Unit 2

Question 1

What are other names for Bovine Ketosis?

Answer 1

Acetonemia, ketonemia

Question 2

When does bovine ketosis usually occur?

Answer 2

Mainly disease in dairy cows 4-6 following parturition

Question 3

What happens when an animal has bovine ketosis?

Answer 3

Ultimately, body fat ends up being utilized for energy, and they produce more ketones than their body can utilize

Question 4

What is the cause of bovine ketosis?

Answer 4

1. Heavy lactation resulting in high glucose demand – lactose production
2. Any factor that reduces the absorption of carbohydrates – secondary to decreased appetite
3. Majority of carbohydrates are metabolized into fatty acids

Question 5

What is bovine ketosis often associated with?

Answer 5

Often associated with underfed cattle, poor quality hay or silage (leads to decrease propionic acid production)

Question 6

What is lactose and why is it important with bovine ketosis?

Answer 6

Lactose = a major enzyme in milk. Made from glucose and galactose. A cow needs to be able to convert carbohydrates into glucose due to increase demand but is not able to do this.

Question 7

What happens to cattle when ketone levels increase? When does this happen?

Answer 7

As ketone levels increase, appetite with DECREASE. They may also go off-feed when they have their calf. At any point, if the cow is not getting enough nutrients, this will happen.

Question 8

What happens when carbohydrates are metabolized into fatty acids in the case of bovine ketosis?

Answer 8

The majority of carbohydrate microbial fermentation happens in the rumen. Creates volatile fatty acids (acetic, propionic, butyric acid). Cows do not absorb glucose from the GI tract; they need to make their own.

Question 9

What is the purpose of propionic acid?

Answer 9

Used to metabolize/ make glucose

Question 10

How does insufficient feed intake cause bovine ketosis?

Answer 10

1. Feed intake does not meet energy demand
2. Insufficient ruminal production of propionic acid, a precursor of glucose
3. Not enough glucose, so cow becomes hypoglycemic (low blood sugar)
4. Low blood sugar makes cows metabolize fatty acids & glycerol supplies
5. Fatty acids and glycerol are oxidized to form acetyl-CoA
6. Lack of energy, the liver cannot cope
7. Excess of acetyl-CoA (due to lack of energy) so it is converted to ketone bodies
8. KETOSIS = ketone bodies accumulate and excreted in milk and urine

Question 11

What are the signs of bovine ketosis?

Answer 11

1. Inappetence, anorexia, depression
2. Incoordination
3. Drop in milk production
4. Weight loss
5. Lethargy
6. Haircoat dull

Question 12

How can bovine ketosis be diagnosed?

Answer 12

A metabolic disorder, meaning you won’t see any elevation in body temperature. History is important – recent parturition and ketone odor in milk or breath (sweet acetone-like smell)

Question 13

What is the treatment for bovine ketosis?

Answer 13

Need to reestablish blood glucose levels
1. Glucose –> IV glucose (usually more than one time over 3-4 days)
2. Propylene glycol (glucose precursor) –> given orally. It needs the liver to be functioning and the rumen to be contracting to be absorbed
3. Glucocorticoids –> Leads to increase gluconeogenesis. It can suppress the immune response.
4. Sodium propionate (glucose precursor) –> Mix in with feed

Question 14

How can bovine ketosis be prevented?

Answer 14

Nutritional management is important. BCS useful. We want to maintain body condition during the dry period but don’t want to over OR underfeed right before she calves. Since calving can throw off appetite, a couple of weeks before calving, we want to change diet (more energy, get used to it). Grain will allow bacteria in the rumen to adjust. After she has a calf, ensure her energy requirements are met with good quality feed (good quality hay).

1. Decrease energy in the diet in late lactation and continue in the dry period (BCS 3.5).
2. Increase energy post-partum

Question 15

What is another name for Fat Cow Syndrome?

Answer 15

Fatty Liver Disease

Question 16

What is the cause of fat cow syndrome?

Answer 16

Feeding too high energy & too low roughage in late lactation & dry period

Question 17

What is the mechanism of fat cow syndrome?

Answer 17

Fat cells replace functioning liver cells. This is a cumulative process. Each time, she is getting liver cells are being replaced by fat cells (happens over long period of time). At some point, liver will not be able to produce enough glucose to support increased ketones.

Question 18

What are the effects of fat cow syndrome?

Answer 18

Fat cows have increased susceptibility to ketosis. Fat metabolism results in ketones

Question 19

How can fat cow syndrome be prevented?

Answer 19

BCS 3.5 at dry off

Question 20

What are other names for ovine ketosis?

Answer 20

Pregnancy disease, Pregnancy toxemia, Pregnancy ketosis, Twin lamb disease

Question 21

When does ovine ketosis occur?

Answer 21

This is a pregnancy disease in sheep and goats. It tends to occur in late gestation / advanced pregnancy. We see it more frequently in ewes that are carrying multiple fetuses.

Question 22

What are the causes of ovine ketosis?

Answer 22

1. Rapid growth of multiple fetuses –> Towards the end of gestation, this is when fetuses are growing fast. During last 6 weeks, majority of glucose production is going to support the growth of the fetuses, so ewe starts to metabolize fat.
2. Stressors
3. Demand for glucose is not met and hypoglycemia develops
4. Excess ketones are produced

Question 23

What are the clinical signs of ovine ketosis?

Answer 23

Develop anywhere from 1-4 weeks before partition. Progressive clinical signs. They may go off feed (partially), depression, separation. Because not enough glucose, may see some CNS signs, incoordination, weakness. If not corrected, they could die from this
1. Stand alone
2. Head pressing, teeth grinding
3. Anorexia, incoordination, weakness
4. Lethargy
5. Coma, death

Question 24

How is ovine ketosis diagnosed?

Answer 24

1. Clinical signs
2. Close to parturition

Question 25

What is the treatment for ovine ketosis?

Answer 25

1. Propylene glycol (glucose precursor) 2. Supplemental feed -->adding oats 3. Cesarean section --> If fetuses are still alive and ewe is close to deliver date AND not severely depressed, may be justified to do c-section. Producer must decide if it is economically viable. If fetuses are dead or too pre-mature to survive c-section and ewe is still in good shape, may be situation where we want to induce labor.

Question 26

How can ovine ketosis be prevented?

Answer 26

Rising plane of nutrition in late gestation. Nutritional management -- BCS should be moderate (no less than 2.5). Add grain for source of carbohydrates.

Question 27

When does Bovine Parturient Paresis occur?

Answer 27

1. Onset at or near parturition 2. Associated with high milk production This can be an acute onset or peracute onset (can be fast). We tend to see it in mature dairy cows. No increase in temp, develop flaccid paralysis (reduced muscle tone), usually seen right at or after partition (within first 72 hours). We can see it at any age, but usually in mature/ high producing (usually in 3rd parturition).

Question 28

What is the cause of Bovine Parturient Paresis?

Answer 28

1. Sudden loss of calcium into colostrum 2. High calcium in diet during dry period

Question 29

How does having high calcium during dry period effect cows?

Answer 29

Sudden loss of calcium going into colostrum / milk. Usually during dry period, getting too much calcium in diet. Hormones in the body help regulate calcium levels. These hormonal mechanisms to maintain Ca shut down. So when they need calcium, systems need time to amp up.

Question 30

Where are the normal sources of calcium in cattle?

Answer 30

Diet, skeleton (via bone resorption). Normally, get it from diet. If more calcium is needed can resorb calcium out of her bones. Enhances absorption of Ca from GI tract and reduced kidneys from losing calcium.

Question 31

What should normally happen with calcium in cattle, compared to what happens with milk fever?

Answer 31

Parathyroid hormone is part of what helps regulate Ca levels in the blood. Effects kidneys (won’t be excreted in urine), GI tract, calcium from the bone if needed. 1. Parathyroid gland --> senses low blood calcium 2. Increased parathyroid hormone secretion 3. Decreased excretion of calcium from kidneys --> increase absorption through intestine 4. Increased Ca release from bone

Question 32

What happens when there is high calcium in diet during dry period?

Answer 32

High blood Ca+ --> + calcitonin --> inhibits PTH. When not fed correctly or too much Ca during dry period, she will always have normal Ca in blood levels. Calcitonin becomes dominant and inhibits parathyroid hormone. When she does need calcium, is now not being conserved from kidneys, GI tract, or bones. Hormonal regulatory mechanisms shut off and can't immediately come on.

Question 33

What are the clinical signs of milk fever?

Answer 33

1. Stage 1 -->Ambulatory, hypersensitivity, excitable. Mild tremors. 2. Stage 2 --> Unable to stand but maintain sternal recumbency. May be dull, extremities will be cold (blood profusion decrease), potentially could bloat, no urinating/defecating. 3. Stage 3 --> Lose consciousness, coma, Unable to maintain sternal recumbency, unresponsive, will only survive a few hours if left untreated

Question 34

What is the treatment of milk fever?

Answer 34

Calcium - 25% Calcium gluconate IV (SQ calcium is not sufficient alone).Needs to go directly into blood stream. Start treatment as soon as possible. If tissue/muscle is not working well, there could muscle or nerve damage and they will never stand, even with calcium.

Question 35

How can milk fever be prevented?

Answer 35

Balance Ca & P ratio; 1:1 (not over 2:1)

Question 36

What is Downer Cow Syndrome?

Answer 36

Inability to rise on her own (recumbent)

Question 37

When does Downer Cow Syndrome occur?

Answer 37

1. Parturition 2. Peak lactation age 3. History of parturient paresis

Question 38

What is the cause of Downer Cow Syndrome?

Answer 38

1. Milk fever (parturient paresis) 2. Trauma --> difficult birth, nerve damage, slipping, infection, etc.

Question 39

What are the risk factors for Downer Cow Syndrome?

Answer 39

1. Delay treatment of milk fever --> Longer she is down, more likely she will be downer cow 2. Housing --> Facilities / flooring, make sure they can get good footing 3. Fat --> - High BCS, bad partition, will lead to dystocia. 4. Infections --> Mastitis, metritis, 5. Malnutrition

Question 40

How is Downer Cow Syndrome treated?

Answer 40

1. Treat milk fever 2. Treat infections

Question 41

How can Downer Cow Syndrome be prevented?

Answer 41

1. Nutrition 2. Environment 3. Supervise parturition

Question 42

How can calving injuries be prevented?

Answer 42

1. Heifer size / bull selection 2. Supervise parturition

Question 43

How can you get cows up that have Downer Cow Syndrome?

Answer 43

If we think it is not permanent, we need to get cow UP. Don’t want muscle or nerve damage. - Slings - Hip lifters (Need to be used correctly)

Question 44

Why is it important to get Downer Cows up?

Answer 44

Getting up allows for better examination. Put feed + water right in front of her. Treat if you know cause, otherwise supportive care.

Question 45

How should downer cows be treated if there is no sign of recovery?

Answer 45

Humane euthanasia; captive bolt or gunshot. Need to know where to target in head to not cause more stress or damage than needed. Call a veterinarian if unsure.

Question 46

What are other names for Hypomagnesemia?

Answer 46

Grass Staggers, Grass Tetany

Question 47

What is the cause of hypomagnesemia?

Answer 47

Complex metabolic disturbance 1. Low plasma concentration of magnesium 2. Mechanism is not known

Question 48

When does hypomagnesemia occur?

Answer 48

1. Lush pastures Dry matter < 0.2% Mg 2. Lactating cattle, sheep, and goats Loss of Mg in milk 3. Top-dressed pastures Mg absorption ↓ when K and N ↑ in soils

Question 49

What type of cattle do we see hypomagnesemia in?

Answer 49

Nursing calves <2 months, beef > dairy

Question 50

What are the clinical signs of hypomagnesemia?

Answer 50

Acute vs. chronic, progressive signs 1. Nervous 2. Muscle tremors 3. Impaired vision (wide eyes, looking around) 4. Unthrifty, anorexia 5. Dullness 6. Convulsions and death

Question 51

How is hypomagnesemia treated?

