Unusual tumor of the zygomatic arch in a Dog

HISTORY: 10 year old female spayed Japanese Chin developed a mass on the right zygomatic arch. Radiographs showed regions of bone lysis and proliferation and invasion of the right temporalis muscle.


The zygomatic bone is effaced by an expansile locally infiltrative, poorly cellular neoplasm of mesenchymal cells arranged in small whorls and streams in an abundant sclerotic collagenous stroma with ossification of the stroma and remodeling forming marrow spaces in the central regions. Neoplastic cells have indistinct cell borders, scant cytoplasm, and are fusiform. Nuclei are flattened, ovoid, and often hyperchromatic, with some at the periphery having finely stippled chromatin. At the leading edge of the tumor the reactive bone forms a shell around the tumor, and is being lysed as the tumor expands and infiltrates. In some areas the neoplasm infiltrates and expands the surrounding skeletal muscle, and forms small whorls which advance out from the main mass.

1509180018 zygomatic 2x2

Low power view of zygomatic arch tumor, showing some connection to the bone in the lower left corner, and the extension into the muscle into the upper left corner. The mass is haphazardly ossified, and interspersed with dense hypocellular fibrous tissue.

1509180018 zygomatic 10x1

High power magnification at one edge of the tumor where it was less ossified, showing a hypocellular whorling mass of fibrous tissue eroding the surrounding reactive bone to the right of the image. This shell of reactive bone is indicative of a moderately growing mass. Slower growing tumors may have lamellar bone at the periphery while more rapidly growing tumors efface any reactive bone.

1509180018 zygomatic 10x2

Moderate magnification of the center of the mass, in a region where the fibrous tumor is effacing islands of reactive woven bone. The woven bone is bordered by flattened to plump osteoblasts and loose connective tissue, but in some areas the fibroblastic tumor erodes them. In the center there is a whorl of fibrous tumor with a small area of mineralization. This is deceptive, as it can be interpreted as bone produced by the tumor. But in this case, this is simply mineralization of a dense collagenous stroma, which can occur in the right microenvironment.

1509180018 zygomatic 20x1

High magnification view of a region of mineralizing tumor stroma. Notice the blending of collagen fibers of the tumor with the surrounding bone, and in the center the slight stippling of basophilic stroma indicating small areas of mineral deposition that are independent of osteoblasts.


Right zygomatic arch: Low grade sclerosing fibrosarcoma with osseous metaplasia


This is an uncommon tumor which most likely arose from either the periosteum or medullary cavity of the zygomatic bone.  Differentials included were benign fibro-osseous tumors such as ossifying fibroma, or fibrous dysplasia, however the bone produced seemed to be eroded by the tumor stroma as it advanced, and did not seem to be produced by it. The central regions of osseous metaplasia were formed by calcification of the haphazard collagenous fibers produced by the tumor, which can be seen using polarized light microscopy.  As the tumor matrix mineralized it then became fair game for the resident osteoclasts and osteoblasts to begin laying down reactive woven osteoid thereby forming the ossified portions of the tumor. The remodeling that has occurred is a factor of the prolonged time course and slow growth rate of this tumor.

A google search for the term sclerosing fibrosarcoma will find a medical diagnosis of “sclerosing epithelioid fibrosarcoma”, which has a particular histological appearance that this tumor did not share. The term “sclerosing fibrosarcoma” is more a descriptive term, and one given to me Dr Roy Pool from Texas A&M when I consulted him on this tumor. Perhaps this may become a distinctive entity in veterinary medicine as more cases are described and recognized. The biological behavior appears to be less aggressive than other fibrosarcomas of bone, and should be differentiated from the highly aggressive entity of the “histologically low-grade, biologically high-grade fibrosarcoma” of the mandible and maxilla.

