Unit 2 Flashcards
What are other names for Bovine Ketosis?
Acetonemia, ketonemia
When does bovine ketosis usually occur?
Mainly disease in dairy cows 4-6 following parturition
What happens when an animal has bovine ketosis?
Ultimately, body fat ends up being utilized for energy, and they produce more ketones than their body can utilize
What is the cause of bovine ketosis?
- Heavy lactation resulting in high glucose demand – lactose production
- Any factor that reduces the absorption of carbohydrates – secondary to decreased appetite
- Majority of carbohydrates are metabolized into fatty acids
What is bovine ketosis often associated with?
Often associated with underfed cattle, poor quality hay or silage (leads to decrease propionic acid production)
What is lactose and why is it important with bovine ketosis?
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.
What happens to cattle when ketone levels increase? When does this happen?
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.
What happens when carbohydrates are metabolized into fatty acids in the case of bovine ketosis?
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.
What is the purpose of propionic acid?
Used to metabolize/ make glucose
How does insufficient feed intake cause bovine ketosis?
- Feed intake does not meet energy demand
- Insufficient ruminal production of propionic acid, a precursor of glucose
- Not enough glucose, so cow becomes hypoglycemic (low blood sugar)
- Low blood sugar makes cows metabolize fatty acids & glycerol supplies
- Fatty acids and glycerol are oxidized to form acetyl-CoA
- Lack of energy, the liver cannot cope
- Excess of acetyl-CoA (due to lack of energy) so it is converted to ketone bodies
- KETOSIS = ketone bodies accumulate and excreted in milk and urine
What are the signs of bovine ketosis?
- Inappetence, anorexia, depression
- Incoordination
- Drop in milk production
- Weight loss
- Lethargy
- Haircoat dull
How can bovine ketosis be diagnosed?
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)
What is the treatment for bovine ketosis?
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
How can bovine ketosis be prevented?
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).
- Decrease energy in the diet in late lactation and continue in the dry period (BCS 3.5).
- Increase energy post-partum
What is another name for Fat Cow Syndrome?
Fatty Liver Disease
What is the cause of fat cow syndrome?
Feeding too high energy & too low roughage in late lactation & dry period
What is the mechanism of fat cow syndrome?
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.
What are the effects of fat cow syndrome?
Fat cows have increased susceptibility to ketosis. Fat metabolism results in ketones
How can fat cow syndrome be prevented?
BCS 3.5 at dry off
What are other names for ovine ketosis?
Pregnancy disease, Pregnancy toxemia, Pregnancy ketosis, Twin lamb disease
When does ovine ketosis occur?
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.
What are the causes of ovine ketosis?
- 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.
- Stressors
- Demand for glucose is not met and hypoglycemia develops
- Excess ketones are produced
What are the clinical signs of ovine ketosis?
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
How is ovine ketosis diagnosed?
- Clinical signs
- Close to parturition
What is the treatment for ovine ketosis?
- Propylene glycol (glucose precursor)
- Supplemental feed –>adding oats
- 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.
How can ovine ketosis be prevented?
Rising plane of nutrition in late gestation. Nutritional management – BCS should be moderate (no less than 2.5). Add grain for source of carbohydrates.
When does Bovine Parturient Paresis occur?
- Onset at or near parturition
- 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).
What is the cause of Bovine Parturient Paresis?
- Sudden loss of calcium into colostrum
- High calcium in diet during dry period
How does having high calcium during dry period effect cows?
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.
Where are the normal sources of calcium in cattle?
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.
What should normally happen with calcium in cattle, compared to what happens with milk fever?
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
What happens when there is high calcium in diet during dry period?
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.
What are the clinical signs of milk fever?
- Stage 1 –>Ambulatory, hypersensitivity, excitable. Mild tremors.
- 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.
- Stage 3 –> Lose consciousness, coma, Unable to maintain sternal recumbency, unresponsive, will only survive a few hours if left untreated
What is the treatment of milk fever?
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.
How can milk fever be prevented?
Balance Ca & P ratio; 1:1 (not over 2:1)
What is Downer Cow Syndrome?
Inability to rise on her own (recumbent)
When does Downer Cow Syndrome occur?
- Parturition
- Peak lactation age
- History of parturient paresis
What is the cause of Downer Cow Syndrome?
- Milk fever (parturient paresis)
- Trauma –> difficult birth, nerve damage, slipping, infection, etc.
What are the risk factors for Downer Cow Syndrome?
- Delay treatment of milk fever –> Longer she is down, more likely she will be downer cow
- Housing –> Facilities / flooring, make sure they can get good footing
- Fat –> - High BCS, bad partition, will lead to dystocia.
- Infections –> Mastitis, metritis,
- Malnutrition
How is Downer Cow Syndrome treated?
- Treat milk fever
- Treat infections
How can Downer Cow Syndrome be prevented?
- Nutrition
- Environment
- Supervise parturition
How can calving injuries be prevented?
- Heifer size / bull selection
- Supervise parturition
How can you get cows up that have Downer Cow Syndrome?
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)
Why is it important to get Downer Cows up?
Getting up allows for better examination. Put feed + water right in front of her. Treat if you know cause, otherwise supportive care.
How should downer cows be treated if there is no sign of recovery?
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.
What are other names for Hypomagnesemia?
Grass Staggers, Grass Tetany
What is the cause of hypomagnesemia?
Complex metabolic disturbance
1. Low plasma concentration of magnesium
2. Mechanism is not known
When does hypomagnesemia occur?
- Lush pastures
Dry matter < 0.2% Mg - Lactating cattle, sheep, and goats
Loss of Mg in milk - Top-dressed pastures
Mg absorption ↓ when K and N ↑ in soils
What type of cattle do we see hypomagnesemia in?
Nursing calves <2 months, beef > dairy
What are the clinical signs of hypomagnesemia?
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
How is hypomagnesemia treated?
- Herd problem –> Even if you only see a few with clinical signs, need to treat WHOLE herd
- Ca and Mg solutions IV
- 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.
How can hypomagnesemia be prevented?
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.
What is the cause of Parakeratosis?
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.
What type of pigs does Parakeratosis occur in?
Confinement swine, 6 weeks – 4 months old
What are the clinical signs of parakeratosis?
- Skin lesions (not itchy)
- Crust formation on skin
How is parakeratosis treated and prevented?
Zinc additive to rations; rapid recovery
Why is differential diagnosis important in the case of parakeratosis?
Greasy pig disease caused by bacteria Staphylococcus hyicus. Occurs in pigs < 7 wks of age
What is another name for White Muscle Disease?
Nutritional Muscular Dystrophy
What type of animals does White Muscle Disease occur in?
All farm animal species. Especially rapidly growing calves, lambs, kids, and foals (3 weeks-3 months)
What does White Muscle Disease lead to effects on?
Cardiac muscle and SKM
What is the cause of White Muscle Disease?
Selenium and/or Vitamin E deficiency
Why can vitamin E and/or selenium deficiencies cause White Muscle Disease?
These are both important to keep cellular membranes healthy, help prevent damage from free radicals. Deficiency results in damage to cellular membranes.
What are the clinical signs of White Muscle Disease?
- Stiffness
- Inactive
- Sudden death
How can White Muscle Disease be diagnosed?
- Clinical signs (stiff gait)
- Elevated muscle enzymes (creatinine and aspartate)
- Low Vit E and Se in (diet, tissue and serum)
- Muscle degeneration
- Necropsy
What will necropsy of tissue effected with White Muscle Disease show?
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.
What do pathologists look for when diagnosing White Muscle disease?
