Food Ani. Med- Small Ruminant Diseases 4

wilsbach's version from 2016-01-22 16:59

Neuro 2

Question Answer
Who gets PEM? is there any age preference?Cattle, Sheep, Goats, Pigs, (Humans); Any age group but young more susceptible
what's PEM stand for?polioencephalomalacia
what is seasonality like for PEM?Sporadic and any time of year. Region dependent, when food is in short supply
what are the two different ways an animal can get PEM?(1) sulfur toxicosis (2) Thiamine deficiency
what are some situations where you might ingest too much sulfur?might be too much in concentrate diets, pasture near high sulfur concentrated areas, water with a high sulfur content.
Thiamine deficiency might occur when..Intake, absorption or production deficiencies, or probs with Thiaminase
if I say sulfur or thiamine, you say what dz?PEM
thiamine deficiency and sulfur toxicosis both interfere with what?Interference with glycolysis and cellular metabolism --> The brain is reliant on glycolysis for energy!!!
why does the body need thiamine?Thiamine plays an important role in metabolism: Kreb’s cycle (inactivity of the alpha-ketoacid dehydrogenase pathway) and the hexose monophosphate pathways for glycolysis
Thiamine is aka?vit B1
How do adult ruminants get and get rid of thiamine (B1)? How about pre-ruminants (babies)?ADULTS: Production by rumen microbes, Destruction by thiaminases. PRE-RUMIS: Pre ruminants rely on dietary thiamine (dietary insufficiency or mal-absorption) (their rumen isnt developed enough, don't have enough bugs in there to make the B1)
explain pathophys of High sulfur intake leading to PEMIncreased production of Sulfide in rumen--> Sulfide is toxic to cellular metabolism. If produced in high amounts it can overwhelm hepatic detoxification and so diffuse into brain
what is the main lesion of PEM? why is the brain predisposed to PEM?The main lesion is neuronal edema with secondary compartment syndrome: caused by ATP depletion and insufficient functioning of the Na+/K+ pump. (fluid accumulates in cells --> swelling). The skull limits expansion leading to pressure necrosis of the brain. The brain is predisposed to PEM as it has extremely high energy and oxygen requirements
what are the clinical signs of the subacute (between acute and chronic) form of PEM?Signs develop with in hours to days and progress From dull and disinterested to stuporous and comatose. Central blindness is a prominent sign (will have PLR but not menace, she said). Some become hyper excited, develop hyperesthesia with muscle tremors and may eventually have seizures. Opisthotonus is a prominent sign. Head pressing, repetitive chewing and ptyalism is open seen. Ultimately … Death
what are the clinical signs of the ACUTE form of PEM?Animals found recumbent and comatose, Episodic tonic-clonic convulsions
what's a simple test you can perform to check if the sulfur levels in the animal are too high?Rumen gas cap sulfur content (obv check diet also, Presumptive diagnosis on history and clinical signs as well as response to treatment)
how can you dx PEM from histology?Diffuse laminar necrosis, Intracellular and intercellular edema, Neuronal necrosis, gliosis, and neuronophagia
how can you dx PEM from necropsy?Cortical swelling, softening, flattening, and yellowish discoloration of the gyri. Necrotic areas of cerebral cortex autofluoresce under UV light
how can you tell if a part of the cerebral cortex is necrotic? (PEM)will autofluoresce under UV light
how can you tx PEM?Thiamine IV and then subQ, supportive therapy
how can you help prevent PEM?Careful dietary management, If anorexic as the result of another disease supplement thiamine and transfaunate
who (breed) is specifically prone to getting scrapie? age?suffolk sheep (again....)....but all sheep can get it. Goats have also been reported to get it, but rarely. 2-5yrs on average
is scrapie zoonotic?It can spread between different species but there are no reports of this being zoonotic
how is scrapie transmitted?Oral route is the natural infectious route. It is found endemically worldwide, so it is suspected to occur naturally in the soil. Eating placental membranes of an infected sheep/ abortion is also a transmission route
what causes scrapie, and what is the resultant pathophysiology?The PrPsc prion protein, which folds irregularly, enters the alimentary system via oral route. It is transported to peripheral lymphoid tissue and spreads to the CNS, all the while causing the sheep PrP proteins to fold irregularly. The prion replicates in the lymphoid tissue of the animal
which genes make sheep more susceptible to scrapie, and which genes confer resistance?susceptible: VV RR QQ. Resistant: AA RR RR
what are the clinical signs of scrapie?Slow onset! Extremely pruritic with increasing intensity (Sheep rub on any fixed objects, get wool loss dermatitis, skin infections and excoriations.) Get a nibble reflex when scratched. Bruxism and ptyalism. (Scrapie aka Mad Itch) ). Weight loss. Nervousness/restless, tremors starting with head and progressing down the body. Advanced cases have convulsions, collapse, are stuporous. Death during convulsion or from starvation if the disease is allowed to run course
to definitively dx scrapie, you a post-mortem
how can you try to dx scrapie pre-mortem?Premortem testing for presumptive diagnosis Using nictitating membranes, anal lymph nodes and tonsil LN, as well as blood and CSF
how can you dx scrapie post-mortem?Samples of brain and spinal cord for microscopic exam. If tissues are autolyzed, PrPsc can be ID’d by immunohistochemistry, Western blot, ELISA
how do you tx scrapie?It is fatal and irreversible, there is no treatment
is there a vx for scrapie?no
how might you be able to prevent scrapie?Genetic testing for susceptibility and culling of susceptible animals and only breeding resistant stock can be used to help control disease

