FAMS final Flashcards
Purposes of new pig quarantine (3)
- prevent disease transmission from new pig -> resident pig
- allow for better observation of new pigs
- ID disease, behavioral issues, or nutritional issues in new pigs
NOT done to allow socialization b/w new and resident pigs across a fence
What pig needs to be quarantined?
Every NEW pig that enters farm, no matter where they come from and what their known health status is
What is a “vet-to-vet” call?
Calls between veterinarians of different production units to discuss health histories of respective herds
- allows for complete transparency
- farm A purchases from farm B herd -> farm A is able to call B and ask for serology results, vax records, what antimicrobials are being used in feed/water, etc.
purchase breeding stock from known source w/ known health statuses
How are most diseases transmitted between pigs?
via direct contact
others ways: vectors (rodents, birds), fomites, environmental
Describe the ideal quarantine area (4)
- Completely separate building from main population, at lease one mile apart
- surfaces are easy to disinfect (floors, walls, etc.)
- foot bath and hand-washing stations
- changing area for PPE (boots, coveralls, glvoes)
one mile is max. distance viral aerosol transmission / bird travel can r
You are performing a herd physical. In what order should you examine the herd?
- Healthy pigs
- Immunocompromised pigs (young, old)
- Sick pigs
- Quarantined pigs
also goes for feeding/watering/handling them
A pork producer is purchasing replacement animals from the same genetic supplier & health monitoring program as they have for the last 2 years. Because they trust their supplier, they omit from quarantining the new pigs. As the veterinarian, why do recommend against this? (4)
- Regardless of how much you trust your supplier, there is always the chance that an animal could have contracted a disease.
- Transport is stressful for animals, so even if they were healthy at the supplier, they could contract disease during this time.
- The incubation period varies so much for different disease agents, and even if your supplier says their animals are healthy, they could still be infected but not show any signs until they are in quarantine/are already in your herd.
- It is essential replacements stay in quarantine until test results & observation verify they are healthy!
Describe in between receiving a new animal and finally introducing them to the resident population.
-
Quarantine period: 30 days
- goal = if sick, incubation period ENDS while still in quarantine (I.P. can be ≥ 7 days, ≤ 14 days)
- test swine for specific diseases they may be bringing (PRRS, Coronavirus-TGE, PED, Influenza) -
Acclimatizaion period: 15-30 days
- animals are immunized, dewormed, etc. for diseases that are proven to be an issue in the resident herd
- expose to Sentinel Pig
Describe antibiotic protocol for quarantine pigs.
- Add ABX into water bowls as they are transitioning into new environment (intial 5-7 days of quarantine) as prophylaxis treatment
- If an animal becomes clinically ill, begin injectable ABX +/- anti-inflammatories
- Always keep records of antibotics used for withdrawal times!
What type of samples should be submitted for antibody tests in quarantined pigs?
Pooled samples - allows for efficient screening of a larger group of animals with fewer individual tests (cost- and time-effective)
What is a sentinel pig?
- used to monitor herd health of resident population
- new pigs in acclimation period are exposed to sentinel pig so that they can be exposed to common pathogens of the resident herd
- this pig should be YOUNG (older sows not preferred b/c she is most likely not shedding anymore)
When is mortality the highest in the swine industry?
Pre-weaning period (younger than 3 weeks old / less than 10-15 lbs.)
Perinatal conditions
- definition
- examples
- Perinatal Conditions: conditions that affect piglets within first 1-2 days of life
- congenital disorders (skin, CNS, urogenital)
- trauma (crushing from sow), hypoglycemia, hypothermia
skin: epitheliogenesis imperfecta, polydactyly, cleft palates
CNS: tremors, splayed legs, hydrocephalus
urogenital: atresia ani (no anal opening), intersex conditions
ID the abnormalities
Image A: epitheliogenesis imperfecta (absence of discrete areas of skin)
Image B: severe cleft palate (failure of tissues of palate to join together) - piglet aspirated every time they nursed
What management measures should be implemented prior to farrowing? (5)
- Completely clean & disinfect farrowing facilities
- Bathe sows prior to entry
- Make sure all farrowing equipment is in place (heaters, lamps, piglet processing tools)
-
Vaccinate all sows for transmissible diseases (diarrheal diseases Abs/IgG in colostrum)
- E. coli
- Clostridium C+D
and 5. Treat sows for parasites (fenbendazole)
What are the 3 main risks for piglets during perinatal period?
