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6/17/2013
Gross Photos
• Sources
– UT Gross Photos website
Equine
Gross Pathology
• http://vetgrosspath.utk.edu/
• Email me for access: [email protected]
– Noah’s Arkive
– Dr.King’s Necropsy Show and Tell
C.L.Davis Gross Course
July 2013
Kim Newkirk, DVM, PhD, DACVP
University of Tennessee
• Organization
– Alphabetically, by system
Cardiovascular
1
2
3
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5
6
7
8
9
2
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10
12
11
13
Endocrine
14
3
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15
16
17
18
19
20
4
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21
22
Gastrointestinal
23
24a
24b
5
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26
27
28
29
30
6
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33
35
32
34
36
7
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37a
37b
38
39a
39b
40
8
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41
42
43
44
45
9
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46
47
48
49
50
51
10
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52
53
54
55
56
57
11
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58
59a
59b
60
61a
61b
12
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62
63a
63b
64
65
66
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68
69
70
71
72
14
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73
74
75
76
Hemolymphatic
77
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79
80
81
82a
82b
16
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Hepatobiliary
83
84
85
86
87
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89
90
91a
• Hepatobiliary
91b
http://www.horsejournals.com/sunburn‐photosensitivity‐too‐much‐good‐thing
92
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Integument
93
94
95
96
97
19
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Dermatophilosis
http://fchshorsejudging.blogspot.com/
115
98a
116
98b
99
100
101
102
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104
105
106
107
108
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Musculoskeletal
109
110
111
112
113
22
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115
116
117
118
119
23
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121
122
123
124
125
24
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127
Neurologic
128
129
130
25
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131
132
133
134
135
136
26
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137a
137b
138
139
140a
140b
27
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141
142
143
144
Horse
145
146
28
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Horse
Reproductive
147
148
149
150
151
29
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152
153
154
155
156
157
30
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158
159
160a
160b
161
162
31
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Respiratory
163
164
165
166
167
32
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168
169
170
171
172
173
33
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174
175
176
177
178
179
34
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180
181
182
183
184
185
35
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187
Urinary
188
189
190
36
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191
192
193
194a
194b
195
37
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196a
196b
197
198
199
200
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Other
203
204
205
39
Equine Gross Pathology
C.L.Davis Gross Course
July 2013
Kim Newkirk - University of Tennessee
[email protected]
Cardiac
Ventricular septal defects (Image 1)
 Most common site is subaortic
Thebesian veins scar
 Thebesian veins comprise all the small coronary veins that connect the chambers of the
atria and ventricles the coronary vessels (rather than via the coronary sinus), enabling
continuous blood flow in the heart.
 Infarction results in an angular scar in the right atrium (Image 2).
 Dr. King’s website has several pictures (see Vet Record 2011 v.168 p.161 Clinical and
pathologic findings associated bovine Thebesian vein anomalies for more info).
Fibrinous pericarditis (Image 3)
 Mare reproductive loss syndrome. Associated eastern tent caterpillars exposure and
secondary sepsis (Mare Reproductive Loss Syndrome. Vet Pathol 45:710–722; 2008)
o Fibrinous pericarditis - Actinobacillus spp.
o Unilateral uveitis
o Meningoencephalitis
o Early fetal losses no lesions
o Late term abortions bronchopneumonia and funisitis (inflammation of the
umbilicus)
Aortic rupture (Image 4)
 Usually occurs distal to the aortic valves or at the junction of the aorta and left ventricle
 Cause:
o Sudden movement of the whole body towards the ground (falling, mating etc.)
 Possible underlying causes:
o Fragmentation, degeneration and mineralization of elastic arteries may
predispose
o Intimal thickening and medial fibrosis of the vasa vasorum → medial ischemia
and necrosis → rupture
 Sequelae:
o Taponade → sudden death
o May dissect into the myocardium and disrupt the atrioventricular node or bundle
of His → sudden death
o May dissect into the right ventricle (aortocardiac fistula) and cause right heart
failure
o Aortic aneurysm → rupture → sudden death
 JKP 5th ed. vol.3 p.62
Equine Gross Pathology – Newkirk. CLDavis Gross Course July 2013 Page 1
Valvular endocarditis (Image 5)
 Rare
 Pathogenesis:
o Bacteremia/sepsis → endothelial changes → thrombosis → endocarditis →
embolic shower → lung and systemic abscesses
 Causes:
o Streptococcus equi, Actinobacillus equuli, E. rhusiopathiae, E.coli, Pseudomonas
aeruginosa, Candida parapsilosis
o Strongylus vulgaris L4 larvae get confused and end up in aorta →
granulomatous endarteritis thrombosis ± aneurysm
 Acutely there is vegetative endocarditis (similar to that seen bacterial
causes) (Image 6)
 Chronically caseous or calcareous nodules form (Image 7)
 Associated conditions:
 Cranial mesenteric arteritis
 Infarct of the colon – especially the pelvic flexure
 Saddle thrombus
Cranial mesenteric arteritis (Images 8, 9)
 Pathogenesis:
o Strongylus vulgaris the 4th stage larvae penetrate mucosal arterioles and
migrate up to the cranial mesenteric arteries → proliferation of the intima and
endothelium with hemorrhage, necrosis, fibrin, cellular debris→ verminous
arteritis
 After wreaking havoc, the 4th stage larvae then return to the cecum/colon
via the artery and again induce hemorrhage and inflammation →
subserosal nodules → rupture out and enter the lumen and mature to
adults that shed eggs
o Chronically the wall can be very thickened
o Or the wall can be thickened and dilated → aneurysm
o Can cause infarction of the intestines → colic etc.
 Cranial mesenteric artery branches off the aorta just cranial to the kidneys
 Adults are small red worms, usually attached to the mucosa of the cecum
 They don’t even go the anterior mesenteric artery for a good reason!!
Endocardial mineralization (Image 10)
o Gross:
o Thickening and increased opacity of the endocardium and valves
o Causes:
o Vitamin D toxicity
 Cestrum diurnum (day blooming jasmine), Solanum malocoxylon,
Trisetum flavescens etc…
o Hypercalcemia (chronic renal failure etc.)
o Uremia – usually secondary to gentamicin toxicity
o JKP 5th ed. vol.3 p.61
Myonecrosis
 Gross:
o Areas of pallor
 Causes:
o Monensin (Image 11)
o Rhabdomyolysis (Monday morning; tying up etc.)
o Phenylbutazone (high doses)
o Cantharidin (blister beetle) (often hemorrhage)
o Cassia occidentalis (senna, coffee senna)
o Adonis aestivalis (summer pheasant’s eye)
o Taxus (yew)
o Oleander (report in a donkey JVIM 2002)
o Foxglove, lily of the valley, false hellebore, rhododendron/azaleas etc.
Petechiae (Image 12)
 Gross:
o Small red dots
 Causes:
o Thrombocytopenia (disseminated intravascular coagulation, ITP, tick borne etc.)
o Vasculitis (herpes, uremia, mycotic, immune etc.)
Purpura hemorrhagica (Image 13)
 Sequel to infection (especially β-hemolytic streptococcal infection) (S.equi associated)
 Pathogenesis:
o Unclear
o Thought to be due to deposition of antigen-antibody complexes in small vessels
and glomeruli → systemic leukocytoclastic vasculitis and glomerulonephritis →
protein & blood loss
 Gross:
o Edema (especially head and limbs)
o Petechia: mucosal, serosal, muscular
 JKP 5th ed, vol.2 p.633
Endocrine
Pituitary pars intermedia dysfunction (PPID)
 Gross:
o Enlargement of the pituitary (Image 14, 15)
 Histologic findings:
o Focal, multifocal or diffuse hyperplasia of the pars intermedia
o Micro or macro adenomas of the pars intermedia
 Associated lesions:
o Laminitis
o Hirsuitism
o NO adrenal changes
Nodular adrenal cortical hyperplasia (Image 16)
 Common in the adult to aged animals
 Incidental finding. No hormonal disturbances
 Gross:
o Small (<5mm), yellow to tan nodules in the capsule, cortex or medulla
Adrenal hemorrhage and necrosis (Friedricheson-Waterhouse syndrome) (Image 17)
 Cause:
o Acute endotoxic shock
 Associated with Actinobacillus equuli, Salmonella
Adrenal pheochromocytoma (Image 18)
 Uncommon
 Gross:
o Grey or red mass arising from the medulla
 Make epinephrine and norepinephrine
Adrenal cortical adenoma (Image 19)
 Uncommon
 Gross:
o Tan to yellow mass arising from the cortex
Nutritional secondary hyperparathyroidism
 ‘Big head disease,’ ’Bran disease’
 Cause:
o High phosphorous diet (bran)
o Low calcium diet (less common)
 Gross:
o Bilaterally enlarged parathyroid glands (Image 20)



