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CVSOH 4 > Bovine and Ovine Gastrointestinal > Flashcards

Bovine and Ovine Gastrointestinal Flashcards

1
Q

What is some important history questions to ask for bovine diarrhoea?

A
  • Herd or single animal
  • Previous occurrence?
  • Age group
  • Duration of diarrhoea
  • Nutrition?
  • Water source? Is this contaminated?
  • Production effects – understanding if this is affecting growth rate or welfare
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2
Q

Why might calves have diarrhoea if put onto lush pasture?

A

Calves being on lush pasture with diarrhoea as a normal physiological response to nutrition, need gut microflora to adapt in order for diarrhoea to settle down. Knowing when to do nothing.

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3
Q

What should be looked for when examining a group or individual cow?

A
  • Drooling saliva
  • Abdominal pain
  • Tenesmus
  • Clinical examination, especially assessing level of dehydration
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4
Q

What is examined from the faeces when assessing bovine diarrhoea?

A

Consistency
Colour
Smell
Mucoid
Blood
Sample

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5
Q

What is assessed upon examination of an cow with diarrhoea?

A
  • Oral cavity for lesions
  • Perineal region
  • Any abdominal pain?
  • TPR
  • Body condition?
  • Any lameness?
  • Any nervous signs?
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6
Q

What are the plant and chemical poisoning differential diagnoses for bovine diarrhoea?

A
  • May become confined to area with little food
  • May be exposed to dumping of potentially harmful material
  • May be exposed to excessive lush pasture or acorns blowing into field (tannins are toxic and cause kidney damage and diarrhoea)
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7
Q

What are the dietary induced differential diagnoses for bovine diarrhoea?

A
  • History of husbandry changes important
  • Ruminal overload, frosted foods, grass scour, excess fodder beet
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8
Q

What is the epidemiology of coccidiosis causing bovine diarrhoea?

A
  • Increasing incidence due to indoor intensification - in housed confined calves, often insufficient bedding
  • Oocysts survive months in faeces but only a few hours in sunlight. Parasites are ubiquitous but disease due to build up of predisposing factors
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9
Q

What is the pathogenesis of coccidiosis causing bovine diarrhoea?

A
  • Acute to chronic diarrhoea, smelly, often greenish, can get mucoid/blood
  • Poor weight gain or actual weight loss
  • Self-limiting, diagnose by examining group
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10
Q

How is coccidiosis treated in cows?

A
  • Diclazuril orally or perhaps sulphonamides
  • Decoquinate in feed preventive medication
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11
Q

What are 2 examples of helminths causing bovine diarrhoea?

A

Ostertagiasis type I and II
Fasciola hepatica

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12
Q

What does salmonellosis cause in cows?

A

Enteritis
Abortion
Septicaemia

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13
Q

How is salmonella transmitted in cows?

A
  • Faecal-oral
  • In feed, on vet, in slurry, rodents and birds
  • Conjunctival
  • Respiratory
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14
Q

What is the infective dose of salmonella in cows?

A

10^10 in adults, 10^8 in calves

Clinical cases excrete 10^8/g faeces

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15
Q

What is the incubation period of salmonella in cows?

A

1-4 days

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16
Q

What is the epidemiology of salmonella typhimurium?

A
  • October-December
  • Not host specific
  • Causes enteritis or septicaemia
  • Resolved after 3-16 weeks
  • Epidemic
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17
Q

What is the epidemiology of salmonella dublin?

A
  • Endemic in wetter areas
  • Host-adapted
  • Active carriers shed for up to a year
  • Passive carriers shed while exposed
  • Latent carriers shed when stressed
  • May even get congenital infection as it can be spread from the reproductive tract in calf from cow that aborted
  • Association with Fasciola hepatica
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18
Q

What are the sites of carriage of salmonella in cows?

A
  • Caecal contents
  • Terminal ileum
  • Ileal/caecocolic lymph nodes
  • Gall bladder
  • Shed in faeces
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19
Q

Distinguish carriage in cows of salmonella typhimurium and dublin.

A

Carriage for around 4 weeks with Typhimurium but carriage for years with Dublin

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20
Q

How is salmonellosis diagnosed in a laboratory?

A
  • Faecal culture
  • Environmental samples
  • Pathology especially gut lesions
  • Histopathology
  • Culture of lesions
  • Culture at abattoir
  • Serology – this will only tell you that the animal has antibodies, not if came from active or previous infection or vaccination
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21
Q

Why is salmonella difficult to treat and control in cows?

A
  • Antimicrobial sensitivity testing aids selection of therapy
  • S. Dublin largely sensitive
  • Vaccines containing killed culture
  • Organisms sensitive to disinfectants, but resistant to drying
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22
Q

What are the clinical signs of salmonella in cows?

A
  • Adult cattle enteric syndrome
  • Lethargy, pyrexia, milk drop
  • Diarrhoea, possibly preceded by firm, bloody faeces
  • Sometimes profuse and watery
  • Often blood, mucus and casts
  • Abdominal pain
  • Recumbency
  • Death
  • Adult cattle abortion – abortion, with or without diarrhoea. More common with S. Dublin infection
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23
Q

What are the clinical signs of salmonella in calves?

A
  • Lethargy, pyrexia, inappetence
  • Diarrhoea
  • Dehydration
  • Death
  • Sudden death
  • Sloughed extremities in some recovered cases esp. S. Dublin
  • Polyarthritis, pneumonia and meningitis are less common
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24
Q

How are individual cases of bovine salmonellosis diagnosed?

A
  • Clinical signs and PM findings suggestive
  • Faecal bacterial count
  • Faecal/gut content culture – repeat cultures?
  • Tissues to culture
  • Haematology
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25
Q

How are cases of bovine salmonellosis on a herd level diagnosed?

A
  • Herd culture – representative faecal samples, slurry samples
  • Herd ELISA – many high titres indicate recent/active infection
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26
Q

How is salmonellosis in cows treated?

A
  • Systemic antibiotics
  • Supportive care – fluids (IV/PO), nursing, diet
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27
Q

How is bovine salmonellosis prevented and controlled?

A
  • Biosecurity
  • Vaccinate – active and passive
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28
Q

What are the consequences of salmonellosis causing peripheral gangrene in cows?