- Trauma (laid on by sow)
- Hypothermia
- Hypoglycemia/starvation
What piglet weight at birth is at an increased risk for death?
piglets born < 2.5-2.75# (they should be between 2.5-5#)
Stillbirths are more likley to occur in what litters?
Those from gilts and older sows
Farrowing Piglets vs Nursery Pigs vs Grower/Finisher
- Farrowing: birth to wean (0 days-3 weeks old; 2.5#-10/15#)
- Nursery: weaned (~ 3 weeks old, ~10-15#; stay until ~60#/2.5months old)
- Grower/Finisher: 60#/2.5 months old until market weight (280# / ~4.5 to 6 months old)
2-day-old piglets are suckling well but they are having yellow-whiteish, profuse secretory d+. They are huddling and have stained haircoats. Does not appear to be spreading between litters.
- diagnosis?
- treatment?
E. coli
TX:
1. rehydrate with e-lyte PO (put into bowls)
2. +/- SpectoGard (spectinomycin) PO 1-3d
E. coli d+ (Colibacillosis) usually is signaled by the appearance of diarrhea. Piglets from gilts may be more severely affected than piglets nursing sows. The severity of the diarrhea varies. The hypersecretory diarrhea usually has an alkaline pH but varies in color. It may be clear and watery, especially in neonates, but may be white or yellow, influenced by type of ingesta and duration of the disease. Sick pigs occasionally vomit but vomiting is not as prominent as with transmissible gastroenteritis (TGE).
As diarrhea continues, there is progressive dehydration and the hair coat becomes roughened. Body temperature often is subnormal. Shivering often is noted unless an adequate supplementary heat source, such as heat lamps, is available. Signs are similar in pigs of various ages but tend to be more severe in younger pigs. Death losses can be severe if husbandry and environmental conditions are poor. Diarrhea tends to persist until intervention is accomplished.
E. coli is one of the most common causes of neonatal septicemia and polyserositis. Often, strains associated with septicemia are not enteropathogenic.
Within 24h of birth, piglets are huddled, not suckling, and are having watery d+. They appeared healthy at birth.
On days 2-3, this appeared to spread to other litters. The piglets continued to have watery d+, and began v+. They were very dehydrated, hypothermic/huddled, with starvation apparent. Mortality rates started increasing.
- Diagnosis?
- What are the key signs with this infection?
- Coronavirus - TGE++ or PEDV
- profuse watery d+, v+, not suckling, severely dehydrated, cold, high mortality, signs began within 24h of birth
Highest mortality rates for piglet d+ are with TGE + PEDv
TGE: In acute outbreaks, the incubation period is very short, 18 hrs to three days. In baby pigs the disease spreads rapidly to affect all susceptible pigs. Signs include profuse diarrhea, frequent vomiting, rapid dehydration, shivering and marked thirst. The pigs weaken rapidly and usually die within one to two days. Pigs suckling immune dams may remain well as long as they receive adequate antibody in the dam’s colostrum and milk. Pigs infected after 4 weeks of age often survive.
PEDV: The main sign in all age groups is watery diarrhea. The disease closely resembles TGE but spreads more slowly than TGE on a site and among adjacent farms. Infected piglets up to one week old die from dehydration after three to four days. Mortality averages about 50% but usually is lower than that of TGE. Older piglets recover in about one week. In other outbreaks, weaned pigs and older animals are severely affected but younger animals may not sicken and have little or no diarrhea. The severity of disease is quite variable.
What ages do clinical signs from Clostridial diseases appear in piglets? Which is the most severe? How does d+ appear?
- 1-5 days old
- C. perfringens type C (CptC) - has necrotizing beta toxin that causes severe necrotizing enteritis
- CptC-infected piglets can be found dead within 4-8hrs post exposure and some die before even developing d+
- If d+ develops, is usually brown-red/hemorrhagic
CptC: Susceptible neonates can become ill in just a few hours after exposure to virulent CptC and may be found dead in as little as 4-8 hours. Sick piglets soon become weak, prostrate and then moribund. Weakened piglets are at high risk of being overlaid by the dam. Piglets with a little more resistance live a few days and may have a bloody diarrhea. Occasionally, piglets may live several weeks, develop a yellow or gray, mucoid diarrhea and remain unthrifty. In acute outbreaks, death can occur even prior to the piglet developing diarrhea. Morbidity is variable but mortality is high, up to l00%, in very susceptible litters.
10-day-old piglets have developed malabsorptive d+ (grayish color) with decline in body weight, but are still eating some. No deaths have occurred.
- diagnosis?
- how would you treat?
