Specialty Reading Q's Flashcards
CS, Articles
DPJ is associated with a poor prognosis when
abdominal fluid T.P. > 3.5g/dL
anion gap increases to 15mEq/L or above
Which point mutation of the beta-2 integrins cause bovine leukocyte adhesion deficiency?
CD18
What does bovine leukocyte adhesion deficiency cause?
marked and persistent neutrophilia
hypergammaglobulinemia
chronic, recurrent bacterial infections and death
Clinical signs in calves appear within a couple of weeks after birth and include anorexia, fever, chronic pneumonia, chronic diarrhea, severe ulcers on oral mucosal membranes, ulcerative stomatitis, gingivitis, periodontitis, loss of teeth, impaired wound healing, chronic dermatitis, decreased growth rate, and death
Lethal Trait A46 in cattle causes
- bovine hereditary zinc deficiency
- reduced lymphocyte numbers
- Calves with skin lesions, diarrhea, and bronchopneumonia.
- Death occurs at approximately 4 months, secondary to bronchopneumonia or complicated diarrhea
IN CALVES - Catabolism of plasma derived immunoglobulins occurs when?
rapidly in the first 12 hours
What is the point of using oligosaccharides (OS) in unpasteurized colostrum?
to decrease adverse effects of colostral bacterial contamination
Which Salmonella species stimulates antibody production and secretion in colostrum in vaccinated cows?
Newport
What drug increases absorption of colostral IgG when administered orally?
cisapride
what causes digital dermatitis
treponema
common dermatophyte in cattle
Trichophyton verrucosum
Which site is most affected by bovine ocular squamous cell carcinoma?
lateral limbus
immunosuppression associated with BVDV infection in calves is due to?
increased neutrophil destruction
Which clinical manifestation is the most economically important in pigs with disease caused by Erysipelothrix rhusiopathiae?
endocarditis
A 100–cow grazing dairy fed total mixed ration once has had increase in incidence of clinical mastitis due to several Gram-negative infections.
Which one of the following management methods will most likely reduce the incidence of mastitis?
adding selenium to the TMR
What is the infective stage of dermatophilosis in cattle?
zoospores
In cohort studies of the role of a risk factor in the etiology of disease, it is essential that:
The exposed and non-exposed groups under study be as similar as possible with regard to possible confounding factors.
Consensus statement definition of EPIH
the presence of blood detected on tracheobronchoscopic examination after exercise, presence of red blood cells in bronchoalveolar lavage fluid, or both.
There is no consensus about the concentration of red blood cells in bronchoalveolar lavage fluid that is diagnostic of EIPH, and the definition varies among reports.
Does EIPH adversely affect the health / welfare of horses?
This question is important because evidence of an adverse effect of EIPH on the health or well-being of horses has potential ramifications for use of horses for racing.
-no evidence of increased risk of sudden death in horses with EIPH.
EIPH Grade 1-3 is not associated with a shorter racing career of Thoroughbred horses
Thoroughbred horses with epistaxis or Grade 4 EIPH have shorter careers.
some horses with EIPH have extensive and characteristic pulmonary lesions.
moderate quality evidence that EIPH is progressive and related to load of racing.
There is no published evidence regarding the heritability of EIPH. There is very low quality evidence of an association of pedigree with occurrence of epistaxis.
Does EIPH affect the athletic capacity of horses? An adverse effect of EIPH on athletic capacity might influence decisions on the use of interventions to decrease the severity or incidence of EIPH.
moderate to severe EIPH in Thoroughbred race horses is associated with increased likelihood of inferior finishing position in a race.
There is very low quality of evidence that EIPH in Standardbred racehorses is not associated with finishing time in a race.
There is moderate quality evidence that Thoroughbred racehorses with more severe EIPH finish farther behind the winning horse in a race.
There is moderate evidence that severity of EIPH in Thoroughbred racehorses is negatively associated with a horse’s race earnings.
There is low quality evidence of a dose-response relationship between severity of EIPH in Thoroughbred racehorses and severity of impaired performance.
Are there effective prophylactic interventions for EIPH? The capacity to manage EIPH is dependent on the existence of medications or interventions that decrease the severity or incidence of EIPH.
There is high quality evidence that furosemide (0.5–1 mg/kg administered IV 4 hours before strenuous exercise) decreases the severity and incidence of EIPH.
There is moderate quality evidence that furosemide reduces pulmonary vascular pressure during strenuous exercise.
There is very low quality evidence that nasal strips, herbs, aminocaproic acid, NSAIDs, corticosteroids, pentoxifylline, or bronchodilators affect EIPH severity.
Does furosemide affect the athletic capacity of horses? An association of furosemide administration with superior performance has been suspected since the drug was first used in race horses and continues to be contentious.
