Pig GI diseases Flashcards

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
Q

Can we vaccinate for rotavirus in pigs

A

No

26
Q

What are the two enteric coronaviruses of pigs and which is notifiable

A
  • Transmissible gastroenteritis virus TGEV
  • Porcine epidemic diarrhoea virus PED = notifiable; absent from UK

Neither are signficant in the UK

27
Q

Transmissible gastroenteritis virus pathogenesis

A

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
Q

Porcine epidemic diarrhoea virus

A

Notifiable
100% mortality in those <7 days old
Vomiting, diarrhoea, inappetance, agalactia in affected sows

29
Q

What two things make weaning stressful

A

GI tract callenge when changing from milk to solid food

Immune challenge; decline in passive immunity from colostrum and milk, environmental

30
Q

What is the causative agent of proliferative enteropathy

A

Lawsonia intracellularis
= obligate intracellular gram -ve pathogen that infects immature crypt cells in terminal ileum

31
Q

What are the two presentations of proliferative enteropathy

A

Proliferative intestinal adenomatosis = chronic; more common

Proliferative haemorrhagic enteropathy = acute

32
Q

Pathogenesis of lawsonia intracellularis (proliferative enteropathy)

A

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
Q

What age pigs does lawsonia intracellularis tend to affect; in PIA form and PHE form

A

PIA = 10-24 week old growing pigs
PHE = 5-8 month gilts after stress

34
Q

What would thickening/corrugation of terminal ileal or caecal mucosa and ileum muscle hypertrophy suggest infection with

A

Lawsonia intracellularis
Proliferative intestinal adenomatous chronic form

35
Q

What is the epidemiology of lawsonia intracellularis

A

shed in faeces, survives 2 weeks outside cells, spread by people as fomites, carrier pigs, may survive in rodents

36
Q

What do we need to remember when vaccinating pigs for lawsonia intracellularis

A

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
Q

What is the cause of swine dysentery

A

Brachyspira orgnaisms = motile and very haemolytic on culture

Mostly B hyodysenteriae
[Also B hampsonii]

38
Q

What predisposing factors are involved in swine dysentery

A

Diet with soluble non starch polysaccharides being able to reach the colon
e.g from course cereals or dense pellets

39
Q

Signs of swine dysentery

A

loss of appetite, abdominal discomfort, soft yellow-grey diarrhoea, later is watery dark and mucohaemorrhagic

40
Q

Pathogenesis of swine dysentery

A

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
Q

PCR is not necessarily clinically relevant for brachyspira in swine dysentery; what is a good indicator of significance?

A

How strong it haemolyses on culture
[atypical strains that aren’t strongly haemolytic not relevant]

42
Q

What diseases have rodents been implaicated in spreading in pigs

A

Lawsonia intracellularis
Brachyspira (swine dystenery_

43
Q

What spirochaetes cause spirochaetel diarrhoea with spontaneous recovery after a few weeks

A

Brachyspira pilosicoli
Brachyspira mudrochii

= less virulent that B hypodystenteriae

44
Q

What are the two disease manifestations os post-weaning E coli and which is more common

A

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
Q

Pathology of oedema disease from E coli in weaned piglets

A

GOod condition
Fluid in pericardial and pleural cavities
Oedema of gastric submucosa

46
Q

Whcih salmonella enterica serotype causes enteritis and septicaemia

A

Typhimurium

47
Q

What salmonella enterica serotype causes septicaemia but is not in UK

A

Cholerasuis

48
Q

Characteristics of salmonella

A

Hardy, ubiquitous gram -ve bacilli; persist for months in organic material

49
Q

Pathogenesis of septicaemia and enterocolitis S enterica forms

A

Septicaemia: endotoxin and host cytokines drive mucosal inflammation and necrosis

Enterocolitis: enterotoxins (shiga, cholera-like) cause diarrhoea; decrease Na+ resorption, increase Cl- secretino

50
Q

Why is it not possible to totally remove S enterica

A

UBiquitous in environment
Carriage in tonsils and terminal ileum

51
Q

How can we control/treat S enterica

A

Water or feed acidification to improve microbiome –> inhibits salmonella
Separate pigs from faeces
Remove sick animals
Reduce stress
Vacinate

52
Q

How would we diagnose S enterica

A

Faecal sample of >15g for culture and isolatino
Or from spleen/lung/liver in septicaemic cases

53
Q

Risk factors for torsion in pigs

A

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
Q

RIsk factors for gastric ulceration

A

Stress, starvation, infection, very small particle size (in diets designed for efficiency food conversion)

55
Q

What is pathognomic for gastric ulceration

A

VOminiting blood

56
Q

What is significant if a hernia is touching the ground or ulcerated

A

Not fit to transport e.g to slaughter

57
Q

Risk factors for rectal prolapse

A

 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
Q

Treating helminths in pigs

A

injectible ivermectins, oral benzimidazoles

59
Q

What is the main economic impact of ascaris suum

A

Liver rejection due to milk spot liver
Also cause reduction in growth rate and feed conversion

60
Q

How to vaccinate for post-weaning E coli

A

Oral live vaccine with F4 and F18

61
Q

Why can we not get oedema disaese until pigs a few weeks old

A

Bceause the F18 fimbriaecan only attach when glycan receptors are fully expressed on enterocytes