Answer 51

1. Herd problem --> Even if you only see a few with clinical signs, need to treat WHOLE herd 2. Ca and Mg solutions IV 3. Magnesium oxide --> If you know what they are grazing on is low in Mg, need to supplement this. Put Mg in with hay, even with those that we treat. If you don’t start adding Mg to diet, ones that have been TX will relapse in a day or two.

Question 52

How can hypomagnesemia be prevented?

Answer 52

Magnesium oxide. If you cannot graze pasture until it gets mature, tend to have >Mg in plants. Graze pasture with animals that aren’t as susceptible. With beef cattle, use cows >4 months, dry cows/heifers. Legumes / mixes are good sources of Mg and Ca. Supplement with Mg.

Question 53

What is the cause of Parakeratosis?

Answer 53

Zinc deficiency that causes skin disease. Result of ration not being mixed properly (too much/too little) OR not absorbing zinc correctly from GI tract.

Question 54

What type of pigs does Parakeratosis occur in?

Answer 54

Confinement swine, 6 weeks – 4 months old

Question 55

What are the clinical signs of parakeratosis?

Answer 55

1. Skin lesions (not itchy) 2. Crust formation on skin

Question 56

How is parakeratosis treated and prevented?

Answer 56

Zinc additive to rations; rapid recovery

Question 57

Why is differential diagnosis important in the case of parakeratosis?

Answer 57

Greasy pig disease caused by bacteria Staphylococcus hyicus. Occurs in pigs < 7 wks of age

Question 58

What is another name for White Muscle Disease?

Answer 58

Nutritional Muscular Dystrophy

Question 59

What type of animals does White Muscle Disease occur in?

Answer 59

All farm animal species. Especially rapidly growing calves, lambs, kids, and foals (3 weeks-3 months)

Question 60

What does White Muscle Disease lead to effects on?

Answer 60

Cardiac muscle and SKM

Question 61

What is the cause of White Muscle Disease?

Answer 61

Selenium and/or Vitamin E deficiency

Question 62

Why can vitamin E and/or selenium deficiencies cause White Muscle Disease?

Answer 62

These are both important to keep cellular membranes healthy, help prevent damage from free radicals. Deficiency results in damage to cellular membranes.

Question 63

What are the clinical signs of White Muscle Disease?

Answer 63

1. Stiffness 2. Inactive 3. Sudden death

Question 64

How can White Muscle Disease be diagnosed?

Answer 64

1. Clinical signs (stiff gait) 2. Elevated muscle enzymes (creatinine and aspartate) 3. Low Vit E and Se in (diet, tissue and serum) 4. Muscle degeneration 5. Necropsy

Question 65

What will necropsy of tissue effected with White Muscle Disease show?

Answer 65

Lesion in muscle. Pale, dry, bilateral. Histologically tissue gets very pale and dry (looks like fish meet). Depends on extend. This happens because of excess Ca being deposited in muscle.

Question 66

What do pathologists look for when diagnosing White Muscle disease?

Answer 66

Looking for calcification, damage to muscle fibers

Question 67

How is White Muscle Disease treated?

Answer 67

1. Sodium selenite 2. Vitamin E When given IM or SQ --> respond quickly. Better response if most damage is within SKM and not heart. Cardiac damage may not be able to handle animal as they get bigger.

Question 68

How can White Muscle Disease be prevented?

Answer 68

Administration of Vitamin E/Se to dam about 4 weeks prior to parturition

Question 69

What type of animals are gastric ulcers a major problem in?

Answer 69

Major problem in intensive swine raising facilities, especially sows and growing pigs. This is where we have lots of stress with them. 2-6 months of age, growing rapidly, pressure to feed.

Question 70

What are the clinical signs of gastric ulcers?

Answer 70

(Most cases are subclinical, found at necropsy) 1. Anorexia and depression --> relucent to eat 2. Anemia due to gastric hemorrhage 3. Blood (melena) in stool 4. Sudden deaths due to blood loss

Question 71

Why do gastric ulcers occur?

Answer 71

Develop where esophagus goes into stomach (not protected from acidic fluid).

Question 72

How are gastric ulcers treated?

Answer 72

Tx usually not economical. Prevention is key. 1. Antacids 2. Vitamin E and selenium 3. Reduce stress

Question 73

How are gastric ulcers prevented and controlled?

Answer 73

Bottom line: need to keep things economical 1. Coarsely ground feed --> use > 3.5mm screen Finely ground --> better feed efficiency, but moves through GI tract more quickly. 2. Selenium supplementation 3. Add zinc if copper is added to feed 4. Reduce stress

Question 74

What are other names for salt poisoning?

Answer 74

Salt Toxicity, Hypernatremia, Sodium ion toxicity, Water deprivation

Question 75

What species do we see salt poising occur in?

Answer 75

We can see salt positioning in all spp. but most prevalent in swine and poultry

Question 76

What is the direct cause of salt poisoning?

Answer 76

Consumption of excess salt a. Excess salt in ration --> Ration may not be mixed properly / miscalculated salt concentration b. Access to brine --> (elevated salt) c. Feeding milk by-products --> such as whey

Question 77

What is the indirect cause of salt poisoning?

Answer 77

Water deprivation a. Frozen pipes b. Malfunctioning waters c. Insufficient waterer space d. Forgetting to turn water back on after repairs e. Medicated water unpalatable

Question 78

What are the clinical signs of salt poisoning?

Answer 78

1. Thirst 2. Constipation 3. Restlessness 4. Depression, blindness, deafness, convulsions, and death

Question 79

How is salt poisoning diagnosed?

Answer 79

1. Clinical signs 2. History!!! --> Look at water / diet intake 3. Clinical pathology --> We can look at BW for elevated blood Na level 4. Necropsy --> May see some inflammation in brain / NS with edema / fluid accumulation

Question 80

What will the pathology of tissue samples taken from animals with salt poising look like?

Answer 80

Looking for vacuolated areas around blood vessels, might be a lot of WBC (eosinophils)

Question 81

How is salt poising treated?

Answer 81

Access to water. Not any other specific tx than provide access to H2O. If there is a problem with the ration, need to replace with properly mixed feed. - Small amounts initially - Limit to 0.5% of BW hourly - Slow return to normal water intake over 2-3 days

Question 82

Why don’t we want animals with salt poisoning to drink all they want immediately?

Answer 82

Don’t want free access to water. The reason being water is going to go where salt is in tissue. High conc. Salt in tissue in NS and allow to drink freely, water will go into tissue. Will worsen problems. Want to try to dilute salt content SLOWLY. Little water at a time, period of over several days. Limit H2O by ½% body weight / hour.

Question 83

What is the mortality rate of animals who show clinical signs of salt poisoning?

Answer 83

Mortality rate in animals with clinical signs, regardless of TX, is usually over 50%. If showing clinical signs, likely to lose them

Question 84

How can salt poisoning be prevented and controlled?

Answer 84

1. Allow free access to clean water 2. Generally recommended salt content should be in feed (<1%) and water (<0.5%) for all animal species

Question 85

What is baby piglet anemia?

Answer 85

Iron deficiency in piglets, Causes anemia, depressed growth

Question 86

Why does baby piglet anemia happen?

Answer 86

Piglets iron requirement cannot be met by sow’s milk

Question 87

When does baby piglet anemia occur?

Answer 87

Piglet becomes anemic within 2-3 days of birth, but peak incidence is 3 weeks

Question 88

What are the clinical signs of baby piglet anemia?

Answer 88

1. Decreased growth 2. Lethargy 3. Pale skin and mucus membranes 4. Difficulty breathing 5. Edema 6. Diarrhea

Question 89

Why can baby pig anemia cause difficulty breathing?

Answer 89

Because there are not enough blood cells to carry oxygen

Question 90

How is baby piglet anemia diagnosed?

Answer 90

1. Clinical signed 2. BW --> Hemoglobin <6 g/100 ml (normal 12-14 g/100 ml)

Question 91

How is baby piglet anemia treated and controlled?

Answer 91

1. 200 mg iron dextran IM at 1 to 3 days of age OR 100 mg at 1-3 days and 7-14 days later 2. Iron (oral)

Question 92

What is the problem with giving oral iron as a treatment for baby piglet anemia?

Answer 92

Inconsistently absorbed; oral iron is unreliable.

Question 93

What is a synonym for Mulberry Heart Disease?

Answer 93

Microangiopathy of pigs

Question 94

What is the cause of Mulberry Heart Disease?

Answer 94

Vitamin E and/or selenium deficiency

Question 95

What is Mulberry Heart similar to?

Answer 95

Pig version of white muscle disease

Question 96

What is the primary damage to in Mulberry Heart Disease?

Answer 96

Primary damage is to SKM in pigs

Question 97

What type of animals is Mulberry Heart Disease most common in?

Answer 97

Most common in nursery or grower pigs

Question 98

What can lead to Vitamin E deficiency that results in Mulberry Heart Disease?

Answer 98

Improper feed processing or storage can destroy vitamin E. If fats have become rancid, this can destroy vit. E. Some grains can be deficient in Se, esp. if grown in deficient soil.

Question 99

What geographic region most has the most common incidence of Mulberry Heart Disease because of selenium deficiency?

Answer 99

Selenium deficient grains in lower Midwest.

Question 100

What is the most common sign of Mulberry Heart Disease?

Answer 100

The most common sign of MHD is sudden death of the best pigs with no symptoms. The heart will appear dark and mottled

Question 101

What are the clinical signs of Mulberry Heart Disease?

Answer 101

- Sudden death - Stiffness --> SKM impacted - Unable to stand

Question 102

How is Mulberry Heart Disease Diagnosed?

Answer 102

- Necropsy - BW: Liver selenium levels <0.5 μg/g

Question 103

What will heart tissue of animals with Mulberry Heart Disease look like when necropsied?

Answer 103

Extensive interstitial hemorrhages (H) and necrotic cardiomyocytes with dystrophic mineralization

Question 104

How is Mulberry Heart Disease treated and controlled?

Answer 104

1. Vitamin E and/or selenium injections (B0-SE) 2. Supplementation of feed

Question 105

What is neonatal hypoglycemia?

Answer 105

Low blood glucose/sugar concentration in neonates

Question 106

What is the cause of neonatal hypoglycemia?

Answer 106

Inadequate intake of milk - MMA (mastitis, metritis, agalactia) - Inability of piglet to nurse – infection, not enough teats

Question 107

What can worsen to neonatal hypoglycemia?

Answer 107

Low environmental temp. may exacerbate. If not 90-degree temp, then they will be shivering trying to maintain body temp., which wastes lots of energy

Question 108

Why are baby piglets susceptible to neonatal glycemia?

Answer 108

Piglet has limited glycogen and body fat stores, depends on frequent meals.

Question 109

When does baby piglets have non-functioning gluconeogenesis capability?

Answer 109

Not able to have good gluconeogenesis ability until >1 week old.

Question 110

What age of piglets will neonatal hypoglycemia occur in?

Answer 110

Piglets <7 days of age

Question 111

What are the clinical signs of neonatal hypoglycemia?

Answer 111

1. Difficulty walking 2. Convulsions 3. Shivering 4. Hypothermia 5. Death

Question 112

When will neonatal hypoglycemic pigs succumb to death by if impacted?

Answer 112

Death usually occurs within 24-36 hr. of onset (1.5 days)

Question 113

How is neonatal hypoglycemia diagnosed?

Answer 113

1. Blood glucose <50 mg/dl 2. Empty stomachs (not nursing)

Question 114

How is neonatal hypoglycemia treated?

Answer 114

1. Glucose injections (Intraperitoneal) 2. Gradually warmed to 1020F 3. Oral supplementation with milk replacer or commercial nutritional supplements after CNS signs goes away

Question 115

How can neonatal hypoglycemia be prevented and controlled?

Answer 115

Make sure piglets are getting adequate milk supply, keep environmental temp normal, minimize stress

Question 116

What is Yew poisoning?

Answer 116

Japanese Yew is a common ornamental shrub. Used for lots of landscaping, not native to NE. Very toxic.

Question 117

What causes Yew poisoning?

Answer 117

Ingestion of Yew plant (Taxus spp.).