Associated lesion:
o Fibrous osteodystrophy (Image 21)
 Bilaterally symmetric, hyperostotic
 Gross:
 Swollen maxillary bones obliterate the maxillary sinuses and
compress the nasal passages
Pathogenesis:
o Low calcium/High phosphorous → hypertrophy and hyperplasia of parathyroid
chief cells → hyperparathyroidism → increased PTH → increased osteoclastic
bone resorption (to increase calcium) replacement by woven bone and fibrous
connective tissue.
 Growth plates normal
Renal secondary hyperparathyroidism is NOT reported in the horse because renal
failure in horses causes hypercalcemia, not hypocalcemia (JKP 5th ed. vol.1 p.83)
Thyroid adenomas (Image 22, 23)
 Found in 75% of horses over 20yrs old
 Incidental finding
 Gross:
o Unilateral or bilateral, single or multiple, 0.1-2cm diameter tan nodules
 Historically believed to be of follicular origin, but recently found to be non-functional C
cell adenomas
o Immunohistochemistry:
 Calcitonin +, NSE +, thyroglobulin –
 JComp Path 2004. Vol.131 p.157
Gastrointestinal
Oral cavity
Mandibular/Maxillary masses
 Hard to differentiate grossly

Squamous cell carcinoma
o Mandibular (Image 24a,b)

Odontogenic/Dentigerous cysts
o Odontogenic cysts are epithelium-lined cysts derived from cell rests of Malassez,
cell rests of dental laminae, reduced enamel epithelium or malformed enamel
organs
o Dentigerous cysts are cysts that contain part or all of a tooth
 The tooth is often malformed
o Most odontogenic cysts are dentigerous
o The most common odontogenic dentigerous cysts involve the vestigial wolf
teeth and vestigial canines
o The most common non-odontogenic dentigerous cyst is the ear tooth
o JKP 5th ed. vol. 2 p.7

Odontomas (Image 25)
o Malformations in which fully differentiated dental tissues are represented
o Complex (disorganized), compound (tooth-like structures) or ameloblastic
o Mandibular or maxillary
o JKP 5th ed. vol. 2 p.27

Ossifying fibroma (Image 26)
o Normal bone is replaced by a fibroosseous stroma composed of irregular
trabeculae of osteoid and woven bone rimmed by osteoblasts
o More cellular than an osteoma, more collagen, and no periosteum

Osteoma (Image 27)

Halicephalobus gingivalis (Image 28)
o Granulomas containing larval nematodes
o See Urinary section for more information
Neonatal glossal hyperkeratosis (Image 29)
 Not eating roughage, so squamous epithelium isn’t getting worn away
 May also have esophageal and gastric hyperkeratosis
Thrush (oral candida) (Image 30)
 Proliferation of yeasts and hyphae in the parakeratotic superficial layers of the oral
epithelium



Predisposing condition:
o Anorexia – allows accumulation of keratin and debris etc.
Gross:
o Patchy, pale-gray pseudomembranous material on the oral mucosa and back of
the tongue
JKP 5th ed. vol.2 p.15
Tongue and oral ulcers
 Rare
 Associated phenylbutazone ± water deprivation (Image 31)
Esophagus
Gonglyonema pulchrum (Image 32)
 Incidental finding!
 Gross:
o Thin, red, serpentine worm 10-15cm long in the epithelium. No associated
inflammation.
 Cockroaches and dung beetles are the intermediate host
Choke (Image 33)
 Pressure necrosis and ulceration → perforation
Esophageal ulceration
 Reflux (usually linear) (Image 34)



Cantharidin (blister beetle, Epicauta spp.) (Image 35)
o Pathogenesis:
 Beetles contain cantharidin → necrosis, ulceration, congestion and
hemorrhage
o Gross:
 Congestion and hemorrhage of mucous membranes (gastrointestinal and
urinary)
Associated lesions:
o Myocardial necrosis
o Hemorrhagic gastroenteritis and cystitis
Clinical pathology:
o Hypocalcemia, hypomagnesemia
Hypertrophy of the smooth muscle of the distal esophagus (Image 36)
 Usually the circular layer
 May have concurrent terminal ileal muscular hypertrophy
Stomach
Ulceration
 More common in the squamous portion because no innate buffering capacity
o Usually most severe at or near the margo plicatus
 Often associated with other gastrointestinal diseases (that may cause stress or reflux)
 Causes
o Cantharidin (blister beetle) (glandular)
o Foals <4mos – most severe in squamous epithelium at margo plicatus
 Associated with toxicoinfectious botulism (C.botulinum type B)
o Steroids and NSAIDs (Phenylbutazone) (Image 37a,b)
 On margo plicatus (glandular)
 Pathogenesis:
 Inhibition of prostaglandin synthetase → decreased vascular tone
and perfusion → ischemia → necrosis and ulceration
o Stress
o Fasting
Gastric parasites
 Gastrophilus sp
o Gastrophilus intestinalis lives in squamous stomach (Image 38)
o Gastrophilus nasalis lives in 1st ampulla of duodenum and pylorus
o Gastrophilus pecorum, G.hemorrhoidalis, G.inermis on rectal mucosa
o Associated lesions:
 Gastric ulceration, hyperkeratosis and proliferation

Draschia megastoma (Image 39a,b)
o Adults penetrate gastric mucosa and cause granulomatous nodules (brood
pouches) with pore in the submucosa of the glandular portion, especially along
the margo plicatus
o Indirect life cycle
 Eggs passed in feces and are ingested by maggots of the stable fly
(Stomoxys calcitrans) and develop in the fly, then migrate to the
proboscis and are deposited on the lips of horses → swallowed →
develop into adults in the stomach

Trichostrongylus axei (Image 40)
o Little worms live deep inside dilated gastric glands (inside adenomatous polyp) in
glandular stomach
o Chronic gastritis
o Multifocal gastric papilloma/hyperplasia and metaplasia
o Lives in the abomasum of ruminants, causes this lesion in horses

Habronema sp
o Found on the mucosa
o May be associated mild ulceration (no nodules)

Gastrointestinal parasites (Vet Record 2005)
o Anaplocephala perfoliata > Gastrophilus intestinalis > T.axei > Habronema
Gastric dilation and rupture (Image 41, 42)
 Primary:
o Grain overload, gastric impaction, excess water, aerophagia
 Secondary:
o Obstruction, anterior enteritis, ileus or grass sickness etc.
 Idiopathic
 Rupture occurs along the greater curvature (muscular, serosa, then mucosa) → death
because shock, peritonitis
Gastric squamous cell carcinoma (Image 43)
 Arises from the squamous portion of the stomach
 Associated lesion:
o Carcinomatosis
 Clinical pathology:
o ± Hypercalcemia
Intestines
Hemomelasma ilei (Image 44)
o Hemorrhage, hemosiderin, hemosiderophages and granulation tissue
 Strongyle-associated??
Peyer’s Patches (Image 45)
 Normal structure, often appear black
Anterior enteritis (duodenitis, proximal jejunitis) (Image 46)
 Occurs in horses > 9yrs
 Pathogenesis:
o Idiopathic – Salmonella and Clostridia are suspected causes (Enterobacteria,
E.coli)
o Adynamic ileus → pain → small intestine distension → gastric reflux
 Gross:
o Abundant gastric reflux and intestinal distension
o Increased abdominal fluid
o Acute segmental mucosal necrosis
o Edema and neutrophils in the submucosa and lamina propria
o Duodenum is ALWAYS involved ± jejunum
Liver:
 Congestion, vacuoles, biliary hyperplasia, inflammation, necrotizing
hepatitis
 Due to ascending infection, absorption of endotoxin, or hypoxia from
shock
 ↑ GGT, AST, ALP
Sequela:
o Gastric dilation and rupture
o