- Coccidiosis (Isospora suis)
- appears in piglets 7-11 days old
- TX: there is NO FDA-approved antiparasitic drug- use Amprolium + sanitize & avoid wooden farrowing crates (are difficult to clean/disinfect)
Amprolium: coccidiostat
What findings on diagnostics + necropsy of SI for Coccidiosis??
- fibronecrotic membrane in SI
- intestines are thickened; greenish-gray
- see coccidial parasires on cytology
4-day-old piglets have developed bright yellow d+ and are moderately dehydrated. Husbandry is good on the farm. All piglets recovered and survived. Likely diagnosis?
Rotavirus
Rotavirus: The onset and severity of signs depends on dose ingested and amount of protective antibody in the dam’s colostrum and milk. Outbreaks on specific premises often occur repeatedly when the piglets reach an age at which lactogenic immunity is no longer adequate to protect against the degree of exposure.
Diarrhea appears, usually white to yellow in color, and generally continues for a few days until the pigs develop an active immunity. There is moderate dehydration. Vomiting occurs but is not a major clinical sign. Morbidity is variable but mortality usually is low or none when good housing and husbandry is present. Signs, morbidity and mortality are enhanced if there is concurrent disease, poor husbandry or exposure to cold.
For all piglet diarrhea cases, what are the most important prevention & treatment measures?
- Adequate hygiene + biosecurity in farrowing house + farm
- Supportive care!: e-lytes, warm/dry environment, nutritional support, colostrum or milk replacer
When should piglets begin creep feeding?
~7 days of age
- Creep feeding = feeding a solid diet to piglets while they are suckling the sow, preparing their digestive system for weaning.
Other management tools for farrowing house (4)
- provide waterers at piglet level
- maintain + transition environmental temps (sows like 60-70ºF; piglets like 90-92ºF so keep mats warm)
- monitor for other diseases like exudative dermatitis
- observe normal behavior + locomotor activity (watch for swollen joints, skin lesions, kyphosis, lethargy, ears back)
Diagnose
umbilical hernia
Diagnose
inguinal hernia
Likely diagnosis
Septic arthritis/swollen joints (strep, staph, pyogenes)
How are farrowing piglets euthanized (3)? Which method should never be used?
- blunt-force trauma (AVMA approves for suckling piglets ONLY)
- non-penetrating captive bolt
- injectable barbituate (req. vet)
- NEVER electrocution!!- young pigs do not have enough body water content to carry electrical signals throughout body
When do swine form social hierarchy/pecking order?
Can develop as early as 1 week old (in farrowing) -> “ranks”/groups are already sorted out when they all get moved out together into nursery (3 weeks old) or wean–to-finish facilities
How to help minimize stress in nursery pigs? (4)
- Keep nursery HOT (insulated/rubber mats at 95ºF, air temp 83ºF)
- feed on mats for first few days
- Sort pigs according to size/hierarchy +/- sex
- Water medicators > in feed (sick pigs will stop eating before they stop drinking)
Nursery pigs are stressed b/c they are weaned/are without their moms
What are the most common diarrheal diseases in nursery pigs?
- E. coli (5-7 weeks old) +++
- Rotavirus (1-6 weeks old)
- Coronavirus
- Coccidiosis (usually farrowig piglets, 7-11 days old but can appear just before weaning)
- Salmonellosis
What age group are CNS disorders most commonly seen?
Nursery pigs (3-10 weeks old)
ataxia, staggering, down + paddling; seizures, convulsions
6 common CNS disorders in nursery pigs
1. Edema disease
2. Streptococcal Meningitis (S. suis II -> septicemia)
3. Na+ toxicity/water deprivation -> cerebral edema
4. Ascending paralysis from tail infection (why we cut tails short)
5. Otitis interna +/- aural hematomas (no tx b/c will reoccur)
6. Pseudorabies virus (Aujeszky’s Disease/herpes virus- incoordination, opisthotonos, death)
Top 4 agents causing polyserositis/arthritis in nursery pigs
- Strep. suis type 2
- Hemophilus parasuis
- Mycoplasma hyorhinis + hyosynoviae
- Erysipelas (Diamond Skin Disease- swollen, painful hocks, knees)
Nursery pig has acute signs of suppurative polyarthritis, and later developed signs of meningitis ( incoordination, tremors, paralysis, paddling, opisthotonus). Dx?
Streptococcus suis type 2
How does Atrophic Rhinitis cause disease in pigs?