There is moderate quality evidence that furosemide administered IV 4 hours prior to racing is associated with improved racing outcomes in Thoroughbred and Standardbred racehorses.
There is low quality evidence that furosemide administered IV 4 hours before treadmill exercise results in delayed onset of fatigue and improved energetic cost of locomotion.
Increased expression of genes encoding for TNF-a, IL-1b, and IFN-c and protein concentrations (TNF-a and IFN-c) have been repeatedly linked with abnormal BALF cytology findings, both in the presence and in the absence of clinical signs, suggesting that activation of the____________ and TH-? response are often involved in the pathogenesis of IAD and most likely drive the luminal neutrophilia
innate immune system and TH-1 response
mRNA expression of IL-17 and IL-23 have been also linked with increases in BALF neutrophil percentage, and increases in IL-4 and IL-5 with the mastocytic form of IAD, which would support an implication of the _______ in  some IAD phenotypes.
adaptive immune response, including Th-2 type polarization
Diagnosis of IAD is based on?
(1) the presence of clinical signs of lower airway disease (poor performance, cough)
(2) the documentation of lower airway inflammation based on excess mucus on endoscopy >2-3/5, BALF cytology >10% neutrophils, >5% mast cells and >5% eosinophils or abnormal lung function, and
(3) the exclusion of severe equine asthma (RAO/heaves) as well as infectious and other respiratory diseases (see differential diagnoses).
Definitive host for s-neurona in north America
The opossum Didelphis virginiana
S. neurona life cycle
Sarcocystis neurona has a 2-host life cycle
- definitive host: opossum (Didelphis virginiana)
- multiple mammal intermediate hosts
Sexual reproduction by the parasite in the intestinal epithelium of the infected opossum results in the production of sporozoite-containing sporocysts that are passed in the feces.
The sporozoites are infectious for the intermediate hosts, which include skunks, raccoons, armadillos, and cats.
S. neurona forms latent sarcocysts in the muscle tissue of the intermediate host; sarcocyst-laden muscle is the source of infection for the opossums
Horses are infected with S. neurona by ingesting food or water that has been contaminated with feces from an infected opossum.
EPM seasonal risk
Fall 6x higher
Spring/summer 3x higher
Winter lowest risk
Factors affecting EPM risk on farms
+ previous EPM diagnosis
+ presence of opossums
+ presence of wooded areas
- wildlife prevented from feed
- river or creek present
Which EPM tests are currently offered commercially that provide information regarding intrathecal antibody production based on serum and CSF titers?
The SnSAG2, 4/3 ELISA serum:CSF titer ratio
NhSAG1 ELISA serum:CSF titer ratio
diclazuril and ponazuril are
benzeneacetonitrile compounds
anticoccidial
these drugs are related to the herbicide atrazine and are thought to target the parasite’s apicoplast organelle.
Sulfonamides and pyrimethamine act synergistically by
interfering with folic acid metabolism and biosynthesis of purine and pyrimidine nucleotides necessary for the parasite’s survival.
Lyme disease-The primary North American genospecies
Borrelia burgdorferi sensu stricto, with Ixodid ticks being the vector for transmission
Ixodes scapularis in eastern North America and Ixodes pacificus on the North American west coast.
B burgdorferi life cycle
2-year enzootic cycle
East: ixodes scapularis and white footed mouse
West: ixodes Pacificas and grey squirrels
- reservoir host for spirochetes and infect tick larvae and nymphs
Deer + large mammals maintain adult ticks
Organism transferred to mammal when the tick feeds
Lyme diagnosis in horses
Diagnosis of current or previous infection with B. burgdorferi is most commonly achieved via serologic testing.
Positive test results indicate presence of antibodies against B. burgdorferi at the sampling time point and might represent different infection stages depending on the test utilized.
Commercially available laboratory tests currently include IFAT, ELISA, whole cell Western blot, and a bead-based multiple antigen ELISA assay (Multiplex). A point of care C6 SNAP marketed for dogs has also been utilized for testing horses. None of the tests consistently detect antibody until 3 or more weeks after infection.
A positive test result in the absence of previous vaccination indicates exposure from either a current or previous infection. Regardless of test methodology, a positive result does not prove causation of current clinical signs (clinical infection) nor does a positive result predict whether infection is likely to cause clinical signs in the future. There is no known correlation between magnitude of titer and likelihood of disease.
Borrelia-associated uveitis
Clinical findings usually include severe and most often bilateral ocular disease consistent with chronic uveitis, including a yellow-green fibroid aqueous humor, aqueous flare, synechiae, miosis, preiridal fibrovascular membrane formation, and other iris changes such as rubeosis iridis and loss of corpora nigra.
Prognosis for vision is poor.
Cutaneous pseudolymphoma associated with B. burgdorferi infection
characterized by dermal, papular to nodular lesions that occurred at the site of the tick bite.
