Hind limb lameness – immature Large breed dog

Approach to lameness

  • Hip dysplasia
  • Osteochondrosis
  • (Patellar luxation)
  • (Cranial cruciate ligament disease)
  • Other causes
  • –      Metaphyseal osteopathy
  • –      Nutritional secondary hyperparathyroidism


Approach to the lame dog

  • What are you trying to achieve?

–      Why is the dog lame? Dx

–      Txt & prognosis

  • How are you going to get there?
  • History

–      Onset (acute or chronic, inciting cause?), duration, progression, previous lameness, response to any previous tx, general health

–      History and signalment guide you towards diagnosis


Approach to the lame dog

General physical examination

Orthopaedic examination

  • Systematic
  • Lameness (yes, no, maybe),  severity, which leg(s)
  • Muscle atrophy
  • Joint effusions, fibrosis, range of motion, crepitus, instability, PAIN
  • Bone pain
  • Neurological abnormalities
  • Findings guide you towards diagnosis and focus further investigation


Hip dysplasia

  • Developmental disease
  • Laxity and secondary osteoarthritis

–      Both cause pain and lameness

–      Laxity source of pain in immature dog, OA in adult dog (combination)

bilateral hip dysplasia dog arthritis

Aetiology – genetic and environmental factors


How does a dog with hip dysplasia present?

  • Often characteristic gait – swings pelvis from side-to-side
  • Lameness may be uni or bilateral
  • Difficulty rising
  • Audible click / clunk
  • Poor muscle mass of hindlimbs

Are there characteristic orthopaedic exam findings?

  • Pain on hip extension

Hip dysplasia How are you going to confirm the diagnosis?

1.  Radiography under sedation

  • Ventrodorsal extended
  • Lateral

2.  Palpation under sedation

  • The Ortolani test


BVA/KC Hip Scoring Scheme

Hip dysplasia diagnosis – beyond the basics

  • Orthopedic Foundation for Animals hip grading system (www.offa.org)
  • Has recently been compared to PennHip:



  • Conservative management

–      Usually considered first

  • Surgery

–      Reduce degree of hip laxity – pelvic osteotomy or pubic symphysiodesis

–      Salvage procedures – joint excision or prosthesis

What do you need to know?

  • Good understanding of conservative management
  • Awareness of surgical options and when they are appropriate


Conservative management

  • Bodyweight and body condition
  • Non-steroidal anti-inflammatory drugs
  • Low impact exercise / physiotherapy
  • Neutraceuticals / alternative therapies
  • Beneficial to maintain slender body condition
  1. Bodyweight and body condition

–      Reduces lameness in dogs with HD and OA

–      Reduces development of HD in genotypically predisposed dogs


  1. Non-steroidal anti-inflammatory drugs
  • Many different ones out there
  • E.g. meloxicam, carprofen, firocoxib
  • Differences in COX selectivity
  • Good evidence to support efficacy
  • Mainstay of osteoarthritis treatment in dogs
  • Possible side effects – gastrointestinal, renal


  1. Low impact exercise / physiotherapy
  • For example swimming
  • Not much evidence other than opinion to support this
  • Still worth discussing with owners / adding to treatment plan
  • Polysulfated glycosaminoglycans (PSGAG)
  • Semisynthetic product structurally similar to GAG
  • Stimulate collagen synthesis, inhibit breakdown in vitro
  • Some (limited) evidence to support improvement in lameness in dogs with HD and OA
  • Diets
  • Omega 3 fatty acid (fish oil) supplemented foods (e.g. Hills® J/D)
  • Increasing tissue levels of omega 3 FA decreases levels of omega 6 FA and overall effect is to suppress inflammation
  • Evidence supports use of these diets in dogs with OA, including hip OA
  • Acupuncture
  1. Neutraceuticals / alternative therapies


Surgical options – decreasing joint laxity

1.  Triple pelvic osteotomy

  • Not for everyone- generally less than 1yr old
  • They have a positive Ortolani sign
  • With no radiographically obvious secondary OA
  • Hip OA will still progress post operatively
  • Performed in puppies 12-20 weeks old
  • W/ radiographic abnormalities not CS
  • Premature closure of pubic symphysis induced by electrocautery
  • Usually combined with neutering procedure
  • Not well established in UK
  1. Juvenile pubic symphysiodesis