Large colon torsion (Image 47, 48)
 Venous infarction
Strangulating lipoma (Image 49, 50)
 Often hard because of central necrosis etc.
 Venous infarction of strangulated bowel
Impaction (Image 51)
Enteroliths (Image 52)
Clostridial enteritis in foals (Image 53)
 Gross:
o Necrohemorrhagic enteritis
 Various species of Clostridium implicated
 May be antibiotic associated
Muscular hypertrophy of the distal ileum (Image 54)
 Hypertrophy of the tunica muscularis
o Can occur anywhere in the small intestine, but the distal ileum is the most
common site
 May be associated Anaplocephala spp. infection
 Significance:
o Usually incidental
o Can cause impaction and rupture of the ileum
 Clinical signs:
o May have intermittent or subacute colic; exaggerated gastrointestinal noises
o Possible cachexia
o Muscular hypertrophy of the distal esophagus
 JKP 5th ed. vol.2 p 101
Intussusceptions (Image 55)
 Intussuscipiens – the portion of the intestines containing the intussusceptum
Tapeworms
 Anaplocephala perfoliata (large, flat, segmented)
o Intussusception (Image 56)
o Cecal inversion (Image 57)
o Rupture at base of cecum
o Most common gastrointestinal parasite of horses (in England)
 Anaplocephala magna
 Paranaplocephala mamillata (small, long and thin)
Ascarids (Parascaris equorum, roundworms) (Image 58)
 Impactions/obstructions
 Intussusceptions
 Linear foreign body
 Intestinal rupture (Image 59a,b), rare
Strongylus vulgaris (double-toothed, large strongyle)
 Adults are small red worms, usually attached to the mucosa of the cecum (Image 60)
 Pathogenesis:
o Strongylus vulgaris the 4th stage larvae penetrate mucosal arterioles and
migrate up to the cranial mesenteric arteries → proliferation of the intima and
endothelium with hemorrhage, necrosis, fibrin, cellular debris→ verminous
arteritis (Image 61)
o Chronically the wall can be very thickened
o Or the wall can be thickened and dilated → aneurysm
o Can cause infarction of the pelvic flexure → colic etc. (Image 62)
 After wreaking havoc, the 4th stage larvae then return to the cecum/colon via the artery
and again induce hemorrhage and inflammation → subserosal nodules → rupture out
and enter the lumen and mature to adults that shed eggs
 They don’t even go the anterior mesenteric artery for a good reason!!
Cyathostomes (small strongyles)
 Very tiny
 Life cycle: Eggs from luminal adults (7-25mm long) are passed in the feces and develop
into L3 infective stage larvae, when ingested, these enter the cecum/colon, where they
become surrounded by a thin fibrous capsule (hypobiotic) – or inflammatory nodules
(Image 63)
o Adults are non-pathogenic
o Migration of larval stages is limited to wall of cecum & colon, some larva may
penetrate small intestine (they don’t got systemic or enter blood vessels)
 They usually incite minimal inflammation and no clinical signs
o Severe diarrhea and death of the host occurs when large numbers of these
hypobiotic larvae leave the mucosa and enter the lumen (often synchronously,
maybe because adults leave the host after deworming)
o Granulomatous and eosinophilic typhlitis/colitis around encysted larva
Fibrinonecrotic enteritis

Cantharidin (blister beetle, Epicauta sp.) (Image 64)

Salmonellosis (Images 65, 66, 67)
o Usually S. typhimurium
o Lesions:
 catarrhal to fibrinous to fibrinonecrotic enterocolitis (ileum thru
colon) with hemorrhage, edema, necrosis, fibrin thrombi and leukocytes
 paratyphoid nodules – small aggregates of macrophages in the liver ±
areas of hepatic necrosis
 ± sepsis, disseminated intravascular coagulation
 Associated condition:
 severe lymphopenia

Other possible causes…
Stretch ulcers
 Linear ulcers in the colon (Image 68)
o Secondary to edema and inflammation from Salmonella, NSAID-associated
colitis, etc.
Equine proliferative enteropathy (EPE) due to Lawsonia intracellulare
 Horses 3mos-2yrs
 Gross:
o Thickened intestines rugae and folds (Image 69)
o Proliferative enteritis villous blunting, fusion and crypt abscesses
o Silver stain: myriad apical, intraepithelial, curved bacilli
o Variable ulceration and inflammation
o Hypoproteinemia (especially young horses)
 Differential:
o Lymphosarcoma
Rhodococcus equi
 Foals
 Pathogenesis:
o Bacteria in the soil get inhaled → suppurative to pyogranulomatous
bronchopneumonia → bacteria are coughed up and swallowed, they enter the M
cells in the intestines → bacteria are not killed by the macrophages →
pyogranulomas in the gut-associated lymphoid tissue (GALT) and mesenteric
lymph nodes → pyogranulomatous and ulcerative typhlocolitis and
lymphadenitis
o Ingestion of contaminated soil/feed can also result in lesions



Gross:
o Mesenteric and colonic lymph nodes enlarged and replaced by purulent or
necrotic debris (Image 70)
o Mucosal ulcers 1-2cm diameter covered by purulent or necrotic debris (Image
71)
Differential:
o Lymphosarcoma
JKP 5th ed. vol.2 p.226, p.630
Lethal white foal syndrome (colonic aganglionosis)
 White foals of American Paint Horses Overo markings (Image 72)
o Rarely American Quarter Horses or Thoroughbreds
 Ile118Lys endothelin receptor B (EDNRB) mutation
o Autosomal recessive
 Gross:
o Small/hypoplastic descending colon ± secondary distension of the proximal
colon and intestines (Image 73)
o The myenteric and submucosal enteric ganglia are absent in the walls of the
terminal ileum, cecum and colon
Lymphosarcoma (Images 74, 75)
 Differentials:
o Rhodococcus equi
o Lawsonia intracellulare
Gastrointestinal Stromal Tumors (GISTs)
 May originate from
 GIST also may originate from the interstitial cells of Cajal (ICC) or from pluripotential
neural crest or mesenchymal cells of the gastrointestinal tract that can differentiate
partially or completely into myoid or neural elements
o ICC are located in the connective tissue between the inner and outer layer of
smooth muscle cells and are in contact both nerve endings and muscle cells and
are believed to participate, perhaps as pacemakers, in electrical and mechanical
coordination of the circular muscle layer of the small intestine
 Gross:
o Arise anywhere from stomach to colon – most common in the cecum and colon
(Image 76)
o Solitary or multifocal
o Well-demarcated, dense to loosely arranged spindle cells often separated by a
myxoid matrix
o May be composed of myogenic, neurogenic, mixed or undifferentiated
mesenchymal cells
o Composed of cells resembling the interstitial cells of Cajal




Immunohistochemistry:
o Vimentin +
o Potentially: KIT+ and CD34+
o ± SMA and S-100
o Negative for GFAP, desmin, factor VIII, chromogranin and NSE
Electron microscopy:
o No features of neuroendocrine cells
o Subplasmalemmal dense plaques of vinculin and talin
o Irregular distribution of dense bodies, subplasmalemmal densities, filaments and
caveolae
o May look like smooth muscle cells or Schwann cells
Behavior:
o In humans, dogs and NHPs they metastasize, but NO metastases reported in
horses
o Usually an incidental finding
Vet Path 2001 38.689; JKP 5th ed. vol.2 p. 128
Hemolymphatic
Anasarca (Image 77)
 May be associated with pulmonary hypoplasia
Normal extruded red pulp (Image 78)
Normal clefts (Image 79)
Splenomegaly
 Usually secondary to barbiturate euthanasia
Bone marrow, serous atrophy of fat (Image 80)
 Gelatinous bone marrow
 Emaciation
Neonatal isoerythrolysis (Hemolytic disease of the newborn)
 Pathogenesis:
o Antibodies versus blood groups Aa, Qa, R, S are most commonly involved
 Because they’re more common in the general population and because
they’re so antigenic)
o Mare sensitized to fetal blood antigens (from sire) → produces antibodies → foal
drinks colostrum containing antibodies versus self red blood cells → isoimmune
hemolysis (direct cell lysis or agglutination) → icterus, hemoglobinuria → hepatic
necrosis (hypoxic) and hemoglobinuric nephrosis
 Gross:
o Icterus (Image 81)
o Splenic infarcts/hematomas
o Hemoglobinuric nephrosis
o Hepatic necrosis (± hepatic encephalopathy)
o Splenic hemosiderosis
o Anemia ± thrombocytopenia
Lymphoma (Image 82a, b)
Hepatobiliary
Fibrous tags on the diaphragmatic liver capsule (perihepatis filamentosis) (Image 83)
 Possible causes:
o Migrating Strongylus edentatus larvae (JKP 5th ed. vol.2 p248)
o Friction rubs (McGavin 4th ed. p.419)
Hepatic granulomas (Image 84)
 Heterobilharzia americana
o Often mineralized
o May also have granulomas on the small intestine, colon, mediastinum, lung,
heart
o Incidental finding
o Gulf Coast of US and SE Texas
o Vet Path 49(3):552-556, 2012 and JAVMA 239:1117–1122, 2011
 Differentials:
o Nematode larva migration
 Parascaris equorum
 Strongylus spp.
Miliary hepatic necrosis

Equine herpesvirus-1 (Image 85)
o Foals

Salmonella
o Paratyphoid nodules – small aggregates of macrophages in the liver ± areas of
hepatic necrosis

