Horses 6 Flashcards
Tricuspid valve insufficiency what murmur present, when normal and when problematic, what causes severe and clinical signs
○ Murmur PMI R heart apex
§ Usually soft, grade 2-3/6 murmur - no worried at this point
§ No obvious leaflet abnormalities
○ Tricuspid regurgitation may increase with athletic training
○ Tricuspid murmur considered problematic if ≥ grade 4/6
○ Endocarditis may be secondary to jugular thrombophlebitis (colitis - SIRS)
○ Abnormal systolic jugular venous pulsations if severe
Aortic valve regurgitation what murmur present, how lesions common, performance effect, when more problematic and effects on the heart
○ Murmur (diastolic) PMI L heart base/aortic valve
○ Degenerative lesions common, esp. older horses (second most common)
○ Often mild, normal performance (may not be able to detect of exercise)
○ More problematic if moderate-severe regurgitation, younger horses - increased risk
§ L ventricular dilation, increased aortic root diameter
Bounding arterial pulse if significant LV volume overload
Aortic valve regurgitation diagnosis and monitoring
○ Diagnosis
§ Exercising ECG if poor performance, cardiac remodelling (presence VPCs, HR for level exercise)
§ 24 hour Holter - if worried about sporadic arrythmia
○ Monitor for progression, esp. moderate-severe AR
§ Monitor for development arrhythmias
□ VPCs
□ A fib
Pulmonic valve lesions common and treatment
- Pulmonic valve ○ Acquired valvular lesions uncommon ○ Relative stenosis –NORMAL valve, murmur systolic Treatment? - Benazepril - reduce volume overload - NOT LOTS OF TREATMENT OPTIONS
Ventricular septal defect what occurs with the murmur, common causes and what can lead to
- R-sided murmur = L→R shunt (loudest)
- L-sided murmur = relative pulmonic stenosis
- Most common congenital cardiac defect
○ Most are membranous - Some breed predispositions
○ Welsh Mountain Ponies
○ Standardbreds
○ Arabians - L-sided volume overload - increase venous return from pulmonary system - left sided congestive heart disease
Ventricular septal defect diagnosis and prognosis
- Diagnosis ○ Echocardiography - Prognosis ○ Unlikely to be a successful athlete ○ Size important
Lung disease when does it affect performance and the 2 main differentials
- Lung disease resulting in no changes at rest, but affects performance
○ Large respiratory reserve - Two main differential diagnoses
○ Exercise-induced pulmonary haemorrhage (EIPH)
○ Inflammatory airway disease (IAD)
Excercise induced pulmonary haemorrhage likely mechanism, what occurs and diagnosis
- Likely mechanism
○ Rupture alveolar capillary membranes as transmural pressures increase during exercise
○ Mucociliary clearance leads to blood in bronchi, trachea
○ Epistaxis in severe cases - Breeds that perform intense exercise predisposed
- Diagnosis
○ Epistaxis associated with exercise
○ Endoscopy - MOST IMPORTANT
§ Within 30-60 minutes of racing
○ BAL
Endoscopic grades for EIPH
○ 0: no blood in upper airway, trachea or bronchi
○ 1: flecks of blood in trachea taking up < 10% tracheal surface area and extending < ¼ tracheal length
○ 2: long stream of blood taking up < 1/3 trcaheal circumference and > ½ tracheal length
○ 3: multiple distinct streams blood covering > 1/3 tracheal circumference; no blood pooling
○ 4: multiple coalescing streams blood > 90% tracheal circumference, blood pooling in thoracic inlet
BAL cytology for EIPH and treatment
○ Haemosiderophages present for ≥ 21 days
○ RBCs/RBCs in macrophages if recent (< 7 days)
Treatment
○ None specific
○ Furosemide
§ OK for training
§ Cannot be given day of race
§ Consider effects on electrolytes
○ Possible association with IAD –treat that?