The closest human analog to this tumor is the desmoplastic fibroma, but again the histological appearance is distinctive.  The word “desmoplastic” refers to the crimped collagen fiber appearance in this tumor which resembles tendon fibers (desmos: A bond, fastening or chain; ie desmitis -inflammation of a tendon). The tumor in this bone does not share this type of collagenous fiber arrangement.

Initially, prior to histopathology, I was expecting a multilobular tumor of bone (MLTB; Multilobular osteochondrosarcoma) given the location. These tumors appear to be associated with bone symphyses and suture lines (skull, hard palate, maxilla, mandible, zygomatic bone). The microscopic architecture is usually characteristic, however it is said that as these become high grade this architecture is lost. Differentiating a high grade MLTB from an osteo- or chondrosarcoma can be difficult, but in my experience there are regions of spindle cell sarcomatous sheets and bundles that are not seen in chondrosarcoma, and there is no convincing bone produced. This probably reflects the fibro-osseous origin of the tumor. Nevertheless the tumor in this case is very low grade, and had no features in common with a MLTB.

If anyone has seen a similar tumor in the skull or long bones I would appreciate hearing about it.


Desmoplastic fibroma of bone: A report of 8 cases and review of the literature. J Bone Joint Surg Am. 1985 Jun;67(5):732-47.

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VetPath Services

It’s been so long since my last post. Partly because I was keeping busy examining racehorse breakdowns for New York. You can see the results of these exams here.


Since then I’ve traveled to Brisbane for 6 months, and worked at Idexx. As fun as it was to work in Brisbane, when VetPath Services, in Stone Ridge, NY opened a position I couldn’t pass up the opportunity.

Let me tell you about VetPath Services, and why this is a superior lab.

  • Experience: Jim Walberg founded this lab after years of experience in diagnostic pathology labs, and his expertise extends into many areas within anatomical and clinical pathology, dermatopathology, gastrointestinal diseases, bone diseases and oral tumors, primate pathology, and lab animal pathology. Check out Jim‘s and my blurb at the website. Add to this my own experience in bone and joint pathology, oral and dental and nasal diseases, as well as well-rounded knowledge of skin disease, GI, liver, renal, and reproductive diseases.
  • Quality: Jim and I review every slide that comes out of the lab, and take direct part in trimming complex cases, processing fluids, and reviewing reports. It is rare to find such quality control in a busy diagnostic lab, and this often results in delays, errors, or miscommunication.
  • Consistency: Jim and I work together to review complex cases and those that require additional expertise. Its rare to find a lab with consistent diagnoses between pathologists. We strive to come to agreement on difficult and complex cases, and can offer a wealth of advice on additional testing that can help make the diagnosis.

I’m looking forward to many great years getting to know the clients of VetPath Services.

I will continue to post interesting cases I’ve collected from Kansas, Cornell, Brisbane, and Stone Ridge, and I am working on adding a more extended Orthopedic Path section, as well as oral tumors, and nasal disease sections. Stay tuned….

Brian G. Caserto


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Diagnosis- What’s your diagnosis #6

What’s your diagnosis #6

See original post here

Continue for Diagnosis…

History: a 15 month old Angus steer went down acutely and was euthanized.

Gross findings were unremarkable.


Brain: In the gray and white matter of the caudal cerebrum, midbrain, and cerebellar peduncle there are multifocal perivascular infiltrates of lymphocytes and fewer neutrophils. There are randomly scattered multifocal areas of necrosis with moderate numbers of neutrophils, lymphocytes, macrophages, microglia and astrocytes (microabscesses). There is a single arteriole with a predominantly eosinophilic infiltrate with fewer lymphocytes.

Brainstem:  There are bilaterally symmetric focal areas of severe necrosis with large numbers of macrophages, neutrophils, lymphocytes, and a few multinucleated giant cells. The meninges are multifocally thickened with moderate numbers of lymphocytes and macrophages. Within areas of necrosis are large expanses of spongiosis with myelin sheath swelling, axonal spheroid formation and digestion chambers with Gitter cells (foamy macrophages).