Histologic evaluation was suggestive of lymphoma but immunohistochemistry revealed mixed lymphoid hyperplasia and Borrelia PCR performed on the tissue was positive.
Borrelia-associated cutaneous pseudolymphoma should be considered for horses in endemic regions with focal infiltrative skin lesions, particularly if the site corresponds to that of a known tick bite.
Abx treatment yielded good outcome
Milk from mares that have recovered from strangles contains immunoglobulin ?
IgGb and IgA
Coxiella burnetii
Small, pleomorphic, intracellular, gram negative bacterium
Infections principally occur through inhalation or ingestion, although infection by blood transfusion occurs.
Infections in animals are termed coxiellosis.
Where does coxiella replicate
within the trophoblasts of the placenta
after the logarithmic growth phase, produces a spore-like bacterial form termed a small cell variant (SCV)
- these SCVs are responsible for persistence of the organism in dust, manure, and the air of farms
- Aerosols originating from infected farms can act as a source of infection for humans
How can coxiellosis be most accurately diagnosed at the herd/flock level with consideration of the individual animal level?
qPCR: animals with abortion caused by C. burnetii. fetal tissues (liver, abomasal fluid, and lung) can also be PCR-positive. High numbers of organisms as evidenced by qPCR values combined with histopathologic placental lesions provide strong evidence that the abortion is caused by C. burnetii.
ELISA: Preferred for large scale screening of livestock, Good agreement with IFA results
Immunofluorescence Assay (IFA): Definitive serological test in human medicine.
Complement Fixation Test (CFT): Less sensitive than most ELISA (as low as 10% in aborting animals); good specificity (>98% • Negative ELISA samples may show low CFT titres, possibly detecting IgM • Limited utility in livestock.
What testing programs are recommended for infected herds and flocks to control clinical and subclinical coxiellosis, including shedding of the agent and transmission to other herds and flocks?
BTM ELISA is a useful test for large scale screening programs to detect flocks that have been previously infected
BTM PCR is more sensitive for detection of actively infected/shedding flocks.
In dairy goat herds, BTM ELISA also is similarly predictive of shedding status when measured with BTM PCR (cut-off 100 bacteria/mL milk) and also for detecting previously infected herds with seroprevalence of >15% (SP ratio of 43%)
Bulk tank milk containing >105 C. burnetii/mL as estimated by qPCR is associated with herd seroprevalence of ≥50% in dairy cattle.
The most beneficial tool that has been described for management of clinical disease is the implementation of vaccination using phase I form of the killed bacteria.
Once coxiellosis is confirmed on a premises, infections should be considered endemic in the population.
How can the transmission and zoonotic risks of coxiella be mitigated?
- Segregate periparturient animals from other high-risk animals (gestating and young). This may decrease exposure to the high level or organisms in aborted fluids.
- Manage parturient animals in an enclosed environment with controlled airflow to lower risk for down-wind transmission. This may increase risk of seroconversion for animals housed within the same environment.
- Eliminate land application of fresh manure.
- Compost manure for 90 days before land application and transport manure and apply only on damp low-wind days
- Promptly remove and dispose of aborted fetus and uterine fluids either by closed composting or burning.
- Move naïve or gestating animals to areas of the farm that are upwind of aborting animals.
- Minimize development of excessively dry and dusty environments in animal housing areas (mist or gently wetting down dusty environments) and around barns.
resistant to the action of abx drugs due to inherent structure or physiology of the bacteria
constitutive resistance
mechanisms:
1- lack of cellular mechanisms required for antimicrobial action (eg penicillin resistance dt lack of correct binding proteins)
2- growth rates too slow for effective action (beta-lactams)
3- resistance in anaerobic bacteria to aminoglycosides dt lack of oxygen-dependent uptake of the antimicrobial into the cell
developed mechanisms to circumvent action of the drugs through genetic mutation or through acquisition of genetic elements
acquired resistance
mechanisms: drug inactivation, drug modification, production of competitive metabolites, target mutation, target substitution, target modification, decreased cell wall permeability to drugs, active efflux of drugs, and failure to metabolise a drug to its active form
chloramphenicol, nitroimidazoles, nitrofurans in food animals
FDA banned over concerns of harmful residues
glycopeptides, extra-label use of fluoroquinolones and cephalosporins in food animals
FDA banned because they pose a risk for causing AMR that can be transferred to people
mechanism of resistance to benzimidazoles
beta-tubulin
mechanism of resistance to ivermectin
P-glycoprotein gene
anthelmintics recommended for small ruminants
ORAL ONLY
DO NOT ROTATE WITHIN A GRAZING SEASON
make sure the drench gets into the rumen so appropriate contact time can ensure killing