○ REST
IAD what is it, diagnosis, what see endoscopically, how do you mange the horse
- Diagnosis - BAL - - non-degenerative neutrophils, mast cells, eosinophils, mixed inflammatory
- What might you see endoscopically? - tracheal mucus
Management
○ Environmental management - NOT INDOORS, feed (wet it down, less dusty, not in hay nets), increase ventilation if in a barn
○ Inhaled or systemic corticosteroids
§ Break from racing until off these medications
Arrhythmia how common, causes and are some normal
- Most common of the cardiac causes of poor performance
- May be isolated electrical disorder or secondary to other factors
○ Structural heart disease
○ Metabolic/endocrine disorders
○ Systemic inflammation
○ Hypotension, haemorrhage, anaemia, ischaemia
○ Autonomic influences
○ Toxins
○ Drugs - Some arrhythmias “normal”, especially athletes
Normal arrhythmias what caused by, the 3 main ones and when normal
- Common in athletic horses –high vagal tone - vagally mediated brady arrythmias
○ Second degree AV block - more common
○ Sinus arrhythmia - increase length between p waves
○ Sinoatrial block - Normal at rest and immediately post-exercise
- May be due to cardiac disease on rare occasions (in which case not normal!)
Second degree AV bock is it normal or pathological, HR, rhythm, auscultation and when bad
- Low-normal HR
- Regularly irregular rhythm
○ Several conducted beats before “dropped” beat - S4 alone may be auscultated at dropped beats
- Abnormal if
○ P:QRS is 2:1 or greater - dropping every other beat or multiple beats
§ “high grade”
Pathologic arrhythmias what is the main effect what is the main one and 4 others
1) Atrial fibrillation - IMPORTANT Other arrhythmias (less common) 1. Atrial premature complexes (APCs) 2. Ventricular premature complexes (VPCs) 3. Ventricular tachycardia (VT) 4. AV block ○ 3rd degree
Atrial fibrillation how common, what occurs, HR, types and cause
- Most common cardiac cause of poor performance
- Loss of organised atrial conductivity; disorganised self-sustained electrical activity
- Resting HR usually normal
- Types -> “Lone” A fib (normal structural heart - TB after racing) vs. secondary (underlying heart disease)
- Electrolyte disturbances - bicarb, frusemide
Atrial fibrillation pathogenesis short and longer term
- Reduction of CO due to ↓ SV due to loss of atrial contribution to ventricular filling (15-20%)
○ No effect at rest (high cardiac reserve) - Inappropriately high HR for level of exercise
○ Compensate for decreased SV by increasing HR
○ Exercise reduces vagal tone and allows more conduction through AV node - Cardiac remodelling occurs if A fib longstanding
○ After 3 months becomes irreversible
Atrial fibrillation common history and physical exam findings
Common history
- Poor performance at high intensity exercise
- May not affect performance at low-level exercise
- May be sudden “pulling up” during fast work
- Development of A fib during fast work
Physical exam
- Cardiac auscultation
○ “Irregularly irregular” rhythm
○ Murmur, increased HR might suggest underlying cardiac disease
○ Absence S4
- Can be paroxysmal
○ Resolves spontaneously in minutes-hours-days after exercise
○ Exercising ECG can be important to detect in these cases
Atrial fibrillation what are the 4 important tests for diagnosis and the best one
- ECG
○ Exercising ECG (Certain circumstances) - Echocardiography - ideal
○ Determine presence of underlying heart disease
§ Structural normal heart or not? - changes prognosis - CTnl
- Electrolytes
In terms of trying to get atrial fibrillation to convert what are the main considerations and ideally what should you do
○ How long has horse been in A fib?
○ Is there any underlying cardiac disease?
○ Are there other underlying causes (e’lyte, acid-base disturbances)?
