skin n soft tissue infections Flashcards
—– Staph. epidermidis
(>90% of skin flora)
—– e.g. Staph. aureus, gut flora
– Colonisation vs. infection
( what lies in our skin vary in – as hand vs groin )
- resident flora
- transient flora
- site
life threaten skin n soft tissue infections:
1- cellulitis:
– Most cases are — and may even be managed with— antibiotics from home
– Has potential to lead to —-if not treated appropriately
2- —-
3- —-
- mild
- oral
- severe sepsis
- nectosting fasciitis
- gas gangrene
- cellulites:
1- — infection in – and — tissues
2- precipitate is often a - in the skin
3- pathogens:
4- clinical fecature:
5- risk factors:
- acute
- skin and subcutaneous
- break
- pathogens include:
– Staphylococcus aureus
– Streptococcus pyogenes (Group
A beta-haemolytic streptococci)
– Less commonly Group C or G
beta-haemolytic streptococci - clinical features:
- Erythema, swelling, pain,
hot to touch - Often well-demarcated
- May be evidence of
precipitating skin break
– although most often not - Patient may be
systemically unwell
– i.e. febrile, tachycardic - risk factors:
1. Previous cellulitis
2. Diabetes mellitus
3. Obesity
4. Peripheral vascular
disease
5. Lymphoedema
6. Skin breaks:
– Leg ulcers
– IV drug use
– Trauma
– Insect bites
cellulites management:
1- blood cultures or skin swab if detected
2- mark boundaries of cellulites
3- iv antibiotic or PO in less severe
- start smart empiric by using —- for staph autos and strep phosgene but consider MRSA risk factors
- then focus aka directed which his based on — and — example:—- if s.pyogene confirmed
- manages any underlying cause
- fluxaciliin
- culture and suspectbilites
- benzylpeniclin
-Severe destructive bacterial
infection of skin, subcutaneous
& peri-muscular fat
-with necrotic liquefaction of fatty
tissue
- this is known as:
- participants:
- pathogens
necrosi fasciitis
participants include: minor trauma, stab wounds, surgery
- pathogens include:
– Type 1: Polymicrobial
– Type 2: Group A beta-haemolytic
streptococci (flesh-eating bug)
– (Type 3: Gas gangrene)
necorstinf fasciitis clinical features:
1- – infection — progressive
2- pain out of prioportion to clinical appearance as skin can initially look —
3- — skin or —
4- skin color changes due to deprived — due to —
5- patient is systemically well
6- high mortality of 20-47
- severe rapid
- normal
- shiny or blisters
- blood supply due to necrosis
encrusting fasciitis management:
- promot diagosis
- urgent — assessment and debridement of dead tissue by sneidg tissue for culture n suspecibitlyu N.B fresh and not in formalise
- blood culture
* anitbitoics:
tissue w clinical microbiology/ID
- start smart w :
- then focus:
- supportive management in ICU
- surgical
- Broad-spectrum empiric therapy
e.g. vancomycin + piperacillin-tazobactam+clindamycin
-If group A strep, benzylpenicillin +
clindamycin (suppresses toxin production)
A form of necrotising fasciitis
occurring in the perineum is known as —
by which we will have full — necrosis of perineal skin and may involve; scortum penis and abdominal wall which is severe and disfiguring
- pathogens:
- managed:
- fourniers gangrene
- full thickness
- pathogen : usually polymicorbial includes anearobes
- managed:
- Extensive debridement vital
- Broad-spectrum antibiotics
gas gangrene - clostridial myonecrosis:
- is a necrosing myosyists
- pathogens :
- participants
- Pathogens: toxin-producing
Clostridium spp.
