27 Infections of skin, soft tissue, muscle Flashcards
How does skin control its own flora and prevent growth of pathogens?
acid pH - fatty acids, sebum
salty sweat
competition between flora/ pathogens
surface temperature is too low for many pathogens
How can infection (of any site) cause skin disease?
Direct damage/ infection of skin
Skin manifestations of systemic infections from blood e.g draining sinus from actinomycotic lesion
Toxin-mediate skin damage due to microbial toxin at another site in body e.g Scarlet fever (strep pyogenes, toxic shock syndrome (staph aureus)
Which layers of skin are affected?
Ringworm Impetigo Erysipelas Folliculitis Cellulitis Necrotising fasciitis
Ringworm - epithelium
Impetigo - epidermis
Erysipelas - dermis
Folliculitis - hair follicles
Cellulitis - dermis/ subcutaneous fat
Necrotising fasciitis - fascia
What sign can be produced by pseudomonas sepsis?
Ecythma gangrenosum - bloody pustule evolves into black ulcer at any site of body
Perivascular bacterial invasion, with associated ischaemic necrosis
Usually immunocompromised or severely unwell
Staph aureus is most common cause of skin infection
Can cause minor or serious infection.
How does boil form?
Infection around hair follicle
organism multiples rapidly
Inflamation with neutrophils
Fibrin produced walls off infection. Neutrophils create pus, which expands
What is scalded skin syndrome?
Staph aureus can infect small lesion, and release toxin knwon as exfoliatin.
This causes destruction of intercellular connections, and separation of top layer of epidermis.
Large blisters form. In 2 days they rupture, leaving normal skin underneath.
Baby is usually irritable, but rarely severely ill.
Treat with antibiotics, and fluid replacement
What is toxic shock syndrome, and what are clinical manifestations?
Multi-organ failure with fever, hypotension and macular rash. Which then begins desquamation - particularly soles/ palms
Due to TSST1 exotoxin
Seen in tampon use, but can occur in any skin wounds
Which bacteria cause impetigo?
Can be staph aureus or/and strep pyogenes
Strep pyogenes can cause infection in respiratory tract, but also skin infections.
Species have different M/ T proteins which specialise it to each site
What toxins can strep pyogenes produce?
hyaluronidase - helps organism spread in tissue
Strep pyogenes exotoxin (SPE)
Toxins are super-antigens and stimulate massive immune response e.g diffuse erythematous rash of scarlet fever
Streptococcal infections cause immune complex deposition on various organs.
What complications can it produce?
Glomerulonephritis
Rheumatic fever
reactive arthritis
erythema nodosum
PANDAS
Cellulitis involves infection of subcutaneous tissue/ fat
Why should it be treated?
Decision to treat clinically
Risk of bacteria seeding into bloodstream causing sepsis
SSTI is usually due to staph/ strep.
What infections can develop in damaged/ devascularised tissue?
Anaerobic infection
Surgical/ traumatic wound
Diabetic feet
Cellulitis with possible anaerobic cause (e.g diabetic foot/ surgical wound)
What is treatment?
Debridement
Penicillin + metronidazole
May progress to osteomyelitis
Staph/ strep are common causes of necrotising fasciitis
Infection spreads along fascia, and rash far outgrows the size of initial infection site. If affects scrotum/ perineum called Fournier’s gangrene
What is treatment?
Radical debridement
antibiotics
Human bite/ animal bite
what infections to be concerned about?
HBV
HCV
HIV
bacterial infection - oral flora
cat - pasteurella
dog - capnocytophagia
Tetanus
rabies
Which organism causes gas gangrene?
Clostridium perfringens
Found in soil and human/ animal faeces. Causes infection by wound contamination
Organism multiplies in subcutaneous tissue, causing gas formation, which may be clinically detectable.
alpha toxin produced causes massive cell lysis
Progresses rapidly
What is management of gas gangrene due to Clostridium perfringens?
surgical debridement is mainstay. Remove dead tissue which anaerobes use for growth
How do blackheads form?
Which bacteria are implicated?
Increase responsiveness to androgenic hormones increases sebum production.
Proprionibacterium/ staph/ microccoi act on sebum to form fatty acids. In combination with neutrophils, this causes inflmamation of skin
keratin/ neutrophil/ bacteria and layer of melanin form plug which blocks pilosebaceous duct
Clostridium tetani itself does not cause a problem, but infection with toxin causes rigidity and lockjaw which can progress to death
Lives in soil, can never be eliminated
Most people vaccinated against it
when is routine vaccination given?
