5. Diagnostics and treatment of liver diseases in ruminants. Flashcards

1
Q

Ruminant energy supply?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Measurement of insulin resistance?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

NEFA in the liver?

A

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

  1. If the liver is unable to utilise it, it will become re-esterified triglycerides, leading to fatty infiltration

(worst)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Jaundice haemolytic icterus causes?

A

Jaundice

Haemolytic icterus

  • Leptospirosis (calf), babesiosis, anaplasmosis
  • Food (cabbage, onion)
  • Copper-toxicosis (sheep)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hepatic icterus?

A

Hepatic icterus

• Common in sheep (toxic hepatopathies), rare in cattle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Obstructive icterus?

A

Obstructive ileus

  • Obstruction of the bile duct (extrahepatic)- very rare
  • Intrahepatic bile capillary compression (e.g., fatty liver): more frequent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical signs and diagnosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Liver enzymes in cattle?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Total bile acids?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Dry chemistry NH3 analyser: blood ammonia checker

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Summary of clinical diagnostics in liver diseases?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Clinical diagnosis of subclinical and clinical ketosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Ultrasound in ruminants?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Liver biopsy in cattle?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Non- Purulent hepatitis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Predisposing factors, clinical signs and treatment non purulent hepatitis?

A

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
17
Q

Infectious necrotic hepatitis-black disease?

A

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

18
Q

Fasciolosis?

A

Fasciolosis

Acute

• Causes liver failure

Chronic

• Most common, liver is cirrhoticallly infiltrated with connective tissue

19
Q

Hepatic abscess?

A

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

20
Q

Hepatitis?

A

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

21
Q

Fatty liver syndrome?

A

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

22
Q

Cause of fatty liver?

A

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
23
Q

Clinical signs of fatty liver?

A

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

24
Q

Diagnosis of fatty liver?

A

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)

25
Q

Therapy of fatty liver?

A

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

26
Q

Prevention of fatty liver?

A

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
27
Q

Therapeutic approach of liver diseases in ruminants-ketosis?

A

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