International Poultry Production — Volume 15 Number 1 11

Various skeletal disorders affectmost fast growing meat birdsand also laying hens. A num-

ber of factors are known to influ-ence normal bone development andthese are discussed in relation tofast growth rate. The incidence ofleg problems is generally higher inmales than females.Nutritional factors include proteinand amino acids, vitamins, mineralsand electrolyte balance as well asrole of mycotoxins.Genetics, sex of the bird andgrowth rate are also major factorsaffecting potential bone disorders.The anatomical difficulty in freemovement and dominance of nor-mal birds make the lame birdsdeprived of normal feeding andwatering.Furthermore, broilers with lame-ness are difficult to eviscerate prop-erly with the automatic evisceratingmachines, thereby, rendering themliable for discard, despite betterbody weights.Most poultry are afflicted withvarying degrees of skeletal disordersat some time during their productivelife cycle. These problems are pro-nounced when fast growth rate isinvolved, and so broilers, turkeys,and ducks are most susceptible.Infectious agents such as bacteria,viruses and mycoplasma can alsoplay a role in abnormal bone, carti-lage or joint development.The leg bones are one of thefastest growing bones in the skele-ton and coupled with their weightbearing characteristics it is not sur-prising that femur, tibiotarsus andtarso metatarsus bone problems areso prevalent.In broilers and turkeys, leg prob-lems occur early in life and leadeventually to morbidity with failureto eat and drink or in extreme cases,mortality.

Normal bone development

Bone is cartilaginous connective tis-sue with the unique property ofbeing mineralised. To some extent,the limit of muscle growth is alsodictated by skeletal size. The mineralcomponent is essentially calcium

phosphate. The ratio of calcium:phosphorus in bone is around 2:1and this essentially is the reason forthe maintenance of this importantratio during feed formulation.Bone is the major mineral reservein the body, representing about 99%of calcium, 88% of phosphate, 80%of bicarbonate, 50% of magnesiumand 35% of total mineral bodyreserves.Both the longitudinal growth andbone thickness are controlled by theactivity at the growth plate in themetaphysis region. Bone growth isaccomplished by two basicprocesses.First, there is formation of bonematrix (collagen and mucopolysac-charides) followed by calcification,mainly as calcium phosphate. Boneabsorbing cells called osteoclastsbreak bone down and discard worncells. After a few weeks the osteo-clasts disappear and osteoblastscome to repair the bone. During thecycle calcium is deposited and with-drawn from the blood.The periosteum, a fibrous mem-brane, covers the outside of bone.This membrane is rich with capillar-ies, which are responsible for nour-ishing bone. The outer layer of boneis called cortical bone. Skeletal bone

mass is 80% cortical bone. Canc-ellous bone (also called trabecularbone) is an inner spongy structurethat resembles honeycomb, whichaccounts for 20% of bone mass.Potential contributors to abnormalbone development include:� Body weight/growth rate.� Nutrition.� Protein and amino acids.� Vitamins and minerals.� Electrolyte balance.� Mycotoxins (see Table 1).� Dietary ingredients.Various skeletal disorders found inpoultry are known to have beeninfluenced by mycotoxins as the eti-ological factor.

Tibial dyschondroplasia

Tibial dyschondroplasia (TD) ischaracterised by an abnormal carti-lage mass in the proximal head oftibiotarsus. TD is seen most com-monly in broiler chickens. Symptomsare first seen at 21-35 days.Birds are reluctant to move andwhen forced to walk, do so withswaying motion or with stiff gait. TDrelates to disruption of the normalmetaphyseal blood supply in theproximal tibiotarsal growth plate,

where the resultant disruption innutrient supply means that the nor-mal process of ossification does notoccur. A typical cartilage plug, there-fore, develops and as bone growsthere is lateral displacement of thegrowth plate causing characteristicbowing or bending of the legs.Riddell, 1975b, suggests thatbetween 21-24 days of age, theproximal tibiotarsus showed thegreatest development of TD.Among many causes like genetics,electrolyte balance, Ca, P leading todevelopment of TD, mycotoxinsdoes also play a vital role in itsdevelopment. Mycotoxins producedby various Fusarium moulds areknown to affect TD. Lee et al.,1985, isolated Fusarium roseum inoats and tested various fractions ofthe mycotoxins produced, as theyaffected TD.

