In frequency, diseases of the gastrointestinal tract rank number one in large animals. Great economic losses may arise from disorders of the gastrointestinal tract. Although many gastrointestinal tract diseases are preventable due to available protective medication or vaccines, and improved management and feeding practices, others continue to occur in the horse, simply as the result of anatomic and genetic peculiarities of this species.
Due to the anatomic length of the gastrointestinal tract, an orderly investigation is recommended and to separate the tract into four segments: stomach, small intestine, colon-cecum, and transverse colon-rectum.
Figure 6.1. Horse. Gastrointestinal Tract. Normal. For more detailed inspection, the gastrointestinal tract has been divided into four segments. (Reprinted from Equine Medicine and Surgery, Colahan et al., Figure 3-55, Page 122, Copyright Elsevier, 1999.)
I. Diseases of the oral cavity
Careful examination of the oral cavity structures is mandatory for both clinicians and pathologists.
Figure 6.2. Horse. Jaws. Examination for Dental Wear. Separation of the mandible from the maxilla facilitates examination of molar teeth.
1. Anomalies
The normal development of the oral cavity depends largely on the organized growth of a synchronized embryologic process. Failure of tissue integration and of tissue fusion may lead to a variety of malformations, the most frequent of which are facial fissures, brachygnathia, and cleft palate (palatoschisis).
2. Dental diseases
Dental diseases are frequently overlooked as the single cause of cachexia. Equine dentistry is a regular service of practitioners to the equine industry. Pathologists have a relaxed attitude toward careful inspection of teeth during the equine necropsy. The few dental disorders presented here do not do justice to equine dentistry as a clinical specialty and are simply individual occurrences to share with practitioners and pathologists.
Figure 6.3. Horse. Incisors. Equine Odontoclastic Tooth Resorption and Hypercementosis (EOTRH). A painful disorder of mainly the incisor teeth, it is thus far of unknown etiology in horses older than 15 years. Macroscopic examination reveals bulbous enlargement by a rough cemental surface at the apical aspect. (Courtesy Dr. R. Smedley, Michigan State University.)
Figure 6.4. Horse. Incisors. Equine Odontoclastic Tooth Resorption and Hypercementosis Syndrome (EOTRH). The enlargement observed on the surface is best seen as thickening on cross section. The dental changes should not be confused with cementoma. (Courtesy Dr. R. Smedley, Michigan State University.)
Figure 6.5. Horse. Incisors. Equine Odontoclastic Tooth Resorption and Hypercementosis (EOTRH). In some incisors depressions, perforations and focal lytic changes with necrotic tissue and focal remnants of the periodontal ligament can be found. Inflammatory lesions in the pulp cavity and alveolar bone can be present in some cases. (Courtesy Dr. R. Smedley, Michigan State University.)
Figure 6.6. Horse. Teeth. Incisors. Diagonal Incisors. The condition leads to malocclusion. (Courtesy Dr. T. Banner, Gainesville, FL.)
Figure 6.7. Horse. Teeth. Incisors. Double Incisors. The condition may lead to periodontal disease. (Courtesy Dr. Toots Banner, Gainesville, FL.)
Figure 6.8. Horse. Teeth. Geriatric Teeth. Much of the enamel is gone, leaving dentin and cementum exposed. The worn occlusal surfaces have reduced grinding functions. (Courtesy Dr. T. Banner, Gainesville, FL.)
Figure 6.9. Horse. Teeth. Molar. Split Molar. Acts like a fractured tooth. (Courtesy Dr. T. Banner, Gainesville, FL.)
Figure 6.10. Horse. Teeth. Molar. Points and Hooks. Can injure soft tissue and predispose to abnormal masticatory motion. (Courtesy Dr. T. Banner, Gainesville, FL.)
Figure 6.11. Horse. Teeth. Molar. Wave. Leads to malocclusion and gingival margin displacement, usually involving fourth premolar and first molar teeth. (Courtesy Dr. T. Banner, Gainesville, FL.)
