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??
- Fibrinonecrotic membrane in SI -> greenish-gray d+
- intestines are thickened
- 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) .
Nowadays, wean-finish facilities becoming much more common. This helps decrease stress of pecking order b/c they are all together in their nurseries and then go grow together after.
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)
Salmonellosis: see d+, septicemia, pneumonia
Swine dysentery: mild & severe syndromes.
- Mild = mucoid d+ w/ flecks of blood. Not absorbing nutrients = NOT growing!
- Severe = profuse, bloody d+ w/ mucus, leading to death.
Proliferative Enteritis: chronic, mild d+ resulting in poor feed conversion (aka not growing!)
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
- 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.
- Mycoplasma hyosynoviae is common in swine herds and can be found in the nasal and pharyngeal secretions and lungs of healthy pigs. Stress or other predisposing factors can lead to systemic spread resulting in arthritis in pigs between the ages of 12-24 weeks with a morbidity of 1-50% within affected herds. The optimal sample to submit is joint fluid. Joint swabs or joint tissue such as synovium are also acceptable. Samples should be transported chilled on ice but not frozen.
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 in flank fold
or
- Calcium gluconate subQ in flank fold
calcium sloughs skin SC
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
Clinical signs of H. contortus
anemia, weight loss, bottle jaw; NEVER causes diarrhea!
Typical herd history for Haemonchus contortus
- Graze on pasture
- “Sudden death” in late summer, kids > adult goats
- Weak + not nursing prior to death
Why is “sudden death” when describing small ruminants who have died from Haemonchus contortus usually not actually true? Why are kids/lambs more affected than adults?
- the animals are usually anemic for awhile, but when they “suddenly die” it’s bc the anemia progressed for so long that it caused severe hypovolemia
- Kids/lambs have not developed immunity yet (usually occurs at sexual maturity)
H. contortus = blood-sucking abomasal nematode
If a SR dies, how can H. contortus infection be confirmed as cause of death? (3)
- Necropsy on dead animals & search ABOMASUM
- Perform FAMACHA on rest of herd (anemia)
- McMaster test- if summer/end of grazing season, can assume most eggs are H. contortus
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!!
Common HX for coccidiosis (Eimeria spp.) infection in small ruminants
- 1-6 months of age
- Stressful conditions: weaning, feed changes, transport
- Diarrhea
- Fecal staining-> dermatitis & alopecia develop if lasts ≥ 2 weeks
Severe: anorexia, dehydration, weakness, weight loss, death
How is coccidia diagnosed in SRs?
Clinical diagnosis (presence of d+)
Not all species of Eimeria are pathogenic, so presence of oocysts on fecal float is not clinically significant as healthy animals often shed small numbers of oocysts.
Treatment for coccidiosis/Eimeria in affected SRs?
Extra-label use of FDA-approved drugs:
1. Amprolium (Corid)
2. Sulfa ABXs
3. Triazine Antiprotozoals (Ponazuril, Diclazuril)
1, 2 and 3 can kill coccidial organism in asexual stage (clinical dz is from destruction of SI epithelium in asexual repro phase)
True or false: Toltrazuril (Baycox) can be used in SRs to treat coccidia.
FALSE
- It is NOT FDA-approved for use in ANY species in the U.S., so extra-label use is illegal
- The only Triazine antiprotozoals that can be used in the U.S. extra-label for coccidia = Ponazuril (Marquis) and Diclazuril (Vecoxan)
What is the Food Animal Residue Avoidance Databank’s (FARAD) suggested withdrawal time for Ponazuril?
120 days for 1 dose
Ponazuril = triazine antiprotozoal, off-label tx for Eimeria in SRs
Coccidiosis prevention in SRs
- Keep environment dry, improve sanitation
- Prevent overcrowding (decr. stress and buildup of manure)
- Ensure proper nutrition an dcolostrum intake
- Coccidiostats (feed additive- slow down shedding but take 21 days to be effective so give in advance ot risk periods)
True or false: coccidiostats (Decoquinate, Lasalocid, Monesin) are approved for lactating small ruminants.