– Clostridium perfringens
– C. septicum - Precipitated by:
– Direct inoculation of wound (trauma or
surgery)
– Haematogenous – C. septicum from
GIT if colon cancer
gas gangrene clinical features and diagnosis:
treatment:
Clinical Features
– Acute onset of severe pain
– Devitalisation of limb, mottled skin
– Fluid or gas-filled blisters on skin
– Systemically unwell
– Foul odour, crepitus
Diagnosis
– CT/ X-ray: Gas in tissues
– Wound swab/ blister fluid/tissue for
culture
– Blood cultures
* Surgical debridement
* Antibiotic therapy
– Broad-spectrum empirically
– Change to benzylpenicillin
when Clostridia confirmed
* Supportive care in ICU
* Hyperbaric oxygen
- Impetigo
- Folliculitis
- Furuncules
- Carbuncles
- Abscesses
- Erysipelas
- Scalded skin syndrome
- Acne
- Bites
10.Diabetic foot infection
11.Surgical site infection
are all examples of —-
10 and 11 may form —
- less serious bacterial skin n soft tissue infections
- form n progress to severe sepsis
impetigo:
- infection confined to — skin layers
- — infectious and outbreaks in —
pathogens include :
clinical :
diagnose:
treatment
- superficial
- highly
- cretches
- group a c g streptococci
- staphylococcus. aureo
- clinical features : exposed sites as face arms legs
- vesicles initially –> golden crusted lesions
- diagnsosis by clinical , cultural of exudate
- treatment : flucoaxilline
Superficial infection of hair
follicles & apocrine structures is known as —
pathogen :
clinical/diganos:
treatment:
- foliculities
- mostly s. aureus
- Small pruritic papules with
central pustule - often not required but flucolxaclin if pressman/extensive
Deep inflammatory nodule,
usually develops from preceding
folliculitis is known as —-
and this is found in —-
- treatment: spontaneous or surgical drainage
- furuncles
- axilla and buttocks ( skin w hair follicles )
1-carbuncle’s are larger and deeper than —
extending into —
- nape of neck back or thighs
- patient is unwell
2- absences : is a localised collection of —- and pathogen is s.auroes and poly microbial
- treatment by incision n drainage and NO role for anitbitocis
- furncle
- subcutaneous fat
- pus
Superficial form of cellulitis with
lymphatic involvement is known as —
- epidemiology in :
-pathiegns:
- clinical/diagnos:
– Painful erythematous lesion with elevated,
well-defined border
– Face or legs
– May be febrile/ unwell
- treatment:
- erysipelas
- children elderly diabetics
- mostly group A strep
- treatment:
– IV benzylpenicillin
– PO switch to oral amoxicillin
– Or oral antibiotics from outset
Multi-factorial skin disorder is known as —
which can be due to: — sebaceous secretion by follicles or – sebaceous glands which leads to pestles
- pathogens :
- treatment;
- acne
- excess , blocked
- Secondary infection with
Cutibacterium spp.
– Inflammation & scarring - treatment ;
Broad-spectrum antibiotics
e.g. doxycycline
traumatic wounds - clostridirum:
- tetanus is life-threatening illness
manifested by muscle— &— caused by the— forming organism Cl. tetani
- the symptoms n signs are caused by — produced by the vegetative form of cl.tetani
- tetanus is a — preventable disease
- muscle rigidity and spams
- spores
- neurotoxins ( tetanospasmim )
- vaccine
- Cl. tetani spores survive in environmental
- Spores are introduced via —-
, often a puncture wound, burns, trivial
wounds, the umbilical stump in the
newborn infant – spores may contaminate heroin - —-transmission does not occur
- skin
- person to person
pathogens of tetanus:
1- spores found in —–