Figure 6.12. Horse. Teeth. Step Mouth and Molar Step. Abrupt changes in crown height along the arcade are known as “step mouth.” Excessive length is due to lack of an opposing tooth. (Courtesy Dr. T Banner, Gainesville, FL.)
Figure 6.13. Horse. Teeth. Caudal Hook. (Courtesy Dr. T. Banner, Gainesville, FL.)
Figure 6.14. Horse. Teeth. Rostral Hook. (Courtesy Dr. T. Banner, Gainesville, FL.)
3. Dental tumors
Contributed by Dr. Julie B. Engiles, University of Pennsylvania
Figure 6.15. Horse. Head. Peripheral Compound Odontoma (“ear tooth”) in a 2-year-old warmblood gelding with a hard swelling caudal to the right ear. (a) Ventral-dorsal digital radiographic projection of the skull shows a discrete radiopaque mass just caudal to the zygomatic arch (arrows) that protrudes laterally. (b) Transverse T1-weighted short tau inversion recovery. Magnetic resonance imaging (MRI) shows a well-defined mass of low signal intensity, consistent with dense mineralized material, containing curvilinear arrays of high signal intensity, consistent with fluid (arrows). The brain (B) is labeled for orientation. (c) Gross photograph of a sagittal section from the surgically excised mass shows two dysplastic but well-formed mineralized odontogenic structures that contain curvilinear fluid-filled cysts as seen in the MRI.
Figure 6.16. Horse. Head. Peripheral Compound Odontoma of decalcified H&E-stained sections of the mass in Fig. 6.15. (a) There is a well-organized odontogenic structure that includes an outer margin of alveolar bone (AB), a cystic cavity formed by the enamel organ (double-headed arrows), underlying dentin (a and b; D) subtended by odontoblasts (arrows), and an inner core of pulp (P). Higher magnification photomicrograph of the framed region 1. shows arrays of dentin tubules (D in b) that abut enamel tubules (E in b and c), which are lined by ameloblasts (arrows in b and c). Higher magnification photomicrograph of the framed region 2. shows Hertwig sheath composed of inner and outer enamel epithelium responsible for induction of root dentin. Remnants of Hertwig sheath become cell rests of Malassez, which are thought to be the origin of fibromatous/ossifying epulis, most common in dogs.
Figure 6.17. Horse. Mandible. Ameloblastic Fibro-Odontoma. Digital radiographic projections and gross photos of a juvenile horse that presented with a rapidly enlarging rostral mandibular mass. Although the mass effaced the entire right and part of the left mandibular rami, and displaced the incisors and canine teeth, the mass had well-defined caudal margins (a, b). Gross photos taken prior to partial mandibulectomy show severe enlargement of the mandible with focal ulceration of the lingual mucosa (c). A sagittal section of the surgically excised mass shows irregular nodules of hard to gritty gray-white mineralized foci admixed with firm red-tan tissue (d).
Figure 6.18. Horse. Mandible. Ameloblastic Fibro-Odontoma. H&E-stained decalcified sections of the mass show lobules of basophilic cells interspersed by eosinophilic islands of mineralized bone/cementum/dentin and spindle-shaped cells embedded in a collagenous matrix (a, c). Higher magnification of the basophilic lobules show primitive hyperchromatic blunt spindle-shaped cells that palisade along the external margin and also form rosettes, resembling ameloblastic epithelium (b). In other regions, the spindle cells have slightly different morphology with frequent mitoses (d, arrows), and surround small islands of unmineralized osteoid/dentin/cementum (d, arrowhead).
Figure 6.19. Horse. Mandible. Primary intraosseous odontogenic squamous cell carcinoma in an adult horse that presented with weight loss and mandibular swelling. Lateral digital radiographic projection (a) that shows multiloculated radiolucencies infiltrating the mandibular ramus. Computed tomography of the same region shows loss of the first molar (b, arrowhead) lysis of the fourth premolar tooth roots and similar radiolucent cavities. Gross photo shows a multinodular proliferation of firm tan tissue that infiltrates the mandibular ramus and extends to the gingival surface (c). Some nodules contain fluid-filled centers (d). The remaining structures in the oral cavity and draining lymph nodes were unaffected.