§ Ensure normal electrolytes and acid-base before treatment
○ CHF –not candidate for conversion
IDEALLY - refer
What are the 2 main options for conversion of atrial fibrillation and how works
1) Quinidine
§ Class 1A antiarrhythmic drug (sodium channel blocker)
§ Prolongs action potentials and lengthens myocardial cell refractory period
2) Transvenous electrocardioversion (TVEC)
§ Deliver
§ Whole atria refractory and so sinal node takes over again
§ Reserve for horses that develop complications during quinidine OR those who don’t convert with quinidine
Quinidine for atrial fibrillation conversion, how often successful, when don’t use and the 2 main types, which most common
§ Successful conversion in approx. 80-90% cases lone A fib -i.e. likely but NOT guaranteed
§ Don’t use if: complex VPCs, rapid ventricular rate, CHF
§ Types
1. Quinidine gluconate (IV) –only if A fib known to be < 2 weeks duration
® NOT IN AUS
2. Quinidine sulfate (via NGT) - most common- IMPORTANT
Quinidine sulfate for atrial fibrillation conversion, how to give, when stop, what monitoring for and common signs seen through treatment
® Repeat q 2 hours until convert to sinus rhythm –then STOP
® If no conversion after 4 treatments↓ frequency to q 6 hours
If signs of toxicosis develop –STOP!
Monitoring essential
◊ Heart rate
◊ ECG (ideally continuous) - or give ECG prior to give second dose (don’t want to go into ventricular tachycardia)
◊ Plasma quinidine concentrations
◊ Signs of toxicosis
® Commonly seen during quinidine treatment - NOT SIGNS OF TOXICOSIS
◊ Dull mentation
◊ Paraphimosis
What are the main signs of qunidine toxicosis
- Diarrhoea
- Ataxia
- Weakness
- Colic
- Anorexia
- Tachycardia
- Laminitis
- Nasal oedema
- Sudden death! Rare
- Prolongation of QRS > 25% baseline
- Development other arrhythmias (SVT, VPCs, VT)
- Plasma quinidine concentration > 4 μg/ml
Atrial fibrillation what to do post successful conversion and prognosis
After successful conversion ○ Rest (minimum one week) ○ Gradual return to work ○ Regular monitoring of HR and rhythm Prognosis - Depends on: ○ Presence underlying heart disease § 95% recurrence within short time period ○ Duration of A fib (cardiac remodelling) ○ How many times gone into A fib § The more you go into the more - Young racehorses with lone A fib have best prognosis
Atrial premature complexes what also called, how common, performance issues, diagnosis and treatment
supraventricular complexes SAME THING) ○ Occasional APCs occur not uncommonly ○ Rarely cause of poor performance if no underlying heart disease Diagnosis ○ Auscultation ○ ECG ○ Check for underlying heart disease § Echo § CTnI (Cardiac troponin) ○ Exercising ECG § Most disappear with exercise Treatment often not required § May need to treat underlying heart disease if present ○ Risk for A fib
Ventricular premature complexes what associated with, can lead to and when cause for concern
○ Most often associated with other disease
§ May be due to primary cardiac disease
○ Runs VPCs = ventricular tachycardia
○ Isolated VPCs common when HR slowing after exercise
○ VPCs during exercise
§ Cause for concern
§ May occur in normally performing horses
§ Further research needed…
Ventricular premature complexes what are the 6 ways to diagnose and expected results
- Auscultation - –premature beats interrupting an otherwise regular rhythm. VT –usually regular, rapid rhythm
- ECG - abnormal QRS with no preceding P wave. Wide bizarre QRS with abnormally large T wave of opposite polarity. Compensatory pause = sinus impulses often blocked at AV node
- Exercising ECG - VPCs should be overridden by exercise. DO NOT DO EXERCISING ECG IF SEVERE ARRHYTHMIA –e.g. VT
- Echo (underlying heart disease) - Echo if increased CTnI, murmur detected or arrhythmia persists
- CTnI
- Electrolytes, blood gas
Ventricular premature complexes and ventricular tachycardia when treat, with what and when can go back to work
§ Underlying heart disease/other body system disease
§ Ventricular Tachycardia
□ Treatment indicated if: - increased risk of ventricular fibrillation
® HR > 100-120
® Multiform VT - different shapes of QRS - multiple ventricular premature complexes
® R on T
□ Treat with
® Magnesium sulfate(50 mg/kg = 25 g/500 kg horse)
® Lidocaine (1.3 mg/kg bolus followed by 0.05 mg/kg/min CRI)
□ Implications for work?