Brain: At low power there are multifocal areas of necrosis and suppurative inflammation, and perivascular cuffing

Brain: At high power the neuropil is fragmented, and neurons are not visible, instead there is cell debris and neutrophils and increased numbers of glial cells including microglia

Brain: Some areas have large macrophages, or reactive astrocytes with abundant eosinophilic cytoplasm which are cleaning up and repairing the damaged neuropil

Brain: Some areas have focal gliosis, which is interpreted as a region of healing (glial scarring)

Brain: Perivascular cuffing ins prominent in some areas; cells consist of lymphocytes, macrophages and some neutrophils.

Brainstem: At low power there are areas of spongiosis (clear spaces; swollen myelin sheaths).

Brainstem: At higher power there is loss of axons, and numerous clear spaces containing large eosinophilic spheroids (swollen damaged axons), and Gitter cells in axonal spaces.

Morphologic Diagnosis:

Brain and brainstem: Meningoencephalitis, necrotizing, suppurative, multifocal, severe, with lymphocytic cuffing


Immunostaining revealed the presence of Listeria monocytogenes in the CNS microabscesses.

Brain, Immunohistochemistry: The red foci indicate positive staining for Listeria monocytogenes

Diagnosis: Listeriosis


Listeria sp are Gram-positive facultative anaerobic bacilli found in the environment. It is hardy, and able to survive in temperatures ranging from 4-45 degrees C. It is an intracellular pathogen of macrophages, neutrophils,  and epithelial cells. Virulence factors include the surface protein internalin,  which internalizes with E-cadherin to overcome the intestinal, placental, and blood brain barriers. It also has a cholesterol-binding hemolysin to lyse phagosomes and escape into the cytoplasm. The organism proliferates in the host cytoplasm and migrates against the cell membrane to form protrusions that can be taken up by other cells. It can use the host cell actin filaments to help cell-cell transfer.

Disease syndromes usually dont overlap. Infection can cause abortions, septicemia, and encephalitis. Septicemia Listeriosis occurs in fetuses, neonates and young large animals up to 1 year of age resulting in generalized visceral abscesses.  Encephalitis is almost solely found in adult ruminants, and may be sporadic or associated with outbreaks.  Listeria can grow in spoiled silage that is incompletely fermented. It invades the oral mucosa and invades the trigeminal nerves traveling to the brain.  Lesions not seen in this case include vasculitis.

Of the competing differentials most can be confirmed by histopathology.

BSE: Histologic lesions include vacuolation of brainstem neurons and immunohistochemical confirmation is possible.

Polioencephalomalacia: Characteristic laminar cortical necrosis, with possible mild endothelial hypertrophy, and perivascular histiocytic cells. The same lesion occurs with thiamine deficiency and lead toxicity.

Rabies: Characteristic Negri bodies (eosinophilic intracytoplasmic inclusions) in neurons with perivascular lymphocyte cuffing.

Urea/Ammonia toxicity: There are no characteristic histologic lesions that I am aware of. In horses ammonia toxicity causes Type II Alzheimer cells, which are a type of reactive astrocyte. This has not been described as a feature of cattle with ammonia toxicity. The alkaline rumen pH may have made this a consideration.  7.4 is pretty alkaline for the rumen, and may indicate the presence of ammonia, the by product of urea metabolism by rumen flora.

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Cerebral abscess in a foal- Streptococcus equi

Cerebral Abscess in a foal- Streptococcus equi


A 4 month old intact female Quarterhorse with nasal discharge and mandibular lymphadenopathy. Despite treatment the foal became neurologic: ataxia, wobbly, and head pressing.  Neurologic exam revealed an intention tremor when head raised and no left menace but direct PLRs were normal. A CBC revealed 600mg/dl fibrinogen and 11,100/ul neutrophils. A CT scan performed 7/14/09 revealed large mass in the right cranium. The owner elected euthanasia.

