Pathology of the distal third metacarpal/metatarsal bone and incidence of lateral condylar fractures in New York State Thoroughbred race horses:42 cases from 2013-2014

Pathology of the distal third metacarpal/metatarsal bone and incidence of lateral condylar fractures in New York State Thoroughbred race horses:42 cases from 2013-2014

N-14 ACVP Atlanta, GA 2014

Brian G Caserto, Cornell University College of Veterinary Medicine, Department of Biomedical Sciences, Ithaca, NY


Degenerative changes in the distal metacarpus/metatarsus are commonly recognized in racehorses. Grading is based on the appearance of the surface cartilage which has limitations in evaluating the underlying subchondral and epiphyseal bone. Progressive changes in the bone density of the distal metacarpal condyles can be observed and categorized by gross examination of longitudinal sections through the midpoint of the condyles. In this series, condylar fractures occurred in lateral condyles only. Condyles from thirty-nine (42) racehorses from 2013-2014 were graded according to an established scoring system, and were additionally categorized by newly described patterns of epiphyseal sclerosis; Normal, Focal subchondral, Bridging , or Diffuse.  Eight horses with 9 lateral condylar fractures (4 left unilateral; 3 right unilateral; 1 bilateral) were found with 77.8% (7/9) of fractured condyles having Bridging epiphyseal sclerosis and 22.2% (2/9) having Focal subchondral sclerosis. No condylar fractures occurred in horses having normal epiphyseal trabecular bone density or diffuse epiphyseal sclerosis. Pre-existing pathology is often cited as a risk factor for catastrophic musculoskeletal injury in racing horses. In this series, grade of condylar arthrosis had no correlation to the pattern of subchondral sclerosis, epiphyseal bone density, or incidence of fracture.  However, gross examination of distal metacarpal/metatarsal condyles is able to  subjectively categorize the pattern of epiphyseal sclerosis, and the large proportion of bridging sclerotic condyles incurring catastrophic fractures suggests that this maladaptive change in bone density is a possible risk factor for lateral condylar fractures resulting in breakdowns in New York State Thoroughbred race horses.

Metacarpal arthrosis vs Palmar/Plantar Osteochondral Disease:

Pathology involving the palmar/plantar aspect of the subchondral bone has been called a variety of names including “metacarpal arthrosis” and palmar/plantar osteochondral disease”. Whichever term is used this refers to several progressive degenerative changes occurring on the palmar apical region of the distal metacarpal/metatarsal condyles of athletic horses. This suite of changes begins with suhchondral sclerosis in a semi-circular pattern:

Distal condyle, early subchondral sclerosis in a focal pattern, with relatively porous (normal) epiphyseal bone

From here several things can happen:

1) The epiphysis progresses to bridging or diffuse sclerosis with no osteochondral disease:

Advanced case of bridging sclerosis, nearly progressed to diffuse, but as yet no subchondral bone defect

Severe bridging sclerosis also with no osteochondral disease


2) The subchondral bone becomes damaged by repeated impact during exercise. What happens to the subchondral bone progresses in stages:

– Microcracks can form in the zone of mineralized cartilage and subchondral bone, and shrunken vascular spaces are damaged causing hemorrhage and localized hypoxia.

Microcracks form in the subchondral bone and zone of mineralized cartilage adding to the devitalization of the subchondral bone, that prevents proper repair.

Larger cracks and fissures form as a precursor to morselization

Hemorrhage within vascular spaces is an early lesion of repetitive injury

-Followed by disruption of the subchondral bone into many small pieces called “morselization” – This grossly looks yellow to brown due to hemorrhage and necrosis.

The subchodnral bone is fragmented into many small pieces by repeated impact trauma. The overlying cartilage is relatively normal.

–  This often causes a depression, flattening or defect in the overlying articular cartilage since the subhcondral bone plate is destroyed focally.

Grade 3 arthrosis/osteochondral disease in both condyles. The discoloration is due to the hemorrhage and necrosis of the underlying bone.

Severe subchondral necrosis (osteochondral disease) in a diffusely sclerotic epiphysis. The surface is flattened, and the bone has only begun to heal.

What Happens to these lesions over time?