FALSE
What are the deterimental effects of lameness in the cattle industry?
#2 cause of low productivity on herd level
- makes her less competitive for resources like food and water -> weight loss, decr. milk production
- ≤2,000 lbs. of milk lost
- prevents her ability to ride other cows during estrus, reducing bull’s ability to detect heat = increased calving -conception intervals
- In feedlots, 70% of revenue is lost to lameness (20-30% of cattle suffer from severe lameness in feedlots. Methods of fattening steers increases laminitis incidences; transport stress increases toe abscesses in yearling steers; feedlots have higher incidences of traummatic injuries in general)
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
When do most feedlot cattle suffer from lameness?
During the first 60 days post arrival
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.).
What are the overall success factors for managing lameness? (4)
1. Early detection (via lameness scoring) + early tx
2. Low opportunities for infection to occur (biosecurity, hygiene, health status of new cattle, management, etc.)
3. Low forces on feet (comfort, flooring, handling, overcrowding)
4. Good horn quality & shape (trims, nutrition
How to hygiene score cows (1-4)
Score based on dirtiness above coronary band
What is the goal Hygiene Score in cows? Why?
< 25% of herd should be grades 3 & 4 (>75% should be 1 or 2
- higher hygiene score, higher chance for DD and FR
wet/damp/anaerobic conditions -> skin maceration –> DD, FR
How many hours/day should cows spend at the milk parlor?
< 3.5 hours per day (includes time it takes to walk there, get set up, and walk back)
- Time management?
◦ Resting - 12-14 hours/day
◦ Eating - 3-5 hours/day
◦ Milking - < 3.5 hours/day (includes time taken out from pen, walked to dairy & back)
◦ Social - 2-3 hours/day
◦ Drinking - 0.5 hours/day
Cattle Lameness
What are the “bricks and mortar” of hoof keratin formation?
Zinc + biotin
Cattle Lameness
Function of the digital cushion in cattle feet? How does lactation cycle influence its thickness?
Digital Cushion: tissue filled with soft fat that acts as a shock absorber. Thickness decreases as BCS decreases (so thickness is lowest during early lactation)
What are the lameness benchmarks in cattle
- 15-25% of herd should have clinical lameness (LS 3, 4 and 5)
- 75-85% of herd should be LS 1 & 2
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.
What is the priority in functional claw trimming in cattle?
Unload the weight-bearing (affected) claw and transfer weight to the non weight-bearing (normal) claw
- remember: the overloaded claw cannot be relieved if the other claw is not stable under load, longitudinally & latitudinally
- TL: medial claw = weight bearer
- PL: lateral claw = weight bearer
re-establishing balanced weight bearing => lat. stability
Describe the 5-Point Dutch Method
FUNCTIONAL TRIMMING (ROUTINE/ALL CATTLE):
1. Measure and trim claw
2. Match trim with the opposite claw (equalize lengths + levels)
3. Dish out/model sole ulcer site (transfers weight from sole center out to wall/toe/heel)
CORRECTIVE/THERAPEUTIC TRIMMING (AFFECTED CATTLE):
4. Relieve weight from affected claw (trim down; place block on healthy claw)
5. Remove any loose horn (manure/dirt etc. can get lodged b/w loose horn & hoof wall, exacerbating problem)
5-Point Dutch Method
How do you decide how much to trim off claws?
Based on amt. of excess hoof present:
- coronary band to hoof apex: 7-7.5cm
- trim any excess from front of toe and down longitudinally, and trim the sole but SPARE 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
5-Point Dutch Method
When trimming the unaffected claw to transfer load over from the overburdened claw, why is it imperative to never trim at the heel?
Example: hind limbs
- the medial claw needs to be able to carry an appropriate share of the load to relieve load off the overburdened lateral claw.
