Organ Path Test 1

Front 1

Etiology;
Equine prtozoal myeloencephalitis

Back 1

Sarcocystis neurona

Front 2

Etiology
Equine Polioencephalomyelitis
WEE: Western Equine Encephalitis
EEE: Eastern
VEE: Venezuelan
WNV: West Nile Virus

Back 2

WEE: Arbovirus
EEE: Arbovirus
VEE: Arbovirus
WNV: West Nile Virus

Front 3

Equine leukoencephalomalacia
Etiology:

Back 3

Fusarium verticillioides toxin
(Fumonisin B1 in moldy corn)

Front 4

Equine leukoencephalomalacia
Pathogenesis

Back 4

Toxic vasculitis of selected brain microvasculature

Front 5

Equine Viral Rhinopneumonitis
Etiology

Back 5

Equine herpesvirus

Front 6

Equine Viral Rhinopneumonitis
Pathogenesis

Back 6

bronchointerstitial pneumonia
secondary bact infections
abortions in mares

Front 7

Equine Influenza
Etiology

Back 7

Opportunistic bacteria:
-Streptococcus spp
- E.coli
-Klebsiella pnemonia
-Rhodococcus equi

Front 8

Equine Influenza
Pathogenesis

Back 8

Sperimposed bacterial infections leading to fibrinous or suppurative bronchopneumonia

Front 9

Rhodococcus equi
pathogenesis

Back 9

small whitish foci (abscesses) distributed anteroventrally.
inhalation

Front 10

Verminous Arteritis
Etiology

hemomelasma ilei

Back 10

Strongylus vulgaris

Strongylus edentatus

Front 11

Guttural Pouch Mycosis
etiology

Back 11

Aspergillus fumigates
Aspergillus Spp

Inhalation of spres from moldy hay

Front 12

Guttural pouch mycosis
Pathogenesis

Back 12

Proximity to interanl carotid artery
vascular erosion and epistaxis
Aneurysm & fatal bleeding
Fugi: angioinvasive: mycotic thromboemboile into carotid -> cerebral infarcts
Dysphagia: damage to pharyngeal brances of the vagus & glossopharyngeal nerves
Horner's syndrome: Cr cervical ganglion & sympathetic fibers

Front 13

Hepatic lipidosis
pathogenesis

Back 13

excessive lipid w/in liver
-lactation
-starvation
-abnormal hepatocyte function
-diabetes mellitus
-hypothyroidism

Front 14

hepatic lipidosis
Clinical signs

Back 14

Ponies (especially Shetland ponies) and miniature horses are predisposed
Clinical Signs
• Hepatomegaly
• Friable
• Greasy
• Yellow
• Floats in formalin
Must differentiate from steroid hepatopathy

Front 15

Hepatic Encephalopathy

Back 15

• Young animals
• Congenital anomaly
• Spider-like arranged vessels
• Stomach is somewhat large, liver is somewhat smaller
• Portocaval shunt

Front 16

Equine Serum Hepatitis
etiology

Back 16

infectious agent
This condition occurs, for the most part, in horses that have received an injection of a biologic that contains equine serum:
• Equine antisera
• Tetanus antitoxin
• Pregnant mare serum gonadotropin

Front 17

Streptococcal meningitis
etiology

Back 17

Streptococus suis

Front 18

Streptococcal meningitis

Back 18

Inflammation of the leptomeninges (pia matter, subarachnoid space, adjacent aracnoid mater.
Type 1: causes dz in suckling pigs ranging from 1-6 weeks
Type 2: affect older pigs 6-14 weeks
more important can cause dz in humans
Fibrinopurent, necrotic foci

Front 19

Streptococcal meningitis
C/S

Back 19

• Clinically affected animals are initially ataxic and then become laterally recumbent with rhythmic paddling of the limbs.
• As disease progresses they may become comatose and die.

Front 20

Salt poisoning: aka Eosinophilic Meningoencephalitis

Etiology

Back 20

Excessive Dietary Na
Restrcted H2O intake

Front 21

Eosinophili meningoencephalitis
Pathogenesis

Back 21

• Laminar cortical neuronal degeneration
• Edema
• Eosinophilic leukocyte and lymphomonocytic perivasculitis and meningitis.
• Necrosis with glitter cells
• Osmotic encephalitis:

• Hypernatremic syndrome

• Movement of water back and forth across osmotic barriers in relationship to osmotic gradients.

• Inhibition of glycolysis in neurons and/or damage to BBB with edema (vasogenic).