– Over time these regions can become re-vascularized and begin to heal:

1) first resorbing the crushed subchondral bone, and forming new dense trabeculae in its place.

Early remodeling of moralized subchondral bone, showing reversal lines perpendicular to the lamellar bone, with woven born added to it

-Healing may take place before collapse of the articular surface, and in mild cases the surface may retain its shape and contour with no lasting effects.

-In more severe cases, the articular surface is changed permanently.

Secondary changes to the overlying cartilage include initially thickening of the cartilage, as it swells with absorbed joint fluid. This then becomes softer, and more prone to mechanical damage, and results eventually in fibrillation or a flap forming.

Late stage of osteochondral disease with fibrillation of the articular cartilage. Notice the subchondral bone is composed of woven osteoid indicating proliferative response and attempt at repair. In this case the contour of the surface is relatively unchanged

In some cases the cartilage collapses and dips into the subchondral bone forming a fold:

Aging healing osteochondral defect with a folding of the articular cartilage and a small rim of brown discoloration indicating past hemorrhage

A gross image of the above lesion, an advanced case of arthrosis/osteochondral disease. On the left side there is swelling of the overlying cartilage secondary to subchondral bone changes. On the right the surface is collapse as seen in the cross section above.

Progressive degenerative joint disease is possible in the long term, however these are nearly clinically undetectable without CT or MRI, and in most cases do not affect racing performance or cause lameness.

The pathogenesis of these lesions is a subject of debate. Increased bone density is thought to lead to ischemia of the bone. However ischemic bone is still structurally sound, so by itself the reduction in vascular supply secondary to sclerosis is only a predisposing factor.

Microcracks in the zones of mineralized cartilage, and subchondral bone often occur at the periphery of the morselized regions, and in my opinion are a precursor to moreselization.  Increased bone density does lead to reduced size of vascular channels, and rigid brittle bone, which predisposes these regions for micro cracks without healing, and further moreselization that will occur.

Epiphyseal Bone Density

In this case series I focused on the gross appearance of the lateral condyles. Serial longitudinal sections through lateral and medial condyles of the right and left limbs provided insights into the variety of progressive bone changes in the epiphyses of these bones.

Sclerosis of the condylar epiphyseal trabeculae was grouped into 4 categories with. Osteochondral defects were not considered in these categories and were treated separately

Mechanical forces acting on the condyles influence the degree of bone density and the pattern of progression. In most horses the medial condyles are larger, wider, and progress to increased bone density faster than the lateral condyles. Undoubtedly there are conformational factors affecting the weight distribution onto the condyles that affect the forces and therefor the bone remodeling in the distal metacarpal bones.

Fractures occurred in the lateral condyles only in these horses, with roughly equal distribution between left and right forelimbs, and the right hind limbs in 3 cases.

Often the degree of density is directly related to the time in training, and not necessarily to age. Based on my observations, I can see several patterns of increased bone density. Young horses with only 1-2 years of training often have a mild increase in bone density, with the bone appearing porous throughout the epiphysis. This I categorized as “Normal”.

With more high speed training a focal region corresponding to the palmar apical area becomes sclerotic, and is distinctly less vascular, and appears as a continuous white region beneath the cartilage. This can occur with or without arthrosis. This pattern I have categorized as Focal subchondral sclerosis, or “Focal”.

In several cases, it can be demonstrated that  with more exercise, the focal regions can extend through the epiphysis, widening and eventually bridging the opposite side of the condyle at the dorsal base of the condyle. This pattern often excludes the subchondral bone adjacent to the palmar apical crescent, and because of this I call this a “Bridging” pattern.   This pattern can eventual progress to  the next category.

The final category can arise in two ways. First, it can progress from the bridging sclerotic change. Secondly it can also develop without going through the bridging phase, and arise simply as a uniform increase in bone density throughout the epiphysis.   The reason for this I believe is simply a mechanical influence resulting from conformation and training.

Osteochondral disease and the relationship to lateral condylar fractures

All lateral condyles were graded, in the left and right limbs of each horse examined. Fractures decreased in incidence as the prevalence of each grade decreased. Most horses fell into the grade 0 category, and the least number in grade 3.