Bordetella destroys nasal turbinates & then pasteurella invades & causes pneumonia
Common respiratory disorders of nursery pigs (6)
- Atrophic Rhinitis
- Porcine Repro & Resp Syndrome (PRRS)
- Porcine Circovirus-Associated Disease (PCVAD)
- Swine Influenza (SIV - H1N1, H1N2, H3N2)
- Salmonellosis
- Mycoplasma hyopneumoniae
all cause pneumonia
Common etiology + pathogenesis for Greasy Pig Disease in nursery pigs
Stress/overcrowding in facility leads to pigs attacking/biting each other (fighting wounds), esp on face, ears –> Staphylococcus hyicus invades –> brown exudative spots on head, axillae, back, groin
How is Greasy Pig disease usually treated?
Topically with dilute bleach (dunk)
How much feed to grower/finisher pigs consume daily? What is their market-ready weight?
- consume 6-10 lbs. of feed/daily (corn, soybean meal)
- 280# = market weight (can reach as early as 4.5 months, to 6 months old)
What respiratory diseases are most common in grower/finsher pigs? (7)
- PRRS
- PCVAD
- SIV
- Mycoplasma hypopneumoniae
- Pasterella multocida *
- Actinobacillus pleuropneumoniae *
- Ascaris sum * (large roundworm of pigs- verminous pneumonia)
*ones not also found in nursery pigs
Nursery Pigs:
1. Atrophic Rhinitis
2. Porcine Repro & Resp Syndrome (PRRS)
3. Porcine Circovirus-Associated Disease (PCVAD)
4. Swine Influenza (SIV - H1N1, H1N2, H3N2)
5. Salmonellosis
6. Mycoplasma hyopneumoniae
Difference in lung lesion distribution in Mycoplasma hyopneumoniae compared to Actinobacillus pleuropneumoniae
M. hyopneumoniae = cranioventral bronchopneumonia
Actinobacillus pleuropneumoniae = caudodorsal fibronecrotic pleuropneumonia
Which porcine resp. diseases cause interstitial pneumonia? (wet/plump lungs)
- SIV
- PRRS
- PCVAD
How do Ascaris suum cause resp. disease =?
Large roundworm of pigs: hepatotracheal migration
- (eggs ingested and L3 hatch/mature in SI, enter systemic circ. by penetrating SI wall -> larvae reach liver and enter hepatic portal system -> larvae reach lungs and cause verminous pneumonia -> larvae are coughed up and either exit host or are swallowed again and return to SI where they mature into adults)
How is roundworm treated compared to whipworms in pigs?
- Roundworm (Ascaris suum): ivermectin (feed or inj.)or pyrantel
- Whipworm (Trichuris suis): fenbendazole - cannot use ivermectin or pyrantel!!
Ascaris suum: hepatotracheal migration - respiratory parasite
Trichuris suis: L3-L4 in small intestine, mature in cecum
What are the most common causes of diarrhea in grower/finisher pigs? (5)
- Salmonellosis
- Swine Dysentery (Brachyspira hyodysenteriae)
- Proliferative Enteritis (Lawsonia intracellularis)
- PEDV
- Whipworm (if on pature)
Gastric ulcers in grower/finisher pigs
- Arise 2º to stress from anorexia + commonly occur when being fed too finely ground feed
- Ulcers appear in cranial GIT + see black tarry feces
- TX: gastroprotectants (NSAIDs are contraindicated w/ ulcers!)
- Goal = get back to eating!
Rectal prolapse in grower/finisher pigs
- Cold temperatures often cause b/c pigs will pile atop one another to keep warm, and the pig at the bottom is most likley to prolapse due to increased abdominal pressure
- Pigs with resp. dz / are coughing
- Keep affected pig isolated from others! (they will chew on the prolapsed tissue)
3-month-old pig dies suddenly overnight with no prior clinical signs. Found pale with bloated apppearance. Likely dx?
Hemorrhagic Bowel Sydrome
etiology unknown w/ peracute death
What is this pig most likely suffering from?
Dermatitis from blood-feeding mosquitoes or biting gnats
ID lesion
Immune-mediated sequel to Porcine Circovirus Associated Disease (PCVAD), called porcine dermatopathy and nephropathy syndrome (PDNS)
Occasionally, pigs may develop blotchy purple skin lesions and nephropathy, likely as an immune mediated sequel to viral infection, which is termed porcine dermatopathy and nephropathy syndrome (PDNS).
PDNS: Is mainly a condition of pigs from 8-18 weeks of age. There are red-purple blotches on the skin, sometimes slightly raised, most obvious on the hind legs and perineum but can extend over the abdomen eventually covering the whole body. Most pigs with PDNS eventually die.
