Inflammation and Infection Flashcards
(111 cards)
1
Q
What are the 5 cardinal signs of Inflammation?
A
- RUBOR- redness
- CALOR- heat
- DOLOR- pain
- TUMOUR- swelling
- FUNCTIO LAESA- loss of function
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
3
Q
Describe what happens when bacteria envade the musculoskeletal system?
A
- The inital response is an acute inflammatory reaction with phagocytosing of bacteria
4
Q
What are the 3 outcomes to acute inflammation?
A
- COMPLETE RESOLUTION
- HEALING BY SCARRING
- PROGRESSION -> CHRONIC INFLAMMATION
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)
6
Q
What are the key cells in chronic inflammation?
A
- Mononuclear cells- principally MACROPHAGES , lymphocytes, plasma cells
- Fibroblasts and eosinophils (in immune reactions)
7
Q
Macrophages are activated in inflammation how?
A
- By Lymphokines ( e.g. gamma-interferon) produced by immune-activated T cells or
- non immune factors such as EXOTOXINS
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
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
10
Q
What are bacteria?
A
- PROKARYTOIC CELLS- as they have no NUCLEUS
11
Q
Where do bacteria keep their genetic material ?
A
- In the NUCLEIOD ; an area of the CYTOPLASM
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
13
Q
What are the 2 groups bacteria are divided into?
A
- GRAM POSITIVE
- GRAM NEGATIVE
- depending on the structure of their cell wall
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
15
Q
How can bacteria be further classified?
A
- Due to SHAPE
- COCCI= ROUND
- BACILLI= SMALL RODS
16
Q
Name some GRAM +ve COCCI BACTERIA?
A
- STAPHYLOCCUS AUREUS
- S.EPIDERMIS
- ENTEROCOCCUS spp
- STREPTOCOCCUS
17
Q
Name some GRAM NEGATIVE COCCI?
A
- Branhamella catarrhalis
- Neisseria gonorrhoea
- N.Meningtides
18
Q
Name some GRAM +ve bacilli BACTERIA?
A
- Clostridium tetani
- C.perfringens
- Bacillus anthracis
- Actinomyces spp
- Corynebacterium spp
- Nocardia asteriodes
- Listeria monocytogenes
19
Q
Name some GRAM NEGATIVE bacilli BACTERIA?
A
- Pseudomonas aeruginosa
- Eiknella corrodens
- Haemphilius influenzae
- Escherichia coli
- Salmonella typhi
- Klebsiella pneumoniae
- Bacteriodes fragilis
20
Q
What is septic arthritis?
A
- A condition characterised by INFECTION OF THE SYNOVIUM and JOINT SPACE
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
22
Q
What is osteomyelitis?
A
- It is an ACUTE or CHRONIC INFLAMMATORY PROCESS OF THE BONE and its structures 2ARY TO INFECTION
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
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
25
Where are the locations most risk to septic arthritis / osteomyelitis?
* Hip
* prox shoulder
* elbow
* ankle of in children
* due **intra- ARTICULAR METAPHYSIS** (within joint capsule)
* **osteomyelitis** In these bones can cause **septic arthritis**
26
Describe the process of destruction of the articular cartilage?
* 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**
27
What is lost by this process from the articular cartilage?
* **Proteoglycans -** by day 5
* **Loss of collagen** - by day 9
28
What also plays a role in the process of articular destruction?
* **impairment of the intracapsular vascular supply** secondary to **elevation** of the **intracapsular pressure** and **thrombosis** of the vessel
29
Describe the clinical presentation of septic arthritis in a child?
* **Acute o**nset, child **irritable** and **febrile \>38.5C**
* if the infection involves the lower limb= child usually **LIMPS** and **REFUSES TO WEIGHT BEAR**
30
If you examined a child with septic arthritis what would you find?
* **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**
31
If you examined a neonate with septic arthritis what would you find?
what are their risk factors for developing SA?
* **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
32
What would your initial investigations be?