Musculoskeletal 1

Question Answer
Caseous Lymphadenitis is aka?Contagious abscesses, CLA, CL, "cheesy gland" or "boils"
if you see a sheepie or goatie like this, what do you think?CLA
signalment for CLA?All animals susceptible, common in sheep and goats tho
CLA--> what kinda abscesses are SHEEP prone to getting? GOATS?SHEEP: internal abscesses. GOATS: external abscesses
causative agent of CLA?Corynebacterium pseudotuberculosis
what is the seasonality of CLA? Once the environment has been contaminated, it (Corynebacterium pseudotuberculosis) can survive harsh weather conditions for several weeks to months and affects animals year round
what age does CLA affect?all ages
how is CLA transmitted?C. pseudotuberculosis enters the body through broken and intact skin, mucous membranes, inhalation, or ingestion
Corynebacterium pseudotuberculosis--> what is this/ what does it cause?causes CLA, it's a gram-positive*, ***intracellular, coccobacillus
what biotype of C. pseudotuberculosis affects sheep and goats?A nitrate-negative biotype infects sheep and goats
what is it that makes corynebacterium pseudotuberculosis so shitty and virulent? All strains produce an exotoxin that enhances dissemination of the bacteria by damaging endothelial cells and increasing vascular permeability
where does C. pseudotuberculosis replicate and how does it form abscesses?Replication of bacteria occurs in the phagocytes, which then rupture and release bacteria. The ongoing process of bacterial replication, followed by attraction and subsequent death of inflammatory cells, forms the characteristic abscesses associated with CL
3 big predisposing factors to CLA?(1) Lack of strict biosecurity and/or poor sanitation can facilitate infection (2) Injury may result from shearing, tagging, tail docking, castration, or other environmental hazards resulting in skin trauma (3) External parasites are a predisposing factor as pruritic stock will rub and put breaks in skin
what are the clinical signs of CLA?Abscesses, weight loss, Other signs associated with abscess location Internal organ affected, External – skin, locomotion, eating and swallowing etc.)
what can you observe that is highly suggestive of CLA?Presence of an abscess in small ruminants
how do you get a definitive dx for CLA?bacterial culture of the purulent material from an intact abscess
for the internal form of CLA, what are some diagnostic tests that you can use?radiography and ultrasound can be useful along with trans-tracheal aspirates where there exists lung involvement
how do you treat CLA? What is the best tx?Treatment is possible but culling is advised. However, if the owner wishes to pursue treatment... EXTERNAL ABSCESS: Lance, drain, debride **Ensure strict biosecurity**, Excise entire abscess without opening, Antibiotics with Gram Positive spectrum, Intralesional tulathromycin has been shown to be effective. INTERNAL ABSCESS: Long term systemic antimicrobials
what abx is effective intralesionally with CLA? tulathromycin
why is CLA (Corynebacterium pseudotuberculosis) so difficult to control?Stability of infectious agent in environment makes it difficult to control
is there a vx for CLA?yes
*what should you def know about the vx for CLA?These vaccines should only be used in the species they are labeled for because adverse reactions have been reported in goats given vaccine labeled for sheep. Also know that Efficacy of these vaccines is not 100%, and vaccination will not clear infected animals
when is it not recommended to use the vx for CLA?In "clean" herds or flocks that have no history of CL, vaccination is not recommended
if there is a farm with CLA endemic, what is an economical solution for treatment?Vaccination of young replacement stock, and culling of older infected animals should be considered as economics allow
Uhhhhhhh what exactly is goin' on hur? Spider lamb dz
Who (breeds) is prone to spider lamb dz?Suffolk lambs and Suffolk X Hampshire lambs (suffoks AGAIN??? That's spider lamb, Scrapie, and abomasum emptying defect. Remember?)
What causes spider lamb dz?Mutation within the gene for fibroblast growth factor receptor 3 (FGFR3)
how is spider lamb dz transmitted?A congenital semi lethal autosomal recessive skeletal abnormality. Both parents must be carriers for phenotypic disease
What are the clinical signs of spider lamb dz for lambs with OBVIOUS abnormalities at birth? (prognosis?)Usually nurse well but don’t grow and die of secondary infections by 4 weeks of age. You will see Generalized chondrodysplasia of appendicular and axial skeleton: Kyphosis, scoliosis, concavity of sternum, deviated maxilla, angular limb deformity, long bones of limbs are very long and very fine. Also poor muscling.
What are the clinical signs of spider lamb dz for lambs with NO OBVIOUS abnormalities at birth? (prognosis?)develop abnormalities at 3 – 8 weeks of age. You will see Progressive malformations, chondrodysplasia of appendicular and axial skeleton. They will usually nurse well but don’t grow and die of secondary infections by 6 months of age. they will also have poor musculing.
How can you dx spider lamb dz?Clinical signs and history, Radiographs, Post mortem and histology. Genotyping is available in some labs, and it is recommended to have new breeding stock tested and to cull carrier positive animals

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