Dealing with lameness in Italian beef cattle rearing N...Lameness is one of the main health and economic issues concerning dairy and beef cattle production systems. Lameness is a Lameness

Dealing with lamenessin Italian beef cattle rearing

SUMMARYLameness is one of the main health and economic issues concerning dairy and beef cattle production systems. Lameness is aclinical condition characterized by multiple triggering (microbial, mechanical, nutritional, and genetic) and predisposing fac-tors (subjective and environmental). Locomotor apparatus diseases (LAD) often become a chronic condition characterized byreduction of feed intake and production performance and increases in nervousness and other health issues. The aim of thiswork was to review the causes and risk factors for the onset of lameness in beef cattle reared in the most often used intensivesystem in Italy. The results of the survey show that in Italian intensive beef cattle rearing, LAD are an important problem char-acterized by variable incidence and a variety of risk factors. Heavy Charolaise bullocks are the most predisposed to LAD. Typeof flooring is one of the main risk factors. Choosing cattle of the appropriate size to be housed on slatted floor facilities canstrongly limit arthropathies incidence. Proper litter management can prevent foot diseases. Other livestock facilities and man-agement can limit or promote LAD incidence and severity. Lowering animal density, better staff training, heat stress reductionduring hot periods, appropriate structures and procedures for animal restraint and handling, can reduce the occurrence oftraumatic injuries because of the reduction of cattle restlessness and competitive behavior. Ration formulation, feed qualitycontrol, proper vitamins and minerals supplements together with a gradual transition from arrival to finishing diet, will re-duce the risk for acidotic events and consequent episodes of laminitis. Accurate diagnosis together with the knowledge of themain LAD related features can help not only in speeding up the decision-making process concerning a specific lame animalbut also in identifying eventual contributing factors to the problem at a herd level. An accurate diagnosis and determinationof causal factors will allow for a better timing of the intervention strategies and limit the need for the administration of drugs,not essential for each case of lameness.

KEY WORDSLocomotor apparatus disease, lameness, arthropathy, foot disease, beef cattle.

R. COMPIANI*, C.A. SGOIFO ROSSI*, G. BALDI*, A. DESROCHERS**

*Dipartimento di Scienze Veterinarie per la Salute, la Produzione Animale e la Sicurezza Alimentare (VESPA),Università degli Studi di Milano**Département des Sciences Cliniques, Faculté de Médecine Vétérinaire, Université de Montréal, 3200 Sicotte, St-Hyacinthe, QC, Canada, J2S 7C6

INTRODUCTION

Locomotor apparatus diseases (LAD) in cattle are gainingmore attention because of welfare issues and economic loss-es1,2. In dairy cattle, lameness was associated with decreasemilk yield and fertility3-5. Digital dermatitis and claw horndisruption are the most significant diseases affecting dairycattle locomotor apparatus around the world6-10. In dairyherds, LAD are one of the main causes of early culling just af-ter low fertility and mastitis11. LAD are also common in beefcattle but there is scant literature on the subject in Europe.Prevalence of lameness in Norwegian beef cows was studiedin 12 herds. Lameness was recorded in 1.1% of the animalswith laminitis like lesions and infectious hoof problems werethe most common diseases12. In the US beef industry theeconomic loss due to lameness is significant. The sellingprice of a lame animal is significantly decreased13. A nation-al survey on bull beef quality in the US concluded that a highpercentage of carcasses from lame animals had inadequate

muscling, arthritic joints and bruises14. Other economic loss-es due to LAD are well quantified and include costs for ther-apies, laboratory analysis, reduction of weight gain, earlyculling and, in the most severe cases, the death of those ani-mals which do not respond to treatments15. Based on the lit-erature, it seems that the origin of lameness in beef cattle ismore varied than in dairy cattle16-28. Causes of LAD include:trauma, osteochondrosis, septic arthritis and epiphysitis. Ac-cording to one study, lameness originates from the foot innearly 90% of the lameness cases in dairy cows and approx-imately only in 70% of the cases in beef cattle15,29. Surveysconducted in North America (Table 1) show that LAD inci-dence lies between 16 and 22% of total morbidity29-31. It is al-so important to stress that, in these studies, the incidence ofLAD in beef cattle was second only to that of bovine respira-tory disease (BRD), which is the main problem in beef cattlerearing all over the world29,32,33.The aim of this paper was to review the literature on lame-ness causes and risk factors of beef cattle reared in the inten-sive system common in Italy. In addition we wanted to de-scribe the main beef LAD in order to better understand thereal incidence of this problem. Finally, we will review someof the main LAD risk factors.

R. Compiani et al. Large Animal Review 2014; 20: 239-247 239

Autore per la corrispondenza:Riccardo Compiani ([email protected]).

N

Compiani_imp:ok 20-06-2016 9:55 Pagina 239

240 Dealing with lameness in Italian beef cattle rearing

Italian beef cattle production systemBeef cattle rearing in Italy is mainly based on fattening youngcattle imported mostly from France to dedicated facilities inNorthern Italy. The most common breeds imported fromFrance are: Charolaise, Limousine and crossbreed. Gender(female and intact male) and weight are variable with aweight of 220-500 kg upon arrival. Cattle are generallyhoused indoors on slatted floor or straw litter. LAD in thisscenario are mainly ration based. In order to achieve appro-priate weight, conformation and fatness to meet the Italianconsumer requirements in the shortest time possible, ani-mals receive diets characterized by high nutritional level andhigh quantity of fermentable carbohydrates which can leadto acidosis and therefore to laminitis34. Many other factorsmay predispose to LAD or complicate the clinical findingsincluding gender, breed, weight, season, housing type andquality of management.

