Food Ani. Med- Bovine - Musculoskeletal Disorders - 4

drraythe's version from 2018-01-20 19:48

Nutritional Myodegeneration (white mm dz)

Question Answer
white mm dz is caused by a dietary deficiency in what?Vit E/ selenium
what is the pathological mechanism behind white mm dz?Not enough Vit E/selenium--> oxidative damage to striated muscle because of a Reduction of Glutathione Peroxidase activity.
the most severely affected areas of WMD are?Myocardium & Large muscle groups. (also see Abortion, Infertility, retained placenta, & stillborn or weak neonates.)
what is good to know about distribution of selenium deficiency?depends on if soil has enough, so is regional (blue is deficient areas)
where do adults usually get vit E? neonateS?Pasture forage is typically adequate. Neonates get Vit. E from dam while nursing.
what should you know about storing vitamin E? Vit. E oxidizes with storage
which types of food require greater fortification with vit E? Processed feeds & feeds that are high in fats / oils require greater fortification
what age is often affected by WMD? Most commonly affects rapidly growing animals.
CSs of WMD?(1) Cardiac= Sudden death. Frothy nasal discharge due to pulmonary edema. (so may look like a resp dz) (2) Skeletal= Muscle weakness (Stiffness). Dysphagia if tongue weakness, risk of aspiration. Acute onset. Unable to stand or stiff gait. mm pain on palpation. (3) +/- myoglobinura. Dark urine --> + for blood on urine dipstick.
what will CK and AST levels be like with WMD?CK= 10 – 50 times normal. AST= 3 – 20 times normal
taking selenium samples from which locations can tell you about whole body selenium?whole blood, serum, liver
if you suspect WMD, is it easier to try to look at levels of selenium or Vit E?Selenium you can test from blood or liver. Vit E Measurement is inconsistent.
which enzyme Parallels the animals Se levels? Where do you measure this enzyme? Glutathione PeroxidaseMeasured in RBC’s. (GP is incorporated into the RBC during erythropoiesis.)
what does WMD look like post mortem?Do a Gross exam of myocardium & sk. Muscle to see White streaks of necrosis. Muscle will resemble raw chicken
how do you tx WMD?Administer Vitamin E & Se. Diuresis to flush myoglobin & prevent kidney damage. Stall rest. Carefully follow directions on Vit E / Se supplement.
(not sure if important) legal limit of Se supplementation in feeds?90PPM
2 times its good to suppliment vit E/selenium?(1) Se / Vit. E supplementation to Dam during dry period. (2) Se / Vit E to neonate at birth


Question Answer
polioencephalomalacia is caused by?This is a metabolic disturbance associated with a deficiency in thiamine (vitamin B1). Also caused by an inhibition of thiamine
why do you need vitamin B1/thiamine?Essential cofactor of glucose metabolism.
how can rumis get B vitamins?product of rumen fermentation
PEM (CCN) can be caused by (5 things)(1) Thiamine deficiency (2) Lead Toxicity (3) Amprolium Toxicity (4) High Sulfates (5) Water intoxication
Disruptions in rumen microflora associated with what 2 kinds of diets can lead to CCN?(1) high grain: low roughage diets (2) diets high in sulfates (molasses, DDG’s)
which 2 bacterial species can multiply in the rumen and produce thiaminase, causing a deficiency? Clostridium sporogenes and Bacillus spp
what is the major bad problem that happens from impaired glucose metabolism due to B1 (thiamine) deficiency?cerebral edema
clinical signs of polioencephalomalacia/ cerebral cortical necrosis?Initially see isolation/disorientation of individual ( Can occur in multiple animals). Afebrile, depression and head pressing. Bruxism, Abnormal head carriage (star gazing= nose higher than the poll). Also see BLINDNESS with papilloedema around the optic disk, and Opisthotonos and Convulsions. Clinical course in calves may be several days
(not sure if we need to know DX) CSF looks like what with CCN?Normal cell count [< 20/microliter, mononuclear].Normal to slightly elevated protein, Pandy’s.
(not sure if we need to know DX) what can you look at in RBCs to try to dx CCN?Transketolase levels in rbc.
PEM related to _________ will not respond to thiamine administrationsulfates
1* signs you might see with PEM/CCN?blindness or convulsions
(not sure if we need to know DX) sulphates over what might indicate CCN?Sulfate analysis > 1500 ppm (feed or water) or 0.083 g/kg BW.
ddx for CCN if blindness is the first sign? DDx if Convulsions as 1* sign?BLINDNESS: vitamin A deficiency, lead poisoning, brain abscess, polioencephalomalacia.... CONVULSIONS: lead poisoning, nervous coccidiosis, familial epilepsy, complicated frontal sinusitis, thrombotic meningoencephalitis, polioencephalomalacia
what will gross path/ histopath look like with CCN? Grossly, may see flattening of the sulci and gyri of the cerebrum. Also will see Autofluorescence due to lipofuchsin pigments.. Will see Laminar cortical necrosis on histopathology..
how do you tx CCN?Thiamine HCl @ 5 mg/lb (11 mg/kg) every 4-6 hours
is CCN reversible? The quicker treatment (giving thiamine) is initiated, the faster the clinical signs reverse.Clinical signs tend to improve in the reverse order they appeared. However, Some animals may be left with deficits.
poor response to thiamine tx with CCN most likely implies that the cause is...Poor response= sulfate-induced CCN
what can you give to reduce cerebral edema in CCN pts?Mannitol
General Brainer Treatment (4 things)Thiamin, Oxytetracycline, Anti-inflammatory, and if a camelid, Fenbendazole