A
  • Jelly looking lesion and clear demarcation of healthy skin
  • Extremities would be very cold and are not lamb as they cannot feel it, so end up damaging it more
  • Stink because they are gangrenous and necrotic
  • Eventually toes will fall off
  • Often the scruff end of tails and ears too, as infection has gotten into peripheral tissues and has affected the blood supply and has caused the peripheral tissue to die off
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29
Q

What are the risk factors for enteric disease in neonatal lambs?

A
  • Pathogen/disease build up under intensive conditions in lambing sheds
  • Overcrowding
  • Overworked staff
  • Contact between neonates and older lambs
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30
Q

What is the cause of watery mouth in noenatal lambs?

A

E.coli

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31
Q

What are the risk factors of watery mouth?

A
  • Usually very young lambs (12-48hrs old)
  • Often twins/triplets
  • Poor colostrum intake
  • Flocks housed at lambing
  • Thin ewes
  • Low birth rate
  • Contaminated environment
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32
Q

What are the clinical signs of watery mouth in lambs?

A
  • Dull, weak, unwilling to suck
  • Drooling saliva
  • May be acidotic (suppresses suck reflex)
  • Hypothermia follows
  • Abdomen becomes distended with gas
  • Gut stasis (as opposed to diarrhoea)
  • Retained meconium
  • Die within 12-24 hours
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33
Q

How is watery mouth treated in lambs?

A
  • Treat clinical signs
  • Prevent starvation – intraperitoneal glucose as for hypothermic lambs
  • Pain relief – NSAIDS via cascade
  • No antibiotics – these will not work and will only cause resistance
  • Prevention is better than cure
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34
Q

How are ewes managed to prevent watery mouth in lambs?

A
  • Monitor body condition score
  • Nutritional management
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35
Q

How are lambs managed to prevent watery mouth in lambs?

A
  • Consider lambing outdoors
  • Sufficient space
  • Maintain hygiene
  • Dry clean bedding – completely cleaned out regularly
  • Clean utensils
  • Isolation pen for sick lambs
  • Avoid mixing of ages
  • Lamb management – colostrum intake (50ml/kg within 4-6 hours of birth)
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36
Q

What is colisepticaemia?

A
  • Lambs up to 7 days old
  • May be in conjunction with watery mouth
  • Systemic E.Coli infection
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37
Q

How does diarrhoea in neonatal lambs cause death?

A

Neonatal scour > dehydration > high mortality

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38
Q

How is diarrhoea in neonatal lambs diagnosed?

A

10 faecal samples from scouring lambs and/or PME

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39
Q

What is the pathogenesis of enteric colibacillosis?

A
  • Non K99 E.coli strains
  • Invasive strains enter via gut or navel
  • Colonise and proliferate in upper SI
  • Toxins cause secretion of fluid into intestinal lumen
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40
Q

What are the clinical signs of enteric colibacillosis?

A

Diarrhoea
Dehydration
Recumbency
Stop nursing
Death

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41
Q

How is enteric colibacillosis treated?

A
  • Supportive fluid therapy
  • NSAIDS
  • Antibiotics? Can interfere with normal gut flora. IM amoxicillin may be beneficial
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42
Q

What causes lamb dysentery/cherry gut?

A

Clostridial perfringes type B

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43
Q

What are the clinical signs of lamb dysentery in lambs 1-3 days old?

A
  • Haemorrhagic enteritis
  • Abdominal pain
  • Sudden death
  • Mortality 100% in affected
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44
Q

What are the clinical signs of lamb dysentery at post mortem examination?

A
  • Haemorrhagic enteritis, mainly with ileum
  • Ulceration of mucosa
  • Serosanguinous peritoneal fluid
  • Toxins in intestinal content
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45
Q

What causes yellow lamb disease?

A

Clostridial perfringes type A/haemorrhagic enteritis

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46
Q

What are the clinical signs of yellow lamb disease in lambs?

A

Diarrhoea
Sudden death
Can sometimes appear as if they have icterus

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47
Q

What are the clinical signs of yellow lamb disease at post mortem examination?

A
  • Generalised haemorrhagic enteritis
  • Bloody diarrhoea
  • Toxins ins intestinal content
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48
Q

How is yellow lamb disease treated and prevented?

A

No treatment

Prevention – ewe vaccination (as this affects new borns so ewes can pass on antibiotics in colostrum), colostrum, hygiene at lambing

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49
Q

What are the clinical signs of cryptosporidium parvum in lambs and kids?

A
  • Diarrhoea – liquid and yellow
  • Lambs often remain alert, active and nursing
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50
Q

What is the epidemiology of cryptosporidium parvum in lambs and kids?

A
  • Often associated with E.coli and rotavirus as they are immunosuppressed from the cryptosporidium
  • Predisposed by poor hygiene, bad weather, inadequate energy intake
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51
Q

How is diarrhoea treated in lambs?

A
  • Oral fluids and allow to suck dam - prevents villous atrophy
  • If severe – fluid therapy. Hartman’s solution and sodium bicarbonate to combat acidosis until stops scouring
  • NSAIDs under cascade: flunixin, ketoprofen
  • Antibiotics rarely indicated – avoid using
  • Suitable disinfectant (check will work against causative agents)
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52
Q

Distinguish diarrhoea in neonatal lambs and older lambs?

A

Neonatal scour > high mortality due to dehydration

Diarrhoea in older lambs – ill thrift

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53
Q

How is diarrhoea in older lambs investigated with history?

A
  • Age
  • Grazing history
  • Clinical signs
  • Treatment history (anthelmintics)
  • Environment – hygiene, overcrowding?
  • Diet – check for overfeeding with concentrates (acidosis), check for low dry matter forage intake (very lush pasture) or fertiliser application without rainfall
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54
Q

How is diarrhoea in older lambs investigated with diagnostic testing?

A
  • Post mortem examination of dead animals
  • Faecal samples for worm egg count, oocyst count, salmonella culture
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55
Q

What are the clinical signs of coccidiosis eimeria in sheep?

A
  • Dehydration
  • Dull coat
  • Diarrhoea which is often bloody and mucoid
  • Depression and lethargy
  • Tenesmus (straining)
  • May get rectal prolapse due to severe tenesmus
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56
Q

How is coccidiosis eimeria in sheep treated?

A
  • Diclazuril
  • Toltrazuril
  • In-feed coccidiostats but prevents immunity developing
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57
Q

How is coccidiosis eimeria in sheep controlled?

