Gout - Uric acid deposits in the joints and surrounding tissues due to kidney damage cause gout.

There is
difficulty in movement with red and swollen joints.

Gout is a musculo-skeletal disorder affecting the muscles and bones around the joints of the mammals
and bird. It is a common disease among humans and reptiles, and is also seen in birds, especially
budgies, waterfowl and poultry

Etiology

Although some instances of gout are hereditary, others may be aggravated by environmental or
nutritional factors. Gout is mainly due to damaged kidneys (nephropathy). When they stop functioning
normally, it results in an accumulation of uric acid and urates in the muscles and joints. Kidney damage
leading to gout can be due to the following causes (12.45)

High calcium and vitamin D, with low phosphorus amounts in food.

High amount of salt (> 0.3%) in food. Not enough water in the diet (dehydration)

High amount of sodium bicarbonate in food. High amount of protein (>30%) in food.

Viral infection like Avian nephritis

Consumption of water with a high amount of minerals (Ca & CuSO4) Poisoning by disinfectants (i.c.
cresol, phenol) Antibiotics like gentamicin, nitrofurosones and sulfonamides

Pathogenesis

⚫ Uric acid is one of the end breakdown products of dietary protein in bird and other animals.

The uric acid is removed from the blood by the kidneys and excreted in the urine.
Gout can occur if the level of uric acid (a by-product of the breakdown of dietary proteins usually
excreted in the urine) in the blood exceeds the ability of the kidneys to remove it.

In articular or synovial gout, the uric acid crystallizes in the joints, ligament and tendon sheaths.

In visceral gout, uric acid deposits are found in the liver, spleen, pericardial sac, kidneys and air sacs.

When the uric acid crystallizes in tissues it forms small, white nodules called "tophi."

Gout can be primary, when the high uric acid level is caused by an abnormal breakdown of protein or
secondary in which case the kidneys are not able to adequately excrete uric acid. Primary gout is
thought to be hereditary in humans. Secondary gout can be caused by medications, chronic diseases,
kidney disease, overeating, improper diet (high protein and possibly high vitamin D or low vitamin A,
dehydration, some infections and other environmental factors that affect the

kidneys' ability to eliminate uric acid.

Symptoms-There are two types of gouts, and symptoms depend on the type on which bird is affected.

Articular gout

It is the chronic form of the disease which occurs when uric acid and urates are deposited in the
ligaments and tendons, but

more commonly in the legs or wing joints. • Male birds are generally susceptible to articular gout and
the common age for this affliction is four months and above.
The joints may be enlarged, stiff and painful and warm to touch. •The affected birds may continually
shift weight from one foot to the other and have a shuffling gait.

The bird may be unable to perch, spending most of his time on the floor of the cage. • If the wings are
affected, the bird may be unable to fly. If forced to walk the bird becomes noisy due to discomfort. • It
may also be depressed and dehydrated with greenish diarrhea. In addition, the bird will look dull and
depressed.

Visceral gout

Visceral gout occurs in the tissues of the internal organs and if the internal organs are involved, signs
include: Weight loss

•Decreased appetite • Lethargy

Diagnosis

Abnormal droppings

•Change in temperament

Diagnosis of gout involve analyzing the diet, environmental factors, availability of fresh, clean water and
a thorough history of previous health problems and treatments (12,31,45).

Examination of x-rays, blood tests, joint fluid or biopsy samples are required for diagnosis.

Uric acid Treatment

crystals in joint fluid and tissues will confirm the diagnosis.

Treatment depends greatly on underlying cause of gout. However, following management can be
suggested ( If the bird is dehydrated, administration of fluid orally or parentally is required. If the cause
of gout is due to improper nutrition, supply low protein diet and may supplement with vitamin A.

Urinary acidifiers should be administered to decrease the uric acid.

45):

Reducing proteins, calcium, vitamin D, and salt, in-combination with an increase of phosphorus and soft
water intake are all important dietary changes to treat gout. The drug allopurinol or probenecid or
colchicines which decreases the amount of uric acid produced in the body. But the

exact dosage and safety of these drugs in birds have not been determined.