Figure 6.20. Horse. Mandible. Primary intraosseous odontogenic squamous cell carcinoma: H&E-stained nondecalcified sections from the cystic nodules. Neoplastic stratified squamous epithelium surrounds cystic cavities filled with pale eosinophilic fluid and sloughed cells (a, “C”). Islands of neoplastic cells show prominent keratinization (b, asterisk) or little keratinization, resembling basal cells (b, asterisk). Immunohistochemistry for AE1/AE3 cytokeratin shows abundant antigen expression by neoplastic cells that form large discrete lobules as well as infiltrative thin cords/trabeculae (c). Neoplastic squamous epithelium also demonstrates vimentin expression (d), which can be seen in a squamous cell undergoing mitosis (d, arrow).
4. Diseases of the buccae and tongue
Color changes associated with the normal pink of the visible oral mucous membrane may include pallor, cyanosis, petechiae, ecchymoses, congestion, and icterus, all important clues for the identification of disease entities affecting different internal organ systems.
Figure 6.21. Horse. Oral Mucosa. Muddy Red. Color change in shock or cyanosis.
Figure 6.22. Horse. Oral Mucosa. Multifocal Red. Color change after drug reaction to nonsteroidal anti-inflammatory drugs (NSAIDs), infection such as infectious equine anemia, or immune dyscrasia such as pemphigus or purpura hemorrhagica. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China)
Figure 6.23. Donkey. Oral Mucosa. White. Color change from anemia. (Courtesy Dr. J. Roberts, National Zoo, Washington, DC.)
Figure 6.24. Horse. Mouth. Plant-induced Ulcerative Stomatitis and Cheilitis. Fleshy ulcers are present in the mucosa of the upper lips and in the gingiva above the incisors. The skin of the lips is ulcerative and eczematous. These lesions have developed from consumption of yellow foxtail (Setaria lutescens) grass barbs. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 6.25. Horse. Mouth. Plant-induced Ulcerative Stomatitis and Cheilitis. After consumption of the grass, spikelets of seed heads burrow into the equine oral gingiva to cause an ulcerative, granulomatous, fibrous foreign body inflammation. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 6.26. Setaria lutescens. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 6.27. Barbs of Setaria lutescens. These are penetrating the gingiva or lips. (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 6.28. Horse. Mouth. Plant-induced Ulcerative Stomatitis and Cheilitis. Microscopically, a plant barb is embedded within a dense foreign body pyogranulomatous reaction with eosinophils. (H&E) (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Differential diagnoses should include immune-mediated bullous diseases such as pemphigus, vesicular stomatitis, bacterial infection, and reaction to treatment with nonsteroidal anti-inflammatory drugs.
Figure 6.29. Horse. Lips. Vesicular Stomatitis. Muzzle. Some focal erosive changes are present in the mucosa.
Vesicular stomatitis is a RNA viral disease caused by a vesiculovirus belonging to the family of Rhabdoviridae that periodically infects horses, swine, cattle, and other ruminants. Clinical signs include excessive salivation and blisters. A coronitis characterized by inflammation and ulcers involves the lower portions of the legs. Vesicular stomatitis in horses occurs in the United States as sporadic outbreaks and requires extensive restriction in the trade including quarantine.
Figure 6.30. Horse. Tongue. Glossitis and Parakeratosis. Multifocal dry exudate on the surface from bacterial infection. Differential diagnosis is candidiasis (thrush).
Figure 6.31. Horse. Tongue. Ulcers. Multifocal chronic ulcerative glossitis from dental attrition. Differential diagnosis: nerve paralysis from intraglossal neoplasia (squamous cell carcinoma).
II. Diseases of the esophagus
As a tubular organ, the esophagus provides the route of passage for masticated food to the stomach. It is divided into three anatomic segments: cervical, thoracic, and abdominal. There are four anatomic narrowings: at the caudal larynx, thoracic inlet, base of the heart and diaphragmatic hiatus. Esophageal diseases in the horse are relatively rare compared with diseases in other compartments of the gastrointestinal tract.