Looking for calcification, damage to muscle fibers
How is White Muscle Disease treated?
- Sodium selenite
- 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.
How can White Muscle Disease be prevented?
Administration of Vitamin E/Se to dam about 4 weeks prior to parturition
What type of animals are gastric ulcers a major problem in?
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.
What are the clinical signs of gastric ulcers?
(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
Why do gastric ulcers occur?
Develop where esophagus goes into stomach (not protected from acidic fluid).
How are gastric ulcers treated?
Tx usually not economical. Prevention is key.
1. Antacids
2. Vitamin E and selenium
3. Reduce stress
How are gastric ulcers prevented and controlled?
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
What are other names for salt poisoning?
Salt Toxicity, Hypernatremia, Sodium ion toxicity, Water deprivation
What species do we see salt poising occur in?
We can see salt positioning in all spp. but most prevalent in swine and poultry
What is the direct cause of salt poisoning?
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
What is the indirect cause of salt poisoning?
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
What are the clinical signs of salt poisoning?
- Thirst
- Constipation
- Restlessness
- Depression, blindness, deafness, convulsions, and death
How is salt poisoning diagnosed?
- Clinical signs
- History!!! –> Look at water / diet intake
- Clinical pathology –> We can look at BW for elevated blood Na level
- Necropsy –> May see some inflammation in brain / NS with edema / fluid accumulation
What will the pathology of tissue samples taken from animals with salt poising look like?
Looking for vacuolated areas around blood vessels, might be a lot of WBC (eosinophils)
How is salt poising treated?
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
Why don’t we want animals with salt poisoning to drink all they want immediately?
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.
What is the mortality rate of animals who show clinical signs of salt poisoning?
Mortality rate in animals with clinical signs, regardless of TX, is usually over 50%. If showing clinical signs, likely to lose them
How can salt poisoning be prevented and controlled?
- Allow free access to clean water
- Generally recommended salt content should be in feed (<1%) and water (<0.5%) for all animal species
What is baby piglet anemia?
Iron deficiency in piglets, Causes anemia, depressed growth
Why does baby piglet anemia happen?
Piglets iron requirement cannot be met by sow’s milk
When does baby piglet anemia occur?
Piglet becomes anemic within 2-3 days of birth, but peak incidence is 3 weeks
What are the clinical signs of baby piglet anemia?
- Decreased growth
- Lethargy
- Pale skin and mucus membranes
- Difficulty breathing
- Edema
- Diarrhea
Why can baby pig anemia cause difficulty breathing?
Because there are not enough blood cells to carry oxygen
How is baby piglet anemia diagnosed?
- Clinical signed
- BW –> Hemoglobin <6 g/100 ml (normal 12-14 g/100 ml)
How is baby piglet anemia treated and controlled?
- 200 mg iron dextran IM at 1 to 3 days of age
OR
100 mg at 1-3 days and 7-14 days later - Iron (oral)
What is the problem with giving oral iron as a treatment for baby piglet anemia?
Inconsistently absorbed; oral iron is unreliable.
What is a synonym for Mulberry Heart Disease?
Microangiopathy of pigs
What is the cause of Mulberry Heart Disease?
Vitamin E and/or selenium deficiency
What is Mulberry Heart similar to?
Pig version of white muscle disease
What is the primary damage to in Mulberry Heart Disease?
Primary damage is to SKM in pigs
What type of animals is Mulberry Heart Disease most common in?
Most common in nursery or grower pigs
What can lead to Vitamin E deficiency that results in Mulberry Heart Disease?
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.
What geographic region most has the most common incidence of Mulberry Heart Disease because of selenium deficiency?
Selenium deficient grains in lower Midwest.
What is the most common sign of Mulberry Heart Disease?
The most common sign of MHD is sudden death of the best pigs with no symptoms. The heart will appear dark and mottled
What are the clinical signs of Mulberry Heart Disease?
- Sudden death
- Stiffness –> SKM impacted
- Unable to stand
How is Mulberry Heart Disease Diagnosed?
- Necropsy
- BW: Liver selenium levels <0.5 μg/g
What will heart tissue of animals with Mulberry Heart Disease look like when necropsied?
Extensive interstitial hemorrhages (H) and necrotic cardiomyocytes with dystrophic mineralization
How is Mulberry Heart Disease treated and controlled?
- Vitamin E and/or selenium injections (B0-SE)
- Supplementation of feed
What is neonatal hypoglycemia?
Low blood glucose/sugar concentration in neonates
What is the cause of neonatal hypoglycemia?
Inadequate intake of milk
- MMA (mastitis, metritis, agalactia)
- Inability of piglet to nurse – infection, not enough teats
What can worsen to neonatal hypoglycemia?
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
Why are baby piglets susceptible to neonatal glycemia?
Piglet has limited glycogen and body fat stores, depends on frequent meals.
When does baby piglets have non-functioning gluconeogenesis capability?
Not able to have good gluconeogenesis ability until >1 week old.
What age of piglets will neonatal hypoglycemia occur in?
Piglets <7 days of age
What are the clinical signs of neonatal hypoglycemia?
- Difficulty walking
- Convulsions
- Shivering
- Hypothermia
- Death
When will neonatal hypoglycemic pigs succumb to death by if impacted?
Death usually occurs within 24-36 hr. of onset (1.5 days)
How is neonatal hypoglycemia diagnosed?
- Blood glucose <50 mg/dl
- Empty stomachs (not nursing)
How is neonatal hypoglycemia treated?
- Glucose injections (Intraperitoneal)
- Gradually warmed to 1020F
- Oral supplementation with milk replacer or commercial nutritional supplements after CNS signs goes away
How can neonatal hypoglycemia be prevented and controlled?
Make sure piglets are getting adequate milk supply, keep environmental temp normal, minimize stress
What is Yew poisoning?
Japanese Yew is a common ornamental shrub. Used for lots of landscaping, not native to NE. Very toxic.
What causes Yew poisoning?
Ingestion of Yew plant (Taxus spp.).
Why are Yew shrubs so toxic when ingested?
Taxine: alkaloid = cardiotoxin (toxin to heart)
When does Yew poising occur?
a. All species
b. Ingestion –> Most cases are associated with accidental ingestion
What are the acute and subacute clinical signs of Yew poisoning?
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.
How is Yew poising diagnosed?
a. History of ingestion
b. Postmortem exam –> Rumen or gastric contents
What is the treatment of Yew poisoning?
Nonspecific. No antidote, all supportive (decontaminate stomach, activated charcoal, rumenectomy). If HR is decreased – could give atropine.
What are the food safety guidelines with animals who have been diagnosed with Yew poisoning?
- Milk withholding – 2 days
- Meat – 35 days
- Drugs - variable
What is Hydrocyanic (Prussic) Acid Poisoning?
Basically, cyanide poisoning. What happens here is our livestock spp. ingest / forage on type of plant that tends to produce cyanogenic glycosides
What are the sources of Hydrocyanic (Prussic) Acid Poisoning?
Many plant sources – Burmuda, milo, sudan grass, chokecherry
What is the toxic compound in Hydrocyanic (Prussic) Acid Poisoning?
Cyanogenic glycosides –> HCN
When does Hydrocyanic (Prussic) Acid Poisoning occur?
a. Wilted, frosted plants –> Higher concentration in leaves than the stems. Crushing, freezing, wilting
b. Rapid consumption
What animals does hydrocyanic (prussic) acid poisoning effect?
Seen in cattle and sheep (most sensitive) although can see in most spp.
Why is dry matter more likely to cause hydrocyanic (prussic) acid poisoning?
If plant is dry, then this increases cyanogenic potential b/c in dry matter it concentrated.