- the medial claw therefore must be left “high” and stable enough to act as a supporting structure
5-Point Dutch Method
Which claw should you dish out more in the hind claws: medial or lateral claw?
The lateral claw (weight-bearing/affected claw)- need to take weight off the sole ulcer site (where pinching occurs and sole ulcers develop)
dishing purpose in medial claw = reduce amt. of material trapped in interdigital space
5-Point Dutch Method
What entails step 4 in the Dutch method?
Trimming down weight-bearing/affected claw even more and then placing a block on healthy claw
- block gives height & prevents weight on affected claw; stays on for at least 21 days
- block must be aligned with the level of the heel AND orientation of the hoof
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)
Ruminant Fluid Therapy
What are available basic field diagnostic tools when determining fluid/acid-base/e-lyte imbalances? (7)
- Ketostix - acetoacetate in urine
- Dipstick - urine blucose, bilirubin, acetoacetate, pH, protein, blood
- Azostix - BUN
- Glucometer
- Ketometer - beta hydroxybutyrate (BHB) in blood
- pH papter - ruminal fluid, urine
- U/S w/ rectal probe
Ruminant Fluid Therapy
Ruminant shock: causes + CS
Causes of shock:
- acute hemorrhage
- septicemia
- acute endotoxemia (LPS)
Clinical Signs of Shock
- tachycardia, tachypnea, pale mm, increased CRT, weakness, profound depression
Ruminant Fluid Therapy
What is the volume of the rumen in adulate cattle?
50 gallons (more in larger cattle/bulls)
Ruminant Fluid Therapy
Describe the upper eyelid skin tent duration in…
- Mild (6-7%)
- Moderate (8-9%)
- Severe (10-12%)
dehydration in adult ruminants
Mild: 2-3s
Moderate: 3-6s
Severe: indefinite
Bulls & bos indicus breeds always eyelid tent > neck or rear quarter
Ruminant Fluid Therapy
In dehydrated ruminants, what 3 electrolytes are deficient and need to be replenished?
sodium, potassium, and chloride
Ruminant Fluid Therapy
Electrolyte abnormalities in acute grain overload (rumen acidosis)
hypocalcemia, hyperkalemia
acidic rumen tries to compensate by shfiting K+ into bloodstream
metabolic status defined by decreased blood pH and bicarbonate, caused by overproduction of ruminal D-lactate. It will appear when animals ingest excessive amount of nonstructural carbohydrates with low neutral detergent fiber. d-lactate is a metabolite originating from bacterial metabolism that accumulates as a result of dietary disturbances in cattle, leading to ruminal acidosis.
Ruminant Fluid Therapy
Metabolic acidosis vs alkalosis
Metabolic Acidosis: acidic blood pH due to ↑ [H+] and ↓ [HCO3-]
- SI strangulation, intussusception, enteritis/d+ (calves), choke (salivary loss of bicarb)
Metabolic Alkalosis: alkalotic blood pH due ↑ [HCO3-] and ↓[H+]
- abomasal/cecal displacement/volvulus, vagal indigestion, DEHYDRATED, MATURE CATTLE
PCO2 = acidic -> compensatory responses (tachy- vs bradypnea)
alkalosis: gut stops working/ileus present -> hypochloremia (bc sequestered in GIT)
Ruminant Fluid Therapy
IVC size for short-term vs. long-term use
Short-term: 2”, 14G
Long-term: 5.25”, 14G
Ruminant Fluid Therapy
What are extra steps you need to take when placing long-term IVCs in ruminants?
- Suture in + cap it
- Provide O w/ heparinized saline flush
Ruminant Fluid Therapy
Why does every med given IV need to ALSO be given PO in ruminants?
IV absorption = rapid (for quick relief), but need that SLOW RUMINAL ABSORPTION from enteral administration. Also, some minerals are much more effective when given PO (Mg2+. K+, P)
How does osmolality relate to rehydrating ruminants?
