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Inflammation and Infection Flashcards

1
Q

What are the 5 cardinal signs of Inflammation?

A
  1. RUBOR- redness
  2. CALOR- heat
  3. DOLOR- pain
  4. TUMOUR- swelling
  5. FUNCTIO LAESA- loss of function
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2
Q

What is the initial phase in inflammation and what follows it?

A
  • VASCONSTRICTION
  • followed then immediate VASODILATION and INCREASED VASCULAR PERMEABILITY
  • further events include** LEUKOCYTIC MARGINATION** and EMIGRATION of NEUTROPHILS/MONOCYTES
  • PHAGOCYTOSIS - intracellular degradation of ingested particles and extracellular release of leukocyte products e.g .lysosomal enzymes
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3
Q

Describe what happens when bacteria envade the musculoskeletal system?

A
  • The inital response is an acute inflammatory reaction with phagocytosing of bacteria
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4
Q

What are the 3 outcomes to acute inflammation?

A
  1. COMPLETE RESOLUTION
  2. HEALING BY SCARRING
  3. PROGRESSION -> CHRONIC INFLAMMATION
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5
Q

Why does chronic inflammation occur?

A
  • Persistent infection by intracellular microbes that are of low toxicity but evoke an immunological reaction
  • Prolonged exposure to non degradable but potentially toxic substance ( e.g. lung silicosis/ abestosis ) and immune reactions ( particuarly autoimmune)
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6
Q

What are the key cells in chronic inflammation?

A
  • Mononuclear cells- principally MACROPHAGES , lymphocytes, plasma cells
  • Fibroblasts and eosinophils (in immune reactions)
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7
Q

Macrophages are activated in inflammation how?

A
  1. By Lymphokines ( e.g. gamma-interferon) produced by immune-activated T cells or
  2. non immune factors such as EXOTOXINS
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8
Q

What do the secretory products of macrophages induce?

A
  • Induce the characteristics of chronic inflammatory change such as
    • TISSUE DESTRUCTION - Protease and o2 derived free radicals
    • NEOVASCULARISATION- growth factors
    • FIBROBLAST PROLIFERATION- ( growth factors)
    • CONNECTIVE TISSUE ACCUMULATION- IL1, TNF-ALPHA
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9
Q

What is the role of lymphocytes in chronic inflammation?

A
  • Activated lymphoyctes produce lymphokines esp gamma- interferon are major stimulators of macrophages
  • activated macrophages produce monokine which in turn influence B and T cell function
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10
Q

What are bacteria?

A
  • PROKARYTOIC CELLS- as they have no NUCLEUS
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11
Q

Where do bacteria keep their genetic material ?

A
  • In the NUCLEIOD ; an area of the CYTOPLASM
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12
Q

Describe some other characteristics of prokaryotic cells? How is this an advantage ?

A
  • CELL WALL
  • NO MITOCHONDRIA OR LYSOSOMES
  • The presence of a cell wall allows bacteria to RESIST OSMOTIC STRESS
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13
Q

What are the 2 groups bacteria are divided into?

A
  • GRAM POSITIVE
  • GRAM NEGATIVE
  • depending on the structure of their cell wall
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14
Q

How are these 2 groups of bacteria determined?

A
  • Depending on whether the cell membrane RETAINS CRYSTAL-VIOLET INDIUM DYE after an ALCOHOL RINSE.
  • GRAM +VE - RETAIN THE DYE = BLUISH under light microscope
  • GRAM -VE - DON’T RETAIN THE DYE BUT RETAIN THE SAFRANIN O COUNTER-STAIN= PINK under a light microscope
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15
Q

How can bacteria be further classified?

A
  • Due to SHAPE
  • COCCI= ROUND
  • BACILLI= SMALL RODS
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16
Q

Name some GRAM +ve COCCI BACTERIA?

A
  • STAPHYLOCCUS AUREUS
  • S.EPIDERMIS
  • ENTEROCOCCUS spp
  • STREPTOCOCCUS
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17
Q

Name some GRAM NEGATIVE COCCI?

A
  • Branhamella catarrhalis
  • Neisseria gonorrhoea
  • N.Meningtides
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18
Q

Name some GRAM +ve bacilli BACTERIA?