Forage –> silage – will reduce cyanide content.
What is the pathogenesis of Hydrocyanic Acid Poisoning?
a. Anoxia, tissue asphyxia
b. Cerebral anoxia
After ingesting, when do animals show clinical signs of Hydrocyanic Acid Poisoning?
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.
What are the clinical signs of hydrocyanic acid poisoning?
a. Acute
b. Dyspnea, restlessness
c. Convulsions
What does cyanide do biologically?
Cyanide prevents hemoglobin from releasing O2 to tissues. Tissues are starving of oxygen.
How is Hydrocyanic acid poisoning diagnosed?
Test plants if concerned
What is the treatment / control protocol for hydrocyanic acid poisoning?
Graze on forage that is naturally low in cyanogenic glycosides (has been accomplished through genetic modification), change feed silage
What is the cause of sweet clover poisoning?
Sweet clover normally produces Coumarin, but when moldy creates dicoumarin.
Coumarin –> Mold –> Dicoumarin
What is Dicoumarin?
Antagonist of vitamin K
What happens when Dicoumarin antagonizes vitamin K?
Blood does not clot. Vitamin K is needed to activate clotting factors in the body.
What drug is sweet clover poisoning similar to in terms of effects?
Warfarin
When does sweet clover poisoning occur?
a. We see this often in cattle
b. Moldy sweet clover
What are the clinical signs of sweet clover poisoning?
a. Hemorrhages –> Nose bleeds (potentially), SQ swelling (bleed under skin), If surgery performed (dehorning), could bleed to death
b. Stiffness –> - Bleed into joints
How is sweet clover poisoning diagnosed?
History (hemorrhaging or bleeding to death)
How is sweet clover poisoning treated?
Vitamin K, if they are showing signs, could have blood transfusion (depends on value of animal), change feed
How is sweet clover poisoning prevented?
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).
Why does Mycotoxicosis occur?
Due to feed contaminated with toxins from fungi or molds
What is the cause of Mycotoxicosis?
Mycotoxins
Why do fungi or molds produce mycotoxins?
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
What are the effects of Mycotoxicosis?
Major effect: feed refusal - leads to poor performance
1. Irritate digestive tract mucosa
2. Destroy vital organs
3. Cause neoplasia
4. Hormonal effects
Where do Aflatoxins come from and how to the effect animals?
Aspergillus flavus and Aspergillus parasiticus (from corn).
- Reduced productivity
- Slow growth
- Hepatotoxicosis –> toxic to the liver
Where do Zearalenone toxins come from and how to the effect animals?
Fusarium fungi. Causes Hyperestrogenic effects:
- swollen vulva
- Polycystic ovaries
- Pseudopregnancy
Where do Ergot mycotoxins come from and what animas do they effect?
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.
What do Ergot mycotoxins cause?
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.
Where does Ochratoxin mycotoxins come from and what clinical signs to they cause?
Aspergillus sp. and Penicillium sp.
- Edema –> around kidneys (enlarged, cysts), increased pu/pd
- Food refusal
- Decreased growth rate
Where do Vomitoxin aka Deoxynivalenol (DON) mycotoxins come from and what effects do they cause?
Fusarium graminearum. Animals can vomit after consuming, feed refusal, decreased growth rate
How is Mycotoxicoses diagnosed?
- Identify mycotoxins –> feedstuffs, animal tissues
- Lesions and clinical signs
Does fungal growth always lead to mycotoxins?
Just b/c you see fungal growth, doesn’t mean mycotoxins (and vice versa)
What species is nitrate poisoning seen in?
Many species are susceptible, but cattle most frequently.
What is the cause and occurrence of nitrate poisoning?
- Nitrates and nitrites in growing plants
- Ingestion of nitrate fertilizers
- Water sources
What is the pathogenesis of nitrate poisoning?
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
When do we most commonly see nitrate poisoning?
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.
What are the clinical signs of nitrate poisoning?
Anoxia, convulsions, coma, death. Rapid, weak HR
What do nitrate poisoning clinical signs result from?
Methemoglobin not able to carry O2, clinical signs are because of hypoxia.
What is the mechanism of action of nitrate toxicity?
High nitrate forage –> (RUMEN) nitrate –> nitrite (normally produces ammonia) –> excess nitrite –> (BLOOD) –> hemoglobin –> methemoglobin
What happens with normal levels of nitrates?
With normal levels, we get ammonia production, eventually converted to proteins
What is the treatment for nitrate toxicity?
Remove source of nitrate; methylene blue. Adjunct treatment = lavage the rumen with cold water. Will reduce activity of bacteria and conversion to nitrite.
What is the mechanism of action of methylene blue? Why is its use controversial?
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.
What is the occurrence of lead poisoning (what species does it happen in, how does it happen)?
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).
What are the systems effected by lead poisoning?
Enters bloodstream, tissues, and will redistribute to the bone.
a. Digestive system – GI irritation
b. Nervous system – damage as a result to peripheral nerves
What are the clinical signs of lead toxicity?
DX made based on clinical signs, determining lead concentration
a. Salivation, drooling
b. Anorexia, decrease activity of rumen
c. Dullness, muscle tremors
d. Death
What is the treatment for lead toxicity?
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.
Why is treatment for lead poisoning controversial?
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.
What species does copper poisoning effect?
Seen in several species, but most common in sheep (they are sensitive)
What is acute vs. chronic copper poisoning?
- Acute –> excessive amount of copper salts in feed, given mineral mixes
- 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.
What are the clinical signs of copper poisoning for chronic and acute symptoms?
a. Acute copper poisoning: Gastroenteritis -Anorexia, abdominal pain, diarrhea
b. Chronic copper poisoning: Hemolytic crisis
How is copper poisoning diagnosed?
Tissue concentration of Cu and Mb
How is copper poisoning prevented and treated?
a. Prognosis poor if a hemolytic crisis occurs
b. Symptomatic treatment
c. Remove the source of copper poisoning
What is selenium toxicity called in horses?
Alkali Disease
Why does selenium toxicity occur?
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.
What are the clinical signs for selenium toxicity?
- Acute – Due to over consumption of plants; nervous system, death
- Chronic – Retarded growth, inhibited reproduction (estrous cycle not going as it should, low birth rate), hair loss, abnormal hoof growth
What is the treatment for selenium toxicity?
No specific treatment. Eliminate source, support symptomatically
What is urea normally used for? Why does urea poisoning occur?
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.
What is the cause of urea toxicity?
- Ammonia collects in rumen
- Absorption occurs - too much ammonia in bloodstream
- Toxicity results
How long does urea toxicity take for it to show clinical signs?
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.
What are the clinical signs of urea poisoning?
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.
How is urea poisoning diagnosed?
Check feed, ammonia odor on breath
What is the mechanism of urea poisoning (why does it convert to ammonia)?
Conversion of urea to ammonia is result from bacteria in rumen called urease.
How is urea poisoning treated?
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.
How is urea poisoning prevented?
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.
What is the cause of Organophosphate Poisoning?
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.
When does organophosphate poisoning occur?
Fields – drift - after pesticide application.
What is the pathogenesis of organophosphate poisoning?
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.
What are the clinical signs of Organophosphate Poisoning in cattle, swine, and horses?
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
How is organophosphate poisoning treated?
- Atropine – muscarinic antagonist (antidote). Decreases salivation, GI motility. Not going to have effect on SKM, specific to receptors.
- Charcoal – for ingestion
- Wash skin
What do infectious agents do?
Invade host, evade host defenses, cause inflammation
How does an infectious agent get from one host to another?