HISTOPHILUS SOMNI SEPTICEMIA/ Thrombotic Meningoencephalitis (TEME)/ Sleeper Syndrome

Question Answer
Histophilus (Haemophilus) is a common pathogen which tends to inhabit which 2 body systems?resp and repro
CNS dz due to histophilus might be seen after an infection of which other system?resp
how common is TEME compared to histophilus?Only a very small percentage of Histophilus infected calves will develop signs of TME
explain the pathogenesis of TEME (where it starts to how it leads to thrombi)H. somni is commonly found in the trachea and upper airway. H. somni is an opportunist that colonizes the lung after viral injury. Creates vascular endothelial damage. Damage & cytotoxin --> microthrombi formation. Thrombi --> ischemic injury to cerebral cortex
what age is most commonly affected by TEME? Most commonly a problem in calves 6 moa - 2 yoa (emphasis on the early ages).
clinical signs of a H. somni/TEME infection?Respiratory disease, otitis, Swollen joints, stilted gait, Knuckling of the fetlocks, Down and stuporous, death
(not sure if will ask dx) what will CSF look like with a TEME infection?inc neutrophils, inc globulin protein (pandy test) (Pandy's test (or Pandy's reaction) is done on the CSF (cerebrospinal fluid) to detect the elevated levels of proteins (mainly globulins).Proteins (globulin and albumin) are precipitated by a saturated solution of phenol in water.)
what does gross/histopath look like with TEME?GROSS: Ischemic infarcts throughout the cerebral cortex and spinal cord, Synovitis of joints, evidence of penumonia. HISTO: Vasculitis with fibrinoiddegeneration
When must you treat TEME? Must be initiated before the animal becomes recumbent.
H. somni is routinely sensitive to what abx?Penicillin's & cephalosporin's, Oxytetracycline, Tilmicosin, Florfenicol
*what should you know about your choice of abx and the bbb?Vascular damage --> B-B barrier is not major concern for AB penetration with this dz
how effective are vx with TEME?Histophilus vaccines are more efficacious against TEME than in the prevention of respiratory disease.