Question 118

Why are Yew shrubs so toxic when ingested?

Answer 118

Taxine: alkaloid = cardiotoxin (toxin to heart)

Question 119

When does Yew poising occur?

Answer 119

a. All species b. Ingestion --> Most cases are associated with accidental ingestion

Question 120

What are the acute and subacute clinical signs of Yew poisoning?

Answer 120

a. Acute --> Sudden death; leads to heart failure b. Subacute --> ataxia, colic, diarrhea, dyspnea, coma, seizures. May see over period of 3 days – when not getting large amount.

Question 121

How is Yew poising diagnosed?

Answer 121

a. History of ingestion b. Postmortem exam --> Rumen or gastric contents

Question 122

What is the treatment of Yew poisoning?

Answer 122

Nonspecific. No antidote, all supportive (decontaminate stomach, activated charcoal, rumenectomy). If HR is decreased – could give atropine.

Question 123

What are the food safety guidelines with animals who have been diagnosed with Yew poisoning?

Answer 123

1. Milk withholding – 2 days 2. Meat – 35 days 3. Drugs - variable

Question 124

What is Hydrocyanic (Prussic) Acid Poisoning?

Answer 124

Basically, cyanide poisoning. What happens here is our livestock spp. ingest / forage on type of plant that tends to produce cyanogenic glycosides

Question 125

What are the sources of Hydrocyanic (Prussic) Acid Poisoning?

Answer 125

Many plant sources – Burmuda, milo, sudan grass, chokecherry

Question 126

What is the toxic compound in Hydrocyanic (Prussic) Acid Poisoning?

Answer 126

Cyanogenic glycosides --> HCN

Question 127

When does Hydrocyanic (Prussic) Acid Poisoning occur?

Answer 127

a. Wilted, frosted plants --> Higher concentration in leaves than the stems. Crushing, freezing, wilting b. Rapid consumption

Question 128

What animals does hydrocyanic (prussic) acid poisoning effect?

Answer 128

Seen in cattle and sheep (most sensitive) although can see in most spp.

Question 129

Why is dry matter more likely to cause hydrocyanic (prussic) acid poisoning?

Answer 129

If plant is dry, then this increases cyanogenic potential b/c in dry matter it concentrated. Forage --> silage – will reduce cyanide content.

Question 130

What is the pathogenesis of Hydrocyanic Acid Poisoning?

Answer 130

a. Anoxia, tissue asphyxia b. Cerebral anoxia

Question 131

After ingesting, when do animals show clinical signs of Hydrocyanic Acid Poisoning?

Answer 131

Acute cyanide poisoning usually occurs within few minutes/hours after ingestion. Once they start to show clinical signs, tend to not survive over >2 hours.

Question 132

What are the clinical signs of hydrocyanic acid poisoning?

Answer 132

a. Acute b. Dyspnea, restlessness c. Convulsions

Question 133

What does cyanide do biologically?

Answer 133

Cyanide prevents hemoglobin from releasing O2 to tissues. Tissues are starving of oxygen.

Question 134

How is Hydrocyanic acid poisoning diagnosed?

Answer 134

Test plants if concerned

Question 135

What is the treatment / control protocol for hydrocyanic acid poisoning?

Answer 135

Graze on forage that is naturally low in cyanogenic glycosides (has been accomplished through genetic modification), change feed silage

Question 136

What is the cause of sweet clover poisoning?

Answer 136

Sweet clover normally produces Coumarin, but when moldy creates dicoumarin. Coumarin --> Mold --> Dicoumarin

Question 137

What is Dicoumarin?

Answer 137

Antagonist of vitamin K

Question 138

What happens when Dicoumarin antagonizes vitamin K?

Answer 138

Blood does not clot. Vitamin K is needed to activate clotting factors in the body.

Question 139

What drug is sweet clover poisoning similar to in terms of effects?

Answer 139

Warfarin

Question 140

When does sweet clover poisoning occur?

Answer 140

a. We see this often in cattle b. Moldy sweet clover

Question 141

What are the clinical signs of sweet clover poisoning?

Answer 141

a. Hemorrhages --> Nose bleeds (potentially), SQ swelling (bleed under skin), If surgery performed (dehorning), could bleed to death b. Stiffness --> - Bleed into joints

Question 142

How is sweet clover poisoning diagnosed?

Answer 142

History (hemorrhaging or bleeding to death)

Question 143

How is sweet clover poisoning treated?

Answer 143

Vitamin K, if they are showing signs, could have blood transfusion (depends on value of animal), change feed

Question 144

How is sweet clover poisoning prevented?

Answer 144

Select a clover variety with low coumarin. Don’t mix feeds together / don’t feed potentially moldy sweet clover prior to parturition (< 3 weeks before).

Question 145

Why does Mycotoxicosis occur?

Answer 145

Due to feed contaminated with toxins from fungi or molds

Question 146

What is the cause of Mycotoxicosis?

Answer 146

Mycotoxins

Question 147

Why do fungi or molds produce mycotoxins?

Answer 147

Results from ingesting contaminated feed OR bedding material with toxins that they are being exposed to. Fungi will grow on cereals, hay, pasture. The toxins have no benefit to fungal organism, not meant for survival. If organism is stressed, produced toxins. If mold is on feed, does not automatically mean toxins are present

Question 148

What are the effects of Mycotoxicosis?

Answer 148

Major effect: feed refusal - leads to poor performance 1. Irritate digestive tract mucosa 2. Destroy vital organs 3. Cause neoplasia 4. Hormonal effects

Question 149

Where do Aflatoxins come from and how to the effect animals?

Answer 149

Aspergillus flavus and Aspergillus parasiticus (from corn). - Reduced productivity - Slow growth - Hepatotoxicosis --> toxic to the liver

Question 150

Where do Zearalenone toxins come from and how to the effect animals?

Answer 150

Fusarium fungi. Causes Hyperestrogenic effects: - swollen vulva - Polycystic ovaries - Pseudopregnancy

Question 151

Where do Ergot mycotoxins come from and what animas do they effect?

Answer 151

Claviceps purpurea. Grows on the seed head of cereal grains and grasses. Historically, rye was the common one effected by it also grows on wheat, barley, oats. All animals are susceptible, but cattle are the ones that are most effected.

Question 152

What do Ergot mycotoxins cause?

Answer 152

Causes very severe vasoconstriction of the arterial supply. No blood supply distally – can develop gangrene / limb loss. Effects limbs, tail, tips of ear. Acts like a tourniquet. Once limping or showing lameness, indicated infection, won’t be able to save tissue.

Question 153

Where does Ochratoxin mycotoxins come from and what clinical signs to they cause?

Answer 153

Aspergillus sp. and Penicillium sp. - Edema --> around kidneys (enlarged, cysts), increased pu/pd - Food refusal - Decreased growth rate

Question 154

Where do Vomitoxin aka Deoxynivalenol (DON) mycotoxins come from and what effects do they cause?

Answer 154

Fusarium graminearum. Animals can vomit after consuming, feed refusal, decreased growth rate

Question 155

How is Mycotoxicoses diagnosed?

Answer 155

1. Identify mycotoxins --> feedstuffs, animal tissues 2. Lesions and clinical signs

Question 156

Does fungal growth always lead to mycotoxins?

Answer 156

Just b/c you see fungal growth, doesn’t mean mycotoxins (and vice versa)

Question 157

What species is nitrate poisoning seen in?

Answer 157

Many species are susceptible, but cattle most frequently.

Question 158

What is the cause and occurrence of nitrate poisoning?

Answer 158

1. Nitrates and nitrites in growing plants 2. Ingestion of nitrate fertilizers 3. Water sources

Question 159

What is the pathogenesis of nitrate poisoning?

Answer 159

Nitrate is converted to nitrite. Normally, nitrate is then converted into ammonia. Nitrate is absorbed into the bloodstream and attached to iron on hemoglobin. Methemoglobin is not able to transport oxygen. Animals are getting too much nitrate production where it outpaces conversion to ammonia

Question 160

When do we most commonly see nitrate poisoning?

Answer 160

We can see it when animals are ingesting certain plants with high concentrations of nitrate such as Clover and cereals. A common source is fertilizer - maybe when bags of fertilizers are left out in field, or when pasture is over fertilized, or access to nitrate from runoff of water. Spring is the most common time we see nitrate poisoning.

Question 161

What are the clinical signs of nitrate poisoning?

Answer 161

Anoxia, convulsions, coma, death. Rapid, weak HR

Question 162

What do nitrate poisoning clinical signs result from?

Answer 162

Methemoglobin not able to carry O2, clinical signs are because of hypoxia.

Question 163

What is the mechanism of action of nitrate toxicity?

Answer 163

High nitrate forage --> (RUMEN) nitrate --> nitrite (normally produces ammonia) --> excess nitrite --> (BLOOD) --> hemoglobin --> methemoglobin

Question 164

What happens with normal levels of nitrates?

Answer 164

With normal levels, we get ammonia production, eventually converted to proteins

Question 165

What is the treatment for nitrate toxicity?

Answer 165

Remove source of nitrate; methylene blue. Adjunct treatment = lavage the rumen with cold water. Will reduce activity of bacteria and conversion to nitrite.

Question 166

What is the mechanism of action of methylene blue? Why is its use controversial?

Answer 166

Converts methemoglobin back to hemoglobin. Not approved for use in food animals. Would call Food Animal Residue Avoidance Bank and if you have to administer this, must follow their protocols. They will give recommendations before you administer and tell recommended withdrawal times.

Question 167

What is the occurrence of lead poisoning (what species does it happen in, how does it happen)?

Answer 167

Cattle. Licking. Most of the time with activity to pasture (seeding, harvesting), often associated with leaded oils. Batteries left in field. Cattle are curious, will come up and lick and ingest lead. Lead paint (old barn).

Question 168

What are the systems effected by lead poisoning?

Answer 168

Enters bloodstream, tissues, and will redistribute to the bone. a. Digestive system – GI irritation b. Nervous system – damage as a result to peripheral nerves

Question 169

What are the clinical signs of lead toxicity?

Answer 169

DX made based on clinical signs, determining lead concentration a. Salivation, drooling b. Anorexia, decrease activity of rumen c. Dullness, muscle tremors d. Death

Question 170

What is the treatment for lead toxicity?

Answer 170

Prevent exposure from continuing. find sound and remove it. If tissue damage is extensive, showing neurological signs, treatment likely is not going to be successful.

Question 171

Why is treatment for lead poisoning controversial?

Answer 171

Treatment for lead poisoning is controversial because it effects bone and it can continue to leach into tissues, products, etc. Half-life of lead is 9 weeks. Can take over a year for lead levels to be where cow could produce milk, go to slaughter. Is it worth keeping these animals for <1 year until they can be used? Only way you will know when it is safe will be repeatedly testing blood Pb levels.

Question 172

What species does copper poisoning effect?

Answer 172

Seen in several species, but most common in sheep (they are sensitive)

Question 173

What is acute vs. chronic copper poisoning?

Answer 173

1. Acute --> excessive amount of copper salts in feed, given mineral mixes 2. Chronic --> What we tend to see most commonly. With this, they are ingesting excessive copper amounts over a long period of time. Toxicity remains subclinical, copper accumulated within liver. When they undergo stress (parturition, lactation, transportation), liver will release Cu and cause lysis of RBC and causes hemolytic crisis.

Question 174

What are the clinical signs of copper poisoning for chronic and acute symptoms?

Answer 174

a. Acute copper poisoning: Gastroenteritis -Anorexia, abdominal pain, diarrhea b. Chronic copper poisoning: Hemolytic crisis

Question 175

How is copper poisoning diagnosed?

Answer 175

Tissue concentration of Cu and Mb

Question 176

How is copper poisoning prevented and treated?

Answer 176

a. Prognosis poor if a hemolytic crisis occurs b. Symptomatic treatment c. Remove the source of copper poisoning

Question 177

What is selenium toxicity called in horses?

Answer 177

Alkali Disease

Question 178

Why does selenium toxicity occur?