A
  • Oocysts survive better in wet environments
  • Hygiene
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58
Q

What are the clinical signs of salmonellosis in sheep?

A
  • Pyrexia
  • Diarrhoea
  • Putrid smell, with mucous and flecks of blood
  • Tucked up’ abdomen
  • Rapid dehydration
  • Peracute – found dead
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59
Q

How is salmonellosis in sheep treated?

A
  • Isolate
  • Oral rehydration
  • Antibiotics
  • Move remaining animals from contaminated area
  • Disinfect area
  • Biosecurity
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60
Q

What is the epidemiology of Johne’s disease in sheeo?

A
  • Very common in goats, sporadic in sheep
  • 18 month+ incubation period
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61
Q

What does Johne’s disease cause in sheep?

A
  • Chronic granulomatous enteritis but doesn’t really cause diarrhoea in sheep
  • Johnes in sheep is not associated with diarrhoea, it is associated with chronic weight loss (wasting)
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62
Q

When might Johne’s in sheep be associated with diarrhoea?

A

Animals with Johnes may have concurrent parasitism which produces diarrhoea

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63
Q

Where is mycobacterium avium subsp paratuberculosis located?

A

Bacteria localise and multiply in mucosa of intestines and their associated lymph nodes (also tonsils)

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64
Q

Why is Johne’s hard to eliminate?

A

Survive on pasture for up to a year and rabbits implicated as reservoirs of infection, so very difficult to eliminate

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65
Q

How is Johne’s in sheep controlled?

A
  • Cull thin animals
  • Do not keep offspring
  • Alternate lambing areas each year (reduce spread)
  • Vaccinate breeding animals within one month - they will become infected but will not develop clinical signs
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66
Q

What are the clinical signs of scour in claves?

A
  • Fever
  • Change in abdominal contour
  • Diarrhoea – colour, consistency, blood
  • Weight loss
  • Inflammation in another body system (umbilicus)
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67
Q

Name 4 endemic pathogens causing calf scour.

A

Rotavirus
Coronavirus
Cryptosporidia
Enterotoxigenic E. coli

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68
Q

Name 2 exotic pathogens causing calf scour.

A

E.coli K99/F41
Salmonella

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69
Q

Name 2 pathogens of unknown prevalence causing calf scour.

A

E.coli AEEC (adherent)
Calicivirus

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70
Q

How does a calf’s age suggest the scouring agent?

A

0 – 6 days = enterotoxigenic E. coli (ETEC)

6 – 21 days = rotavirus, coronavirus, cryptosporidium

> 21 days = coccidiosis

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71
Q

What is the epidemiology of rotavirus in calves?

A
  • Infection in almost 100% of calves
  • Cows shed virus, colostrum contains specific antibodies
  • Several strains, some avirulent
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72
Q

How does rotavirus cause scour in calves?

A

Destruction of microvilli in enterocytes

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73
Q

How is immunity affected by rotavirus in calves?

A
  • Immunity requires local antibody
  • Immunity overcome by heavy challenge
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74
Q

What are the clinical signs of rotavirus in calves?

A

Thin, yellow white diarrhoea, second week of life

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75
Q

How is rotavirus in calves prevented against?

A

Vaccine available (administered to the dam, immunity via colostrum)

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76
Q

Describe the normal intestinal function in calves.

A

Lactase cleaves lactose into glucose and galactose. Sodium glucose cotransporter 1 then transports glucose and galactose across the luminal (gut) side of enterocytes with sodium ions.

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77
Q

What is the pathogenesis of rotavirus in calves?

A
  • The non-structural virus protein NSP4 can specifically inhibit this sodium glucose symporter, meaning water cannot be reabsorbed and is lost.
  • Calcium ion movement from the ER to the cytoplasm and a loosening of intracellular junctions, which loses fluid from intracellular space to gut lumen
  • It is further thought that this can lead to a release of amines and peptides from infected cells that stimulate the enteric neural system, elevating crypt cell sodium secretion and gut motility.
  • This takes a while to get over which stunts their growth rates
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78
Q

What is the epidemiology of coronavirus in calves?

A
  • Widespread infection, virus in faeces of 65% cows (winter dysentery)
  • Commonly subclinical
  • Virus causes diarrhoea that can be acute and severe leading to rapid death in calves or more commonly causes chronic debilitating diarrhoea in older calves
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79
Q

What is the pathogenesis of coronavirus in calves?

A
  • Massive loss of intestinal epithelium and villus stunting
  • Greatly reduced absorption of intestinal fluid
  • Basal crypt cells less affected, recovery can be rapid
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80
Q

What is the epidemiology of cryptosporidium in calves?

A
  • Extracellular protozoan, not host specific
  • Zoonosis
  • Infection widespread, favoured by dirty conditions
  • Mixed infections common
  • Earliest cases 5-7 days, age immunity at three weeks
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81
Q

What are the clinical signs of cryptosporidium in calves?

A

Profuse watery diarrhoea for about 7 days

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82
Q

Why is cryptosporidium hard to treat in calves?

A
  • Poor response to anti-protozoals
  • Oocysts resistant to disinfectant
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83
Q

What are the pathogenic E.coli serotypes?

A
  • Enterotoxigenic E. coli (EETEC)
  • Verotoxigenic E. coli (VTEC)
  • Attaching and effacing E. coli (AEEC)
  • Enteroinvasive E. coli (EIEC)
  • Unclassified
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84
Q

What is the pathogenesis of enterotoxigenic E.coli in calves?

A
  • Rare over 5 days old due to loss of receptors on the gut epithelium for E. coli adhesins/toxins
  • Specific antibody blocks the adhesion
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85
Q

What are the clinical signs of enterotoxigenic E.coli in calves?

A

Sudden onset
Profuse watery diarrhoea
Severe dehydration leading to collapse of calf
Recovery takes a while

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86
Q

How does the normal calf gastrointestinal tract digest milk?

A
  1. Milk bypasses the rumen via oesophageal groove
  2. Acid (and rennin) causes paracasein to clot quickly
  3. Abomasum acts as reservoir, releasing small amounts of clot into SI by action of gastric enzymes
  4. The whey, containing lactose and globulins, moves quickly into SI
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87
Q

What are the causes of poor clotting of casein that can cause nutritional scour in calves?