Vector (biological or mechanical), fomites, or biological material
What is a vector?
Vector is a living agent that carries and transmits infectious agent / pathogen from one living organism to another.
What is the difference between a biological vector and a mechanical vector?
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).
What is a fomite?
Inanimate objects capable of carrying infectious organisms (boots, trailers, feed bags)
What is biological material?
Blood, tissues, urine, etc
What is vertical and horizontal transmission?
Vertical transmission –> Spread: mother to offspring
Horizontal transmission –> Spread: animal to animal
What are the portals of entry for infectious diseases?
- Ingestion
- Inhalation
- Genitourinary
- Teat canal
- Bites
What is tropism? T
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?
How are infectious disease prevented and controlled?
- Break disease cycle
- Alter host susceptibility
What are the problems due to parasites?
- Obstruction
- Nutrients
- Tissue destruction
- Irritation
- Vector
- Toxins
What are the characteristics of parasites?
- Host specific
- Most problems: young, malnourished
- Larvae harmful
- Does not cause death
- Prolific
- Complex life cycles
How are parasites prevented and controlled?
Decrease exposure via management, use anthelmintics
What is Pediculosis?
Louse infestation, lousiness
What are the different types of lice?
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.
What season to lice prefer?
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.
What species to lice prefer?
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.
What is the life cycle of lice?
Entire life on host (Eggs, nymphs, adults)
How are lice transmitted?
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.
What are lice carriers?
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.
What is the economic importance of lice?
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.
How are lice diagnosed?
Clinical signs, inspection
What is the chemical treatment for lice?
a. Self-treatment – limited
b. Sprays – not cold weather
c. Pour ons – cold weather
d. Injectable – sucking lice
What is mange?
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.
What are the three types of cattle scabies mites?
- Psoroptic (common scabies)
- Sarcoptic
- Chorioptic (common mange)
What are the mange regulations?
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.
How is mange transmitted?
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.
What is the occurrence of mange?
Duration of life cycle – 2 weeks –> Eggs, larvae, nymph, adult
Seasonal –-> the worst time of the year is fall through spring
What is the survival of mange like?
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.
What are the chemical compounds used to control mange?
i. Lime sulphur
ii. Toxaphene (banned in the USA)
iii. Coumaphos
iv. Injectable (eg. Ivermectin)
What are Swine Mange Mites?
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.
What are the clinical signs of swine mange mites in nursery/grower pigs and those with chronic mange?
Nursery-grower
- Acute allergic
- Intense itching
- Small sores
- Decreased growth rates
Chronic mange
- Usually, adults
- Mild itching
How are swine mange mites diagnosed?
Clinical signs, skin scrapings
How are swine mange mites treated and controlled?
a. SPF
b. Topical sprays & dips
Reapply: 14 days
Spray adults: 6 months
c. Injectable
Single dose: 100% kill of adult mites
How can swine mange mites be eradicated?
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
What is another name(s) for cattle grubs?
Warble fly larvae, heel flies
What is the occurrence of cattle grubs?
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.
What is gadding?
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
What internal effects to cattle grubs cause?
Hide and carcass damage
What is the life cycle of cattle grubs?
- Heel flies
- Eggs
- Larvae grub (mature larvae)
- Pupae
How are cattle grubs prevented and controlled?
- Housing –> Keep animals inside when flies are out in late spring / early summer, but this is not practical.
- 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).
What are the 4 main types of flies, and what kind of cattle to they affect?
- Pastured cattle
a. horn flies
b. face flies - Confined cattle
a. stable flies
b. house flies
What is the life cycle of horn flies?
Eggs–fresh manure. It is within these feces you are going to get larval and pupal development.
What mouth appendages to horn flies have?
Piercing-sucking mouth parts
Where do horn flies spend a majority of their time?
On the host
How do horn flies cause economic loss?
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
What is the life cycle of face flies?
Eggs–fresh manure
What mouth appendages do face flies have?
Spongy mouth parts. Their mouth appendages are adapted to sponging up fluid (tears, saliva, mucous, blood)
Why are face flies important?
Economic importance. Annoying to host, interfere with productivity.
What are face flies a vector of?
Moraxella bovis
What is Moraxella bovis and how do face flies transmit it?
Pink eye. Rough spines on mouth cause irritation to cornea and predispose for developing PINK EYE
How can horn flies and face flies be controlled?
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
What is another name for the stable fly?
Biting house fly
What mouth appendage does the stable fly have?
It has needle sharp proboscis designed to: penetrate skin, get into blood vessels, suck blood
What is the life cycle of stable flies (where to they lay their eggs)?
Eggs – decaying organic material
Where to stable flies spend most of their time?
Spend time off host
What is the importance of stable flies?
Bite is painful. Decreased productivity
What are house flies?
Very common insect in livestock facilities, poultry operations. Vomit feeders –> anything they do ingest, they regurgitate out
Where do house flies lay their eggs?
Fresh manure and decaying organic material
What type of mouth appendages do house flies have?
Spongy mouth parts
What is the importance of house flies?
Important for disease transmission, they are a public nuisance
How can stable and house flies be controlled?
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
What are parasitoids?
Miniature wasps, used to control stable flies.
What are miniature wasps?
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
What are biting midges and what they feed off of?
Tiny gnats, blood feeders
Where are biting midges found?
Swamps & streams
What species do biting midges affect?
Affects all classes of livestock
What do biting midges transmit?
Transmit blue tongue virus and Epizootic Hemorrhagic Disease virus
What do Horse Fly & Deer Flies do that is bothersome?
Bite. BOTH larvae and adult stage can bite. Adult has scissor like mouth parts.
What do horse and deer flies transmit?
Transmit Anaplasmosis
What animals to horse and deer flies affect?
Affect cattle and horses
What is another name for Sheep Keds?
Sheep ticks
What are sheep keds?
NOT ticks, they are wingless flies that suck blood
What do sheep keds cause?
Wool damage. Cause discoloration of wool (decreased value)
How are sheep keds treated?
Sheer, administer insecticide and re-treat in 3-4 weeks
What is another name for sheep bots?
Nasal bot fly
How do sheep bots infect their host?
Larvae – nasal passage. The female fly likes to lay larvae around the nostrils. Not eggs, larvae are deposit. Larvae migrate to nasal cavity / sinuses
How can you tell if sheep are being infected with sheep bots?
Nose to the ground / huddled together
What is the life cycle of mosquitos?
a. Eggs
b. Wrigglers (larvae)
c. Pupae (tumblers)
d. Adults
What diseases can mosquitos transmit?
Venezuelan equine encephalitis, canine heartworm
Where does the mosquito life cycle need to occur?
In water
How can mosquitos be controlled?
Destroy breeding grounds, fill low areas, get rid of tires. Aerating pond / getting water movement will help
What are ticks?
Blood sucking arthropods, able to transmit dz and cause irritation
What are the ticks found in NE?
Rocky mountain spotted tick, American dog tick, brown dog tick, Lone star tick, Winter tick, Spinous ear tick, Deep tick
What are the two classifications of ticks?
- Hard ticks (Ixodidae)
- Soft ticks (Argasidae)
What are characteristics of hard ticks?
Flattened, mouth parts visible, dorsal plate
What are the characteristics of soft ticks?
Can’t see mouth parts, oval, leathery
What is the life cycle of ticks? ELNA
- Eggs
- Larvae – seed ticks
- Nymphs – re-attach if 2 or 3 tick host
- Adult
What is the morphological difference between larvae and nymphs?
Larvae = 6 legs. Nymphs = 8 legs
How many hosts does the rocky mountain wood tick have?