Answer 178

Vegetation with high Se. Selenium is needed by the body, is used by enzymes, proteins in the body. They need a certain level, but there is a narrow level between what is needed and what is considered toxic. All spp. affected, but more common in forage eating animals. Esp. when grazing ^ Se containing plants. Plants deriving Se from soil. Most available to soil when it is alkaline (higher pH) and when there is low rainfall / dry period.

Question 179

What are the clinical signs for selenium toxicity?

Answer 179

1. Acute – Due to over consumption of plants; nervous system, death 2. Chronic – Retarded growth, inhibited reproduction (estrous cycle not going as it should, low birth rate), hair loss, abnormal hoof growth

Question 180

What is the treatment for selenium toxicity?

Answer 180

No specific treatment. Eliminate source, support symptomatically

Question 181

What is urea normally used for? Why does urea poisoning occur?

Answer 181

Urea is used in ruminants as a source of non-protein nitrogen. Is targeted by the rumen microflora, converted to ammonia, goes onto protein synthesis. Improper feed mix. Usually, ingestion of excess urea due to it not being added to feed properly.

Question 182

What is the cause of urea toxicity?

Answer 182

1. Ammonia collects in rumen 2. Absorption occurs - too much ammonia in bloodstream 3. Toxicity results

Question 183

How long does urea toxicity take for it to show clinical signs?

Answer 183

Period from ingestion to clinical signs can be as short as 20 minutes, especially in cattle. Takes a little longer in horses. Once clinical signs are seen, death usually seen in 2 hours in cattle, 4 hours in sheep, 12 hours in horses.

Question 184

What are the clinical signs of urea poisoning?

Answer 184

Acute, weakness/paralysis, salivation, muscle tremors, ataxia, fluid accumulation in lungs (pulmonary edema), gasping for breath, death. If they survive and urea is removed from feed, will usually recover and won’t see any consequences.

Question 185

How is urea poisoning diagnosed?

Answer 185

Check feed, ammonia odor on breath

Question 186

What is the mechanism of urea poisoning (why does it convert to ammonia)?

Answer 186

Conversion of urea to ammonia is result from bacteria in rumen called urease.

Question 187

How is urea poisoning treated?

Answer 187

Remove suspect feed. Not a whole lot we can do. Test feed. Replace feed. Can infuse rumen with 5% acetic acid solution that will acidify rumen contents, infuse cold water (will dilute ammonia) and will slow down metabolism of bacteria in rumen.

Question 188

How is urea poisoning prevented?

Answer 188

Limit urea and read labels. Urea should be < 1/3 of total Nitrogen content and should not exceed < 3% of grain. Adaptation; need to acclimate ruminal microflora to non-protein nitrogen source. Do not switch food right away. Bacteria need to adjust. If we take off, will need to readjust again. Keep on consistent amount.

Question 189

What is the cause of Organophosphate Poisoning?

Answer 189

Pesticides – highly toxic. Saw more when field were being sprayed with these. Would drift off and then absorbs quite readily through skin. Co-Ral = Organophosphate spray. Warnings for people spraying, can expose humans.

Question 190

When does organophosphate poisoning occur?

Answer 190

Fields – drift - after pesticide application.

Question 191

What is the pathogenesis of organophosphate poisoning?

Answer 191

Cholinesterase is inhibited. Neurons release AcH (autonomic NS, skeletal muscle) and acts on receptors to give effect. NT needs to be degraded (can't be continuously activated). Cholinesterase degrades acetylcholine. Acetylcholine remains in synapse + accumulates. In autonomic NS, will be parasympathetic NS side.

Question 192

What are the clinical signs of Organophosphate Poisoning in cattle, swine, and horses?

Answer 192

Animals essentially die from asphyxia --> fluid accumulates in lung, rib area can’t contract 1. Cattle - salivation, dyspnea, diarrhea, bloat, death 2. Swine - salivation, muscle tremors, recumbency 3. Horses - abdominal pain, diarrhea, dyspnea

Question 193

How is organophosphate poisoning treated?

Answer 193

1. Atropine – muscarinic antagonist (antidote). Decreases salivation, GI motility. Not going to have effect on SKM, specific to receptors. 2. Charcoal – for ingestion 3. Wash skin

Question 194

What do infectious agents do?

Answer 194

Invade host, evade host defenses, cause inflammation

Question 195

How does an infectious agent get from one host to another?

Answer 195

Vector (biological or mechanical), fomites, or biological material

Question 196

What is a vector?

Answer 196

Vector is a living agent that carries and transmits infectious agent / pathogen from one living organism to another.

Question 197

What is the difference between a biological vector and a mechanical vector?

Answer 197

Biological --> part of infectious agents' lifecycle has to be in vector (tick). Mechanical --> when it does not need to complete life cycle in vector (fly).

Question 198

What is a fomite?

Answer 198

Inanimate objects capable of carrying infectious organisms (boots, trailers, feed bags)

Question 199

What is biological material?

Answer 199

Blood, tissues, urine, etc

Question 200

What is vertical and horizontal transmission?

Answer 200

Vertical transmission --> Spread: mother to offspring Horizontal transmission --> Spread: animal to animal

Question 201

What are the portals of entry for infectious diseases?

Answer 201

1. Ingestion 2. Inhalation 3. Genitourinary 4. Teat canal 5. Bites

Question 202

What is tropism? T

Answer 202

he capability of a virus to infect a distinct group of cells in the host is referred to astropism. For many viruses, tropism is determined by the availability of virus receptors on the surface of a host cell. Once pathogen enters host, what tissue does it prefer?

Question 203

How are infectious disease prevented and controlled?

Answer 203

1. Break disease cycle 2. Alter host susceptibility

Question 204

What are the problems due to parasites?

Answer 204

1. Obstruction 2. Nutrients 3. Tissue destruction 4. Irritation 5. Vector 6. Toxins

Question 205

What are the characteristics of parasites?

Answer 205

1. Host specific 2. Most problems: young, malnourished 3. Larvae harmful 4. Does not cause death 5. Prolific 6. Complex life cycles

Question 206

How are parasites prevented and controlled?

Answer 206

Decrease exposure via management, use anthelmintics

Question 207

What is Pediculosis?

Answer 207

Louse infestation, lousiness

Question 208

What are the different types of lice?

Answer 208

Sucking lice vs biting lice. Sucking lice have mouth parts that are pointed, and they are designed to actually penetrate the skin, blood vessels, and feed off of blood. If there is enough of these, then they could lead to anemia in animals and problems there. Biting lice, on the other hand, have mouth parts that are designed for CHEWING. These tend to be lice that chew on feathers, hair, skin, etc.

Question 209

What season to lice prefer?

Answer 209

Lice are cold season insects. The population of lice on our livestock increase during the winter. Dec, Jan, Feb. As spring comes on and the weather starts warming up, the lice populations start to decrease.

Question 210

What species to lice prefer?

Answer 210

Host specific. In general, each species of louse is only associated with one kind of animal host. Helps us as far as control. Usually, entire life cycle of the louse occurs on that individual single host.

Question 211

What is the life cycle of lice?

Answer 211

Entire life on host (Eggs, nymphs, adults)

Question 212

How are lice transmitted?

Answer 212

Direct contact (carriers). Since the lice tend to stay on one animal/host, then transmission is essentially via direct contact. So, when the animals rub up against each other, this is how the lice get spread.

Question 213

What are lice carriers?

Answer 213

There are some animals that tend to have lice populations all year round. Not just during cold weather, also during the warmer weather. These are called carrier animals. They end up being the ones that are continuing to infect herd.

Question 214

What is the economic importance of lice?

Answer 214

Feeding activity. Lice are economically important b/c they cause irritations, which then causes the animal to want to rub, decreases productivity, they eat less, produce less milk. These lice can serve as another potential source of predisposition for some other diseases.

Question 215

How are lice diagnosed?

Answer 215

Clinical signs, inspection

Question 216

What is the chemical treatment for lice?

Answer 216

a. Self-treatment – limited b. Sprays – not cold weather c. Pour ons – cold weather d. Injectable – sucking lice

Question 217

What is mange?

Answer 217

Cattle scabies infestation. These infections / infestations with mites tend to cause a lot of itching, hair loss, scabs, lesions on skin, very stressful for animals.

Question 218

What are the three types of cattle scabies mites?

Answer 218

- Psoroptic (common scabies) - Sarcoptic - Chorioptic (common mange)

Question 219

What are the mange regulations?

Answer 219

Quarantine and treat. Psoroptic and Sarcoptic require that the herd be quarantined and treated. Will be guided by state/federal veterinarians on the proper means of treating these animals and how long. They will then lift quarantine so animals can be moved again.

Question 220

How is mange transmitted?

Answer 220

One host, traffic. All of the scabies mites are considered one host parasites – so, they live on one host, lay eggs, hatch, and then die all on the same animal. While some of them can drop off during transportation and it could potentially be a source of infection for other cattle, transmission is mainly direct from animals rubbing up against other animals. Fairly contagious.

Question 221

What is the occurrence of mange?

Answer 221

Duration of life cycle – 2 weeks --> Eggs, larvae, nymph, adult Seasonal –-> the worst time of the year is fall through spring

Question 222

What is the survival of mange like?

Answer 222

The Psoroptic and Sarcoptic mites – they are not gong to survive very long off of the host. They may survive if humidity and temperature are just right, but normally direct sunlight, wind will cause them to die in about 48 hours. Chorioptic can survive for quite a while. Humidity and temperature are important.

Question 223

What are the chemical compounds used to control mange?

Answer 223

i. Lime sulphur ii. Toxaphene (banned in the USA) iii. Coumaphos iv. Injectable (eg. Ivermectin)

Question 224

What are Swine Mange Mites?

Answer 224

This is caused by another scabies mite (Sarcoptes scabei var. suis). It is very contagious. The mite burrows into the skin, causes intense itching. All stages of the mite develop within or on the skin. Often infections in pigs start around ear and will spread through the rest of the body. Direct contact, this is spread very easily.

Question 225

What are the clinical signs of swine mange mites in nursery/grower pigs and those with chronic mange?

Answer 225

Nursery-grower - Acute allergic - Intense itching - Small sores - Decreased growth rates Chronic mange - Usually, adults - Mild itching

Question 226

How are swine mange mites diagnosed?

Answer 226

Clinical signs, skin scrapings

Question 227

How are swine mange mites treated and controlled?

Answer 227

a. SPF b. Topical sprays & dips Reapply: 14 days Spray adults: 6 months c. Injectable Single dose: 100% kill of adult mites

Question 228

How can swine mange mites be eradicated?

Answer 228

a. Inject every animal in herd to eradicate Steps 1.Decrease breeding herd 2. Summer 3. Remove bedding and spray premises 4. Inject all animals in 1–2-day period

Question 229

What is another name(s) for cattle grubs?

Answer 229

Warble fly larvae, heel flies

Question 230

What is the occurrence of cattle grubs?

Answer 230

These flies want to lay eggs on the hair of cattle, especially the legs, lower body region. This occurs during the late spring and early summer.

Question 231

What is gadding?

Answer 231

May see the cattle running around in pasture, have characteristic behavior (tail is up, running frantically, kicking hind legs up) – this is called Gadding. What they are trying to do is get away from flies that are trying to lay eggs. Gadding activity causes: - Loss in production - Animals may hurt themselves

Question 232

What internal effects to cattle grubs cause?

Answer 232

Hide and carcass damage

Question 233

What is the life cycle of cattle grubs?

Answer 233

1. Heel flies 2. Eggs 3. Larvae grub (mature larvae) 4. Pupae

Question 234

How are cattle grubs prevented and controlled?

Answer 234

1. Housing --> Keep animals inside when flies are out in late spring / early summer, but this is not practical. 2. Systemic insecticide --> ivermectin. The timing of this is critical b/c we do not want to tx these animals when grubs have reached back of animal. Killing grubs at this stage is going to cause a lot of tissue damage. Recommended to treat animals as soon as you start seeing gadding behavior stop (usually within a month).

Question 235

What are the 4 main types of flies, and what kind of cattle to they affect?

