principals of animal diseases internal metabolik diseases

DI SIAPKAN OLEHPROF . DR.PRATIWI TS

Principals of Animal DiseasesInternal metabolik diseases

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poultry metabolik diseases-pts-2

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Membahas gejala, kausa serta pathogenesis dan patofisiologi berbagai jenis penyakit interna yang bersifat sistemik, diakibatkan oleh gangguan metabolism, hormonal, faktor keturunan atau genetik, serta ketepatan penegakan tindakan diagnostik sehingga dapat melakukan terapi yang tepat sesuai dengan penyebabnya pada berbagai spesies hewan.

Deskripsi materi

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Tujuan

Diakhir kuliah mahasiswa diharapkan dapat memahami dan menjelaskan jenis penyakit interna disebabkan gangguan metabolisme dan genetik meliputi gejala dan penyebab serta dapat melakukan diskusi untuk menentukan diagnosa, tindakan prevensi dan memilih tindakan kuratif yang tepat.

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APA YANG DIMAKSUD DENGAN METABOLIC

DISEASES

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What is a metabolic disease?

“Inborn errors of metabolism”inborn error : an inherited (i.e.

genetic) disordermetabolism : chemical or physical

changes undergone by substances in a biological system

“any disease originating in our chemical individuality”

In toxication

OUTPUT INPUT

ENERGY BALANCE

EBAL = Feed Intake – (Maintenance (BW0.75) + Milk Production (yield and composition))

Especially fat!

Energy Balance

OUTPUT

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METABOLIC DISEASES OCCUR WHEN HOMEOSTATIC

AND FUEL MECHANISMS FAILWhen the rate of “input” of dietary nutrientsis out of balance with the rate of “output” of

production (lambs, kids, milk)

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Caused of metabolic disease?

Small molecule disease Carbohydrate Protein Lipid Nucleic Acids Toxin

Organelle disease Lysosomes Mitochondria Peroxisomes Cytoplasm

Noninfectious DiseaseNot contagiousGenetic diseasesCaused by defects in the genes

Problem or disease can be passed from parent to offspring

Genetic Diseases

Cannot be spread through contact with other animals

Control of genetic diseases, using good selection practices

Avoid breeding animals that are known to have genetic defects in their line

Nutritional Diseases

Milk fever in dairy cattle

Cows lie down and are unable to stand

Insufficient amount of Ca in the bloodstream

Poisoning

Moldy feed can contain toxins

Aflatoxins and ergot – fungi that grow on grains

Grazing on poisonous plants

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13How do you recognize a metabolic disorder ??

• SIMPLE LABORATORY TESTS, CLINICAL EXAMINATION

Glucose, Electrolytes, Gas, Ketones, BUN (blood urea nitrogen), Creatinine, Kalsium

Lactate, Ammonia, Bilirubin, LFT

Amino acids, Organic acids, Reducing subst

Health is determined by interaction of interrelated variables

1. Genetic or biological determinants,

2. Behavior (diet and lifestyle habits),

3. Pre-and postnatal environments (physical, biologic, economic, and social),4. The health care system

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1-Stage of pre-pathogenesis (pre disease) (susceptibility) = well:

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The disease has NOT developed ( animal is not yet involved) but animal is very much exposed to risk factors which increase the likelihood that the disease will develop.

2-Stage of pathogenesis:

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a) starts with entry of the agent Pre-symptomatic stage (latent disease):

No signs or symptoms (incubation period)

b) start of pathologic changes Clinical disease stage (symptomatic disease):

TREATMENT Antibiotics

Useful in controlling bacteria – not viruses

Are drugs that originate from living sources

Usually those living sources are molds and fungi

BUKAN UNTUK TERAPI PENYAKIT METABOLIK TETAPI SIDE EFFECT (KONTAMINASI

SEKUNDER)

Non-infectious health problems differ from infectious

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Examples of non-infectious problems:

Genetic defects

Nutritional disorders

Poisoning

Metabolic disorders (ketosis, diabetes)

Outcome (end results) of the disease process:

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Recovery (cure).Chronicity.Disability (any limitations of person's activities -

mental or physical- as a result of acute or chronic condition).

Death.

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PENYEBAB LAIN ?