A
  • Failure of sufficient acid and enzyme secretion
  • Poor quality milk product
  • Farmer uses incorrect concentration of milk powder
  • Farmer feeds at incorrect temperature
  • Feeding times irregular
  • Infection of the abomasum
  • Overfeeding
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88
Q

What is the consequence of poor clotting of milk in calves?

A

Casein “spills” over into SI which results in poor digestion leading to poor growth rates as well as possibly nutritional scours

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89
Q

What is the pathogen responsible for calf diphtheria?

A

Opportunist Fusobacterium necrophorum infection

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90
Q

What is the epidemiology of calf diphtheria?

A
  • Occurs in pre-weaned calves and those up to about 6-9 months age
  • Usually single animal, poor hygiene
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91
Q

What causes calf diphtheria?

A

Need physical abrasion to allow bacteria in – such as feeding bedding hay instead of barley hay, rougher and causes abrasions in the mouth that allow bacteria in

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92
Q

What are the clinical signs of calf diphtheria?

A

Necrotic infection of oral cavity and often larynx
Extensive salivation
Some swelling
May be dull

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93
Q

How is calf diphtheria diagnosed?

A

Diagnose on examination of mouth, halitosis, enlarged draining lymph nodes and pain

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94
Q

How is calf diphtheria treated?

A
  • Treat with Penicillin or similar
  • Avoid coarse food and improve hygiene
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95
Q

What are the 2 forms of ruminal bloat in pre-weaned calves?

A

Firstly milk fermentation in immature rumen due to defective oesophageal groove closure or abomasal overfill/rapid drinking

Secondly immature rumen syndrome

96
Q

What are the clinical signs of ruminal bloat in pre-weaned calves?

A

Pasty scours, bloat and colic

97
Q

How is ruminal bloat in pre-weaned calves treated?

A
  • Treat by stomach tube and occasional use of surfactants
  • Withdraw milk and feed ORS for 24 hrs, may need fistula
  • Correct feeding errors, provide hard food and wean early
98
Q

What causes immature rumen syndrome?

A
  • Calves eat large volumes of fibre and immature rumen cannot digest adequately
  • Rumen dilated, calf still hungry, vicious circle
99
Q

What are the clinical signs of immature rumen syndrome?

A

A pot-bellied appearance with thin pasty faeces

100
Q

How is immature ruminal syndrome treated?

A

Drastic reduction in roughage
Use shavings as bedding
Palatable concentrates
Inoculate rumen with adult rumenal fluid

101
Q

What are the clinical features of calf scours?

A
  • Demeanour
  • Hydration status – sunken eyes, skin tent?
  • Age of calf and duration of scour – over a week old calves are more likely to get metabolic acidosis due to development of gut microbiota from loss of bicarbonate
  • Condition score – indication of energy status
  • Faecal score
  • Other conditions
  • TPR
102
Q

What does presence of suck reflex in scouring calves determine?

A

Will directly affect treatment option pertaining to fluids

103
Q

Why do calves scour and sometimes die?

A
  • Pathogen multiplication leads to epithelial damage
  • Diarrhoea can be hypersecretory or malabsorptive, or both
  • Loss of water and electrolytes (Na, K, Cl, HCO3) = alkaline faeces
  • Dehydration and metabolic acidosis
  • Calf hyperventilates to correct acidosis
  • Acidosis leads to loss of potassium and sodium from cells
  • Hyperkalaemia causes disruption of the P-wave, arrhythmia and eventually cardiac arrest
104
Q

What is the best indicator of likelihood of severe acidosis?

A

Age

Under 6 days of age = mild/moderate acidosis
Over 6 days = more severe acidosis

105
Q

What are the clinical signs of metabolic acidosis in calves?

A

Ataxia/recumbency
Hydration status
If do not respond to appropriate fluids, may still be acidotic

106
Q

What is the problem with investigating calf scouring on farms?

A

Rotavirus, cryptosporidium, coronavirus/winter dysentery are ubiquitous so likely on every farm. So the question is, why is this a problem on this farm and in this calf? Ascertaining which can be problematic

107
Q

What are the factors affecting the degree of susceptibility to scour in calves?

A

Inadequate colostrum
Environmental stress
Nutritional errors
Concurrent disease

108
Q

How are scouring calves treated regardless of aetiology?

A
  • Antibiotics unnecessary (contraindicated) except for E. coli and Salmonella – as well as cryptosporidium, an antiprotozoal will be more of a prevention to reduce shedding and so spreading and oocyst excretion
  • Major aspects of treatment are fluid therapy, nursing and improved environment
109
Q

What are the clinical signs at each stage of dehydration in scouring calves?

A

<5% = normal, increased thirst

6-8% = dry muzzle, mouth, sunken eyes, reduced skin elasticity

9-10% = cold legs and mouth, recumbent

11-12% = comatose and shocked

13-14% = death

110
Q

When might dehydration and haemoconcentration occur in calves?

A
  • Decreased tissue perfusion
  • Decreased liver function
  • Increased lactic acid production
111
Q

What are the clinical signs of metabolic acidosis in calves?

A

Hyperpnoea
Bradycardia
Cardiac arrhythmia due to effect on P wave
Poor pulse volume

112
Q

What is the pathogenesis of metabolic acidosis caused by scouring calves?

A
  • Increased lactic acid production in tissues
  • Colon-derived acids
  • Bicarbonate loss via gut
  • H+ loss via kidneys
113
Q

What are the effects of diarrhoea in calves?

A
  • Dehydration and haemoconcentration
  • Metabolic acidosis
  • Reduction in plasma Na+
  • Plasma K+ fall, then later rises
  • BUN rises
  • Reduced renal perfusion
  • Plasma glucose falls
114
Q

What is the reason for reduced plasma sodium ions in scouring calves?

A

Intestinal loss. Sodium needs to be pumped from gut lumen and co-transported with glucose, which will allow water to follow by osmosis, so this is the basis of treatment

115
Q

What is the reason for fluctuations in plasma potassium ions in scouring calves?

A

Plasma K+ fall, then later rises – exchange of intracellular K+ for extracellular H+ to buffer extracellular fluid as H+ is being lost

116
Q

How is diarrhoea in calves diagnosed?

A
  • Several samples – minimum 6 pots of faeces
  • Postmortem examination
117
Q

How is diarrhoea in calves treated?

