5. Diagnostics and treatment of liver diseases in ruminants. Flashcards
Ruminant energy supply?
Ruminant energy supply
• The blood glucose is lower than in monogastric species because most of the energy supply comes from the
rumen (VFA).
• During gluconeogenesis in the liver glucose is formed. A lot of the produced glucose goes to the udder to
form milk glucose in dairy cattle. After calving there can be insulin resistance
Measurement of insulin resistance?
Measurement of insulin resistance
• Gold standard
o Hyperinsulinemia euglycemic (HEC) test
§ The gluconeogenesis of the liver can be supressed at 100-120uU/ml insulin concentration
- Intravenous glucose tolerance test
- Intravenous insulin tolerance test
NEFA in the liver?
NEFA in the liver (non-esterified fatty acids)
2-6 weeks after calving there is a major negative energy balance. The cow will burn its body fat stores, BCS
decreases. In the blood we measure non-esterified fatty acids, they go to the liver and 3 things can happen:
1. They join gluconeogenesis (best)
2. Ketone body formation (hyperketonaemia)- Beta- hydroxy butyrate, acetoacetate, and acetone. In high
amounts they appear in the urine and milk
- If the liver is unable to utilise it, it will become re-esterified triglycerides, leading to fatty infiltration
(worst)
Jaundice haemolytic icterus causes?
Jaundice
Haemolytic icterus
- Leptospirosis (calf), babesiosis, anaplasmosis
- Food (cabbage, onion)
- Copper-toxicosis (sheep)
Hepatic icterus?
Hepatic icterus
• Common in sheep (toxic hepatopathies), rare in cattle
Obstructive icterus?
Obstructive ileus
- Obstruction of the bile duct (extrahepatic)- very rare
- Intrahepatic bile capillary compression (e.g., fatty liver): more frequent
Clinical signs and diagnosis?
Clinical signs
- Yellow sclera, MM, and skin
- Dark urine
o Bilirubinuria and/or haemoglobinuria
• Increase in plasma Br rarely results in clinical icterus in ruminants
o TBr > 3mg/dl
Diagnosis
• Liver Enzymes in Cattle
o AST can come from the RBCS, brain and muscles- it is less specific in Ru
Liver enzymes in cattle?
Total bile acids?
Total bile acids (TBA)
• Normal
o <90umol/L
• Fatty liver
o 1.5-2 x increase
- High variability between individuals
- No importance of pre- and postprandial level
Dry chemistry NH3 analyser: blood ammonia checker
Dry chemistry NH3- analyser: blood ammonia checker
• Reference value
o 25-50umol/L
• Energy deficiency, protein overload
o 50-80umol/L
• Severe fatty liver, coma hepaticum
o >100umol/L
Summary of clinical diagnostics in liver diseases?
Summary of clinical diagnostics in liver diseases
• Plasma/ sera
o AST, ALT, ALKP, GLDH, bilirubin, ammonia, BHB, NEFA
• Urine
o Acetic acid, acetone
- Ultrasound
- Biopsy
o TL, TAG
Clinical diagnosis of subclinical and clinical ketosis?
Clinical diagnosis of subclinical and clinical ketosis
On farm ketone body measurement
• Beta-hydroxy butyrate (BHB)
o Blood from tail vein (v. coccygea)
o Clinical ketosis
§ >2.5mmol/L
o Subclinical ketosis
§ >1.2-1.4mmol/L
Ultrasound in ruminants?
Liver is on the right side, can scan it through the ICS, there is no criteria in cows for hepatomegaly
• In normal animals it is triangle shaped. Caudal vena cava thrombosis can occur in seriously septic conditions
blood clots in the caudal vena cava
Liver biopsy in cattle?
Liver biopsy in cattle
• In upper 3rd of 11th intercostal space (13 ribs and 12 ICS in total) there is the puncture place of the blind
liver biopsy
• Use special biopsy needles
Non- Purulent hepatitis?
Non-purulent hepatitis
• Metabolic
o Energy deficiency- fatty liver
• Toxic
o Cu, P, As, CCl4
o Cabbage
o Lupinosis: phomopsin
o Plant toxins
o Poor quality silage, mycotoxins
• Infectious
o Bacterial
§ Cl novyi, salmonella, enteriditis
o Hepatic fascioliasis
§ Acute hepatitis, cholangitis
Predisposing factors, clinical signs and treatment non purulent hepatitis?
Predisposing factors
• Energy deficiency, acidosis, Co deficiency
Clinical signs
• Subclinical
o Decreased meat and milk production
o Reproductive disorders
• Secondary hepatopathies
o Clinical signs of the underlying disease
• Clinical signs indicating hepatic disease
o Anorexia, ruminal atony, weight loss, jaundice
o Hepatomegaly, photodermatitis, watery diarrhoea
o Recumbency, hepatic coma
o Laboratory examination is important
Treatment
- Find and eliminate the underlying cause
- Optimal nutrition, supportive therapy
Infectious necrotic hepatitis-black disease?
Infectious necrotic hepatitis- Black disease
- Histotoxic clostridium novyi type B
- Frequent in sheep, less common in cattle
- Fasciolosis triggers the disease
o Tissue damage near spores’ triggers Clostridium growth and production of toxins
Fasciolosis?