most important factor contributing to selection for anthelmintic resistance
levels of refugia
1) stages of parasites in the host that are not affected by the drug tx
2) parasites residing in animals that are left untreated w a partic drug
3) free-living stages in the environment at the time of tx
biosecurity recommendations for small ruminant parasites
Current recommendation is to quarantine (on dry lot where faeces can be removed) every new addition, dose w triple-class anthelmintic therapy, and perform FECRTss
Feed should be withheld for 24 h before tx, then moxidectin, levamisole, and albendazole should be administered consecutively (do not mix drugs together)
Retest 14 d later: FEC should be zero, and flotation should yield very few or no eggs
After this tx, animals should be placed on a contaminated pasture. Never should an animal be placed onto a clean pasture after a triple anthelmintic class treatment regimen is administered, bc any surviving worms will be triple resistant and there will be no refugia on pasture to dilute the future transmission of any eggs that are shed
what sheep breed has high heritability of FAMACHA scores
merino
signs of grey matter involvement
focal muscle atrophy and severe muscle weakness
signs of white matter involvement
ataxia and weakness in limbs caudal to site of infection
test of choice for detection of EHV-1
PCR on NASAL SWAB
acyclovir
Thymidine kinase inhibitor
synthetic purine nucleoside analog that selectively inhibits the replication of herpesviruses
this drug phosphorylated initially by viral thymidine kinase, followed by 2 other phosphorylations by host cell kinases à triphosphate acyclovir compound binds to and inhibits the viral DNA polymerase for the formation of viral DNA
PK of acyclovir after single po admin (10 and 20 mg/kg) to adult horses has been associated w high variability in serum acyclovir-time profiles and poor bioavailability below the concentrations required for viral inhibition
on culture, which strep ferments sorbitol and lactose
strep equi zoo, NOT strangles
immune complex is a type ? hypersensitivity
III
negative prognostic factors in for horses with structural heart disease
progressive chamber remodelling (dilatation and altered chamber shape) and dysfunction
great vessel enlargement
the development of pulmonary hypertension, CHF, and potentially dangerous arrhythmias
Any left-sided holodiastolic murmur I an adult horse
assumed aortic regurg until proven otherwise
Often mild and associated w normal performance and life expectance
If moderate to severe or first recognised in younger horse (<10) risks for reduced performance life and longevity higher
Continuous machinery murmur loudest on right side of thorax w bounding arterial pulses is characteristic of ?
aorta-cardiac fistula
Ultrasound monitoring of ascarids in foals
- Can detect burdens of > 10 worms
- most reliable findings were in loops within 5cm of the abd wall
Tapeworm species in horses
Anoplocephala perfoliata, A. magna and Anoplocephaloides mamillana (formerly known as Paranoplocephala mamillana).
Of these, A. perfoliata is by far the most prevalent and the other two species are reported only sporadically
Equine tapeworm treatment
Pyrantel pamoate paste 13.2mg base/kg
praziquantel 1mg/kg
Equine ascarids
Parascaris equorum or univalens
P. univalens has only one chromosome pair, whereas P. equorum has 2
Parascaris spp. Life cycle
- Hepatotracheal
- ingest eggs containing L2
- larvae penetrate small intestinal barrier, go through portal vein to liver
- migrate through liver and lungs for 14 days
- cough up and swallow
- after 90 days in small intestine are patent adults
Glanders recommended test
Complement fixation
varying sensitivities and specificities depending on the antigen and methodology used. False positives are problematic for the horse-owner and veterinary authority, whereas false negatives may allow the reintroduction of B. mallei into B. mallei-free areas. These gaps in knowledge of the epidemiology of glanders, and weaknesses in its diagnosis, coupled with the increased movement of equids, indicate that infection with B. mallei remains a major risk in the context of international movement of equids.
Burkholderia mallei
Glanders
Contagious zoonotic disease
40% mortality rate in man
Very treatment resistant
Acute glanders
Most common in donkeys
Fatal in 7-10 days
Fever, septic, bronchopneumonia, weight loss, swollen lymph nodes and nasal discharge
Chronic glanders
Horses
Acute episodes that recur but get progressively worse
Farcy
Cutaneous glanders
Crater shaped ulcers in muzzle and limbs - associated with lymph vessels
Definitive diagnosis of burkholderia mallei infection
Isolation and culture from lesions- limited by low concentrations in tissues and fluids
How does b mallei evade host immunity?
Formation of a protective capsule
hiding in the cytosol
Mycobacteria in horses
M. Avium spp hominissuis
CS - weight loss, d+, fever, v edema, hypoalbuminaemia and hyperfibrinogenaemia
rectal biopsy - mild multifocal neutrophilic or mild granulomatous proctitis
Equine coronavirus
+ fever, depression, anorexia
+- colic and d+
Fecal PCR Or intestinal biopsy IHC or e- microscopy
self limiting dz
What percent of foals with R. equi on PM did not have any clinical signs?