Dehydrated ruminants are hypoosmotic. They need supplemented e-lytes to increase plasma osmolality in order to drive free water absorption from the rumen into the blood plasma.
Osmolality = relative to [solute]. Water flows from low -> high [solute]
When supplementing electrolytes to the dehydrated ruminant, how much (general) should you provide?
- Physiologcal levels of Na+ and Cl-
- Elevated levels of K+ (only source is from diet and these animals are anorexic, + is constantly excreted in urine)
Almost all dehydrated ADULT ruminants are __1. ?__, so fluids need to be __2. ?__
- alkalotic
- non-alkalinizing (hypertonic saline (7.2%), or water + NaCl, KCl, CaCl2)
Since most dehydrated cattle have a metabolic alkalosis, it is important to use a non-alkalinizing oral electrolyte solution that does not contain bicarbonate, acetate, or propionate. We generally don’t attempt to correct an alkalosis by administering acid, instead our goal is to provide extracellular anions in relative excess to cations.6 In practice, this is accomplished with chloride-rich, high potassium solutions. By simply adding NaCl (7 grams/L), KCl (1.25 grams/L) and CaCl2 (0.5 grams/L) to a liter of water (or 140 grams NaCl, 25 grams KCl, and 10 grams CaCl2 in 20 liters or roughly 5 gallons of water), a non-alkalinizing oral electrolyte solution for adult ruminants can be created that will effectively rehydrate animals without alkalinizing the blood pH. Most of the commercial oral electrolyte solutions made for cattle are designed for dehydrated calves which typically have a metabolic acidosis. The majority of these products contain bicarbonate and are not indicated for use in adult ruminants.
When rehydrating ruminants, why is it imperative to ALWAYS give PO drenches as well?
She will eventually dehydrate again PLUS her rumen will be dried out if only getting IV. Need to give PO water drench or non-alk. oral e-lyte fluids.
Fluid Therapy in Ruminants
Describe fluid therapy for 1. Mild vs. 2. Moderate vs. 3. Severe dehydration in adult cattle
- Mild: Drench- AAS (nutritional) in 10 gallons of water PO
- Moderate: IV HTS + drench- AAS in 10 gallons of water PO
- Severe: IV HTS + drench KCl in 10 gallons of water PO (KCl > AAS b/c this cow is down and so is at risk of aspiration w/ a nutritional drench)
Fluid Therapy in Ruminants
What is in AAS mix?
AAS mix: calcium propionate (replenish Ca2+ & propionate for energy ) + 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).
Fluid Therapy in Ruminants
Describe fluid therapy tx for persistent ketosis/hepatic lipidosis in ruminants.
- IV dextrose (250mLs) q12h for 2 days, + Vit B supplementation (good for anorexic cows)
- Drench either propylene glycol or AAS mix for 5 days
Propylene glycol: can be fermented into propionate in the rumen or absorbed & metabolized into glucose in the liver
50% Dextrose dose per adult cow = 250mls (1/2 a bottle)
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).
Fluid Therapy in Ruminants
Describe fluid therapy tx for the hypocalcemic cow.
-
Calcium gluconate 23% IV
- for the post-partum, housed dairy cow who develops hypoca2+ within the first 24-48h -
CMPK (Cal-Dex) IV - can ONLY go IV!
- for the 2nd tx of 1.
- periparturient recumbency in field (for any cow)
- suspected grass or winter tetany
- recumbent bovine w/ severe endotoxemia or septicemia (e.g., mastitis or peritonitis)
CMPK is usually a dextrose-based solution ➡️ glucose SQ is irritating/will cause skin to slough
Fluid Therapy in Ruminants
What is the most important thing about giving IV calcium?
Give SLOWLY!!!! 500 mL (one bottle) over >5 minutes!!
- giving too quickly can lead to bradycardia-induced death!
Fluid Therapy in Ruminants
How does fluid therapy differ when treating rumen acidosis?