Another ECG performed before back into work
Myocardial disease cause, when may be normal, what may auscultate and diagnosis
- Causes poorly understood ○ Toxic ○ Inflammatory ○ Necrosis ○ Fibrosis ○ May follow other disease (e.g. viral disease) ○ Nutritional ○ Neoplastic - If mild, may be normal at rest - May auscultate arrhythmia, murmur - Diagnosis ○ ECG ○ Echocardiography ○ CTnI - INCREASE - KNOW THERE IS MYOCARDIAL DAMAGE
Ionophore toxicosis leading to myocardial damage what toxins, how cause damage and when generally seen
- Monensin, salinomycin, lasalocid
- Direct myocardial damage
○ Cell death
○ Fibrosis
○ Arrhythmia
○ Poor contractility - Na+ and K+ transport across membranes inhibited → mitochondrial failure, ↓ ATP activity, ↓ Ca+ availability
- Results in hypercontractility, cellular necrosis, eventually CV system failure and death
- May be seen in outbreaks (contaminated common feed source)
Ionophore toxicosis leading to myocardial damage clinical presentation and diagnosis
Clinical presentation depends on dose ingested ○ Skeletal muscle may be involved § Myoglobinuria § Increased CK, AST ○ Recumbency, collapse, death ○ Arrhythmias Diagnosis (field) ○ History ○ Clinical signs ○ Feed analysis ○ CK, AST; CTnI ○ Myoglobinuria ○ ECG ○ Post mortem - pale myocardium, subendocardial haemorrhage, myocardial necrosis
Ionophore toxicosis leading to myocardial damage treatment
Treatment
○ None specific
○ Seek specialist advice, but stress induced by transport to a hospital might exacerbate signs
○ Supportive - hoping heart will recover itself
§ Activated charcoal
§ Correct electrolyte abnormalities
§ Rarely successful
§ Digoxin contraindicated - increase contractility bad
Ionophore toxicosis leading to myocardial damage prognosis and management
- Prognosis
○ Guarded if clinical disease is apparent or contractility affected - Management of survivors
○ Strict rest
○ Thorough cardiac evaluation before gradual return to work
What are some other toxicoses that lead to myocardial damage
- Toxins and their metabolites that interfere with beta-oxidation (if in negative energy balance - cannot metabolise fatty acids - muscles die)
○ Hypoglycin A (seasonal pasture myopathy/atypical myopathy)
○ Cyclopropene fatty acids –found in many plants, common weeds (marsh-mallow) - Skeletal and cardiac muscle affected - can have cardiomyopathy
- Negative energy balance
What are the 5 main mechanisms of weight loss
1) decreased intake of nutrients
- good appetite OR reduces desire to eat
2) Maldigestion.malabsorption
3) inappropriate utilisation of absorbed nutrients
4) increased requirements for nutrients
5) increased losses of nutrients
Good appetite leading to weight loss what are the 3 main causes
1) Protein/energy malnutrition - reduced nutrition available to horse
□ Inadequate quantity of feed, quality of feed or access to feed
- Herd dynamics (competition), musculoskeletal disease (neck pain, laminitis), neurologic disease (flavivirus)
2) Dysphagia and dental disease (uncommon to cause PHYSICAL obstruction) - reduced ability to consume available to feed
- problem with prehension, mastication, deglutition - due to neurologic, pain and physical/musculoskeletal obstruction
3) Stereotypes - horse diverted away from eating -> wind sucking
Prehension nervous control and clinical signs with issues
® Voluntary control ◊ Cranial nerve 7 : Facial nerve } Muscles of facial expression (lips) ® Clinical signs - Ptyalism, dropping feed, head tossing, exaggerated head movements, submerging head in feed/water
Mastication nervous control and clinical signs with issues
® Voluntary control
◊ Cranial nerve 5 : Trigeminal N.
} Masticatory muscles : masseter, temporalis, digastricus.