ID lesion
Pityriasis rosea
- ventral abd, inner thighs
- circular, coalescing, raised, red lesions
- non-pruritic
- usually affects light-skin pigs
Pityriasis rosea is a dermatitis usually seen in four to twelve week old pigs and is characterized by 1- to 20-cm raised, reddened, ring-shaped lesions on the skin. Lesions first develop on the skin of the ventral abdomen but occasionally start in other areas. The cause is unknown. Papules first develop on the ventral abdomen and inner thighs. These early lesions expand to form circular, coalescing lesions with an expanding rim. Older lesions often have healed centers. Lesions heal in about four weeks without intervention. Pityriasis rosea is easily diagnosed by gross examination and does not require any treatment. The condition is not pruritic and seems to have no apparent effect on the health or growth rate of affected pigs.
How are mites treated in pigs
pyrethrin spray
ID
Erysipelas rhusiopathiae (Diamond Skin Disease)
Erysipelas is an infectious disease mostly of growing or adult swine. It may be clinically inapparent, may cause acute illness involving many animals, or be a chronic disease characterized by enlarged joints, lameness, and endocarditis. Rhomboid skin (diamond-skin) lesions are an inconsistent feature only associated with acute cases.
Why do grower/finisher pigs experience a lot of OA/lameness?
because they are fast-growing and mostly live on concrete
OA is also most common in pot-bellied pigs
Porcine Stress Syndrome
Genetic syndrome of york or landrace pigs, aka malignant hyperthermia or transport myopathy.
- triggered by stress or excitement, or by halothane
- tremors, muscle rigidity, inability to walk; resp. distress, hyperthermia, blotchy dermal hyperemia, acute right heart failure, death
make sure york or landrace animals are negative before breeding!
Pig has swollen joints + stiffness. Likely dx?
Erysipelas rhusiopathiae or Mycoplasma hyosynoviae infection
Important considerations when selecting breeding stock
- health status/history of breeding stock since its inception + that of any daughter herds that have been established from it
- breeding history + any evidence of infectious repro disease
- biosecurity measures of donor herd when new pigs or genetic material are brought into their herd
How is monitoring for reproductive failure in swine breeding operations different between sows vs. boars?
- What are the most important factors for the sow? The boar?
Sows are more difficult/time-consuming because evaluation of her entire repro cycle takes time (anestrus, estrus, periparturition, etc.)
- Anestrus
- Abortions, mummies, stillbirths
- Pregnant sows that fail to farrow
Boars are easier to work up b/c you just need to do semen evaluation, testes/penis assessment, assess feet/leg conformation (for mounting)
- failure to mate
- bleeding at mating
Hypocalcemia is a common periparturient disorder in sows. How would you treat it?
- CPMK subQ
or
- Calcium gluconate subQ in flank fold (glucose subQ sloughs skin//can cause abscesses!)
When + how do preg check sows?
- Preg check @ 28-30 days gestation
- Observe her behavior around a boar- she will be uninterested/actively avoid him, + be aggressive if he approaches her
Sow gestation: 3mo, 3wks, 3days = 115 days
What factors cause lameness in sows and boars? (2)
- Improper flooring (they need flooring that can wear their claws down like fiberglass grit or solid concrete; can injure themselves on slatted flooring)
- Improper conformation
Whilst conformation and stance of the sow will vary widely, the normal stance of the front limb is more upright (vertical) than the hind limbs. However, the latter is highly variable. As sows age the pasterns tend to drop, which alters the angle of contact of the foot with the floor. This may in part be associated with discomfort on certain floor types or simply the result of tendon stretching under load. The sloping of the hind limb may of course reduce wear, allowing overgrowth of the front of the claw, especially the outer claw. https://www.pig333.com/articles/overgrown-claws-and-foot-problems-in-sows_14592/
Why are sows prone to shoulder sores?
Sows in low BCS// have low body fat, so when they are lying laterally often in farrowing crate they develop pressure sores
Why are pigs’ hind legs more prone to lameness?
- hind legs bear more weight
- hind legs have a steeper angle => more prone
- larger outer claws of hind legs more prone to injury/overgrowth
How does heat stress impact breeding stock?
it decreases fertility (summertime!) -> to compensate, 30% more pigs are bred during this time of year in order to fill all available farrowing crates
What causes most vaginal & vulvar injuries in sows?
injuries in farrowing crate
Post-partum metritis in sows is most commonly caused by? How to treat?
repeated palpation/intervention during a dystocia - give Banamine and PenG
banamine: 1cc/100#
PenG: 4cc/100#
How is uterine prolapse in sows treated?