Fluids need to be non-acidifying - IV sodium bicarbonate
- DIY supplemented sodium bicarb (severe acidemia- blood ph < 7.20) : 3/4c baking soda in 1 gallon distilled water IV, then switch to 3Tb BS in 1 gallon distilled water IV (5% bicarb solution -> 1.3% bicarb solution)
Fluid Therapy in Ruminants
Dehydrated Adult Ruminant fluid calculation formulas (Guynn) :
1. Dehydration
2. Maintenance
3. CRI shock dose
- Dehydration = % dehydrated x BWkg
- Maintenance = 50ml/kg/24h
- CRI shock dose = 90ml/kg/hr
In the real world, the shock dose is impossible for bovine (e.g., 45L/hr for a 500kg cow) -> just give the fluids as fast as you can
What is the maintenance fluid rate for…
- Adult beef, small ruminant and non-lactating dairy cow
- A neonatal ruminant
- Adult beef, small ruminant and non-lactating dairy cow - 50 ml/kg/day
- A neonatal ruminant - 80 ml/kg/day
- A lactating dairy cow OR an adult bovine or small ruminant in a very warm environment - 70ml/kg/day is more appropriate
- A small ruminant until ~2 months of age or a bovine until 6-7 months of age could benefit from 80/ml/kg/day
Fluid Therapy in Ruminants
In reality, why is it impossible to meet the calculated replacement fluid volume in adult cattle?
e.g., for 500kg cow, her total replacement = 17 gallons (65L) - NO ONE carries anywhere near this amt. of HTS for IV administration- this is why we drench w/ isotonic fluids
Fluid Therapy in Ruminants
What are important considerations in small ruminant fluid therapy?
- significantly smaller ruminal capacity (5 gallons), so need to use SLOWER FLUID RATES to prevent inducing pleural effusion!
- administer CRIs for no longer than 1 hour at a time
- never do long-term CRIs (animal will chew fluid line/get twisted in it)
- if long-term IVC in place, the SR must be isolated (herdmates will chew out IVC)
Fluid Therapy in Ruminants
What are important considerations in fluid therapy for calves? (4)
- underdeveloped rumen, so drenching is very difficult
- their metabolic/e-lyte imbalances are typically more severe, so can’t treat them in a “drive-by” situation like you can with adults
- must consider body temp!! if < 99ºF, they will NOT absorb any PO fluids b/c gut not working
- Always heat fluid bags prior to giving, no matter their body temperature
Calf has upper eyelid skin tent of >4 seconds and her extremities are cold. What is her estimated dehydration status?
Severe ( >10% dehydrated)
Pathogenesis of Scrapie in small ruminants
- PrPsc (prion) shed from placental & fetal fluids @ lambing/calving -> neonates ingest
- PrPsc has incubation period of 2-5 years -> clinical signs arise from PrPsc invading CNS
- Causes non-inflammatory, vacuole (spongiform) degeneration of gray matter
- FATAL, progressive neurodegenerative disease
Signs arise in young sheep (2-5 years old)- less common in goats
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
How is Scrapie treated + prevented?
- TX = culling
- Prevention = selective breeding for resistant genes:
- codon 171 (Q, R) -> RR 100% resistant, QR rarely susceptible, QQ highly susceptible with no clinical signs
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
What are the common cause of thiamine deficiency in small ruminants (3)?
Ruminal acidosis
1. Lambs & kids being fed low roughage, high concentrate
2. SRs being treated for coccidiosis with amprolium (a thiaminase)
3. Plant-derived thiaminases (bracken fern, horsetail, nardoo fern, pigweed
How is thiamine deficiency diagnosed + treated?
- Dx = clinical signs, signalment, history, rapid response to tx
- TX = immediate thiamine replacement (10mg/kg IV, SC or IM
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
In small ruminants, how is Listeria infection most commonly sourced?
