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Pathology lab 5 unit 2

Terms in this set (13)

1. description: red with multifocal darker areas, friable/dry tissue with gas bubbles
2. MORPH: hindlimb, gas gangrene (or coagulative necrosis), severe, and acute
3. black leg
4. Clostridium chauvoei
5. PATH: Clostridium chauvoei ingested from environment > chauvoei lays dormant > trauma (usually to muscle) > creates low O2 environment > allowing spores to produce toxins > toxins produce hemorrhage or gas > kills animals rapidly
case 1:
this is skeletal muscle from a 6 month-old steer that acutely died with no previously noted clinical signs; you vaccinated and dewormed a week ago; lesions are mainly seen in the left hind limb

1. describe the lesion
2. what is the morphological diagnosis?
3. what is the common name of this disease?
4. what is the known causative agent?
5. propose a pathogenesis for this lesion based on clinical history
1. description: sharply demarcated, crusty, dry, and shrunken, bilateral
2. MORPH: pinna of the ear, dry gangrene (or arterial infarction with dehydration), chronic, severe
3. PATH: trauma at site > staff infection in wound > localized bacterial infection produces toxins that cause cell death and thrombus > infarction

this kind of injury is common on the ear tip and tail
case 2:
this piglet presented with its littermate to the food animal department with multiple skin wounds from fighting
1. describe what you see
2. what is the morphologic diagnosis for the ear pinna?
3. what is proposed pathogenesis for this lesion?
gangrene: necrosis that develops at the distal aspect of extremities (limbs, tail, pinnae) or in dependent portions of organs (mammary glands, lungs)

dry gangrene (coagulative necrosis): seen in extremities due to vascular compromise or ischemia (tail, ears, toes); ergot toxicity; form of infarction resulting in coagulative necrosis, few to no bacteria present, black discoloration results from interaction of hemoglobin and hydrogen disulfide = iron sulfide

wet gangrene: necrotic tissue invaded by saprophytic bacteria (putrefactive), results in a liquefactive necrosis component, typically occur in moist tissues, develops rapidly due to blockage of venous blood flow (less so with arterial obstruction), presence of accumulated blood = rich medium for bacterial growth, toxic bacterial byproducts can be absorbed > sepsis, swollen, soft, pulp, dark in color with putrefactive smell, no viable blood supply; cold to touch

gas gangrene: wet/moist gangrene with anaerobic fermentation of Clostridium spp. and gas production; life-threatening; clostridium spp. enters tissue through a contaminated would or pathogenically proliferates in GI tract (normal flora in most species), bacteria rapidly spreads through tissues (especially in muscles) > extensive necrosis and edema, gas released by the organisms form bubbles in the tissues > crepitations on palpation
summarize the differences between
dry gangrene, wet gangrene, and gas gangrene
(Clostridium chauveoi)
spores ingested and become latent in muscle > bruising injury cause hemorrhage > anaerobic environment > bacteria proliferate, produced toxins > necrosis and emphysema production
pathology of blackleg in cattle
1. description: locally extensive, yellow-white, chalky mineralization > calcium deposit >saponification of fat
2. MORPH: pancreatic fat, fat necrosis with saponification, severe, subacute, chronic
case 3:
this is a tissue from a cat that presented with severe abdominal pain.
1. describe the changes you see within the tissue around the pancreas
2. what is your morphological diagnosis?
1. dystrophic mineralization: means of neutralizing the effects of necrotic tissue, can have mechanical effects depending on location; calcium overload in areas of necrosis - expected sequela of irreversible cell injury and death
2. metastatic: targets of intima and tunica media of vessels (lungs, pleura, endocardium, kidneys, stomach), imbalance in calcium and phosphate
what are the two types of calicifation?
enzymatic fat necrosis

pancreas is inflamed > leaky vessels > release of lipase and other enzymes that break down peripancreatic fat > lipase damage fat cells > release and splitting of triglycerides into fatty acid components > FAs bind to calcium > saponification
this cat was diagnosed with pancreatitis. What is the pathogenesis for this lesion?
1. enzymatic fat necrosis (pancreatic)
2. nutritional fat necrosis (yellow fat disease) due to diet high in unsaturated fatty acids and low in vitamin E (or other antioxidants)
3. traumatic fat necrosis (blunt trauma or chronic pressure on adipose tissue against bony prominences)
4. Idiopathic fat necrosis (mesenteric and omental fat becomes firm (necrotic) around the viscera, lead to obstructive lesions in the bovine abdomen)
what are the causes of fat necrosis?
1. dark purple vessels with shading of pink around it, no sharp demarcation
2. hemoglobin imbibition: staining of tissues by free hemoglobin
case 4:
this is the abomasum of a cow that has been dead for 18 hours.
1. describe the changes that you see.
2. what is the postmortem change responsible for the red to pink color in this image?
1. grey/black/green discoloration with locally extensive red patches
2. the black coloring is key - pseudomelanosis is the most common post mortem change; bacteria produce hydrogen sulfide that bind with hemoglobin and create a black color - common within the guts and any structure touching the guts
case 5:
this is a section of jejunum from a horse that died the previous day.
1. describe the changes
2. what is the change you are seeing?
1. description: light tan, breakable, gas bubbles
2. gas accumulation create post mortem enphysema (post mortem bacteria invading the tissues)
case 6:
this is a picture of the liver of the same horse (with pseudomelanosis of the jejunum) as the previous slide.
1. describe the changes you see.
2. what is this post mortem change?
1. diffusely pale cortex, slightly enlarged
2. this is a lugol Iodine stain, that stains for amyloid

(bonus: amyloid is a beta pleated sheet protein that was folded incorrectly, so it cannot be broken down, causing it to accumulate - it's an extracellular product)
case 7:
these are the kidneys of a dog that presented with generalized subcutaneous edema.
1. Describe the changes you see?
2. do you know what stain is applied to the kidney in the bottom right and what this stain is used for?
1. eosinophilic homogenous protein
2. congo red proves it is amyloid
case 7:
these are the kidneys of a dog that presented with generalized subcutaneous edema.
1. describe the kidney changes
2. what is the stain used in the bottom right image and what is it staining?
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