® Clinical signs
◊ Ptyalism, prehension with no chewing attempts, exaggerated chewing movements, reluctance to open mouth, holding or packing feed into the oral cavity, dropping feed
Deglutition what are the 2 phases, nervous involved and what occurs
1) Part 1: Pharyngeal phase
◊ Involuntary reflexes
} Cranial nerve 9 & 10 : Glossopharyngeal & Vagus
◊ Ingesta bolus propelled by constrictor muscles of pharynx into relaxed upper oesophageal sphincter
2) Part 2: Oesophageal phase
◊ Involuntary reflex
} Cranial nerve 10 : Vagus N
◊ Primary peristaltic waves initiated by closure of cricopharynx
Reduces desire to eat leading to weight loss causes and most common
§ Gastric ulceration - VERY COMMON □ Squamous vs glandular § Chronic pain § Systemic illness § Advanced renal disease □ Intrinsic renal □ Nephrolithiasis, urolithiasis § Unpalatable food
Maldigestion leading to weight loss causes and most common cause
1. Dental disease - COMMON □ Physical act of mastication -> break down FIRST STEP OF DIGESTION 2. Gastrointestinal dysfunction □ Gut flora imbalance/diarrhoea □ Secondary lactose intolerance 3. Chronic liver disease 4. Pancreatic disease - NOT COMMON
Malabsoprtion leading to weight loss causes and most common
§ Infiltrative GI disease (can have a reduced appetite as well)
□ Inflammatory cells
® Primary: IBD - lymphocytes, eosinophils, macrophages
® Secondary: colitis, parasites, flora imbalance, sand, infectious, toxins (NSAID) - right dorsal colitis
□ Neoplastic cells - lymphoma
§ Parasites - COMMON
□ Larval cyathostomins
® Physical obstruction
® Inflammation
Inappropriate utilisation of absorbed nutrients leading to weight loss 4 causes
a. Inappropriate processing § Chronic hepatic disease § Neoplasia § Metabolic/endocrine disease □ PPID, hyperthyroid (VERY RARE - cancer common BUT GENERALLY ALWAYS BENGIN) b. Advanced renal disease c. Redirection of nutrients § Neoplasia § inflammatory conditions □ Focal (Abscess) □ Diffuse (body cavity) Advanced cardiac disease
Increase requirements for nutrients leading to weight loss physiologic and pathologic causes
○ Physiologic § Intense exercise - increase basal requirements by 2 § Pregnancy (final trimester) § Lactation § Breeding (stallion activity) § Environmental conditions (cold) ○ Pathologic § Stereotypes - box weaving (moving head back and forth in the stall) § Inflammation □ Focal abscess, diffuse (body cavity) § Neoplasia § Pain § Immune mediated disorders § Dyspnoea (RAD - recurrent airway obstruction), Rhodococcus equi) □ Taking so much energy JUST TO BREATHE
Increased losses of nutrients leading to weight loss 5 causes
a. Gastrointestinal tract § Protein losing enteropathy § Diarrhoea § Parasites § Sand b. Losses into body cavities c. Renal loss § Protein losing nephropathy d. Cutaneous losses § Burn injury § Extensive wounds e. Miscellaneous Inflammatory diseases
What are the 3 most common causes of weight loss
- Dental disease - induced maldigestion (NOT reduced appetite or dysphagia)
- Diet inadequate to caloric requirements
- Gastrointestinal parasitism
Multiple concurrent contributing factors
What are key features to ask during history of a weight loss case
- Horse usage
○ Exercise, breeding, pregnancy, lactation - Housing and environmental conditions
○ Herdmates – environment or individual problem - Feeding protocol
○ Composition (quantity, quality), frequency, location, competition - Feed intake
○ Observed problems with prehension, mastication and deglutition - Medical history
○ Medications administered (NSAIDs, Abx)
○ Previous illness, colic, colic surgery, respiratory disease… - Preventative health care practices
○ Anthelmintics
○ Dentistry – lay dentist or veterinarian
○ Vaccinations - Management changes
- Problems other than weight loss
○ Concurrent problems = concurrent diseases
What are the key features of the physical exam for a horse with weight loss
- Indication of a primary disease from history
- Signs of systemic disease
○ Demeanour, fever - Oral exam
○ Tongue, teeth, oral cavity (foreign body, abscess) - Observe eating
○ Prehension, mastication, swallowing - Auscultation:
○ Cardiac, respiratory, gastrointestinal - Examine faeces :