Feeding improperly fermented silage w/ pH of > 5.5
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
Common etiologies of bacterial meningitis in small ruminants
- Bacteremia associated w/ pneumonia, omphalophlebitis, mastitis, endocarditis, or other septic processes
- Hematogenous infection in neonatal septicemia from FPT (E. coli, salmonella, pasteurella)
CSF findings in SR bacterial meningitis
- marked increases in protein concentration, total leukocyte count, proportion of neutrophils
- CSF glucose lower than serum
Treatment for SR bacterial meningitis
- Case fatality rate is HIGH (due to late recognition)
- Aggressive + prolonged IV ABX (ceftiofur)
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
4 main causes of lameness in small ruminants
- Foot Rot
- Caprine Arthritis Encephalitis
- Ovine Progressive Pneumonia
- White Muscle Disease (Nutritional Muscular Dystrophy)
Causative agent in small ruminant foot rot
Dichelobacter nodosus
- opportunisitc bacterial pathogen that is a part of the normal flora of ruminant GIT
- requires breach in foot skin from wet conditions that lead to maceration of tissue
- Invades subQ interdigital tissues/dermis
Bovine: Fusobacterium necrophorum
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
How is foot rot treated in small ruminant herds in the U.S.?
Treatment initiated within 3 days of lameness occurring can reduce to only 2% of herd!
Trims + inj. ABX + local therapy:
- proper hoof trimming
- footbath containing zinc
- injectable antibiotics (oxytet, nuflor, zactran; all off-label)
- topical treatments (powder tetracycline; zinc sulfate)
How long should new animals be quarantined in small ruminant herds in order to prevent foot rot?
30-60 days
Pathogenesis of CAE
A retro/lentivirus in goats that causes lifelong infection by infecting monocytes and macrophages. Target tissues include joints, mammary glands, lungs, and brain, inducing chronic inflammation via invoking host I.R.
Which clinical syndrome of CAE is most common?
Arthritis
- chronic, progressive arthritis in goats > 6 months old
- causes non-suppurative synovisitis of carpal joints
How is CAE spread?
via transmission of fluids w/ infected MØs
- colostrum ingestion +++
- close contact w/ infected goats
- improper disinfection of milking equipment
What clinical syndrome of CAE do caprine kids get?
Leukoencephalomyelitis
- 1-5 months old
- short, choppy gait
- unilateral-bilateral paresis and ataxia
How is CAE treated/prevented?
- TX = test + cull
- Prevention: if herd is known positive, separate kids from does at birth and administer heat-treated or pastuerized colostrum. Test herd q6 months b/c time to seroconversion varies greatly (years)
How is CAE diagnosed post mortem?
nonsuppurative demyelinating encephalomyelitis and lymphocytic infiltration of any target tissue (joints, mammary glands, lungs, brain)
What are the predilection sites of Ovine Progressive Pneumonia? (OPP)
“Maedi-visna”
- Lungs (pneumonia)
- Udder (mastitis- hardbag)
What age group is OPP seen in?
Older animals due to long incubation period (adult sheep > 2 years old)
Pathogenesis of White Muscle Disease
Deficiencies in selenium and/or Vitamin E, affecting skeletal & cardiac muscle of young, rapidly growing animals (2-4 months of age).
- Selenium & VitE are antioxidants -> deficiency allows for free radicals to increase and therefore cause oxidative damage to muscles
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
What are the two syndromes of White Muscle Disease?
- Cardiac - acute to peracute C.S. of recumbency, resp. distress, frothy nasal discharge from P.E., tachycardia
- Skeletal - subacute/more common. C.S. of stiff gait, tremble when standing, weak, unable to nurse
Necropsy findings of animal infected with White Muscle Disease
- friable muscles
- pale streaks corresponding with regions of degenration & mineralization
How is White Muscle Disease treated & prevented?
Tx: Vit E/Selenium single injection +/- repeat in 24h
Prevention: supplement diet w/ selenium & vitE to susceptible animals. Inject dam 30 days prior to lambing w/ selenium/vitE.