LOCOMOTOR APPARATUS DISEASES

Hereinafter are reported some of the main LAD that can af-fect cattle. Table 2 summarize some features about lamenesscharacterized by body area of onset. The table also indicatesthe possible severity of lameness, the position adopted of theaffected limb, the degree of pain at palpation and swelling foreach of the listed conditions. The chart also recommendsspecific physical exam or particular diagnostic test that theveterinarian needs to formulate a correct diagnosis, progno-sis, treatment and future prevention strategies. Table 2 re-ports some problems with a very poor prognosis as specificfractures that can be confused with joint problems. Theknowledge of these problems is important because a decisionmust be taken rapidly from an animal welfare standpointand to salvage optimal value of the meat.

Laminitis or claw-horn disruptionClaw-horn disruption is by definition any event, pathologythat will influence claw-horn growth. Subclinical laminitis isoften associated with horn growth abnormalities. The clinicalmanifestations are poor horn quality, sole hemorrhage, soleulcers and white line disruption. Laminitis is one aspect ofclaw-horn disruption. Laminitis by definition is the inflam-mation of the lamella of the hoof. The term laminitis was bor-rowed from the equine condition because of similar clinicalsigns. The events leading to the ultimate sinking of the pedalbone seems to be different in cattle35,36. In horses and cattle, thehorn is attached to the corium (sensitive part of the claw) bylamellae which are very small leaflets providing nutritive sup-ply to the non sensitive horn. The corium is attached to the

pedal bone. In horses, the inflammation of the lamellae willcreate a separation of the sensitive and non sensitive lamellaeprovoking pain and moreover sinking or a rotation of the ped-al bone in severe cases. This separation is permanent. The voidbetween the lamella will be filled with poor quality connectivetissue and secondary horn (white line horn production). Thewhite line will then be wider and weaker. The corium will bedamaged to various degrees depending of the pedal bone dis-placement. The origin of the detachment is different in cattlebut unfortunately the results are the same. It varies from focalhemorrhages to apical protrusion of the pedal bone.Subclinical rumen acidosis has been frequently associated asa causative agent of laminitis in cattle34. Toxin, endotoxinand inflammation by-products37 produced by the rumen flo-ra during ruminal acidosis often have a detrimental effect onthe vascularisation of the foot or directly on the suspensorytissues of the pedal bone. Using the oligofructose overloadmodel, Dansher showed that in fact, there are clinical(weight shifting, solar hemorrhages) and histologicalchanges at the lamellar level consistent with laminitis. How-ever, it does not decrease the strength of suspensory tissue ofthe bovine claw38.

OsteochondrosisOsteochondritis is a focal disturbance of the endochondralossification for which the exact underlying disease mecha-nisms remain unknown. The consequence is an abnormalthickening of the cartilage known as cartilage retention. Evo-lution of the lesion is highly dependent of the type of forcesapplied to the dysplasic cartilage area. Fissures or fractures ofthe cartilage occur in areas subjected to shear forces. Thosefractures and focal cartilage weakness can evolve to a com-plete separation of the cartilage from the underlying sub-chondral bone to form a typical osteochondritis dissecans le-sion (OCD). Osteochondral fragments are formed when car-tilage flaps do separate entirely. In contrast high compressiveloading on dysplasic cartilage areas create cartilage infoldingand resorption evolving to a subchondral bone cyst (SBC)39.Predisposing factors are not well established. High energyand protein diet have been investigated and proposed as acause of osteochondrosis26,39,40. Animals on high energy dietswere more affected and the lesions more severe. Low con-centration of dietary calcium was also suspected as a con-tributing factor. Other nutrients like phosphorus, vitamin A and D may playa role in osteochondrosis as well23. Inheritance has been sus-pected in grazing beef cattle where affected bulls shared acommon ancestral sire. However, the caloric intake ratherthan the concentration of any minerals is the most impor-tant predisposing factor among all the studies and all fast

Place Canada Kansas, USA Nebraska, USA

Number of animals 294,144 250,521 1,843,652

Total morbidity, % 12.87 9 13.1

BRD incidence, % (% of morbidity) 7.55 (58.66) 6.03 (67) –

LAD incidence, % (% of morbidity) 2.73 (21.21) 1.98 (22) 2.1 (16)

foot disease among LAD cases, % 97 70 70

Table 1 - Total morbidity and BRD and LAD incidence in north America feedlot.

Reference Church and Radostits, 1981 Edwards, 1984 Griffin et al., 1993



STIFLE

Septic joint ++++ Flexed ++++ +++ Joint palpation/find origin (lungs) ArthrocentesisJoint lavage,

antibiotics 2 weeks

OCD +Extension,

+ ++ Examine contralateral stifleArthrocentesis, Correct diet,

circumduction X-Ray soft bedding

HIP

Dorsal luxation +++Internal

+ 0Abduction and palpation

X-Ray Slaughterrotation hock of greater trochanter (crepitation)

Ventral luxation ++++Limb abducted

+ 0Trochanter medially displaced,

X-RayEuthanasia/emergency

downer excessive abduction slaughter

Septic joint ++++ Toe touching + +/–Abduction, flexion (pain) Arthrocentesis,

Antibiotics for 2 weeksFind origin (lungs) X-Ray

Femoral head++

Greater++ 0

Abduction and palpationX-Ray

Euthanasia/fracture trochanter higher of greater trochanter (crepitation) emergency slaughter

ELBOW

OCD ++ Normal + + Flexion/extensionArthrocentesis, Correct diet,

X-Ray soft bedding

Septic joint +++ Normal ++ ++ Flexion/extensionArthrocentesis,

Antibiotics for 2 weeksX-Ray

Ulnar fracture +++ Dropped elbow +++ +++ Olecranon palpation X-Ray Stall rest

HUMERUS

Diaphyseal2 months of stall rest

fracture+++ Dropped elbow +++ +++ Humerus palpation and abduction X-Ray (prognosis 50%)

Emergency slaughter

SHOULDER

Septic joint ++++ Normal +++ ++ Joint palpation, flexion/extensionArthrocentesis,

Antibiotics for 2 weeksX-Ray

OCD ++ Normal + + Flexion/extensionArthrocentesis, Correct diet,

X-Ray soft bedding

FOOT

Septic coffin++++ Toe touching ++++ +++

Swelling/draining tract Probe in the Amputation,joint at the coronary band fistula, X-Ray joint resection

