Ruminants Flashcards
What are the predisposing factors to displacement of the abomasum?
Hypocalcaemia Genetic predisposition Strenuous activity Abomasal atony Increased gas production (e.g. grain rich feed) Concurrent diseases e.g. metritis
What is the general underlying cause of erosive and ulcerative gastritis in cattle?
What are some examples of causes?
Increased contact time between epithelium and abomasal acid.
e.g. Dietary change, acidosis, BVD, impact, displacement, long periods with empty abomasum
What are the consequences of parasitic gastritis in cattle, such as that caused by ostertagiosis?
Ill-thrift Oedema Diarrhoea Protein loss Impaired acid secretion and elevation of gastric pH Epithelial necrosis Secondary bacterial infection
What does conservative treatment of a left displaced abomasum typically entail?
Casting and rolling (right lat. to dorsal, pause, to left lat.)
NSAIDs +/- Buscopan
Oral fluid therapy
Treatment and correction of metabolic imbalances
What are the surgical approaches to correcting a left displaced abomasum?
Right paralumbar with pyloro/omento-pexy
Bilateral paralumbar with pyloro/omento-pexy
Left paralumbar fossa with abomaso/omento-pexy
Right paramedian with abomasopexy
Toggle pin suture with or without laparoscopic correction
What are the complications associated with abomasal surgery?
Abomasitis +/- ulceration Hypomotility / atony Peritonitis Wound infections Pexy failure +/- redisplacement Adhesions Intestinal incarceration
What are the signs of potential endotoxic shock in cattle?
HR 100BPM+ Congested mucous membranes CRT >3secs Weak peripheral pulses Cold extremities
What would be the indications for surgical treatment of hardware disease?
Signs of acute cranial abdominal pain (elbow abduction, fast and shallow respiration, arched back)
Pyrexia
Grunting associated with reticular contraction
No response to conservative management within 24hrs
What medication is recommended in the conservative management of traumatic reticulopericarditis?
Broad spectrum systemic antibiotics
NSAIDs
Oral fluid therapy
How does primary “frothy” bloat develop?
Change to fermentable diet that lowers the rumen pH (e.g. high concentrates, lush grass, legumes)
Gas bubbles and RR contents form a stable foam
This blocks the cardia so eructation cannot occur
Rumen distends as nowhere for gas to go
What are possible causes of secondary bloat?
Oesophageal/cardial obstruction
Innervation disorders
Failure of oesophageal groove closure
What is the difference between primary and secondary bloat?
Primary: dietary change leads to gas build up, which causes the obstruction
Secondary: obstruction occurs first, which then causes build up
What is a ‘bloat line’ on post mortem?
Demarcation of congested proximal oesophagus (sign of potential bloat)
How does ruminal acidosis develop and lead to death?
High carb diet causes increase in lactic acid production due to microbiota changes
This reduces the pH of the RR
The osmotic pressure in the RR increases, drawing water from circulation
This leads to dehydration, circulatory collapse, rumen atony and death
How can ruminal acidosis progress into ruminitis?
Excess acid can damage squamous epithelia
Lesions can allow secondary bacterial infection to develop
Or opportunistic fungi to penetrate wall
What are the effects of bacterial ruminitis as an infection secondary to ruminal acidosis?
Necrosis of rumen with ulcers and scars
Embolism to liver leading to abscesses
Development of necrotising hepatitis
What are potential consequences of mycotic rumenitis?
Peritonitis
Vasculitis leading to thrombosis and infarction of ruminal mucosa
Abortion through spread to placenta
What are the four types of Vagal indigestion?
I: Damage to vagus nerve leading to eructation failure and bloat
II: Damage leading to a failure of omasal emptying into abomasum
III: Damage leading to abomasal impaction or displacement
IV: Compression of nerve due to pregnancy-related abomasal shifting
What are the main causes of calf diarrhoea?
Rotavirus
Coronavirus
Cryptosporidia
Enterotoxigenic E. coli
Nutritional diarrhoea in calves is due to poor clotting of casein. What can cause this?