OBESITAS

BODY COMPOSITION SBORE

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BCS and Increased Health Risk

Excess Body Condition Fat Cow Syndrome Ketosis Displaced Abomasum Milk Fever Metritis Mastitis Lameness Limited Dry Matter

Intake

Thin Body Condition Lameness

Metabolic problems can set the stage for consequences of other nutritional-stress complications, including infections such as mastitis.

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JENIS-JENIS PENYAKIT

Milk Fever = hypocalcemia Pregnancy Toxaemia / Ketosis / Fatty

Liver DiseaseKetosis

(Acetonemia, acetonuria, ketonemia, ketonuria

Hepatic LipidosisFatty liver disease, fat cow syndrome, pregnancy toxemia (small ruminants)

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JENIS-JENIS PENYAKIT

Lactational Ketosis / Fatty Liver DiseaseNervous ketosisHypomagnesemia (Grass Tetany,

Lactation Tetany, Milk Tetany)Lactic Acidosis (Grain Overload)Zinc Deficiency

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KULIAH KE 2

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Periparturient Hypocalcemia (Milk Fever)

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Milk Fever = hypocalcemia (low blood calcium)

When: within 2 days of calving on 3rd or later lactation

Why: rapid synthesis of milk draining calcium from blood

D: no fever, cow staggering or down, off feed, glazed eyes

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Hypocalcemia (1)

Hypocalcemia is a disease commonly seen in dairy cattle on or immediately following calving.

Small ruminants can experience hypocalcemia during late pregnancy associated with rapid calcium loss to the developing fetus(es) for bone mineralization.

Other species can experience hypocalcemia at or near the time of peak lactation (lactational

eclampsia).

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Hypocalcemia (2)

Hypocalcemia during late pregnancy is a result of insufficient dietary calcium to meet fetal needs. Insufficient calcium intake during late pregnancy or early lactation will require the body to mobilize calcium from bones to meet the need.

If the hormonal mechanisms are not properly prepared, mobilization will be delayed and low blood calcium concentration will result

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Pregnancy Toxaemia

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39Pregnancy Toxaemia / Ketosis / Fatty Liver Disease

Pregnancy toxemia (pregnancy ketosis or twin lamb/kid disease) is a metabolic disease of goats and sheep commonly occurring in the last six weeks of gestation, especially in those dams with multiple fetuses.

Negative energy balance with associated mobilization of fatty acids (NEFA) from adipose stores is the underlying problem.

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Factors inducing a reduction in feed intake (pregnancy, poor quality forages, feeding management) or increasing energy requirement (rapid fetal growth, lactation, environmental conditions) contribute to the duration and magnitude of negative energy balance and predisposition to aberrant metabolism leading to subclinical or clinical disease.

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Faktor eksternal

Addition of external stressors such as severe weather, sudden changes in feed, other disease or transportation further accentuate negative energy balance.

Mortality rate is high in affected animals when liver function is compromised as a result of fatty infiltration.

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Ketosis

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Ketosis(Acetonemia, acetonuria, ketonemia, ketonuria)

Definition of ketosis:Abnormally elevated concetrations of the

ketone bodies acetoacetic acid, acetone, and Betahydroxybutyrate, in body tissues and fluids

KetosisOccurs 2 to 4 weeks after calving (peak

incidence is about 3 week)Affect most high producing cows (sub-

clinically) in early lactation

“Typical” ketone (acetone) smell in the breath;

Lack of appetite Decreased rumen mobility and

production of “dry feces” Loss of weight, gaunt appearance, and

dullness

Occurrence:

Symptoms:

Ketosis

Two changes in the blood related to liver functions Drop in blood glucose (<50 mg/dl) Rise in -hydroxy butyrate (>14.4 mg/dl)

Presence of ketones in urine (“Ketostick”):-hydroxy butyrate; Acetone; Aceto-

acetic acid.