Front 22

Edema Disease
Etiology

Back 22

E. Coli

Front 23

Edema Disease
Pathogenesis

Back 23

Edema disease principle (EDP)
• Gram negative bacterial endotoxin that is neurotoxic
• Acts at BBB (vasogenic edema)
• Affects vascular endothelial function
• Alters function of neurons

Front 24

Mycoplasma hypopneumoniae

Aka

Back 24

porcine enzootic pneumonia

Front 25

Mycoplasma hypopneumoniae
Etiology:

Back 25

Mycoplasma hypopneumoniae

Front 26

Mycoplasma hypopneumoniae
Pathogenesis

Back 26

• M. hyopneumoniae is present in the air.
• Adheres to cilia of the bronchi
• Colonizes the ciliated epithelial cells
o Trachea and bronchi of the cranioventral regions of the lungs. This changes the chemical composition of mucus and predisposes the lung to secondary bacterial infections.
• Influx of neutrophils into the trachebronchial mucosa
o Extensive loss of cilia and reduce phagocytic activity of neutrophils.
• Intense hyperplasia of lymphocytes in the BALT
o Mononuclear cells into the bronchoalveolar interstitium.

Front 27

Acinobacillus Plueropnemoniae
aka APP

Etiology

Back 27

Actinobacillus pleuropneumoniae (Haemophilus pleuropneumoniae)

Front 28

Acinobacillus Plueropnemoniae

Etiology

Back 28

• Transmission occurs by the respiratory route.
• Can sporadically produce septicemia in young pigs and otitis media and interna with vestibular syndrome in weaned pigs.
• Virulence factors allow for attachment to cells.
• Produce pores in cell membranes
• Damage capillaries and alveolar walls, resulting in vascular leakage and thrombosis.
• Impair phagocytic function and elicit failure of clearance mechanisms

• Gross lesion in the acute form consist of fibrinous bronchopneumonia characterized by severe consolidation and a fibrinous exudates on the pleural surface.
• A common site that is affected is the dorsal area of the caudal lobes.
• A large area of fibrinous pleuropneumonia involving the caudal lobe of a pig’s lung is considered almost diagnostic for this disease.

Front 29

Atrophic rhinitis

etiology

Back 29

: Bordetella bronchioseptica and Pasturella multocida

Front 30

Atrophic Rhinitis

Pathogenesis

Back 30

• B. bronchioseptica:
o Mild to moderate turbinate atrophy
o Promotes the colonization by P. multocida
• P. multocida:
o Potent cytotoxins inhibit osteoblastic activity
o Promote osteoclastic reabsorption in nasal bones. Abnormal bone remodeling results in atrophy of turbinates.

Increased incidence of bronchopneumonia

Front 31

Mulberry Heart Disease

etiology

Back 31

• Deficiency of Vitamin E (antioxidant)
• Deficiency of selenium (glutathione peroxidase)

Front 32

Mulberry Heart disease
Pathogenesis

Back 32

• Lack of antioxidants and reducing agents
• Lipid peroxides (oxygen-free radical) damage myocardial cells
• Usually die of fatal ventricular arrhythmia
• Often seen with hepatosis dietetica

• 3-4 month old pigs
• Excellent condition
• Animals found dead

Front 33

Interventricular septal defects
pathogenesis

Back 33

• Left to Right shunt
• Right ventricular hypertrophy/dilation

Front 34

Ascaris suum (milk spots)
etiology

Back 34

Ascaris suum

Front 35

Ascaris suum
Pathogenesis

Back 35

• Larvae migration through the liver.
• Larvae produce local tracts of hepatocellular necrosis that are accompanied by inflammation.
• These tracts are replaced with connective tissue that matures into fibronous scars.
• Scars are prominent on the capsular surface and term milk spotted fever.
Other Notes: Remember that you can also have pulmonary interstitial edema with hemorrhage.

Front 36

Aflatoxicosis
etiology

Back 36

• Aspergillus flavus (main one in book), and Aspergillus parasiticus
• Toxin: Aflatoxin B1 elaborated during storage of fungal-contaminated feed

Front 37

Aflatoxicosis

Pathogenesis

Back 37

• Chronic intoxication:
o Affected livers are firm and pale.
o Lipidosis and necrosis
o Biliary hyperplasia
o fibrosis

Front 38

Hepatosis dietetica
etiology

Back 38

nutritional deficiency Vitamin E or selenium
• Enzymes are antagonists of free radical formation
• Maintenance of stability and integrity of cellular membranes (i.e. lipid peroxidation)

Front 39

Hepatosis dietetica

Back 39

• Hemorrhagic centrolobular necrosis
• Massive hepatic necrosis
• Disease a.k.a. nutritional hepatic necrosis (Syndrome of acute hepatic necrosis)
• Young, rapidly growing pigs