Colibacillosis in neonates

Actinobacillus equuli in neonates

Tyzzer’s disease (Clostridium piliforme)
o Obligate intracellular parasite
o Gram **negative** Clostridium
o Histologic findings:
 Widespread, multifocal portal to periportal hepatic necrosis with
neutrophilic infiltration – organisms present in hepatocytes at the
periphery of lesions
 ± Necrotizing enteritis, colitis, myocarditis or lymphadenitis
o JKP 5th ed. vol.2 p356
Theiler’s disease (serum sickness, equine serum hepatitis)
 Occurs in horses 2-3mos post-injection with equine serum or tissue emulsions
o outbreaks
 Cause:
o Theiler’s disease-associated virus (TDAV), pegivirus, flaviviridae
 www.pnas.org/cgi/doi/10.1073/pnas.1219217110
 Clinical signs:
o Acute onset icterus, ‘blind staggers’, hyperexcitability, ataxia
o Death in 6-24hrs
 Gross:
o Icterus, ascites, petechia,
o Dishrag liver (flaccid) (Image 86)
o Almost complete loss of hepatocytes; remaining hepatocytes are swollen,
vacuolated or distended lipid
o Acute hepatic necrosis is not usually seen
o Bile accumulation in hepatocytes and Kupffer cells
o Diffuse mild fibroplasia
o Mild infiltration by lymphocytes, plasma cells, neutrophils, macrophages
o Biliary hyperplasia
o JKP 5th ed. vol.2 p344
 Associated condition:
o Hepatic encephalopathy (severe diffuse ↑ in type II astrocytes)
o Severe unresponsive colic (develops 41-60d later in some horses – JVIM 2005)
Hydatid cyst (Image 87)
Echinococcus granulosus granulosus
 Multiple hydatid cysts (Image 88)
 Pathogenesis:
o Dog intestines → horses (intermediate host with hydatid cysts and scolices) →
dogs
Hepatic amyloidosis
 Secondary capsular fractures (acute and chronic) (Image 89)
Hepatic lipidosis (Image 90)
 Gross:
o Yellow, tan
o Friable
 Equine hyperlipidemia
o Ponies (especially Sheltlands); miniature horses and donkeys
o Usually pregnant or lactating mares that are fat, anorexic, stressed
o Pathogenesis:
 Insulin resistance and hyperlipemia in periods of negative energy balance
Increased triglycerides indicate that the liver is working, but maybe the
plasma transport mechanisms are saturated, so triglycerides accumulate
in hepatocytes
 Also decreased ability of other tissues to use VLDLs and there’s
continued synthesis by the liver
 Also maybe insulin resistance combined with stress and
glucocorticoids that interfere with insulin function
Clinical pathology:
 Increased plasma triglycerides, VLDLs
 Increased plasma insulin levels (insulin resistance??)
 Metabolic acidosis
 Disseminated intravascular coagulation
Associated lesions:
 Lipidosis in other tissues (heart, skeletal muscle, kidneys, adrenal
cortices)
 Lipid emboli
JKP 5th ed. vol.2 p313

o
o
o
Cirrhosis (Image 91a, b)
 Lesion:
o Nodular hyperplasia/regeneration and fibrosis
o Photosensitivity dermatitis (secondary) (Image 92)
 Many causes
o Pyrrolizidine alkaloids
 Crotalaria, Senecio, Cynoglossum, Heliotropum, Echium, Amsinckia,
Symphytum
 Pathogenesis:
 Ingested alkaloids are metabolically activated to
dehydropyrrolizdines in the liver → mitosis inhibited, but DNA
synthesis occurs → hepatocellular polyploidy → megalocytosis
 Ingestion of large amounts: centrilobular necrosis
 Repeated, low level exposure: atrophy regenerative nodules and
megalocytosis also biliary hyperplasia ± periportal fibrosis
o Atrophy because hepatocytes die and can’t be replaced
o Some hepatocytes can still divide so there can be
regenerative nodules
 JKP 5th ed. vol.2 p.373
Cholelith (Image 93)
Integument
Epitheliogenesis imperfecta (Image 94)
 In normal skin, collage VII fibrils lay below the lamina densa, and they bind to and
interact with the laminin-5-anchoring filaments which traverse the lamina lucida and
interact with the α6β4-integrin (part of the hemidesmosome, and it’s found on basal
keratinocytes)
o The disease in foals is likely NOT caused by a defect in α6β4 integrin, but it may
be a laminin-5 defect – which is the lethal variant of junctional epidermolysis
bullosa
 Clinical signs:
o Missing epithelium on hooves, limbs, tongue, anterior esophagus ± irregularly
pitted teeth
o Skin and oral mucosa: Sharply demarcated discontinuities of squamous
epithelium and adnexa
 No lesions in internal organs
 Vet Path 2002
Nutritional panniculitis (yellow fat disease)
 Pathogenesis:
o Diet high in polyunsaturated fats (fish) and low in antioxidants → peroxidation of
lipids and membranes → free radicals → necrosis, inflammation, ceroid etc.
 Gross:
o Fat is grey to yellow to orange (Image 95)
o May be firm or edematous
o Fat necrosis stimulates a neutrophilic, then granulomatous reaction
o Deposition of globules of ceroid in the interstitium, macrophages etc.
 Ceroid is acid fast and autofluorescent
Cutaneous papillomatosis
 Cause: ECPV-1 (Equus caballus papillomavirus 1)
 Gross:
o Usually small, discrete, and attached by a narrow stalk on the muzzle and lips
(Image 96)
o Hyperplastic folded layers of squamous epithelium with acanthosis and
hyperkeratosis ± ballooning degeneration supported by a thin core of CT
o Koilocytes (keratinocytes with swollen grey/clear cytoplasm, nuclear
enlargement and atypia)
o Hypomelanosis
o Prominent granular cell layer
 May spontaneously regress
 Can be congenital in foals (not viral, probably hamartoma)
Aural plaques
 Cause:
o ECPV-1 (Equus caballus papillomavirus 1)
 Gross:
o Solitary or multiple, raised, non-pigmented, scaly lesions on the inner pinna
(Image 97)
o Same as cutaneous papillomatosis
 Usually don’t regress on their own
Dermatophilus (Dermatophilus congolensis)
 “rain scald”, “mud fever” Transmission:
o Via the motile zoospore (coccoid form) – direct, indirect, arthropod
 Pathogenesis:
o The organism invades and multiplies in the epidermis as branching filaments,
which divide yielding multiple rows of coccoid organisms
o Large numbers of neutrophils infiltrate the epidermis – this inflammation inhibits
further penetration of the bacteria
o The invaded/infected epidermis then cornifies prematurely, which stimulates
reactive hyperplasia of the epidermis, and a new epidermis is produced under
the exudate
o This new epidermis then gets invaded by bacteria at the periphery of the lesion
→ vicious cycle → laminated
 Gross:
o Raised, alopecic, sometimes papillomatous lesions covered by thick scabs, hair
removable (paintbrush with moist pink skin underneath)- lower limbs, back
(Image 98a,b)
o Alternating layers of keratin and neutrophils
o Epidermal hyperplasia and superficial perivascular dermatitis
o Bacteria form ‘railroad’ tracks (they divide longitudinally and transversely)
Fistulous withers (Image 99) and Poll evil
 Lesions:
o Chronic suppurative to granulomatous supraspinous bursitis or nuchal bursitis
(respectively)
o Tends to erode into the overlying skin
 Cause:
o Onchocerca cervicalis; Brucella abortus or B.suis; Actinomyces bovis,
Streptococcus equi zooepidemicus
o Ill-fitting tack, saddles etc.
o Penetrating trauma
 JKP 5th ed. vol. 1 p.172
Most common non-neoplastic skin masses

Exuberant granulation tissue (proud flesh) (Image 100)

Phycomycosis (Basidiobolus haptosporus, Conidiobolus coronatus)
o On lower limbs, usually wet, macerated skin (‘swamp sores’)
o Pyogranulomatous and eosinophilic rare, indistinct, fungal agents (PAS, GMS),
and kunkers – cores of inspissated pyogranulomatous pus, often mineralization
 Pleomorphic, irregular, coarse, branching, rarely septate hyphae (3-25um
diameter)
 Branching is irregular, and usually at perpendicular, and branches
are smaller than the parent hyphae
Pythiosis (Pythium insidiosum) – looks the same, but called Pythiosis, not
Phycomycosis – need to culture to see which one it is
o Leeches, kunkers (Image 101)


Cutaneous habronemiasis (Image 102)
o “Summer sores”
o Cause:
 Larvae of the stomach worm Draschia megastoma (also Habronema
muscae, H.majus)
 The adults live in the stomach, and eggs and larvae are passed in the
feces and are eaten by maggots – then when they grow up to be flies,
they deposit larvae on the horses
 Larvae that are eaten become bots
 Larvae in wounds/MCJs → habronemiasis
o Hypersensitivity reaction to dead/dying larvae
o Vector:
 Stomoxys calcitrans
o Gross:
 Often mucocutaneous junction (medial canthus, 3rd eyelid, penis)
 Distal extremities
 Proliferative, moist, nodular granulomatous dermatitis and panniculitis
 Larvae penetrate deeply into the dermis → eosinophilic granulomas ±
ulcers
 Sulfur granules: necrotic, caseous or mineralized material around
larvae
 Only see nematode larvae in 44% (if you don’t see larvae, it’s just an
eosinophilic granuloma)
o Differentials:
 Sarcoid, phycomycosis, pythiosis, eosinophilic granuloma syndrome,
squamous cell carcinoma
o JAVMA 2003

