I. Upper respiratory tract
1. Structures of normal nose
Figure 4.1. Horse. Nose. Midsaggital Section. Normal structures of the nasal passages are exposed.
2. Sinonasal disorders
a. Paranasal sinus cyst
Figure 4.2. Horse. Head. Nasal Deviation. A unilateral facial deformity is associated with nasal septum deviation. Differential diagnoses include branchial cyst, paranasal cyst, ossifying fibroma, congenital dental deformities, abscessation, nutritional osteodystrophy, and nasal neoplasia.
Figure 4.3. Horse. Nasal Cavity. Paranasal Cyst. A multiloculated cystic growth has occupied and expanded into half of the nasal cavity thus slightly deviating the septum. The surrounding molar tooth has been dislodged. The paranasal sinuses of the opposite nasal cavity are filled with mucin. The cyst mainly arises from the caudal maxillary sinus.
b. Ethmoid hematoma
This slowly growing tissue proliferation arises from the mucosa of the caudal nasal cavity or ethmoid labyrinth. The pathogenesis is not understood because this tissue proliferation acts like a locally invasive neoplasm but morphologically is not. It clinically leads to small volume epistaxis.
Figure 4.4. Horse. Sinus. Ethmoid Hematoma. A reddish granular tissue mass expands cranially from the ethmoid plate and is evident after fenestration of the sinus.
Figure 4.5. Horse. Caudal Nasal Cavity. Ethmoid Hematoma. An amorphous, soft, jelly, grapelike growth has been surgically removed from the ethmoid plate of a horse with repetitive nose bleeding.
Figure 4.6. Horse. Ethmoid Hematoma. Mixed cellular inflammation that includes histiocytes and giant cells is one microscopic feature of ethmoid hematoma. (H&E)
Figure 4.7. Horse. Ethmoid Hematoma. Mineralized collagen and hemosiderin-laden macrophages are additional microscopic features. (H&E)
c. Nasal polyp
Figure 4.8. Horse. Nasal Cavity. Polyps. Oval, partially cystic growths are deep in the caudal nasal passages. Nasal polyps originate from the ethnoturbinates. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 4.9. Horse. Nasopharynx. Polyp. A single round mass has obliterated the pharynx. Nasopharyngeal polyps originate from the middle ear. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 4.10. Horse. Nasal Polyps. Pedunculated, gelatinous tissue surgically removed from the nose. (Courtesy Dr. J. King, Cornell University.)
d. Sinonasal inflammation
Viruses, bacteria, and fungi have to be considered as etiologic agents. If bacteria are involved, these usually are Streptococci sp. or Fusobacterium sp. Noninfectious causes may be environmental, irritants, or trauma. The inflammatory response can be classified depending on the nature of the exudate as catarrhal, mucinous, hemorrhagic, purulent, and granulomatous.
Figure 4.11. Horse. Nose. Midsaggital Section. Fibrinohemorrhagic Rhinitis. Fusobacterium sp. Destruction of nasal conchae. Trauma. Differential diagnosis should be nasal neoplasia or ethmoid hematoma.
Figure 4.12. Horse. Nose. Midsaggital Section. Fungal Hemorrhagic Sinusitis. Aspergillosis. Differential diagnosis should be trauma or hemangiosarcoma.
Figure 4.13. Horse. Nose. Midsaggital Section. Caseous Rhinitis Aspergillosis (Aspergilloma). A fibrinonecrotic inflammation is considered more common with fungal infections.
Other fungi to affect the nasal cavity are Coccidioides immitis and Cryptococcus neoformans.
Figure 4.14. Horse. Nose. Rhinosporidiosis. This granulomatous disease typically affects the nasal septum and sinuses. Tumorlike, soft, polypoid, glistening nodules are grossly visible. (Courtesy Dr. D. Meuten, North Carolina State University.)
Figure 4.15. Horse. Rhinosporidiosis. The pyogranuloma histologically is characterized by large oval sporangia containing numerous endospores. Rhinosporidium seeberi, the causative organism, is now considered an aquatic protistan parasite. (H&E)
Figure 4.16. Horse. Nose. Midsaggital Section. Granulomatous Rhinitis. Pythiosis. Differential diagnosis: nasal amyloidosis. (See Chapter 13, “Diseases of the Skin (Integument).”)
The nasal form of glanders is an example of infection with an exotic, zoonotic bacillus. The agent (Burkholderia mallei) causes granulomas and ulcers in the nasal septum.