20%
Polysynovitis with rhodococcus
- should resolve with abx treatment for the pneumonia
- effusion in multiple joints without lameness; occurs in 33%
- rheumatoid factor, IgG, or immunofluorescence in synovial fluid points to immune complex deposition as the cause of the nonseptic synovitis
African horse sickness in partially immune horses
Or reservoir species
Horse sickness fever
Mild subclinical fever
Dunkop
Peracute pulmonary form (‘Dunkop’)
-characterised by rapidly progressive respiratory failure and usually occurs when AHSV infects fully susceptible horses
CS: pyrexia (up to 41°C), severe respiratory distress, forced expiration, profuse sweating and paroxysmal coughing
- onset of dyspnoea can be sudden, with death occurring as soon as 30 min after the onset of clinical signs
- >95% case fatality rates common
dikkop
Cardiac form (‘Dikkop’)
- characterised by oedema preceded by 3–4 days of pyrexia
- oedema starts in the supraorbital fossa before extending to the conjunctiva, head, and neck
- distal limbs and ventral abdomen are rarely affected
- dyspnoea, cyanosis, abdominal pain and heart failure also occur
- cardiac form is less clinically severe and more protracted than the pulmonary form, with fatality in >50% of cases
African horse sickness diagnosis
Any suspected cases of AHS in OIE disease–free countries must be reported to the state authorities and subject to laboratory confirmation
Virus isolation is considered the gold standard for diagnosis
however the OIE accepts molecular evidence of viral presence by PCR and serological evidence of infection via enzyme-linked immunosorbent assays (ELISAs)
Reservoir hosts for AHS
South Africa-zebras
North Africa-donkeys
Clinical signs of primary hyperparathyroidism in the horse
weight loss, facial swelling, inappetence, difficulty eating and shifting lameness
Persistent hypercalcaemia, hypophosphataemia and increased parathyroid hormone (PTH) concentrations are consistent with a diagnosis of primary hyperparathyroidism
How to differentiate primary and nutritional secondary hyper-pth
While nutritional secondary hyperparathyroidism results in increased blood concentrations of PTH and similar clinical findings to primary hyperparathyroidism (including osteodystrophia fibrosa, shifting lameness, difficulty eating and weight loss), important clinicopathological differences exist.
Hyperphosphataemia and normocalcaemia or hypocalcaemia are evident in nutritional secondary hyperparathyroidism — In contrast, primary hyperparathyroidism is characterised by persistent hypercalcaemia, hypophosphataemia and phosphaturia
gold-standard techniques for identifying insulin dysregulation
frequently sampled i.v. glucose tolerance test or hyperinsulinaemic–euglycaemic clamp
OGT vs OST
The results of the present study show that ponies defined as insulin resistant by the OGT may not be defined as insulin resistant by the OST. When previously established, but not validated, cut-off values for insulin resistance [15] were applied to each test, the OGT identified more ponies as insulin resistant than the OST. It is not possible to say which test more correctly identifies ponies with insulin dysregulation; this requires future studies in which the 2 tests are compared in the same conditions in conjunction with direct tests of insulin sensitivity.
Lamellar pathology in PPID animals is:
- unrelated to duration of laminitis
- Most lesions were located abaxially within the lamellar tissue and included increased length and width of the lamellae, chronic abnormal keratinisation, interlamellar epidermal bridging and cell death with more acute lamellar tearing in some cases.
- The lamellae of PPID animals without laminitis were normal
Conclusions: Whether PPID and hyperinsulinaemia have a causal inter-relationship or not, it may only be the hyperinsulinaemia that is associated with lamellar morphological alteration and pathology consistent with laminitis.
the predominant receptor present in lamellar tissue
IGF-1R
Our results not only demonstrate that IGF-1R is the predominant receptor present in lamellar tissue but also show
The iso form InsR-A
Foal microbiota: mainly compromised of
- Newborn: firmicutes
- 2-30 days: akkermansia, decreeased diversity
- weaning plus: more fibrobacteres
Most frequently diagnosed equine tumors
sarcoid (24% cases)
squamous cell carcinoma (SCC) (19%)
lymphoma (14%)
melanoma (6%), gonadal stromal tumour (6%) and mast cell tumour (MCT) (4%)
What breed has an increased risk of mast cell tumors
Arabs, cobs
Hypoglycin A causes?
Multiple acyl CoA dehydrogenase deficiency
These enzymes are crucial for the oxidation of fatty acids and the generation of energy within type 1 muscle fibres.
—> increased concentrations of blood acylcarnitines and urinary organic acids
How is hypoglycin metabolized?
by transamination and oxidative decarboxylation to the toxic compound MCPA by the liver.
MCPA then inhibits long chain fatty acid metabolism through the inhibition of acyl CoA dehydrogenases. MCPA is subsequently conjugated and excreted in urine.