Halicephalobus gingivalis (Image 103)
o 2005 AFIP case (conf 1, case 2) of penile
o Uncommon, usually nasal/oral, renal, spinal cord
o See Urinary section for more information

Nodular necrobiosis (eosinophilic collagenolytic granuloma)
o Gross:
 Nodules on withers or under saddle girth, high friction areas, no ulceration
 Multifocal granulomatous dermatitis
o Thought to be hypersensitivity reaction to microfilaria
Most common cutaneous neoplasms
 Sarcoids (51%) > SCC (18%) > melanocytic tumors > papillomas > mast cell tumors
Sarcoids (Image 104)
 Cause:
o Bovine papillomavirus type 1 and 2 (BPV-1, BPV-2)
 Transferable from one part of the body to another
 Abnormal proliferation is primarily epidermal, but later the dermis gets involved and may
predominate
o Fibropapillomas – acanthosis with long fronds of epidermis extending deep into
the mass AND interlacing bundles of spindle-shaped cells that may form
whorls/bundles
o Fibroblasts at the dermo-epidermal junction are frequently oriented perpendicular
to the basement membrane (picket fence)
Squamous cell carcinoma
 Locations:
o Lightly pigmented areas…
 Periocular, conjunctival (Image 105)
o Penile (Image 106)
o Vulvar (Image 107)
 Gross:
o Often ulcerated
 Causes:
o Solar/Ultraviolet exposure
o ECPV-2 (Equus caballus papillomavirus 2)
 Penile, not periocular
Melanomas (Image 108)
 Grey horses (Arabs, Lippizaners) are predisposed
o Tumors increase in number with age
o Usually perineal, ventral tail, lips, eyelids
 Non-grey horses may develop melanocytomas too as they age
o More likely to be malignant
 3 Distinct growth patterns in grey horses
o Slow growing without metastases (most common!)
o Malignant transformation of a benign lesion
o Starts out malignant (rare)
 Hard to predict the behavior from the histologic features
 EqVetJ 2003
Musculoskeletal
Thyroid hyperplasia musculoskeletal deformities (TH-MSD) in foals (in western Canada)
 Prolonged gestation and signs of prematurity
 Foals are presumed to be hypothyroid
 Gross:
o Thyroids range from small to normal (not enlarged/goiter)
o Musculoskeletal deformities
 Flexor deformities
 Domed head (Image 109)
 Mandibular prognathism (Image 110)
 Incomplete skeletal ossification
 etc.
o Thyroid follicular hyperplasia
 Can Vet J 1994; 35: 31-38
 Cause:
o May be due to high nitrate diets or iodine deficient diets (Can Vet J. 1996 June;
37(6): 349–358.)
Brachygnathia inferior (micrognathia; parrot mouth) (Image 111)
 Common
Palatoschisis (secondary cleft palate) (Image 112)
 4% of thoroughbred foals
o Aspiration pneumonia
o Primary cleft palate (harelip, cheiloschisis)
Polydactyl (Image 113)
Laminitis
 Normal hoof (Image 114)
 Causes:
o Endotoxemia, pneumonia, endogenous/iatrogenic corticosteroids, fever, plant
alkaloids
 Acute Laminitis:
o Gross:
 Congestion ± hemorrhage
 Elongation and disorganization of the keratinocytes of the secondary
epidermal laminae → pulls away from the basement membrane →
separation of the dermal and epidermal laminae



As the keratinocytes in the secondary epidermal lamina move
away from the secondary dermal lamina they move away from
their blood and nutrient supply…
Chronic laminitis (Image 115)
o Gross:
 Rotation of P3
 Irregular epidermal laminar hyperplasia and hyperkeratosis
Degenerative joint disease
 Cartilage fibrillation and erosion and eburnation (to make like ivory) (Image 116)
 Synovial villous hyperplasia (Image 117)
Osteochondrosis (developmental orthopedic disease)
 Gross:
o Dimpling and wrinkling of articular cartilage (Image 118)
o Retained or thickened cartilage
o Cartilage flap (osteochondritis dissecans, OCD)
 Predilection sites
o Lateral trochlear ridge
o Medial condyle of the femur (Image 119)
o Patella
o Dorsal edge of the sagittal ridge of the distal tibia
o Various sites in the tarsus and fetlock
o Articular process of cervical vertebrae (predisposes to Wobbler syndrome)
(Image 120)
 Pathogenesis:
o At the articular-epiphyseal (AE) complex:
 The articular cartilage of neonates is vascularized and the vessels recede
maturity
 Premature death of vessels (or infarction etc.) in the AE complex →
ischemic necrosis of cartilage or delayed endochondral ossification →
extension of necrotic cartilage into the subchondral bone
 Clefts can form in the deep layers of necrotic cartilage (the trauma of
weight bearing etc.) → cartilage flaps (± ossification of cartilage flaps) →
osteochondritis dissecans (OCD)
 Predisposes to subchondral cystic lesions
o At the physis:
 Metaphyseal dysplasia viable hypertrophic chondrocytes
 NOT cartilage necrosis
 May be secondary to microfractures which interfere vascularization and
endochondral ossification etc. → persistence of the zone of hypertrophic
chondrocytes
 Causes:
o Copper deficiency
o High calcium diet; over nutrition
o Prolonged dexamethasone because it increases MMPs

o Genetic
o Trauma
JKP 5th ed. vol.1 p.136, 143
Physitis and Osteomyelitis (Image 121)
 Pathogenesis:
o Sepsis → bacteria get trapped in the sharp loops of the physeal vessels and
escape through the fenestrations → edema, neutrophils, trabecular necrosis
(possible sequestrum formation) ± bone resorption, proliferation of granulation
tissue (involucrum) etc. (Image 122)
 Causes:
o E.coli
o Klebsiella spp.
o Rhodococcus equi
o Salmonella spp.
o Streptococcus spp.
Metastatic vertebral hemangiosarcoma (Image 123)
Osteopetrosis (Image 124)
 Usually lethal (malignant) form lesions present at birth
 Newborns, lethal
 Recessive
 Pathogenesis:
o Defective osteoclastic bone resorption → accumulation of primary spongiosa in
marrow cavities → no marrow spaces
o Increased fragility of bone because primary spongiosa isn’t replaced by thicker
trabeculae mature lamellar bone
o Metaphyses are relatively avascular
o Medulla filled dense chondro-osseous tissue (cartilage matrix lined by a thin layer
of woven bone)
o Normal to increased numbers of osteoclasts – they are larger than normal, but
lack a ruffled border (suggests functional defect)
 Predisposed breed:
o Peruvian Paso’s
 Associated conditions:
o Brachygnathia inferior, malpositioning and impaction of teeth
o Rib fractures (birthing trauma)
Hypertrophic osteopathy (Image 125)
 Gross:
o Diffuse periosteal new bone formation along the diaphysis and metaphyses (not
epiphyses) of the distal limbs
 Pathogenesis is obscure