- 3 doses - at 2/3/4 months of age as part of routine immunisation.
- 1st booster dose aged approximately 4 years
- 2nd booster dose 10 years after 1st booster
- Not vaccinated in childhood - give adult 3 doses, each a month apart
- always give a booster dose if any doubt about immunisation status
Which injuries are considered to be at risk of tetanus?
Clean cuts are not at risk e.g knife in kitchen. As superficial injury, and unlikely to be contaminated with spores
Tetanus- prone wounds
- puncture in garden
- IVDU at risk
- wound foreign body
- compound fracture
- burns with systemic sepsis
- animal bites - certain ones
High risk tetanus-prone wounds
- heavy wound contamination with soil
- wounds requiring surgery which is delayed >6 hours
What is management of tetanus-prone wound?
Wound cleaning
Previously vaccinated (within past 10 years) no action required
Previously vaccinated (last dose >10 years ago) -
tetanus booster vaccine
Tetanus immunoglobulin only if very high risk - e.g >6 hours, soil exposure
Unvaccinated -
tetanus vaccine
Tetanus immunoglobulin if medium or high risk - e.g >6 hours, soil exposure
see green book table
what is incubation period of tetanus?
4-21 days
What is tetanus treatment in following cases following injury?
Fully tetanus vaccinated (3 doses) (in past 10 years)
Fully tetanus vaccinated (3 doses) (last does >10 years ago)
Fully tetanus vaccinated (3 doses) (in past 10 years)
- No further vaccine or IM-TIG required
Fully tetanus vaccinated (3 doses) (last does >10 years ago)
- vaccine booster
- IM-TIG if high risk tetanus prone injury
What is tetanus treatment in following cases following injury?
Not completed initial tetanus immunisation (3 doses) or uncertain immunisation status
- give booster vaccine
- give IM-TIG
What is dose of IM-TIG if high risk injury in unvaccinated person?
250 IU usual dose
500 IU if >24 hours since injury, or severe contamination
Dose same for adults/ children
What are four forms of tetanus presentation?
Generalised muscle spasms
Cephalic tetanus is localised tetanus after a head or neck injury, involving primarily the musculature supplied by the cranial nerves
Localised tetanus is rigidity and spasms confined to the area around the site of the infection and may be more common in partially immunised individuals. Localised symptoms can continue for weeks or may develop into generalised tetanus
Neonatal - umbilical stump infection from use of manure. Muscle rigidity, unable to feet, 70-100% mortality
How to diagnose tetanus infection?
Mostly a clinical diagnosis - muscle rigidity/ spasms/ trismus. Can lead on to autonomic dysfunction, and respiratory difficulties
Wound sample - clostridium tetani PCR
Serology - check toxin in serum
Serology - check antibody status. Although cases of patients with sufficient antibody developing infection. So reasonable antibody level cannot exclude tetanus infection
What is management of suspected tetanus case?
- wound debridement
- antimicrobials including agents reliably active against anaerobes such as intravenous benzylpenicillin, metronidazole can used
- IM-TIG or intravenous Immunoglobulin (IVIG) given IM
- vaccination with tetanus toxoid following recovery
- supportive care (benzodiazepines for muscle spasms, treatment of autonomic dysfunction, maintenance of ventilation, nursing in a quiet room etc)
Leprosy causes by Mycobacterium leprae. Also known as Hansen’s disease
How is it transmitted?
Direct contact skin lesion - particularly overcrowding. Requires prolonged contact as not very contagious
Aerosol - nasal secretions contain bacteria
Infects armadillos, chimpanzee, mangabey monkeys, but little evidence of transmission
What is life cycle of M. leprae?
grows intracellulary within endothelial cells/ histiocytes/ Schwann cells of peripheral nerves
After several years, disease presents - which depends on immune response
What are names of stages of M leprae infection?
Tuberculoid leprosy
Borderline/ intermediate leprosy
Lepromatous leprosy
What are clinical stages of these forms of leprosy?