Failure of sufficient acid and enzyme secretion Poor quality milk product Incorrect concentration of milk powder Feeding milk at incorrect temperature Irregular feeding times Abomasal infection Overfeeding
Calf diphtheria is caused by…
Fusobacterium necrophorum
Treatment for Calf Diphtheria
Penicillin, Improved hygiene, avoid coarse food
Clinical signs of immature rumen syndrome
Pot-belled appearance, thin pasty faeces, hungry calf (vocalisation)
Cause of immature rumen syndrome
Often if weaned too early
Calves eat large volumes of fibre which immature rumen cannot fully digest
Rumen becomes dilated and calf is still hungry
Treatment for immature rumen syndrome
Drastic reduction in roughage
Swap straw bedding for shavings
Feed palatable concentrates
Inoculate rumen with adult ruminal fluid
Advantages of right paralumbar laparotomy for LDA
Good visualisation of right abdomen
Low recurrence risk
Animal can stay standing
Assistant not required
Advantages of left paralumbar approach to LDA
Good visual of abomasum Can break down adhesions Low recurrence Animal can stay standing Useful in cows in late gestation
Advantages of right paramedian approach to LDA
Allows visualisation of abomasal fundus and other abdominal viscera Adhesions can be managed More rapid than other procedures Low risk of recurrence Surgeon arm length is not restrictive Appropriate for any size of displacement
Advantages and disadvantages of toggle-pin suture for LDA
Quick and cheap
Can’t visualise viscera as doing blind
Potential risk of trauma to personnel and cow
Requires rolling space and man power
How should poisoning in cattle be treated?
Ruminal contents removed
Rumen lavaged with copious amounts of warm water
Provide activated charcoal
Manage and correct any effects of poison
Clinical signs of urachal abscess
Poor growth / ill-thrift Pollakiuria / polyuria Stranguria / pyuria / haematuria \+/- Pyrexia \+/- Purulent umbilical discharge
Causes of stillbirth in cattle.
Dystocia/anoxia (foetal oversize) Pre-partum infection: BVD, Leptospira, Trueperella pyogenes Twinning Iodine deficiency in mother Vitamin E/Se deficiency in mother
Signs of intra-partum deaths
Hypoxia lesions
Subcutaneous oedema (esp of head and neck)
Atelactic / inflated lungs
Possible traction injuries
Signs of post-partum neonatal death.
Evidence of dystocia
Blood clot in navel
Lungs partially or fully inflated
Colostrum in stomach
Neonatal septicaemia signs
Sudden onset dullness Pyrexia Inappetence Sticky, mucoid saliva drooling Prostration Diarrhoea Sudden death
Bacterial meningitis signs in calves
Depression, lethargy Hypopyon Opisthotonus Blindness Hyperaesthesia Paddling Convulsions Coma Diarrhoea Acidosis Hyperkalaemia
Bacterial meningitis treatment in calves
ABx:
TMS I/V twice a day
Amoxyclav I/M
Anticonvulsants:
Xylazine
I/V fluids if unable to feed
Causal agents of navel/joint-ill
E.coli
Fusobacterium necrophorum
Less common:
Strep
Staph
Pasteurella
Prevention and control of Johne’s Disease
Segregation and culling of infected
Separation of calves from infected dams and feed colostrum from known uninfected dams
Pasteurisation of colostrum
Avoid pooled colostrum
Cull offspring from infected cows
Ensure calf pastures free of adult faeces
Don’t use calves as followers on pasture
Aetiology of Johne’s Disease
Mycobacterium avium paratuberculosis Organism acquired: From faeces Contaminated items Vertical transmission
Survives on pasture for around 6 months
Diagnosis of Johne’s
Based on clinical signs
Serology ELISA
Faecal culture +/- PCR
Clinical signs of Johne’s Disease
Usually 2y+
Diarrhoea (homogenous, no blood)
Weight loss
Ventral oedema
Malignant Catarrhal Fever cause
Ovine Herpesvirus 2 (OHV-2)
Malignant Catarrhal Fever epidemiology
No cattle to cattle spread
Spread by close contact between sheep (neonates particularly good spreaders) and cattle
Does not cause disease in sheep - silent carriers
Differentials for abdominal distension in calves