Toe+++

High heels+++ 0 Sole exam and hoof tester

Probe in a tract, Debridement Subtotalulcer/abscess (overgrowth) X-Ray amputation

Footrot ++/+++ Toe touching +++ ++ Pastern is swollen, feverInterdigital Debridement,necrosis Short term antibiotics

Laminitis +/+++ Abnormal stance ++ 0 Hoof tester and sole examinationLongitudinal cut of Correct diet,the feet at autopsy soft bedding

Septic fetlock ++++Toe touching,

++++ +++ Swelling/draining tract or lacerationArthrocentesis, Joint lavage,

flexed fetlock X-Ray antibiotics 2 weeks

Physitis ++ Tiptoes walking ++ ++ Distal radial physis swelling X-RayCorrect diet,soft bedding

CARPUS

Septic joint ++++Toe touching,


flexed carpus X-Ray antibiotics 2 weeks

Hygroma 0 Normal +/– ++ Soft, painless UltrasoundIf many animals

affected, verify stalls

Physitis ++ Tiptoes walking + + Distal metacarpal physis swelling X-RayCorrect diet,soft bedding

DJD +/++ Flexed carpus + ++Bilateral carpal swelling in flexed Arthrocentesis,

Soft bedding, slaughterposition X-Ray

HOCK

Septic joint ++++Toe touching,


flexed tarsus X-Ray antibiotics 2 weeks

OCD + Extension + ++ Often bilateral painless swellingArthrocentesis, Correct diet,

X-Ray soft bedding

Hygroma 0 Normal +/– ++ Lateral soft swelling, painless UltrasoundIf many animals

affected, verify stalls

Gastrocnemius+++

Dropped+ ++

Flexion of the hockPhysical exam

Euthanasia/emergencyrupture hock/downer with the stifle extended slaughter

Peroneus++

Hyperextension+/– +/–

Complete extension of the hockPhysical exam Stall restrupture hock with stifle extended

Table 2 - Characteristics of the main causes of lameness in cattle.

Lameness Limb position Pain Swelling Specific physical exam Specific test Treatment/prevention(palpation)



growing farm animals. The only exception is the bull wheresome research results are contradictory. American studies re-port a frequency of 8.5% for osteochondrosis lesion atslaughter whereas the incidence seems higher in middle agebulls with 12%26. Lack of exercise was incriminated as a fac-tor in one study. Based on the literature, osteochondrosis ismore frequent in males. However, it is most likely over rep-resented because only high genetic value bulls have been ex-amined and the condition reported41. Hard flooring wasshown to exacerbate methaphyseal osteochondrosis lesionsin Holstein calves42.In cattle, joints commonly affected are the stifle and the tar-sus. But osteochondrosis lesions have been diagnosed in thecarpus, shoulder, and distal interphalangeal joint. In a studywhere 28,235 atlanto-occipital joints were examined, 3.8%had lesions compatible with osteochondrosis. In the samestudy, 8.5% of the 106 lame cattle had lesions of osteochon-drosis mostly in the stifle26. Final diagnosis is often based onradiographic findings. Osteochondrosis dissecans, bone cystsand physitis can be observed.

Septic joint diseaseSeptic arthritis is the most common condition affecting thejoints of cattle43. It can be caused by a direct trauma to the ar-ticulation (primary), an adjacent infection to the articulation(secondary), or a systemic infection (tertiary)44. The distallimb, being less protected by soft tissue, is more exposed toexternal trauma especially if the environment favors it. Septicarthritis in cattle is of bacterial origin. The most commonbacterial pathogens in adult cattle are: Trueperella pyogenes,Escherichia coli, and other environmental bacteria. A retro-spective study on bacterial culture of 172 cases of septicarthritis showed that Trueperella pyogenes was the most com-mon bacteria isolated (35% of positive culture in young ani-mal and 48% in adult)45. Sixty percent of cases had a positiveculture. Cattle affected by Histophilus somni as well as My-coplasma spp may have more than one articulation infected.If the incidence of septic joint disease increases in a herd with-out umbilical involvement, Mycoplasma and Histophilus som-ni should be considered as a possible cause. Incidence of sep-tic arthritis will increase in the presence of Mycoplasma pneu-monia and mastitis in a herd46. Arthritis was present in 25 of54 calves with Mycoplasma bovis pneumonia in a feedlot18. Infeedlots of eastern France, Mycoplasma bovis was isolated in 8of 9 operations included in a study on bovine respiratory dis-ease. Mycoplasma bovis was isolated in broncho-alveolarlavage from 79% of normal calves and 82 of the sick calves47.

PhysitisIt’s a clinical syndrome of young rapidly growing animals af-fecting mainly the physeal regions of the appendicular skele-ton. Affected animals will walk on their toes therefore theirheels will be higher with over worn toes. There is obvious en-largement or flaring of the distal physeal area of the metacar-pus or metatarsus in chronic cases. In a study looking at 4612 month-old bulls clinical lameness, physitis was found in34 animals48. Limb deformities will be present in severe cas-es (rotation, valvus or varus). At palpation, there is a hardswelling just proximal to the fetlock over the physis. It can beeither septic or a type of osteochondrosis. Distal metacarpalor metatarsal physis are more commonly affected, however,distal radius could be affected as well. The pain engendered

by the process is significant with consequences on appetiteand growth rate.Trauma or intrinsic abnormalities of focal blood supply ofthe cartilage could be at the origin of osteochondrosis lesionof the physis. Same etiologic factors contributing to osteo-chondritis dissecans have been incriminated as causingphisitis. Housing on slatted floor was suspected in one studyand confirm the theory of trauma to the physeal cartilage28.However, 2 out of 4 affected animals had a streptococcus iso-lated from the physis. In another study on calves raised onhard flooring, osteochondrosis lesions were found on lamecalves42. Harder flooring exacerbated the clinical signs of af-fected animals. Septic physitis is most likely secondary to asepticemia or local trauma. If no wound is observed then aremote infection origin must be suspected and investigated.