Tuberculoid leprosy
Borderline/ intermediate leprosy
Lepromatous leprosy
Tuberculoid leprosy - hypopigmented skin, anaesthesia, thickening of nerves
Borderline/ intermediate leprosy - numerous tuberculoid lesions
Lepromatous leprosy - generalised involvement of the skin/ nerves with evidence of nodules. Enlargement of nostrils/ ears/ cheeks - Lion like appearance
How does immune response effect clinical presentation of leprosy?
If vigorous cell-mediated immunity response, then can contain bacteria - tuberculoid leprosy with single lesion
If poor CMI - organism multiplies unhindered
How to diagnose leprosy?
Skin biopsy - stain Ziel-Neelsen or auramine to see acid-fast rods
does not grow in culture, as compared to M Tb which does grow in culture
What is treatment for leprosy?
Dapsone, rifampicin and clofazimine given between 6 months- 2 year depending on stage
Repeat skin biopsies to confirm clearance
BCG vaccine has some protection against leprosy
Mycobacterium TB can rarely infect skin when it is damaged. What condition does it cause?
Ulcerating lesion extends from skin to lymph node - scrofuloderma
What species of mycobacterium is associated with fish tanks/ swimming?
M marinum
At risk - aquarium owners marine biologist fishermen swimmer
Injury allows mycobacteria to enter wound. Incubates for 2-8 weeks, then small papule appears. May ulcerate
What is treatment of M marinum skin infection?
Clarithromycin + ethambutol
6-18 months treatment
What disease does M. ulcerans cause?
What is its geographical spread?
Buruli ulcer - necrotic ulcers. Can spread over skin surface, and can invade and cause osteomyelitis
Africa - primarily
SEA
SA
Aus
What is M ulcerans route of infection?
Direct skin inoculation through traumatic wound
Has been found in possums/ mosquitoes. Speculated may occur after infected mosquito bite
Fungal infectious can either be -
superficial
cutaneous or
deep/ subcutaneous
What are most common superficial fungal infection?
Pityriasis versicolor
tinea species (other name is ringworm)
white piedra
black piedra
What is cause of pityriasis versicolor?
How does it present?
M pityrosporum furfur
common skin inhabitant, unclear why/ when becomes pathogenic
Hypo- or hyperpigemtned macules form, which can coalesce into sclaing plaques
How to diagnose pityriasis versicolor?
Treatment
Direct microscopy of scrapings - round yeas forms
topical azole
What are causes of cutaneous fungal infections?
Tinea -
- capitis (head)
- corporis (body)
- cruris (crotch)
- manuum (hands)
- unguium (nails)
- pedis (feet)
Tinea means maggot, and is uses interchangeable with ringworm to describe cutaneous fungal infection of different sites.
Causes of tinea include various Tinea species, and microsporum/ trichophyton.
Tinea/ microsporum species have natural hosts in humans/ soil/ animals
Tinea infection (cutaneous dermatophyte) - what does lesion look like?
Annular patch with raised margin
dry/ scaly
itchy
hair loss
How to diagnose cutaneous dermatophyte infection?
Skin scrapings to look for fungi - tinea/ microsporum/ trichophyton
Culture - can take 2 weeks
Fluorescence under UV light
What is treatment of cutaneous dermatophyte infection?
Skin - topical azole - ketoconazole/ clotrimazole/ miconazole
Nails/ hair - oral terbinafine/ itraconazole
Why does candida grow in mouth/ groin?
Requires moist area for growth
Can invade deeper if patient becomes immunosuppressed
What are causes of subcutaneous mycoses?
Rare
Sporotrichosis
Blastomycocsis
Actinomyces if gram negative which can mimic appearance
sporotrichosis is fungi widespread in soil and rose bushes. Most common route of infection is via thorn
What happens after initial inoculation?
Small papule/ nodule forms at site 1 week - 6 months after inoculation
Infection spreads along lymphatics, producing a series of nodules
Can cause disseminated disease and pulmonary infection. More common if immunocompromised, but can occur in immunocompetent. Prognosis poor
How is sporotrichosis diagnosed?
What is treatment?
Culture of drained/ aspirated material
Itraconazole/ fluconazole
What parasites can cause skin lesions?
Leishmaniasis
Schistosomiasis
Cutaneous larva migrans - hookworm (ancylostoma/ necator)
Guinea worm
Onchocerciasis
How does hookwrom infections cause disease?
