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Pig GI diseases Flashcards

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1
Q

Aetiology of E coli causing disease in piglets

A

Adhesion to villi via fimbrial adhesions
O antigen (LPS) causing inflammation and epithelial damage
LT enterotxin increases electrolye secretion
ST enterotoxin reduce electrolyte reabsorption

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2
Q

Two manifestations of E coli infection in neonates

A

Septicaemia: pyrexia, convulsions, coma, death; 100 mortality
Diarrhoea: water/yellow diarrhoea; 70% mortality

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3
Q

How do E coli LT and ST toxins work

A

LT enterotoxin increases electrolyte secretion
ST enterotoxin reduce electrolyte reabsorption

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4
Q

How does E coli diarrhoea in slightly older piglets 1-3 weeks differ from neonatal

A

Lower severity diarrhoea; grey colour
Related to change in diet; having some creep

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5
Q

What are the 3 main differentials for watery diarrhoea in young piglets

A

E coli
C perfringens (bloody diarrhoea)
Rotavirus (tend to be older; 3-5 weeks)

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6
Q

Pathological lesions in diarrhoea form of neonatal E coli

A

Dehydrated carcase
Dark liver
Congestion of small intestine with watery content
Villi intact or mildly atrophic

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7
Q

Pathological lesions in neonates with septicaemia E coli

A

Good condition carase
Muscle congestion
Enlarged spleen
Meningitis/polyserositis/polyarthritis if haven’t died immediately from septicaemia

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8
Q

What are the two important types of clostridium perfringens in piglet diarrhoea and which toxins do they make

A

Type A - makes alpha toxins
Type C - makes alpha and beta toxins

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9
Q

Which litters is C perfringens more common in

A

Littesr born to gilts due to immature immunity of mother so poorer colostral immunity

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10
Q

Characteristics of type A vs type C C perfringens disease

A

A = milder; creamy pink diarrhoea, dramatic loss of condition, dull, sunken eyes, high morbidity low mortality

C = sudden death, high mortality up to 100% in non-immune herds, necrotic haemorrhagic diarrhoea [can get chronic infections in older piglets with loss of condition]

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11
Q

Pathology of C perfrigens carcase

A

Pale carcase
Very inflamed intestines filled with haemorrhagic content
Villous atrophy on histopath

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12
Q

What does bloody diarrhoea in first few days of life point towards

A

Clostridium perfringens

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13
Q

How to prevent risk of C perfringens

A

Kill spores using flames or lime wash
Wash sows before they enter farrowing house
Vaccinate
Can use long acting amoxycillin for litters at high risk

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14
Q

When does coccidiosis cause issues in piglets

A

at 2-3 weeks old

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15
Q

Signs of coccidiosis

A

Pasty-watery, yellow foamy with blood streaks, loss of condition, may get other pathogens, vomit

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16
Q

Which coccidia species might piglets get and which is more significant

A

Isospora suis; more important; amplifies in piglets and passes batch to batch

Eimeria suis = less signficant; carried by cows

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17
Q

Pathology of coccidiosis and diagnosis

A

Thickened small intestine with creamy/watery contents, necrosis, villous atrophy

Definitive diagnosis = oocysts in pooled faecal sample

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18
Q

Treatment of coccidiosis

A

Give toltrazuril prophylactically in first week of life

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19
Q

Signs of cryptosporidium parvum and when might it be more severe

A

90% asymptomatic
But can get severe signs when assocaited with rotavirus

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20
Q

When do piglets tend to be affected by rotavirus

A

3-5 weeks old

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21
Q

What type of virus is rotavirus and which strain is most significant in pigs

A

RNS virus
Type A most important

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22
Q

Signs of rotavirus infection

A

Profuse yellow diarrhoea, rapid condition loss, anorexia, up to 30% mortality, slow growing after recovery

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23
Q

Pathology of rotavirus infectino

A

Just small intestine affected
= distended with creamy fluid, thin walled with villous atrophy, fusion and crypt hyperplasia

