Skin and soft tissue infections

Question 1

Clinical syndromes caused by staphylococcus aures

Answer 1

Folliculitis
Furuncles
Carbuncles
Impetigo
Cellulitis
Toxic shock syndrome
Post-operative wound infections

Question 2

Clinical syndromes caused by streptococcus pyogenes

Answer 2

Impetigo
Erysipelas
Cellulitis
Necrotising fasciitis
Toxic shock syndrome

Question 3

Impetigo

Answer 3

• very superficial infection involving the epidermis
• commonest in children and is usually on the face often around the mouth and nose
• two forms

Question 4

What are the two forms of impetigo?

Answer 4

• non-bullous (‘honey-crust’) lesions, most commonly due to Strep pyogenes (Group A strep)
• bullous, when bullae rupture they appear instead as thin ‘varnish’like’ crusts due to staph aureus

Question 5

Folliculitis

Answer 5

• infection of the hair follicles
• may occur after exfoliation, use of a loofah sponge, shaving or spontaneously
• whirlpool (hot tub or spa) folliculitis can be caused by pseudomonas aeruginosa
• self-limiting so there is no specific treatment

Question 6

Abcesses and furuncles

Answer 6

• staph aureus is the leading community pathogen causing abcesses and furuncles
• certain phage types are associated with recurrent episodes of furunculosis and may spread among family members
• staphylococcal blood stream infection from a minor skin lesion or a furuncle may rarely result in severe complications, including osteomyelitis, septic arthritis and endocarditis

Question 7

What’s an abcess?

Answer 7

A collection of pus in any tissue

Question 8

What’s a furuncle?

Answer 8

An abcess in the skin, commonly called a boil

Question 9

What’s a carbuncle?

Answer 9

Larger abcesses, interconnected furuncles

Question 10

What is cellulitis and what are the 3 categories?

Answer 10

Acute spreading inflammation involving soft tissues but excluding muscle.

• Erysipelas
• Acute cellulitis
• Necrotising fasciitis

Question 11

Erysipelas

Answer 11

• involve the superficial dermis
• extremes of age
• usually Group A strep (but can be group G, B, C)
• face and leg commonest sites
• distinction from acute cellulitis is unimportant clinically
• blood cultures, aspirates, biopsies are usually negative
• may recur in the same area (possibly related to local lymphatic insufficiency)

Question 12

Treatment of erysipelas

Answer 12

Benzyl penicillin (iv)
High does iv flucloxacillin will cover both strep and staph infection if doubt about aetiology

Question 13

Acute cellulitis

Answer 13

• ‘wild fire’ onset
• often high fever then cellulitis 12 hours later
• rapidly spreading inflammation of the deep dermis and subcutaneous fat.
• often subtle portal of entry
• usually group A strep (sometimes staph aureus)
• redness and pain, systemic signs and symptoms
• lymphangitis can occur (streak of redness on lymphatics)
• blood cultures/aspirates usually negative unless there is a purulent collection

Question 14

Necrotising fasciitis

Answer 14

• life threating
• involves superficial fascia and underlying fat
• two main bacterial causes: strep pyogenes and synergistic infections with anaerobic organisms mixed with aerobes (abdo surgery or perineal infection/trauma)

Question 15

When would you suspect necrotising fasciitis instead of cellulitis?

Answer 15

• nec fasc failure to respond to antibiotics
• marked pain
• very unwell
• in mixed infection there could be crepitus or a foul smell

Question 16

What’s fourniers gangrene?