RISK FACTORS

To evaluate the main LAD risk factors in the intensive beefcattle rearing, incidence of lameness in 10 farms was ana-lyzed. The farms selected were located in the north of Italyand all of them import young cattle from France. Data werecollected from each farm animal health database. Farm man-agement policy calls for a veterinarian to perform an animalhealth inspection in each pen once a day in the morning. Theherd veterinarian observes each animal to detect any signs ofpathology (lameness, swelling, asymmetry, abnormalstance). A more thorough physical examination was per-formed on affected animals and appropriated therapy wasstarted. Animals with severe problems and deserving specialcare or prolonged therapy were moved to hospital pens.Lameness was defined by an abnormal gait and divided in 2categories based on location: arthropathies and foot diseases.Arthropathies were defined by any swelling located at the fol-lowing joints: fetlock, carpus, tarsus and stifle. A more spe-cific diagnosis could not be attempted in this study consid-ering the facilities and the management of the farms.The risk factors evaluated in this study were divided in 2 cate-gories: animal and environment. Data regarding gender, breed,weight at arrival, season, floor surface and overall managementin relation to LAD morbidity were analyzed by one-way ANO-VA, using proc GLM of SAS 9.3 (SAS Inc.); animal weight wasnot used as a covariate because it was considered as an inher-ent characteristic of the different variables analyzed.

Factors related to the animalTo evaluate the animal related risk factors, data were collectedon about 18.000 animals from January 2010 to January 2011.In this farm, animals were kept in pens on concrete coveredwith wheat straw litter for 30 day after arrival. During this pe-riod they received a transition diet that gradually move to thefattening one characterized by high nutritional level. After 30days, cattle are moved to straw-bedded fattening pens of 8-12animals. Stables are covered and open on all 4 sides. Collectedanimal data included: gender, breed and weight. The weightwas subdivided in 4 categories based on the typical differenttypologies of newly received beef cattle imported from France.Males were not castrated. Table 3 summarizes the results relat-ed to the signalment of the affected animals.Results show that there is a higher lameness incidence inmales than in females. It is most likely related to the natural


*Lm: limousine; Ch: charolaise; Cr: crossbreed.**Cattle moved to hospital pen.a,b,c Different small letters indicate significant difference among means in the same row (P<0.05).A,B,C Different capital letters indicate significant difference among means in the same row (P<0.01).


competing behavior of males and because males generallyreceive diets characterized by a higher nutritional level thanfemale exposing them to higher risk of acidosis and thereforenervousness. European consumers ask for lean and tenderbeef, and considering the greater capacity and speed of fatdeposition of female, their diets have lower energy contentthan males.Breed is a risk factor for LAD incidence but there is a strongrelationship with animal weight. It has been shown thatsome foot diseases have a partial genetic basis, and that cer-tain morphological characteristics are associated with thedevelopment of lameness in dairy cattle49,50. To our knowl-edge these findings were not described in beef breeds. Thehigh LAD incidence in Charolaise could be related to theweight and the size of these animals, factors that predisposeto severe traumatic events during social fighting. Anotherfactor could be the origin of animals; indeed Charolaise cat-tle generally come from flat pastures and in these circum-stances joints are not adapted to intense solicitations or tosudden movements typically present on mountain pastures.We hypothesize that their limb conformation is not adaptedfor feedlot as in other breeds coming from uplands such as

Limousine or Aubrac. Charolaise cattle have also a higher in-cidence of lameness due to nutritional causes, probably be-cause those subjects have a higher feed intake than otherbreeds both in total volume per day and in volume per meal,with consequent higher risk of rumen acidosis. Whilst takinginto account the importance of several environmental riskfactors, several nutritional foot diseases in newly receivedbeef cattle could be influenced by the dramatic changes inthe diet composition that occur between pasture, arrival andfinishing diet. So it is important to implement an adequateand appropriate nutritional management policy.In the end, collected data show that LAD incidence is alsohigher among heavier animals at arrival. LAD in heavier cattle could be caused by a higher socialcompetitiveness during the adaptation period and to a high-er protein and energy concentration of diets administered toolder and heavier cattle during adaptation and the followingrearing phases.

Factors related to environmentTo verify the effects of season as a risk factor for LAD, anoth-er study has been conducted in the previous farm (Figure 1).

Number of animals 9,261 8,435 10,646 4,323 2,727 5,226 4,360 4,594 3,516Average weight, kg 434 ± 52 285 ± 50 328 ± 82 443 ± 66 372 ± 70 254 ± 31 338 ± 24 416 ± 20 486 ± 31

LAD, % 3.97A 0.42B 2.11a 3.83b 2.03a 0.45a 1.38b 4.09c 3.83c

Foot diseases, % 2.24A 0.38B 1.13a 2.61b 1.31a 0.33a 0.83b 2.35c 2.30c

(% LAD) (56) (90) (54) (68) (79) (73) (60) (57) (60)Arthropathies, % 1.73 0.04 0.98a 1.22b 0.72a 0.12a 0.55b 1.74c 1.53c

(% LAD) (44) (10) (46) (32) (21) (27) (40) (43) (40)

Problem cattle**, % 6.37a 4.42b 5.48 6.38 3.81 5.28 4.75 5.92 5.88Hoof diseases, % 25.64A 1.07B 7.54a 19.56b 16.34b 4.35a 14.49b 33.82c 33.34c

Arthropathies, % 16.94a 6.97b 16.95a 31.17b 16.34a 2.17a 3.87a 15.08b 23.19c

Table 3 - LAD incidence and animal signalment60.

Risk factorsGender Breed* Weight

Male Female Lm Ch Cr < 300 300-380 380-450 > 450

Figure 1LAD incidence and season60.

a,b,c Different small lettersindicate significant differenceamong means (P<0.05).A,B,C Different capital lettersindicate significant differenceamong means (P<0.01).