* **FBC**
* acute- phase reactants i.e. **C- reactive protein** (CRP)
* **Erthrocyte sedimentation rate (**ESR)
* **Blood cultures**
33
What are the predictors of SA and who describes them?
**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
34
What is the mainstay of diagnosis?
* **Joint aspiration with immediate gram stain and miscropscopy + culture and sensitivity**
35
What value of wcc, lactate, glucose is found on hip aspiration with SA?
* **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
36
what further tests aid diagnosis?
* **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
37
What is the tx for septic arthritis?
* 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
38
what surgical approach would you use for SA hip joint in pads? Can you describe the inter nervous plane?
* 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)_
39
Can you describe how you would do the medial approach to the hip?
* 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
40
What are the dangers with this approach?
* **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
41
what are the 4 bad prognostic signs of a child with Septic arthritis?
* **Age \< 6 months**
* **Joint effusion** with underlying **osteomyelitis**
* **Hip** involvement
* **Delay in treatment \> 4days**
42
Name the organisms most likely found in an infant \<1yr? what tx would you suggest?
* **GROUP B STREPTOCOCCI**
* most common tx ***1st gen cephalosporin***
* **STAPHYLOCOCCUS aureus**
* **ESCHERICHIA coli**
43
How long are iv antibiotics are given for?
* 2 weeks and converted to oral for 4-6 weeks depending on clinical response
44
Name the organisms most likely found in an child 1-16yr? what tx would you suggest?
* **STAPHYLOCOCCUS aureus**- most common-
* 2/3rd gen cephalosporin
* STREPTOCOCCUS pyrogens
* HAEMOPHILUS INFLUENZA
* **Pseudomonas aeruginosa**- foot puncture wound
* salmonella- sickle cell
45
Name the organisms most likely found in an ADULT \>16yr?what tx would you suggest?
* **NEISSERIA Gonorrhoea** - adolescent most common
* tx with cephalosporin
* ** Staphylococcus epidermidis **
* **Staphylococcus aureus**
* Pseudomonas aeruginosa
* Serraria marcescens
* Escherichia coli
46
Can you describe paediatric Acute osteomyelitis pathology on a macroscopic level?
* **SUBPERIOSTEAL ABSCESS DEVELOPMENT**
* when the _purulence breaks thru the metaphyseal cortex_
47
Can you describe paediatric acute osteomyelitis pathology on a microscopic level?
* **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
How does paediatric acute osteomyelitis occur?
* Most thru HAEMATOGENOUS
* initial bacteraemia thru skin lesion, infection, or even trauma
49
What X-ray changes in a child with OM would you see ?
* 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
Can you describe the pathology of paediatric chronic osteomyelitis
* **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
what radiographic signs do you see in chronic ostomyelitis?
* **Necrotic bone = Sequestrum**
* **periosteal new bone= INVOLUCRUM**
52
What further investigations would you do in a child with OM?
* 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
What investigation aids treatment of OM?
* **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
what is the tx of paediatric om?
* _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
What is the tx for chronic osteomyelitis?
* **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
What are the complication of OM in pads?
* **DVT**
* **Meningitis**
* **Chronic osteomyeltitis**
* **Septic arthritis**
* **Growth disturbance** and **limb length discrepancies**- \> **gait abnormalities**
* **Pathological fractures**
57
What risk factors increase the risk of DVT in a Paeds pt with OM?
* **Age \>8 yrs**
* **MRSA**
* **Surgical treatment**
* **CRP \>6**
58
How can antibiotics be delivered?
* **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
What are antibiotics used for?
* Prophylaxis
* Eradicate infection
* Initial care in open fractures/wounds
60
Name the different actions antibtiocs and the groups that they belong to?
* 1) **_INHIBIT CELL WALL SYNTHESIS_**
* *Pencillins*
* *Cephalosporins*
* *Glycopeptides- vancomycin, teicoplanin*
* *Carbapenems- imipenem*
* 2) _I**NHIBITION OF NUCLEIC ACID SYNTHESIS**_
* i) **INHBIT DNA GYRASE** (enzyme that compresses dan into super-coils)
* *Quniolones = Ciprofloxacin*
* ii) **INHIBITS DNA DEPENDENT **_R_**NA 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
Describe the subgroup of Pencilins with examples?
