is the most important consideration in a yersinosis outbreak?
Zoonosis - personal hygiene, important to talk to staff
33
How is yersinosis controlled?
Hygiene and AIAO measures
34
How common is GI torsion in pigs?
Very common
35
Where do GI torsions occur in pigs?
- Long length SI volvulus at the mesenteric root | - Gastric dilatation/volvulus in older pigs
36
When are pigs most likely to get SI volvulus at the mesenteric root?
Growers 8-12wks Tend to eat a lot and jump, fight and roll Usually single cases of sudden death
37
When are pigs most likely to get a GDV?
Older pigs | Usually when there has been a change in feed or they eat a lot and fight
38
How common are stomach ulcers in pigs?
Very common >60% of growers at slaughter
39
What are the 3 main factors that cause stomach ulcers in pigs?
Finely ground feed components Cessation of feed intake for one day Wet fed with whey (can also be secondary to lung infections)
40
What are the clinical signs of stomach ulcers in pigs?
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
How are stomach ulcers treated?
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
What are the important gut parasites of pigs?
Ascaris suum- large roundworm Trichuris suis- large intestine whipworm Oesophagostomum sp - nodule worm Hyostrongylus rubidus- red stomach worm Strongyloides ransomi- intestinal threadworm
43
What are the clinical signs of Trichuris suis?
Weight loss, bloody diarrhoea, anaemia, worms or autopsy
44
What are the clinical signs of oesophagostomum?
Not pathogenic, nodules in the small and large intestines at slaughter, not a problem
45
How can GI parasites in pigs be controlled?
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
How can an outbreak of GI disease in pigs be managed?
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
What are the common vaccinations in pigs?
Clostridia perfringens a, b or c | E. coli (vaccines for both toxins and bacteria)
48
What samples do you need to submit for a definitive diagnosis to distinguish between commensal and virulent E.coli?
Necropsy samples – samples from ilium and jejunum for histo and culture Euthanised piglet – samples are taken and processed rapidly after death
49
What diagnostic tests need to be performed to identify virulent enterotoxigenic E coli likely to cause disease in neonatal piglets?
Agglutination or PCR for fimbriae | PRC for e.coli toxin genes
50
Which quick tests would allow you to distinguish between diarrhoea likely caused by rotavirus from that likely caused by E. coli?
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
How is coccidiosis controlled in pigs?
Hygiene - oocysts are very resistant to conventional disinfectants, limewashing is effective, burning/removal of any bedding Coccidiostats e.g. toltrazuril
52
What traits should poultry litter have?
Absorbent, biodegradable, minimal dust, bio-secure source, pure source, comfortable, affordable, concrete floors underneath for better biosecurity and litter management
53
Why does poultry litter become wet?
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
Why is it important for birds to have dry litter?
Can lead to pododermatitis, increased coccidial development, increased bacterial and viral damage
55
If you have 500 or more meat chickens, what is the maximum stocking density?
33kg per square metre | Can increase up to 39kg per square metre but there are additional requirements
56
What additional requirements are needed when stocking birds above 33kg per square metre?
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
What is dysbacteriosis in the context of chicken GI health?
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
How common is clostridium perfringens in poultry?
Ubiquitous – present in the intestines and environment
59
When will C. perfringens affect poultry?
Cp waits for an opportunity e.g. coccidial challenge or immunological stress Uncontrolled growth will lead to disruption of intestinal integrity
60
What is the pathogenesis of Clostridium perfringens in poultry?
Disruption of intestinal integrity by Cp toxins  dysbacteriosis  clostridial enteritis (NE) or cholangiohepatitis
61
How is bacterial enteritis treated in poultry?
Oral antibiotics in the water e.g. amoxicillin, tylosin
62
How is bacterial enteritis controlled in poultry?
``` Prophylactic antibiotics? Probiotics Competitive exclusion products Prebiotics (Nondigestible compounds) Supplementary enzymes & acids Husbandry Feed manipulation No vaccines available ```
63
What are the common GI viruses in poultry?
Infectious bronchitis – also causes kidney damage Gumbo virus (infectious bursal disease IBD) – GIT damage and immunosuppression Adenovirus – gizzard erosion and scour
64
What is the most economically important mycotoxin in poultry?
Aflatoxins produced by Aspergillus flavus +/- Aspergillus parasiticus Aflatoxin B1 is the most toxic
65
What is the source of aflatoxins in poultry?
grains, maize, soyabeans, peanuts, millet | warm and humid conditions in storage
66
Which birds are most at risk from aflatoxins?
Ducklings > turkeys > goslings >chickens
67
What are the clinical signs of aflatoxicosis in poultry?
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
How can aflatoxicosis be treated in poultry?
No treatment Recovery is possible after moderate intoxication Need to remove contaminated feed
69
How can aflatoxicosis be prevented/controlled in poultry?
``` 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
What are the common manifestations of coccidiosis in poultry?
``` Poor FCRs Poor/variable weights Poor bone mineralization Dehydration Decreased pigmentation? Increased mortality Assists onset of enteritis ```
71
Which types of immunity play a part in coccidiosis control?
Cell mediated immunity – involves heterophils and heterophages (most important) Humoral – antibody production and NK cells
72
Why is the peak challenge of coccidiosis in chickens at around 24 days of age?
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
What are the internal stages of coccidia replication in the bird?
Schizogony (2 phases) Gametogony (1 phase) Release of unsporulated oocysts The internal phase is where anticoccidials / vaccines act
74
What is the external stage of coccidia replication in the bird?
External phase where the oocysts become sporulated | This is where litter management and terminal hygiene are critical
75
Where does Eimeria acervuline infect?
The upper intestine
76
Where does Eimeria maxima infect?
The upper and middle intestine
77
Where does Eimeria tenella infect?
The caeca
78
How is coccidiosis diagnosed?
PM, faecal samples (OPG or AST)
79
What is OPG and how is it done?
Oocysts per gram – oocyst count in the faeces or litter | Done using a microscope and mcmaster counting chamber
80
What is AST and how is it done?
Anticoccidial sensitivity testing – used to monitor the efficacy of anticoccidial products Products are compared for efficacy against field isolates
81
What is total mean lesion scoring?
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
How many birds are need for post mortem in a coccidiosis case?
Live birds needed! Minimum 5 birds (18-24days old) needed per house.
83
How can coccidial disease be treated in poultry?
Vaccines – not commonly used Alternative products – no evidence they work Anticoccidial drugs – most common
84
What different anticoccidial drugs are available?
Synthetic anticoccidials ‘chemicals’ | Polyether ionophore anticoccidials ‘ionophores’ – monovalent, monovalent glycoside, divalent
85
Why are anticoccidial drugs rotated?
Changing the anticoccidial drugs to another class after a few cycles allows recovery of anticoccidial activity and limits the build up of resistance.
86
What are the possible reasons for coccidial outbreaking poultry?
``` 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
Sulphonamides have been used in the past for control of coccidiosis. Why is their use being limited?
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
What is Amprolium and how does it work?
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
What is Toltrazuril?
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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