Occurrence:

Detection:

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Fatty liver disease

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Hepatic LipidosisFatty liver disease, fat cow syndrome, pregnancy toxemia

(small ruminants)

DefinitionExcessive triglyceride formation and

deposition in the liver, resulting in further severe impairment of liver function

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52Pathophysiology

As ruminants approach end of gestation and/or enter early lactation are greater energy demands:

• Increased fetal needs in last trimester • Preparation for lactation (colostrum) • High milk production postpartum

At the same time energy intake from feeds is reduced:• Lower rumen capacity prepartum• Depressed appetite around time of parturition• Result: animal enters negative energy balance

Fatty liver

Associated with increased metabolic and infectious diseases: Ketosis Displaced abomasum Milk fever Downer cow syndrome Infertility Mastitis Endometritis

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Ammonia Intoxication

• Rations low in digestible energy• High non-protein nitrogen feeding (Urea)• Excessive or highly degradable protein in the dietDecreased liver

detoxifying capacity

• Fatty Liver• Acidosis• Ketosis• Intoxications• Infectious diseases

Gluconeogenesis from aminoacids

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Protein-Energy Malnutrition (PEM)(Pregnancy Toxemia of Beef Cows)

Blood glucose concentration decreases as pregnancy progresses (hypoglycemia) from a normal 35-45 mg/dl to 20-25 mg/dl.

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KETOSIS ACETONEMIA

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64Fate of Ketone bodies

Used as an energy source – in TCA cycle of tissues such as heart,

skeletal muscle, kidney (not liver)Excreted in milk, urine

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Clinical vs Subclinical Ketosis

It is normal for ketone bodies to increase to some degree in high producing cows in early lactation: 35 % or more of cows have subclinical ketosis Accumulation in tissues/fluids beyond certain levels results in clinical signs of ketosis (appetite suppression, etc.) and exacerbate Free Fatty Acid (FFA) mobilization.

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Occurrence of Ketosis & Hepatic Lipidosis• Usually 0-6 weeks postpartum

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Treatment.

Glucose Replacement (propylene glycol (15-30 ml twice daily) for at least 3 days

Inhibit Adipose Mobilization (Insulin (20-30 U Ultra Lente) may be used with glucose treatments for better utilization of glucose and to inhibit fat mobilization

Address Dehydration, Acid-Base Balance (Intravenous administration of large volumes of electrolyte

solutions with sodium bicarbonate may be important. Corticosteroids may not be effective in the laterstages unless given at dosages utilized to combat endotoxic shock )

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68Treatment.

Similar to pregnancy toxemia, glucose supplementation in the form of intravenous

dosing followed by 3 days of oral propylene glycol is needed

Corticosteroid therapy is also used to stimulate the dam’s ability to generate glucose from

amino acids. In refractory cases, insulin therapy in conjunction with glucose infusions may be necessary.

Supportive therapy to stimulate intake and dietary modification to increase glucose availability are also

warranted

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Lactational Ketosis

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Lactational Ketosis / Fatty Liver Disease

Similar to the disease process described for pregnancy toxemia, glucose demand to support mammary lactose production exceeds the body’s ability to maintain glucose homeostasis, thus resulting in aberrant metabolism and excessive ketone body production.

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71Diagnosis.

In severe cases, neurologic signs (nervous ketosis) similar to those described for pregnancy toxemia will be observed

Lactating dams will initially reduce milk production

Dams will rapidly lose body condition during early lactation.

Body temperature, pulse rate and respiratory pattern will be within normal limits.

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15 APRIL 2012

Nervous ketosis

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73Nervous ketosis

10% of cases: • Acute onset of neurological signs: • circling, head pressing, apparent blindness • Aggression, excessive grooming behaviour, • Excessive salivation, bellowing, • Muscle tremeors, hyperesthesia, ataxia • Hypoglycemia? or isopropyl alcohol? (breakdown product of acetoacetic acid in rumen) Differental Dx : rabies, hypo-Mg, lead poisoning, milk fever (stage 1)

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• History: - May be obese/well conditioned cow in early postpartum period

• Physical exam: - Clinical signs (previous) - Cow-side ketone tests: Ketonuria, Ketolactia - 50% of people can smell ketones on breath – * look for other primary concurrent diseases(differentiate between primary & secondary ketosis)

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Etiology - Result of negative energy balance in last 6 wks. Of pregnancy due to increased energy drain by fetusRisk factors: – Fat animals – Twins – Heifers (need additional energy for growth) – Unpalatable or restricted feed – Snow cover – Concurrent diseases