A
  • Rehydration using oral/IV fluids
  • Nutrition – milk with/without oral fluids
  • Antibiotics – often not needed unless E.coli or salmonella
118
Q

What are the aims of therapy with scouring calves?

A
  • Maintain calf growth rates
  • Return calves to normal feeding
  • Minimise mortality
  • Reduce spread to other calves
  • Reduce risk of human infection – if suspicion of zoonosis
119
Q

When is oral route for fluids of a scouring calf effective?

A

If dehydration is less than 8%. Get to suckle if possible due to oesophageal reflex as ST goes into rumen

120
Q

Why do oral fluids not correct acidosis themselves?

A

Problems with low energy and poor correction of acidosis – these are not substitutions for food so this itself will not combat acidosis but may get kidneys working again and so get the animal back to normal plasma pH

121
Q

What is the WHO formulation for rehydration fluids?

A

0.6% NaCl, 2% glucose

122
Q

What may be needed in fluids for acidosis to be corrected?

A

Do not assume that the lactate in Hartmann’s is enough to correct any acidosis, may need some additional bicarbonate. If more bicarb, best to put in with saline

123
Q

How is IVFT given to calves?

A
  • Cut-down to vein – no.11 blade, suture catheter and giving set
  • Positioning calf with head down so that head is below the heart before inserting IV catheter
124
Q

What are the clinical signs and therapy required for no acidosis in scouring calves?

A

Alert
Standing
Strong suck reflex

Oral electrolyte solutions

125
Q

What are the clinical signs and therapy required for mild acidosis in scouring calves?

A

Tired
Almost secure standing

20-30g sodium bicarb (for 34kg calf)

126
Q

What are the clinical signs and therapy required for moderate acidosis in scouring calves?

A

Tired/listless
Wobbly
Has to be helped up

30-40g sodium bicarbonate (per 34kg calf)

127
Q

What are the clinical signs and therapy required for severe acidosis in scouring calves?

A

Apathetic to comatose sternal or lateral recumbency

40-60kg sodium bicarbonate (per 34kg calf)

128
Q

How much fluid is given to scouring calves?

A

Usually 5 – 10 litres over 24 hours

129
Q

What is done after adding sodium bicarbonate to fluids?

A
  • Then added more glucose as a source of energy to address nutritional demands
  • Now assists in gut repair by including glutamine (promotes villus repair and regeneration)
130
Q

How are fluids administered to scouring calves?

A

When to give = as soon as scour starts
Which route = teat and bucket is best
How much = 4-8L daily
How often = little and often
Milk feeding = yes

131
Q

What are the fluids requirements of scouring calves?

A

Total fluid requirements of the average diarrhoeic calf = 4L oral fluids and 4L milk = 8L total fluid daily, may need substantially more

132
Q

What are the advantages of milk feeding scouring calves?

A
  • Feed the calf (maintain body condition)
  • Feed the gut mucosa and microbes (assists in repair)
  • Ensure intake of Ca, Mg, vitamins, etc.
  • Improve renal function (supplies energy, thus assisting in fluid and electrolyte correction)
133
Q

When are antibiotics used in calf scouring cases?

A
  • E. coli
  • Salmonella
  • Lack of colostrum, low IgG levels
  • Damage to gut
134
Q

When are antibiotics not used in calf scouring cases?

A
  • Viruses
  • Protozoa
  • Normal gut bacteria
  • Development of resistance
135
Q

What are the main reasons for poor treatment success in scouring calves?

A
  • Electrolyte given too infrequently
  • Electrolyte given at the wrong dilution
  • Removal of milk feeding for too long
  • Failure to give electrolyte in favour of a “jab of antibiotic”
  • Failure to give appropriate nursing care
  • Delaying treatment
  • Hopeless case due to lack of colostrum
  • Treatment missed as “someone else was doing it”
  • Presence of concurrent disease
136
Q

How is scour in calves prevented against?

A
  • Adequate colostrum essential
  • Store colostrum from the dam and feed diluted (10%-20%) with milk or milk replacer for first 7-10 days
  • Immunise dams against rotavirus and coronavirus– 1 injection, 3-12 weeks prior to calving
  • Improve hygiene
  • Depopulate and clean out infected calf accommodation
  • More bedding
  • Reduce stocking density
  • Individual accommodation if possible
137
Q

What is the disadvantage of vaccinating against pathogens causing calf scour?

A

These will not protect the calf if the calves do not have colostrum

138
Q

What population are most susceptible to Johne’s disease?

A

Calves most susceptible, a small proportion become carriers and a few of these then develop clinical signs mostly between 2-5 years of age

139
Q

What are the clinical signs of Johne’s disease in cows?

A

Specific progressive enteritis
Drop in milk yield early sign
Profuse watery diarrhoea but no blood or mucous, homogenous
Gluteal muscle wastage
Skin loses suppleness – this is because of PLE
Ventral oedema in some cases - protein loss reduced oncotic pressure

140
Q

How is Johne’s disease diagnosed in cows?

A

Diagnose on history and clinical signs, definitively by bacteria in faeces and more lately an ELISA/PCR

141
Q

How is Johne’s prevented against?

A
  • No effective treatment, consider vaccination, but now difficult to get permission (effect on TB test)
  • Prevention based around breaking passage from mother to daughter and between cows – avoid pooling colostrum
  • Improvements in hygiene and husbandry
142
Q

What is the incubation period of Johne’s disease?

A

Over 15 months

143
Q

Why is Johne’s difficult to get rid of?

A
  • For every advanced clinical case, 15-25 others are likely to be infected
  • Difficult to diagnose as they do not seroconvert for years
  • Wild rabbits and their faeces
144
Q

What is the appearance of mycobacterium avium paratuberculosis on histology?

A

Organisms clump together as they live in macrophages

145
Q

What is the appearance of mycobacterium avium paratuberculosis on histology?

A

Find in lower part of small intestine and large intestine – find very thickened gut that cannot be stretched out/corrugates.

Sheep can produce an orange pigment that gives brick red appearance to intestinal folds

146
Q

How can Johne’s disease be diagnosed at herd level?

A
  • Faecal smears
  • Stained by ZN
  • Acid alcohol fast bacilli red
  • Single organisms inconclusive
  • Clumps pathognomonic
  • Culture - difficult, takes 12 weeks
  • PCR
  • Serology - complement fixation test
  • ELISA - best. Herd screening using milk now common place – sensitivity and specificity may be less good
147
Q

What is delayed type hypersensitivity to Johne’s disease and the consequence of this?