1. Obstruction of the lumen
This can be the result of impaction, choke, and strictures. Narrowing of the lumen also occurs from compressive changes due to disease processes outside the esophagus (soft tissue inflammation from trauma). Of additional critical clinical importance are perforations because they induce severe cellulitis.
Figure 6.32. Horse. Megaesophagus. Impaction. The esophagus is diffusely distended.
Figure 6.33. Horse. Megaesophagus. Ingesta as the result of gastric functional stricture or impaction occupy the lumen. Aspiration pneumonia may occur as a complication. Differential diagnosis: diffuse idiopathic megaesophagus, megaesophagus from vascular ring anomaly.
Figure 6.34. Horse. Esophagus. Foreign Body (Choke). Foreign object entrapment occurs at the site of the esophageal narrowings. The entrapped object causes pressure necrosis of the adjacent mucosa. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China)
Figure 6.35. Horse. Esophagus. Foreign Body (Choke). When prolonged, the entrapment may lead to weakening of the wall to cause an inflammatory pseudo-diverticulum and cellulitis of the periesophageal soft tissue. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China)
Figure 6.36. Horse. Esophagus. Foreign Body (Choke). Stricture developed from the healing process of the necrotic mucosa after removal of the object. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China)
Figure 6.37. Horse. Esophagus. Perforation. Result of injury from passing a medical instrument (gastric tube). Erosion and ulceration of the esophagus are described in the section on gastroduodenal ulcer disease in Chapter 2, “Diseases of Foals and Juveniles.”
Figure 6.38. Horse. Esophagus. Stricture interfering with food passage resulted in perforation, septic fibrinous pleuritis, and empyema.
2. Inflammation
Figure 6.39. Horse. Esophagus. Reflux Esophagitis. Ascending linear erosive and ulcerative changes are present in the mucosa that also exhibits hyperkeratosis. Differential diagnosis: corrosive and chemical burns.
Figure 6.40. Horse. Esophagus. Parakeratosis due to Candida sp. Opportunistic infection in a leukopenic horse infected with Salmonella sp. and treated with antimicrobials.
3. Idiopathic hypertrophy of the distal esophagus
Older horses (12.5 ± 5.6 years) frequently develop along the caudal 20 cm of the distal esophagus a thickening of the wall without exhibiting clinical signs of dysfunction, an incidental finding at necropsy. This is due to hypertrophy of the smooth muscle cells involving the circular layer of the tunica muscularis without fibrosis or inflammation. The cause remains elusive. The condition does not develop in the proximal portions of the esophagus that is composed of skeletal musculature or in the middle 20 cm that is skeletal muscle intermixed with smooth muscle cells.
Figure 6.41. Horse. Distal Esophagus. Muscular Segmental Distal Hypertrophy.
Figure 6.42. Horse. Distal Esophagus. Muscular Hypertrophy (Courtesy Dr. P. Habecker, University of Pennsylvania.)
Figure 6.43. Horse. Distal Esophagus. Muscular Hypertrophy. Several smooth muscle myocytes exhibit hydropic changes in sarcoplasm. (H&E)
4. Neoplasia
Primary tumors arising from the esophageal mucosa are rare and generally squamous cell carcinomas.
Figure 6.44. Horse. Esophagus. Squamous Cell Carcinoma. The mucosa is characterized by small discrete elevations distorting the longitudinal mucosal folds.
Figure 6.45. Horse. Distal Esophagus. Papilloma. This small, cauliflower-like, single elevation of the mucosa of the distal esophagus represents equine papillomavirus-induced papilloma.
III. Diseases of the stomach
1. Gastric rupture
Most of the cases are the result of overeating, impaction, ileus, or intestinal obstruction; some of the cases are simply idiopathic. Horses with histories of both acute and chronic colic are susceptible to gastric ruptures. Death occurs before there is time for peritonitis to develop. Gastric rupture is one of the causes of sudden death in the horse. Gastric rupture typically occurs at the greater curvature. Rupture sequence is: (1) muscularis, (2) serosa, (3) mucosa.