A
  • Clostridium tetani
  • C.perfringens
  • Bacillus anthracis
  • Actinomyces spp
  • Corynebacterium spp
  • Nocardia asteriodes
  • Listeria monocytogenes
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19
Q

Name some GRAM NEGATIVE bacilli BACTERIA?

A
  • Pseudomonas aeruginosa
  • Eiknella corrodens
  • Haemphilius influenzae
  • Escherichia coli
  • Salmonella typhi
  • Klebsiella pneumoniae
  • Bacteriodes fragilis
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20
Q

What is septic arthritis?

A
  • A condition characterised by INFECTION OF THE SYNOVIUM and JOINT SPACE
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21
Q

In septic arthritis what does the infection do?

A
  • Causes an INTENSE INFLAMMATORY REACTION
  • RELEASE OF PROTEOLYTIC ENZYMES leading to RAPID DESTRUCTION OF THE ARTICULAR CARTILAGE
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22
Q

What is osteomyelitis?

A
  • It is an ACUTE or CHRONIC INFLAMMATORY PROCESS OF THE BONE and its structures 2ARY TO INFECTION
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23
Q

Is septic arthritis and osteomyleitis common in paeds and adults?

A
  • YES
  • In adults usually secondary to an IMMUNOCOMPROMISED STATE or UNDERLYING MEDICAL CONDITION- DM
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24
Q

How do septic arthritis and osteomyelitis occur?

A
  • PRIMARILY- SEEDING OF SYNOVIAL MEMBRANE
  • SECONDARY
    • INFECTION IN ADJACENT METAHYSEAL BONE
    • or DIRECTLY from INFECTION IN A JOINING EPIPHYSIS
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25
Q

Where are the locations most risk to septic arthritis / osteomyelitis?

A
  • Hip
  • prox shoulder
  • elbow
  • ankle of in children
  • due intra- ARTICULAR METAPHYSIS (within joint capsule)
  • osteomyelitis In these bones can cause septic arthritis
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26
Q

Describe the process of destruction of the articular cartilage?

A
  • begins quickly
  • secondarily due to proteolytic enzymes released from Synovial cells
  • ** IL-1 Triggers** the release of proteases from the Chondrocytes and Synoviocytes in response to Polymorphonuclear leukocytes and bacteria
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27
Q

What is lost by this process from the articular cartilage?

A
  • Proteoglycans - by day 5
  • Loss of collagen - by day 9
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28
Q

What also plays a role in the process of articular destruction?

A
  • impairment of the intracapsular vascular supply secondary to elevation of the intracapsular pressure and thrombosis of the vessel
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29
Q

Describe the clinical presentation of septic arthritis in a child?

A
  • Acute onset, child irritable and febrile >38.5C
  • if the infection involves the lower limb= child usually LIMPS and REFUSES TO WEIGHT BEAR
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30
Q

If you examined a child with septic arthritis what would you find?

A
  • RESISTANCE to passive motion of the attempted joint
  • SEVERE PAIN on MOVING the joint
  • INCREASED SWELLING, ERYTHERMA, EFFUSION
  • POSITION of joint in MAX COMFORT
    • HIP=FLEXION, ABDUCTION, EXT ROTATION
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31
Q

If you examined a neonate with septic arthritis what would you find?

what are their risk factors for developing SA?

A
  • Lethargy
  • irritability
  • difficulty in feeding
  • pseudo-paralysis of the affected limb
  • in osteomyelitis tenderness most acute over the involved area of bone- usually metaphyseal

Risk factors

  • PREMATURITY
  • CAESARIAN SECTION
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32
Q

What would your initial investigations be?

A
  • FBC
  • acute- phase reactants i.e. C- reactive protein (CRP)
  • Erthrocyte sedimentation rate (ESR)
  • Blood cultures
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33
Q

What are the predictors of SA and who describes them?

A

KOCKER JBJS1999- PREDICTORS OF SA

  • 1) WCC >12,000/mm3 with 40-60% polymorphonuclear leukocytes
  • 2) ESR elevated usually > 40mm/hr
  • 3) REFUSAL to WB
  • 4) FEVER >38.5C
  • ALL 4 chance of SA cf transient synovitis hip 99.6%, 3= 93%, 2=40%, 1=3% cf none 0.2%
  • ***CRP >2mg/dL added by CAIRD 2006 so all 5 positive predictor =98% chance of SA
  • Blood cultures positive in 30-50% of cases
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34
Q

What is the mainstay of diagnosis?

