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Microbiology > Skin and Soft Tissue Infections > Flashcards

Skin and Soft Tissue Infections Flashcards

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1
Q

Describe cellulitis and the most common causative organisms.

A

Bacteria breach the skin barrier and infect and spread throughout the deeper dermis and fat

  • characterised by oedema, erythema and warmth
  • most common in the lower extremities
  • S.aureus, beta-haemolytic streptocci (A, B, C and G)
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2
Q

Which group of people are most likely to get cellulitis?

A

Middle aged and elderly people

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3
Q

Where does S.aureus normally live?

A

Carried by 30-40% of normal people, in the nose or moist areas of the skin
Type carried is stable
2% MRSA prevalence

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4
Q

What and where is the average carriage of strep pyogenes?

A

5-15% carriage

Normally in the respiratory tract and vaginal tract

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5
Q

What are the non-modifiable risk factors for cellulitis?

A 
Pregnancy
White caucasian 
Trauma
Animal/insect bites
Tattoos
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6
Q

What are the modifiable risk factors for cellulitis?

A 
Venous insufficiency
Lymphoedema
Ulcers
Eczema
Athletes foot
Burns
Surgery
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7
Q

What factors are incorporated when considering the management decisions in SSTI?

A

Severity
Anatomical site
Health Care Associate Infections
Co-morbidities

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8
Q

When deciding between treating at home or treating in the community, what criteria mean they have to remain in hospital?

A 
Severe, localising pain
Confusion
Rapidly evolving skin lesions or skin blistering 
Systolic blood pressure  <100mmHg
Sepsis syndrome 
- heart rate >100
- RR >20/min
- temp >38 or <36
- WCC >12 or <4/mm3
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9
Q

Describe a class 1 soft tissue/skin infection.

A

No sign of systemic toxicity
No co-morbidities
Oral antibiotics
Treated as an outpatient

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10
Q

Describe a class 2 soft tissue/skin infection.

A

May have a systemic illness
Has PVD, obesity or venous insufficiency
IV antibiotics
Hospital treatment for at least 48 hours, then community treatment

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11
Q

Describe a class 3 soft tissue/skin infection.

A

Significant systemic illness
Unstable co-morbidities
IV antibiotics
Hospital treatment

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12
Q

Describe a class 4 soft tissue/skin infection.

A

Sepsis syndrome/necrotising fasciitis
Unstable co-morbidities
IV antibiotics and surgery
Hospital treatment

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13
Q

What is the organism and associated treatment for typical cellulitis?

A

S.pyogenes

- ampicillin or flucloxacillin

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14
Q

What is the organism and associated treatment for typical cellulitis with pus?

A

S.aureus (sometimes MRSA)

  • Flucloxacillin
  • Vancomycin
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15
Q

What is the treatment for typical cellulitis when the patient has a penicillin allergy?

A

Doxycycline
Clindamycin
or
Vancomycin

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16
Q

What is the organism and associated treatment for cellulitis caused by cat/dog bite?

A

Pasteurella multocida

  • co-amoxiclav
  • doxycycline and
  • metronidazole
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17
Q

What is the organism and associated treatment for cellulitis after fresh water exposure?

A

Aeromonas hydrophila

- ciprofloxacin

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18
Q

What is the organism and associated treatment for cellulitis after salt water exposure?

A

Vibrio vulnificus

- doxycycline

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19
Q

What is the organism and associated treatment for necrotising fasciitis?

A

C.perfringes/S.pyogenes

- flucloxacillin, clindamycin, gentamicin and metronidazole

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20
Q

What is the organism and associated treatment for cellulitis in butchers/fish handlers?

A

Erysipelothrix

- ciprofloaxacin

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21
Q

What are the differential diagnoses for cellulitis?

A

Stasis dermatitis - bilateral, circumfernetial
Acute arthritis - joint involvement
Pyoderma gangrenosum - ulceration on legs
Hypersensitivity - exposure to allergens, no fever or pain
DVT - no skin changes or fever
Necrotising fasciitis - severe pain, swelling, fever, rapid progression

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22
Q

What things should you consider when someone with cellulitis isn’t improving after treatment?

A

Resistance
Admission to hospital
Underlying conditions (bone infection, abscess, PVD)
Incorrect diagnosis (DVT, abscess, chronic changes)

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23
Q

What is the difference between cellulitis and erysipelas?