3 hosts
How long is the life cycle for the rocky mountain wood tick?
Two year life cycle
What diseases is the rocky mountain wood tick a vector for?
Anaplasmosis, RMSF (rocky mountain spotted fever)
What is the life cycle for an American dog tick?
Life cycle similar to RMWT. 3 host tick. Takes up to 2 years to go through life cycle.
What is the life cycle of the brown dog tick?
3 hosts, short life cycle (2 months)
What is done for tick control?
Difficult, dips are effective. Sprays are not as effective. Look at environment. Woody areas, shrubby areas – need to be cleaned
What are the Abomasal parasites of cattle and sheep?
HOT
Haemonchus
Ostertagia
Trichostrongylus
What is Haemonchus spp?
The barber pole worm, large stomach feeder
Where can Trichostrongylus also be found?
Small intestine
What is the disease production of abomasal parasites of cattle and sheep?
- Blood sucking (anemia due to blood loss)
- Mucosal destruction (Penetrate abomasum, get into glands and cause obstructions, thickening of nodular glands)
What is the life cycle of abomasal parasites of cattle and sheep?
- Eggs – passed in feces
- Larvae – L1 –> L2 –> L3 (infectious stage) –> ingested –> L4 –> L5
- Adult
What are the clinical signs of abomasal parasites of cattle and sheep?
- Anemia, submaxillary edema
- Diarrhea
- Diarrhea
- Weight loss, poor growth, weak
- Rough hair coat
- Pot belly
How are abomasal parasites of cattle and sheep controlled?
- Eliminate crowding
- Nutrition
- Rotate grazing
- Anthelmintic resistance
- Anthelmintics
What is Hypobiosis?
“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.
What is the dormant stage for abomasal parasites?
Dormant stage (L4)
When do abomasal parasites come out of their hypobiosis dormancy?
Late fall/ early winter. Stress –> triggers release of L5
What is type II Ostertagiasis?
a. Large number of larvae
b. Dormant
c. Calves 12-20 months
What is type I Ostertagiasis?
a. Recent infections
b. Most are adults and respond to anthelmintics
c. Calves: 7-15 months
What is the species and location occurrence of liver flukes?
Sheep and cattle, mainly. Wet, moist, swampy areas, ponds, irrigated pastures, etc.
What vector is needed for liver flukes?
Part of life cycle involves a specific snail.
What is the life cycle of a liver fluke?
- Bile duct – adult
- Snail – larvae
- Aquatic vegetation – larvae
- Ruminant ingestion
- Gut penetration: liver migration
What are the clinical signs of liver fluke infestation in cattle and sheep?
- Cattle – anemia, emaciation, diarrhea
- Sheep – sudden death, anemia, bottle jaw
How are liver flukes treated and controlled?
- Anthelmintics
- Eliminate snails (copper sulfate, but is toxic to sheep)
- Keep animals off wet pasture
What species do Large Strongyles affect?
Horses
What is the life cycle of Large Strongyles?
- Eggs are passes out in feces
- Eggs in feces develop into L1, L2, and then L3 larvae stage
- L3 larvae on grass
- The horse eats the grass and ingests L3 stage larvae
- The L3 penetrates the intestinal wall
- L4 larvae develop into adults and lay eggs
What system do large strongyles penetrate once ingested?
Circulatory system
Where do adult Large Strongyles form and how do they affect this organ?
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.
What is the pathogenesis of large strongyles?
Larval migration – mechanical damage associated with migration. Adult worms—attach to mucosa, suck blood.
What are the clinical signs of large strongyles?
Anemia, colic, diarrhea, anorexia
How are large strongyles diagnosed?
History and clinical signs, fecal examination
How are large strongyles treated and controlled?
- Drugs
- Isolate, deworm
- Fecal tests
- Rotate pastures
- Break fecal piles
- Sanitation
What are Ascarids (Parascaris equorum)?
This is a large worm (up to 1 ft long). Found in small intestine
What is the life cycle of ascarids?
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
What are the clinical signs of ascarids?
Unthrifty Loss of energy, colic b/c of migration. Lung damage, cough
How are ascarids treated and controlled?
Anthelmintics. Broad spectrum anthelmintics effective against adults and larvae
Where are Gasterophilus intestinalis eggs laid?
limbs / shoulder region –> requires stimulation
Where are Gasterophilus haemorrhoidalis eggs laid?
around face, nose, lips –> requires stimulation
Where are Gasterophilus nasilis eggs laid?
Underneath throat area –> no stimulation required
Where (in general) are eggs of Gasterophilus spp. found?
Hair
What is the life cycle of Gasterophilus spp.?
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.
What are the clinical signs of Gasterophilus spp.?
Subclinical (colic), mild gastritis, stomatitis (mouth), painful to eat.
How are Gasterophilus spp. treated and controlled?
Medication. Current recommendations is to tx horse once / year
What are Oxyuris equi?
Pinworms
Where are adult and eggs of pinworms found?
Adults – large intestine (cecum, colon). Eggs – perianal.
What are the clinical signs of pinworms?
Tail rubbing. Don’t cause a lot of significant clinical signs. Can be irritating (itching, hair loss)
How are pinworms treated and controlled?
Drugs. Most broad spectrum anthelmintics will take care of these.
What are swine ascarids?
Large worm in swine, found in small intestine
What is the life cycle of ascaris in swine?
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.
What are the clinical signs of swine ascarids?
a. Thumps – abdominal breathing, heavy contractions while breathing
b. Failure to gain weight
c. Stunting
How are swine ascarids treated and controlled?
Treatment is supportive. Secondary infection should be treated with antibiotics
a. Anthelmintics
b. Deworm – before breeding, before farrowing
What is the life cycle of lung worms?
- 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
What are the clinical signs of lungworms?
a. Parasitic pneumonia
b. Coughing
c. Anorexia
How are lungworms treated and controlled?
Levamisole, slatted floors
Where are swine nodular worms found?
Large intestine
What is the life cycle of nodular worms?
Direct life cycle
- Eggs passed in feces
- L3 in pasture, ingested
- Once ingested, form nodules in large intestines
What are the clinical signs of nodular worms?
Subclinical
How are nodular worms treated and controlled?
a. Drugs – Levamisol, pyrantel
b. Sanitation
How big are viruses?
Microscopic
Where can viruses survive?
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.
What is the structure of viruses?
- Nucleic Acid - DNA or RNA
- Capsid – protein coat
- Some have lipid envelope
- Virus-specific proteins
- No cell wall, no nucleus
What is a nucleocapsid?
Nucleocapsid = Nucleic Acid + Capsid
What is an antigen?
Any foreign protein that can induce an immune response
Where are viral antigens located?
Capsid, envelope
Are antigens synonymous to antibodies?
NO
What is Hemagglutinin?
binds to sialic receptor on host cell and initiates entrance into host cell
What is Neurominidase?
involved in getting virus out of host cell
How long can viruses survive out of a host?
Only able to survive for short period of time out of the host.
What are some routes of entry of viruses?
Oral, urogenital tract, respiratory tract, bites
What are some mechanisms of spread for viruses?
Aerosolized (cough, sneeze), body fluids
What are viral disease characteristics?
- Rapid onset
- Fever
- No pus
- No response to antibiotics
How are viral disease spread through carriers?
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
What does replication of a virus entail?
Replication: attachment, penetration, uncoating, macromolecular synthesis, viral assembly, and release
What are the types of virus cell interactions?
Cytocidal, noncytocidal
What does it mean for a virus to be cytocidal?
KILL host cell; usually once they have reproduced
What does it mean for a virus to be noncytocidal?
