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?