A
  • Joint aspiration with immediate gram stain and miscropscopy + culture and sensitivity
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35
Q

What value of wcc, lactate, glucose is found on hip aspiration with SA?

A
  • WCC > 50,000/mm3 with >75% polymorphonuclear leukocytosis
  • synovial protein lactate >40mg.dl and less than serum protein lactate = SA
  • aspirated glucose level is lower than serum level
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36
Q

what further tests aid diagnosis?

A
  • USS of hip= effusion which can be aspirated
  • Radiographs
    • ap and frog lateral = subluxation/ dislocation hip suttle widening of joint space in SA and metaphsyeal rarefaction in OM
    • in chronic OM- necrotic bone (sequestrum) and new bone formation (involucrum)
  • Bone scan
    • initally cold in early phase
    • ‘hot’ , increased uptake later on
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37
Q

What is the tx for septic arthritis?

A
  • An emergency
  • tx expedited to prevent any permanent damage to the articular cartilage
  • prompt diagnosis, surgical drainage and irrigation of the involved joint with appropriate constitutional support in the form of fluids and antibiotics
  • If surgery is not followed by rapid recovery- consider reexploration surgery
  • Iv antibiotics should be commenced immediately after aspiration of the joint.
  • Broad spectrum antibiotics commenced initally and change to specific depending on culture and sensitivity
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38
Q

what surgical approach would you use for SA hip joint in pads? Can you describe the inter nervous plane?

A
  • Medial approach
  • superificial -
    • no inter nervous plane as both ADDUCTOR LONGUS and GRACILIS innervate by ANT division of OBTURATOR N.
  • Deep-
    • inter nervous plane between ADDUCTOR BREVIS ( ANT div Obturator n) and ADDUCTOR MAGNUS (dual innervation - post div OBTURATOR and ischial portion by tibial portion of SCIATIC N)
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39
Q

Can you describe how you would do the medial approach to the hip?

A
  • patient supine, hip flexed abducted and ext rotated
  • incision- begin 3cm below PUBIC TUBERCLE
  • INCISE long over ADDUCTOR LONGUS
    • Sup- develop plane between add longs and GRACILIS - no in plane both ANT DIV OBTURATOR N
    • Deep- develop plane between ADD BREVIS ( ant div Obutrator N ) and ADD Magnus ( dual inneravation)
    • UNTIL you feel the LESSER TROCHANTER on FLOOR of the WOUND
    • PROTECT POST DIV OF OBTURATOR N
    • Isolate PSOAS tendon by placing narrow retractor above and below lesser trochanter
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40
Q

What are the dangers with this approach?

A
  • Medial FEMORAL CIRCUMFLEX ARTERY
    • passes medial side of distal psoas tendon
    • must isolate psoas tendon and cut under direct vision
  • ANT DIV OF OBTURATOR N
    • supplies add longus, add brevis and gracilis
  • POST DIV OF OBTURATOR N-
    • lies within substance of obturator externus, supplies adductor portion of add magnus
  • DEEP EXT PUDENDAL ARTERY
    • at risk proximally , lies ant to pectinous nr origin of adductor longs
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41
Q

what are the 4 bad prognostic signs of a child with Septic arthritis?

A
  • Age < 6 months
  • Joint effusion with underlying osteomyelitis
  • Hip involvement
  • Delay in treatment > 4days
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42
Q

Name the organisms most likely found in an infant <1yr? what tx would you suggest?

A
  • GROUP B STREPTOCOCCI
    • most common tx 1st gen cephalosporin
  • STAPHYLOCOCCUS aureus
  • ESCHERICHIA coli
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43
Q

How long are iv antibiotics are given for?

A
  • 2 weeks and converted to oral for 4-6 weeks depending on clinical response
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44
Q

Name the organisms most likely found in an child 1-16yr? what tx would you suggest?

A
  • STAPHYLOCOCCUS aureus- most common-
    • 2/3rd gen cephalosporin
  • STREPTOCOCCUS pyrogens
  • HAEMOPHILUS INFLUENZA
  • Pseudomonas aeruginosa- foot puncture wound
  • salmonella- sickle cell
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45
Q

Name the organisms most likely found in an ADULT >16yr?what tx would you suggest?