- euthansia most common
- amputate or try to replace uterus
Why are overgrown dewclaws in pigs of particular concern?
can get caught on things and rip off, allowing for 2º bacterial invasion from environment leading to osteomyelitis (poor prognosis)
How short should nails be trimmed in pigs?
2.5cm from the coronary band
Common health issues in boars (6)
- decreased libido
- overuse issues (collect sperm MWF to allow sperm to relocate to tail of epididymis)
- penile injuries/prolapsed penis (young/novel boars who jump on fence, etc.)
- Enlargement of preputial diverticulum
- Overgrown tusks
- Behavioral issues
Why can’t overgrown tusks be removed in boars?
They grow down to jaw- removal can break the jaw. Tx = trim/tipped w/ Gigli wire to just above the gumline
What is the most important parasite sheep/goat?
Haemonchus contortus
- abomasum
- L3 = infective stage
- Causes anemia, weight loss, bottle jaw
- Tx: ivermectin, albendazole, fenbendazole, levamisole
ALL GRAZING ANIMALS HAVE WORMS
Which SR species requires higher doses of anthelmintic drugs for treating H. contortus?
Goats- double the sheep dose (except levamisole 1.5x)
metabolize anthelmintics faster
When is Haemonchus contortus the most problematic?
SUMMER
- Warmth + humidity of summertime provides favorable environment for eggs in pasture to hatch/develop into L3 (min. 5-7 days) and migrate out of the feces (to then be ingested by host during grazing)
- See highest # of cases in LATE summer
L4 = hypobiotic stage (can arrest development in cold or very hot temps)
If H. contortus egg survives and develops into L3 during the winter, why will it die come early springtime?
B/c they will hatch but no hosts will be out grazing, + lack of humidity
What is Integrated Parasite Management in H. contortus prevention in small ruminants?
IPM = coordinated use of refugia + grazing practices + genetic slection to limit H. contortus resistance, ingestion, and infection rate.
- Refugia = targeted selective treatment: only some animals in herd are treated for nematodes in order to maintain genetic pool of susceptible nematode larvae on pasture to help dilute out resistant genes that survive treatment. Important management practice bc of widespread reisstance of nematode to anthelmintics.
- Rotate pastures
- Breed those who are resistant to infection/clinical disease
How is Duddingtonia flagrans a part of integrated control for Haemonchus contortus in SRs?
It is a naturally occurring fungus/”bioworm”that is added to their feed -> will completely pass in the feces and then the fungus will feed on the nematode larvae in pasture
How should you select anthelmintics for treating H. contortus?
- oral > injection (oral selcts for resistance more slowly)
- Use combo tx (2 or 3 drugs from different groups at same time- do not mix in syringe)
- Do NOT treat all animals routinely w/ combos- use selective deworming program like refugia
NONE have approved/established milk withdrawal times!!
True or false: coccidiostats (Decoquinate, Lasalocid, Monesin) are approved for lactating small ruminants.
FALSE
When/why do most dairy cows suffer from lameness?
Early stage of lactation (the first 100 days in milk)
- Cow BCS declines during this time b/c she is mobilizing large amt. of fat reserves in order to meet NRG demands of milk production
- The rapid physiological changes she undergoes during this transition period can put stress on her feet/joints, making her more susceptible to lameness conditions.
DIM 305 days
Dairy cattle BCS @ calving: 3/5
Beef cattle BCS @ calving: 6/9
Cattle Lameness Scoring
Describe the 5 lameness scores in cattle
1. Normal- flat back when standing & walking. Long, confident strides
2. Mildly lame- flat back when standing arched back when walking. Slightly abnormal gait.
3. Moderately lame- arched back when standing + walking. Short strides.
4. Lame- arched back when standing + walking. Favors certain legs.
5. Severely lame- constantly arched back. Great difficuly moving.
Lameness scoring can be used as a preventive measure for detecting prevalence EARLY so that those affected can be treated SOONER. Can also estimate lost profits within a herd and determine how effective current preventatives are (claw trims, occurrence of lameness scoring, foot baths, etc.).
How to hygiene score cows (1-4)
Score based on dirtiness above coronary band
Why is routine claw trimming in cattle important in preventing lameness?
- relieves pain caused by overgrown claw, which ultimately improves the cow’s wellbeing + direct positive effect on productivity
- decreases pressure on the sole which redirects weight to abaxial wall, allowing for lateral stability under load
Lateral stability: helps resist tendency of foot to slip
Load: the proportional distribution of weight on the solar surface of the claw.