Answer 235

1. Pastured cattle a. horn flies b. face flies 2. Confined cattle a. stable flies b. house flies

Question 236

What is the life cycle of horn flies?

Answer 236

Eggs–fresh manure. It is within these feces you are going to get larval and pupal development.

Question 237

What mouth appendages to horn flies have?

Answer 237

Piercing-sucking mouth parts

Question 238

Where do horn flies spend a majority of their time?

Answer 238

On the host

Question 239

How do horn flies cause economic loss?

Answer 239

The feeding of these flies causes pain, is annoying to animal, will see blood loss. B/c animals are so stressed and irritated, likely to see weight loss, reduced milk production. Considerable economic loss associated with horned flies

Question 240

What is the life cycle of face flies?

Answer 240

Eggs–fresh manure

Question 241

What mouth appendages do face flies have?

Answer 241

Spongy mouth parts. Their mouth appendages are adapted to sponging up fluid (tears, saliva, mucous, blood)

Question 242

Why are face flies important?

Answer 242

Economic importance. Annoying to host, interfere with productivity.

Question 243

What are face flies a vector of?

Answer 243

Moraxella bovis

Question 244

What is Moraxella bovis and how do face flies transmit it?

Answer 244

Pink eye. Rough spines on mouth cause irritation to cornea and predispose for developing PINK EYE

Question 245

How can horn flies and face flies be controlled?

Answer 245

Insecticides a. Self-treatment – early Rubs – stand alone Dust bags – same as rubs b. Direct sprays c. Ear tags – convenient 5 months d. Feed additives – adult flies problem, pour-ons --> blood feeders

Question 246

What is another name for the stable fly?

Answer 246

Biting house fly

Question 247

What mouth appendage does the stable fly have?

Answer 247

It has needle sharp proboscis designed to: penetrate skin, get into blood vessels, suck blood

Question 248

What is the life cycle of stable flies (where to they lay their eggs)?

Answer 248

Eggs – decaying organic material

Question 249

Where to stable flies spend most of their time?

Answer 249

Spend time off host

Question 250

What is the importance of stable flies?

Answer 250

Bite is painful. Decreased productivity

Question 251

What are house flies?

Answer 251

Very common insect in livestock facilities, poultry operations. Vomit feeders --> anything they do ingest, they regurgitate out

Question 252

Where do house flies lay their eggs?

Answer 252

Fresh manure and decaying organic material

Question 253

What type of mouth appendages do house flies have?

Answer 253

Spongy mouth parts

Question 254

What is the importance of house flies?

Answer 254

Important for disease transmission, they are a public nuisance

Question 255

How can stable and house flies be controlled?

Answer 255

a. Sanitation and manure management b. Residual sprays c. Space sprays d. Direct sprays e. Larvicidal sprays f. Feed additives g. Baits – only house flies

Question 256

What are parasitoids?

Answer 256

Miniature wasps, used to control stable flies.

Question 257

What are miniature wasps?

Answer 257

Natural type of fly control measure. Miniature wasps don’t harm animals. Lay eggs on pupae of stable flies. When their eggs hatch, the larvae feed from fly pupae. Indirect means of control. If chemicals are used, will kill these off too

Question 258

What are biting midges and what they feed off of?

Answer 258

Tiny gnats, blood feeders

Question 259

Where are biting midges found?

Answer 259

Swamps & streams

Question 260

What species do biting midges affect?

Answer 260

Affects all classes of livestock

Question 261

What do biting midges transmit?

Answer 261

Transmit blue tongue virus and Epizootic Hemorrhagic Disease virus

Question 262

What do Horse Fly & Deer Flies do that is bothersome?

Answer 262

Bite. BOTH larvae and adult stage can bite. Adult has scissor like mouth parts.

Question 263

What do horse and deer flies transmit?

Answer 263

Transmit Anaplasmosis

Question 264

What animals to horse and deer flies affect?

Answer 264

Affect cattle and horses

Question 265

What is another name for Sheep Keds?

Answer 265

Sheep ticks

Question 266

What are sheep keds?

Answer 266

NOT ticks, they are wingless flies that suck blood

Question 267

What do sheep keds cause?

Answer 267

Wool damage. Cause discoloration of wool (decreased value)

Question 268

How are sheep keds treated?

Answer 268

Sheer, administer insecticide and re-treat in 3-4 weeks

Question 269

What is another name for sheep bots?

Answer 269

Nasal bot fly

Question 270

How do sheep bots infect their host?

Answer 270

Larvae – nasal passage. The female fly likes to lay larvae around the nostrils. Not eggs, larvae are deposit. Larvae migrate to nasal cavity / sinuses

Question 271

How can you tell if sheep are being infected with sheep bots?

Answer 271

Nose to the ground / huddled together

Question 272

What is the life cycle of mosquitos?

Answer 272

a. Eggs b. Wrigglers (larvae) c. Pupae (tumblers) d. Adults

Question 273

What diseases can mosquitos transmit?

Answer 273

Venezuelan equine encephalitis, canine heartworm

Question 274

Where does the mosquito life cycle need to occur?

Answer 274

In water

Question 275

How can mosquitos be controlled?

Answer 275

Destroy breeding grounds, fill low areas, get rid of tires. Aerating pond / getting water movement will help

Question 276

What are ticks?

Answer 276

Blood sucking arthropods, able to transmit dz and cause irritation

Question 277

What are the ticks found in NE?

Answer 277

Rocky mountain spotted tick, American dog tick, brown dog tick, Lone star tick, Winter tick, Spinous ear tick, Deep tick

Question 278

What are the two classifications of ticks?

Answer 278

1. Hard ticks (Ixodidae) 2. Soft ticks (Argasidae)

Question 279

What are characteristics of hard ticks?

Answer 279

Flattened, mouth parts visible, dorsal plate

Question 280

What are the characteristics of soft ticks?

Answer 280

Can’t see mouth parts, oval, leathery

Question 281

What is the life cycle of ticks? ELNA

Answer 281

1. Eggs 2. Larvae – seed ticks 3. Nymphs – re-attach if 2 or 3 tick host 4. Adult

Question 282

What is the morphological difference between larvae and nymphs?

Answer 282

Larvae = 6 legs. Nymphs = 8 legs

Question 283

How many hosts does the rocky mountain wood tick have?

Answer 283

3 hosts

Question 284

How long is the life cycle for the rocky mountain wood tick?

Answer 284

Two year life cycle

Question 285

What diseases is the rocky mountain wood tick a vector for?

Answer 285

Anaplasmosis, RMSF (rocky mountain spotted fever)

Question 286

What is the life cycle for an American dog tick?

Answer 286

Life cycle similar to RMWT. 3 host tick. Takes up to 2 years to go through life cycle.

Question 287

What is the life cycle of the brown dog tick?

Answer 287

3 hosts, short life cycle (2 months)

Question 288

What is done for tick control?

Answer 288

Difficult, dips are effective. Sprays are not as effective. Look at environment. Woody areas, shrubby areas – need to be cleaned

Question 289

What are the Abomasal parasites of cattle and sheep?

Answer 289

HOT Haemonchus Ostertagia Trichostrongylus

Question 290

What is Haemonchus spp?

Answer 290

The barber pole worm, large stomach feeder

Question 291

Where can Trichostrongylus also be found?

Answer 291

Small intestine

Question 292

What is the disease production of abomasal parasites of cattle and sheep?

Answer 292

1. Blood sucking (anemia due to blood loss) 2. Mucosal destruction (Penetrate abomasum, get into glands and cause obstructions, thickening of nodular glands)

Question 293

What is the life cycle of abomasal parasites of cattle and sheep?

Answer 293

1. Eggs – passed in feces 2. Larvae – L1 --> L2 --> L3 (infectious stage) --> ingested --> L4 --> L5 3. Adult

Question 294

What are the clinical signs of abomasal parasites of cattle and sheep?

Answer 294

1. Anemia, submaxillary edema 2. Diarrhea 3. Diarrhea 4. Weight loss, poor growth, weak 5. Rough hair coat 6. Pot belly

Question 295

How are abomasal parasites of cattle and sheep controlled?

Answer 295

1. Eliminate crowding 2. Nutrition 3. Rotate grazing 4. Anthelmintic resistance 5. Anthelmintics

Question 296

What is Hypobiosis?

Answer 296

“Below life.” Hypobiosis or facultative arrested development represents such an adaptation which, by facilitating the persistence of the larval forms for prolonged periods in the host, enables the parasite to capitalize on optimal opportunities for transfer.

Question 297

What is the dormant stage for abomasal parasites?

Answer 297

Dormant stage (L4)

Question 298

When do abomasal parasites come out of their hypobiosis dormancy?

Answer 298

Late fall/ early winter. Stress --> triggers release of L5

Question 299

What is type II Ostertagiasis?

Answer 299

a. Large number of larvae b. Dormant c. Calves 12-20 months

Question 300

What is type I Ostertagiasis?

Answer 300

a. Recent infections b. Most are adults and respond to anthelmintics c. Calves: 7-15 months

Question 301

What is the species and location occurrence of liver flukes?

Answer 301

Sheep and cattle, mainly. Wet, moist, swampy areas, ponds, irrigated pastures, etc.

Question 302

What vector is needed for liver flukes?

Answer 302

Part of life cycle involves a specific snail.

Question 303

What is the life cycle of a liver fluke?

Answer 303

1. Bile duct – adult 2. Snail – larvae 3. Aquatic vegetation – larvae 4. Ruminant ingestion 5. Gut penetration: liver migration

Question 304

What are the clinical signs of liver fluke infestation in cattle and sheep?

Answer 304

1. Cattle – anemia, emaciation, diarrhea 2. Sheep – sudden death, anemia, bottle jaw

Question 305

How are liver flukes treated and controlled?

Answer 305

1. Anthelmintics 2. Eliminate snails (copper sulfate, but is toxic to sheep) 3. Keep animals off wet pasture

Question 306

What species do Large Strongyles affect?

Answer 306

Horses

Question 307

What is the life cycle of Large Strongyles?

Answer 307

1. Eggs are passes out in feces 2. Eggs in feces develop into L1, L2, and then L3 larvae stage 3. L3 larvae on grass 4. The horse eats the grass and ingests L3 stage larvae 5. The L3 penetrates the intestinal wall 6. L4 larvae develop into adults and lay eggs

Question 308

What system do large strongyles penetrate once ingested?

Answer 308

Circulatory system

Question 309

Where do adult Large Strongyles form and how do they affect this organ?

Answer 309

Develop in large intestine. Blood feeding parasites. If they are in large quantities, could see anemia in host. Damage to mucosa; able to ingest chucks of mucosa.

Question 310

What is the pathogenesis of large strongyles?

Answer 310

Larval migration – mechanical damage associated with migration. Adult worms—attach to mucosa, suck blood.

Question 311

What are the clinical signs of large strongyles?

Answer 311

Anemia, colic, diarrhea, anorexia

Question 312

How are large strongyles diagnosed?

Answer 312

History and clinical signs, fecal examination

Question 313

How are large strongyles treated and controlled?

Answer 313

- Drugs - Isolate, deworm - Fecal tests - Rotate pastures - Break fecal piles - Sanitation

Question 314

What are Ascarids (Parascaris equorum)?

Answer 314

This is a large worm (up to 1 ft long). Found in small intestine

Question 315

What is the life cycle of ascarids?

Answer 315

Eggs are passed in feces. Adults are found in the small intestine. - Larvae do not erupt from eggs. L2 larvae still enclosed in eggs. Once this is ingested eggs hatch in the gut - L2 migrate through SI and enter portal circulation (blood flow that drains GI tract and goes to liver). - L3 once in liver, can reach within 24 hours of ingestion - Migrate to lungs. Break into capillaries, enter alveoli. - Coughed up, swallowed down into GI tract. Finish maturation into adult worms at this point

Question 316

What are the clinical signs of ascarids?

Answer 316

Unthrifty Loss of energy, colic b/c of migration. Lung damage, cough

Question 317

How are ascarids treated and controlled?