*40% traumatic injuries; 60% septic arthritis.**16% traumatic injuries; 84% septic arthritis.a,b,c Different small letters indicate significant difference among means in the same row (P<0.05).A,B,C Different capital letters indicate significant difference among means in the same row (P<0.01).


In spring time, LAD incidence was higher than in the otherperiods of the year. The increasing temperature that char-acterized Italian climate condition during spring time iscertainly a factor that makes litter administration morecomplicated and, in case of poor management, bacterialproliferation and moisture in the environment can weakenfoot tissues contributing to increasing LAD34. The lower in-cidence detected in summer is in contrast with that view,indicating that other factors intervene in spring in increas-ing lameness susceptibility. In this period, in fact, tempera-ture, humidity and day light conditions are ideal for fungiand mold development in hay and silage, increasing the riskof presence of mycotoxins. Mycotoxicosis, especially thosesupported by toxins produced by Fusarium fungi, interfer-ing with ruminal microbial populations, can lead to a moreor less severe ruminal acidosis with all the systemic effectsthat contribute to laminitis51. Furthermore, some cases oflimb subcutaneous tissue diffuse edema caused by vasoac-tive mycotoxins, can be misinterpreted as arthritis and thenLAD incidence could be overestimated. We think that thisincrease of lameness during spring in Italy is related to theraising of called cattle “repouse”. Those animals have spentthe previous winter in stable in their country of origin andare imported older and heavier. It makes them at risk forLAD as explained earlier.Among the environmental factors, an important role is cer-tainly played by flooring and in particularly by its hardness,abrasiveness and slipperiness. In Italy, beef cattle are fre-quently housed on slatted floor and lameness are often asso-ciated with traumatic injuries as a result of mating and com-petitive behavior. Insufficient wear and overgrowth are ob-served on slatted floor. As a consequence, cattle are moreprone to white line disease, sole ulcer and abscesses34. If aconcrete floor is covered with litter, it must be kept as dry aspossible to avoid excessive pathogen bacterial growth like fu-sobacterium, spirochetes and dichelobacter. Among differentbedding materials, wheat straw has the highest insulatingproperties and good absorbing capacity. Sand and sawdusthas higher absorbing capacity but very low insulating prop-erties and moreover, high amounts of sawdust can increaseirritation of upper airways52,53.In Table 4 are reported the results of LAD incidence in 5 dif-ferent farms which differ mainly in the floor surface of fat-tening pens. Those farms imported young cattle from Franceand managed them as the first farm described above. Sincefloor type is certainly a LAD risk factor, in our study the type

of surface was not strictly related to joint or foot diseases asexpected. The incidence of foot diseases in litter housingranged from 24 to 65% of total LAD, similar to the range ob-served on the slatted floor (21 to 68%). Comparable trendswere also recorded for arthropathies (litter: 35-76%; slatted:32-79%). Even in this case, the association with other sub-jective risk factors or those related to the environment, caninfluence LAD incidence.Indeed, in addition to the type of floor, other environmentalfactors may increase the risk for LAD such as safe handlingfacilities with adequate animal density per pen. Farm staffmust be well trained to recognize not only sick animals butto understand the behavior of cattle. Sudden change of di-rection, strong competition between animals increases therisk of injury34. Under field conditions is very difficult toevaluate how each environmental factor could influenceLAD morbidity individually, so we chose 3 different farms inthe same area of North of Italy which import same typologyof animals but which differ in management level as reportedin Table 5. In case of poor (farm 3) or fairly good (farm 2)management level, LAD incidence is higher than under verygood managerial conditions (farm 1). Indeed, in farm 1, thedensity per pen is ideal (> 4.5 m2/head), each day new bed-ding material is added, water troughs are proportional in

Number of animals 66,428 32,380 45,608 3,520 17,300 16,800 11,800 3,780

Floor surface Litter Slatted Litter Litter Litter Slatted Slatted Slatted

LAD, % 1,99 2,87 1.19a 3.31b 3.82b 2.89 2.80 2.97Foot diseases, % 0,88 1,43 0.77 0.81 1.18 1.27a 1.91a 0.62b

(% LAD) (44) (50) (65) (24) (31) (44) (68) (21)Arthropathies, % 1,11 1,44 0.42a 2.5b,* 2.64b 1.62a 0.8b 2.35c,**(% LAD) (56) (50) (35) (76) (69) (56) (32) (79)

Table 4 - LAD incidence and floor type in 5 different beef cattle rearing in north of Italy between 2009 and 201060.

Farm

1 2 3 3 4 5

Floor surface(overall results)

*Very good: density >4.5 m2/head, bedding straw added daily, watertroughs with float valve, very good interaction between animals and hu-mans, more than 5 dietary steps.**Fairly good: density 3.5-4.5 m2/head, bedding straw added every 2 days,water troughs with float valve, very good interaction between animals andhumans, 3 to 5 dietary steps.***Poor: density <3.5 m2/head, bedding straw added every 5 days, nose-activated water troughs, poor interaction between animals and humans, 2to 3 dietary steps.a,b,c Different small letters indicate significant difference among means in thesame row (P<0.05).A,B,C Different capital letters indicate significant difference among means inthe same row (P<0.01).

Management Very good* Fairly good** Poor***

Number of animals 9,844 2,082 3,403

LAD, % 1.85a 3.53b 6.03c

Foot diseases, % 0.24A 0.88B 3.46C

(% LAD) (13) (25) (57)Arthropathies, % 1.61a 2.65b 2.57c

(% LAD) (87) (75) (43)

Table 5 - LAD incidence and management in 3 different farms60.