Causes cutaneous larva migrans
Hookwrom ivnades via skin after contact with soil
Life cycle takes it through blood to intestine
As humans are not natural hosts, larva fail to escape via skin. So can creep along parallel to skin, leaving intensely itchy rash
What is treatment of scabies?
Norweigan scabies is extensive thickening and crusting, which may occur in severely immunocompromised
Permethrin topical
Oral ivermectin - if severe/ Norweigan scabies
What other tropical diseases can have rash? (maculopapular)
Dengue
Marburg
Hepatitis B
Rickettsia - RMSF
Typhus
Kawasaki syndrome can form part of differential diagnosis for skin rash.
What is pathophysiology?
Children <4
acute vasculitis due to dysregulated T-cell activation to infectious trigger.
Mortality 2%
More common Asian population
What are symptoms of Kawasaki’s disease?
Dryness/ redness of lips/ palms/ soles
Desquamation of palms/ soles
Oedema
Arthralgia
Myocarditis - 20% can develop coronary artery aneurysms
What is treatment of Kawasaki’s?
Immunoglobulin
Aspirin
Both can prevent coronary artery damage
Trypanosoma cruzi invades via skin. Reduviid bug deposits parasite on skin during feeding. This is then rubbed into wound/ mucus membrane. Can invade muscle
What are common symptoms?
Skin - chagoma/ Romanas sign
95% have cardiac defects - conduction/ heart failure due to myocardial invasion
megaoesophagus
megacolon
Parasitic worms are primarily intestinal parasites. Larval stages of non-human tape worms can invade muscle
What species invade muscle?
Tapeworms -
Echinococcus granulosus - sheep tapeworm
Taneia solium - pork tapeworm. Can cause neurocysticercosis
Roundworm (nematode) -
Trichinella - pork roundworm
What are viral causes of arthritis?
HBV
Rubella - post vaccination
Mumps
Parvovirus
Togaviruses - Chikungunya, Ross River, Eastern Equine virus, Western Equine virus
What are causes of reactive arthritis?
Associated with HLA B27
Due to immunogenic phenomena, as opposed to bacteria within joint
Campylobacter
Salmonella
Shigella
Yersinia
Chlamydia trachomatis - Reiter’s syndrome urethritis, arthritis, conjunctivitis
gonorrhoea
streptococcal
viral - many causes
What are causes of septic arthritis?
Knees most commonly affected. Followed by hips, ankles, elbows. Occurs more commonly in damaged joints e.g RA
Staphylococcus - most common Streptococci - A/B Haemophilus influenzae - children Kingella - age <4 Neisseria gonorrhoea E. Coli
Rarer - Salmonella - disseminated infection Mycobacterium TB Borrelia burgdorferi Sporotrichosis - fungal
What are symptoms of septic joint?
Fever
joint pain
swelling
reduced movement
What is treatment of native joint septic arthritis?
Flucloxacillin 2g QDS or
Vancomycin or
Clindamicin or
ceftriaxone
Oral options (depending on sensitivities) - flucloxacillin ciprofloxacin linezolid clindamicin
6 weeks therapy
Minimum 2 weeks IV
What is treatment of prosthetic joint septic arthritis?
DAIR/ revision - see separate cards
Vancomycin + rifampicin
Duration 6 weeks at least
What are risk factors for septic joint?
Overlying skin infection
recent surgery
OA/ RA
diabetes mellitus/ HIV
immunosuppressive medication
IVDU
Soil exposure
Animal bite
What is treatment of discitis/ vertebral osteomyelitis?
Ceftriaxone 2g OD or
Vancomycin - aim higher level 15-20
Add metronidazole 400mg TDS if epidural abscess
Bone can become infected directly, or from haematogenous spread
What bacteria are common causes of osteomyelitis?
Staph aureus
Staph epidermidis
GroupB strep - neonates
Neisseria gonorrhoea
Pseudomonas - diabetic
Enterococci
Enterobacter
Rarer - salmonella - sickle cell TB - Potts disease pasteurella - cat bite serratia
What is treatment of osteomyelitis?
Flucloxacillin 2g QDS or
Vancomycin + rifampicin
6 weeks therapy
Minimum 2 weeks IV
How to diagnose osteomyelitis?
CRP/ ESR
Blood cultures
Imaging
Bone biopsy
Which infective agents replicate in erythrocytes?