Answer 317

Anthelmintics. Broad spectrum anthelmintics effective against adults and larvae

Question 318

Where are Gasterophilus intestinalis eggs laid?

Answer 318

limbs / shoulder region --> requires stimulation

Question 319

Where are Gasterophilus haemorrhoidalis eggs laid?

Answer 319

around face, nose, lips --> requires stimulation

Question 320

Where are Gasterophilus nasilis eggs laid?

Answer 320

Underneath throat area --> no stimulation required

Question 321

Where (in general) are eggs of Gasterophilus spp. found?

Answer 321

Hair

Question 322

What is the life cycle of Gasterophilus spp.?

Answer 322

The larvae once they are hatched from the egg they migrate to the stomach. Start at mouth (mucous membranes / tongue). Once within stomach, stay here for 8-10 months continuing to grow. After they attach / develop , eventually detach and are excreted in feces. Pupate in soil and adult fly emerges.

Question 323

What are the clinical signs of Gasterophilus spp.?

Answer 323

Subclinical (colic), mild gastritis, stomatitis (mouth), painful to eat.

Question 324

How are Gasterophilus spp. treated and controlled?

Answer 324

Medication. Current recommendations is to tx horse once / year

Question 325

What are Oxyuris equi?

Answer 325

Pinworms

Question 326

Where are adult and eggs of pinworms found?

Answer 326

Adults – large intestine (cecum, colon). Eggs – perianal.

Question 327

What are the clinical signs of pinworms?

Answer 327

Tail rubbing. Don’t cause a lot of significant clinical signs. Can be irritating (itching, hair loss)

Question 328

How are pinworms treated and controlled?

Answer 328

Drugs. Most broad spectrum anthelmintics will take care of these.

Question 329

What are swine ascarids?

Answer 329

Large worm in swine, found in small intestine

Question 330

What is the life cycle of ascaris in swine?

Answer 330

Larvae developing w/in eggs, gets to infective stage in 3-4 weeks. Migrate to liver from SI --> lung --> coughed up / swallowed / back to intestinal tract.

Question 331

What are the clinical signs of swine ascarids?

Answer 331

a. Thumps – abdominal breathing, heavy contractions while breathing b. Failure to gain weight c. Stunting

Question 332

How are swine ascarids treated and controlled?

Answer 332

Treatment is supportive. Secondary infection should be treated with antibiotics a. Anthelmintics b. Deworm – before breeding, before farrowing

Question 333

What is the life cycle of lung worms?

Answer 333

- Adults --> Adult worms found in the lungs - Eggs --> Eggs coughed up, swallowed, deposited in feces. Larvae hatch, larvae are ingested by earth worms - Larvae --> ingested by earth worm - Earthworm --> ingested by pig

Question 334

What are the clinical signs of lungworms?

Answer 334

a. Parasitic pneumonia b. Coughing c. Anorexia

Question 335

How are lungworms treated and controlled?

Answer 335

Levamisole, slatted floors

Question 336

Where are swine nodular worms found?

Answer 336

Large intestine

Question 337

What is the life cycle of nodular worms?

Answer 337

Direct life cycle - Eggs passed in feces - L3 in pasture, ingested - Once ingested, form nodules in large intestines

Question 338

What are the clinical signs of nodular worms?

Answer 338

Subclinical

Question 339

How are nodular worms treated and controlled?

Answer 339

a. Drugs – Levamisol, pyrantel b. Sanitation

Question 340

How big are viruses?

Answer 340

Microscopic

Question 341

Where can viruses survive?

Answer 341

Obligate Intracellular parasite. They live and multiply within a living host cell. Outside a host they are metabolically inert. May survive outside host for limited time, but to replicate they are going to have to have a host. Without host, they will eventually die in the environment.

Question 342

What is the structure of viruses?

Answer 342

1. Nucleic Acid - DNA or RNA 2. Capsid – protein coat 3. Some have lipid envelope 4. Virus-specific proteins 5. No cell wall, no nucleus

Question 343

What is a nucleocapsid?

Answer 343

Nucleocapsid = Nucleic Acid + Capsid

Question 344

What is an antigen?

Answer 344

Any foreign protein that can induce an immune response

Question 345

Where are viral antigens located?

Answer 345

Capsid, envelope

Question 346

Are antigens synonymous to antibodies?

Answer 346

NO

Question 347

What is Hemagglutinin?

Answer 347

binds to sialic receptor on host cell and initiates entrance into host cell

Question 348

What is Neurominidase?

Answer 348

involved in getting virus out of host cell

Question 349

How long can viruses survive out of a host?

Answer 349

Only able to survive for short period of time out of the host.

Question 350

What are some routes of entry of viruses?

Answer 350

Oral, urogenital tract, respiratory tract, bites

Question 351

What are some mechanisms of spread for viruses?

Answer 351

Aerosolized (cough, sneeze), body fluids

Question 352

What are viral disease characteristics?

Answer 352

1. Rapid onset 2. Fever 3. No pus 4. No response to antibiotics

Question 353

How are viral disease spread through carriers?

Answer 353

Often introduced into herd due to carrier animal brought in that is not showing any clinical signs (subclinical), but is able to transmit to naïve animals

Question 354

What does replication of a virus entail?

Answer 354

Replication: attachment, penetration, uncoating, macromolecular synthesis, viral assembly, and release

Question 355

What are the types of virus cell interactions?

Answer 355

Cytocidal, noncytocidal

Question 356

What does it mean for a virus to be cytocidal?

Answer 356

KILL host cell; usually once they have reproduced

Question 357

What does it mean for a virus to be noncytocidal?

Answer 357

Able to happily survive within cell. Allows place for virus to continually produce offspring (persistent + latent infections)

Question 358

What are inclusion bodies?

Answer 358

Aggregate protein type substances. Helps for identification purposes

Question 359

What are the two types of virus-induced death?

Answer 359

Necrosis and programmed cell death

Question 360

What are the laboratory methods used to identify viruses?

Answer 360

Cytologic examination, histopathology, viral culture, viral serology, electron microscopy, fluorescent antibody immunohistochemistry, Polymerase chain reaction

Question 361

What is cytologic examination for viruses?

Answer 361

Cytologic examination is where we are looking at cells. Whether it is a sample we have taken from a lymph node OR infected cells in culture and looking for changes. Not very sensitive. If we see an inclusion body, great, body we don’t see that in all cells. We are looking for cells that are changing (dying, vacuoles, fusion, multinucleated giant cells)

Question 362

What is histopathology for viruses?

Answer 362

Taking tissue sample and looking for structural changes under microscope that correlate with viral infection. Could also treat tissues with viral protein, and will be tagged with substrate/dye.

Question 363

What is viral serology?

Answer 363

Means of evaluating the animal’s immune response and determining level of antibodies in the blood. Depending on levels, gives us indication if we have recent infection, active infection, etc.

Question 364

What are the complications of viral serology?

Answer 364

Sometimes levels from active infection may be at same level of those from animal who has been vaccinated. Hard to differentiate between the two.

Question 365

What is electron microscopy of virus laboratory methods?

Answer 365

Look at the virus (shape, protein projections) used for ID purposes

Question 366

What is fluorescent antibody immunohistochemistry?

Answer 366

Tag antibody with fluorescent color, look under with fluorescent microscope

Question 367

How are viruses treated and controlled?

Answer 367

Interferon, antiviral drugs, classical antibiotics are NOT effective, immunity through vaccination or natural exposure

Question 368

What are interferons and how do they help treat / control viruses?

Answer 368

Cells activate cytokine. Infected cells produce these, and it is meant to help surrounding cells

Question 369

What are the general characteristics of bacteria?

Answer 369

Prokaryotic, microscopic

Question 370

What are the three shapes of bacteria?

Answer 370

Round = cocci Elongated – Bacilli Spirochetes = wavy

Question 371

What is the structure of bacteria?

Answer 371

Unicellular, cytoplasm, ribosomes, nucleoid, cell wall (rigid, for protection), pili / fimbriae, +/- flagella

Question 372

What are the subdivisions of bacteria cell walls?

Answer 372

1. Gram positive – thick peptidoglycan later (stains purple / blue) 2. Gram negative – thinner peptidoglycan later (stains more red / pink)

Question 373

What is the capsule of bacteria?

Answer 373

Slime layer (polysaccharide). Contains K antigen. Protective mechanism for bacteria that allow them to persist on non-favorable conditions. Important for allowing bacteria to adhere to host tissues, helps establish colonization.

Question 374

What is the K antigen?

Answer 374

Located on capsule. Antigen host can develop antibodies to

Question 375

What are Pili and what antigen to they contain?

Answer 375

Short hair like projections. Help bacteria adhere. Contain F antigen

Question 376

What is the function of flagella and what antigen do they contain?

Answer 376

Mobility. Contain the H antigen

Question 377

What are spores?

Answer 377

Help with survival (protective coat). Metabolically inert. If they find themselves in environment where they will die, they will produce spores; survival technique.

Question 378

What are plasmids?

Answer 378

extrachromosomal DNA

Question 379

What do plasmids encode for?

Answer 379

Drug resistance, virulence

Question 380

How do bacteria function metabolically?

Answer 380

Most are independently metabolic. When conditions are appropriate, they can replicate outside of host cells (unlike viruses).

Question 381

What is the mechanism of disease production for bacteria?

Answer 381

A. Adhere to host cell --> this is where capsid and villi help B. Secrete toxin --> penetrated and spreads within host C. Enter cell

Question 382

What are the laboratory methods to evaluating bacteria?

Answer 382

Microscopic exam, growth in media and biochemical reactions, MALDI-TOF, antibiotic susceptibility tests

Question 383

What is MALDI-TOF?

Answer 383

Matrix-assisted laser desorption/ionization time of flight. Sort of like spectrometry, compares to known bacterial spectrums and compares

Question 384

What are the different antibiotic susceptibility tests?

Answer 384

Diffusion techniques and dilution plates. Both works to determine what bacteria is susceptible to. With plates, can produce concentration where bacteria aren’t going to grow

Question 385

How can bacteria be treated and controlled?

Answer 385

A. Antibiotics - - selected on basis of antibiotic sensitivity tests B. Immunization C. Good husbandry and hygiene

Question 386

What are the general characteristics of fungi?

Answer 386

Eukaryotic, structure is filamentous (mold) or unicellular (yeast - unicellular), Dimorphic

Question 387

What are the different types of hyphae filament of fungi cells?

Answer 387

Mycelium and spores

Question 388

What are mycelium of fungi?

Answer 388

Mass of hyphae (mold)

Question 389

What are fungi spores?

Answer 389

Airborne, from hyphae

Question 390

What are the classifications of fungal infections?

Answer 390

Superficial or Deep Systemic Infections

Question 391

What is an example of a superficial fungi infection?

Answer 391

Ringworm

Question 392

What is an example of a Deep Systemic fungi infection?

Answer 392

Blastomycosis

Question 393

What is mycotoxicosis?

Answer 393

Ingestion of fungi toxins (i.e., ergot)

Question 394

What is the mechanism of infection of fungi?

Answer 394

A. Spores enter breaks in skin B. Inhalation of spores C. Opportunistic mycoses

Question 395

What are the laboratory procedures to determine if there is a fungi infection?

Answer 395

Direct microscopic examination, culture

Question 396

How can fungi be treated and controlled?

Answer 396

Fungicides - topical and systemic; Management -- depends on situation. A lot that have superficial, put in dry / sunny environment and it can self-resolve.

Question 397

What are the general characteristics of protozoa?

Answer 397

Eukaryotes, unicellular

Question 398

What us the structure of protozoa?

Answer 398

They have a complex life cycle, and structure varies with age

Question 399

What are the two main worldwide protozoan diseases?

Answer 399

Malaria, Trypanosomiasis

Question 400

What are the main protozoan diseases in North America?

Answer 400

Coccidiosis, Cryptosporidiosis, Trichomoniasis

Question 401

What is the mechanism of infection of Coccidiosis/Cryptosporidiosis?

Answer 401

Transmitted through fecal oral route 1. Feces – ground 2. Ingest oocyte 3. Invade intestine

Question 402

What is the mechanism of infection of Trichomoniasis?