Dehydrated carcase

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24
Q

Diagnosing rotavirus nfection

A

Virus detection
NB: serum antibody not useful

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25
Can we vaccinate for rotavirus in pigs
No
26
What are the two enteric coronaviruses of pigs and which is notifiable
- Transmissible gastroenteritis virus TGEV - Porcine epidemic diarrhoea virus PED = notifiable; absent from UK Neither are signficant in the UK
27
Transmissible gastroenteritis virus pathogenesis
Profuse watery diarrhoea Causes destruction of IMMATURE enterocytes so high mortality in those <7 days old, sows may be agalactic Gastritis, villous strophy, thin walled intestine
28
Porcine epidemic diarrhoea virus
Notifiable 100% mortality in those <7 days old Vomiting, diarrhoea, inappetance, agalactia in affected sows
29
What two things make weaning stressful
GI tract callenge when changing from milk to solid food Immune challenge; decline in passive immunity from colostrum and milk, environmental
30
What is the causative agent of proliferative enteropathy
Lawsonia intracellularis = obligate intracellular gram -ve pathogen that infects immature crypt cells in terminal ileum
31
What are the two presentations of proliferative enteropathy
Proliferative intestinal adenomatosis = chronic; more common Proliferative haemorrhagic enteropathy = acute
32
Pathogenesis of lawsonia intracellularis (proliferative enteropathy)
Infection of immature crypt cells in terminal ileum and prolieration PIA: Get poor growth, wasted appearance, wet cement diarrhoea, can remain stunted, thickening and corrugation of terminal ileum/caecal mucosa PIH: haemorrhagic faeces, blood clots in ileum, pale pigs, found dead
33
What age pigs does lawsonia intracellularis tend to affect; in PIA form and PHE form
PIA = 10-24 week old growing pigs PHE = 5-8 month gilts after stress
34
What would thickening/corrugation of terminal ileal or caecal mucosa and ileum muscle hypertrophy suggest infection with
Lawsonia intracellularis Proliferative intestinal adenomatous chronic form
35
What is the epidemiology of lawsonia intracellularis
shed in faeces, survives 2 weeks outside cells, spread by people as fomites, carrier pigs, may survive in rodents
36
What do we need to remember when vaccinating pigs for lawsonia intracellularis
It is a live attenuated vaccine so the pig must not be on antibiotics or this will kill vaccine; withdraw 3-5 days before minimum
37
What is the cause of swine dysentery
Brachyspira orgnaisms = motile and very haemolytic on culture Mostly B hyodysenteriae [Also B hampsonii]
38
What predisposing factors are involved in swine dysentery
Diet with soluble non starch polysaccharides being able to reach the colon e.g from course cereals or dense pellets
39
Signs of swine dysentery
loss of appetite, abdominal discomfort, soft yellow-grey diarrhoea, later is watery dark and mucohaemorrhagic
40
Pathogenesis of swine dysentery
Faeco-oral Pathogen colonises crypt and goblet cells in colon When fermentable food reaches the colon can ferment this and create irritant metabolites Haemolysin and LPS for submucosal invasion and inflammation Interfere with transport mechanism so get malapsortion and fluid loss Secondary infections
41
PCR is not necessarily clinically relevant for brachyspira in swine dysentery; what is a good indicator of significance?
How strong it haemolyses on culture [atypical strains that aren't strongly haemolytic not relevant]
42
What diseases have rodents been implaicated in spreading in pigs
Lawsonia intracellularis Brachyspira (swine dystenery_
43
What spirochaetes cause spirochaetel diarrhoea with spontaneous recovery after a few weeks
Brachyspira pilosicoli Brachyspira mudrochii = less virulent that B hypodystenteriae
44
What are the two disease manifestations os post-weaning E coli and which is more common
Enteritis disease; very common; >95% of diarrhoea in recently weaned pigs, low mortality Oedema disease: affects best conditioned piglets, get neuro signs, high mortality
45
Pathology of oedema disease from E coli in weaned piglets
GOod condition Fluid in pericardial and pleural cavities Oedema of gastric submucosa
46
Whcih salmonella enterica serotype causes enteritis and septicaemia
Typhimurium
47
What salmonella enterica serotype causes septicaemia but is not in UK
Cholerasuis
48
Characteristics of salmonella
Hardy, ubiquitous gram -ve bacilli; persist for months in organic material
49
Pathogenesis of septicaemia and enterocolitis S enterica forms
Septicaemia: endotoxin and host cytokines drive mucosal inflammation and necrosis Enterocolitis: enterotoxins (shiga, cholera-like) cause diarrhoea; decrease Na+ resorption, increase Cl- secretino
50
Why is it not possible to totally remove S enterica
UBiquitous in environment Carriage in tonsils and terminal ileum
51
How can we control/treat S enterica
Water or feed acidification to improve microbiome --> inhibits salmonella Separate pigs from faeces Remove sick animals Reduce stress Vacinate
52
How would we diagnose S enterica
Faecal sample of >15g for culture and isolatino Or from spleen/lung/liver in septicaemic cases
53
Risk factors for torsion in pigs
Rapid ingestion of lots of liquid food (e.g whey) or water Activity after feeding Excessive gas production by yeasts/C perfringens A/whey
54
RIsk factors for gastric ulceration
Stress, starvation, infection, very small particle size (in diets designed for efficiency food conversion)
55
What is pathognomic for gastric ulceration
VOminiting blood
56
What is significant if a hernia is touching the ground or ulcerated
Not fit to transport e.g to slaughter
57
Risk factors for rectal prolapse
 Persistent coughing  Straining due to chronic diarrhoea  Excessive huddling in cold conditions  Gorging on liquid feed  Flatulent diets  High mycotoxin levels in diet Heavily pregnant sows in gestation crates where hindwaurters lower High lysine supplementations Males with blocked urethra from phosphate
58
Treating helminths in pigs
injectible ivermectins, oral benzimidazoles
59
What is the main economic impact of ascaris suum
Liver rejection due to milk spot liver Also cause reduction in growth rate and feed conversion
60
How to vaccinate for post-weaning E coli
Oral live vaccine with F4 and F18
61
Why can we not get oedema disaese until pigs a few weeks old
Bceause the F18 fimbriaecan only attach when glycan receptors are fully expressed on enterocytes

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