Differences in the rate of hepatic hypoglycin metabolism to the active MCPA could also play a role in the variable incidence of clinical signs. Indeed the difference in the concentration of hypoglycin metabolites was much greater between cases and co-grazers than the difference in unmetabolised hypoglycin concentration.
Atypical myopathy
Sycamore or box elder
Acer pseudoplatanus
acer negudo
Spontaneous aortic rupture in horses
- friesians
- occurs at thoracic aorta near ligamentum arteriosum
Reference range for triglycerides in donkeys
- the upper limit of the range is now 2.8 mmol/l
- previously 4.3 mmol/l
- It is very important that veterinarians note this difference as this upper limit of triglycerides is commonly used to determine the risk of a donkey becoming hyperlipaemic
What is the asocialtion between eiph and sudden death in racing?
Unclear
When should horses with AF be retired or cardio-verted?
Exercising HR at Max exercise exceeds 220 beats/ min or if there are concurrent ventricular arrhythmias
Prodromal signs in cases of sudden cardiac death
extreme tachypnoea or respiratory distress, deep expirations, profuse sweating, agonal trembling, ataxia, staggering, vocalisations, rearing, the rider feeling that ‘there was something wrong’ and the horse slowing down or stopping during exercise
Echocardiograms have been recommended in equine athletes when any of the following are identified:
1) a previously diagnosed “functional” murmur that is louder on serial examinations
2) a grade 3–6/6 left-sided murmur compatible with mitral regurgitation or aortic regurgitation
3) a grade 4–6/ 6 right-sided systolic murmur compatible with tricuspid regurgitation
4) suspected ventricular septal defect or other congenital heart lesion
5) continuous or combined systolic–diastolic murmurs
6) pathologic arrhythmias
7) suspected myocardial injury/damage
In Dembeck EVJ 2016 what were found to be markers of hypoperfusion in foals?
clinical hypoperfusion in neonatal foals is characterised by hyperlactataemia, hyperaldosteronaemia and hypervasopressinaemia
also demonstrated that hypothermic extremities and albumin concentrations are good predictors of hypoperfusion and can be used to assess tissue perfusion
Thoracic pump chest compressions
Chest compressions to aid circulation in foals or mature equine cases involves using the ‘thoracic pump’ method
changes in thoracic volume promote forward blood flow
horses should be positioned on a hard surface in lateral recumbency and hands should be placed over the widest portion of the chest wall (caudodorsally) and the chest should be depressed to approximately 30–50% of its width with a 1:1 compression to relaxation rate at 100 compressions/min (which correlates to the underlying beat of ‘Staying Alive’)
Assessment of success of chest compressions is best measured by
End tidal co2
goal of 18-22mmHg but epi may artificially increase it
How does colitis affect neutrophil apoptosis?
Delays it
The data show that neutrophil apoptosis is delayed in horses following the induction of colitis as a result of interference with the intrinsic and extrinsic apoptotic pathways, which may contribute to the development of equine SIRS. Concurrent development of neutrophilia may contribute to a prolonged neutrophil lifespan through a concentration-dependent delay in apoptosis.
Ulcerative posthitis versus ulcerative dermatitis
Posthitis: caused by c. renale
Does not bleed when you pull scab off
Dermatosis: lip and leg ulcer - caused by a pox virus related to orf (contagious ecythema virus)
Lesions also on legs and lips
Bleeds when you take scabs off and contain non stinky pus
Treatment for ulcerative posthitis
Reduce dietary protein and non-protein nitrogen
Disorders resulting from urolithiasis
Acute urethral obstruction
Chronic urethral obstruction
Urethral rupture
Urinary bladder rupture
Less common: ureterolith and hydronephritis
Common site of urethral obstruction in cattle
Distal sigmoid flexure, near the insertion of the retractor penis muscle
Most common site for bladder rupture
Dorsum of bladder fundus
Why will xylazine exacerbate bladder distention?
Diuretic!
Serum potassium concentration in ruminants with bladder rupture
Variable!
Anorexia may contribute to hypokalemia or normokalemia
- Aldosterone release secondary to volume depletion results in increases in salivary potassium excretion
- Alkalosis, secondary to hypochloremia, may encourage potassium into cells
- Hyperphosphatemia may occur secondary to uroabdomen
- Peritoneal fluid/serum creatinine ratio of 2: 1 or higher indicates uroperitoneum.
What initiates urinary calculus formation?
