Food Animal Disease

Question 1

Bloat results in pressure on what two structures/groups of structures?

Answer 1

(Diaphragm and abdominal vessels → primarily caudal vena cava)

Question 2

A cow presents to you with signs of bloat and you ask about their diet and the farmer tells you they have been feeding clover since they have an abundance of it, what type of bloat would you be leaning towards?

Answer 2

(Frothy bloat)

Question 3

What other feed stuff could induce frothy bloat (so besides lush legumes)?

Answer 3

(Alfalfa hay and high grain diets)

Question 4

The basis of free-gas bloat is that the cardia is not cleared and that results in the cow being unable to eructate. What are three possible causes of the cow not being able to clear the cardia?

Answer 4

(Decreased rumen motility d/t decreased pH or increased VFAs, hypocalcemia, and blockages)

Question 5

Why will a cow with bloat have an increased heart rate?

Answer 5

(To compensate for the decreased cardiac output due to decreased venous return)

Question 6

Drenching a cow with soap solution will work for what kind of bloat?

Answer 6

(Frothy → breaks down the bubbles)

Question 7

Is hardware disease more common in dairy or beef cattle?

Answer 7

(Dairy)

Question 8

You are performing a withers pinch test on a dairy cow and she bows when you apply pressure, is this a positive or negative result?

Answer 8

(Negative)

Question 9

What clinical pathology abnormalities may a chronic hardware disease cow have? Three answers.

Answer 9

(Increased fibrinogen, increased plasma proteins, increased A/G ratio)

Question 10

Changes surrounding what aspect of cattle husbandry is the typical culprit for causing simple indigestion?

Answer 10

(Changes in feed)

Question 11

How long does it take for ruminal microbes to adapt to new feed?

Answer 11

(1-2 weeks)

Question 12

What results from excessive consumption of readily fermentable carbohydrates?

Answer 12

(Rumen acidosis aka grain overload or lactic acidosis)

Question 13

What should you do to diagnose rumen acidosis?

Answer 13

(Rumenocentesis, pH will be less than 5 and there will be no live protozoa)

Question 14

What are the two types of vagal indigestion and which of them is more common?

Answer 14

(Failure of rumen to empty/omasal transport failure (more common) and abomasum fails to empty/pyloric outflow failure)

Question 15

Why does the increased motility of the rumen in omasal transport failure vagal indigestion not result in forward movement of ingesta?

Answer 15

(The contractions are all unorganized, do not move the ingesta correctly)

Question 16

The rumen will be hyper/hypochloremic while the blood will be hyper/hypochloremic in a pyloric outflow failure vagal indigestion.

Answer 16

(Rumen - hyperchloremic, blood - hypochloremic → metabolic alkalosis)

Question 17

If you perform a Liptak test on a cow that does not have an LDA, what do you expect the pH to be?

Answer 17

(pH of the rumen → 5.5-8)

Question 18

What two abnormal urine findings would be suggestive of abomasal displacement?

Answer 18

(Ketonuria and acidic urine)

Question 19

How can you tell the difference between a simple displaced right abomasum and a right torsed abomasum?

Answer 19

(Clinical signs → will be more severe (signs of shock, cool extremities, heart rate 100+ bpm, acutely ill) for right torsed abomasum)

Question 20

(T/F) Both left and right displaced abomasums can undergo torsion.

Answer 20

(F, only right)

Question 21

(T/F) The ‘roll and toggle’ or ‘roll and tack’ method can only be used for left displaced abomasums.

Answer 21

(T)

Question 22

What type of neoplasm is indicated in an abomasal impaction due to pyloric obstructions?

Answer 22

(Lymphosarcoma)

Question 23

What are two possible etiologies of abomasal ulcers in calves?

Answer 23

(Eating solid feed and copper deficiency)

Question 24

Why are high producing dairy cows early in lactation more commonly affected by abomasal ulcers?

Answer 24

(Lots of stress → stress ulcers)

Question 25

What is the most common clinical sign of hepatic disease in ruminants?

Answer 25

(Weight loss)

Question 26

What is a common clinical sign of chronic hepatic disease in ruminants?

Answer 26

(Diarrhea)

Question 27

What type of toxicity is induced by the senecio and crotalaria plant species?

Answer 27

(Pyrrolizidine alkaloid toxicity)

Question 28

What are pyrrolizidine alkaloids converted into that can cross link with DNA, triggering those cells to be unable to divide which leads to megalocytosis and fibrosis of the biliary system?

Answer 28

(Pyrroles)

Question 29

Is pyrrolizidine alkaloid toxicity an acute or chronic disease?

Answer 29

(Chronic)

Question 30

What population of animals is most susceptible to pyrrolizidine alkaloid toxicity?

Answer 30

(Calves)

Question 31

How do you prevent pyrrolizidine alkaloid toxicity since there is no treatment?

Answer 31

(Avoid first cutting alfalfa)

Question 32

What degradation product of chlorophyll that is usually removed by the liver can build up when there is liver damage and cause secondary photosensitization?

Answer 32

(Phylloerythrin)

Question 33

Why are liver abscesses more common in feedlot cattle?

Answer 33

(Because feedlot cattle are on high grain diets which can lead to ruminal acidosis which can then lead to ruminal damage and that all drains to the liver)

Question 34

What two bacterial agents are the typical culprits in liver abscesses?

Answer 34

(Fusobacterium necrophorum and Trueperella pyogenes)

Question 35

How can liver abscesses cause ascites and diarrhea?

Answer 35

(By infiltrating the caudal vena cava and causing thrombosis, that leads to back up of GI tract draining vessels → ascites and diarrhea)

Question 36

In a cow with liver abscesses, will they be painful mostly on their right or left side?

Answer 36

(Right)

Question 37

Ruminants typically have more lymphocytes than neutrophils (which is the opposite of other animals), will this relationship change in an animal with liver abscesses?

Answer 37

(Yes, will shift so that there are more neutrophils than lymphocytes)

Question 38

How are liver abscesses treated?

Answer 38

(Long term penicillin)

Question 39

Fat cow syndrome affects what type of cow and when?

Answer 39

(Overconditioned dairy cows in the postpartum period)

Question 40

What is glucose made from in the liver in ruminants?

Answer 40

(Propionic acid and glycerol)

Question 41

Fat can be broken down into free fatty acids and glycerol to supply glycerol to make more glucose, but if you have an oxaloacetate deficiency, free fatty acids cannot be processed by the Krebs cycle so instead they become what?

Answer 41

(Ketone bodies)

Question 42

Why do cows with fat cow syndrome develop a fatty liver?

Answer 42

(Triglycerides leave the liver via VLDLs but ruminants have limited VLDLs so if they get overwhelmed by lots of triglycerides in the liver → fatty liver)

Question 43

What is a disease of small ruminants that is observed in the last 6 weeks of gestation in females carrying multiple fetuses?

Answer 43

(Pregnancy toxemia)

Question 44

What population of cows is at the greatest risk of protein-energy malnutrition?

Answer 44

(Growing pregnant heifers)

Question 45

What other coinfection is necessary to establish the anaerobic environment necessary for Clostridium novyi type B to proliferate in the liver?

Answer 45

(Coinfection with liver flukes)

Question 46

What is the causative agent of bacillary hemoglobinuria aka redwater disease?

Answer 46

(Clostridium hemolyticum)