* **Natural**
* penicillin G (iv)
* pencilllin v (oral)
* **Penciliiase-resistance**
* Flucloxacillin
* **Aminopencillins**
* ampicillin
* co-amoxiclav
* **antipseudomonal**
* pipercillin
62
What is penicillin spectrum of activity?
* Against **GRAM POSTIVE COCCI**
* clostridium spp
* Anthrax spp
* **inactivated by beta lactamases**
63
What is pencillin's mode of action?
* **BACTERICIDAL:**
* inhibit **bacterial peptidoglycan synthesis** by **binding** to **Pencillin binding proteins** on **BACTERICAL CELL MEMBRANES**
* aka- Beta lactam antibotics
64
What is flucloxacillin spectrum of activity?
* against **Staphylococcus spp**
65
What are pencillin/flucloxacillin's complications?
* **HYPERSENSITIVITY** reactions
* **Hameolytic Anaemia**
* **CNS Toxicity**
* **Colitis** and **Cholestatic Jaundice**
* **Hepatitis**
66
What is CO-AMOXICLAV spectrum of activity?
* **STAPH aureus**
* **ESCHERICHIA COLI**
* **HAEMOPHILUS influenza**
* **BACTEROIDES spp**
* **KLEBSIELLA**
* \*\* co- amoxilcav is **amoxicillin + beta lactamase inhibitor clavulanic acid\*\***
67
What are CO-AMOXICLAV's complications?
SAME AS flucloxacillin
* **Hypersensitivity reactions,**
* **Cholestatic jaundice**
* **Hepatitis**
68
Describe the subgroup of Cephlalosporins with examples?
* **First generation- cefalexin**
* **2nd generation- cefuroxime**
* **3rd generation- ceftriaxone**
* **4th generation- cefepime**
69
What is cephalosporins mode of action?
* **BACTERICIDAL**
* **INHIBIT CELL WALL SYNTHESIS**
70
What are cephalporin's spectrum of activity?
* 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
What are the complications of cephalosporins?
* **Haemolytic anaemia**
* **Colitis**
* **Allergic skin reactions**
* **Disturbance in liver enzymes**
72
What is carbapenems mode of actions and can you name one?
* **Bactericidal - inhibit cell wall synthesis**
* **IMPIPENEM**
73
What is the spectrum of action for impipenem?
* Active against
* **aerobes**
* **anerobes**
* gram positive
* gram negative bacteria
* Given with **cilastin to prevent renal metabolism**
74
What are the complications of impipenem?
* **CNS toxicity **
* **Grand mal seizures**
* **Colitis**
75
What is the mode of action of aminoglycosides?
Can you name some?
* **inhibit bacterial protein synthesis by binding to cytoplasmic rRNA _30S_ subunit**
examples
* **Gentamycin**
* **Neomycin**
76
What is the spectrum of action for gentamycin?
* mainly against **GRAM NEG BACTERIA**
* pseudomonas aeruginosa,
* enterobacteriacee spp
77
What are the complications of gentamycin?
* **ototoxicity**
* **nephrotoxicity**
* **neuromuscular blockage**
78
What is the mode of action of macrolides? Can you name some?
* **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
What is the spectrum of action for erythromycin?
active against
* **STREP** spa,
* **LISTERIA**,
* **MORAXELLA** catarrhalis,
* **MYCOPLASM** pneumoniae,
* **LEGIONELLA** pneumonphilia,
* **CHLAMYDIA** pneumonia
80
What are the complications of erythromycin ?
* potential GI effects
* **nausea**
* **vomiting**
* **abdo cramps**
81
What is the mode of action of Quniolones? Can you name some?
