skin n soft tissue infections

Question 1

—– 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 )

Answer 1

• resident flora
• transient flora
• site

Question 2

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- —-

Answer 2

• mild
• oral
• severe sepsis
• nectosting fasciitis
• gas gangrene

Question 3

• cellulites:
  1- — infection in – and — tissues
  2- precipitate is often a - in the skin
  3- pathogens:
  4- clinical fecature:
  5- risk factors:

Answer 3

• 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

Question 4

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

Answer 4

• fluxaciliin
• culture and suspectbilites
• benzylpeniclin

Question 5

-Severe destructive bacterial
infection of skin, subcutaneous
& peri-muscular fat
-with necrotic liquefaction of fatty
tissue
- this is known as:
- participants:
- pathogens

Answer 5

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)

Question 6

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

Answer 6

• severe rapid
• normal
• shiny or blisters
• blood supply due to necrosis

Question 7

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

Answer 7

• surgical
• Broad-spectrum empiric therapy
  e.g. vancomycin + piperacillin-tazobactam+clindamycin
  -If group A strep, benzylpenicillin +
  clindamycin (suppresses toxin production)

Question 8

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:

Answer 8

• fourniers gangrene
• full thickness
• pathogen : usually polymicorbial includes anearobes
• managed:
• Extensive debridement vital
• Broad-spectrum antibiotics

Question 9

gas gangrene - clostridial myonecrosis:
- is a necrosing myosyists
- pathogens :
- participants

Answer 9

• 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

Question 10

gas gangrene clinical features and diagnosis:
treatment:

Answer 10

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

Question 11

1. Impetigo
2. Folliculitis
3. Furuncules
4. Carbuncles
5. Abscesses
6. Erysipelas
7. Scalded skin syndrome
   (refer to Staphylococci lecture)
8. Acne
9. Bites
   10.Diabetic foot infection
   11.Surgical site infection
   are all examples of —-
   10 and 11 may form —

Answer 11

• less serious bacterial skin n soft tissue infections
• form n progress to severe sepsis

Question 12

impetigo:
- infection confined to — skin layers
- — infectious and outbreaks in —
pathogens include :
clinical :
diagnose:
treatment

Answer 12

• 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

Question 13

Superficial infection of hair
follicles & apocrine structures is known as —
pathogen :
clinical/diganos:
treatment:

Answer 13

• foliculities
• mostly s. aureus
• Small pruritic papules with
  central pustule
• often not required but flucolxaclin if pressman/extensive

Question 14

Deep inflammatory nodule,
usually develops from preceding
folliculitis is known as —-
and this is found in —-
- treatment: spontaneous or surgical drainage

Answer 14

• furuncles
• axilla and buttocks ( skin w hair follicles )

Question 15

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

Answer 15

• furncle
• subcutaneous fat
• pus

Question 16

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:

Answer 16

• erysipelas
• children elderly diabetics
• mostly group A strep
• treatment:
  – IV benzylpenicillin
  – PO switch to oral amoxicillin
  – Or oral antibiotics from outset

Question 17

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;

Answer 17

• acne
• excess , blocked
• Secondary infection with
  Cutibacterium spp.
  – Inflammation & scarring
• treatment ;
  Broad-spectrum antibiotics
  e.g. doxycycline

Question 18

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

Answer 18

• muscle rigidity and spams
• spores
• neurotoxins ( tetanospasmim )
• vaccine

Question 19

• 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

Answer 19

• skin
• person to person

Question 20

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

Answer 20

• soil intestine and facesces of animals
• gitttt
• localised anaerobic environment ( necrotic tissue)
• inhibitory

Question 21

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

Answer 21

• minutes
• 3-4 weeks
• lockajw
• risus sardonicus

Question 22

tetanus prevention :

Answer 22

• 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

Question 23

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

Answer 23

animal flora n staph/ strep

Question 24

human bites:

Answer 24

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?

Question 25

diabetic foot infection:
1- non limb threading :
-pathiegns:
- treatment :
2- severe n limb threatening:

Answer 25

• 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

Question 26

management of severe food infects :

Answer 26

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

Question 27

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

Answer 27

• colonised
• 10-14 days
  -6-12 weeks

Question 28

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)

Answer 28

healthcare
type of procduere and patient factors

Question 29

classification of SSI:
- pathogens;

Answer 29

• 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)

Question 30

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

Answer 30

pre
intra
post

Question 31

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

Answer 31

• superficial
• colonising

Question 32

• Warts
• Cold sores
• Varicella Zoster virus
• Mpox
• Hand, foot & mouth disease
  are all — skin infections

Answer 32

viral

Question 33

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

Answer 33

genital
dna

Question 34

MPOX are enveloped — virus and genus prthopoxivrius pox viridian family
- trasmittion is — transmutation and through direct contact w —

Answer 34

• 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

Question 35

MPOX incubation period is — days
- rash presists for – weeks

Answer 35

• 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)

Question 36

fungal infection include:
parasitic skin infection :

Answer 36

• candid ringworm n pityriasis versicolor
• scabies n lice

Question 37

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

Answer 37

erweigian scabies

Question 38

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)

Answer 38

headline
body lice
pubic lice

Question 39

summary :

Answer 39

• 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