Figure 6.46. Horse. Stomach. Pyloric Sphincter Hypertrophy. A distinct bulge of the mucosa at the pylorus is the result of marked hypertrophy of the sphincter muscle. This might be a cause for gastric rupture. Other causes of gastric rupture are impaction or intestinal obstructions such as strangulating lipoma, ileus.
Events of gastric rupture are shown in Figure 6.47, Figure 6.48, Figure 6.49, and Figure 6.50.
Figure 6.47. Horse. Stomach. Distension. The stomach is markedly distended but not ruptured. Overeating with grass/alfalfa hay induces risk for rupture; grain may reduce risk. Gastric distension also occurs in grass sickness. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China.)
Figure 6.48. Horse. Stomach. Incomplete Rupture. The stretched serosa has dissected from the muscularis. The rent in the serosa usually is the longest; it is less in the tunica muscularis, and the smallest in the mucosa. The tunica muscularis apparently is the weakest of the stomach layers. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China.)
Figure 6.49. Horse. Stomach. Full-Wall Rupture. Feed has spilled to the serosal surface. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China.)
Figure 6.50. Horse. Stomach. Mucosa. The torn mucosa has swollen, ragged, hemorrhagic edges differentiating it as an antemortem rupture from a postmortem rupture. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China.)
2. Gastric ulcers
Gastroduodenal ulcer disease in foals is presented in Chapter 2, “Diseases of Foals and Juveniles.” Mucosal tears at the plicate margin are normal findings due to incomplete keratinization. In the literature they mistakenly have been diagnosed as erosions/ulcers.
Gastric ulcers are largely recognized in performance horses. Ulcers may affect both compartments of the equine stomach. They have to be differentiated from erosions, which are shallow, not extending beyond the basal membrane of the mucosa. There are several causes for gastric erosions and ulcers: dietary, parasitic, trauma (stomach tube), neoplasia, and drugs. Interestingly, an association with Helicobacter sp. has not been convincingly verified with gastric ulcers in the horse. On rare occasions, Salmonella enterica can be isolated from the glandular mucosa ulcers in conjunction with intestinal salmonellosis. Antemortem diagnosis of ulceration is achieved by endoscopy. Scoring systems as to severity and location have been developed. Clinical signs include recurrent colic, poor appetite, and weight loss.
Figure 6.51. Horse. Stomach. Bleeds. Clotted blood is intermingled with ingesta. The blood was ingested and digested from a bleeding guttural pouch mycosis and had an apple cider odor. Differential diagnosis: bleeding ulcer.
Figure 6.52. Horse. Stomach. Bleeding Ulcer. A crater in the nonglandular compartment of the stomach is covered by blood. The mucosal defect was deep enough to involve submucosal blood vessels to cause bleeding into the intestinal tract. This adult horse had a history of being repeatedly treated with NSAIDs. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China.)
Figure 6.53. Horse. Stomach. Chronic Ulcers. These frequently occur in racehorses.
Figure 6.54. Horse. Stomach. Mucosal Breaks and Elevations. Hyperkeratosis of nonglandular stomach. Erosions and shallow ulcers of glandular mucosa are present. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China.)
Figure 6.55. Horse. Stomach. Perforation. This event may be a fatal complication leading to peritonitis. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China.)
In the Southwest of the United States, alfalfa hay when cropped and crimped to hay may be contaminated with entrapped three-striped blister beetles, belonging to the genus Epicauta sp. The beetles contain terpenoid cantharidin. As little as 4–6 mg of dried Epicauta beetles can kill a horse due to hypocalcemia, hypomagnesemia, or cardiac failure from necrosis of myocardial tissue. The mechanism for the metabolic changes is unknown.
- Within the gastrointestinal tract und urothelium, cantharadin causes mucosal blisters, hemorrhage, and necrosis.
- The heart may exhibit myocardial necrosis
Figure 6.56. Horse. Stomach. Hyperemia. Focal reddening in the glandular mucosa is caused by Epicauta sp. Small erosions are present.
Figure 6.57. Horse. Stomach. Epicauta sp. Detection of parts of blister beetles in stomach contents screened via funnel supports the suspicion of cantharides toxicity.