○ Consistency (diarrhoea), (parasites), sand - Abdominal palpation per rectum
- Any chronic painful conditions that limit mobility
○ e.g. laminitis, cervical pain - Body condition scoring (1-9)
Diagnostic testing for weight loss initial evaluation what included
- Guided by any preliminary perspectives ○ e.g. respiratory disease, cardiac disease… - Ration evaluation ○ Proximate analysis - Minimal lab database: ○ CBC – inflammation § ± Infection § Acute phase proteins ○ MBA (Hepatic, renal and immune systems, protein quantitation) - Faecal examination ○ Quantitative parasite flotation (McMasters) – Questionable utility ○ Occult blood ○ Sand
Weight loss case what further investigation may need to occur
- Ultrasound : Abdomen, thorax
- Urinalysis
- Abdominocentesis
- Tests of small intestinal absorption function
○ oral glucose/D-xylose absorption - Endoscopy – Guttural pouches, pharynx, oesophagus, gastroscopy
- Radiography – abdomen – sand, stones
- Endocrine testing – Basal ACTH (PPID)
- Biopsies
○ Transcutaneous (spleen, liver, kidney)
○ Intestinal
§ Trans-endoscopic (proximal duodenum – very superficial)
§ Rectal mucosa (often poorly representative)
§ (Exploratory laparotomy – full thickness, multiple locations)
○ Laparoscopy
○ Exploratory laparotomy (biopsies, masses etc) - Laparoscopy – visualisation, biopsies
- Exploratory laparotomy (biopsies, masses etc)
Chronic colic causes the 5 main ones and the most common
- Same causes as weight loss
1. Decreased intake of nutrients - VIA REDUCED DESIRE TO EAT (not good appetite)
2. Maldigestion and malabsorption
3. Inappropriate utilisation of absorbed nutrients
4. Increased requirements for nutrients - PATHOLOGICAL ONLY
5. Increased losses of nutrients
Number 1 - Sand colitis and enteroliths (ONLY ONE THAT DOESN’T RESULT IN WEIGHT LOSS AS WELL)
what measuring with rectal temperature
- Fever vs hyperthermia
○ Alteration in hypothalamic set point vs imbalance between heat generation and heat dissipation
§ Inability to rid body of excess heat
§ Evaporation, Radiation, Conduction, Convection. - Fever = inflammation
○ Fever hunt = inflammation hunt
○ Infectious and non-infectious inflammation
Fever of unknown origin diagnostic investigation
- Respiratory tract - lung, parenchyma, airways - pneumonia
- Pleural cavity
- Inside GIT
- Peritoneal cavity
- Other abdominal organs - liver, spleen, lymph nodes, pancreas (not common)
- Skin and subcutaneous
- Cardiovascular system - RBC, WBC, myocardium, valves, blood vessels
- Cranial nervous system - brain, CSF
- Musculoskeletal system (muscle, lig/tendon, bone)
- Genital system (penis, accessory glands, testes, uterus, udder)
- Urinary system (kidney, ureter, bladder, urethra)
Euthanasia considerations and what need to be
- Sedatives
○ Slow heart down - will go down quickly
○ Use ace as sedative - Barbiturate
○ Large amount with large catheter - large needle
○ Have the multiple syringes ready - Firearm
- Safety. Safety. Safety.
- Assistants vs Onlookers?
○ NOT CLOSE - Disposal of the body
○ 6 feet down
○ Knackeries generally WILL NOT take barbiturate euthanised horse - Cost
○ Knackeries may charge - Behaviour during - PREPARE FOR WORST CASE SCENARIO
○ Defecate, urinate, whinny, may move - gallop
○ Stay away until completely convinced will not move
Normal PE finding and haemtology and biochem - bright and alert with poor appetite differentials
- Gastric ulceration - squamous, glandular
- Infiltrative bowel disease
○ Neoplastic and inflammatory cells
§ Inflammatory leukogram
THINKING - Inflammatory bowel disease or cancer - Parasites - encysted small strongyles
- Sand (but not in history)
- PPID - endocrine disease
- Chronic pain - severe musculoskeletal disease (not lame)
What are the 3 main reasons antimicrobials are indicated
- When there is high suspicion or confirmation of bacterial infection
- When there is high risk of bacterial infection developing
- When it is considered unlikely that the infection will resolve without antimicrobial treatment
Case - Banjo - 10 month old Thoroughbred colt - Routine castration - Physical examination normal Does Banjo need peri-operative antimicrobials?