Able to happily survive within cell. Allows place for virus to continually produce offspring (persistent + latent infections)
What are inclusion bodies?
Aggregate protein type substances. Helps for identification purposes
What are the two types of virus-induced death?
Necrosis and programmed cell death
What are the laboratory methods used to identify viruses?
Cytologic examination, histopathology, viral culture, viral serology, electron microscopy, fluorescent antibody immunohistochemistry, Polymerase chain reaction
What is cytologic examination for viruses?
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)
What is histopathology for viruses?
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.
What is viral serology?
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.
What are the complications of viral serology?
Sometimes levels from active infection may be at same level of those from animal who has been vaccinated. Hard to differentiate between the two.
What is electron microscopy of virus laboratory methods?
Look at the virus (shape, protein projections) used for ID purposes
What is fluorescent antibody immunohistochemistry?
Tag antibody with fluorescent color, look under with fluorescent microscope
How are viruses treated and controlled?
Interferon, antiviral drugs, classical antibiotics are NOT effective, immunity through vaccination or natural exposure
What are interferons and how do they help treat / control viruses?
Cells activate cytokine. Infected cells produce these, and it is meant to help surrounding cells
What are the general characteristics of bacteria?
Prokaryotic, microscopic
What are the three shapes of bacteria?
Round = cocci
Elongated – Bacilli
Spirochetes = wavy
What is the structure of bacteria?
Unicellular, cytoplasm, ribosomes, nucleoid, cell wall (rigid, for protection), pili / fimbriae, +/- flagella
What are the subdivisions of bacteria cell walls?
- Gram positive – thick peptidoglycan later (stains purple / blue)
- Gram negative – thinner peptidoglycan later (stains more red / pink)
What is the capsule of bacteria?
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.
What is the K antigen?
Located on capsule. Antigen host can develop antibodies to
What are Pili and what antigen to they contain?
Short hair like projections. Help bacteria adhere. Contain F antigen
What is the function of flagella and what antigen do they contain?
Mobility. Contain the H antigen
What are spores?
Help with survival (protective coat). Metabolically inert. If they find themselves in environment where they will die, they will produce spores; survival technique.
What are plasmids?
extrachromosomal DNA
What do plasmids encode for?
Drug resistance, virulence
How do bacteria function metabolically?
Most are independently metabolic. When conditions are appropriate, they can replicate outside of host cells (unlike viruses).
What is the mechanism of disease production for bacteria?
A. Adhere to host cell –> this is where capsid and villi help
B. Secrete toxin –> penetrated and spreads within host
C. Enter cell
What are the laboratory methods to evaluating bacteria?
Microscopic exam, growth in media and biochemical reactions, MALDI-TOF, antibiotic susceptibility tests
What is MALDI-TOF?
Matrix-assisted laser desorption/ionization time of flight. Sort of like spectrometry, compares to known bacterial spectrums and compares
What are the different antibiotic susceptibility tests?
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
How can bacteria be treated and controlled?
A. Antibiotics - - selected on basis of antibiotic sensitivity tests
B. Immunization
C. Good husbandry and hygiene
What are the general characteristics of fungi?
Eukaryotic, structure is filamentous (mold) or unicellular (yeast - unicellular), Dimorphic
What are the different types of hyphae filament of fungi cells?
Mycelium and spores
What are mycelium of fungi?
Mass of hyphae (mold)
What are fungi spores?
Airborne, from hyphae
What are the classifications of fungal infections?
Superficial or Deep Systemic Infections
What is an example of a superficial fungi infection?
Ringworm
What is an example of a Deep Systemic fungi infection?
Blastomycosis
What is mycotoxicosis?
Ingestion of fungi toxins (i.e., ergot)
What is the mechanism of infection of fungi?
A. Spores enter breaks in skin
B. Inhalation of spores
C. Opportunistic mycoses
What are the laboratory procedures to determine if there is a fungi infection?
Direct microscopic examination, culture
How can fungi be treated and controlled?
Fungicides - topical and systemic; Management – depends on situation. A lot that have superficial, put in dry / sunny environment and it can self-resolve.
What are the general characteristics of protozoa?
Eukaryotes, unicellular
What us the structure of protozoa?
They have a complex life cycle, and structure varies with age
What are the two main worldwide protozoan diseases?
Malaria, Trypanosomiasis
What are the main protozoan diseases in North America?
Coccidiosis, Cryptosporidiosis, Trichomoniasis
What is the mechanism of infection of Coccidiosis/Cryptosporidiosis?
Transmitted through fecal oral route
1. Feces – ground
2. Ingest oocyte
3. Invade intestine
What is the mechanism of infection of Trichomoniasis?
Breeding
How are protozoan infections determined in the laboratory?
Direct microscopic exam; PCR
How are Coccidiosis and Cryptosporidiosis treated and controlled?
Management (understand life cycle)
What is the treatment and control for Trichomoniasis?
Cull animals before breeding
What are prions?
Proteinaceous infectious particle; infectious proteins
What are different types of prion diseases?
Agents of TSEs (transmissible spongiform encephalopathy)
- BSE
- Chronic Wasting Disease
- Transmissible mink encephalopathy
- Scrapie
- Human TSEs: CJD, Kuru
How are prions classified?
- Host & disease
- Molecular & biological properties
- Amino acid sequence: host
What are the properties of prions?
normal cellular protein undergoes conformational changes to become pathogenic. Encoded in genome.
Why is the structure of prions important?
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).
Are prions resistant?
Prions are very resistant. Things that denature cell membranes / DNA, won’t affect prions. Requires UV & gamma radiation and environmental insults.
What is important in the infectious mechanism of prions (why are they so effective)?
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.
How are prions PrPsc replicated?
- Transmitted horizontally
- Catalyzes conversion of PrPc into PrPsc
- Template for abnormal folding & polymerization of PrPc
- Process cascades exponentially
What damage do prions cause to the host?
When PrPsc builds up, causes fibrillar masses (plaques). Leads to neuronal degeneration & neurological defects
What are the general considerations in controlling infection while raising livestock?
A. Intensive animal raising
B. Antibiotics
C. Disinfection
What does intensive animal raising entail to control infection?
Physical contact, contaminated feed/water, air movement
What is disinfection?
Destruction of pathogenic microorganisms on inanimate objects
What are the requirements for effective disinfection?
Systematic approach (Depopulate – AIAO, clean, remove equipment, wash – detergent, apply disinfectant, fumigate, dry/rest, restock)
What is detergent important for washing?
decreases surface tension to allow to start breaking down fats, proteins for washing
What are different types of physical disinfection that can be used?
Sunlight, hot air, moist heat, fire, sterilant, thermal death
What is moist heat?
Autoclave – steam w/ pressure
- 121 degrees C / 15 lbs. / 15 mins
- Sterilize surgical lab equipment
What is dry heat?
160 degrees C, 1 hr.
What is the difference for non-spore forming versus spore forming bacteria regarding physical disinfection?
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
What is the mechanism of action for disinfection?
- Denature cell wall –> basically punching bacteria holes and causes to lyse
- Alter microbe permeability
- Damage/destroy nucleic acid
- Damage/destroy proteins
What is a disinfectant?
Germicide with little irritant effect on tissue
What is disinfection?
destruction of pathogens on inanimate objects
What is sterility?
Complete absence of any form of life
What is an antiseptic?
Agent that eliminates infection on a living tissue
What is antisepsis?
Destruction of pathogens on surface of living tissue
What are the characteristics of an ideal chemical disinfectant?
- Broad spectrum
- Effective at low concentration
- Nontoxic
- Stable
- Minimal corrosiveness and caustic
What is boric acid?