Supersaturation exceeds the protective capabilities of crystallization inhibitors
Stone types affected by urine ph
struvite, ca phosphate, and ca carbonate are less soluble in alkaline
Rations high in phosphorus (grain-based rations) make ruminants prone to
struvite (magnesium ammonium phosphate hexahydrate)
apatite (calcium phosphate)
Outbreaks of urolithias is May be caused by
Rations with calcium: phosphorus ratio less than 2:1
Primary route of Phos excretion in ruminants
GI tract
Silica uroliths are a problem in what population
Range cattle - 50-80%
During periods of water deprivation, silicic acid polymerizes to polysilicic acid
Polysilicic acid forms large micelles that become insoluble when bound to urinary mucoproteins
Increased by feeding a high calcium/phosphorus ratio (>2.8:1) and inducing more alkaline urine
What will help increase phosphate excretion?
Increasing long-stem forage: increase salivary flow and fecal phosphate excretion
DCAD diet in small ruminants
0-mEq/kg DCAD diet using ammonium chloride (fed at .5 to 1.5% of dry matter) reduces urinary pH to between 6.0 and 6.5 without significantly decreasing blood pH.
This pH should increase solubility of struvite and apatite crystals.
Most urachal infections in ruminants involve?
Truperella pyogenes or E. coli
Primary Causes of Recumbency Initiating the “Downer Cow Syndrome”
Subclinical hypocalcemia
blood Ca is below 8 mg/dL but above 5.5 mg/dL
- may affect 25% of heifers and more than half of older cows
- not as severe as clinical milk fever
- these cows are more immune suppressed than normocalcemic cows and at greater risk of metritis, ketosis, and retained placenta
- degree of hypocalcemia and the length of time the cow is hypocalcemic greatly influence susceptibility to these secondary disorders.
Parathyroid hormone (PTH) effects at the surface of target bone and kidney cells.
A) Under normal conditions, PTH released in response to hypocalcemia interacts with its receptor, located on the surface of bone and kidney cells, in a lock and key fashion. This stimulates G proteins and adenylate cyclase (adenylate cyclase complex) resulting in production of cyclic AMP, which acts as a second messenger within the cytosol of target cells. This initiates mechanisms such as bone Ca resorption and renal production of 1,25-dihydroxyvitamin D to restore blood Ca concentration to normal levels.
(B) Alkalotic conditions induced by high-potassium diets induce a change in the shape of the PTH receptor protein so that it is less able to recognize and bind PTH, resulting in failure to activate the cell by producing cyclic AMP.
(C) Mg is required for function of the adenylate cyclase complex. Hypomagnesemia reduces ability of PTH stimulated cells to produce cylic AMP, resulting in failure to activate the cell.
the primary mineral causing the metabolic alkalosis that interferes with PTH function
potassium
Dietary absorption of chloride and sulfate
Diet chloride anions are absorbed with nearly 100% efficiency. Sulfate anions can also help acidify the cow, but sulfate is not absorbed as well as chloride and has approximately 60% the acidifying activity of chloride
DCAD of:
0
+ 50 mEq/kg
−75 and −125 mEq/kg
results in average urine pH in cows of approximaely:
- 0
- 5
- 3
most common causes of a decrease in the anion gap
Hypoproteinemia and hyperchloremic metabolic acidosis
The cause of normal to low anion gap hyperchloremic metabolic acidosis often can be differentiated on the basis of the serum potassium concentration. Animals with hyperchloremic metabolic acidosis associated with gastrointestinal fluid losses or renal tubular acidosis most often manifest hypokalemia
high anion gap acidosis
associated with accumulation of a metabolizable acid, most commonly L and D lactic acid associated with anaerobic exercise, grain overload, acute gastrointestinal accidents, or hypovolemic shock (e.g., diarrhea in young calves)
D128G allele
Bovine leukocyte adhesion deficiency (BLAD)
-autosomal-recessive congenital disease of Holstein calves
The molecular basis for BLAD is a single point mutation (adenine to guanine) of the CD18 gene, resulting in aspartic acid to glycine substitution at amino acid 128 (D128G) in the glycoprotein
-Calves with BLAD are homozygous to the D128G allele, whereas β2 integrin expression in heterozygotes occurs in 56% to 90% of cattle not affected by BLAD
Lethal trait A46 causes?
Bovine hereditary zinc deficiency
in a zinc-deficient state, lymphocyte numbers and function are
REDUCED
bovine hereditary zinc deficiency
- autosomal-recessive immunodeficiency disorder
- clinical signs DO respond to zinc oxide therapy (acetate)
- Calves appear normal at birth but develop skin lesions at 4 to 8 weeks of age
- skin lesions are characterized by alopecia, hyperkeratosis, and exanthema
- distribution of the skin lesions includes the perineum, lower legs, head, and neck
Clinical signs associated with lethal trait A46 include
skin lesions, diarrhea, and bronchopneumonia
How does acyclovir work
- phosphorylated initially by viral thymidine kinase, followed by 2 other phosphorylations by host cell kinases
- triphosphate acyclovir compound binds to and inhibits the viral DNA polymerase for the formation of viral DNA
- PK of acyclovir after single po admin (10 and 20 mg/kg) to adult horses has been associated w high variability in serum acyclovir-time profiles and poor bioavailability below the concentrations required for viral inhibition.