2- humans may harbour organism in –
3- Spores in wound germinate when there is a localized —-
4- spores may contaminate —
5-A tiny area with relatively anaerobic conditions is required for Cl. tetani spores to germinate
5- Toxin blocks transmission at— synapse resulting in ‘inhibition of inhibitory neurons’
- sustained muscle contraction/spasm
- soil intestine and facesces of animals
- gitttt
- localised anaerobic environment ( necrotic tissue)
- inhibitory
presentation :
* Muscle Spasms r frequenct n last — and persist for — weeks
– Muscles of the thorax, abdomen and
extremities = flexion of arms,
extension of legs, arching of back
– Trismus or “—–”
– —–”(sardonic
appearance) produced by increased
tone of orbicularis oris
* Complications
– Laryngospasm
– Autonomic nervous system dysfunction (labile BP,
arrhythmias, sweating)
The mortality rate is ≥ 60% in severe cases
- minutes
- 3-4 weeks
- lockajw
- risus sardonicus
tetanus prevention :
- Prevented by immunisation with toxoid vaccines
- Recovery from tetanus does not confer natural immunity
- The majority of cases are birth-associated among newborn babies & mothers not vaccinated
- Toxoid vaccine is part of childhood
vaccination programme in many countries:
DTP (diphtheria-tetanus-pertussis) vaccine
– Clinical efficacy almost 100% but immunity
wanes & after 10 years may not provide protection
animal bites are from —-
diagnosis ; Send swab (or tissue if
debriding) for culture &
susceptibility
management :
* Tetanus prophylaxis
* Usually co-amoxiclav
– Discuss with Micro if deep infection
/ osteomyelitis or not resolving
animal flora n staph/ strep
human bites:
Pathogens
* Mouth flora
– e.g. strep, anaerobes
Management
* Tetanus booster
* Antibiotics (usually co-
amoxiclav)
* Consider blood-borne viruses
* Check for deep infection:
* Is there osteomyelitis?
diabetic foot infection:
1- non limb threading :
-pathiegns:
- treatment :
2- severe n limb threatening:
- cellutlies no vascular compromise no abscess
- staph auras b haemolytic strep
- flucoaxillin :
– Cellulitis: 5-7 days
– Superficial ulcer: 5 days
– Deep ulcer: flucloxacillin
+ metronidazole - 7 days
2- serve:
vascular compromise abscess ad osstemomylitis/gangrene - need radiological
imaging to rule out
osteomyelitis if
this is suspected
management of severe food infects :
Involve MDT:
* Endocrinology i.e.
glycaemic control
* Diabetes nurse
specialist
* Vascular surgeons
re drainage/
debridement
* Radiology: is there
osteomyelitis?
* Microbiology/ID antibiotic
choice
* Podiatrist
* ?OPAT team if osteomyelitis
antibiotic treatment of severe diabetic foot infection :
* Start smart: Empiric broad-spectrum
– Co-amoxiclav
– Piperacillin – tazobactam (If evidence of sepsis, previous inpatient
admission for diabetic foot infection, previous growth of Pseudomonas
aeruginosa from foot specimen)
* Broad spectrum aims to cover S. aureus & streptococci /
Gram-negatives / anaerobes)
– Often ulcers—- with multiple organisms so swabs may not be
helpful
– Tissue or bone specimens from debridement or bone biopsy are the
specimens of choice to identify the pathogen(s)
* Treatment duration: approximately —— days if just soft
tissue /—- weeks if bone involvemen
- colonised
- 10-14 days
-6-12 weeks
surgical sire infections SSI:
very common —- associated infection
risk factors: — and —
- surgery type:
– Clean (no breach of tract e.g. excision of a skin lump)
– Clean- contaminated (breach of GI/ GU/ Respiratory
etc. tract)
– Contaminated (operating in a contaminated field e.g.