- No - most don’t develop infections - AS LONG AS HYGIENE GOOD
Case 3
- 3 yoThoroughbred racehorse
- Elective arthroscopy to remove an osteochondral fragment from the right carpus
Does Superfast need peri-operative antimicrobials?
- No? - depends on the person definitely not passed 12 hours
Case - Boris - 12 yo Standardbred gelding - Laceration over upper radius - Dirt present all over laceration - Muscle exposed, some bone - No synovial structures involved Does Boris need antimicrobials?
- No? - different between infection and contamination - ensure clean out properly
○ If synovial structure involved then YES
How to decide which antimicrobials to choose and when don’t do
- Ideally decision made based on C&S results
- Two scenarios when empirical treatment given
○ Life-threatening infection
§ No time to wait for C&S
○ Minor infections treated in the field
§ Do C&S ONLY if treatment unsuccessful
○ Surgical prophylaxis
What are the 7 main considerations when choosing an antibiotic
- Likely organisms involved
○ Gram stain can help in interim
○ Intracellular organism?
○ Anaerobic vs. aerobic? - Likely susceptibility patterns of these organisms
○ G+vevs. G-ve, anaerobes - Site of infection
○ Organ system, abscess
○ Do we need an antimicrobial that maintains good activity in particular environment (acidic/purulent)
○ Concentrations achieved in different organ systems - Severity of disease, immune function
○ Do we need something cidal or static? - Toxicosis
○ Does our horse have organ system disease that could lead to toxicosis? - Owner compliance
○ How frequently and by which routes, can the drug be administered - Stewardship
Don’t pull out the big guns straight away
pleuropneumonia what antibiotic do you wnat
- Can’t wait for C&S (takes ≈ 48 hours)
- Take samples prior to treatment - if even treated - CULTURE
○ Broad spectrum (strep most likely cause)
§ G+ve, G-ve, anaerobes
○ Ideally has good penetration into infected tissue
§ But will drain pleural fluid, lung abscessation not obvious
○ Bactericidal
§ Severe disease
○ FIRST TIER
Pleuropneumonia what antibiotic would you give and what if not susceptible to
- First line
- Penicillin (Gram positive, aerobic) + gentamicin (gram negative, aerobic) - STOCK STANDARD FIRST LINE FOR HORSES
○ Can add metronidazole (better penetration - if think anaerobe - can also wait for culture)
§ Can lead to inappetence - Not enrofloxacin - doesn’t get streptococcus
- If not susceptible to penicillin
○ Give TMS - still need broad spectrum
what is the difference with giving antibiotics to horses compared to small animals
○ We often start with broad spectrum antimicrobial coverage
○ The consequences of getting it wrong can be severe
○ We don’t typically give antimicrobials for colitis
○ We have to avoid certain antimicrobials that are particularly disruptive to hindgut flora
○ Cost of treatment is a greater factor to consider
How to know how long give antibiotic for
- Duration of antimicrobial courses can be difficult to determine
- Base on:
○ Response to treatment
○ Improvement of clinical signs
○ Improvement/normalisation of clinicopathologic data
○ Empiric decision (minor infections) - Monitoring is essential
what what situations should certain antimicrobials be avoided or are contraindicated
- Organ system disease
○ Liver –rifampin, consider effects of elimination of drugs metabolised by the liver
○ Kidney –aminoglycosides, oxytetracycline
○ Neuromuscular disease –aminoglycosides - Age of patient
○ Macrolides in adult horses (antimicrobial-associated colitis) - NO
○ Enrofloxacinin foals - NO - Physiologic state e.g. pregnancy
○ TMS in early pregnancy? - worry - Previous hypersensitivity reaction
- No good rationale for use
What are 6 ways to minimise bacterial resistance
- By only treating with antimicrobials when necessary
- By treating with appropriate antimicrobial regimens
- By ensuring owner compliance with treatment
- By performing C&S testing
- By not over-prescribing
- By preventing bacterial disease
○ Hygiene!!!!