The water soluble fraction wasfound to be most problematic andof the six major components of thisfraction, one known as TDP-1 wasfound to be causing 100% TD whenfed at 75ppm. TDP-1 has since beenisolated as Fusarochromanone.Krough et al., 1989, reported whatthey claimed to be the first directevidence of TD due to naturallyoccurring fusarochromanone.The morphological characteristicsof the cartilage of affected birdswere classical to TD in that the typi-cal cartilage was not penetrated bythe meta physeal vascular system.Krough et al., 1989, showed that

Effects of mycotoxinson bone structure

by Dr Devendra S. Verma, MVSc, technical director, Biomin, India.

Continued on page 12

SSkkeelleettaall MMyyccoottooxxiinn ddiissoorrddeerrss iinnvvoollvveemmeenntt

Tibial dyschondroplasia �

Cage layer fatigue �

Rickets �

Chondrodystrophy �

Spondylolisthesis/kinky back �

Femoral head necrosis �

Foot pad dermatitis �

Articular gout �

Table 1. Some of the majorskeletal disorders whereininvolvement of mycotoxin hasbeen implicated.

Fig. 1. The structure of bone.

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12 International Poultry Production — Volume 15 Number 1

while these changes were most pro-nounced in tibiotarsus, lesions alsooccurred in the humerus, femur andtarso metatarsus.More recently Wu et al., 1993,indicated that moderately high levels(75ppm) of fusarochromanonecaused 100% incidence of TD inbroilers, and that the minimumdietary level of this toxin needed toproduce leg problems was 20ppm.

Rickets

Rickets most commonly occurs inyoung meat birds, the main charac-teristic being inadequate bone min-eralisation. Ca deficiency is the mainproblem, although this can beinduced by feeding diets deficient inCa, P, or vitamin D3. In most fieldoutbreaks abnormal bird behaviouris seen between 7-10 days of age.

Characteristic weak bones and ribbeading can be see at around 10-14days of age, where 10-100% of theflock is affected. Their bones arerubbery and the rib cage is flattenedand beaded at the attachment to thevertebrae.In most of the cases of rickets, adeficiency of vitamin D3 is often sus-pected. This can be due to a simpledietary deficiency, inadequatepotency of D3 supplement or otherfactors that reduce the absorptionof vitamin D3. Rickets is often moreproblematic when diets containmycotoxins and especially aflatoxins.Normally, Vitamin D2 and D3 isconverted to 25-hydroxycholecalcif-erol (25-OH), which is a circulatoryform of Vitamin D3. This is thenconverted to 1,25 di hydroxychole-calciferol (1,25-OHD) or calcitrol,that is the most biological activeform of the vitamin D. Aflatoxinreduces vitamin D absorption and

liver damage prevents conversion tothe active 25-OH form of vitaminD3 as shown in Fig. 2.However, it is unclear if the myco-toxins create a specific metabolicdeficiency of vitamin D3 and ofother nutrients or if they simplyaffect the bird by reducing the feedintake. In mycotoxins contaminateddiets especially those from Fusariummoulds, it is recommended toincrease levels of vitamin D3.

Articular gout

Gout refers to the condition inwhich high plasma uric acid leads toprecipitation of urate crystals eitherin synovial fluid and tendon sheathsof various joints especially the hockjoint or on serous surface of variousvisceral organs when kidneys aredysfunctional. Sustained hyperure-caemia is most commonly caused by

decreased renal clearance of urate.Deposition of such urate crystalsat joint is referred to as articulargout. Mycotoxins like aflatoxin,ochratoxin, and citrinin are allknown for their kidney dysfunctionmechanism.Mollenhaur et al., 1989, fed afla-toxin at levels upto 5ppm of diet,and after 21 days, observed thicken-ing of glomerular membranes ofglomerular apparatus of chickensleading to articular gout.Another mycotoxin namelyoosporein (formed from mould,Chaetomium spp.) not only severelyaffects epithelium of proximaltubules of the nephron but also thebasement membranes. Thesechanges in kidney lead to hyperure-caemia and ultimately leading togout.