Non irrirating, weak (not really effective)
What is lye (soda lye)?
Caustic, 2%. Essentially sodium hydroxide; dangerous, could burn skin
What is lime (calcium oxide)?
Used in pens, floors. Has drying effect on feet of animals
What is chlorine (sodium hypochlorite / Clorox)?
a. 1 to 50 ppm (5% bleach)
b. Inhibited by organic material
c. Corrosive, kills spores
What are phenolics?
- Toxic – protoplasmic poison
- Kills mycobacteria, not spores
- Uses – umbilicus infection, sterilize instruments
What are quaternary ammonium compounds?
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
What are the uses of quaternary ammonium compounds?
- Tissues (alcohol solutions)
- Sanitization (dairy)
What should quaternary ammonium compounds NOT used for ?
- Sterilization of surgical equipment
- Use with soaps
What are the different preparations of quaternary ammonium compounds?
- Benzalkonium chloride
- Benzethonium chloride
- Cetylpyridium chloride
What is Formaldehyde solution?
A. Bactericidal – excellent / reliable
B. Hazardous, carcinogen
C. 4% used for hoof infections
What are the advantages of formaldehyde solution as a disinfectant?
a. Powerful germicidal action
b. Action not decreased by organic material
c. Noncorrosive
What are the disadvantages of formaldehyde solution as a disinfectant?
a. Irritating gas
b. Skin damage
c. Carcinogen (cancer causing)
What are alcohols used for in disinfecting?
Solvent, antiseptic, disinfection
What is Ethyl alcohol (70%) / isopropyl alcohol?
- Medically, one of the best antiseptic / disinfectants
- Used in combination with other compounds (solubize fat, synergism)
What is the action of ethyl alcohol (70%)?
a. Denatures soluble proteins
b. Decreases surface tension
c. Local effect – brief irritation
What is iodine effective on?
- Kills spores in 15 mins
- Kills most bacteria in 1 min
What is iodine used as?
2% solution – scrubs, presurgical preparation
What are the limitations of iodine?
- Irritates tissues – delays healing
- Diffuses into cell, inhibits cell metabolism
What are iodophores?
- Surface-active agent combines with iodine
- Advantages of iodine without disadvantages
- Used in teat dips – mastitis control
What is Povidone – Iodine (Betadine)?
- Advantages of iodine without irritation, stain, toxicity
- Surgical scrub
What are the general things used for chemotherapy?
- Antiseptics – topical
- Sulfa drugs – 1935
- Antibiotics
What is an antibiotic?
Substance produced by a micro-organism …. that at a low concentration inhibits or kills another micro-organism
What is the mechanism of antibiotic action of penecillin?
Inhibit cell wall synthesis
What is the mechanism of antibiotic action of amphotericin B?
Alter cell membranes
What is the mechanism of antibiotic action of tetracyclines?
Inhibition of protein synthesis
What is the mechanism of antibiotic action of quinolone?
Inhibition of nucleic acid synthesis
What is the mechanism of antibiotic action of sulfonamides?
Antimetabolic activity
How do you test for bacterial resistance?
Antibiotic sensitivity (plate culture or plate dilution assay)
What are we trying to calculate in a plate dilution assay?
Minimum inhibitory concentration
How do bacteria become resistance to antibiotics non genetically?
- Absence of receptors
- Inadequate permeability
- Escape drug action
- Synthesize drug action
- Synthesize enzyme (inactivation)
How can bacteria acquire drug resistance?
Chromosomal or plasmid
How can drug resistance be transferable?
Transduction, conjugation, transposition, integrons
What is transduction?
Plasmid DNA incorporated and transferred by a bacteriophage
What is conjugation?
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.
What are transposons?
A DNA recombination reaction that results in translocation of a discrete DNA segment called a transposon
What are integrons?
Insertion of antimicrobial drug resistance cassette
What is bacterial transformation?
Bacteria take up foreign generic material (naked DNA) from the environment
What are the different resistance mechanisms of bacteria?
- Enzymatic degradation
- Target mutation
- Decreased cell wall permeability
- Active efflux
What is the definition of immunity?
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.
What are the two subcategories of the immune system?
Acquired and innate
What are the characteristics of the innate immune system?
Not antigen driven (nonspecific), immediate, natural
What are the innate defense mechanisms?
- Physical
- Chemical
- Phagocytosis
- Complement
- Interferon
In the innate immune defense, what are non-specific host mechanisms?
Invading organisms repelled at body surfaces by physical and chemical mechanisms
What are the physical barriers of the innate immune system?
Body surfaces (skin, respiratory / digestive / urinary tracts, eyes)
How does the skin act in the innate immune system?
- Mechanical barrier
- Resident bacterial flora
- Regulated by desquamation, desiccation, pH
How does the digestive tract act in the innate immune system?
- Mouth – saliva; flushing
- Low pH – gastric
- Lysozyme – antibacterial, antiviral
- Bile
- Pancreatic enzymes
Is the innate immune system specific or non-specific?
Non-specific
How does the urinary system act in the immune system?
- Low pH
- Flushing action
How does the udder act in the innate immune system?
- Flushing action
- Inhibitors in milk (lactenins)
a. Lactoferrin
b. Lysozyme
How does the respiratory tract act in the innate immune system?
- Filters – turbinates’, trachea, mucous
- Mucous
- Alveolar macrophages – phagocytosis
What are the mechanisms of blood bourn innate immunity?
Phagocytosis and complement cascade
What is the function of phagocytes?
Trapping and eliminating system for material that evades the outer defenses
What is the complement cascade?
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.
What is phagocytosis?
Trapping system acts through cells that bind, ingest, and destroy invaders through phagocytosis
What ate the categories of phagocytic cells?
Granulocytes, mononuclear, Natural killer cells
What are granulocytes and how do they act?
Neutrophil, eosinophils, basophils. Rapid, not sustained.
What is an example of a mononuclear phagocyte and how does it act?
Macrophage. Slow, sustained
What is a neutrophil?
Major function is phagocytosis. Rapid, not sustained
What is a macrophage?
Develops from monocyte. Delayed phagocytosis, sustained.
What are eosinophils?
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.
What are basophils?
Do not infest foreign cells. Produce substances that attract neutrophils and eosinophils to trouble spots.
What are natural killer cells?
Important in initial defense against viral infections. Produce cytokines that regulate some functions of T cells, B cells, and macrophages.
What are the steps of the process of phagocytosis?
- Chemotaxis and adherence of microbe to the phagocyte
- Ingestion of microbe by phagocyte
- Formation of a phagosome
- Fusion of the phagosome with a lysosome to form a phagolysosome
- Digestion of ingested microbe by enzymes
- Formation of residual body containing indigestible material
- Discharge of waste materials
What is the role of inflammation?
Role is to combat infection and tissue injury
How is inflammation triggered?
Triggered when innate immune cells detect infection or tissue injury
What are the signs of inflammation?
Redness, heat, swelling, pain, loss of function
What are the tissue macrophages in broken skin?
Histocytes
What are the tissue macrophages in muscles?
Histiocytes
What are the tissue macrophages in lymph nodes?
Reticular cells in LM, spleen, BM
What are the tissue macrophages in GI tract?
Kupffer cells in liver
What are the tissue macrophages in the lung?
Alveolar macrophages
How many proteins are in the enzyme cascade of the complement system?
> 30 proteins
What are the actions of the complement system?
- Mediated inflammation
- Controls bacterial infections
What are interferons?
Glycoproteins that control viral infections by signaling other cells to increase resistance to viruses. Not virus specific.
What sections is acquired immunity split into?