Associated condition:
o Ovarian tumors (dysgerminoma)
 Not usually associated pulmonary disease as it is in other species
Onchocerca cervicalis
 Adult filarid worms (27-75mm long, <1mm thick) live between the fibers of the
ligamentum nuchae over the shoulder/neck → when the worms die they are surrounded
by a granulomatous reaction fibrosis and mineralization (Image 126)
o Larvae (microfilaria) migrate through the connective tissue to the skin (ventral
midline, inner thighs, eyelids) and may be picked up by biting vectors and
transmitted to other animals.
 If the larvae die they incite an inflammatory reaction → nodular skin
lesions
 JKP 5th ed, vol.1, p.279
Malignant edema and gas gangrene (Image 127)
 Malignant edema is technically more of a cellulitis than myositis
 Most common in the cervical musculature
o Secondary to wound contamination; dirty needles; inadvertent perivascular
injections
 Causes: Clostridium septicum, C. perfringens, C. novyi, C. sordelli, C. chauvoei
 Pathogenesis:
o Spores present in tissues → trauma etc. → low oxygen, alkaline pH → spores
germinate → toxins produced → necrotizing myositis and cellulitis
o Death due to systemic intoxication
 Gross:
o Edema
o Emphysema
o Hemorrhage (discoloration)
o Necrosis
Myonecrosis
 Gross:
o Pale streaks
 Causes:
o Exertional rhabdomyolysis (Image 128)
o Polysaccharide storage myopathy
o Nutritional myopathy (E/Se deficiency)
o Ischemic from anesthesia
o Plant toxicity (Cassia occidentalis, coffee weed)
o Ionophore toxicity (monensin)
o Clostridial myositis (malignant edema, botulism)
o Protozoal myopathy (sarcocystis)
o Streptococcus associated myopathy
Nervous
Spina bifida (Image 129)
Meningocoele (Image 130)
 Fluid-filled meninges protruding through a defect in the cranium (crania bifida)
Cerebral aplasia (prosencephalic hypoplasia) (Image 131)
 No cerebral hemispheres
 True anencephaly there is no brainstem etc.
Hydranencephaly (Image 132)
 Complete absence of the cerebral hemispheres, leaving only membranous sacs filled
CSF and surrounded by meninges
 Usually the head shape is normal
 Normal brainstem, hippocampus and choroid plexus
 Pathogenesis:
o Usually results from full thickness necrosis of the cerebral hemisphere
Hydrocephalus (Image 133)
 Internal
o Fluid is maintained within the ventricular system
o Associated conditions:
 Cavitating cerebral defects
 Hydranencephaly
 Porencephaly
 Cranial malformations
 External
o Fluid is in the arachnoid space
o Rare
 Communicating
o Fluid is in both locations
o Rare
Cerebellar hypoplasia (Image 134)
 Likely genetic in Arabian foals and Gotland ponies
o These breeds also predisposed to cerebellar abiotrophy (Image 135)
Herniation, parahippocampal gyrus (Image 136)
Skull fractures (Image 137a, b)
Cholesteatoma (cholesterol granulomas)
 Pathogenesis:
o Chronic congestion and edema → macrophage infiltration → cholesterol crystals
deposited and become foreign bodies → granulomatous inflammation
o Can get large and obstruct the interventricular foramen → hydrocephalus →
pressure atrophy of the ventricles
 Gross:
o Firm, crumbly, grey nodules (Image 138)
o 4th ventricle > lateral ventricle
 JKP 5th ed, vol.1 p.346
Nigropalladial encephalomalacia (toxic equine parkinsonism)
 Gross:
o Bilaterally symmetric areas in the globus pallidus and/or substantia nigra that are
slightly bulging, yellow and gelatinous (Image 139)
o Lesions may progress to form a pseudocystic cavity
 Cause:
o Centaurea solstitialis (Yellow star thistle)
o Centaurea repens (Russian knapweed)
 Pathogenesis:
o A sesquiterpene lactone from C.repens, called repin → glutathione depletion →
increased ROIs → membrane damage → malacia
th
 JKP 5 ed, vol.1 p.357; VetPath 49(2):398-402. 2012
Equine leukoencephalomalacia (moldy corn poisoning) (Image 140a, b)
 Pathogenesis:
o Fumonisin B1 toxin from Fusarium verticillioides (previously F.monoliforme)
 Inhibits ceramide synthase and interfere with the synthesis of
sphingolipids → accumulation of bioactive intermediates of sphingolipid
metabolism → interferes function of membrane proteins (Vet J 186:157161; 2010)
 Microcirculatory damage → necrosis of the white matter of the cerebral
hemispheres
 Gross:
o Gyri slightly flattened and discolored
o Multifocal, random soft (malacic), pulpy, grey areas in the white matter
 ± Hemorrhage
 May be diffuse, yellow, edema in the surrounding white matter (Image
141)
o Usually bilateral, but unequal in severity (not symmetrical)
o Brainstem and spinal cord are also affected, but the necrosis is primarily in the
grey matter
o Malacia in the white matter edema and cavitations that tend to follow blood
vessels


o Eosinophils and plasma cells, lipofuscin-laden macrophages
o Thickening of the adventitia of vessels, especially in the brainstem
Associated lesion:
o Centrilobular hepatic necrosis and fibrosis (similar to Aflatoxicosis)
JKP 5th ed, vol.1 p.358
Meningitis and brain abscesses (Image 142)
 Primary sites of infection include paranasal sinuses, periorbital tissues, submandibular
and retropharyngeal lymph nodes
 Causes:
o Rhodococcus equi
o Streptococcus equi var equi (bastard strangles)
o S.equi zooepidemicus
 JAVMA 2004
Spinal cord hemorrhage

Equine protozoal myelitis (Sarcocystis neurona) (Image 143)
o Pathogenesis: focal parasitic activation and replication → inflammation → axonal
damage → axonal swelling and degeneration → Wallerian degeneration
o Segmental granulomatous myelitis myelomalacia and hemorrhage
 Necrosis, axonal swelling, hemorrhage lymphocytes, macrophages,
neutrophils, eosinophils, and occasionally multinucleated giant cells;
lesion usually at cervical and lumbar intumescence
 Banana-shaped organisms associated with lesions, free or encysted in
macrophages, neurons, vascular endothelium
 Random lesions, grey matter and white matter
 Rule out Neospora