A feed analysis is also necessary, ensures the bird receives an appropriate intake of minerals, protein
and vitamins Multivitamins including vitamin K may be used to help the liver and kidneys function
normally and can help control the Most birds with gout must be treated for the rest of their lives. If
therapy is discontinued, there is a possibility that the disease will reappear if the therapy is discontinued

Although there is no cure for gout, it's important for every bird owner to keep an eye out for symptoms,
while also providing proper nutrition, an adequate source of vitamin A, either from leafy, green
vegetables or vitamin supplements and fresh clean water.

Gout

Both visceral gout and articular gout occur in poultry.

• Visceral gout is caused by renal failure and the diffuse deposition of urate crystals may involve joints
and tendon sheaths as well

as other parts of the body.

• Articular gout in which only the musculoskeletal system is affected, is relatively less common, and
appears to be multifactorial in origin but with a strong hereditary basis. • Clinical signs include swellings,
which may ulcerate, especially around the metatarso phalangeal and interphalangeal joints. •Affected
joints, periarticular tissue, tendon sheaths and musculature contain extensive, paste like deposits of
urate crystals.

Gout in birds

Gout is a condition in which crystals of uric acid (UA) or urates are deposited in tissues. Uric acid is the
relatively water- insoluble nitrogenous end product of protein and purine nucleotide metabolism. Gout
is a common discase among humans, reptiles and birds. It is more common in budgies, waterfowl and
poultry

What causes gout?

Uric acid is one of the end breakdown products of dietary protein in birds and other animals. The uric
acid is removed from the blood by the kidneys and excreted in the urine.

Gout can occur if the level of uric acid in the blood exceeds the ability of the kidneys to remove it

Types of gout

thought to be hereditary in humans.

Secondary gout - In secondary gout, the high level is due to the inability of the kidneys to adequately
excrete the uric acid.

This can be caused by medications, chronic diseases, kidney diseases, overeating, improper diet (high
protein and possibly

high vitamin D or low Vitamin A). poor blood circulation, inactivity, decreased water intake or chronic
dehydration, some

Excessive levels of uric acid, slightly soluble in the blood (uriaciduria) may lead to the formation of
insoluble salts (urates). A. There are two types of gout based on etiology, viz. O Primary gout and
Secondary gout (21-23.31,44). Primary gout In primary gout, the high uric acid level is a result of an
abnormal breakdown of protein. Primary gout is

infections, and other environmental factors which affect the kidneys' ability to eliminate uric acid. B.
There are two types of gout based on lesions produced, viz. Visceral gout and Articular gout (Table 278).

Visceral gout - Uric acid deposits are commonly found in the serous membranes of visceral organs
especially in the liver. spleen, pericardial sac, kidneys and air sacs (Photo 366 and Photo 368). Articular
(synovial) gout. The uric acid crystallizes in the joint, ligaments and tendon sheaths. When uric acid
crystallizes in

tissues it forms small, white nodules called "tophi' (Photo 367).

Humans Common sites of involvement include articular and periarticular tissues.

There are multiple forms and causes of gout, the concentration of uric acid in the blood is generally
elevated (hyperuricemia). a. Deficiency or increased activity of specific enzymes involved in purine
metabolism.
Causes include:

b. Impaired renal excretion of urates caused by renal disease or nephrotoxic drugs and chemicals. c.
Genetic factors

d. Environmental influences. Birds and reptiles

The kidneys eliminate semisolid urates rather than urine and uric acid. • Factors associated with gout in
these species include: impaired renal function and clearance of urates, nephrotoxic drugs, various

dietary excess (protein and calcium), and deficiencies (vitamin A) and dehydration.

The kidney damage can arise from infection with certain strains of Infectious bronchitis virus (IBV),
exposure to some

mycotoxins or inadequate water intake. • Baby chick nephropathy in the first week of life (kidney
damage) can be due to inappropriate egg storage conditions, excessive

water loss during incubation or during chick holding/transport, or inadequate water intake during the
first few days of life.

Very low humidity in brooding will also increase the likelihood of this problem.

⚫ in Pekin / mallard ducks the condition is almost always due to inadequate water intake, whereas in
muscovy ducks it is seen in breeders allowed to continue laying for over 24 weeks without a rest.