A

Cellulitis - bacterial infection of the lower layers of the skin
Erysipelas - bacterial infection of the upper layers of the skin, and superficial lymphatics
- raised lesion with clear line of demarcation

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24
Q

Describe what parts of the body erysipelas involves

A

Classically butterfly involvement of the face (20% of cases)
Legs are affected (80% of cases)
Can also involve the ear

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25
Q

What are the most common causative organisms of erysipelas?

A

Group A strep

  • more rarely you can get B, C and G as well
  • staph aureus also a rare cause
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26
Q

How is erysipelas diagnosed?

A

Elevated ASOT for 10 days

Mainly a clinical diagnosis, based on how the skin looks

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27
Q

Describe the appearance of an impetigo skin infection.

A

Sores and blisters, commonly in a perioral location

- honey coloured

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28
Q

What causes an impetigo skin infection?

A

Highly transmissible staphylococcus infection of the epidermis

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29
Q

Who would an impetigo infection most commonly affect?

A

Children

Sports people

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30
Q

What is the treatment for an impetigo skin infection?

A

Gently remove the crust
Treat with flucloxacillin
- be aware of the risk of a secondary infection (e.g. HSV)

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31
Q

What is the definition of necrotising fasciitis?

A

Severe inflammation of the muscle sheath that leads to necrosis of the subcutaneous tissue and adjacent fascia

32
Q

What bacteria (and virulence factors) cause necrotising fasciitis?

A

Most commonly a mixed infection (aerobes and anaerobes)

Toxin mediated - superantigens and cytokine release

33
Q

What are the important differentiating factors between cellulitis and necrotising fasciitis?

A 
Initial pain becomes painless
Rapid spread
Systematically unwell
Dusky skin and necrosis
May have skin crepitus
34
Q

What are the clinical manifestations of necrotising fasciitis?

A

Rapid progression
Most common on the extremities
Initially erythema and swelling without shapr margins
Pain and tenderness
Lymphatic involvement is rare
Colour change from red-purple to blue-grey
Skin breakdown and bullae with development of anaethesia
Probing of the lesion reveals easy through the tissues

35
Q

Describe the management of necrotising fasciits.

A

Surgical debridement
Antibiotics
Activated protein C (evidence is limited and can’t b used within 24 hours of surgery)

36
Q

Which antibiotics are used in the management of necrotising fasciitis?

A 
Penicillin
Flucloxacillin
Clindamycin
Gentamicin
Metronidazole
37
Q

When is prophylactic treatment for bites needed?

A

If the bite is deep, on the hands or the patient is immunocompromised/ splenectomised

38
Q

What is the treatment for a bite?

A

Gram stain of the wound and blood cultures
Debridement and abscess drainage
Antibiotics
- cover staph, anaerobes, pasteurella and capnocytophaga
Rabies immunoglobulin and vaccination is appropriate

39
Q

Describe pasteurella and it’s associated treatments.

A 
Gram negative bacteria
Most common pathogen which infects bites
Treated with
- penicillins
- cephalosporins
- tetracyclines
- quinolones
- macrolides
Co-amoxiclav, doxycycline and metronidazole
40
Q

Aeromonas species are associated with what clinical syndrome?
- caught after exposure to fresh water

A

Rapidly developing infection with fever and sepsis

41
Q

Edwardsiella tarda are associated with what clinical syndrome?
- caught after exposure to fresh water

A

Cellulitis, occasionally fulminant infection with bacterameia

42
Q

Erysipelothrix rhusiopathiae are associated with what clinical syndrome?
- caught after puncture wounds from crabs

A

Indolent localised cutaneous eruption, erysipeloid

43
Q

Vibrio vulnificus are associated with what clinical syndrome?
- caught after exposure to salt or brackish water

A

Rapidly progressive necrotising infection, bullous, cellulitis, sepsis

44
Q

Mycobacterium marinum are associated with what clinical syndrome?
- caight after exposure to fresh or salt water

A

Indolent infection, papules to ulcers, ascending lesion may resemble sporotrichosis

45
Q

What is tinea?

A

A superficial dermatophyte infections characterised by scaly, inflammatory or non-inflammatory patches
- generally limited to the epidermis and expands in a centrifungal pattern

46
Q

What is classification of tinea based off?

A

The affect region

  • tinea pedis for feet (athletes foot)
  • tinea corporis for the body
  • tinea capitis for head/scalp
  • tinea curis for groin (jock itch)
47
Q

What is tinea caused by?