Overloading: an increase in pressure on the dermis of the sole due to an abnormally thick or irregular sole horn. Overloading also occurs on the abaxial wall as the result of abnormally thick solar horn.
Overburdening: an obvious buildup of horn at the heel.
5-Point Dutch Method
After trimming excess, what should the angle between the hoof wall and the sole be at the hoof apex?
52º
What knot should you use to tie up the foot effectively in the chute when performing claw trims in cattle?
Clove Hitch (using quick release + Pulley system)
Fluid Therapy in Ruminants
What is in AAS mix?
AAS mix: calcium propionate (replenish Ca2+ & propionate) + alfalfa (provides
beneficial microbes that produce volatile FAs, plus protein)
Fluid Therapy in Ruminants
Describe fluid therapy tx for nervous ketosis in ruminants.
Require aggressive IVF w/ added dextrose
- 50% dextrose = 50g/100mL -> most come in 500mL bottles which = 250g/bottle
- dose per adult cow = 250mLs (1/2 a bottle)
supplementing glucose helps prevent KB production in liver
Nervous ketosis cows’ livers have decreased ability/capacity to perform normal gluconeogenesis and clear lactate. Supplementing glucose via dextrose helps prevent increasing gluconeogenesis demands onto the liver, helping prevent ketone body production
Ketosis state: When adipose tissue is mobilized (metabolic fuels low and/or energy demand is high- fasting, exercise, cold exposure), NEFAs are released and then stored as fat in the liver OR used to synthesize KETONE BODIES. Ketone bodies are produced in excess during excessive breakdown of fatty acids like NEFAs. This causes hyperketonemia (elevated levels of acetone, acetoacetic acid, and beta-hydroxybutyric acid in the blood).
Main clinical signs of Scrapie
intense body wasting; intense pruritus that leads to self mutilation
others: gait abnormalities; aggression toward people/obkects
How can Scrapie be diagnosed?
- Antemortem: biopsy of lymphoid tissue (3rd eyelid) w/ presence of PrPsc
- Postmortem: degenerative changes in CNS grey matter
What are 4 causes of polioencephalomalacia in small ruminants? How do these cause it?
PEM = the histiologic change in cerebral gray matter
- Thiamine deficiency
- Sulfur toxicosis
- Lead toxicosis
- Sodium toxicosis/water deprivation
All disrupt cerebral energy metabolism -> intracellular sodium & water accumulation -> edema, swelling, pressure necrosis of cerebral neurons
𝐏𝐨𝐥𝐢𝐨 means “gray”, and in this case, refers to the 𝐠𝐫𝐚𝐲 𝐦𝐚𝐭𝐭𝐞𝐫 of the brain. The gray matter is the outer layer of the brain, where all of the 𝐜𝐞𝐥𝐥 𝐛𝐨𝐝𝐢𝐞𝐬 (main processing center) of the neurons live. The center of the brain is the 𝐰𝐡𝐢𝐭𝐞 𝐦𝐚𝐭𝐭𝐞𝐫, which contains all of the 𝐚𝐱𝐨𝐧𝐬 (the main electrical conducting fibre of neurons).
𝐄𝐧𝐜𝐞𝐩𝐡𝐚𝐥𝐨 means brain. This is an important distinction to make, because there is also gray and white matter in the spinal cord. If this disease affected the spinal cord, we would use 𝐦𝐲𝐞𝐥𝐨.
𝐌𝐚𝐥𝐚𝐜𝐢𝐚 means necrosis, which is death of the tissue. So if you put it all together, polioencephalomalacia means death of the gray matter of the brain!
Thiamine:
1. where is it produced
2. function
3. clinical signs of deficiency in small ruminants
- In rumen by resident microorganisms
- A cofactor of the rate-limiting enzyme (transketolase) of the glycotic pathway that provides most ATP to the brain
- Signs are bilaterally symmetric: wandering aimlessly -> recumbent, central blindness, opisthotonos, tremors, nystagmus
small ruminant neuro diseases
Etiology of Listeria monocytogenes
- ubiquitous in environment of farm animals
- shed in feces, tears, nasal secretions, uterine fluid, and milk (zoonotic!)