A
  • NEISSERIA Gonorrhoea - adolescent most common
    • tx with cephalosporin
  • ** Staphylococcus epidermidis **
  • Staphylococcus aureus
  • Pseudomonas aeruginosa
  • Serraria marcescens
  • Escherichia coli
46
Q

Can you describe paediatric Acute osteomyelitis pathology on a macroscopic level?

A
  • SUBPERIOSTEAL ABSCESS DEVELOPMENT
  • when the purulence breaks thru the metaphyseal cortex
47
Q

Can you describe paediatric acute osteomyelitis pathology on a microscopic level?

A
  • SLUGGISH BLOOD FLOW IN METAPHYSEAL CAPILLARIES due to SHARP TURNS->VENOUS SINUSOIDS
  • give bacteria time to LODGE in this region
  • the LOW pH and O2 tension around the growth plate assist bacterial growth
  • infection occurs after local bone defences have been overwhelmed
  • bacteria spread thru bone via Haversian and volkmann canals
48
Q

How does paediatric acute osteomyelitis occur?

A
  • Most thru HAEMATOGENOUS
  • initial bacteraemia thru skin lesion, infection, or even trauma
49
Q

What X-ray changes in a child with OM would you see ?

A
  • early- nothing/ loss of soft tissue planes/soft tissue oedema
  • new periosteal bone formation 5-7days
  • osteolysis 10-14 days
  • late films- metaphsyeal rarefaction (reduction in metaphyseal bone density) or possible abscess
50
Q

Can you describe the pathology of paediatric chronic osteomyelitis

A
  • Periosteal elevation deprives the underlying cortical cone of blood supply -> NECROTIC BONE (SEQUESTRUM)
  • an outer layer of new bone is formed by the PERIOSTEUM (INVOLUCRUM)
  • Chronic abscesses may be surrounded by sclerotic bone and fibrous tissue -> BRODIE’S abscess
51
Q

what radiographic signs do you see in chronic ostomyelitis?

A
  • Necrotic bone = Sequestrum
  • periosteal new bone= INVOLUCRUM
52
Q

What further investigations would you do in a child with OM?

A
  • Ct- helpful later
  • MRI
    • T1 signal decreased
    • with gadolinium- increased T2 increased 88%-100% sensitivity
  • Bone scan- 92% sensitivity
      • cold bone scan -can be more aggressive infections
  • bone aspiration- definitive diagnosis
53
Q

What investigation aids treatment of OM?

A
  • CRP- ELEVATED IN 98% with acute haematological spread, WITHIN 6 HOURS
  • most sensitive to monitor therapeutic response - declines rapidly.
  • failure for crp to decline in 48-72hrs after tx commences should indicate tx may need alliterating
54
Q

what is the tx of paediatric om?

A
  • non op
    • aspiration
      • helps to guide medical management
      • when organism identified antibiotics
      • controversial duration most 4-6 weeks, generally oxacillin
  • surgical drainage and antibiotics
    • Need to evacuate all purulence, deride devitalised tissue and drill needed into intraossesous collections.
    • Remove sequestrum in chronic cases, send tissue to pathology to rule out neoplasia and miscobiology
    • close wounds over pack/drans and redebride in 2-3 days
55
Q

What is the tx for chronic osteomyelitis?

A
  • Drainage and Debridement of ALL NECROTIC TISSUE with PRESERVATION OF THE INVOLUCRUM
  • OBLITERATION OF DEAD SPACES
    • ​ Vaccum assisted closure/ vascularised bone graft
  • ADEQUATE SOFT -TISSUE COVERAGE
      • local /free flaps
  • PRESERVATION OF SKELETAL STABILITY
56
Q

What are the complication of OM in pads?

A
  • DVT
  • Meningitis
  • Chronic osteomyeltitis
  • Septic arthritis
  • Growth disturbance and limb length discrepancies- > gait abnormalities
  • Pathological fractures
57
Q

What risk factors increase the risk of DVT in a Paeds pt with OM?

A
  • Age >8 yrs
  • MRSA
  • Surgical treatment
  • CRP >6
58
Q

How can antibiotics be delivered?

A
  • Oral
  • Intramuscular
  • Intravenous
  • Antibiotics beads and spacers
    • amino glycosides are added to bone cement and used to tx osteomyelitis/ infected arthroplasty.
    • Elution of the antibiotic is for a max of 6-8 weeks.
    • this gives a very high local concentration of the antibiotic
  • Osmotic pump- high conc of antibiotic
59
Q

What are antibiotics used for?