post GI perforation)
healthcare
type of procduere and patient factors
classification of SSI:
- pathogens;
- classification : superficial deep/incisional organ/space
Pathogens: - Staphylococcus aureus (most common irrespective of type of
surgery) - Beta-haemolytic streptococci
- Gram-negative bacilli (mostly only seen post clean-contaminated or
contaminated surgery) - Anaerobes (post clean-contaminated or contaminated surgery)
- Coagulase-negative staphylococci (if prosthetic material)
prevention of SSI:*
—-operatively
– optimise risk factors such as diabetes mellitus
– MRSA decolonisation before some procedures if carriage
*—–operatively:
– No shaving, skin asepsis, choice/timing of antibiotic
prophylaxis
– surgical technique, theatre conditions, short duration
procedure
– Glycaemic control, oxygenation
*—-operatively:
– Removal of drains, asepsis when reviewing wound
pre
intra
post
wound colonisation:
*—- swabs taken from diabetic ulcers likely represent— flora if wound has not beenappropriately cleaned and debrided
* If a swab is being sent from a diabetic ulcer shouldbe done so after cleaning and debridement of any
dead skin / tissue and taken from base of ulcer
* Avoid debridement if foot ischaemic
- superficial
- colonising
- Warts
- Cold sores
- Varicella Zoster virus
- Mpox
- Hand, foot & mouth disease
are all — skin infections
viral
HPV : human papilloma virus
— warts - STI
- common warts:
– Children
– Infection by direct contact
– Palms, wrists, dorsum of
hand
– — virus infects
epidermal cells -
hypertrophy & multiply
leading to keratinised
nodular papilloma
- treatment;
* Childhood: self-resolution
* Excision, salicylate &
lactic acid ointment
* Freezing, cryoprobe or
liquid nitrogen
genital
dna
MPOX are enveloped — virus and genus prthopoxivrius pox viridian family
- trasmittion is — transmutation and through direct contact w —
- DS DNA virus
- Epidemiology
o Identified as cause of human disease in 1970s, sporadic cases
in central and West Africa
o 2022 WHO reports endemic in multiple African countries
o Global outbreak/PHEIC 2022 (Clade IIb)
o Public Health Emergency of International Concern (PHEIC)
declared by WHO 2024 (Clade I) - Transmission
o Human to human transmission
▪ Direct contact with lesions (Skin/genital/mucous membranes)
▪ Through the air
▪ Indirect contact (Fomites)
▪ Percutaneous
▪ Vertical
MPOX incubation period is — days
- rash presists for – weeks
- 5-21days
- 2-3 weeks
(info: * Rash
o Persists for 2-3 weeks
o Macules papules vesicles pseudopustules
o Well circumscribed, umbilicated
o May be painful and then itchy once crusted
o Distribution has differed in outbreaks v infections in endemic
areas - Systemic symptoms
o Fever, headache, myalgia, lymphadenopathy - Timing of onset of systemic symptoms and rash has
differed during some outbreaks when compared with
clinical course in countries with endemic infection)
fungal infection include:
parasitic skin infection :
- candid ringworm n pityriasis versicolor
- scabies n lice
scabies :
* Scabies mite (Sarcoptes scabiei)
* Mite burrows into epidermis
* Clinical features
– Characteristic burrows in finger webs
– Itch ++ (worse at night)
– ‘——: diffuse crusted lesions (same parasite but in
immunocompromised patients)
* Highly infectious Outbreaks: Household, boarding school
* Treatment
– Topical permethrin- messy, need to leave on overnight
– Wash clothes/ sheets etc. as well
erweigian scabies
lice - pediculosis:
*—- (Pediculus capitis)
– Common in children, outbreaks in
schools, spread by direct contact
– ‘Nits’ (eggs) attached to bases of
hairs
– Itch / papular lesions
– Treatment: Malathion or 1%
permethrin. Fine combing to remove
nits. Bathing/ washing clothes
*—- lice (Pediculus humanus)
*—- lice (Phthirus pubis)
headline
body lice
pubic lice
summary :
- Skin & soft tissue infections are common but most
are relatively minor - Bacterial causes are often found on the skin, e.g.
Staph. aureus or the respiratory tract, e.g. Group A
streptococci - Common, usually minor infections include impetigo,
carbuncles & SSI (healthcare-associated) - Warts, tinea & scabies are relatively common viral,
fungal & parasitic infections, respectively, requiring
specific treatment