Evan’s Syndrome
Immune mediated anaemia and thromocytopenia are recognised to occur concurrentl
Direct coomb’s test
detects the presence of IgG antibodies or complement on the surface of red blood cells, and is a highly specific but not particularly sensitive test for erythrocyte agglutination and immune mediated disease
IMHA is what type of reaction
secondary type II hypersensitivity antibodies directed against RBC surface antigens
The mode of action of trimethoprim sulfonamide antimicrobials
sulfonamides act as competitive agonists for para-aminobenzoic acid (PABA), preventing the production of dihydrofolic acid.
Dihydrofolic acid is a precursor for tetrahydrofolate, an essential component of folic acid formation and bacterial replication.
Trimethoprim inhibits the enzyme dihydrofolate reductase, responsible for the conversion of dihydrofolic acid to tetrahydrofolic acid preventing folic acid formation.
In horses and foals, hyperglycaemia (glucose
?? mmol/l) has a negative association with survival in
critically ill patients (Hollis et al. 2008; Hassel et al. 2009),
> greater than 7.5
Folic acid
- required for mammalian and bacterial cellular nucleic acid synthesis
- haematopoietic cells are particularly sensitive to deficiency due to their rapid cell division
- Mammalian cells do not require the action of PABA for folic acid synthesis, but rather folate is absorbed directly through the gastrointestinal tract or following gut microbial production. In horses treated with potentiated sulfonamide antimicrobials, the lack of gut microbial folic acid production and reduced synthesis following absorption due to failure of dihydrofolate reductase result in folic acid deficiency.
- Dietary supplementation is not sufficient to prevent the clinical syndromes associated with folate deficiency (Toribio et al. 1998), as dihydrofolate reductase is required for oral absorption of folate (Zimmerman et al. 1987) and therefore do not respond favourably to oral folate supplementation.
inhibit the cellular membrane Na+/K+-ATPase,
resulting in an electrolytic disturbance that affects the
electrical conductivity of the heart
cardiac glycosides
most common autoimmune diseases in horses
- purpura hemorrhagica
- pemphigus foliaceus
ab tap findings consistent with haemoperitoneum
sanguineous abdominal fluid
elevated RBC (>20,000 RBC/ll)
WBC counts (>2500 cells/ll)
hyperproteinaemia (>2.5 g/dl)
erythrophagocytosis and evidence of nondegenerate neutrophilic inflammation
chronic colic
evidence of colic signs being observed daily for 3 or more days
causes of recurrent colic
parasites
ulcers
large intestinal obstructions
intestinal
neoplasia
small intestinal stenosis, obstruction or muscular
hypertrophy
abdominal abscess
abdominal adhesions,
chronic grass sickness
enteroliths
intra- or extra-luminal masses resulting in partial obstructions
inflammatory bowel disease (such as eosinophilic or lymphoplasmacytic enteritis or enterocolitis)
spasmodic colic
colonic displacements
…
recommended feed for horses with IBD
no hay - can have trouble with transit through thickened intestines
complete pelleted diet
high protein - 14%
high digestible fibre like beet pulp
high fat
parascaris should be assumed resistant to ____ until proven otherwise
ivermectin
where does a. perfoliata like to hang out
caecum / ileocaecal junction
where do a. mamilana and a. magna like to hang out
smallies
causes of primary abdominal abscesses in horses
corynebacterium
strep
rhodococcus
e. coli
most common mycobacterial infections in horses
mycobacterium avian spp. avium and hominissuis
GRANULOMATOUS ENTERITIS
mycobacterium spp
Confirmation of ECoV infection
- Specific ECoV nucleic acid detection in faeces by quantitative PCR (qPCR)
- demonstration of coronavirus antigen by immunohistochemistry or electron microscopy in intestinal biopsy material obtained ante or post mortem
which rhodococcal EPD’s are associated with worse survival?
uveitis
bacteremia
septic synovitis
intra abdominal abscesses
non septic polysynovitis is seen in up tp __% of foals with rhodococcus?
33%
metoclopramide is a
serotonin agonist dopamine receptor antagonist crosses the BBB prevents inhibitory effects on intestinal smooth muscle - no effect on colon
paresis
deficiency in generation of the gait (upper motor neuron) or the inability to support weight (lower motor neuron)
Abnormalities associated with abomasal obstructions
Hypochloremic hypokalemic metabolic alkalosis - sequestration of abomasal contents - ex LDA, outflow obstructions
impact of selection bias
overestimation of test accuracy, sensitivity, and specificity
impact of classification bias
Potential underestimation of index test accuracy because
the reference standard is treated as a gold standard test (even though it isn’t)