LISTERIOSIS (silage dz, circling dz) / BOTULISM

Question Answer
what causes listeriosis? (describe it a little, where does it live?)Etiology is Listeria monocytogenes, a gram + rod. Bacteria is common to the environment of the ruminant.
most common source of infection for listeria?corn silage
explain pathogenesis of listeriosis (how does it enter, what damage does it do, where does it go) CNS infections occur via the oral route, as Bacteria gain access to the trigeminal n. through lacerations of the oral mucosa. Bacteria then migrate up the nerve to the brainstem (takes about 7 days). Infection of the brain is unilateral spreading along one side of the brainstem.
Cranial Nerve V--> does what (what will you see CSs wise when listera damages this nerve)Motor to muscles of mastication, palpebral reflex
Cranial Nerve VII--> does what (what will you see CSs wise when listera damages this nerve)Droopy ear & eyelid, lip droop
Cranial Nerve VIII--> does what (what will you see CSs wise when listera damages this nerve)Head tilt and loss of equilibrium, nystagmus
Cranial Nerve IX--> does what (what will you see CSs wise when listera damages this nerve)Difficult swallowing
Cranial Nerve XII--> does what (what will you see CSs wise when listera damages this nerve)Dropping cuds, difficult prehension of food, protrusion of the tongue
(not sure about if we need to know diagnostics) what will CSF be like with listeria? Elevated WBC’s, principally lymphocytes (70-200 cells/microliter) (<--remember that H. somni was neuts) Elevated protein (but +/- on the pandy test)
*what should you know about the presentation of the cranial nerve dysfunction caused by listeria?UNILATERAL usually (hence circling in one direction towards the lesion)
how do you tx listeriosis (/what are some of the drugs you can use)Early antibiotic therapy: Oxytetracycline, Florfenicol, Penicillin (?). Maintain hydration and acid-base balance (stomach tube, rumen fistula), Tarsorrhaphy if they can’t blink (Tarsorrhaphy is a surgical procedure in which the eyelids are partially sewn together to narrow the eyelid opening)
what causes botulism (say a little about it)Clostridium botulinum: a G+ spore former which survives well in the environment
where in the animal's enviro do you find clostridium botulinum?Found in spoiled feed stuffs: Moist, alkaline silage, Brewer’s grains, Decaying vegetation, animal carcasses
CSs of botulism?Flaccid paralysis w/in weeks of ingestions, flaccid tongue.
which age is LESS susceptible to botulism?adults LESS susceptible.
what exactly is it that causes the problems with botulism? (pathophys)Ingestion of preformed toxin!! Small ruminants must ingest toxin (horses can get toxicoinfectious form tho). Toxin binds at neuromuscular junction
one easy way to test CSs of botulism?pull tongue out of mouth, they wont put it back in
how do you tx botulism?supportive care only :(
how can you help control botulism? get rid of rotting things. Don’t feed silage to small ruminants.

BORDER DISEASE (hairy shaker lambs) / NERVOUS COCCIDIOSIS / PSEUDORABIES OF CATTLE (Aujeszky's disease, Mad Itch)

Question Answer
what is the etiological agent of border dz? Non cytopathic flavivirus
CSs of border dz? Abortion & stillbirths, infert, deformed lambs
explain pathogenesis of border dz- how and when are they infected? what does it do to them?Congenital infection, where Severity of signs depends on fetal stage. There can be EED, or Immunotolerance w/ persistent viremia depending on the stage infected. It causes hypomyelination and can spread horizontally and vertically.
(prolly dont need to know) how do you dx border dz?IFA to detect viral antigens, Necropsy (brain malformations)
what kinda brain/head malformations can border dz cause?Hydranencephaly, Porencephaly, Microencephaly, cerebellar hypoplasia, Brachygnathia
how do you tx border dz?no tx :(
what causes NERVOUS COCCIDIOSIS?Etiology has not be definitively agreed upon! Thought to be caused by the elaboration of neurotoxin. There is no direct involvement of the CNS by the organisms. (Eimeria zurnii, E. bovis), but Affected cattle will have signs of intestinal coccidiosis.
what are the coccidia involved in nervous coccidiosis, and what is important to remember about them as causative agents?Eimeria zuernii, E. bovis-- remember they don't directly cause the problem. They theorize that it is a neurotoxin they produce
clinical signs of nervous coccidiosis? Diarrhea (± blood), Ill-thrift, Muscle tremors, Convulsions, Opisthotonos, nystagmus
3 ddx for convulsions that aren't nervous coccidiosis?Hypomagnesemia, Polioencephalomalacia, Brain abscess
prog for nervous coccidiosis?The prognosis for calves with nervous coccidiosis is very poor - most die.
how can you tx nervous coccidiosis? (what are the coccidiostats?)(very poor prog) Tranquilizers and anticonvulsants. Try administering coccidiostats: Amprolium, Sulfadiamethoxine, Decoquinate
what is the etiological agent of pseudorabies? Etiology is a herpesvirus whose natural host is the pig (horses & humans are resistant).
pseudorabies is aka? Disease is also called Aujeszky’s disease or Mad Itch.
what kinda host are cattle with pdeudorabieS?dead-end host (natural host pig-- horses and humans resistant)
what are the clinical signs and how long is the clinical course for pseudorabies?Clinical course from 8-72 hours. Intense localized pruritus leading to self-mutilation, Elevated temperature, Some show aggressive behavior, paralysis, muscular twitching, convulsions, & staggering gait.
explain the pathogenesis of pseudorabiesVirus is neurotrophic: Attaches itself to peripheral nerves, from which it migrates to the spinal cord.
you need to send suspected pseudorabies to the state diagnostic lab..what samples do you use?Spinal cord from the areas that innervate the dermatomes affected by the mutilation.