Fracture incidence by sclerotic pattern

Lateral condyles were compared in both left and right limbs. The majority of these were categorized as diffuse sclerosis, having sufficiently dense bone throughout the epiphysis. The next frequent categories were focal, and normal, and these two had the least number of fractures. By far the smallest category was bridging, but it had the majority of fractures, and these outnumbered the cases of bridging sclerosis where no fracture occurred.


Bridging sclerosis may be a risk factor for lateral condylar fractures that could potentially be identified by CT or MRI.  Several studies, and also a poster in this conference have studied the subchondral osteochondral disease in racehorses and attempted to correlate the grade of arthrosis with incidence of fractures or breakdowns. I think the focus on these defects is not warranted based on the above results. Rather, the entire epiphysis should be examined since it seems to have a better association with lateral condylar fractures.

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What’s Your Diagnosis #6

What’s your diagnosis #6

History: A 15 month old Angus steer became recumbent and could not rise.

What are some differential diagnoses for acute weakness and recumbency in cattle?


The steer was treated with thiamine and penicillin, but  was eventually euthanized for diagnostic purposes. Three other animals have died acutely.

Gross Necropsy Findings:

The steer was in good body condition. The rumen contained coarse plant fibers and chopped cornstalks, with no grain. The rumen pH was 7.4. The brain did not fluoresce under UV light.

There were no significant gross lesions.


Differential Diagnoses for acute recumbency:


Polioencephalomalacia (thiamine deficiency, lead toxicity)

Lymphoma (spinal)


Thrombotic Meningoencephalitis



Septic meningitis


Calcium deficiency

Magnesium deficiency (grass tetany)

Salt toxicity/water deprivation


Blackleg (Clostridium chauvoei)





Urea toxicity

Nervous Ketosis

Nervous Coccidiosis

Abomasal displacement


Systemic bacteremia


Considering the signalment and gross necropsy findings many of these diseases can be ruled out or down.  This is not a lactating cow (its a steer), so hypocalcemia, and hypomagnesemia are less likely. There is no evidence of septic peritonitis, abomasal bloat, or meningitis.  There is no enteritis suggesting coccidiosis, and no rumen acidosis. There was no sign of skeletal muscle necrosis, fractures, or joint diseases, and no sign of lymphoma.

Remaining differentials include: Polioencephalomalacia, Urea toxicity, BSE, Rabies, Listeriosis, or TME

What would you expect to see histologically in each of these conditions?

Stay tuned for histopath…

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Polioencephalomalacia in a calf

Polioencephalomalacia in a calf

History:  A 1 month-old Charolais cross was submitted for necropsy, from a herd where several were found acting “goofy” and walking in circles with foam and blood coming from their mouths. They died within 1 hour of symptoms. The calves were fed “wet cake” from an ethanol plant.

Gross Necropsy Findings:

The calf was in good body condition. There were no gross abnormalities. The brain did not fluoresce under UV light.


Brain, cerebrum: there is mild multifocal necrosis and degeneration of the superficial to middle laminar cortical neurons, characterized by cellular and nuclear pyknosis, hypereosinophilic, angular cell borders, and occasional rarefaction of the surrounding neuropli. There is multifocal hypertrophy of capillary endothelial cells, and a few macrophages in Virchow-Robbins spaces surrounding vessels.

Cerebrum, low power: The arrow marks the junction of the normal neuropil (lower left)from the rarefaction (upper right) indicating the abnormal neuropil

Cerebrum, higher power: A closer view shows the rarefaction (clear spaces) centerer around neurons in the superficial to middle lamina of neurons

Cerebrum, high power: The arrows indicate neurons undergoing necrosis, with eosinophilic cytoplasm, angular cell borders, and pyknotic nuclei. There is also few perivascular mononuclear cells (macrophages) around small blood vessels.

Morphologic Diagnosis:

Brain, cerebrum: Mild, multifocal laminar cortical necrosis and endothelial hypertrophy

Lab Results:

Listeria culture: Negative

Lead Toxicology: Liver =  24.67 ppm (toxic)/ Kidney = 99.29 ppm (toxic)


This is a case of lead toxicity causing laminar cortical necrosis or Polioencepahlomalacia in calf.  The mild lesions pose a contrast to the severity of clinical signs, probably as a function of the acute nature of the illness. The source of the lead was never discovered int his case.