- survives for months-years in soil, feces and contaminated feed
Pathophysiology of Listeriosis in small ruminants
Most common: enters CNS & induces formation of microabscesses, focal neuronal necrosis, and neurophagia
- leads to unilateral loss of function in cranial nerves & brainstem
- rapidly progresses and is 100% fatal w/out tx
- Unilateral loss of function in multiple cranial
nerves - Fever only in early stages
- Facial hypalgesia, dropped jaw, dysphagia– CN V
- Drooped lips, ears, nasal deviation, ptosis– CN VII
- Head tilt, circling, nystagmus– CN VIII
- Pharyngeal paresis, dysphagia– CN IX and X
- Unilateral tongue paresis and dysphagia– CN XII
Pathogenesis of the meningeal worm in small ruminants
Parelaphostrongylus tenius
- Sheep & goats dead-end hosts; larvae cannot complete their life cycle like normal within the spinal cord (which they can do in their normal host, the white-tailed deer)
- The larvae aberrantly migrate within the spinal cord, inciting inflammation
How do small ruminants contract the meningeal worm?
Parelaphostrongylus tenius
- ingestion of the intermediate host (snails or slugs)
- close contact with deer feces
Clinical signs of meningeal worm infection in small ruminants
Unilateral to bilateral hindlimb paresis and ataxia
SR Neuro
What finding on CSF is diagnostic for meningeal worm?
Eosinophilic pleocytosis w/ 7-97% eosinophils present
eosinophils: WBCs that respond to parasites, allergens, foreign bacteria
Ways to prevent bacterial meningitis from developing in neonates
- timely administration of colostrum = imperative
- when disbudding kids, hold NO LONGER than 5 seconds (3s -> cool -> 3s)! Their sinuses are not developed yet and PORTASOL cautery can fry their brains
Benign vs. Virulent Foot Rot in small ruminants
BOTH: 1º infection w/ D. nodosus
Virulent: 2º infection w/ F. necrophorum
Benign: inflammation + necrosis of interdigital tissue w/ underrun soft horn (sole)
Virulent: severe lameness, underrunning of hard horn beginning near heel; separation of hoof horn from underlying tissue; malodorous exudate, flystrike
Which clinical syndrome of CAE is most common?
Arthritis
- chronic, progressive arthritis in goats > 6 months old
- causes non-suppurative synovisitis of carpal joints
What are the predilection sites of Ovine Progressive Pneumonia? (OPP)
“Maedi-visna”
- Lungs (pneumonia)
- Udder (mastitis- hardbag)
How do animals become deficient in selenium and vitamin E?
- Fed poor-quality hay or straw; lack of access to pasture
- Forage with < 0.1 PPM
- If on pasture, live in areas where selenium concetrations are low
Necropsy findings of animal infected with White Muscle Disease
- friable muscles
- pale streaks corresponding with regions of degenration & mineralization
Pathogenesis of pregnancy toxemia in small ruminants
Body in negative energy balance
- mobilization of adipose tissue & transportation to liver to be converted into NEFAs for Kreb’s cycle to theoretically provide energy to produce glucose. However, since these animals are anorexic, they are not producing glucose precursor propionic acid, so the Kreb’s cycle cannot function properly -> NEFAs accumulate –> converted into ketone bodies or stored as fat (lipoproteins) in the liver -> liver becomes overwhelmed –> ketosis + fatty liver
ruminants ≠ efficient at transporting lipoproteins back out into adipose
Treatment of mild vs severe pregnancy toxemia in SRs
Mild
1. PO propylene glycol + insulin
2. calf oral e-lyte drench
Severe (in field)
1. Single IV 50% Dextrose injection +/- IV hypertonic bicarb 8.4% (if acidotic)
2. Plus above mild treatments
hospital: 2x maint. IVF w/ dextrose, and isotonic bicarb IV
Propylene glycol: can be fermented into propionate in the rumen or absorbed & metabolized into glucose in the liver
other supportive txs: appetitie stimulant, thiamine, antioxidants, anti-inflammatories (be careful b/c flunixin is nephrotoxic), transfaunation, high-energy feed/limit roughage intake
Pregnancy toxemia
What is the gestational age of the ewe vs. doe for safe parturition induction?
Ewe: 140th day
Doe: 143rd day
gestation = ~150 days
Severe/later stages of pregnancy toxemia; fetuses must be removed ASAP, w/ tx aimed at saving the life of the dam at the expense of the lambs or kids. Choose C-section mostly, but can induce if animal is NOT critically ill or the dam’s value does not warrant surgery.
Signalment + clinical signs of SR hypomagnesemia
- ewes 2-4 weeks post partum, esp. females w/ twins
- excitable, paddling convulsions; clonic-tonic muscle spasms; tachypnea