Pathogenesis of pain
The predilection site in humans includes articular and peri-articular tissues, where the urate crystals
attract and

are phagocytized

by neutrophils and macrophages. These cells release lysosomal enzymes and mediators of inflammation,
which, in turn, exacerbate the acute inflammation and cause intense pain. Articular gout is stubbornly
recurrent in human patients (21-23.31.44). Clinical findings

Joint may be enlarged, stiff and painful and the bird may continually shift weight from one foot to the
other and have a shuffling gait. The bird may be unable to perch and so remains on the floor of the cage.
If the wings are affected, the bird may be unable to fly.

If the internal organs are involved, there may be a decrease in appetite, lethargy, weight loss and
abnormal droppings. The bud may show a change in temperament or die suddenly.

Diagnosis

Based on necropsy lesions which include chalky white nodular deposits known as 'tophi" on
pericardium, liver, air sac. Based on history of diet, environmental factors, availability of water and
previous health problem and treatment.

The serous surfaces of visceral organs, especially the parietal surfaces of pericardium are encrusted by a
thin layer of grayish peritoneum? Similar deposits may be present in joints and are usually present in the
kidney (Photo 366-368) granular material that may have a metallic sheen and this appearance is enough
to make a diagnosis.

Radiographs and blood tests for uric acid help to substantiate the diagnosis.

The identification of uric acid crystals in joint fluid, biopsies or "tophi' confirms it.
Treatment

Any underlying dietary or environmental cause will need to be remedied. Birds with gout will be placed
on a low protein diet

Vitamin A may be given to birds who had received an improper diet. Proper hydration is necessary and
fluids may need to be administered. Medications such as allopurinol. probenecid or colchicine may be
used but the exact dosage and safety of these drugs in birds

have not been determined,

Most birds will need to be treated for life or the condition will quickly reappear if therapy is
discontinued.

Table 278. Differences between visceral gout and articular gout in birds (21-23,31,44)

S/N

Features

Visceral gout

Articular gout

Onset
It is usually an acute condition but can be chronic

It is usually a chronic disease

Frequency

It is very common

It is rare or sporadic

Age

I day and above

4-5 months and above

Sex

Both males and females are susceptible

Mostly males
Main causes

• Genetics

High protein in the diet

Others?

• Dehydration Nephrotoxicity-calcium, mycotoxins (ochratoxins. oosporein, aflatoxins etc.), certain

antibiotics, heavy metals (lead), ethylene glycol, ethoxyquin etc.

Infectious agents- nephrotropic IBV, avian nephritis virus (chickens), polyomavirus, PMV-1 (pigeons),
Salmonella sp.. Yersinia sp.. Chlamydia psittaci. Eimeria truncate, Cryptosporidia. Aspergillus sp.

• Vitamin A deficiency

• Urolithiasis

Neoplasia (lymphoma, primary renal tumors) Immune mediated glomerulonephritis

Anomalies

It is generally due to failure of urate excretion

Pathogenesis (renal failure)

It is probably due to a metabolic defect in the secretion of urates by the kidney tubules. Kidneys are
normal grossly. Kidneys may

Gross lesions Kidney

Kidneys are almost always involved and they look grossly abnormal with deposition of white, chalky

precipitates.

become abnormal with white urate deposits

if the bird get dehydrated.

Soft tissues

Visceral organs like liver, myocardium, spleen or serosal surfaces like pleura, pericardium, air sacs.
mesentery are commonly involved.

Soft tissues around the joints are always involved, especially feet. Other joints of the legs, wings, spine
and beak are also involved.

Joints

Soft tissue around the joints may or may not be involved. Surfaces of muscles, synovial sheaths of
tendons and joints are involved in severe cases.
Soft tissue around the joints are involved especially feet. Other joints of the legs, wing, spine and beak
are also commonly involved.

Granulomatous inflammation in synovium and other tissues.

Microscopic

Generally no inflammatory reaction in synovium or visceral surfaces. Kidney has inflammatory reaction
around tophus

If arthritis from gout is severe, it is possible to surgically remove the uric acid crystals from the joint. Pain
medications such as aspirin may be given. The prognosis for a bird with gout is generally poor.