Based on the history and described clinical signs initial differentials were thiamine deficiency (Wet Cake = distiller grain = high sulfur = thiamine deficiency), and listeriosis (unusual in a calf this young, but considered based on “circling” and multiple animals affected).  Listeria culture was negative, and based on the lead toxicology results thiamine deficiency is less likely.

Poliencephalomalacia in ruminants can be caused by thiamine deficiency (Bracken fern, Sulfur, grain overload), lead, and cyanide poisoning. It has also been described in salt poisoning in swine. In young animals PEM may cause acute death with only swelling of the brain or cerebral edema.


Maxie, M.G. and Youssef, S. Nervous System. Chapter 3 in Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals, 5th edition, M. Grant Maxie editor. 2007. Saunders, Elsevier.

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Glycogen Branching Enzyme Deficiency in a foal

Glycogen Branching Enzyme Deficiency in a foal

History: A 1 week-old male Quaterhorse was submitted for necropsy. At 12 hours old he nursed 3 times but became progressively recumbent and failed to nurse. Upon arrival to the referral hospital he was laterally recumbent with poor mentation. Initial blood chemistry revealed blood glucose of 93 mg/dL, BUN 27 mg/dL, Creatinine of 4.3 mg/dL, lactate of 2.2 mmol/L, CK > 30,000 u/L, and hypoproteinemia. Muscle biopsies were sent to the University of Minnesota. CBC indicated left shift. Later CBC/Chem indicated leukopenia, anemia, hypoproteinemia, hyperfibrinogenemia, and hyperglycemia. He died acutely.

Gross Findings:

The foal was thin with minimal body fat stores. The cranial lung lobes were bilaterally dark red, and firm. There was mild interlobular edema and collapse of the cranial lung lobes. The trachea, primary bronchi, and itra-lobular bronchi contained serous and fibrinous exudate.

The skeletal muscles were diffusely soft pale and pink.


Skeletal muscle: There is mild multifocal myocyte degeneration and necrosis. Diffusely large numbers of myocyes contain intracytoplasmic pale basophilic round inclusions which replace the sarcoplasm. Myocytes also have pale vacuoles in the cytoplasm.

Heart: Cardiac myocytes are similar to skeletal muscle. The most striking feature is the large basophilic inclusions in Purkinje fibers.

Heart, Skeletal muscle PAS w/ glycogen digestion: Both the pale basophilic inclusions and the pale vacuolar areas in the cytoplasm are positive with PAS/with glycogen digestion (using diastase or amylase).

Heart, H&E stain: Cardiac myocytes contain pale basophilic inclusions and often have pale vacuolated areas

Heart, PAS/Amylase: PAS positive material (dark purple) is found as clumps of granular subtance in myocytes, and as smooth round inclusions. This is not digested with amylase indicating its not normal glycogen, rather some abnormal polysaccharide

Hear, H&E stain: IN the center the Purkinje fibers contain large pale basophilic inclusions

Heart, PAS/amylase: Amylase resistant polysaccharide bodies coincides with the pale basophilic inclusions, and the pale vacuolar areas

Normal Heart, PAS/amylase: Normal glycogen is digested by amylase and is not present in normal heart from a control animal

Normal Muslce, PAS/amylase: Normal glycogen is digested by amylase leaving no PAS positive material in cells

Morphologic Diagnosis:

Skeletal muscle: Generalized multifocal myocyte necrosis, with diffuse pale basophilic amylase resistant sarcoplasmic inclusions, and amylase resistant polysaccharide.

Heart: Diffuse cardiomyocyte and Purkinje fiber inclusions and amylase resistant polysaccharide.