Plasmodium
Babesia
Bartonella
Rickettsia
Parvovirus
Colorado tick fever
All infections can cause anaemia
Why do EBV/ CMV cause thrombocytopenia?
Antibodies to virus cross-react and adhere to platelets
HTLV 1/2 infects T-cells in bone marrow.
Which countries is it found in?
West Indies
Japan
Can have up to 15% population infected
Rarer cases in SA/ Africa
How is HTLV primarily transmitted?
Maternal breast milk - most common
sexual
IVDU
What are symptoms of HTLV infection?
mild febrile illness
lymphadenopathy
pleural effusion/ aseptic meningitis can develop
tropical spastic parapesis - myelopathy
acute leukaemia
PCP/ strongyloides and other opportunistic infection
Cellulitis is erythema of skin, with pain, swelling, fever. Can have systemic features
What grading system can be used to help decide about treatment/ admission?
Eron grading
Class I - no systemic signs
Class II - systemically unwell, but reasonably stable
Class III - significant systemic upset - confusion/ tachycardia/ hypotension
Class IV - septic/ life-threatening
Class I - oral
Class II - I 48 hours, then oral or OPAT
Class III/ IV - IV
What are differential diagnosis of cellulitis?
DVT
Ruptured Baker’s cyst
Septic arthritis
gout
superficial thrombophlebitis
varicose eczema
lymphoedema
lipdoermatosclerosis - subcutaneous panniculitis in lower limbs of obese women with venous insufficiency
Skin and soft tissue infection, with history of animal contact.
What are possible organisms?
Cat bite - pasteurella
dog bite - capnocytophaga
bartonella
Francisella tularensis
bacillus anthracis
yersinia pestis
Skin and soft tissue infection, with history of water contact.
What are possible organisms?
vibrio vulnificus
aeromonas hydrophilia
mycobacterium marinum
pseudomonas
Skin and soft tissue infection, with history of IVDU
What are possible organisms?
MRSA
C botulinum
C tetani
B anthracis
Skin and soft tissue infection, with history of foreign travel
What are possibyle organisms?
cutaneous leishmaniasis
cutaneous larva migrans
myiasis
What are virulence factors of strep pyogenes in SSTI?
Adherence factors
Exotoxins
Superantigen
Adherence factors -
fimbrillae - binds host epithelial cells
M protein - binds fibrinogen and blocks complement binding
Protein F - allows invasion into epithelial cells
Exotoxins -
Haemolysin (Streptolysin O) - tissue damage
Hyaluronidase - digest host tisse
Superantigens -
streptococcal pyrogenic exotoxins (SPEs) - bind to T cells causing mass cytokine release - toxic shock
What are virulence factors of staph aureus in SSTI?
Adherence factors
Exotoxins
Superantigen
Adherence factors -
clumping factor - bind host epithelial cells
Protein A - prevents opsonisation
Exotoxin -
PVL (5% of isolates) - causes membrane pore formation in neutrophils, leading to skin lysis/ necrosis
Superantigen -
Enterotoxin, TSST, Exfoliative toxin A/B - bind to T cells causing massive cytokine activation
What is treatment duration for cellulitis?
7-14 days depending on severity
prolonged course if underlying disease e.g PVD, lymphoedema
What scoring system is used to assess for probability of necrotising soft tissue infection?
If high clinical suspicion, then do not check score, proceed to debridement
Laboratory Risk Indicator for Necrotising Fasciitis - LRINEC
CRP WCC Hb Na+ Cr Glucose
Gardener presents with lump over left leg. Was ulcer, but now hard red nodule. Nodules in distribution of lymphatics
What is treatment?
Dapsone Doxycycline Cidofovir Itraconazole Peg-IFN
Itrazoncaole
Sporotrichosis
Diabetic foot ulcer.
What are indications of treatment for infection?
Inflammation
cellulitis
tissue loss
IDSA uses PEDIS to grade diabetic foot infections Perfusion Extent Depth Infection Sensation
HCA has skin abscess. Swab shows PVL staph which is treated. What is advice about returning to work?
Repeat screen one week after treatment, and return to work once lesion healed
Repeat screen on last day treatment, return to work if negative
Repeat screen one week post-decolonisation, return to work if three negative screens
Return to work after completing antibiotics
PVL is notifiable disease
Repeat screen one week after treatment, and return to work once lesion healed
If unwell/ cellulitis/ boils - treat with antibiotics
If well - chlorhexidine decolonisation wash
If repeat screen positive, then for further decolonisation.