Active or passive immunity
What is acquired immunity?
Defense system which can distinguish, differentiate and remember different pathogenic invaders (viruses, bacteria, etc.)
What are characteristics of acquired immunity?
- Specificity: Can differentiate between foreign molecules (antigens)
- Diversity: Can recognize a variety of foreign molecules (antigens)
- Differentiates between self and non-self
- Remembers (memory)
What are the components of acquired immunity?
- Antibody-Mediated Immune System
- Cell-Mediated Immune System
- Lymphokine Production
What is the Antibody-Mediated Immune System?
Humoral immunity, antibodies/ Bcells (memory and plasma)
What does the Antibody-Mediated Immune System Protect the body from?
Viruses, some bacteria, toxins
What is the main cell of the Cell-Mediated Immune System?
Lymphocytes
What are the different types of lymphocytes in the Cell-Mediated Immune System?
- Helper T cells
- Cytotoxic T cells
- Memory T cells
- Regulatory T cells
What are lymphokines?
Cytokines that are released by lymphocytes. Important in stimulating immune response. Help coordinate humoral and cell mediated response.
What is an antigen?
Agents that stimulate production of antibody and bind specifically to that antibody or provoke immune cell function or is recognized by immune cell
What is an antibody?
Immunoglobulin formed in response to antigen
What do antibodies bind to?
High affinity binding to antigenic determinants = site on antigen to which antibody binds.
What is a key property of antibodies?
Specificity
What is the structure of antibodies?
Consists of 2 classes of polypeptide chains (heavy + light chains)
What is a domain of an antibody?
Functional regions of antibody
What are the 2 domains of an antibody?
- Binding domain – interacts with antigen
- Effector domain of processes
What is Immunoglobin M (IgM)?
First antibody following antigenic stimulation. Second highest concentration. Major Ig with initial immunization.
What is immunoglobulin D (IgD)?
Receptor (B cell receptor). Primates, rodents, cattle, sheep, and pigs.
What is Immunoglobulin G (IgG)?
Main serum antibody. Major role in antibody defenses. Smallest Ig.
What is Immunoglobulin E (IgE)?
In tissues / allergic reactions
What is immunoglobulin A (IgA)?
Dimeric – two molecules held together. Secretory component. Mucosa surfaces (lungs, intestines, skin, mammary gland)
What immunoglobulin is part of mucosal immunity?
IgA
What is plasticity of the immune system?
Ability to recognize the whole universe of potential determinants
What is the cellular strategy for plasticity is the selective theory?
Immune system generates many specific molecules and antigens are bound to the ones that fit
What is the primary response of the immune system?
First encounter of B cell with an antigen
What is the secondary response of the immune system?
Second encounter of B cell with same antigen leads to a more rapid and greater response
What is Immune system memory based on?
Based on long-lived “Memory B cells”
How do T lymphocytes become T cells?
Must bass through thymus
What is the T cell receptor?
Antigen binding site on surface of T cell
What does the T cell receptor react with?
React with antigens on the surface of other cells (APCs). Macrophages, dendritic cells
What do cytotoxic t cells (killer T cells) do?
Recognize other cells that display foreign antigens on their surfaces. Eliminated unwanted substances.
What is the function of Helper T cells?
Function is to recognize degradation products of antigens and secrete protein factors that stimulate other cells
What do lymphokines do?
Secreted factors that promote antibody production by B cells. Stimulate macrophages or CTLs, CMI
Where are macrophages found?
Found in all tissues. Circulate in blood (monocytes)
How do macrophages encounter foreign substances?
Generally, first cell to encounter foreign substance in the body. Nonspecifically engulf. Degrade.
What are the degradation products of macrophages?
Peptides bind to protein and surface expression
How do T cells recognize macrophage surface?
Displayed peptides
What are the two compartments of the immune system in the body?
Primary and secondary organs
What are the primary organs of the immune system in the body?
Bone marrow and thymus.
What are the secondary organs of the immune system in the body?
Peripheral lymphoid tissue. Tonsil (throat), lymph nodes (limbs), Peyer’s patches (intestines)
What is tolerance in the immune system?
Central concept of immunology. Immune system can differentiate between self and non-self.
What are the parts of innate (non-specific, native) immunity?
Phagocytosis, inflammation, complement, interferon
What are the parts of humoral immunity?
Antibody (IgG or IgM), B cells (plasma cells)
What is the component on cell-mediated immunity?
T lymphocytes
What is part of mucosal immunity?
Secretory IgA (secretory component)
What is the purpose of a vaccination?
Give antigen, mount immune response, develop resistance
What is the criteria to determine if vaccination is desirable / possible?
- Identify cause
- Protection
- Risks –> reaction and costs
What are the types of immunization procedures?
Passive immunization and active immunization
What is passive immunization?
Transfer of antibodies through administration (oral / parenteral) or by ingesting (colostrum)
What is the duration of passive immunization?
Limited, depends on amount of antibody
When is the onset of passive immunization?
Immediate
What are the important considerations regarding colostrum?
Neonatal calf losses (infectious enteric diseases or failure of passive antibody transfer).
When and how much colostrum should be consumed?
Two liters (5% body wt; 6-8 hrs; repeat in 12h)
When does absorption of colostrum decrease?
> 6 hours
What calf factors could cause failure of passive transfer from colostrum?
Ability to absorb decreases with age. Amount absorbed in 4-12 hours. Premature, cow not allowing to nurse, etc.
What maternal factors could cause failure of passive transfer from colostrum?
- Dams serum antibodies are concentrated in colostrum
- Diet. Protein deficient = no effect. Energy deficiency = decreased volume
What colostrum factors could cause failure of passive transfer from colostrum?
Normally 22% solids, compared to 12% in milk. Could have extra solid (Ig) or amount of Ig is variable.
What impacts colostrum quality?
- First milking
- Breed difference
- Exposure of cow
- Parity of cow
- Freeze
- Do not pool
When should commercial colostrum supplements be used?
Not a replacement or substitute for high quality colostrum. May be beneficial if all you have available is low-medium quality.
What is active immunization?
Development of immune response by the host in response to antigenic stimulation
What is the duration of active immunization?
Prolonged
What is the onset of active immunization?
Delayed
What is a vaccine?
Biological agent used to produce active immunity
What things does the ideal vaccine have?
Prolonged immunity, cheap, stable, safe
What are the different types of vaccines?
- Bacterin – inactivated bacteria or bacterial components
- Live bacterial suspension
- Toxoid – detoxified toxin
- Live virus vaccine – unmodified virus
- Modified live virus vaccine (MLV)
- Sub-unit vaccine
- Inactivated (Killed virus vaccines)
- Marker vaccine
What are the advantages of a live vaccine?
- Strong – long lasting immunity
- Interferon – possible
- Fewer doses
- Cheaper
What are the disadvantages of a live vaccine?
- Virulence risk
- May cause abortion
- May be immunosuppressive
- Contamination risk
- Stability
What are the advantages of an inactivated vaccine?
- Safe
- Stable
What are the disadvantages of an inactivate vaccine?
- Less immunogenic
- More frequent administration
- Not good inducers of CMI
- Require adjuvants for maximal response
What are adjuvants?
- Combine with vaccine
- Enhance immune response
- Not involved with specificity of response
What are the different routes of vaccine administration?
- Parenteral
- Intranasal
- Oral
- Aerosolization
How does the USDA determine vaccine efficacy?
Purity, Potency, Efficacy, Safety
What is serology?
Study of blood serum (antibody)
What is serology used for?
Indicator of infection / response to vaccination
What is a titer?
Level of specific antibody