Abomasal torsion Abomasal dilatation Abomasal ulcers (perforated or not) Torsion of root of mesentery Acute diffuse peritonitis Intussesception Atresia coli (Per)acute enteritis Umbilical abscess Ruminal bloat
Clinical signs of Malignant Catarrhal Fever in cattle
Sudden death Marked pyrexia Superficial lymphadenomegaly Mucopurulent nasal and ocular discharge Mucous membrane ulceration Head pressing (or other neuro signs) Increased salivation Dyspnoea Joint swelling Dermatitis Increased corneal opacity Urticaria
Clinical signs of Bovine Papular Stomatitis
Lesions confined to muzzle, nostril, buccal mucosa
Small circular reddish papules
Cause of Bovine Papular Stomatitis
Parapox virus
Differentials for poor growth rate in an individual calf
Chronic suppurative pneumonia Congenital cardiac lesions Chronic joint-ill Chronic enteritis Omphalophlebitis Liver abscess Chronic ruminal maldigestion Chronic nephritis Congenital defects BVD persistently infected
Winter dysentery in cattle - pathogenesis and epidemiology
Acute, sometimes severe diarrhoea Usually November (into January) Caused by coronavirus infection First lactation heifers more severely affected High morbidity, low mortality
Copper deficiency clinical signs in cattle
Depigmentation
Diarrhoea without anorexia or fever
Reduced milk yield
Weight loss
Differentials for salivary loss / hypersalivation in cattle
Malignant Catarrhal Fever Foot and Mouth Disease Vesicular stomatitis Listeria meningoencephalitis Actinobacillosis Calf diphtheria Abscess/lesion in mouth Foreign body Dental disease Botulism
Wooden Tongue cause
Actinobacillus lignieresii
‘Rough’ forage causing initial lesion for infection to invade
Wooden Tongue clinical signs
Painful tongue
Swelling of tongue at base
Involvement of local draining lymph nodes
Sudden onset salivation
Wooden Tongue / Actinobacillosis treatment
5-7 days IM Streptomycin
Actinomycosis in cattle - cause, signs, treatment
Actinomyces bovis
Hard, painless swelling on jaw
Potential dysphagia and weight loss
Treat early with tetracyclines
Watery Mouth predispositions and cause
Very young lambs (<2 days)
Often twins/triplets
Common in housed lambing
Inadequate / delayed colostrum intake
+ concurrent NON-enterotoxigenic E Coli
Watery Mouth signs
Dullness / weakness Unwilling to suck Drooling saliva Acidosis (which leads to suck reflex suppression!) Hypothermia Abdominal gas distension Death within 12-24 hours
Watery Mouth treatment
Intraperitoneal glucose (as for hypothermic lambs)
ABx PO/Systemic
Buscopan
NSAIDs (meloxicam)
Watery Mouth control and prevention
Avoid having thin ewes Ensure adequate colostrum intake Avoid early stress e.g. castration, docking Good hygiene (bedding, stomach tubes) Use lots of bedding in between ewes Early turn out of lambs where possible
Lamb Dysentery Pathogenesis and Control
Clostridium perfringens Type B
Haemorrhagic enteritis in lambs 1-3d old
Sudden death - 100% mortality
CLOSTRIDIAL VACCINATION - LAMBIVAC
Coccidiosis in lambs - cause and signs
Eimeria spp.
Dehydration Dull coat Tenesmus Bloody and mucoid diarrhoea Possible rectal prolapse
Coccidiosis treatment in lambs
Diclazuril / Vecoxin
Toltrazuril / Baycox
Decoquinate / Deccox
Nematodirosis - when and who affected?
Late spring / early summer
Only lambs show signs:
Profuse watery diarrhoea
Ovine skin disease examples
Contagious pustular dermatitis / Orf virus Dermatophytosis Dermatophilosis Photosensitisation Cullicoides hypersensitivity Staphylococcal dermatitis Psoroptes ovis / Sheep scab
Bovine foot lameness causes
Sole ulcers White line disease Sole bruising Digital dermatitis Foul / Interdigital necrobacillosis Interdigital hyperplasia FB penetration
Treatment of hock cellulitis / bursitis
Not usually necessary unless secondary infection
ABx will usually relieve lameness
DO NOT INCISE AND DRAIN
Osteomyelitis causes in calves and foals
Trueperella Streptococcus Staphylococcus Salmonella E. coli
