Introduction:
“Avian
urolithiasis’’ or Gout is a metabolic disorder occurs in poultry and other domestic
birds related with kidney dysfunctions. It is characterized by high level of
uric acid in the blood (hyperuricemia) and leads to deposition of urates on the
surface of visceral organs or various joints particularly hock joint (articular
gout). In avian, uric acid is end product of protein or nitrogen metabolism due
to absence of uricase enzymes. In gout, blood levels of uric acid are higher
than the normal when it exceeds 10mg/dl lead to gout. It can be as high as 44mg/100ml
compared to 5-7mg/100ml in a normal bird. The syndrome occurs usually in two separate
form visceral gout and articular gout. Visceral gout is a condition in which
white chalky uric acid or urate crystals (tophi) (monosodium urates) deposits
are seen in soft tissues of various organs in body. Due to its striking
lesions, visceral gout has also been describe as acute toxic nephritis, renal gout,
kidney stones, nutritional gout and nephrosis. It is responsible for high
morbidity and mortality in fast growing and high producing broilers. Visceral gout
has emerged as a syndrome of major concern causing heavy economic losses in
broiler industry, particularly of broiler chicks and poses a challenge to
control because of its multi factorial etiology .The syndrome occurs worldwide
which is most common cause of mortality in growing broiler chickens. In worst situation
mortality had been seen up to 90% in past. However, 8-15 % mortality is most
common in broilers.
Prevalence:
The visceral
gout in fowls was first time described in India by Iyer (1941). Visceral gout is
a condition of chickens that has been recognized for more than 30 years. This
condition can occur as an individual problem at any age but outbreaks are seen
in young chicks in the first or second week of life (baby chick nephropathy)
and could be of multi factorial origin. Year wise incidence of the disease
ranged between 4.01 to 9.37% with an overall average relative incidence of
7.15% (Chaudhary, 2016). Sayed (2001) reported the incidence of visceral gout
was increased during winter months which were attributed to environmental cold
stress, making the birds more susceptible to visceral gout followed by summer and
monsoon. The highest incidence 93.07% was recorded in colder season in broilers
by Shrivastava (2001). He reported higher susceptibility of this condition in broiler
between 0-3 weeks of age. Greater the severity of gout resulted in poor feed conversion
ratio (FCR) and lower body weight gain. Visceral gout assumes prime economic
importance in poultry industry due to increased incidence causing production
loss, mortality and lack of availability of specific treatment.
Etiology:
Visceral
gout is a metabolic disease and multi etiological factors alone or in
combination are known to influence occurrence of this syndrome.
This comprises of
Nutritional and metabolic causes
1. Excess dietary calcium and vitamin D3 with low
phosphorous supplementation in the diet of immature pullets.
2. Rearing diets that contain limestone and sodium
bicarbonate in particle form which may results in excess calcium intake and
imbalance of Ca: P ratio.
3. Marginally low available phosphorus in rearing diets
has been associated with higher gout incidence.
4. Sodium bicarbonate can contribute to gout by making
the urine more alkaline, which, with high levels of calcium, is an ideal medium
for the formation of kidney stones.
5. Vitamin A deficiency over a long period of time can
cause damage to the lining of the ureters, which leads to urethral ducts get
occluded by the desquamated metaplastic squamous epithelium preventing the
excretion of uric acid and facilitating its accumulation in the blood (Ali et
al., 2012).
7. Excess of dietary protein (30–40 %)
8. High amount of salt (more than 0.3 %)
9. Poor quality of protein (High amount of nonessential
amino acids)
Managemental causes
1. Water deprivation either because of mechanical malfunction
or less water in the diet (dehydration).
2. Consumption of hard water with a high amount of
minerals (i.e., calcium and copper sulfate).
3. Brooding management (type of brooder, temperature).
Infectious causes:
Viral agents known to be involved in gout are infectious bronchitis, avian
nephritis virus, reo virus and astro virus. Nephropathogenic or nephrotropic
strains of infectious bronchitis have a special predilection for the kidneys in
youngpoultry causing enlargement of kidney and distended with urates.