A
  • Injected intradermally in prepared site
  • Skin thickness measured before and at 72 hours
  • Reactions to avian TB common – interferes with test so needs permission to vaccinate
148
Q

What are 2 disadvantages of vaccinating against Johne’s disease?

A
  • Produce large nodules
  • Induce sensitivity to other mycobacteria
149
Q

How can Johne’s disease be diagnosed on an individual level?

A
  • Clinical signs
  • Rectal scraping and smear
  • Faecal smear
  • Faecal culture – 6-18 weeks or 10 d + PCR
  • Mesenteric, ileocaecal LN biopsy
  • Haemotology/biochemistry – hypoproteinaemia, anaemia, hypocalcaemia, hyponatraemia, hypokalaemia
  • Herd diagnosis – mostly using milk ELISA
  • Serological
  • ELISA
150
Q

How is Johne’s prevented against?

A
  • Segregation and culling
  • Cull infected cattle
  • Breed dairy cows to a beef bull
  • Separate calves from dams and feed colostrum from known uninfected dams
  • Pasteurisation of colostrum
  • Avoid pooled colostrum
  • Cull offspring of infected cows
  • Ensure calf pastures not contaminated with adult faeces
  • Don’t use calves as followers on pastures
  • Vaccination
151
Q

What is the epidemiology of malignant catarrhal fever?

A
  • An almost invariably fatal disease of cattle of worldwide distribution
  • A herpesvirus that shouldn’t be in cattle, should be in sheep
  • Invariably fatal – recently has been shown that you can nurse them through it
  • From sheep to cattle at lambing
  • Occasional mild cases occur, recover spontaneously
152
Q

What are the clinical signs of malignant catarrhal fever in cows?

A

Diarrhoea
Almost all cases involve lesions on head/eyes and occasional urticaria
Profuse mucopurulent nasal discharge
Superficial lymph nodes enlarged
Occasional nervous signs
Dermatitis
Very marked pyrexia – over 40
Centripetal oedema of cornea
Generalised vasculitis - destruction of tissues

153
Q

What is the onset of malignant catarrhal fever in cattle?

A

Days to weeks

154
Q

How is malignant catarrhal fever treated?

A

No treatment - kindest thing is to put them down

155
Q

How is malignant catarrhal fever controlled?

A

Based on keeping cattle separate from sheep, especially at lambing time

156
Q

What done bovine popular stomatitis cause?

A
  • Little clinical importance
  • Does not cause diarrhoea but often occurs with coccidia or ostertagia
  • Lesions confined to muzzle, nostril and buccal mucosa, not tongue
  • Small circular shaped reddish papules
  • Heals quickly, good immunity
157
Q

How is winter dysentery spread in cattle?

A

Faeco-oral transmission. Highly contagious

158
Q

What are the incubation and recovery periods of winter dysentery?

A

Incubation period 3-7 d
Recovery in 5-7 days - good immunity

159
Q

What is the cause of winter dysentery in cows?

A

Coronavirus
November
Acute, and sometimes severe diarrhoea

160
Q

What are the clinical signs of winter dysentery in cows?

A
  • Acute onset of diarrhoea, sometimes containing blood
  • Milk drop, lethargy and inappetance
  • Possible dehydration
  • Not usually pyrexic
  • Rumen motility might decrease
  • Intestinal borborygmi might decrease
  • Dilated loops of intestine on rectal exam
  • Spontaneous recovery in 2-3 days
161
Q

How is winter dysentery treated in cows?

A
  • Supportive therapy
  • Only treat individual cases with antimicrobials if unable to distinguish from salmonellosis on clinical examination and history
162
Q

What are the clinical signs of copper deficiency in cows?

A

Depigmentation
Reduced milk yield
Weight loss
Persistent diarrhoea
Not anorexic or febrile

163
Q

How is copper deficiency causing diarrhoea in cows diagnosed?

A

Check copper levels in blood and liver

164
Q

What are the infectious differential diagnoses of saliva loss in cattle?

A
  • Malignant catarrhal fever
  • FMD
  • Vesicular stomatitis
  • Listeria meningoencephalitis
  • Actinobacillosis
  • Calf Diphtheria
  • Abscess/lesion in mouth
165
Q

What are the toxic differential diagnoses of saliva loss in cattle?

A
  • Buttercups/rhododendron
  • Organophosphorus toxicity
  • Botulism
166
Q

What are the physical differential diagnoses of saliva loss in cattle?

A
  • Oral foreign body
  • Pharyngeal foreign body
  • Oesophageal foreign body
  • Teeth problems
  • Jaw fracture
  • Choke
  • Rupture/damage to pharyngeal area or oesophagus
  • Teeth problems
  • Facial Nerve Paralysis
167
Q

What pathogen causes wooden tongue?

A

Actinobacillus lignieresii

168
Q

What are the clinical signs of wooden tongue?

A
  • Often sudden onset, salivation
  • Tongue very painful and swollen at base
  • Local draining lymph nodes can be involved
169
Q

How is wooden tongue treated?

A

Treatment by 5-7 days of IM Streptomycin

170
Q

What are the clinical signs of choke in cows?

A
  • Just behind mandible or by thoracic inlet
  • Profuse salivation and then bloat
171
Q

How is choke treated?

A
  • Gag, examine, manipulate (sedate?), stomach tube
  • Smooth muscle relaxant if necessary
  • Prevention
172
Q

What is caused by actinomyces bovis?

A

Hard painless swelling on jaw, may lead to dysphagia and weight loss

173
Q

How is actinomyces bovis treated?

A

Early with tetracyclines

174
Q

What is pasture bloat?

A
  • Rumen distension due to normal gas of fermentation, trapped in a foam
  • Occurs soon after moving cattle to lush (legume) pastures and rumen produces foam in fermentation if rumen microflora is not adapted to this. cannot eructate and bloats.
  • Sudden death
175
Q

What are the clinical signs of pasture bloat?

A
  • Mild “colic” signs
  • Abdominal distension (upper left side)
  • Rumen hypermotility causes rumen hypomotility – as rumen expands it cannot contract
  • Tachypnoea, tachycardia, and progressive respiratory and CV compromise leads to death within minutes of animal assuming lateral recumbency
176
Q

How is pasture bloat treated in cows?