Surgical options – salvage

  1. Femoral head and neck ostectomy
  • Eliminates contact between femoral head and acetabulum = ↓discomfort
  • Pseudoarthrosis (false joint) forms
  • Limb function should improve but will probably never be normal
  • Better results in smaller dogs
  • Consider as “plan C” for hip dysplasia i.e if all else fails and dog is not a candidate for THR

–        Aim for complete removal of head and neck

  • Performed through craniolateral approach
  • Straightforward surgery
  • Useful technique for other conditions e.g. Perthes’ disease, hip luxation salvage – in practice


  1. Total hip replacement
  • Replacement of diseased hip with prosthesis
  • Better function than FHNO, best option for large breed dogs
  • Much more technically demanding procedure
  • Much more expensive
  • Risk of significant complications
  • Good outcome if all goes well
  • Cemented and cementless systems available
  • Micro systems available for toy dogs and cats
  • Potential complications include luxation, infection and fracture
  • Referral procedure



Osteochondrosis dissecans in the hindlimb

–        Young dog.

Osteochondrosis dissecans

  • Disorder of endochondral ossification
  • Affects articular cartilage surface
  • Dissecans describes formation of a cartilage flap
  • Secondary osteoarthritis will develop
  • Stifle – femoral condyles (lateral usually)
  • Tarsus – trochlear ridges of talus (medial usually)
  • Hip – uncommon but can affect femoral head



  • Lame young (4-8 months) large breed dog
  • Affected joint is effused and painful
  • Radiographically look for defect in articular surface


1. Conservative management – most appropriate where OA is already advanced

2. Removal of cartilage flap by arthrotomy or arthroscopy

–      Removes source of inflammation and discomfort

–      Defect heals by fibrocartilage formation

–      Clinical outcome better for some joints than others

3. Osteochondral grafts are now being explored

  • Cores of cartilage and bone harvested from non-weightbearing regions
  • Implanted in OCD defect
  • Cartilage and bone become integrated in new location
  • Initial results encouraging



patellar luxation in large breed dogs

  • Why is the patella luxating?
  • Tibial or femoral deformity?
  • Need to correct deformity
  • Referral situation


Cranial cruciate ligament disease

  • Increasingly common in skeletally immature dogs
  • Treatment options may be more limited
  • Useful to be able to differentiate “puppy” from pathological cranial drawer- Puppy drawer has a distinct “end point”

Cranial cruciate ligament disease

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Veterinary public health review

Category 1- stained Patent blue V

  • all SRM-  Specific risk material
  • entire bodies of dead animals and carcases
  • all body parts (incl hides) of animals suspected or confirmed as having TSE
  • All material (cludge) collected from waste water in ruminant slaugterhouses
  • animals killes as TSE eradication measures
  • others: e.g drugs not licences

Category 2 (medium risk)- stained Black PN or Brilliant black BN

  • Animal by products not included in 1 or 3. 
  • e.g post mortem rejects with lesions indicating disease communicable to man or animals e.g septicaemic carcases
  • sludge from 6mm waste water non ruminant slaughter house
  • products containing residues of veterinary drugs and contaminants
  • animals and part of animals that die other than being slaughtered for human consumption (unless cat 1)
  • manure and digestive tract contents
  • blood from any animal that has not passed ante mortem inspection
  • imported material from 3rd countried that does not comply with GB requirements

Category 3 (low risk)

  • parts of animals passed as fit but not going for human consumption – pet food
  • parts of animals rejected as unfit but no risk to humans or animals (carcase passed)
  • e.g fluke liver
  • blood from ruminants that pass meat inspection
  • hides, skins etc
  • foodstuff containing meat no longer intended for human consumption

Exemption from staining:

  • category 3 by products
  • blood
  • entire body (except poultry- black)
  • products for examination or scientific purposes
  • manure and digestive content


  1.  approved incinerators, renders, intermediate plants
  2. as above + manure to land, gut room waste to non pasture land
  3. as above + petfood plants, technical plants, biogas plants and taneries.