Prevention Careful monitoring of the conditions of hatching egg storage and incubation with a view to
achieving a standard egg weight loss

profile. ⚫ Humidification of holding rooms and chick transporters may also be beneficial.

Gout

Gout is the result of abnormal accumulation of urates and occurs as two indistinct syndromes. These are
visceral gout and articular gout, both occur in poultry.
Visceral gout

Visceral gout, which has also been called visceral urate deposition is characterized by precipitation of
urates in the kidney, and on serous surfaces of the heart liver, mesenteries, air sacs, and peritoneum
(Fig. 161 and Plate V/6) In severe cases, surfaces of muscles and synovial sheaths of tendons and joints
may be involved and precipitation

may occur within the liver and spleen.

The deposits on serosal surfaces appear grossly as a white chalky coating while those within viscera may
only be

recognized microscopically.

Visceral urate deposition is generally due to a failure or urinary excretion, which may be due to
obstruction of

ureters renal damage or dehydration.

A change in concentration of some constituent of the intercellular fluid due to renal disease is probably
needed to

cause precipitation of the urates. Dehydration due to water deprivation is a common cause of viscera;
gout in domestic poultry. Outbreaks of visceral gout in poultry have also been attributed to vitamin A
deficiency excess dietary calcium.

treatment with sodium bicarbonate and a mycotoxin oosporein. Outbreaks of renal gout in which
kidneys are enlarged and often distended with urates result when flocks of young chickens are infected
with nephrotropic strains of infections bronchitis virus.
Articular gout

Articular gout is characterized by tophi, deposits of urates around joints, particularly those of the feet in
which the joints are enlarged and the feet appear deformed. Articular gout in which only the muscular
skeletal system is affected is relatively less common and appears to be

multifactorial in origin but with a strong hereditary basis. Articular gout is a sporadic individual bird
problem of little economic importance in poultry. Raised levels of uric acid in the blood have been
reported in both renal disease and articular gout in the absence of visceral urate deposition.

A change in concentration of some constituent of the intercellular fluid due to renal disease is probably
needed to

cause precipitation of the urates.

Articular gout undoubtedly painful but acute attaches have been described as alternating with periods
of remission. Clinical signs include swellings which may ulcerate especially around the metatarso-
phalangeal and interphalangeal joints.

When these joints are opened and white semifluid deposits of urates may be found within the joints.

VISCERAL GOUT

It is most important to stress at the outset that visceral gout is merely the sequel to renal failure and not
a disease entity in itself. In the uricotelic bird, where the waste product of protein metabolism is uric
acid, a loss of renal tubular function rapidly leads to hyperuricaemia and to visceral gout, that is to say a
deposition of urate crystals on the serous surfaces of the thoracoabdominal viscera and on the synovial
membranes of joints and tendon sheaths (Fig. 9.1). The loss of tubular function may be due to primary
tubular damage or to back pressure following obstruction of the ureter and its branches.

A condition which is clearly differentiated from visceral gout is articular gout, in which urate deposits are
found only in and around joints (Fig. 9.2). It is a hereditary metabolic disease which is not consequent
upon renal failure or indeed kidney involvement. It is accompanied by a painful inflammatory reaction
and the formation of tophi, the typical granulomata of gout.

NEPHROSIS

The term nephrosis, as used in poultry pathology, is non-specific and implies a primary degenerative
affection of the kidney without a significant inflammatory component. The kidneys are often uniformly
pale, but a satisfactory and reliable diagnosis cannot be made merely by gross examination. A large
number of poisons, from simple inorganic to complex organic ones, can cause nephrosis; that is to say
degeneration and even necrosis of the epithelial cells of the kidney tubules. If this tubular damage is
sufficiently severe the birds may die from renal failure which, in the less acute cases, is often
accompanied by visceral gout.

Most primary inflammatory conditions of the kidney also show a degree of the degenerative tubular
change but this does not justify the use of the term nephrosis. Expressions such as 'nephritis-nephrosis
are unnecessary and confusing.

(c) Gout in Poultry

Gout in poultry denotes a condition when there is a deposition of uric and urates in the organs of
poultry, because of increased concentration of uric acid in blood and body fluids as a consequence of
decrease excretion by the kidneys.