A
  • Prophylaxis
  • Eradicate infection
  • Initial care in open fractures/wounds
60
Q

Name the different actions antibtiocs and the groups that they belong to?

A
  • 1) INHIBIT CELL WALL SYNTHESIS
    • Pencillins
    • Cephalosporins
    • Glycopeptides- vancomycin, teicoplanin
    • Carbapenems- imipenem
  • 2) INHIBITION OF NUCLEIC ACID SYNTHESIS
    • i) INHBIT DNA GYRASE (enzyme that compresses dan into super-coils)
      • Quniolones = Ciprofloxacin
    • ii) INHIBITS DNA DEPENDENT RNA POLYMERASAE so prevent RNA transcription
      • _R_ifampicin
  • 3) INHIBIT PROTEIN SYNTHESIS
    • i) Dissociation of PEPTIDYL tRNA From Ribsomes during Translocation by Binding to 50S SUBUNIT
      • Macrolides
      • Clindamycin
      • Linezolid
      • Choramphenicol
    • ii) Inhibit Bacterial Protein Synethesis binds to rRNA 30S Subunit =
      • Aminoglycosides- Gentamycin,neomycin
      • Tetracyclines
    • iii) INHIBIT FOLATE SYNTHESIS- sulphonamides
61
Q

Describe the subgroup of Pencilins with examples?

A
  • Natural
    • penicillin G (iv)
    • pencilllin v (oral)
  • Penciliiase-resistance
    • Flucloxacillin
  • Aminopencillins
    • ampicillin
    • co-amoxiclav
  • antipseudomonal
    • pipercillin
62
Q

What is penicillin spectrum of activity?

A
  • Against GRAM POSTIVE COCCI
    • clostridium spp
    • Anthrax spp
  • inactivated by beta lactamases
63
Q

What is pencillin’s mode of action?

A
  • BACTERICIDAL:
  • inhibit bacterial peptidoglycan synthesis by binding to Pencillin binding proteins on BACTERICAL CELL MEMBRANES
  • aka- Beta lactam antibotics
64
Q

What is flucloxacillin spectrum of activity?

A
  • against Staphylococcus spp
65
Q

What are pencillin/flucloxacillin’s complications?

A
  • HYPERSENSITIVITY reactions
  • Hameolytic Anaemia
  • CNS Toxicity
  • Colitis and Cholestatic Jaundice
  • Hepatitis
66
Q

What is CO-AMOXICLAV spectrum of activity?

A
  • STAPH aureus
  • ESCHERICHIA COLI
  • HAEMOPHILUS influenza
  • BACTEROIDES spp
  • KLEBSIELLA
  • ** co- amoxilcav is amoxicillin + beta lactamase inhibitor clavulanic acid**
67
Q

What are CO-AMOXICLAV’s complications?

A

SAME AS flucloxacillin

  • Hypersensitivity reactions,
  • Cholestatic jaundice
  • Hepatitis
68
Q

Describe the subgroup of Cephlalosporins with examples?

A
  • First generation- cefalexin
  • 2nd generation- cefuroxime
  • 3rd generation- ceftriaxone
  • 4th generation- cefepime
69
Q

What is cephalosporins mode of action?

A
  • BACTERICIDAL
  • INHIBIT CELL WALL SYNTHESIS
70
Q

What are cephalporin’s spectrum of activity?

A
  • 1st gen=cefalexin
    • very active GRAM POSITIVE bacteria
  • 4th gen= cefepime/cefpirome
    • active against GRAM NEG Bacteria
  • ***activity against gram positive decreases from 1-4th generation**
71
Q

What are the complications of cephalosporins?

A
  • Haemolytic anaemia
  • Colitis
  • Allergic skin reactions
  • Disturbance in liver enzymes
72
Q

What is carbapenems mode of actions and can you name one?

A
  • Bactericidal - inhibit cell wall synthesis
  • IMPIPENEM
73
Q

What is the spectrum of action for impipenem?

A
  • Active against
    • aerobes
    • anerobes
    • gram positive
    • gram negative bacteria
  • Given with cilastin to prevent renal metabolism
74
Q

What are the complications of impipenem?

A
  • **CNS toxicity **
  • Grand mal seizures
  • Colitis
75
Q

What is the mode of action of aminoglycosides?

