Ординатура / Офтальмология / Английские материалы / Veterinary Ocular Pathology A Comparative Review_Dubielzig, Ketring, McLellan_2010

Veterinary Ocular Pathology

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INFLAMMATION AND IMMUNOBIOLOGY

Acute inflammation

Morphologic features of acute inflammation (Fig. 2.11) include:

Protein exudation

Leakage of serum protein from blood vessels resulting in:

•Tissue edema

•Proteinaceous exudates within the aqueous, vitreous, or sub-retinal space.

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Figure 2.5  Lysosomal storage disease.

(A)Photomicrograph of a canine retina stained with Luxol-fast blue showing accumulation of storage product in ganglion cells and glial cells (arrows).

(B)Photomicrograph of a bovine retina showing accumulation of storage product in the retinal pigment epithelium

(*) in mannosidosis.

*

Figure 2.6  Cellular necrosis. (A) Photomicrograph of feline post-traumatic sarcoma, round cell variant. Surviving neoplastic cells are only around blood vessels, and cellular necrosis occurs away from vessels. (B) Necrotic ganglion cell profiles (arrow) in acute canine glaucoma are characterized by excessive eosinophilic staining.

Figure 2.7  Cellular apoptosis. (A) Photomicrograph of the retina from a dog with acute glaucoma showing a regional area of apoptosis of cells in all layers (arrows). (B) TUNEL stain of the retina from a dog with acute glaucoma. The brown marker indicates DNA cleavage in a pattern that is typical of apoptosis. (C) Transmission electron micrograph of a canine retina from a dog with day-4 glaucoma showing apoptotic nuclear profiles (arrows) and extruded nuclear fragments.

Initiation of the clotting cascade resulting in the formation of fibrinous exudates within the tissues or within the aqueous, vitreous, or sub-retinal space, and recognizable as:

•Deposition of opaque membranous exudates

•Increase in tissue fragility.

Cellular exudation

Suppurative inflammation, with neutrophilic exudate, is a hallmark feature of acute inflammation initiated by bacteria or fungi. Neutrophilic infiltration is often accompanied by macrophage cells that do not form clusters or granulomas (Fig. 2.12). Examples include:

•Corneal stromal abscess in mycotic keratitis

•Peri-lenticular exudates in cat scratch injuries, where bacteria are implanted into the lens

•Intraocular exudates from a penetrating injury.

Eosinophilic exudate is a hallmark feature of acute inflammation associated with parasitism or hypersensitivity. Examples include:

•Conjunctivitis or episcleritis due to onchocerciasis

•Eosinophilic conjunctivitis/keratitis in cats.

Macrophage exudation is another feature of acute inflammation, however, macrophages, when present in the form of epithelioid cells are the hallmark of granulomatous inflammation. Examples include (Fig. 2.13):

•Inflammatory cellular response to foreign material

•Inflammatory cellular response to many fungi and some bacteria, such as mycobacteria

•Inflammatory cellular response to exposed lens proteins.

Lymphoplasmacytic, non-suppurative inflammation (Fig. 2.14)

Morphologic features of lymphoplasmacytic inflammation include:

•Perivascular accumulations of lymphocytes and/or plasma cells within intact connective tissues

•Absence of protein exudation or tissue destruction

•Formation of lymphoid follicles within the affected tissues.

Significance of lymphoplasmacytic inflammation

•Indicates chronicity (at least several days)

•Septic disease is not likely to manifest as lymphoplasmacytic inflammation

•Indicative of immune-mediated disease such as:

■Equine recurrent uveitis

■Feline lymphoplasmacytic uveitis.

Tissue fibrosis in inflammation

Gross morphologic features of tissue fibrosis include:

•Firmness of affected tissues

•Adhesions within affected tissues

•Loss of color distinctions within affected tissues.

Tissue fibrosis is suggestive of a chronic process (Fig. 2.15).

•When seen in conjunction with acute inflammation, fibrosis defines ‘chronic active’ inflammation

•The uveal tract resists direct fibrosis; however, the chambers and spaces of the globe (anterior chamber, posterior chamber, and vitreous space) are often affected by fibrosis or fibrovascular proliferation. Examples include: (Fig. 2.16)

■Pre-iridal fibrovascular membrane

■Pupillary membrane

■Cyclitic membrane

■Fibrovascular proliferation into the vitreous from the optic nerve head.

Granulomatous inflammation (Fig. 2.17)

Morphologic features of granulomatous inflammation

The diagnostic criteria for granulomatous inflammation are dependent on identifying certain specific features and some pathologists use more restrictive criteria whereas others use more inclusive criteria (Fig. 2.18):

•By the most restrictive criteria, granulomatous inflammation is only diagnosed if ‘classical’ tubercle-like granulomas are seen, such as in tuberculosis

•By moderately restrictive criteria (as used in this book), the phagocytic cells should form ‘epithelioid’ macrophages, forming aggregates with indistinct cell borders in some part of the inflammatory infiltrate

•By the least restrictive criteria, granulomatous inflammation is diagnosed any time macrophage cells predominate in the

cellular infiltrate, even when the macrophage cells fail to form aggregated clusters of epithelioid cells.

Phagocytic cells identified as epithelioid macrophages may take several different forms (Fig. 2.19):

•Aggregated clusters with features that resemble epithelial cells, hence the name ‘epithelioid cell’

•Fusion of phagocytic cells to form multinucleate giant cells which, in turn may be further classified as:

■Langhans giant cell (peripheral rim of nuclei)

■Foreign body giant cell (randomly distributed nuclei)

■Touton giant cell (foamy outer rim of cytoplasm, seen in xanthogranuloma).

Significance of granulomatous inflammation

Suggestive of the persistence of material that is hard to eliminate from the tissues. May be associated with:

•Deep mycoses

•Mycobacteria

•Foreign bodies

•Tissue break-down products

•Idiopathic granulomatous syndromes (commonly encountered in veterinary pathology).

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