Forms of gout

There are two main forms of gout:

(i) Visceral gout

(ii) Articular gout.

In both the forms white chalky deposits occur. Articular form is a chronic form of the disease and it is
less common.

Etiology

Many factors may result in gout in poultry such as:

(1) Excess of protein, especially protein of animal origin (2) Deficiency of vitamin A. the diet of poultry.

(3) Disease involving kidneys.

(4) Specific diseases such as infectious bursal disease (IBD) or infectious bronchitis (IB) in chicks.

(5) Nephrosis due to overmedication with sulpha drugs or other kinds of medicines (Gentamycin and
nitrofurasone have to be carefully given. Ochratoxin and oosporin are important for disease production.

(6) Fungal toxins in the feed.

Some factors may help in aggravation of this condition such as extreme cold or humid- ity. Use of copper
sulphate in drinking water may result in water refusal, dehydration and gout. Disinfectants like phenols
and cresols if wrongly used also cause residual toxicity.
Lesions

donated to eat laroqque sal ben but

The kidneys appear swollen, mottled and greyish in colour due to deposition of urates. The ureters are
dilated with white, pasty material. In advanced cases whitish chalky deposits are also seen on the serous
membranes and surfaces of the liver, heart, etc.

Symptoms of gout

Gout is accompanied by signs of depression, dehydration and sometimes greenish diar- rhoea. Affected
chicks appear dull with ruffled feathers and moist vent. Mortality among chicks is high. Scarified chicks
show chalky deposits in kidneys, ureters and other organs.

Control of gout

• Avoid diet higher in proteins or high calcium.

• Review IB vaccination programme. In areas where IB is endemic, it is advisable to vaccinate chicks with
nephrotoxic strain at about 4 days of age. Day-one beak dip vaccination has been found useful in
broilers.

• Use urine acidifiers; Ammonium sulphate 5.0 g/kg and ammonium chloride 10 g/kg

increase acidity of urine and uric acid excretion. Methionine hydroxy analogue (MHA) or even DL
methionine may be used. • Meet the dietary calcium and phosphorus levels carefully. It is better to
provide at least 50% Ca as grits which dissolves slowly and maintains blood calcium level.
• Analyse the feed for mycotoxins particularly for ochratoxin and take necessary steps . Check water
supply for regular uninterrupted water supply and for proper heights of waterers.

• Examine if nephrotoxic drugs or disinfectants are being used or have been used. • Ensure proper levels
of A, B, D, K and B compiex.

Excessive use of sodium bicarbonate (more than 2 kg/ton) should be avoided. Use of electrolytes
through water may assist in controlling mortality.

In acute cases potassium chloride 1 g/litre can be used.

. Provide broken maize for at least 3 days along with Jaggary, 5 g per litre of water for 3 to 5 days in
acute cases with mortality.

Table 7.2 Differences between Visceral Gout and Articular Gout in Birds*

Visceral gout

1. Onset

It is usually an acute condition but can be chronic

2. Frequency

It is very common. 1 day and above.

3. Age
4. Sex

Both males and females are susceptible.

5. Causes

a. Infectious

b. Nutritional

c. Toxic

6. Pathogenesis

It is generally due to failure of urate excretion (renal failure).

7. Gross lesions (Kidney)

Kidneys are almost always involved and they look grossly abnormal with deposition of white, chalky
precipitates.

Soft tissues

Visceral organs like liver, myocardium, spleen or serosal surfaces like pleura, pericardium, air sacs,
mesentery, etc. are commonly involved.
8. Microscopic lesions

Generally no inflammatory reaction in synovium or visceral surfaces. Kidney has inflammatory reaction
around tophus.

Articular gout

It is usually a chronic disease.

It is rare or sporadic.

4-5 months and above. However, in immature, genetically susceptible chickens, it may be induced by
high protein levels in the diet.

Mostly males.

a. Genetic

b. High protein in the diet

c. Others

It is probably due to a metabolic defect in the secretion of urates by the kidney tutules.

Kidneys are normal. Kidneys may become abnormal with white urate deposits if the bird gets
dehydrated.
Soft tissues other than synovium are rarely involved. However, comb, wattles, and trachea have been
observed to be involved.

Granulomatous inflammation in synovium and other tissues.