* Inhibit nucleic acid synthesis specifically **inhibit DNA GYRASE**- prevents the DNA from supercoiling
* e.g. **CIPROFLOXACIN**
82
What is the spectrum of action for ciprofloxacin ?
* mainly against **GRAM -VE BACTERIA**
83
What are the complications of ciprofloxacin ?
* **GI disturbance**
* **tendonitis** increased achilles tendon rupture
84
What is the mode of action of Glycopetides? Can you name some?
* inhibit cell wall synthesis by interfering with insertion of glycan subunits
* e.g.
* **VANCOMYCIN**
* **TEICOPLANIN**
85
What is the spectrum of action for vancomycin?
* Excellent against **STAPH** aureus
* **STAPH epidermis**
* **enterococcus spa**
* ** mrsa**
86
What are the complications of vancomycin ?
* **Red man syndrome**
* _flushing red head, neck, upper torso_
* assoc with _hypotension_
* **nephrotoxicity**
* ** ototoxicity**
* ** neutropenia**
* **thrombocytopenia**
87
What is the mode of action of tetracylines? Can you name some?
* inhibit bacterial protein synthesis by binding to _cytoplasmic rRNA 30s_ subunit
* e.g. **TETRACYCLINE**
* **doxycycline**
88
What is the spectrum of action for tetracycline ?
* **GRAM POSITIVE BACTERIA**
89
What are the complications of tetracycline ?
* **colitis**
* **staining** of **bone** and **teeth** in children
* **hepatotoxicity in pregnancy**
90
Name the 2 types of antibiotic resistance?
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
2. ** 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
How is extrinsic resistance mediated?
* Via **PLASMIDS**
* *small circles of double stranded DNA*
* carry genes for specialised functions
* can one or more genes for antimicrobial resistance
92
What is MRSA?
* **Methicillin-Resistant Staphylococcus Aureus**
* **Gram positive coccus**
* Major nosocomial Pathogen
93
What is MRSA's prevalence? Why is MRSA infection a problem?
* **1.6%** in orthopaedic dept
* 0.3 general hospital setting
* problem as
* **High morbidity**
* **high mortality** associated
* **financial implications** in infected arthroplasties
94
How do staphylococci acquire their resistance ?
* 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
How are most mrsa infections acquired?
* By **proximity** and **contact** with other colonsationed pts
* 25% hospital personnel are carriers for mrsa.
96
What are known risk factors for mrsa infection?
* **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
How is mrsa prevented?
* **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
If an mrsa carrier is identified what are they tx with?
* Nasal **MUPIROCIN**
* **bathing in antiseptic detergent**- **4% chlorhexidine**
99
Once mrsa infection is established what does management involve?
* 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
MRSA resistance to glycopeptides has been shown what then would be your antibiotic of choice?
* **Linezolid- a oxazolidinones**
* ( _inhibit early step in protein synthesis)_
* problem can cause **bone marrow suppression**
101
What is TB?
* **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
What are the mycobacterium ?
* **Olibigate aerobic acid fast rods**
103
Where does the infection usually begin?
* 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
What is the normal presentation of pt w TB?
* **_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
What can happen to the primary TB infection?
* Completely resolve
* Remain quiescent or spread systemically - locally in lung -\> bronchopneumonia haematogenous -\> military TB - involves lung,bones, joints,spine
106
What does skeletal TB involve?
* 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
What is the basis of skin tests? can you name them?
* **DELAYED Hypersensitivity reaction**
* **Heaf test** or **MANTOUX tes**t
* 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
How is diagnosis made?
* **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
If both ZN and LJ tests are negative what is the next step in dx?
* A biopsy
* classic **GRANULOMA** with **CASEATING CENTRAL NECROSIS**
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How is TB treated ?
* A combination of first line CHEMOTHERAPEUTIC AGENTS "RIPE"
* **Rifampicin**
* **Isoniazid**
* **Pyrazinamide**
* **Ethambutol**
* FOR **6-9 MONTHS**
111
Why is tx for a long time?
* 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**