Farm 1 2 3



number and size and the interaction between humans andanimals aims to maximize animal quietness.Management level was also evaluated on the same farmthrough the years in which there were a considerable effortto improve handling facilities, cattle comfort and operativeprocedures. The data collection on the farm represented inFigure 2 was over 10 years. It has a significant positive impacton the LAD incidence and a decrease in the number of ani-mals in the hospital pen. From 1999 to 2011 improvementswere made to facilities, cattle handling resources and man-agement to optimize the production process throughoutproviding an overall reduction in health problems. For ex-ample, space availability per head was increased from 2.5 to4.5 m2, with the added space per animal cattle can lay downmore often. This probably causes less overload on claw andbetter rumination avoiding laminitis-related lameness. Thedecision to group newly received cattle by weight and con-formation was made with the objective of minimizing com-petitive behaviors and possible injury to cattle. Animal han-dling equipment was installed to carry out the conditioningprocedures in complete safety for animals and operators(vaccinations, antibiotic and antiparasite treatments, clip-ping, etc.). Animals were quarantined and an appropriatetransition diet was fed for this period. Ventilation and heatstress abatement systems were installed. Staff was trainedand every procedure was coded with the aim to avoid eachstressful event in particular in the early stages of interactionwith humans.Animal nutrition, ration formulation and feeding strategyare of critical importance to managing LAD, animal healthand productivity. Transition from a grazing environment toabrupt forced feeding of concentrates, ad libitum feed ad-

ministration and full fermentation while maintaining animalhealth and productivity are major challenges to the cattlefeeder. All these aspects are closely related to ruminal acido-sis, and thus to laminitis. Still today, the prevailing thoughtamong experts is that nutritional issues are necessary but notsufficient alone to cause LAD54. However, Table 5 and Figure2 show how a management plan aimed to reduce LAD andother health problems, shall also include very careful nutri-tional planning. Rapid transition to the finishing diet is pos-sible but should be made through several intermediate stepsto promote the correct animal and rumen microbial meta-bolic adaptation. In fact, sudden changes in diet compositioncontribute to metabolic disorders that can cause laminitis.Moreover, to avoid digestive problems and subsequent nutri-tional based lameness, constant quality control of the animalration and nutrients is fundamental. Precision in loading in-gredients in mixing wagon, appropriate particle size, TMRhomogeneity, appropriate integration of vitamins and min-erals for each specific phase, and also attention to raw mate-rials quality55.

DISCUSSION

The results of the studies reported above show that in Italianintensive beef cattle rearing, LAD is an important problemcharacterized by variable incidence and different risk factorscompared to North American rearing. Incidences of LADobserved were significantly variable not only between farmsbut also among groups of cattle of the same farm but housedin different environmental conditions. The high incidence oflameness, makes it one of the major issues concerning cattle

Figure 2 - LAD incidence and management in the same farm through over 10 years60.

a,b,c Different small letters indicate significant difference among means (P<0.05).A,B,C Different capital letters indicate significant difference among means (P<0.01).



welfare34,56,57. Animals affected by foot pain show several pos-tural changes and anomalies in locomotion, which tend to bemore evident the greater the severity of lameness58. Further-more, a chronic painful condition, besides being very stress-ful, leads to a slow healing process, a reduction of feed intakeand production performances, a weakening of heart andlungs activity and increases nervousness and associated dis-eases (i.e. frequent postural changes can lead to muscleweakness or joint injuries)59.Regarding risk factors, subject characteristics are very im-portant. A male Charolaise has a higher weight at arrival,and is more predisposed to LAD. Floor is certainly a riskfactor, but the right choice of which animal will be housedon slatted floor can strongly limit arthropathy incidenceand a proper litter management can prevent foot diseases.In addition to floor type, other livestock facilities and man-agement can limit or promote LAD incidence and severity.For example, lower animal density per pen, a better stafftraining, cooling devices during hot periods and adequatestructures or procedures for containment and handling,can limit the occurrence of traumatic injuries thanks to areduction of cattle nervousness and competitive behaviors.Furthermore feed quality control, proper vitamins andminerals integration and the gradual transition from ar-rival to finishing diet, limit acidosis events and then lamini-tis. Other LAD risks factors, as length and travel conditionor bunk fighting, have to be evaluated in the future to im-prove preventing strategies in beef cattle rearing respectingthe Italian particular situation.

CONCLUSION

A limit of the studies reported is certainly the lack in detec-tion of lameness diagnosis and severity, but the monitoringprocess has been carried out faithfully reflecting what hap-pens in almost all of the intensive beef production systems.Even in case of high LAD morbidity, seldom is the realcause(s) of lameness clearly identified. Diagnostic misin-terpretations based only on visual inspection likely occuroften. With proper animal handling and confinement aproper and complete clinical examination of the affectedanimal and limb can be made. Furthermore, the use of ad-ditional diagnostic procedures and tools, i.e. centesis, x-rayor ultrasonography, can help and speed up the decision-making process not only about the fate of a specific lameanimal but also to identify the cause behind of a wide-spread problem in the herd. In this way specific preventingstrategies can be formulated and adopted to limit drug ad-ministration which may not be necessary in every case oflameness.In conclusion, considering the multiple triggering (micro-bial, mechanical, nutritional, and genetic) and predisposingfactors (subjective and environmental), the clinical condi-tion of lameness in beef cattle could be considered a multi-factorial complex syndrome.

ACKNOWLEDGMENTS

The authors would like to thank Frank Welcome (DVM,Cornell University, Ithaca, NY) for the editorial review.

References

1. Cha E., Hertl J.A., Bar D., Gröhn Y.T. (2010) The cost of different typesof lameness in dairy cows calculated by dynamic programming. PrevVet Med, 97:1-8.

2. Bruijnis M.R., Hogeveen H., Stassen E.N. (2013) Measures to improvedairy cow foot health: consequences for farmer income and dairy cowwelfare. Animal, 7(1):167-175.

3. Collick D.W., Ward W.R., Dobson H. (1989) Associations between ty-pes of lameness and fertility. Vet Rec, 125:103-106.

4. Hernandez J., Shearer J.K., Webb D.W. (2002) Effect of lameness onmilk yield in dairy cows. J Am Vet Med Assoc, 220:640-644.

5. Hernandez J., Shearer J.K., Webb D.W. (2011) Effect of lameness on thecalving-to-conception interval in dairy cows. J Am Vet Med Assoc,218:1611-1614.