Equine herpesvirus-1
o Pathogenesis:
 Infects the respiratory mucosa and then replicates in the GI or respiratory
mucosa →infection of mononuclear cells → cell associated viremia
 Tropic for endothelial cells of the spinal cord white matter → multifocal
necrotizing vasculitis with thrombosis → hemorrhage, and infarction
(myelomalacia); mononuclear cuffing; multinucleated giant cells
 Cerebrospinal ganglioneuritis, and vasculitis in other tissues too
o Not neurotropic
o No intranuclear inclusion bodies
 Rhinopneumonitis
 Abortion and perinatal foal infections
Cauda equina neuritis (polyneuritis equi)
 Cause:
o Unknown – likely immune mediated versus anti-myelin basic protein; type I
adenovirus has been isolated
 Gross:
o Sacral and caudal/coccygeal nerve roots are thickened, fusiform and discolored
by recent or old hemorrhage (Image 144)
 Extradural parts of the nerves are particularly affected and lesions may
extend through the intervertebral foramina and into the adjacent muscle
 Intradural parts of the nerves are discolored, but not usually enlarged
o Severe granulomatous perinueritis and polyradiculoneuritis fibrosis
 NO granulocytes
o Degeneration and regeneration in the myelin and nerves
o Milder disease may be seen in spinal nerve roots & cranial nerve (especially VII
& VIII) roots
 Differential Diagnoses:
o Halicephalobus gingivalis (See Urinary section for more information)
o Cryptococcus (Tifton case 2013)
Nonsuppurative encephalomyelitis
 Usually no gross lesions
 Possible causes:
o EEE/WEE/VEE (alphaviruses, togaviridae)
o West Nile (flavivirus, togaviridae)
o Japanese B encephalitis virus (flavivirus, togaviridae)
o EHV-1 (alphaherpes)
o EPM (Sarcocystis falculata neurona)
Cervical vertebral stenotic myelopathy- “Wobblers”
 Really hard to get a good gross image…
Ocular
Mycotic keratitis (Image 145)
 Causes:
o Aspergillus, Penicillium, Fusarium, Candida etc.
 Pathogenesis:
o Fungi gain access via trauma and have an affinity for Descemet’s → stromal
abscesses
 Possible lesions:
o Stromal ulcers, abscess etc.
o Corneal vascularization
Equine periodic ophthalmia (Equine recurrent uveitis, ERU)
 Pathogenesis:
o Unclear
o Leptospira interrogans serovar pomona?
 60% have Onchocerca cervicalis – incidental?
o Autoimmune response?
 Repeated episodes of severe acute anterior uveitis
 Lesions vary depending on the chronicity
 Gross:
o Pus and fibrin in the anterior chamber (Image 146)
o Corneal vascularization
o Cataract
o Synechia
o Haab’s stria (breaks in Descemet’s membrane) (Image 147)
o Iris and ciliary body are congested and infiltrated with leukocytes (initially
neutrophils, then lymphocytes)
o Lymphoid follicles in the iris and ciliary body
o Perivascular cuffs of lymphocytes in the optic papilla
o Hyalinized membrane covering the inner aspect of the ciliary body – stains
positive for amyloid!
o Crystalline protein inclusions (Coolie bodies) in the cytoplasm of the inner (nonpigmented) layer of ciliary epithelium
o Retinal detachment
Reproductive
Normal endometrial cups (Image 148)
 Present from 40-120d gestation
Normal cervical star (Image 149)
 No microcotyledons
Allantoic adenomatous (cystic) dysplasia/hyperplasia/plaques (Image 150)
 Uncommon
 Pathogenesis:
o May be secondary to chronic irritation, and, therefore, are associated with
primary placental pathology
o Placentitis
o Placental edema
o Fetal diarrhea
 Gross:
o Multifocal, solid to cystic 1-5cm tan, firm areas near the umbilical stalk
o Classified into 3 stages.
o The first 2 stages: complete loss of chorionic villi and hyperplastic epithelium
forms pseudoglands in the allantoic stroma accumulation of neutrophils and
proteinaceous fluid in the lumen
o 3rd stage (nodular masses)
 Allantois thickened by glandular structures lined by tall columnar to
flattened epithelium
 Lumina of cysts contain proteinaceous and cell debris (inflammation is
usually mild)
 Overlying chorion can be normal OR ulcerated due to associated
chorionitis
Differentials for placental nodules:
 Trophoblastic disease (Partial and complete hydatidiform moles and choriocarcinomas)
 Germ cell tumors
 Metastatic tumors
 Granulomas
 Adenomatous hyperplasia of the allantois
Mycotic placentitis (Image 151)
 Pathogenesis:
o Ascending infection and primarily affects the cervical star
 Gross:
o Peripheral thickening of cotyledons due to inflammatory cells and necrotic debris
o Fetal skin lesions on head and neck – grey-white plaques
Equine placentitis
 Aspergillus fumigatus (most common fungal cause)
 Candida
 Nocardioformes (Amycolatopsis, Crossiella equi)
 Phycomycetes (Absidia, Mucor, Rhizopus)
 Cellulosimicrobium cellulans
 Histoplasma
 E.coli
 EHV-1
 Equine viral arteritis
 Encephalitozoon cuniculi
 Klebsiella pneumonia
 Leptospira
 Pseudomonas aeruginosa (Image 152)
 Rhodococcus equi
 Salmonella
 Streptococcus equi zooepidemicus
Cystic endometrial hyperplasia (Image 153)
 Uncommon in mares!
 NOT associated granulosa cell tumors
Middle uterine artery rupture (Image 154)
 Predisposing conditions:
o Increasing age
o Multiparity
o Pregnancy!
 Pathogenesis:
o Often occurs during parturition
o The artery near the rupture often contains degenerative changes:
 Smooth muscle atrophy fibrosis of the tunica media
 Disruption and/or mineralization of the internal elastic lamina
 Gross:
o Hemorrhage into the broad ligament ± abdomen → exsanguination
o Hemoabdomen
o Pregnancy!
 JKP 5th ed. vol. 3 p.460; McGavin 4th ed. p.598; and Eq.Vet.J. 42(6):529-533. 2010
Uterine prolapse (Image 155)
Contagious equine metritis (Taylorella equigenitalis)
 Transmission:
o Coitus (stallions are asymptomatic carriers)
 Gross:
o Mucopurulent vaginal discharge (Image 156)
o Uterine folds are thickened and edematous
o Cloudy, viscous exudate in the uterus (Image 157)
o Purulent, necrotizing endometritis which progresses to a mild lymphoplasmacytic
endometritis
Coital exanthema (infectious pustular vulvovaginitis)
 Cause:
o Equine herpesvirus-3
 Venereal transmission
 Gross:
o Small vesicles or raised yellow with white necrotic plaques that coalesce and
slough leaving areas of ulceration (Image 158)
 Resolution leaves depigmented spots
o Predilection for the body of the penis, not the glans
o Hydropic degeneration and necrosis with ulceration and eosinophilic intranuclear
inclusion bodies
Normal fetal ovaries (Image 159, 160a, b)
 Very large due to hyperplasia of the interstitial endocrine cells which contain lipochrome
pigment
Ovarian hemorrhage
 Luteinized hemorrhagic anovulatory follicle (AHFs) (Image 161)
o Histological and immunohistochemical characterization of equine anovulatory
haemorrhagic follicles (AHFs). Reproduction in Domestic Animals 44:395-405,
2009
 Ovarian hematoma – controversial, rule out corpus hemorrhagica
 Can result in exsanguination
Granulosa cell tumor (Image 162)
 Most common equine ovarian neoplasm
 Clinical signs:
o Anestrus
o Continuous/intermittent estrus
o Stallion-like behavior
 Gross:
o Usually cystic, can be solid




Histologic findings:
o Gland-like or rosette patterns of abortive follicles, some of which may contain a
secretory globule resembling an ovum (Call-Exner body)
Rarely metastasize (but it’s been reported)
Clinical pathology:
o Elevated testosterone
Associated lesion:
o Contralateral ovarian atrophy (due to inhibin production)
Ovarian teratoma (Image 163)
Respiratory
Rhinitis
 Viral
o




Equine viral rhinopneumonitis
 EHV-4 in weanlings and racehorses (persists latently in trigeminal
ganglion)
 EHV-1 with abortions in mares
o Equine influenza (type A) – rarely progresses to pneumonia
o Equine rhinovirus
o Equine adenovirus
o Equine parainfluenza virus
o Equine viral arteritis
Bacterial
o Streptococcus equi
o Glanders (Pseudomonas mallei) → pyogranulomatous nodules → ulcer
Fungal
o Basiodiobolus (Image 164)
o Pythium, Conidiobolus etc.
o Aspergillus (Image 165)
o Cryptococcus neoformans → granulomas
Rhiestrus purpureus (Russian gadfly) – nasal myiasis
Rhinosporidium seeberi → polypoid stromal proliferation ± granulomatous rhinitis
Progressive nasal/ethmoid hematoma (Image 166)
 Gross:
o Hemorrhagic nasal polyps that arise unilaterally from the ethmoid region
o May be large enough to stick out a naris
o Highly vascular polyps hemorrhage, hemosiderosis, and fibrous tissue (from
repeated episodes from hemorrhage), and edema
o Prominent ferruginous and calcareous encrustations of collagen fibers and
vessel walls
o Giant cells
 Tends to recur
 Meuten 4th ed. p.376
Nasal and Sinus tumors

Squamous cell carcinoma (Image 167)

Adenocarcinoma

Cryptococcus neoformans – granulomas can be really big and aggressive (Image
168)
Chronic pharyngitis with lymphoid hyperplasia (Image 169)
 Thoroughbreds <5yrs
 Gross:
o Polypoid projections of the pharyngeal mucosa
o White plaques/nodules (lymphoid hyperplasia)
 JKP 5th ed. vol. 2 p.537
Entrapped epiglottis (Image 170)
 Epiglottis is entrapped under the arytenoepiglottic fold
 Associated or Predisposing condition:
o Dorsal displacement of the soft palate
o Congenital hypoplasia of the epiglottis
o Other epiglottic deformities
 McGavin 4th ed. p.486
Subepiglottic cysts
 Thought to arise from thyroglossal duct remnants
Epiglottic squamous cell carcinoma (Image 171)
Laryngeal hemiplegia (Roarer)
 Pathogenesis:
o Idiopathic degeneration of the left recurrent laryngeal nerve → denervation
atrophy and fibrosis of the left cricoarytenoideus dorsalis muscle
 Gross:
o Pale, atrophic cricoarytenoid muscle (Image 172)
Guttural pouch empyema (Image 173)
 Causes:
o Streptococcus equi equi (Strangles)
 Gross:
o Suppurative guttural diverticulitis
o Inspissated pus can form chondroids (Image 174, 175)
Guttural pouch mycosis (Image 176)
 Causes:
o Aspergillus fumigatus → thrombosis → infarction → necrosis → erosion of
internal carotid → hemorrhage; also mycotic osteomyelitis
o Pythium insidiosis if eosinophilic and granulomatous


Gross:
o Fibrinonecrotic guttural diverticulitis
Guttural pouch squamous cell carcinoma
Tracheal collapse (Image 177)
Lungworms

Dictyocaulus arnfeldi (donkeys) (Image 178, 179)
o Gross:
 Scattered, wedge-shaped foci of overinflation (especially in the caudal
lung lobes)
 Bronchi packed coiled adult worm
 Goblet cell hyperplasia, lymphocytic infiltrates
 Catarrhal to eosinophilic bronchitis

Parascaris equorum
o Gross:
 Nodules
 Migrating larval stages in interstitium, alveoli or bronchi surrounded by
eosinophils, lymphocytes, fibrosis ± mineralization
th
JKP 5 ed. vol.2 p.635