Economic losses

Leg abnormalities probably causemore economic losses than anyother single abnormality in thechicken house. It has been estimatedthat 2-6% of all broilers display someobservable signs of skeletal prob-lems, while many more will beaffected in a less visible way.Leg abnormalities result in mortal-ity, reduced feed utilisation andgrowth rate, and down-grading inthe processing plant. Unlike in

Continued from page 11

NNuummbbeerr ooff ppoossiittiivvee ssaammpplleess iinn rreessppeeccttiivvee rraannggee ooff mmyyccoottooxxiinn ccoonncceennttrraattiioonnss

AAffllaattooxxiinn BB11 ((ppppbb)) OOcchhrraattooxxiinn AA ((ppppbb)) TT--22 ttooxxiinn ((ppppbb))

00--5500 5500--110000 00--5500 5500--110000 00--5500 5500--110000

Cereals 88 44 68 44 72 44Cereal byproducts 48 8 24 16 32 8Oilseed meals 152 8 64 40 60 24Finished feed 328 76 200 80 268 96

Table 2. Co-occurrence of aflatoxin B1, ochratoxin A and T2 toxin in feed ingredients and fin-ished poultry feeds in India (Devegowda et al., 2005).

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International Poultry Production — Volume 15 Number 1 13

North America, where efforts havebeen made to accurately monitorthe losses incurred in the livestockindustry due to mycotoxicoses, nosuch detailed information is availablefor the Asia-Pacific region.Losses due to mycotoxicoses havebeen estimated at more than $1 bil-lion in Canada and over $2.5 billionin the US during the 1990s.To estimate production lossesfrom skeletal problems, the chickenindustry has been divided into twobroad production systems – broilerflocks and breeder/layer flocks.

Broiler flocks

Broilers have a life span of approxi-mately five to seven weeks afterwhich they are slaughtered for meat.Therefore, the important produc-tion parameters that a disease mayaffect are weight gain, culling andmortality rates and condemnationsat slaughter.� DDiisseeaassee eeffffeeccttss::Weight gain/feed conversion. Nopublished data were found on theeffect of skeletal disorders on weightgain although they are said to havean impact.� MMoorrttaalliittyy aanndd ccuulllliinngg..In a UK trial quoted by Pattison(1992), 0.8% of broilers between 15days of age and slaughter wereculled for lameness. In a 1976 surveyof broiler mortality on six farms inEast Anglia, leg deformities werediagnosed in 2.06% of dead birds togive an overall mortality rate fromleg deformities of around 0.06%.The suggested mortality/cullingrates for skeletal problems areminimum 1%, mean 2% and maxi-mum 3% of broilers placed per year.� CCaarrccaassee ccoonnddeemmnnaattiioonnss..At a large poultry processing plant in1992, 2.09% of broiler carcaseswere rejected in total and 1.57% ofbroiler carcases were rejectedbecause of disease conditions. Jointlesions were responsible for 0.31%of condemnations in broilers fromfarms with rejection rates of 3% ormore. However, the author notes thatthe 19.5% of condemnations foremaciation were probably the resultof leg weakness. If the assumption istrue, around 20% of condemnationsin broilers from farms with high con-demnation rates were directly orindirectly attributable to leg weak-ness (skeletal problems).

If the relative importance of skele-tal problems is the same in flockswith average condemnations rates,then around 0.3% (20% of 1.57%) ofbroilers slaughtered are likely to becondemned for skeletal problems.The suggested carcase condemna-tion rates for skeletal problems areminimum 0.2%, mean 0.3% andmaximum 0.5% of broilers slaugh-tered per year.

Egg laying flocks

Studies of losses due to disease inegg laying birds tend to be concen-trated on birds in lay.However, skeletal problems alsocause losses during the rearingperiod in birds destined for breederand commercial egg laying flocks.The life span of egg laying birds hasbeen divided into two periods: 0-19weeks (growing period) and 20-70weeks (laying period).