Answer 16

A form of necrotising fasciitis affecting the male genitalia

Question 17

Diagnosis and treatment of necrotising fasciitis

Answer 17

• Surgical exploration and debridement
• antibiotic therapy can be guided by initial gram stain of debrided sufgical material and then culture results
• if Strep nec fasc: high dose IV penicillin and clindamycin
• if treating blind or mixed infection: iv cefuroxime, clindamycin and metronidazole

Question 18

Clinical definition of toxic shock syndrome

Answer 18

1. temperature > 38.9
2. systolic BP < 90mmHg
3. rash with subsequent desquamation, especially on palms and soles
4. involvement of three or more systems:
   - GI (vomiting, profuse diarrhoea)
   - muscular (severe myalgias or CPK 5x normal)
   - renal (creatinine twice normal with pyuria)
   - liver (hepatitis: bilirubin AST, ALT twice normal)
   - blood (thrombocytopenia <100000 mm^3)
   - CNS (disorientation without focal neurological signs)

Question 19

Gas gangrene

Answer 19

Clostridial myonecrosis

• a necrotising gas forming process of muscle associated with systemic signs of toxaemia
• approx 80% due to clostridium perfringens type A. Other causes: Clostridium novyi, Clostridium spticum
• alpha toxin (lecithinase) is major toxin
• myonecrosis, shock, haemolysis
• usually related to trauma (can be minor), post-op (abdo), post partum, septic abortion
• can also appear spontaneously often associated with an underlying colonic carcinoma or intra-abdominal abscess

Question 20

Treatment of gas gangrene

Answer 20

Emergency surgical debridement
Antibiotics
Hyperbaric oxygen

Question 21

Pathophysiology of tetanus

Answer 21

• clostridium enters the body through a wound
• spores germinate in anaerobic conditions
• toxins are produced and disseminated through blood and lymphatics
• toxins act at various sites in the NS including the peripheral end plate, spinal cord, brain, and sympathetic NS.
• toxins gain access to the CNS via retrograde axonal transport in motor nerves
• toxins move into the presynaptic inhibitory interneurons with resulting inhibition of release of inhibitory neurotransmitters (GABA in the brain, glycine in the spinal cord)
• this results in heightened muscular activity
• loss of glycine inhibition occurs in the intermediolateral grey matter of the spinal cord results in increased sympathetic activity
• reduction of release of acetylcholine from motor neurons may result in paralysis of cranial nerves in cephalic tetanus

Question 22

Three forms of tetanus

Answer 22

Generalised
Local
Neonatal

In the generalised from the cervical, facial and masticatory muscles are affected first. There is then dysphagia, then generalised weakness, trismus and back spasm (opisthotonus)

Question 23

Clostridium tetani

Answer 23

• in soil and GI tract of animals and humans
• slender, motile, gram positive, anaerobic rod that may develop a terminal spore giving it a drumstick appearance
• insensitive to heat
• cannot survive in the presence of oxygen

Question 24

Clinical features of tetanus

Answer 24

• the earliest manifestation of generalized tetanus are rigidity of the masseter muscle (lockjaw/trismus), and facial muscles, with straightening of the upper lip (grimace/risus sardonicus)
• soon followed by rigidity of axial muscles with prominent involvement of the neck and back muscles (opisthotonus)
• rigidity of axial muscles may precede or accompany trismus
• stiffness of limb muscles may be evident with sparing of distal muscles
• dysphagia and laryngospasm (asphyxiation) due to muscles involved

Question 25

Diagnosis of tetanus

Answer 25

clinical and EMG studies

Question 26

Treatment

Answer 26

``` Supportive (ICU) Benzodiazepines Debridement of wounds Benzylpenicillin Tetanus IVIg ```

Question 27

Organisms that might colonise venous ulcers

Answer 27

``` Staph aureus Gram negatives (pseudomonas) ```

Question 28

When would you give someone with a venous ulcer antibiotics?

Answer 28

Cellulitis Lymphangitis Systemic infection

Question 29

Common cause of malignant otitis externa in diabetics

Answer 29

Pseudomonas

Question 30

Cause of athletes foot

Answer 30

Tinea pedis

Question 31

Onychomycosis

Answer 31

Fungal nail infection

Question 32

Treatment of fungal nail infections

Answer 32

Itraconazole Griseofulvin Terbinafide For prolongued period of time

Question 33

What's pityriasis versicolor?

Answer 33

A common, asymptomatic, chronic infection of the stratum corneum caused by the lipophilic yeast Malassezia furfur. Characterised by discrete scaly depigmented areas of skin mainly on the trunk