6. Amory J.R., Barker Z.E., Wright J.L., Mason S.A., Blowey R.W., GreenL.E. (2008) Associations between sole ulcer, white line disease and digi-tal dermatitis and the milk yield of 1824 dairy cows on 30 dairy cowfarms in England and Wales from February 2003-November 2004. PrevVet Med, 83:381-391.

7. Zecconi A., Sturlesi N., Tarantino S. (2012) Risk factors for hoof disea-ses. Informatore Agrario, 68:68-70.

8. Sagliyan A., Gunay C., Han M.C. (2010) Prevalence of lesions associa-ted with subclinical laminitis in dairy cattle. Isr J Vet Med, 65:27-33.

9. Brizzi A. (2010) Evolution of digital diseases in cattle, structural resear-ch and functional trimming. Which future?. Summa Animali da Red-dito, 5:38-45.

10. Project TADHH (2012) The Alberta Dairy Hoof Helath Project HoofHealth Database.

11. Enting H., Kooij D., Dijkhuizen A.A., Huirne R.B.M., Noordhuizen-Stassen E.N. (1997) Economic losses due to clinical lameness in dairycattle. Livestock Production Science, 49(3):259-267.

12. Fjeldaas T., Nafstad O., Fredriksen B., Ringdal G., Sogstad A.M. (2007)Claw and limb disorders in 12 Norwegian beef-cow herds. Acta VetScand, 49:24.

13. Ahola J.K., Foster H.A., Vanoverbeke D.L., Wilson R.L., Glaze J.B., FifeT.E., Gray C.W., Nash S.A., Panting R.R., Rimbey N.R. (2011) Qualitydefects in market beef and dairy cows and bulls sold through livestockauction markets in the Western United States: II. Relative effects on sel-ling price. J Anim Sci, 89(5):1484-1495.

14. Roeber D.L., Mies P.D., Smith C.D., Belk K.E., Field T.G., Tatum J.D.,Scanga J.A., Smith G. C. (2001) National market cow and bull beef qua-lity audit-1999: a survey of producer-related defects in market cowsand bulls. J Anim Sci, 79:658-665.

15. Miskimins D.W. (2002) Predominant causes of lameness in feedlot la-meness and stocker cattle. Proc: 12th International Symposium on La-meness in Ruminants, Orlando, Shearer J.K., Orlando, 147-151.

16. Persson Y., Soderquist L., Ekman S. (2007) Joint disorder; a contribu-tory cause to reproductive failure in beef bulls. Acta Vet Scand, 49:31.

17. Heinola T., Jukola E., Nakki P., Sukura A. (2006) Consequences of hazar-dous dietary calcium deficiency for fattening bulls. Acta Vet Scand, 48:25.

18. Gagea M.I., Bateman K.G., Shanahan R.A., van Dreumel T., McEwenB.J., Carman S., Archambault M., Caswell J.L. (2006) Naturally occur-ring Mycoplasma bovis-associated pneumonia and polyarthritis infeedlot beef calves. J Vet Diagn Invest, 18:29-40.

19. Gagea M.I., Bateman K.G., van Dreumel T., McEwen B.J., Carman S.,Archambault M., Shanahan R.A., Caswell J.L. (2006) Diseases andpathogens associated with mortality in Ontario beef feedlots. J Vet Dia-gn Invest, 18:18-28.

20. Hewicker-Trautwein M., Feldmann M., Kehler W., Schmidt R., ThiedeS., Seeliger F., Wohlsein P., Ball H.J., Buchenau I., Spergser J., Rosengar-ten R. (2002) Outbreak of pneumonia and arthritis in beef calves asso-ciated with Mycoplasma bovis and Mycoplasma californicum. Vet Rec,151:699-703.

21. Barth A.D., Waldner C.L. (2002) Factors affecting breeding soundnessclassification of beef bulls examined at the Western College of Veteri-nary Medicine. Can Vet J, 43:274-284.

22. Stokka G.L., Lechtenberg K., Edwards T., MacGregor S., Voss K., Grif-fin D., Grotelueschen D.M., Smith R.A., Perino L.J. (2001) Lameness infeedlot cattle. Vet Clin North Am Food Anim Pract, 17:189-207.

23. Davies I.H., Munro R. (1999) Osteochondrosis in bull beef cattle fol-lowing lack of dietary mineral and vitamin supplementation. Vet Rec,145:232-233.

24. Weisbrode S.E., Monke D.R., Dodaro S.T., Hull B.L. (1982) Osteochon-drosis, degenerative joint disease, and vertebral osteophytosis in midd-le-aged bulls. J Am Vet Med Assoc, 181:700-705.

25. Jensen R., Lauerman L.H., Park R.D, Braddy P.M., Horton D.P., FlackD.E., Cox M.F., Einertson N., Miller G.K., Rehfeld C.E. (1980) Limbarthropathies and periarticular injuries in feedlot cattle. Cornell Vet,70:329-343.

26. Jensen R., Park R.D., Lauerman L.H., Braddy P.M., Horton D.P., FlackD.E., Cox M.F., Einertson N., Miller G.K., Rehfeld C.E. (1981) Osteo-chondrosis in feedlot cattle. Vet Pathol, 18:529-535.



27. Reiland S., Stromberg B., Olsson S.E., Dreimanis I., Olsson I.G. (1978)Osteochondrosis in growing bulls. Pathology, frequency and severityon different feedings. Acta Radiol, Suppl 358:179-196.

28. Murphy P.A., Weavers E.D., Barrett J.N. (1975) Epiphysitis in beef cat-tle fattened on slatted floors. Vet Rec, 97:445-447.

29. Griffin D., Perino L.J., Hudson D. (1993) Feedlot Lameness. In: Univer-sity of Nebraska Lincoln Extension: University of Nebraska-Lincoln, 6.

30. Church T.L., Radostits O.M. (1981) A retrospective survey of diseasesin feedlot cattle in Alberta. Can Vet J, 22:27-30.