Toxins:
Products
used on a routine basis that have potential for human error and resulting
toxicity are antibiotics, anti-coccidials, minerals, vitamins, manufactured
chemicals and pesticides. Fungal toxins (Mycotoxins, ocharatoxins, aflatoxins,
oosporein etc.) in poultry feed are nephrotoxic. Other causes includes heavy
metal poisoning and the inappropriate use of antibiotics (such as gentamycin,
nitrofurosones and sulfonamides etc.), anti-coccidials, chemicals, pesticides,
disinfectants (i.e., cresol and phenol) etc.
Development of disease / Pathogenesis
The kidney is a vital organ of the bird with diverse
metabolic and excretory function viz. maintaining the chemical composition of
body fluids, removal of metabolic waste products, regulation of blood pressure
and blood volume and conservation of fluids and electrolytes. Avians are
uricotelic due to that they are more prone to gout. As that uric acid is the
main excretory end product of protein or nitrogen metabolism in the absence of
uricase enzymes in birds. Gout is mainly due to damaged kidneys (nephropathy),
it leads to accumulation of uric acid in blood (Hyperurecaemia). There
isprecipitation of monosodium urate monohydrate (MSU) crystals in joints called
articular gout and on visceral surfaces called visceral gout (Lumeij, 2008).
Visceral gout is an acute form of deposition of urate crystals. These crystals
stimulate phagocytosis by neutrophils and initiate the inflammatory cascade
(Arun and Azeez, 2004).An elevated serum urate level, together with local
factors, can result in the deposition of urate crystals into the joints is more
advanced stage and found rarely. Its crystallization depends on the
concentrations of both urate and cation levels. Chronic cumulative urate
crystal formation in tissue fluids leads to MSUM crystal deposition (tophus) in
the synovium and cell surface layer of cartilage. These “crystal shedding”
facilitates crystal interaction with synovial cell lining and residential
inflammatory cells, leading to an acute gouty flare.
Signs and pathological lesions
• Chalk-like urate deposits on pericardial sac and liver
capsule
• Increased thirst (polydipsia)
• Dehydration and sometimes greenish diarrhea
• Joints may be enlarged, stiff and painful, shifting
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
• Birds often have reddened, swollen feet that progress
to blisters and sores. Joint become painful and joint immobilization due to
depot of urate crystals
• Gouty plaques are found (shiny, raised, whitish
deposits) under skin
• Decreased appetite
• Lethargy
• General debility and weight loss
• Feather plucking, dull plumage and self-trauma
• Abnormal droppings with chalky urates in their stool.
• Change in temperament
The gross lesions include woolen pale kidneys with urate
deposits and dilated ureters filled with chalky white material. The kidneys are
congested and greyish white with a soft in consistency. The other noticeable
findings observed are presences of chalky white masses surrounding the heart,
kidneys, liver intestines, peritoneum, spleen, lungs, air sacs, muscles and
inner lining of proventriculus. Generally no inflammatory reaction in synovium
or visceral surfaces has been observed.
Microscopically, the kidneys shows severe lesions
characterized by moderate to severe tubular dilation, necrosis and large
deposits of radiating fine needle shaped crystals in the tubular lumen and in
the interstitium and also in myocardium. These deposits are surrounded by a
zone of granulomatous inflammation. The crystals appeared black against a
yellow background on DeGalantha staining confirming theme to be of urates and
the cases of gout. Kidney lesions were mainly of nature of visceral gout
characterized by granular degeneration, vacuolation and desquamation of tubular
epithelium, foci of necrosis and massive infiltration of heterophils in the
interstitium in acute stage of the syndrome.
Managemental approaches to prevent gout/
Prevention and control
As described visceral gout is of multifactorial origin
when incidence occurs identifying the cause is often difficult. Different
managemental strategies can alleviate the problems in poultry flocks.
Housing management
Minimize the stress from the hatchery level to the chicks
up to all life stages. With minimizing dehydration. Maintain proper
ventilation, brooding temperature and humidity (60-70%) during early chick
stage. Provide adequate number of drinker to the flock with appropriate height.
Nutritional management
Preventive measures concern with nutrition includes
1. Ensure adequate hydration. Water deprivation should be
avoided in rearing of boiler and laying flocks.
2. Use of Jaggery 2 to 5 grams per liter of water or
recommended electrolyte doses in water.