Answer 402

Breeding

Question 403

How are protozoan infections determined in the laboratory?

Answer 403

Direct microscopic exam; PCR

Question 404

How are Coccidiosis and Cryptosporidiosis treated and controlled?

Answer 404

Management (understand life cycle)

Question 405

What is the treatment and control for Trichomoniasis?

Answer 405

Cull animals before breeding

Question 406

What are prions?

Answer 406

Proteinaceous infectious particle; infectious proteins

Question 407

What are different types of prion diseases?

Answer 407

Agents of TSEs (transmissible spongiform encephalopathy) - BSE - Chronic Wasting Disease - Transmissible mink encephalopathy - Scrapie - Human TSEs: CJD, Kuru

Question 408

How are prions classified?

Answer 408

- Host & disease - Molecular & biological properties - Amino acid sequence: host

Question 409

What are the properties of prions?

Answer 409

normal cellular protein undergoes conformational changes to become pathogenic. Encoded in genome.

Question 410

Why is the structure of prions important?

Answer 410

Normal protein, we don’t really know the function. It ends up developing a different infectious structure. Instead of just alpha helices, you have a helix + beta sheets. Body doesn’t recognize it as abnormal (thus, no inflammatory response).

Question 411

Are prions resistant?

Answer 411

Prions are very resistant. Things that denature cell membranes / DNA, won’t affect prions. Requires UV & gamma radiation and environmental insults.

Question 412

What is important in the infectious mechanism of prions (why are they so effective)?

Answer 412

Prions develop to high titers in the brain. Prions evoke no inflammatory or immune responses in their hosts. Host doesn’t recognize as foreign antigen.

Question 413

How are prions PrPsc replicated?

Answer 413

- Transmitted horizontally - Catalyzes conversion of PrPc into PrPsc - Template for abnormal folding & polymerization of PrPc - Process cascades exponentially

Question 414

What damage do prions cause to the host?

Answer 414

When PrPsc builds up, causes fibrillar masses (plaques). Leads to neuronal degeneration & neurological defects

Question 415

What are the general considerations in controlling infection while raising livestock?

Answer 415

A. Intensive animal raising B. Antibiotics C. Disinfection

Question 416

What does intensive animal raising entail to control infection?

Answer 416

Physical contact, contaminated feed/water, air movement

Question 417

What is disinfection?

Answer 417

Destruction of pathogenic microorganisms on inanimate objects

Question 418

What are the requirements for effective disinfection?

Answer 418

Systematic approach (Depopulate – AIAO, clean, remove equipment, wash – detergent, apply disinfectant, fumigate, dry/rest, restock)

Question 419

What is detergent important for washing?

Answer 419

decreases surface tension to allow to start breaking down fats, proteins for washing

Question 420

What are different types of physical disinfection that can be used?

Answer 420

Sunlight, hot air, moist heat, fire, sterilant, thermal death

Question 421

What is moist heat?

Answer 421

Autoclave – steam w/ pressure - 121 degrees C / 15 lbs. / 15 mins - Sterilize surgical lab equipment

Question 422

What is dry heat?

Answer 422

160 degrees C, 1 hr.

Question 423

What is the difference for non-spore forming versus spore forming bacteria regarding physical disinfection?

Answer 423

Non-spore forming -- If we were to just use heat, most bacteria are susceptible if we can get up to high enough level. Spore forming – must be MUCH higher temp, not practical

Question 424

What is the mechanism of action for disinfection?

Answer 424

1. Denature cell wall --> basically punching bacteria holes and causes to lyse 2. Alter microbe permeability 3. Damage/destroy nucleic acid 4. Damage/destroy proteins

Question 425

What is a disinfectant?

Answer 425

Germicide with little irritant effect on tissue

Question 426

What is disinfection?

Answer 426

destruction of pathogens on inanimate objects

Question 427

What is sterility?

Answer 427

Complete absence of any form of life

Question 428

What is an antiseptic?

Answer 428

Agent that eliminates infection on a living tissue

Question 429

What is antisepsis?

Answer 429

Destruction of pathogens on surface of living tissue

Question 430

What are the characteristics of an ideal chemical disinfectant?

Answer 430

1. Broad spectrum 2. Effective at low concentration 3. Nontoxic 4. Stable 5. Minimal corrosiveness and caustic

Question 431

What is boric acid?

Answer 431

Non irrirating, weak (not really effective)

Question 432

What is lye (soda lye)?

Answer 432

Caustic, 2%. Essentially sodium hydroxide; dangerous, could burn skin

Question 433

What is lime (calcium oxide)?

Answer 433

Used in pens, floors. Has drying effect on feet of animals

Question 434

What is chlorine (sodium hypochlorite / Clorox)?

Answer 434

a. 1 to 50 ppm (5% bleach) b. Inhibited by organic material c. Corrosive, kills spores

Question 435

What are phenolics?

Answer 435

1. Toxic – protoplasmic poison 2. Kills mycobacteria, not spores 3. Uses – umbilicus infection, sterilize instruments

Question 436

What are quaternary ammonium compounds?

Answer 436

A. Cationic surfactant (minimum detergent action) B. Effective on gram +, some gram -, and envelopes viruses C. Not effective on mycobacteria and non-enveloped viruses D. Limited value with blood and tissue

Question 437

What are the uses of quaternary ammonium compounds?

Answer 437

1. Tissues (alcohol solutions) 2. Sanitization (dairy)

Question 438

What should quaternary ammonium compounds NOT used for ?

Answer 438

1. Sterilization of surgical equipment 2. Use with soaps

Question 439

What are the different preparations of quaternary ammonium compounds?

Answer 439

1. Benzalkonium chloride 2. Benzethonium chloride 3. Cetylpyridium chloride

Question 440

What is Formaldehyde solution?

Answer 440

A. Bactericidal – excellent / reliable B. Hazardous, carcinogen C. 4% used for hoof infections

Question 441

What are the advantages of formaldehyde solution as a disinfectant?

Answer 441

a. Powerful germicidal action b. Action not decreased by organic material c. Noncorrosive

Question 442

What are the disadvantages of formaldehyde solution as a disinfectant?

Answer 442

a. Irritating gas b. Skin damage c. Carcinogen (cancer causing)

Question 443

What are alcohols used for in disinfecting?

Answer 443

Solvent, antiseptic, disinfection

Question 444

What is Ethyl alcohol (70%) / isopropyl alcohol?

Answer 444

1. Medically, one of the best antiseptic / disinfectants 2. Used in combination with other compounds (solubize fat, synergism)

Question 445

What is the action of ethyl alcohol (70%)?

Answer 445

a. Denatures soluble proteins b. Decreases surface tension c. Local effect – brief irritation

Question 446

What is iodine effective on?

Answer 446

1. Kills spores in 15 mins 2. Kills most bacteria in 1 min

Question 447

What is iodine used as?

Answer 447

2% solution – scrubs, presurgical preparation

Question 448

What are the limitations of iodine?

Answer 448

- Irritates tissues -- delays healing - Diffuses into cell, inhibits cell metabolism

Question 449

What are iodophores?

Answer 449

1. Surface-active agent combines with iodine 2. Advantages of iodine without disadvantages 3. Used in teat dips – mastitis control

Question 450

What is Povidone – Iodine (Betadine)?

Answer 450

1. Advantages of iodine without irritation, stain, toxicity 2. Surgical scrub

Question 451

What are the general things used for chemotherapy?

Answer 451

1. Antiseptics – topical 2. Sulfa drugs – 1935 3. Antibiotics

Question 452

What is an antibiotic?

Answer 452

Substance produced by a micro-organism …. that at a low concentration inhibits or kills another micro-organism

Question 453

What is the mechanism of antibiotic action of penecillin?

Answer 453

Inhibit cell wall synthesis

Question 454

What is the mechanism of antibiotic action of amphotericin B?

Answer 454

Alter cell membranes

Question 455

What is the mechanism of antibiotic action of tetracyclines?

Answer 455

Inhibition of protein synthesis

Question 456

What is the mechanism of antibiotic action of quinolone?

Answer 456

Inhibition of nucleic acid synthesis

Question 457

What is the mechanism of antibiotic action of sulfonamides?

Answer 457

Antimetabolic activity

Question 458

How do you test for bacterial resistance?

Answer 458

Antibiotic sensitivity (plate culture or plate dilution assay)

Question 459

What are we trying to calculate in a plate dilution assay?

Answer 459

Minimum inhibitory concentration

Question 460

How do bacteria become resistance to antibiotics non genetically?

Answer 460

1. Absence of receptors 2. Inadequate permeability 3. Escape drug action 4. Synthesize drug action 5. Synthesize enzyme (inactivation)

Question 461

How can bacteria acquire drug resistance?

Answer 461

Chromosomal or plasmid

Question 462

How can drug resistance be transferable?

Answer 462

Transduction, conjugation, transposition, integrons

Question 463

What is transduction?

Answer 463

Plasmid DNA incorporated and transferred by a bacteriophage

Question 464

What is conjugation?

Answer 464

Plasmid-mediated transfer resistance. We have donor bacteria that have plasmid DNA (encodes for gene). Connects to adjacent bacteria and draws it close so that the plasmid can replicate and send copy over.

Question 465

What are transposons?

Answer 465

A DNA recombination reaction that results in translocation of a discrete DNA segment called a transposon

Question 466

What are integrons?

Answer 466

Insertion of antimicrobial drug resistance cassette

Question 467

What is bacterial transformation?

Answer 467

Bacteria take up foreign generic material (naked DNA) from the environment

Question 468

What are the different resistance mechanisms of bacteria?

Answer 468

1. Enzymatic degradation 2. Target mutation 3. Decreased cell wall permeability 4. Active efflux

Question 469

What is the definition of immunity?

Answer 469

The quality or state of being immune. A condition of being able to resist a particular disease especially through preventing development of a pathogenic microorganism or by counteracting the effects of its products.

Question 470

What are the two subcategories of the immune system?

Answer 470

Acquired and innate

Question 471

What are the characteristics of the innate immune system?

Answer 471

Not antigen driven (nonspecific), immediate, natural

Question 472

What are the innate defense mechanisms?

Answer 472

1. Physical 2. Chemical 3. Phagocytosis 4. Complement 5. Interferon

Question 473

In the innate immune defense, what are non-specific host mechanisms?

Answer 473

Invading organisms repelled at body surfaces by physical and chemical mechanisms

Question 474

What are the physical barriers of the innate immune system?

Answer 474

Body surfaces (skin, respiratory / digestive / urinary tracts, eyes)

Question 475

How does the skin act in the innate immune system?

Answer 475

1. Mechanical barrier 2. Resident bacterial flora 3. Regulated by desquamation, desiccation, pH

Question 476

How does the digestive tract act in the innate immune system?

Answer 476

1. Mouth – saliva; flushing 2. Low pH – gastric 3. Lysozyme – antibacterial, antiviral 4. Bile 5. Pancreatic enzymes

Question 477

Is the innate immune system specific or non-specific?

Answer 477

Non-specific

Question 478

How does the urinary system act in the immune system?

Answer 478

1. Low pH 2. Flushing action

Question 479

How does the udder act in the innate immune system?

Answer 479

1. Flushing action 2. Inhibitors in milk (lactenins) a. Lactoferrin b. Lysozyme

Question 480

How does the respiratory tract act in the innate immune system?

Answer 480

1. Filters – turbinates’, trachea, mucous 2. Mucous 3. Alveolar macrophages – phagocytosis

Question 481

What are the mechanisms of blood bourn innate immunity?

Answer 481

Phagocytosis and complement cascade

Question 482

What is the function of phagocytes?

Answer 482

Trapping and eliminating system for material that evades the outer defenses

Question 483

What is the complement cascade?

Answer 483

A part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane.

Question 484

What is phagocytosis?

Answer 484

Trapping system acts through cells that bind, ingest, and destroy invaders through phagocytosis

Question 485

What ate the categories of phagocytic cells?

Answer 485

Granulocytes, mononuclear, Natural killer cells

Question 486

What are granulocytes and how do they act?