Glycogen Branching Enzyme Deficiency is an inherited defect in an enzyme that creates branches in glycogen for storage in tissues.  This disease is similar to the Type IV glycogenosis in humans (glycogen storage disease caused by a deficiency in alpha-1,4-glucan 6-glycosyl transferase). It is also similar to adult polyglucosan body disease in humans, also caused by a defect in a glycogen branching enzyme.  Organs affected with these disease include liver, CNS, PNS, and muscles.  The defect is an inherited autosomal recessive mutation in the GBE1 gene, causing a premature stop codon. This mutation results in poorly functional enzyme and therefore poorly branched glycogen, which is not capable of being transformed into glucose by debranching enzyme.

The University of California Davis and Vetgen are  licensed  to conduct testing to test a foal, mare or stallion for carrier status.  You can find more information at and


Ward, T.L. et al. 2004. Glycogen branching enzyme (GBE1) mutation causing equine glycogen storage disease IV. Mammalian Genome vol 15: 570-577.

Valberg, S.J. et al. 2001. Glycogen Branching Enzyme Deficiency in Quarter Horse Foals. J. Vet. Intern. Med. Vol 15:572-580.

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Canine Adenovirus Pneumonia in 2 puppies- CAV-2

Canine Adenovirus Pneumonia in 2 puppies- CAV-2

History: Two English Bulldog puppies (1, and 3 weeks old) had trouble breathing in the morning and by noon had died.

Gross Necropsy Findings:

Lungs: Diffuse dark red to purple, edematous.

Histologic Findings:

Lung: At low power, centered around bronchioles and extending into the interstitium are cellular infiltrates. Bronchiolar epithelium is sloughing off the basement membranes

Lung: At higher power, centered on a bronchiole there is necrosis and sloughing of respiratory epithelium. Epithelia contain nuclear inclusions which fill the nucleus or marginate the chromatin (arrow)

Lung, bronchiole at high power: Intranuclear inclusions are visible, and the lumen of the bronchiole contains necrotic cell debris and degenerate neutrophils, indicating a bacterial component secondary to loss of epithelial defenses.

Lungs, alveolar spaces: The lung is collapsed, alveolar capillaries are congested, and there is necrosis of type 1 pneumocytes, and intranuclear inclusions. There are a few neutrophils present.

Lungs: Multifocal necrosis of bronchiolar respiratory epithelium and alveolar pneumocytes. Alveolar septa are expanded by moderate numbers of macrophages, lymphocytes, plasma cells, and neutrophils (degenerate and intact). Respiratory epithelia contain large basophilic intra-nucelar viral inclusions that displace the chromatin. There is diffuse vascular congestion.

Liver: There are multifocal areas of hepatocellular necrosis with small numbers of macrophages. There are small numbers of macrophages in the portal areas. There is diffuse vascular congestion.

Morphologic Diagnosis: 

Lungs: Multifocal to coalescing broncho-interstitial pneumonia, necrotizing, lymphoplasmacytic and neutrophilic, severe, with intraepithelial intra-nuclear viral inclusions.

Liver:  Multifocal, random, hepatic necrosis, moderate

Bacterial cultures: Small numbers of  non-hemolytic E coli were cultured from the lungs and liver, and small numbers of Klebsiella spp were cultured from the lungs.


The features of the pneumonia are diagnostic for Canine Adenovirus type 2.  This disease affects unvaccinated juvenile dogs and is distinct from disease caused by Canine Adenovirus type 1 (Infectious Canine Hepatitis).  Infections may be mild particularly in vaccinated animals, and limited to the upper respiratory tract, producing a serous or catarrhal rhinitis or tracheitis.  Disease in the lungs is severe when complicated by bacterial pneumonia.  In this case the disease was peracute, the lesions are necrosis with only moderate cellular infiltrates, and no type 2 pneumocyte hyperplasia which takes at least 3-4 days to appear. Bacterial cultures indicate a possible complication with bacterial pneumonia. Common bacterial causes of pneumonia in dogs do include E coli, particularly in newborn pups, as well as Klebsiella pneumoniae, Bordetella bronchiseptica, Pasteurella spp, and Streptococcus spp.  Multifocal hepatic necrosis indicates bacterial sepsis and likely contributed to the acute death in these pups.


Lopez, Alfonso. Respiratory System, Chapter 9 in Pathologic Basis of Veterinary Disease 4th edition, McGavin, M.D., and Zachary, J.F. editors. 2004 Mosby Elsevier.

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