Fasciolosis
Acute
• Causes liver failure
Chronic
• Most common, liver is cirrhoticallly infiltrated with connective tissue
Hepatic abscess?
Hepatic abscess, purulent hepatitis
• Sporadic, but 5-10% of slaughtered animals, 45-50% of feedlot animals (baby beef)
Causes
• Ruminal acidosis (chronic)
o Rumen parakeratosis + pyogenic bacteria via portal circulation
§ Fusobacterium necrophorum, Corynebacterium pyogenes, staphylococcus aureus,
streptococcus equi
• Systemic infection
o Umbilicus, udder, uterus
• Direct bacterial effect
o Traumatic hepatitis
Clinical signs
• Fever, septicaemia, peritonitis, shock
Diagnosis
• Hemogram, glutaraldehyde test
Hepatitis?
Hepatitis (necrobacillosis) caused by Fusobacterium necrophorum
• Sheep, deer, cattle
Cause
• Enteritis/ rumenitis- fusobacterium necrophorum- portal vein
o Other hepatopathies, impaired hepatic blood flow, anaerobic conditions
• Infection via systemic circulation
o Panaritium, disease of the distal extremities, necrotic stomatitis (lamb), umbilical infection
Clinical signs
- Fever, anorexia, lethargy
- Jaundice
- Death after 4-5 days or chronic weight loss
Treatment
• AB
Fatty liver syndrome?
Fatty liver syndrome
- High-producing dairy cattle, postpartum period, older cows, herd disease
- Mild fatty liver (TL 15%)
- Severe Fatty liver (TL >30%)
Lipid (mainly triglyceride) content of the liver
- Dry period <50g/kg
- Early postpartum period 80-100g/kg
- 4 weeks postpartum 40-60g/kg
Fatty liver
• >150g/kg- 300g/kg
Cause of fatty liver?
Cause
- Energy deficit after parturition
- Increased lipid mobilization
- Obesity during the dry period, lipid stores incr
- Anorexia disease/after parturition
- Nutritional anomalies
- Stress- catecholamines, GCC, insulin decr- lipid mobilization incr
- Relative deficiency in lipotropic factors
o Methionine, choline
- Hepatocyte TG incr = liver dysfunction
- Lipoprotein synthesis decr= lipid export decr= hepatocyte TG incr= liver dysfunction
Clinical signs of fatty liver?
Clinical signs
• Acute (peracute) disease
o Anorexia after parturition, lethargy, fast progressing recumbency, behavioural disorders, coma
• Subacute disease
o Slow progression of the disease, gradual worsening, anorexia, weight loss, ketonuria
• Subclinical fatty liver
o Decr resistance= secondary diseases
o Reproductive disorders
o Predisposition to fatty liver disease at next calving
Diagnosis of fatty liver?
Diagnosis
• US
o Diffuse incr echogenicity
• Liver biopsy
o Floating test, total lipid detection
- Incr serum AST, bile acids, blood ammonia
- Ketonuria
- Cholesterol, urea decr, NEFA incr
Floating test
• Placing liver into MgSO4 and CuSO4 solutions of 1.01-1.06 SG (g/ml) and based on floatation we determine
fatty liver
o Normal liver floats
o Fatty liver sinks
Blood ammonia
o Physiological concentration: < 50 μmol/l
o Fatty liver: > 100 μmol/l)
Therapy of fatty liver?
Therapy
• Support liver functions
o Fluid and electrolyte therapy, glucose IV
o Gluconeogenetic substances: propylene glycol drench, glycerol, propionate (Na, Ca), salts
o Glucocorticoids: dexamethasone, prednisolone IM
o Insulin (retard): 100 iu/animal IM
o Lipotropic factors: methionine, choline
Prevention of fatty liver?
Prevention
• Avoid over conditioning around calving
o BCS 3.5-4
- Feeding according to production levels
- Progressive adaptation to concentrated (2-3 weeks) before calving
- Walking
Therapeutic approach of liver diseases in ruminants-ketosis?
Therapeutic approach of liver diseases in ruminants – Ketosis
• Gluconeoplastic materials
o Propylene glycol
o Glycerine
• GCC
o Inhibit insulin, fat, and protein storages
o Help glucose production in the liver
§ Dexamethasone 12-14mg/animal
§ Flumethasone 20mg/animal
• Glucose/dextrose infusion
o 50-70g glucose/hour maintenance, 200g glucose/hour milk production
o Max 250ml 50% dextrose/glucose (125g glucose) PO
• Niacin
o Rumen protection is needed
o Antilipolytic effect, incr in milk production
o B3 vitamin, nicotinic acid
§ PO 6-12g/day/animal
• Insulin
o Slows down lipolysis, fat synthesis improves, improves the utilisation of ketone bodies
o Do not use alone, combine with Lente insulin
• Further additives given PO
o Choline: rumen protection, improves TCA (citric acid) cycle in the liver
§ 40-70g/animal/day
o Chromic acid: decr insulin resistance
§ 4g/day/animal
o Methionine: improves liver amino acid synthesis
§ 20-30g/animal/day
o PUFA: alter fat profile, can decr appetite
§ 5-10g/animal/day
o Molasses
- B12
- After treatment 2-5 days are required for improvement after all the mentioned treatments.
- Check BHB everyday
