Tularemia in a cat and capybara

Tularemia in a cat and capybara

This post combines two cases Tularemia: the cat and capybara have no relation

History: A 2 year-old male DSH cat had a leg wound 1 week prior, then stopped eating and drinking, became laterally recumbent and depressed.  Temperature, pulse and respiration were within normal limits, PCV was 22% with a neutrophilic leukocytosis and left shift.   The capybara was a captive zoo animal living with several capybaras. Several had severe bloody diarrhea and one died.  It was necropsied by the referring veterinarian who described necrotizing enteritis as the primary gross lesion and submitted fixed tissues for histopathology.

Gross findings: 

Cat: The sclera was icteric, and the left hind-limb hada  2 cm ulcer over the left lateral aspect of the tarsus and tibia with swollen subcutis.  The spleen contained many 1mm diameter white foci that were ell-circumscribed. The liver contained many 1mm white foci. The lung was edematous, dark red, and contained many 2-3mm white foci.  The intestines contained tarry black feces but no other lesions. Many lymph nodes were necrotic with white foci.

Spleen from cat: The capsular surface is raised by well-demarcated white foci that extend into the parenchyma diffusely



Spleen: Multifocal random necrotizing suppurative splenitis, severe

Spleen, low power magnification, HE stain: At low power there are multifocal random areas of necrosis and suppurative inflammation (purple foci). These dead cells are most likely neutrophils that migrated into the spleen, or pre-existing lymphocytes.

Spleen from cat, HE stain: The white foci seen grossly correspond to these areas of necrotic debris consisting of necrotic and lysed neutrophils, lymhpocytes and red blood cells and splenic stromal cells lined by a rim of intact neutrophils and macrophages

Liver: Multifocal necro-suppurative hepatitis, moderate, generalized

Cat liver at high magnification, HE stain: The liver also contained grossly visible white foci corresponding to these areas of necrotic neutrophils mixed with necrotic hepatocyte debris. These foci are also circumscribed by macrophages and intact neutrophils.

Skin: Focal necrotizing panniculitis, and ulcerative dermatitis with vascular thrombosis

Skin, low power from the cat: The leg wound had severe necrotizing and suppurative cellulitis involving the panniculus, muscle and dermis, with vascular thrombosis (lower right corner)

Lymph nodes: Diffuse necro-suppurative lymphadenitis, severe

Lungs: Multifocal necro-suppurative pneumonia

Stomach: Suppurative gastritis, multifocal, mild

Large intestine: Intraluminal hemorrhage, severe


Intestine: Diffuse transmural necrotizing enteritis, severe

Lungs: Multifocal necrotizing pneumonia, moderate, generalized

Lymph nodes: Diffuse necrotizing lymphadenitis, severe


All affected tissues in the capybara and cat were positive with IHC for Francisella tularensis.

Ancillary findings:

Cat: Francisella tularensis cultured positive

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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 www.vgl.ucdavis.edu and www.vetgen.com.


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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