There is a current strangles outbreak on the farm. The brain mass indicates strong suspicion of abscess as complication to strangles.

Gross Findings:

The carcass was in good body condition, fresh with no autolytic changes. The guttural pouches bilaterally were filled with thick, firm inspissated pus.

Guttural pouches, ventral view (rostral is left): in the center you can see a thick solidified pasty yellow mass extruding from the guttural pouch.

The mandibular and retropharyngeal lymph nodes were enlarged bilaterally and several were completely effaced with purulent material, and had fibrous capsules enclosing the pus.

Lymph node: several lymph nodes were effaced by thick pale yellow to white pus with some fibrous tissue surrounding them, indicating prolonged timecourse.

The right caudal lung lobe had a focal 2cm firm nodule elevating the pleural surface of the dorsal and medial aspect of the lung lobe. The nodule was composed of a thick fibrous capsule surrounding a 2 mm diameter central zone containing yellow purulent material.

Lungs, dorsal view: The right dorsal aspect of the middle and caudal lobes have a poorly defined expanded area corresponding to a chronic abscess. Rhodococcus equi was cultured.

The right cerebral hemisphere was swollen, with flattened sulci and gyri and contained a 5 cm x 4 cm elliptical abscess filled with yellow to light green pasty pus.

Brain, dorsal view: The right cerebrum is expanded and fluctuant, with flattening of sulci and gyri (Abscess)

Brain lateral view: The right hemisphere is yellowed multifocally with obvious flattening of sulci and gyri

Brain, cross sectioned: THe right cerebrum is effaced by a well circumscribed abscess filled with pasty purulent material (asbcess). cerebral grey matter and white matter tracts are effaced, and the lateral ventricles are mildly dilated. There is deviation of the midbrain to the left.

Brain, cross section with pus removed. The rim of the abscess is composed of some yellow tissue corresponding to suppurative infiltrate and astrocyte proliferation histologically. The red areas are neovascularization in response to the inflammation.

The small intestine contained  moderate numbers of large roundworms (Ascarids) (incidental finding)

Small intestine, opened: The lumen contains large nematodes- (Ascarids), presumably Parascaris equorum

The non-glandular gastric mucos had multifocal to coalescing ulcers.

Stomach: Non-glandular portion is on top, and at the Margo plicatus, and extending upward are multiple coalescing areas of ulceration. Presumably stress related.

Gross Diagnosis:

1. Brain: Focal cerebral abscess, unilateral

2. Mandibular and retropharyngeal lymph nodes: Suppurative lymphadenitis, multifocal, severe, chronic

3. Guttural pouch: Bilateral empyema, severe, chronic

4. Lung: Focal chronic abscess, unilateral

5. Small intestine: intra-luminal ascarids, moderate


The gross findings are consistent with bastard strangles, a disseminated form of Streptococcus equi infection. Typical strangles results in empyema and lymphadenitis of the retropharyngeal lymph nodes. If the infection progresses, septicemia can seed other organs. In this case the brain abscess resulted in severe neurologic disease and euthanasia was elected.  The lung abscess was originally presumed to be a Streptococcus equi infections, however cultures identified only Rhodococcus equi.  This is a common location for Rhodococcus equi infections, and these may be clinically silent for a long time.

Other complications of Streptococcus equi infections include Purpura hemorrhagica, which is a Type III hypersensitivity to certain anitgens related to this bacteria. This conditions requires a first infection that sensitizes the horse to the bacteria, and then when re0infection happens antigens released systemically form complexes with circulating antibodies that lodge in small vessels, activate complement, recruit neutrophils, and cause a leukocytoclastic vasculitis with petechial hemorrhage and edema. Hemorrhages may only be visible in the gingival mucosa. Edema can be seen in the head, neck, and chest.

Ancillary testing:


Lung: Rhodococcus equi

Brain, swab: Streptococcus equi

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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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