A
  • Antifoaming agents
  • Poloxalene
  • Simethicone emulsion
    Oils – break down tension and breakdown foam
    Detergents
177
Q

How is pasture bloat treated with detergents?

A
  • Via a stomach tube, dilute or wash down into rumen as necessary, take care to avoid inhalation
  • In emergency may inject anti-foaming agents directly into rumen
178
Q

How is pasture bloat prevented?

A
  • Pasture management
  • Regular administration of anti-foaming agents
179
Q

What is grain bloat?

A
  • High quantities of rapidly fermentable carbohydrate
  • Grain overload and ruminal acidosis
  • Leads to metabolic acidosis
180
Q

What are the clinical signs of grain bloat?

A
  • Bloat
  • Anorexia
  • Dehydration
  • Collapse
  • Severe metabolic acidosis causing tachypnoea/hyperpnoea
  • Diarrhoea
181
Q

How is grain bloat diagnosed?

A
  • History
  • Clinical signs
  • Rumen pH
  • Plasma pH or TCO2
182
Q

How is grain bloat treated?

A
  • In severe emergency consider rumenotomy
  • Correct rumenal and metabolic acidosis and dehydration
  • Rumen function stimulants
  • Transfer of rumen contents from healthy cattle
  • Consider on farm emergency slaughter
183
Q

What are the causes of interfered eructation that could cause free gas bloat?

A
  • Oesophageal obstruction
  • External pressure on oesophagus
  • Pathology of the oesophagus or reticulum
  • Conditions affecting smooth muscle function
  • Poor management at weaning – may result in chronic rumenal tympany
184
Q

What are the clinical signs of free gas bloat?

A
  • Increased intraruminal pressure resulting in bulging of left sub-lumber fossa
  • Additional signs follow from increased abdominal pressure as for pasture-bloat
  • Additional specific signs related to underlying aetiology
185
Q

What are the aims of treatment for free gas bloat?

A

Relieve obstruction or allow escape of gas by some other means

186
Q

How is free gas bloat treated?

A
  • Stomach tube
  • Probang – more rirgid stomach tube that is used to shove into the rumen
  • Trocar and cannula
  • Treat underlying cause
187
Q

What are the clinical signs of chronic ruminal distension/post-weaning diarrhoea syndrome?

A
  • Abdominal enlargement
  • Weight-loss
  • With/without diarrhoea
  • Impaired eructation
188
Q

What are some other conditions that could lead to chronic ruminal distension as a consequence in adult cows?

A
  • Chronic reticular adhesions
  • Vagal indigestion – something wrong with vagus nerve
  • Sand impaction
  • Alimentary tract carcinoma
  • Rumeno-reticular actinobacillosis
189
Q

How is chronic ruminal bloat treated?

A
  • None
  • Diet change
  • Semi-permanent rumen fistula
  • Indwelling trocar and cannula – not a good idea long term, as rumen contents spill out ad will cause inflammation after a while
190
Q

What are the varied clinical signs of traumatic reticulitis in cows?

A

Dullness
Anorexia
Agalactia
Fever
Anterior abdominal with/without thoracic pain
Abduction of elbows
Alimentary stasis – mild bloat
Grunt

191
Q

What does penetration in traumatic reticulitis coincide with?

A

Penetration may not coincide with time of consumption, but rather with time of increased abdominal pressure, especially parturition

192
Q

What are the possible pathologies caused by traumatic reticulitis?

A
  • Mild discomfort due to pricking of reticulum and reticular abscessation
  • Localised peritonitis, reticulitis
  • Traumatic pericarditis
  • Liver abscess
  • Mediastinal abscess
  • Generalised peritonitis
  • Generalised abscessation
193
Q

What is a crude diagnostic measure of traumatic reticulitis?

A

If they grunt when the rumen contracts, likely got traumatic pericarditis

194
Q

What can be picked up on examination of early cases of traumatic reticulitis?

A
  • Elevated rectal temp. in early stages
  • Ruminal tympany
  • Rumen stasis or weak contractions
  • Abdominal pain, withers test, pole test, Williams test positive
195
Q

How can traumatic reticulitis be treated?

A
  • Rumenotomy and removal of foreign body
  • Magnets?
196
Q

What are the indications for a rumenotomy?

A
  • Removal of foreign body
  • Exploratory surgery
  • Some poisoning cases
197
Q

When do displaced abomasum cases occur?

A

Postpartum dairy cows within 6 weeks of calving

198
Q

Why is good management around drying off important for displaced abomasum cases?

A

Multifactorial disease and can occur with other conditions - hypocalcaemia, ketosis, acidosis, retained foetal membranes, metritis

199
Q

What are the key elements for the aetiology of displaced abomasal cases?

A
  • Anatomical position of the abomasum and other structures such as the rumen
  • Abomasal atony
  • Gas formation within the abomasum
200
Q

What are the clinical signs and diagnosis of LDA?

A
  • Reduced milk yield
  • Reduced appetite especially concentrate feeds
  • Full clinical examination
  • Auscultate and percuss over ribs 9-13 on left – flick here will have high pitched drumming sound
  • Biochemistry
201
Q

What does the biochemistry in an LDA show?

A

Ketosis
Hypochloremic
Hypokalemic
Metabolic alkalosis

202
Q

What are the clinical signs and diagnosis of RDA?

A
  • Auscultate and percuss over ribs 9-13 on right
  • Severe dehydration
  • Biochemistry
  • May have total abomasal outflow obstruction
  • Very sick animal may become shocked and die
203
Q

What does the biochemistry from an RDA show?

A
  • Ketosis
  • Severe hypochloremic (HCl pools in abomasum and can’t escape, glands in stomach continue to produce it)
  • Hypokalemic and metabolic alkalosis
204
Q

How is dry matter intake and displaced abomasum linked?

A
  • Dry matter intake negatively correlated with body condition score
  • Fat cows are at risk of DA
205
Q

What are the metabolic parameters in displaced abomasum cases?

A

Negative energy balance and hypocalcaemia postpartum were therefore shown to be associated with an increased risk of DA

206
Q

How are ketosis and displaced abomasum linked?

A
  • Prevention of sub-clinical ketosis is very important if DA is to be prevented
  • Manage body condition to maximise DMI
  • Optimise transition cow nutrition
207
Q

What feeding practices should be undertaken to prevent displaced abomasum?