3. Feed pullets should not contain more than 1 per cent
calcium in powdered form up to 16 weeks of age. High calcium intake in immature
pullets can cause serious kidney damage.
4. Available phosphorus levels should be 0.45-0.50 per
cent in rearing diets. Insufficient phosphorus predisposes the kidneys to
calcium damage.
5. Pre-lay ration should not be used before 16 weeks of
age, or when the flock shows signs of sexual maturity (blooming of the combs).
A calcium content of 2.50-2.75 per cent should be sufficient.
6. If sodium bicarbonate is used to improve egg shell
quality, use the minimum recommended level and only when needed. A flock with
gout should not be medicated with sodium bicarbonate or fed a ration that is
highly alkaline (high levels of sodium or potassium).
7. Review all calcium and phosphorus levels in the
feeding program. Pullet and layer feeds should be routinely analyzed for
calcium and phosphorus level.
8. Feed samples are assayed for the presence of the
mycotoxins like citrinin, ochratoxin and oosporein routinely.
9. Avoid a diet with higher protein content than the
recommended level as per the age group of poultry. Depending upon severity
manipulate the diet with low protein for few days.
10. Adequate level of phosphorus should be supplied as
per the recommended level in concern with calcium to balance Ca: P ratio.
11. Birds with incidence of gout may be supplement or
rear on natural vegetables, some of the fruit and plant based compounds such as
flavonoid due to richness of vitamin A, antioxidant and anti-inflammatory
actions.
12. Supply adequate amount of vitamin A as per
recommendation and additional supplementation is needed when gout is prevalent
in flock (Omega-3 fatty acids).
13. Use toxin binders and liver tonics to keep minimum
levels of fungal toxins in feed. Use recommended levels of aluminum-free Sodium
bicarbonate (baking soda) in feed during high temperatures.
Other measures:
Field cases and research reported the interaction between
infectious bronchitis (IB) and nutritional as well as managemental factors for
triggering visceral gout in poultry. Considering this point as per recommendations
and following standard of vaccination schedule for IB vaccines should be
administered in poultry birds. Kept in mind for various serotypes of bronchitis
vaccines in endemic areas and specifically against nephropathogenic strains
will improve immunity of birds against this infection. Some of antiviral drugs
should also be helpful for immunity elevation. In broiler breeder and broiler
farms infectious bronchitis virus vaccination programme should be review.
Treatments
• Based on history and incidence occurrence in flock the
supportive treatment should be given to the birds which cannot be corrected
completely kidney damage but may help full to alleviate from this condition and
turns to normal functioning of kidney.
• This condition of kidney damage is linked with loss of
water and electrolytes so check proper hydration and give fluid therapy and
electrolyte supplementation intravenously or in drinking water.
• Techniques involved for reducing gout by using urine
acidifier preparations, such as ammonium chloride, DL-methionine, ammonium
sulfate, potassium chloride and methionine hydroxy analogue (MHA) which
acidifies the urine and increases the solubilization of calcium and urates
crystals in urine.
• Use some of the diuretics preparations like Lasix,
Zyloric have also been used.
• Use some the pain relieving medication generally of
non-steroidal anti-inflammatory (NSAIDs) compounds like meloxicam, aspirin and
Celebrex etc.
• Use some of the herbal compounds like coconut water is
of a good diuretic action.
Conclusion: The
incidence of visceral gout in chicks is indicative of kidney damage occurred at an earlier stage in the poultry. As per the research
findings, strongly inkling this syndrome withnutritional causes of Ca:P imbalance and the viral infection
of IB as principal cause of visceral gout in broilers leads to mortality. Other
factors also likely to be an underlying cause include dehydration, electrolyte
imbalance and mycotoxins possibly need to recognize. The prognosis of affected
flocks with visceral gout is generally poor that cannot be cured but proper
nutritional and housing management and proper endemic strain specific
vaccination can alleviate the problems which reduces mortality in broiler
chicken flocks.
Dr. A. B. Parmar, Dr. V. R.
Patel, Dr. J. M. Patel and Dr. Y. D. Padheriya
College of Veterinary Science & Animal
husbandry, Navsari Agricultural University,
Navsari -396 450. Gujarat, India.
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