Can you name some?

A
  • inhibit bacterial protein synthesis by binding to cytoplasmic rRNA 30S subunit

examples

  • Gentamycin
  • Neomycin
76
Q

What is the spectrum of action for gentamycin?

A
  • mainly against GRAM NEG BACTERIA
    • pseudomonas aeruginosa,
    • enterobacteriacee spp
77
Q

What are the complications of gentamycin?

A
  • ototoxicity
  • nephrotoxicity
  • neuromuscular blockage
78
Q

What is the mode of action of macrolides? Can you name some?

A
  • inhibit bacterial protein synthesis by binding to 50s subunit- actually inhibit the dissociation of peptidyl tRNA from ribosomes during translocation

examples

  • Erythromycin
  • Clarithromycin
  • Azithromycin
79
Q

What is the spectrum of action for erythromycin?

A

active against

  • STREP spa,
  • LISTERIA,
  • MORAXELLA catarrhalis,
  • MYCOPLASM pneumoniae,
  • LEGIONELLA pneumonphilia,
  • CHLAMYDIA pneumonia
80
Q

What are the complications of erythromycin ?

A
  • potential GI effects
    • nausea
    • vomiting
    • abdo cramps
81
Q

What is the mode of action of Quniolones? Can you name some?

A
  • Inhibit nucleic acid synthesis specifically inhibit DNA GYRASE- prevents the DNA from supercoiling
  • e.g. CIPROFLOXACIN
82
Q

What is the spectrum of action for ciprofloxacin ?

A
  • mainly against GRAM -VE BACTERIA
83
Q

What are the complications of ciprofloxacin ?

A
  • GI disturbance
  • tendonitis increased achilles tendon rupture
84
Q

What is the mode of action of Glycopetides? Can you name some?

A
  • inhibit cell wall synthesis by interfering with insertion of glycan subunits
  • e.g.
  • VANCOMYCIN
  • TEICOPLANIN
85
Q

What is the spectrum of action for vancomycin?

A
  • Excellent against STAPH aureus
  • STAPH epidermis
  • enterococcus spa
  • ** mrsa**
86
Q

What are the complications of vancomycin ?

A
  • Red man syndrome
    • flushing red head, neck, upper torso
    • assoc with hypotension
  • nephrotoxicity
  • ** ototoxicity**
  • ** neutropenia**
  • thrombocytopenia
87
Q

What is the mode of action of tetracylines? Can you name some?

A
  • inhibit bacterial protein synthesis by binding to cytoplasmic rRNA 30s subunit
  • e.g. TETRACYCLINE
  • doxycycline
88
Q

What is the spectrum of action for tetracycline ?

A
  • GRAM POSITIVE BACTERIA
89
Q

What are the complications of tetracycline ?

A
  • colitis
  • staining of bone and teeth in children
  • hepatotoxicity in pregnancy
90
Q

Name the 2 types of antibiotic resistance?

A
  1. Innate/INTRINISIC
  • that bacterial cell inherently has properties that do not allow the antibiotic to act on it
  • e.g changes in cell wall permeability, enzyme production that destroys the antibiotic
  1. ** EXTRINSIC**
  • implies the organism ACQUIRES RESISTANCE TO AN ANTIBIOTIC to which is was previously sensitive.
  • Occur due to chance mutation in the genetic material of the cell or acquisition of drug resistance genes form drug resistance cell
91
Q

How is extrinsic resistance mediated?

A
  • Via PLASMIDS
    • small circles of double stranded DNA
    • carry genes for specialised functions
    • can one or more genes for antimicrobial resistance
92
Q

What is MRSA?

A
  • Methicillin-Resistant Staphylococcus Aureus
  • Gram positive coccus
  • Major nosocomial Pathogen
93
Q

What is MRSA’s prevalence? Why is MRSA infection a problem?

A
  • 1.6% in orthopaedic dept
  • 0.3 general hospital setting
  • problem as
    • High morbidity
    • high mortality associated
    • financial implications in infected arthroplasties
94
Q

How do staphylococci acquire their resistance ?

A
  • Due to the presence of an ACQUIRED PENCILLIN-BINDING PROTEIN, PBP2a
  • this protein is encoded by the gene mecA carried on staph chromosome.
  • the levels of resistance depend on production of PBP2a.
95
Q

How are most mrsa infections acquired?