Mortality/culling is the mostimportant production parameteraffected by skeletal disorders in egglaying birds. All breeder and com-mercial egg laying flocks will containbirds with skeletal abnormalities.�� MMoorrttaalliittyy aanndd ccuulllliinngg..Birds aged 0-19 weeks: Little datawere found on mortality and cullingrates for skeletal disorders in grow-ing birds in breeder/ layer flocks.In a survey of mortality in chicksfrom 0-70 days of age in ninebreeder flocks, 1.3% of birds thatdied had deformed hocks to give anoverall mortality rate from the con-dition of around 0.02%. However, as the study only coversthe early part of the birds’ lives, it isan underestimate. The same rateapplied proportionately over 19weeks is 0.04%.The suggested mor-tality/culling rates for skeletal prob-lems in birds during the growingperiod, is minimum 0.04% of birdsaged 0-19 weeks.Birds aged 20 weeks (point of lay)to 70 weeks (slaughter): The sug-gested mortality/culling rates forskeletal problems in birds during layare minimum 0.1%, mean-0.5% andmaximum 1.0% of birds in lay.

Indian perspective

During 2004 and 2005, a survey wasconducted to study the incidence ofaflatoxin, ochratoxin and T-2 toxin

in various feed ingredients and fin-ished feeds collected from differentstates of the country.Out of 984 samples analysed, 824samples were found to be positivefor the presence of aflatoxin, ochra-toxin and T-2 toxin. Of these, 91,94, 97 and 97% of cereals, cereal by-products, oilseed meals and finishedfeeds, respectively, tested positivefor mycotoxins.The authors reiterated that notonly are aflatoxins a problem in theregion; but also ochratoxins and T-2toxin.Over a five year period, Chandra-sekaran et al., 2002, assayed 7,173samples of oil cake, 3,842 samples ofcomplete feed and 2,463 cereals forthe presence of ochratoxin A(OTA), citrinin and aflatoxin.Ochratoxin was detected in all sam-ples while aflatoxin was found in90% of the samples (Table 3).Nevertheless, mycotoxin surveysfrom around the world indicate thatprotein sources such as rapeseedmeal, cottonseed meal, groundnutcake, sunflower cake, copra mealand palm kernel meal are more sus-ceptible to mycotoxin contamina-tion than conventional raw materialssuch as soybean meal.Owing to high prices of conven-tional raw materials during certainyears, feed manufacturers have beenforced to opt for alternatives to soy-bean meal and this has increased thepotential for mycotoxicoses formany livestock species.Similarly, the cost of maize hasforced a look at other energysources, including byproducts suchas rice bran, wheat bran and screen-ings. Many mycotoxins are concen-trated in the outer covering of theseeds and therefore, the chances ofmycotoxin related problems areincreased when such materials areused in animal rations.For example, during the millingprocess DON was found in thehighest concentration in the branand lowest in the flour. Mycotoxinsfrom these byproducts in combina-tion with mycotoxins from moretraditional ingredients can result intoxicological interactions.

Conclusion

It is quite evident that feed contami-nated with mycotoxins play a role ininducing leg weakness.Differential diagnosis will alwaysallow us to determine what actionsmust be needed to control such inci-dences. Controlling all mycotoxin(polar and non polar) with availablecontrol strategy will undoubtedlybring down the leg weakness inci-dences. �

OOcchhrraattooxxiinn AA AAffllaattooxxiinn BB11 ((ppppbb)) TToottaall ssaammppllee((ppppbb)) NNeeggaattiivvee 11--2200 2211--5500 nnuummbbeerr

1-20 4 69 6 7921-50 1 25 1 2751-100 2 18 6 26101-200 4 3 4 11>200 3 0 0 3

TToottaall ssaammppllee nnuummbbeerr 1144 111155 1177 114466

Table 3. Co-occurrence of ochratoxin A with aflatoxin B1 incomplete feed in India (Chandrasekaran et al., 2002).

Fig. 2. Aflatoxin blocking vitamin D absorption.

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