31. Edwards A. (1984) Preventing Toe Abscesses. In: Feedlot ManagementApril, pp 39-42.

32. Townsend H.G., Meek A.H., Lesnick T.G., Janzen E.D. (1989) Factorsassociated with average daily gain, fever and lameness in beef bulls atthe Saskatchewan Central Feed Test Station. Can J Vet Res, 53:349-354.

33. Panciera R.J., Confer A.W. (2010) Pathogenesis and pathology of bovi-ne pneumonia. Vet Clin North Am Food Anim Pract, 26(2):191-214.

34. Greenough P.R. (2007) Bovine laminitis and lameness: a hands-on ap-proach. Philadelphia: Sauders, Elsevier.

35. Lischer Ch.J., Ossent P., Raber M., Geyer H. (2002) Suspensory struc-tures and supporting tissues of the third phalanx of cows and their re-levance to the development of typical sole ulcers (Rusterholz ulcers).Vet Rec, 151:694-698.

36. Ossent P., Lischer C. (1998) Bovine laminitis: the lesions and theirpathogenesis. In Practice 20:415-427.

37. Plaizier J.C., Krause D.O., Gozho G.N., McBride B.W. (2008) Subacuteruminal acidosis in dairy cows: the physiological causes, incidence andconsequences. Vet J, 176:21-31.

38. Danscherm A.M., Toelboell T.H., Wattle O. (2010) Biomechanics andhistology of bovine claw suspensory tissue in early acute laminitis. JDairy Sci, 93:53-62.

39. Ytrehus B., Carlson C.S., Ekman S. (2007) Etiology and pathogenesis ofosteochondrosis. Vet Pathol, 44:429-448.

40. Tryon K.A., Farrow C.S. (1999) Osteochondrosis in cattle. Vet ClinNorth Am Food Anim Pract, 15:265-274.

41. Trostle S.S., Nicoll R.G., Forrest L.J., Markel M.D. (1997) Clinical andradiographic findings, treatment, and outcome in cattle with osteo-chondrosis: 29 cases (1986-1996). J Am Vet Med Assoc, 211:1566-1570.

42. White S.L., Rowland G.N., Whitlock R.H. (1984) Radiographic, macro-scopic, and microscopic changes in growth plates of calves raised onhard flooring. Am J Vet Res, 45:633-639.

43. Russell A.M., Rowlands G.J., Shaw S.R., Weaver A.D. (1982) Survey oflameness in British dairy cattle. Vet Rec, 111:155-160.

44. Desrochers A. (2004) Septic Arthritis. In: S.L. Fubini, N.G. Ducharme

(ed.) Farm Animal surgery. Missouri: Saunders, pp 330-336.45. Francoz D., Desrochers A., Fecteau G. (2002) A retrospective study of

joint bacterial culture in 172 cases of septic arthritis in cattle. Proc. 20thAnnual ACVIM Forum, 774.

46. Houlihan M.G., Veenstra B., Christian M.K., Nicholas R., Ayling R.(2007) Mastitis and arthritis in two dairy herds caused by Mycoplasmabovis. Vet Rec, 160:126-127.

47. Arcangioli M.A., Duet A., Meyer G., Dernburg A., Bézille P., PoumaratF., Le Grand D. (2008) The role of Mycoplasma bovis in bovine respi-ratory disease outbreaks in veal calf feedlots. Vet J 177:89-93.

48. Dutra F., Carlsten J., Ekman S. (1999) Hind limb skeletal lesions in 12-month-old bulls of beef breeds. Zentralbl Veterinarmed A, 46:489-508.

49. McDaniel B.T. (1997) Genetics of conformation. In: P.R. Greenough(ed) Lameness in Cattle, Philadelphia, W.B. Saunders, 75-78.

50. Baggott D.G., Russell A.M. (1981) Lameness in cattle. Br Vet J, 137:113-132.

51. Sgoifo Rossi C.A., Compiani R. (2011) Bovine mycotoxicosis. LargeAnim Rev, 17(6):237-245.

52. Midwest plan service (1976) Livestock waste facilities handbook. IowaState University, 6.

53. Panivivat R., Kegley E.B., Pennington J.A., Kellogg D.W., KrumpelmanS.L. (2004) Growth performance and health of dairy calves beddedwith different types of materials. J Dairy Sci, 87:3736-3745.

54. Brizzi A. (2007) How to manage feeds for preparing efficient rations.Informatore Agrario, 63(38):45-48.

55. Gremmels J.F. (2008) The role of mycotoxins in the health and perfor-mance of dairy cows. Vet J, 176:84-92.

56. Shearer J.K., Stock M.L., Van Amstel S.R., Coetzee J.F. (2013) Asses-sment and Management of Pain Associated with Lameness in Cattle.Vet Clin North Am Food Anim Pract, 29:135-156.

57. Bruijnis M.R., Beerda B., Hogeveen H., Stassen E.N. (2012) Assessingthe welfare impact of foot disorders in dairy cattle by a modeling ap-proach. Animal, 6:962-970.

58. Sprecher D.J., Hostetler D.E., Kaneene J.B. (1997) A lameness scoringsystem that uses posture and gait to predict dairy cattle reproductiveperformance. Theriogenology, 47:1179-1187.

59. Whay H.R. (2009) A decade of pain: a look back over ten years of di-scovery about pain associated with lameness in cattle. In: Proceedingsof Cattle Lameness Conference, School of Veterinary Medicine andScience University of Nottingham, Leicestershire, 19-22.

60. Sgoifo Rossi C.A., (2011) Importanza delle patologie agli arti nell’alle-vamento del vitellone da carne. Proc: XIV Congresso Internazionale SI-VAR, Palazzo Trecchi, Cremona Italy, 6-7 maggio 2011.


Documents

Dealing with lameness in Italian beef cattle rearing N...Lameness is one of the main health and economic issues concerning dairy and beef cattle production systems. Lameness is a Lameness