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