A
  • By proximity and contact with other colonsationed pts
  • 25% hospital personnel are carriers for mrsa.
96
Q

What are known risk factors for mrsa infection?

A
  • Old age
  • previous hospitalisation
  • prolonged hospitalisation
  • open skin lesions
  • chronic medial illness
  • presence of invasive indwelling devices
  • prolonged antibiotic therapy
  • exposure to other colonised/infected patients
97
Q

How is mrsa prevented?

A
  • EFFECTIVE screening to pick up high risk pt
  • ISOLATION and TREATMENT of carriers
  • Education of staff on HAND HYGEINE
    • _ alcohol based hand gel_ effective against mrsa
98
Q

If an mrsa carrier is identified what are they tx with?

A
  • Nasal MUPIROCIN
  • bathing in antiseptic detergent- 4% chlorhexidine
99
Q

Once mrsa infection is established what does management involve?

A
  • Administration of IV GLYCOPEPTIDES
    • VANCOMYCIN/ TEICOPLANIN
    • adv of teicoplanin = better bone penetration, better tolerated and given as a bolus dose ( so can be give as outpatient)
100
Q

MRSA resistance to glycopeptides has been shown what then would be your antibiotic of choice?

A
  • Linezolid- a oxazolidinones
  • ( inhibit early step in protein synthesis)
  • problem can cause bone marrow suppression
101
Q

What is TB?

A
  • A CHRONIC GRANULOMATOUS CONDITION commonly caused by MYCOBACTERIUM tuberculosis.
  • the incidence is low in developed countries cf developing but there is an increase due to hiv, and multiple drug resistances
102
Q

What are the mycobacterium ?

A
  • Olibigate aerobic acid fast rods
103
Q

Where does the infection usually begin?

A
  • In the lungs and the sub pleural region along with lymphatic drainage.
  • the mediastinal lymph nodes are also involved= Primary Gohn Complex
  • local spread into lungs-> Bronchopneumonia
  • homogenous spread-> Military TB
    • ​this involves the lungs, bones, joints and spine ie Secondary TB
104
Q

What is the normal presentation of pt w TB?

A
  • LOW grade fever
  • Productive chronic cough
  • weight loss
  • generalised weakness
  • **skeletal involvement normally follows pulmonary but only half of pt with skeletal have pulmonary
105
Q

What can happen to the primary TB infection?

A
  • Completely resolve
  • Remain quiescent or spread systemically - locally in lung -> bronchopneumonia haematogenous -> military TB - involves lung,bones, joints,spine
106
Q

What does skeletal TB involve?

A
  • Spine- tuberculous spondylitis
  • fingers- tuberculous dactylitis
  • appendicular skeleton- metaphyseal lytic lesions with little/ no sclerosis seen
  • rarely knee/hip - monoarthritis
    • ​florid synovitis
    • preservation of joint space
    • periarticular osteopenia
107
Q

What is the basis of skin tests? can you name them?

A
  • DELAYED Hypersensitivity reaction
  • Heaf test or MANTOUX test
  • both tests expose the pt skin to purified protein derivatives.
  • a positive response includes the formation of paules on the skin after a designated number of hours
  • a positive response implies an active infection or previous BCG ( Bacillus-Calmette-Guerin) vaccination
108
Q

How is diagnosis made?

A
  • MINIMUM OF 3 LARGE VOLUMES OF EARLY MORNING SPUTUM
  • Presence of ACID-FAST BACTERIA ON ZIEHL-NEEELSEN STAIN ( bacteria appear as red acid-fast organisms under the stain
  • If neg ZN then cultured on LOWSTEIN-JENSEN medium for 6weeks at 35-37oC
109
Q

If both ZN and LJ tests are negative what is the next step in dx?

A
  • A biopsy
  • classic GRANULOMA with CASEATING CENTRAL NECROSIS
110
Q

How is TB treated ?

A
  • A combination of first line CHEMOTHERAPEUTIC AGENTS “RIPE”
  • Rifampicin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol
  • FOR 6-9 MONTHS
111
Q

Why is tx for a long time?

A
  • A TB is slow growing and there is a possibility of it becoming dormant.
  • USING 2 OR MORE ANTIBTIOICS AT ONCE REDUCED CHANCE OF RESISTANCE DEVELOPING

Basic Science (31 decks)

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