A

Everything possible should be done to maximise DMI in periparturient cow – palatable forage, ad lib, minimum competition, may warrant a separate management group

208
Q

Which individuals are at risk of displaced abomasum?

A
  • Over-fat body condition at calving
  • Reduced DMI in the immediate postpartum period
  • Dystocia/stillbirths
  • Twins
  • Ketosis
  • Excessive fat mobilisation
  • Hypocalcaemia
  • Retained foetal membranes
  • Periparturient infections including mastitis and metritis
  • Endotoxaemia
  • Acidosis leading to reduced DMI
209
Q

What are some other abomasal conditions affecting cows, other than DA?

A
  • Abomasal ulceration
  • Abomasal impaction
  • Small intestinal obstruction
  • Caecal dilatation and torsion t
  • Fat necrosis
  • Neoplasia
  • Pneumoperitoneum
  • Peritonitis/abdominal abscesses
210
Q

When are cows infected with bovine viral diarrhoea virus?

A

Calf can become infected in utero, calves that are infected before they develop a functional immune system will see antigen from virus as self so become persistently infected as they do not mount an immune response to the virus and produce lots of it throughout their lives

211
Q

What are the syndromes cause by bovine viral diarrhoea virus?

A

Mucosal disease
Reproductive consequences
Immunosuppression
Respiratory disease
Congenital defects

Most of the time it does not even cause diarrhoea - capable of causing, as calves with mucosal disease will have diarrhoea

212
Q

How does bovine viral diarrhoea virus affect calving?

A

If infected it would take them longer to get in calf

213
Q

What does the BVD status on the farm tell you?

A

Whether or not they are naïve to BVDV

214
Q

What congenital defects can be caused by bovine viral diarrhoea virus?

A

Tail shortening
More ribs
Cerebellar hypoplasia - ataxia and mobility abnormalities

215
Q

How may PI calves of BVDV look?

A

Persistently infected calves may look normal or may cause them to lose weight.

216
Q

What clinical signs would you associate with BVDV infection in cattle?

A

Abortion
Poor pregnancy rate
Calf pneumonia
Congenital abnormalities
Immunosuppression
Mucosal disease
Stunted growth
Calf diarrhoea

217
Q

What are the 2 genotypes of BVDV?

A

BVDV 1 – classical form

BVDV 2 – severe acute BVD (haemorrhagic syndrome) – very rare

218
Q

What are the 2 biotypes of BVDV?

A

Non-cytopathic

Cytopathic - if subsequentially infected with this will then not recognise and not mount an immune response and cause mucosal disease

219
Q

What are the clinical syndromes of BVDV in naive adult cattle?

A
  • Usually subclinical
  • Systemic
  • Mild pyrexia with/without diarrhoea
  • Reduced milk yield
  • Reproductive
  • Poor fertility, early embryonic death and abortion
  • Congenital defects
  • Production of persistently infected (PI) calves
220
Q

What are the clinical syndromes of BVDV in naive calves?

A
  • Pyrexia with/without diarrhoea
  • Immunosuppression which increases risk of respiratory disease, calf diarrhoea, other infectious disease
  • Acute haemorrhagic enteritis and death (rare as more associated in BVDV2)
221
Q

What are the clinical syndromes of BVDV in persistently infected calves?

A
  • Poor growth rates
  • Immunosuppression
  • Mucosal disease when infected with cytopathic virus
222
Q

Simplify the outcome of BVDV into 2 broad syndromes?

A
  • Acute infection followed by immunity
  • Persistent infection with/without mucosal disease
223
Q

What is the epidemiology of BVDV?

A
  • Faecal-oral and transplacental spread
  • If infected 0-1 months = early/late embryonic death
  • If infected 1-4 months – PI
  • If 4-9 months = congenital abnormalities
224
Q

Outline the development of mucosal disease.

A
  1. Persistently infected cattle – immunotolerant to NCP
  2. Mutation of NCP or superinfection with CP
  3. Mucosal disease – presence of NCP and CP 6-24 months of age, acute or chronic, 100% mortality
225
Q

What are the clinical signs of oropharyngeal ulcers as a result of mucosal disease?

A

Ulcers
Hyperaemia
Oral pain
Ptyalism
Reduced appetite/anorexia

226
Q

What are the clinical signs of muzzle ulcers as a result of mucosal disease?

A

Ulcers
Dried cracked inflamed rhinarium

227
Q

What are the clinical signs of gut ulcers as a result of mucosal disease?

A

Ulcers
Profuse, homogenous diarrhoea

228
Q

What are the clinical signs of foot ulcers as a result of mucosal disease?

A

Ulcers in interdigital cleft

229
Q

What are the other clinical signs of mucosal disease besides ulceration?

A
  • With/without dermatitis (scabs and skin crusts) – heels, perineal region and between the hind legs
  • Eyes – lacrimation, epiphora with/without crusting
  • Nose – mucopurulent discharge with/without crusting
  • Rapid loss of condition
  • Depression
230
Q

What is found on post mortem examination of mucosal disease?

A
  • Microvesicles causing ulcers
  • Lesions throughout the alimentary tract
  • Transverse palatine ulcers
  • Longitudinal oesophageal ulcers
  • Depletion of gut-associated lymphoid tissue (GALT) with/without underlying lymph nodes
231
Q

What are the differential diagnoses for mucosal disease?

A

FMD
Bluetongue
Malignant catarrhal fever
Bovine Papular Stomatitis
BHV-1 (IBR)
Calf diphtheria

232
Q

What is done next for poorly grown calves that have tested positive for BVD antigens and negative for BVD antibodies?

A

Cull persistently infected animals and test other animals in the herd – bulk tank milk PCR and ELISA to see if virus is in adult herd, if so must go looking for PI adults. If antigen positive, must be culled. If antigen negative, must vaccinate and use biosecurity and monitoring.

233
Q

How is herd status for BVDV?

A

Bulk milk tank - antibody ELISA, antigen PCR

Individual testing - antibody and antigen ELISAs

234
Q

How is BVDV monitored?

A
  • Annual youngstock screen – 9-18 month old animals, unvaccinated. Separately managed groups
  • Quarterly bulk milk PCR
235
Q

What is the aim of vaccination against BVDV?

A

The main aim is to prevent the birth of PI calves

Primary course must be completed before the first service

CVSOH 4 (35 decks)

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