- Inhibition of protein phosphatase 2A
- Change of permeability of mitochondrial membranes
- Mucosal acantholysis
- Ingestion of chemicals or corrosives
- Acute arsenic toxicosis
Figure 6.58. Wood Shavings. Epicauta sp. Hay shook from compressed bails releases blister beetles.
Figure 6.59. Horse. Urinary Bladder. Hyperemia. Reddening of the mucosa indicates hyperemia caused by Epicauta sp.
- Abdominal pain
- Anorexia
- Hypocalcemia, hypomagnesemia
- Chemical analysis for cantharadin in urine or stomach contents by spectrophotometry
- Finding of blister beetles or their remnants in gastric contents
3. Gastric parasites
In a 1998 study of 70 slaughtered horses in the Netherlands, Trichostrongylus axei was the most prevalent gastric parasite (51.4%), followed by Gasterophilus intestinalis (41.4%) and Habronema sp. (4.3%). Gastrointestinal parasites largely have disappeared since the introduction of effective anthelmintics such as ivermectin.
Figure 6.60. Horse. Glandular Mucosa. Fibrinous Hyperplastic Gastritis. Trichostrongylosis. The rugae are largely accentuated and covered by a fibrinous exudate. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China.)
Figure 6.61. Horse. Stomach. Mucosa. Thickening is due to glandular hyperplasia and the presence of nematode larvae and/or adults within the gastric gland lumina with no inflammatory reaction. (H&E)
The adult worm of the nematode Trichostrongylus axei is tiny (0.5–0.8 cm long). The parasite enters the horse’s stomach and intestine when the animal eats grass infected with eggs. The eggs hatch and the larvae move into the stomach and intestine where they mature. They induce a chronic gastroenteritis clinically. Affected horses typically graze with cattle or sheep also shedding eggs of the nematode.
Figure 6.62. Horse. Glandular Stomach. Polypoid Rugal Hypertrophy. This condition is frequently encountered in ponies and should serve as differential diagnosis to trichostrongylosis (Courtesy Dr. L. Roth-Johnson, Eastham, MA.)
Figure 6.63. Horse. Stomach. Botfly. Larvae of botflies are loosely attached to the glandular mucosa just across the margo plicatus. Their location identifies them as Gasterophilus intestinalis. G. nasalis larvae are found embedded in the mucosa of the duodenum near the pylorus, whereas larvae of G. hemorrhoidalis attach to the tongue or mucosa of the mouth. When removed, larval attachment sites are associated with small, round, red ulcers.
Figure 6.64. Horse. Pylorus. Botfly. Larvae of Gasterophilus nasalis.
Figure 6.65. Horse. Tongue. Botfly. Eggs of Gasterophilus hemorrhoidalis attach to the hairs of the lips and larvae migrate into the mouth as seen here on the surface of the tongue. There is also evidence of grade 2 tonsillar lymphoid hyperplasia.
Figure 6.66. Horse. Skin. Botfly Eggs. The adult flies of the three species of horse bots have their eggs glued to the hair of various body parts of the horse, especially forelimbs and shoulder. Larvae hatch usually after the animal’s licks the infested hair.
Figure 6.67. Horse. Stomach. Glandular Part. Parasitic Ulcerative Nodular Gastritis. A tumor-like swelling is present in the glandular mucosa compatible with infestation by Habronema sp. Several mucosal defects represent brood pouches of the adult stomach worms and a route for eggs to be passed into the lumen of the stomach. (Reprinted with permission from the Animal Technology Institute of Taiwan, Republic of China.)
The three species of stomach worms are Habronema muscae, Habronema microstoma, and Draschia megastoma (insulae). Adults may measure 6–25 mm in size. Adults of Draschia burrow into the mucosa; the other species are free on the mucosa. The eggs or larvae are ingested by house flies (Musca domestica) or stable flies (Stomoxys calcitrans). Migrating larvae of Draschia may cause pulmonary nodules. Clinical signs are usually not observed.
- Nematodes: Trichostrongylus axei
Gasterophilus sp.
Habronema sp.; Draschia megastoma
- Glandular stomach, duodenum, tongue, pharynx
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