Fatty liver occurs transiently in early stages of PEM

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Diagnosis• History/demonstrate decreased caloric intake• Physical exam - see above, Rule-out other diseases• Lab tests (not specific for PEM) - Ketonuria (not typical) - Reduced Ca, insulin• Necropsy: - Decreased muscle mass - Serous atrophy of fat (bone marrow, perirenal) - Fatty yellow liver if acute PEM (not advanced)

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The aberrations in calcium homeostasis associated with hypocalcemia in dairy cattle

and this is extrapolated to the situation with small

ruminants

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Hypocalcemia during late pregnancy is a result of insufficient dietary calcium to meet fetal needs.

Insufficient calcium intake during late pregnancy or early lactation will require the body to mobilize calcium from bones to meet the need. If the hormonal mechanisms are not properly prepared, mobilization will be delayed and low blood calcium concentration will result

Additionally, hypocalcemia often occurs secondary to many other periparturient diseases of small ruminants, especially pregnancy toxemia.

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Treatment.

Clinical cases of hypocalcaemia are usually treated with careful intravenous calcium borogluconate solution infusions to effect. Typical dose is 1 g Ca per 100 lbs body weight or about 50 - 75 ml of most commercial solutions.

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Hypomagnesemia (Grass Tetany, Lactation Tetany,

Milk Tetany)

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Hypomagnesemia (Grass Tetany, Lactation Tetany, Milk Tetany)

Hypomagnesemia is a common problem in beef cattle on spring pasture, but sporadically seen is dairy cattle and small ruminants

Lactating does on spring pasture are susceptible (Grass tetany or Lactation tetany) as well as growing kids on milk replacer (Milk tetany).

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Diagnosis.

Hypomagnesemia (< 1.2 mg/dl) usually occurs in early lactation and results in a life threatening disease process characterized by severe tetanic muscle spasms

Affected animals initially show ataxia, stiffness and hyperexcitability.

This rapidly progresses into recumbency and paddling. All muscles are overstimulated resulting in extreme leg

stiffness and observed muscle spasms. This is very different from the paralytic muscle weakness

of hypocalcemia. Convulsions may be triggered by some stimuli including predator attacks, severe weather

changes, transportation and other stressors.

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Lactic Acidosis (Grain Overload)

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Lactic Acidosis (Grain Overload)

Excessive intake of rapidly fermented sugars and starches in conjunction with reduced effective fiber intake, can result in severely depressed rumen pH and clinical ruminal acidosis

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White Muscle Disease (Nutritional Myodegeneration,

Stiff Lamb Disease)

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Most soils around the Northeast are very deficient in selenium, resulting in low selenium content of forages. Selenium functions as an antioxidant, generally in concert with another antioxidant, vitamin

E. Selenium and vitamin E have been shown to be equally or mutually protective against a wide range of disease processes

Border disease

“Hairy Shakers”

Nutritional myodegeneration(white muscle disease)

vitamin E / Se deficiencyyoung rapidly growing lambs / kidstwo syndromes

cardiac form - sudden onset, sudden death skeletal form - slower onset, muscle weakness,

stiffness recumbency death skeletal muscle degeneration, pale

discoloration, white streaks in muscle bundles

treat with vitamin E / SE

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Zinc Deficiency

Reported on an adult llama with mild ataxia and ill-thrift.

Histologic changes were suggestive of Cu-associated necrosis

Pregnancy toxemia

occurs in over-conditioned ewes & does in last 2-4 weeks of gestation

usually multiple fetusesanorexia, depression, weakness, neuro signs

(star gazing, circling, tremors, teeth grinding, appear blind)

negative energy balance d/t fetal demandsketonuria*, acidotic, hypocalcemic

Pregnancy toxemia

pale, friable, fatty liver on necropsytreatment

induce parturition dexamethasone (15-20 mg) in ewes dexamethasone (10 mg) or PGF2 (10g) in does

C-section IV dextrose (5-10%), rumen transfaunations,

15-30 ml propylene glycol P.O. q12h, calcium, lactated ringers, B12 , biotin

prognosis guarded to poor

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DISPLACED ABOMASUM

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