May be positive due to persistent infection, or re-infection from close contact in community
If repeatedly positive, can still return to work if no active skin lesions
What is differential diagnosis for septic arthritis?
Reactive arthritis
bursitis
gout
lyme disease
brucella
whipples disease - mimic RA presentation
What is involved in two-stage revision of infected prosthetic joint?
Infected tissue/ implant removed
4-6 samples of deep tissue taken with new set of instruments (not wound swabs)
6 weeks antibiotics given
Repeat sampling and insertion of prothesis to ensure clearance of infection
48 year old with ESRF, has right hip fracture and surgery. Now has discharging sinus.
- Wound swab grows enterobacter and coagulase-negative staph.
- Deep wound culture grows enterobacter.
Plan for 2 stage revision. He has hip washout, with spacer inserted.
What is plan for antibiotics?
Ignore coagulase negative staph in wound swab. Deep wound swab more indicative of actual infection
Given six weeks therapy (minimum 2 IV), in between first and second stage revision arthroplasty
79 THR 2015. Presents 8 month history pain on weight bearing. Has discharing sinus.
Has single stage revision surgery. Then has teicoplanin IV, and rifampicin oral for 6 weeks via OPAT.
Returns to clinic for 6 week post-operative assessment. Doing well, and pain free. What is plan with antibiotics?
continue antibiotics further 6 weeks
stop teicoplanin, continue rifampicin further 6 weeks
give cipro and rifampicin further 6 weeks
stop all antibiotics
give cipro and rifampicin further 6 weeks
Single stage considered if no co-morbidities, good soft tissue health, and sensitive organism
Total three months therapy, which includes initial 6 weeks therapy
Extend to six months total for knee infection
Why are rifampicin/ cipro useful in prosthetic infections?
Bactericidal
Good joint penetration
Prevent biofilm formation
SJS/ TEN are part of same spectrum of disease, in which there is mucosal loss. Nearly always caused by drugs. CD8 T cells directed towards drug, and cytokines produced cause damage and skin shedding.
What are causes?
Nearly all caused by medication
Antibiotics -
co-trimoxazole
Beta-lactam
Fluroquinolones
Anti-epileptics
NSAIDs
Allopurinol
Symptoms start between 1 week - 1 month after starting drug.
What are symptoms of SJS/ TEN?
Prodromal flu-like illness - fever, coryza, myalgia
Abrupt onset of rash which extends to maximal within 4 days
- erythema
- macules
- blisters
How to diagnose SJS/ TEN?
Clinical diagnosis
Skin biopsy
What is mortality risk of SJS/ TEN?
What scoring systems can be used to predict mortality?
Mortality 10% SJS/ 30% TEN
SCORTEN score - Age > 40 years Presence of malignancy (cancer) Heart rate > 120 Initial percentage of epidermal detachment > 10% Serum urea level > 10 mmol/L Serum glucose level > 14 mmol/L Serum bicarbonate level < 20 mmol/L.
What is differential diagnosis of SJS/ TEN?
Other severe cutaneous adverse reactions (SCARs) to drugs (eg, drug hypersensitivity syndrome)
Staphylococcal scalded skin syndrome and toxic shock syndrome
Erythema multiforme
Mycoplasma infections
Bullous systemic lupus erythematosus
Paraneoplastic pemphigus
What is management of SJS/ TEN?
Stop offending drug
Fluid support
Temperature support
Analgesia
Antibiotics - only if infection develops
Case reports - anti-TNF/ IVIG/ cyclophosphamide
IDSA use PEDIS is grade diabetic foot ulcers
What constitutes the score?
Perfusion Extent Depth Infection Sensation
Uninfected 1
Mild 2 - cellulitis >2cm
Moderate 3 - deep involving muscle/ bone
Severe 4 - sepsis
diagnosis of infection is clinical. Microbiology cannot diagnose infection, but can be used to identify infecting organism
CUH guidelines
Diabetic foot ulcer
What is treatment?
Mild
Moderate
Severe
Mild
- flucloxacillin/ co-amoxicalv
Moderate
- co-amoxiclav
- doxycycline + metro
Severe
- co-amoxiclav IV
- tazocin
- MRSA - vancomycin + tazocin
duration minimum 2 weeks