can also go to diagnostic, educational and research purposes + taxidermy
Most types of cat 2 & 3:
– feeding to zoo and circus animals
– feeding to reptiles or birds of prey
– treatment at approved collection centres for feeding to hound packs, maggot farms etc

Please click on the link for a PDF review of some common clinical findings at the abattoir:

PAPH review practical

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Antimicrobial Pharmacology


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GI Pharmacology


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Analgesia pharmacology


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How antibiotics act selectively against bacteria

How can antibiotics act selectively against bacteria? Why may antibiotics have no effect on bacteria? Describe the main bacterial antibiotic resistance mechanisms.
Antibiotics are selectively toxic against bacteria because bacteria differs greatly from human cells, mainly the bacteria have cell walls that for the outer boundary of the cell. The type of wall a bacterium has is one factor that determines which antibiotic can kill it. Some antibiotics selectively kill either gram positive bacteria or gram negative bacteria (narrow spectrum) eg. Vancomycin that selectively kills gram positive bacteria like staphylococcus, streptococcus and enterococcus. Broad spectrum antibiotics will kill gram positive and negative, but no antibiotic can kill all bacteria. the sites of action of main antibiotics include peptidoglycan synthesis (beta lactams- causing the bacteria to lyse), protein synthesis, nucleic acid synthesis, biosynthesis of folic acid (starve bacteria), DNA replication, transcription and cytoplasmic membrane integrity.

Gram negative bacteria have less peptidoclycan in their cell wall and are more antibiotic resistant than gram positive bacteria. Some of the bacteria might no have an effect on the bacteria unless they are combined with an antibiotic that breaks down the cell wall, because they wont get into the bacteria to have their effect. E.g. sulphonamides, aminoglycosides, tetracylines, cloramphenicols and Linchosamides,macrolides. Efflux pump pumping these out of the bacteria will also be an important reason for developing resistance.

There are resistance genes that inactivated antibiotics.
Hydrolysis that inhibit Beta lactams with beta lactamase occurs in both gram negative and positive bacteria. Penicillin G has a huge resistance and there is therefore need to develop beta lactamase resistant  beta lactams like methicillin. One can also give beta lactamase inhibitor.
Chemical modification: aminoglycosisdes or chloramphenicols are altered so that its prevented to bind to its target site.
Active efflux pump will actively pump antibiotics out of the cytoplasma so that it cant reach its target site.
Alteration of the target site can happen if aquires a gene for altered penicillin binding protein from another organism like MRSA. Macrolides are chemical mediators of antibiotic binding sites with reisitance enzyme methylate 2 adeninne which prevent antibiotic binding.
Metabolic byplass can happen when the plasma codes variance of enzymes giving a lower affinity to the antibiotic. This occurs with suphonamides and trimethoprim.

sometimes the resistance is gene is passed on to clinical bacteria. Evolution of multi R plasmid will help transmit resistant genes to different bacteria. S.typhimuruim was an example of a clone that is multi-resistant to antibiotics, its now banned

Discuss how antibiotics can interfere with peptidoglycan and protein biosynthesis. Discuss why antibiotics may have no effect on bacteria.

Peptidoglycan is in the bacteria cell wall causing rigidity and strength due to the peptide bonds. It causes the cell wall of the bacteria and protects it, because the bacteria will lyse without it. (except for a few.e.g mycoplasma). Peptidoglycan will grow outside the membrane but synthesis precursors in the cytoplasm and transport the precurors across the cell membrane by specific transport proteins. Glucopeptides will inhibit the action of the precursors to the peptidoglycan. Beta lactams will inhibit cross linking (e.g. penicillin).   Penicillin and cephalosporins compromises the largest and most important class of antibacterial drugs which inhibit cell wall synthesis.  Whilst a number inhibit protein synthesis. Aminoglycosides bind to 30s ribosomal subunit and affect a number of different steps in protein synthesis. Macrolides inhibit protein synthesis by inhibiting 50s ribosome subunit. Drugs which act synergistically including sulponamides and trimethorprim act at two different sites in the folic acid pathway, and clavulanic acid and penicillin combination inhibit beta lactamase activity and therefore prevent the inactivation of penicillin.