3. Guttural pouch diseases
Also known as eustachian tube diverticula, the guttural pouches in the horse are large pockets on either side of the caudoventral head, lined by a thin, smooth, shiny mucosa. Each guttural pouch is partially divided by the stylohyoid bone, connected with the pharynx and traversed by the internal carotid artery as well as by cranial nerves and cranial ganglia. Because of this close anatomic relationship of blood vessels, nerves, and pharyngeal opening, the guttural pouches are susceptible to pathogens of the upper respiratory tract with a sometimes serious outcome such as severe fatal epistaxis. Dysphagia and Horner’s syndrome are other clinical signs of guttural pouch diseases resulting from damage of the adjacent cranial nerves and ganglia.
Figure 4.17. Horse. Guttural Pouch. Empyema. The pouch is unilaterally distended and filled by abundant thick, fibrinopurulent exudate. Infectious organisms that may be recovered are Streptococcus equi subsp. equi or Streptococcus equi subsp. zooepidemicus. Intermittent, unilateral mucopurulent nasal discharge is a common clinical sign, often increasing when the horse lowers the head. Epistaxis is uncommon.
Figure 4.18. Horse. Guttural Pouch. Chondroids. Inspissated concretions can form with chronic infection.
Figure 4.19. Horse. Guttural Pouch. Chondroids. Cross sections.
Figure 4.20. Horse. Guttural Pouch. Hematoma Due to Mycosis or Pythiosis. Usually unilateral, it is the result of aspergillosis or in the Southeast of the United States due to pythiosis.
Aspergillus nidulans is a common resident of the guttural pouch. The mycotic infection can spread through the wall of the pouch, with fungi invading the nearby internal carotid artery to induce thrombosis and dissection aneurysm with massive bleeding, sometimes leading to exsanguination. The pathogenesis of the aneurysm may be partially due to fracture of the stylohyoidal apparatus or joint instability due to chronic joint degeneration.
Figure 4.21. Horse. Guttural Pouch. Mycosis. Once the blood is removed, there is evidence of a friable, cauliflower-like dry exudate covering the pouch wall.
Figure 4.22. Horse. Stylohyoidal Bone Apparatus. Guttural Pouch. There is evidence of chronic arthritis with exostoses and fractures in a horse with guttural pouch mycosis. The bone changes might be partially responsible for traumatic damage to the adjacent internal carotid artery and might aid the angioinvasion of resident fungi.
4. Pharynx/Larynx/Epiglottis disorders
Figure 4.23. Horse. Larynx. Epiglottal (Laryngeal) Entrapment. This is the result of redundant mucosa and the cause of upper airway obstruction with exercise intolerance and respiratory noise noticed in racehorses, but also seen in non-racehorses, and is followed by subepiglottic granuloma and subepiglottic cyst formation. Entrapped membranes become thickened. (Courtesy Dr. J. King, Cornell University.)
Figure 4.24. Horse. Epiglottis. Congenital Subepiglottal Cyst. A small cyst surrounds the epiglottis. (Courtesy Dr. J. King, Cornell University.)
Figure 4.25. Horse. Epiglottis. Hypoplasia and Granuloma. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 4.26. Horse. Aryepiglottic Fold. Anaerobic bacterial infection. Necrosuppurative, locally extensive, chronic, moderate laryngitis.
Figure 4.27. Horse. Larynx. Cicatrix Syndrome. The nasopharyngeal cicatrix syndrome occurs in two forms. The acute phase is characterized by inflammation and the presence of a diphtheritic membrane, whereas the chronic condition is characterized by scar tissue in the pharynx rostral to the epiglottis. Also included are deformity of the epiglottis, inflammation of the arytenoid cartilage, scarring and thickening of the vocal cords. The condition has been reported from Texas. Detection is made by endoscopic examination. (Courtesy Dr. J. King, Cornell University.)
Other abnormalities associated with the epiglottis are dorsal abscesses.
5. Sinonasal neoplasia
Nasal neoplasms occur more often than thought and mainly arise from the caudal maxillary sinuses. The common tumor types include squamous cell carcinomas, adenocarcinomas, fibro-chondro-osseous and dental tumors, and hemangiosarcomas. On occasion lymphosarcomas, meningiomas, and carcinoids have been reported. Most of the sinonasal tumors are malignant, destroying nasal structures by local invasion and frequently causing facial deformity, loss of teeth, and breathing difficulty. Spread to regional draining lymph nodes may occur, but distant metastases are very rare. Grossly, the sinonasal tumors are indistinguishable as to histogenesis, and microscopic examination is mandatory for morphologic classification. Figure 4.28, Figure 4.29, Figure 4.30, Figure 4.31, Figure 4.32, and Figure 4.33 are representative of the various tumor lineages.
All of these growths are destructive while invading various tissues of the nose. Their histologic makeup has to be identified by microscopy.
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