Answer 486

Neutrophil, eosinophils, basophils. Rapid, not sustained.

Question 487

What is an example of a mononuclear phagocyte and how does it act?

Answer 487

Macrophage. Slow, sustained

Question 488

What is a neutrophil?

Answer 488

Major function is phagocytosis. Rapid, not sustained

Question 489

What is a macrophage?

Answer 489

Develops from monocyte. Delayed phagocytosis, sustained.

Question 490

What are eosinophils?

Answer 490

Can ingest bacteria and target foreign cells too large to ingest. Less active against bacteria than neutrophils and macrophages. One of main functions is to immobilize and kill parasites.

Question 491

What are basophils?

Answer 491

Do not infest foreign cells. Produce substances that attract neutrophils and eosinophils to trouble spots.

Question 492

What are natural killer cells?

Answer 492

Important in initial defense against viral infections. Produce cytokines that regulate some functions of T cells, B cells, and macrophages.

Question 493

What are the steps of the process of phagocytosis?

Answer 493

1. Chemotaxis and adherence of microbe to the phagocyte 2. Ingestion of microbe by phagocyte 3. Formation of a phagosome 4. Fusion of the phagosome with a lysosome to form a phagolysosome 5. Digestion of ingested microbe by enzymes 6. Formation of residual body containing indigestible material 7. Discharge of waste materials

Question 494

What is the role of inflammation?

Answer 494

Role is to combat infection and tissue injury

Question 495

How is inflammation triggered?

Answer 495

Triggered when innate immune cells detect infection or tissue injury

Question 496

What are the signs of inflammation?

Answer 496

Redness, heat, swelling, pain, loss of function

Question 497

What are the tissue macrophages in broken skin?

Answer 497

Histocytes

Question 498

What are the tissue macrophages in muscles?

Answer 498

Histiocytes

Question 499

What are the tissue macrophages in lymph nodes?

Answer 499

Reticular cells in LM, spleen, BM

Question 500

What are the tissue macrophages in GI tract?

Answer 500

Kupffer cells in liver

Question 501

What are the tissue macrophages in the lung?

Answer 501

Alveolar macrophages

Question 502

How many proteins are in the enzyme cascade of the complement system?

Answer 502

>30 proteins

Question 503

What are the actions of the complement system?

Answer 503

1. Mediated inflammation 2. Controls bacterial infections

Question 504

What are interferons?

Answer 504

Glycoproteins that control viral infections by signaling other cells to increase resistance to viruses. Not virus specific.

Question 505

What sections is acquired immunity split into?

Answer 505

Active or passive immunity

Question 506

What is acquired immunity?

Answer 506

Defense system which can distinguish, differentiate and remember different pathogenic invaders (viruses, bacteria, etc.)

Question 507

What are characteristics of acquired immunity?

Answer 507

1. Specificity: Can differentiate between foreign molecules (antigens) 2. Diversity: Can recognize a variety of foreign molecules (antigens) 3. Differentiates between self and non-self 4. Remembers (memory)

Question 508

What are the components of acquired immunity?

Answer 508

1. Antibody-Mediated Immune System 2. Cell-Mediated Immune System 3. Lymphokine Production

Question 509

What is the Antibody-Mediated Immune System?

Answer 509

Humoral immunity, antibodies/ Bcells (memory and plasma)

Question 510

What does the Antibody-Mediated Immune System Protect the body from?

Answer 510

Viruses, some bacteria, toxins

Question 511

What is the main cell of the Cell-Mediated Immune System?

Answer 511

Lymphocytes

Question 512

What are the different types of lymphocytes in the Cell-Mediated Immune System?

Answer 512

1. Helper T cells 2. Cytotoxic T cells 3. Memory T cells 4. Regulatory T cells

Question 513

What are lymphokines?

Answer 513

Cytokines that are released by lymphocytes. Important in stimulating immune response. Help coordinate humoral and cell mediated response.

Question 514

What is an antigen?

Answer 514

Agents that stimulate production of antibody and bind specifically to that antibody or provoke immune cell function or is recognized by immune cell

Question 515

What is an antibody?

Answer 515

Immunoglobulin formed in response to antigen

Question 516

What do antibodies bind to?

Answer 516

High affinity binding to antigenic determinants = site on antigen to which antibody binds.

Question 517

What is a key property of antibodies?

Answer 517

Specificity

Question 518

What is the structure of antibodies?

Answer 518

Consists of 2 classes of polypeptide chains (heavy + light chains)

Question 519

What is a domain of an antibody?

Answer 519

Functional regions of antibody

Question 520

What are the 2 domains of an antibody?

Answer 520

1. Binding domain – interacts with antigen 2. Effector domain of processes

Question 521

What is Immunoglobin M (IgM)?

Answer 521

First antibody following antigenic stimulation. Second highest concentration. Major Ig with initial immunization.

Question 522

What is immunoglobulin D (IgD)?

Answer 522

Receptor (B cell receptor). Primates, rodents, cattle, sheep, and pigs.

Question 523

What is Immunoglobulin G (IgG)?

Answer 523

Main serum antibody. Major role in antibody defenses. Smallest Ig.

Question 524

What is Immunoglobulin E (IgE)?

Answer 524

In tissues / allergic reactions

Question 525

What is immunoglobulin A (IgA)?

Answer 525

Dimeric – two molecules held together. Secretory component. Mucosa surfaces (lungs, intestines, skin, mammary gland)

Question 526

What immunoglobulin is part of mucosal immunity?

Answer 526

IgA

Question 527

What is plasticity of the immune system?

Answer 527

Ability to recognize the whole universe of potential determinants

Question 528

What is the cellular strategy for plasticity is the selective theory?

Answer 528

Immune system generates many specific molecules and antigens are bound to the ones that fit

Question 529

What is the primary response of the immune system?

Answer 529

First encounter of B cell with an antigen

Question 530

What is the secondary response of the immune system?

Answer 530

Second encounter of B cell with same antigen leads to a more rapid and greater response

Question 531

What is Immune system memory based on?

Answer 531

Based on long-lived “Memory B cells”

Question 532

How do T lymphocytes become T cells?

Answer 532

Must bass through thymus

Question 533

What is the T cell receptor?

Answer 533

Antigen binding site on surface of T cell

Question 534

What does the T cell receptor react with?

Answer 534

React with antigens on the surface of other cells (APCs). Macrophages, dendritic cells

Question 535

What do cytotoxic t cells (killer T cells) do?

Answer 535

Recognize other cells that display foreign antigens on their surfaces. Eliminated unwanted substances.

Question 536

What is the function of Helper T cells?

Answer 536

Function is to recognize degradation products of antigens and secrete protein factors that stimulate other cells

Question 537

What do lymphokines do?

Answer 537

Secreted factors that promote antibody production by B cells. Stimulate macrophages or CTLs, CMI

Question 538

Where are macrophages found?

Answer 538

Found in all tissues. Circulate in blood (monocytes)

Question 539

How do macrophages encounter foreign substances?

Answer 539

Generally, first cell to encounter foreign substance in the body. Nonspecifically engulf. Degrade.

Question 540

What are the degradation products of macrophages?

Answer 540

Peptides bind to protein and surface expression

Question 541

How do T cells recognize macrophage surface?

Answer 541

Displayed peptides

Question 542

What are the two compartments of the immune system in the body?

Answer 542

Primary and secondary organs

Question 543

What are the primary organs of the immune system in the body?

Answer 543

Bone marrow and thymus.

Question 544

What are the secondary organs of the immune system in the body?

Answer 544

Peripheral lymphoid tissue. Tonsil (throat), lymph nodes (limbs), Peyer’s patches (intestines)

Question 545

What is tolerance in the immune system?

Answer 545

Central concept of immunology. Immune system can differentiate between self and non-self.

Question 546

What are the parts of innate (non-specific, native) immunity?

Answer 546

Phagocytosis, inflammation, complement, interferon

Question 547

What are the parts of humoral immunity?

Answer 547

Antibody (IgG or IgM), B cells (plasma cells)

Question 548

What is the component on cell-mediated immunity?

Answer 548

T lymphocytes

Question 549

What is part of mucosal immunity?

Answer 549

Secretory IgA (secretory component)

Question 550

What is the purpose of a vaccination?

Answer 550

Give antigen, mount immune response, develop resistance

Question 551

What is the criteria to determine if vaccination is desirable / possible?

Answer 551

1. Identify cause 2. Protection 3. Risks --> reaction and costs

Question 552

What are the types of immunization procedures?

Answer 552

Passive immunization and active immunization

Question 553

What is passive immunization?

Answer 553

Transfer of antibodies through administration (oral / parenteral) or by ingesting (colostrum)

Question 554

What is the duration of passive immunization?

Answer 554

Limited, depends on amount of antibody

Question 555

When is the onset of passive immunization?

Answer 555

Immediate

Question 556

What are the important considerations regarding colostrum?

Answer 556

Neonatal calf losses (infectious enteric diseases or failure of passive antibody transfer).

Question 557

When and how much colostrum should be consumed?

Answer 557

Two liters (5% body wt; 6-8 hrs; repeat in 12h)

Question 558

When does absorption of colostrum decrease?

Answer 558

>6 hours

Question 559

What calf factors could cause failure of passive transfer from colostrum?

Answer 559

Ability to absorb decreases with age. Amount absorbed in 4-12 hours. Premature, cow not allowing to nurse, etc.

Question 560

What maternal factors could cause failure of passive transfer from colostrum?

Answer 560

1. Dams serum antibodies are concentrated in colostrum 2. Diet. Protein deficient = no effect. Energy deficiency = decreased volume

Question 561

What colostrum factors could cause failure of passive transfer from colostrum?

Answer 561

Normally 22% solids, compared to 12% in milk. Could have extra solid (Ig) or amount of Ig is variable.

Question 562

What impacts colostrum quality?

Answer 562

- First milking - Breed difference - Exposure of cow - Parity of cow - Freeze - Do not pool

Question 563

When should commercial colostrum supplements be used?

Answer 563

Not a replacement or substitute for high quality colostrum. May be beneficial if all you have available is low-medium quality.

Question 564

What is active immunization?

Answer 564

Development of immune response by the host in response to antigenic stimulation

Question 565

What is the duration of active immunization?

Answer 565

Prolonged

Question 566

What is the onset of active immunization?

Answer 566

Delayed

Question 567

What is a vaccine?

Answer 567

Biological agent used to produce active immunity

Question 568

What things does the ideal vaccine have?

Answer 568

Prolonged immunity, cheap, stable, safe

Question 569

What are the different types of vaccines?

Answer 569

1. Bacterin – inactivated bacteria or bacterial components 2. Live bacterial suspension 3. Toxoid – detoxified toxin 4. Live virus vaccine – unmodified virus 5. Modified live virus vaccine (MLV) 6. Sub-unit vaccine 7. Inactivated (Killed virus vaccines) 8. Marker vaccine

Question 570

What are the advantages of a live vaccine?

Answer 570

- Strong – long lasting immunity - Interferon – possible - Fewer doses - Cheaper

Question 571

What are the disadvantages of a live vaccine?

Answer 571

- Virulence risk - May cause abortion - May be immunosuppressive - Contamination risk - Stability

Question 572

What are the advantages of an inactivated vaccine?

Answer 572

- Safe - Stable

Question 573

What are the disadvantages of an inactivate vaccine?

Answer 573

- Less immunogenic - More frequent administration - Not good inducers of CMI - Require adjuvants for maximal response

Question 574

What are adjuvants?

Answer 574

- Combine with vaccine - Enhance immune response - Not involved with specificity of response

Question 575

What are the different routes of vaccine administration?

Answer 575

1. Parenteral 2. Intranasal 3. Oral 4. Aerosolization

Question 576

How does the USDA determine vaccine efficacy?

Answer 576

Purity, Potency, Efficacy, Safety

Question 577

What is serology?

Answer 577

Study of blood serum (antibody)

Question 578

What is serology used for?

Answer 578

Indicator of infection / response to vaccination

Question 579

What is a titer?

Answer 579

Level of specific antibody