- if dam is deficient, her lambs will be born deficient!
When does pregnancy toxemia occur in ewes and does/under what conditions? (3)
- the last month of gestation
- thin or obese; pregnant w/ single large fetus, twins, or triplets
- in association w/ anorexia caused by other diseases or sudden stresses
gestation = ~150 days (21 weeks)
During late gestation,
- in most mgmt. systems, late gestation occur during winter months when less pasture available + poorer quality feedstuffs are offered
- 70-80% of fetal growth occurs during this time
- obese ewes/does: abdominal space filled w/ accumulated fat + ever-expanding uterues -> difficult to consume enough feedstuff to meet energy requirements (decr. rumen capacity)
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
Pregnancy Toxemia
What is a sequela to increased NEFAs in the blood?
Insulin resistance
- cells stop responding to insulin -> lipolysis of triglycerides into NEFAs in adipose tissue continues b/c no signal from insulin to adipose tissue to suppress lipolysis
Clinical signs of pregnancy toxemia in SRs
depressed, anorexic; “star-gazing”, blindness, circling
Small Ruminants
Obesity-related pregnancy toxemia tends to be a(n) __?__ problem, while starvation-related pregnancy toxemia tends to be a(n) __?__ problem.
Obesity-related pregnancy toxemia tends to be a(n) __individual animal__ problem, while starvation-related pregnancy toxemia tends to be a(n) __herd-wide__ problem.
Obesity: Show/pet animals
- BCS ≥4/5 at GREATEST risk
- decr. capacity for rumen to take in feed -> hepatic lipidosis, hypoglycemia, ketosis
Starvation: producers not feeding enough during pregnancy, or she is pregnant while underconditioned.
- singleton but LARGE
- twins
- geriatric
- concurrent pneumonia, foot rot, parasitism, CWD, etc.
- occurs within 1-3 weeks of parturition
- Hypoglycemia & hypocalcemia = 1º metabolic ocnerns
- cause of maternal death losses
What are the primary metabolic issues in starvation pregnancy toxemia in ewes/does?
- Hypocalcemia - 20% of pregnancy toxemia animals
- Hypoglycemia
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.
When does peri-parturient hypocalcemia occur in ewes & does?
Shortly before or after parturition
- greatest calcium demand in non-dairy animals = 3-4 weeks pre-partum (fetal skeleton mineralization)
- high-producing dairy goats’ usually post partum
Why are older ewes/does more susceptible to hypocalcemia?
reduced ability to absorb & mobilized stored calcium
Small ruminants
Clinical signs of hypocalcemia
can overlap those of pregnancy toxemia
- ataxic
- hyperactive -> recumbent (lack of membrane stabilization from calcium -> lack of ACh at NMJ to influence muscle contractility).
Hypocalcemia tx in SRs
1. Uncomplicated
2. Complicated (preg. tox present)
- Uncomplicated: IV calcium gluconate 23% over > 5mins, followed by SC or PO calciumm for prolonged absorption
- Complicated: avoid IV calcium, as solutions are fatal in animals w/ impaired liver function. Manage clinical signs + precaution for sequela dystoica, uterine prolapse
Small Ruminants
Hypomagnesemia can develop either from decreased intake or from reduced absorption in the GIT. What are the specific causes of each?
Decreased Mg intake: grazing lush, rapidly growing pasture w/ decreased Mg content (spring/autmn)
Reduced Mg absorption:
- increased potassium (from alfalfa hay/haylage, fertilizers)
- reduced sodium content + increased milk yield
Signalment + clinical signs of SR hypomagnesemia
- ewes 2-4 weeks post partum, esp. females w/ twins
- excitable, paddling convulsions; clonic-tonic muscle spasms; tachypnea
Treatment of hypomagnesemia
IMMEDIATE MgCl administration + CPMK IV
- death can occur eithin hours of onset of neurological signs
- recovery is quick, but relapses may occur -> additional SC or PO administration 12-24h later recommended