Beta lactam antibiotics involved binding to the receptor known as penicillin binding protein and cause the bacteria to lyse by interfering with the crosslinking of peptidoglycan in the cell wall of the bacteria. Bacteria which produces beta lactamases are resistant to beta lactam antibiotics because beta lactamase cleave the beta lactams rings, rendering the antibiotic ineffective. These enzymes may be plasma mediated, as in staphylococci, or they may be chromosomally encoded as in gram negative bacteria. Resistant genes can be transferred between bacteria through transduction, conjugation, transponsable elements or transformation. Resistance to an antibacterial agent often results in cross resistance to other agents in the same plass. Mechanisms producing resistance to antibacterial drugs include production of enzymes by bacteria which destroy or inactivate the drug and reduction of bacterial cell permeability. Bacteria may also develop alternative metabolic pathways to those inhibited by the drug. The antibiotic may be eliminated from the cell(efflux pump), or the target site of the drug might be structurally altered. Bacterial resistance is widespread and control measures are being put into place to prevent the resistant bacteria reaching the human populations. This will most often result in the antibiotic class being banned for use in animal.

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Staphylococci are gram +ve cocci that form irregular bunches of cocci that resembles bunches of grapes. They occur as commensals of skin and mucosa, and some act as opertunistic pathogen causing pyogenic infections. Staphylococci are non motile and catalase positive. They do not form spores and is stable in the environment.


In the laboratories staphylococci are represented by opaque and rich creamy colonies. One can do a catalase test to distinguish staphylococci from streptococci. Staphylococci are resistant to bile salts and therefore grow on macconkey agar. Staphyolococci will grow on simple media (nutrient agar) and survive well in the environment outside the host. Staphylococcus make cytokines so some will produce a diffuse zone incomplete beta haemolysis.

Staphylococci diseases in domestic animals include mastitis, tick pyaemia, exudative epidermitis, botryomycosis and pyoderma.  There are a lot of different species, most important in the veterinary field is S.aureus which is the most important of pathogens and has the widest host range. S.aureus is the most common cause of mastitis in cattle, but can also cause thick pyaemia in sheep and dangerous dermatitis in poultry. S.pseudintermedius cause pyoderma I n dogs. S.hyicus cause exudative epidermis in pigs (greasy pig disease) or s.epidermidis cause skin commensal in all species.

Staphyolococci has a range of virulence factors to help them avoid the host immune system and maintain in the host. Coagulase will prevent phagocytosis. Protein A bind to Fc portion of IgG to inhibit opsonization and produces a capsule.  Leukocidin will destruct the phagocytes of some species. Alpha and beta toxins will demage cells. Exfoliative toxin will cause desquamation (scaly skin syndrome in humans). And enterotoxins which is a heat stable toxin.


For the majority the pathogenesis is multifactorial so its is difficult to determine precisely the role of any given factor. However there are correlations between strains isolated from particular diseases and expressions of particular virulence determinants that suggest the role they had. Normally the host response to staphylococci is inflammation with swelling, accumulation of pus and necrosis of tissue. Around inflamed areas fibrin clots might form, walling off the bacteria and leukocyutes as characteristic pus filled boil or abscess. If the bacteria invade the blood stream this could cause septicemia which might be fatal. Bacteremia may result in seeding other internal abscesses, other skin lesions, or infections in the lung, kidney , heart, skeletal muscles or meninges.

Binding of the Fc portion of antibody to protein a will interfere with phagocytosis. because it binds the wrong way around which interferes with phagocytosis and therefore its not able to bind to white cell receptors. Staphylococcus have a molecule that has complement inhibitor (SCIN) which will inhibit all complement activation pathways. By producing a capsule it prevents the cell interacting with white cells and therefore wont be opsonized and phagocytosed.  Fibrinogen binding protein are surface bound proteins that inhibits opsonisation (hiding it from phagpcytosis)

Haemolysins and leukocidin toxins are produced  to kill (lyse) or inhibit phagocytosis.

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