Recurrent airway obstruction (RAO; heaves; chronic obstructive pulmonary disease
(COPD))
 Pathogenesis:
o Genetic predisposition?
o Th2 allergic immune response
o Hypereactive airways
o Common allergens: Micropolyspora faeni, Aspergillus fumigatus, Actinomycetes
 Gross:
o Normal or emphysematous (Image 180)
o Goblet cell metaplasia in bronchioles
o Plugging of bronchioles mucus and eosinophils
 Can result in atelectasis and/or emphysema
o Peribronchiolar lymphocytes, plasma cells, mast cells, eosinophils
o Hypertrophy of smooth muscle around bronchi and bronchioles
 McGavin 4th ed. p. 504; JKP 5th ed. vol.2 p.560
Rhodococcus equi
 Foals
 Pathogenesis:
o Bacteria in the soil get inhaled → Bacteria are not killed by the macrophages →
suppurative to pyogranulomatous bronchopneumonia
 Bacteria are coughed up and swallowed, they enter the M cells in the
intestines → pyogranulomas in the gut-associated lymphoid tissue
(GALT) and mesenteric lymph nodes → pyogranulomatous and ulcerative
typhlocolitis and lymphadenitis
 Gastrointestinal form can also come from ingestion of contaminated feed
etc.
 Gross:
o 1-10cm tan firm nodules, especially cranioventral (Image 181, 182)
o Enlarged lymph nodes
o Pyogranulomatous bronchopneumonia
 Central caseous necrosis
 Bacteria in macrophages
o Pyogranulomatous lymphadenitis
 Associated Lesions:
o Pyogranulomatous typhlocolitis and lymphadenitis
o May go systemic with arthritis, hepatic and splenic abscess, hypopyon etc.
 JKP 5th ed. vol.2 p.226, p.630
Multifocal white dit-dots in the lungs (Image 183)

Salmonella bronchopneumonia (Image 184)

Embolic Aspergillosis (Image 185)
o Associated lesion:
 Colitis, often Salmonella
 VetPath 44(2):215-217. 2007; JKP 5th ed. vol.2 p.634

Early Rhodococcus equi – may be more cranioventral

Equine herpesvirus-1

Lots of other possible causes…
Multinodular Equine Pulmonary Fibrosis (Image 186)
 Cause:
o Equine herpesvirus-5 (gamma herpes)
 Gross:
o Multifocal to coalescing tan nodules
o ALL lobes affected
o Interstitium expanded by fibrosis
o Alveolar architecture maintained


 Alveoli lined by cuboidal epithelium and contain mixed inflammation
o Intranuclear inclusion bodies in macrophages (NOT epithelial cells)
”Soft fibrosis of the equine lung” Dr.King
JKP 5th ed. vol.2 p.569 and VetPath 44(6):849-862. 2007
Granular cell tumor (Image 187)
 Most common primary lung tumor in the horse
 Originates from Schwann cells in the peribronchial tissue
 Usually an incidental finding
 NO metastases
 Gross:
o Tan mass, often in large bronchi
o Unilateral, multinodular
o Sheets or lobular aggregates of large, round or angular cells abundant
cytoplasm containing tiny acidophilic granules
 Granules are Luxol fast blue positive; variably PAS positive
 Lysosomes?
 Also tongue of dogs, meninges and urogenital system of rats…
Metastatic hemangiosarcoma (Image 188)
Urinary
Normal mucus in the renal pelvis (Image 189)
Pigmentary nephrosis
 General Pathogenesis:
o Increased serum hemoglobin, myoglobin (or bile) → they enter the glomerular
filtrate → high concentrations of these concurrent ischemia (hypovolemic shock;
anemia) → acute tubular necrosis
 Causes:
o Red Maple (Acer rubrum) (hemoglobinuric nephrosis) (Image 190, 191, 192)
 Pathogenesis:
 Oxidative damage → denaturation of hemoglobin → Heinz bodies
→ extravascular hemolysis
 Oxidative damage → cross-linking of membrane proteins →
eccentrocytes → extravascular hemolysis
 Heinz body formation and oxidation of cell membranes can cause
sufficient cellular damage for hemoglobin to escape from the
cytoplasm → hemoglobinemia (intravascular hemolysis)
 Oxidative damage → methemoglobinemia → interferes oxygen
transport and methemoglobinuria
 Duncan & Prasse, 4th ed. p35
 Rule out Babesia, neonatal isoerythrolysis
o Rhabdomyolysis (myoglobinuric nephrosis)
 Accumulation of myoglobin in tubules
o Bile (cholemic nephrosis)
Renal medullary crest necrosis (it’s not technically a papillae in horses)
 Cause:
o Non-steroidal anti-inflammatory drugs (NSAIDs)
 Pathogenesis:
o NSAIDs → inhibition of prostaglandin (PG) synthetase → decreased PGs →
decreased vascular tone and perfusion → ischemia → necrosis
o NSAIDS → interstitial cell damage decreases PG synthesis → decreased blood
flow → ischemia
o The inner medulla is the least well-perfused area, so any lesion that further
decreases medullary flow → ischemic infarction of the papillae
o Dehydration makes it all worse
 Gross:
o Green to yellow discoloration of the renal crest (Image 193)
o ± Mineralization
Actinobacillus equuli
 Pathogenesis:
o Infection acquired in utero or shortly after birth → sepsis → bacteria lodge in
glomeruli (glomerulonephritis) or in vessels (infarcts)
 Gross:
o Multifocal focal yellow/green foci (<3mm) in the renal cortex (tiny cortical
abscess) (Image 194a,b)
o Suppurative embolic glomerulonephritis intralesional bacterial colonies
o Umbilical infection
o Polyarthritis
 Differentials:
o E.coli (Image 195) or other septicemia
Halicephalobus gingivalis (rhabditid nematode) (previously Micronema deletrix)
 Pathogenesis:
o Parasite from soil invades skin and mucous membrane (nasal/oral) → invasion of
the sinuses and bones of the head, and/or hematogenous spread
 Gains access to the brain via migration along vessels
o Prenatal or transmammary infection of suckling foals
 Organ involvement:
o Brain > kidneys > oral and nasal tissue > lymph nodes > lungs > spinal cord >
adrenal
 Gross:
o Firm, gray-white nodules in the kidneys etc. (Image 196a,b)
o Rule out neoplasia
o Granulomas surrounding adult and larval nematodes ± eggs
 Adult females: 15-20mm diameter, 250-430mm length
 Larvae: ~10mm diameter, rhabditiform esophagus, tapered tail
o Hyperglobulinemia and hyperfibrinogenemia (chronic inflammation)
o Elevated creatine kinase (muscle injury from parasites, trauma, or recumbency)
o Elevated creatinine (postrenal obstruction due to lower motor neuron disease if
cauda equina neuritis).
 JKP 5th ed. vol. 2 p. 479
Renal infarct (Image 197)
 Gross:
o Wedge shaped
o Acute – red
o Chronic – depressed
Bladder infarcts (urinary bladder fundic necrosis) (Image 198)
 Pathogenesis:
Increased pressure in the bladder (neurogenic distention, obstruction etc.) →
compresses blood supply from the trigone (neck) of the bladder and the sides of
the bladder → ischemic necrosis
Dr. King’s website; JKP 4th ed. vol. 2 p.506
o

Bladder hemorrhage (Image 199)
 Cantharidin (blister beetle, Epicauta spp.)
 Thrombocytopenic Purpura
 Purpura hemorrhagica
Bladder rupture (cystorrhexis) (Image 200, 201)
 Occurs on dorsal side because that’s where the fibers come together
o Can be ventral…
 Primarily male foals
 Causes:
o Birthing trauma
 Twists in the amniotic portion of the umbilical cord may compress the
urachus, impair outflow and lead to rupture
o Congenital abnormality (rare)
o Atrophy of the smooth muscle (rare)
o Uroabdomen
o Addison-like
o Hyponatremia
o Hypochloremia
o Hyperkalemia
o Peritoneal fluid:serum ratio > 2:1 for potassium, phosphate, creatinine
 JKP 4th ed. vol. 2 p.507
Bladder squamous cell carcinoma (Image 202)
 Most common urinary bladder tumor in horses
Other
Inguinal hernia (Image 203)
 Herniated viscera pass down the inguinal canal
 May be a genetic predisposition
 Direct
o Less common
o Contents pass through the internal inguinal ring and end up subcutaneously
 Can have necrosis of the overlying skin, strangulation of the intestines
etc.
 Life threatening
o Pathogenesis:
 Increased intraabdominal pressure during birth
 Indirect
o More common
o Congenital or acquired (exercise, breeding)
o Contents pass through the inguinal and vaginal rings within the vaginal sheath
and are retained within the tunica vaginalis of the scrotum
 May have secondary testicular degeneration
 Can rupture out of the tunica vaginalis and end up subcutaneously, in
which case the complications are similar to direct hernias
th
 JKP 5 vol.2 p.93; vol.3 p.602
Diaphragmatic hernia entrapment and venous infarction of intestines (Image 204)
 Congenital
 Acquired (traumatic)
o Usually involves the area where the tendinous portion of the diaphragm meets
the pars costalis
 Postmortem diaphragmatic
o Usually occurs at the ventral midline (xyphoid)
 Usually present colic, not respiratory distress
Pneumoperitoneum (Image 205)
 Causes:
o Traumatic abdominal wall rupture
o Concurrent pneumothorax and diaphragmatic tears
o Gastrointestinal rupture
o Urinary bladder rupture
o Reproductive tract rupture (females)

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