A

Dermatophytes

  • trichophyton (most common)
  • microsporum
  • epidermophyton
48
Q

How is a tinae infection diagnosed?

A

Potassium hydroxide (KOH) preparation from a skin scraping

49
Q

How is erythema infectiosum caused?

A

Parvovirus B19

- transmission via respiratory droplets, blood or blood products

50
Q

What are the symptoms of erythema infectiosum?

A

Fever
Headache
Runny nose
Pruritic rash on the face (slapped cheek), torso and extremities

51
Q

What are the complications of persistent erythema infectiosum?

A 
Persistent arthropathy
Gloves-and-socks syndrome
Papular, purpuric eruptions on the hands and feet
Acute cessation of RBC production
- transient aplastic crisis
- chronic RBC aplasia 
- hydrops fetalis
- congenital anaemia
52
Q

What is hand-foot-and-mouth disease?

A

A viral illness with oral and sital-extremitry lesions

53
Q

What is the cause of hand-and-foot-and-mouth disease?

A

Coxsackie virus A16

- typically affects children and infants

54
Q

How can hand-foot-and-mouth disease cause and epidemic?

A

Highly contagious during the first week of the illness

- direct contact with nasal and oral secretions or faecal material

55
Q

What are the symptoms of hand-foot-and-mouth disease?

A 
Fever
Rash
Headache
Sore throat
Oropharyngeal ulcers
Loss of appetite
56
Q

How can herpes reoccur once it has been treated?

A

Virus doesn’t disappear from the body, lives latent in the sensory never ganglia

57
Q

What is the diagnosis and treatment for herpes simplex?

A 
Clinical diagnosis
- blood or vesicle fluid for PCR
- serology
- be careful as 60% of cases are asymptomatic 
Treatment 
- acyclovir (topical, oral or IV)
58
Q

What two conditions can the varicella zoster virsu cause?

A

Chickenpox

Shingles

59
Q

How is chicken pox diagnosed?

A

PCR of vesicle fluid (or serology)

60
Q

Chickenpox is self-limiting in children; how is it problematic in adults?

A

Can cause congenital abnormalities during pregnany

Pneumonitis

61
Q

If an at risk adult (pregnant, immunocompromised or has contracted penumonitis) contracts chickenpox, how are they treated?

A

Need to be treated within 48 hours of symptoms

- acyclovir PO/IV

62
Q

Describe shingles.

A

Reactivation of dormant VZV (dorsal root ganglia)
Dermatomal distribution
Highly contagious until all the vesicles have crusted over

63
Q

How is shingles treated?

A

Only the immunocompromised patients and those with disseminated infection are treated
- acyclovir
NSAIDs and gabapneitn for the pain

64
Q

Briefly describe burns.

A

Damage to the skin (Heat, chemical, radiation, cold) causing protein denaturing

65
Q

What conditions can occur because a burn has compromised resistance to the environment?

A

Infection - must be diagnosed clinically (burn swabs are rarely sterile)
Hypothermia
Acid-base abnormalities
Dehydration

66
Q

How are burns managed?

A 
Dressings
Topical antimicrobials (e.g. sulfadiazine, may delay re-epithelialisation)
Topical antibiotics (bacitracin)
Systemic antibiotics (directed by culture results) are required in invasive infection
67
Q

What is staphylococcal scalded skin syndrome, and what are its symptoms?

A

Staph aureus strains producing an exfoliative exotoxin
Widespread bullae formation and exfoliation
- known as Ritter’s disease or Pehmphigus neonatorum in the neonate
Symptoms are fever, tenderness and a scarlatiniform rash

68
Q

What is the causative pathogen and virulence factors for Scarlet fever?

A

Infections with a streptococcal strain that elaborates streptococcal exotoxins or erythrogenic toxins
- usually post-pharyngitis but may complicate wound infections and post-partum infections

69
Q

Describe the signs and symptoms of Scarlet fever.

A

Diffuse red blush (2nd day of infection)
- becomes a deeper red blanch on pressure
- starts on upper chest and spreads to trunk, neck and extremities
Mild eosinophilia
Occlusion of sweat glands (skin feel like sandpaper)
Palms, soles and face are normally spared
Circum-oral pallor
White strawberry tongue followed by red strawberry tongue
High fever and systemic toxicity is severe cases

70
Q

What are the major features of cutaneous anthrax?

A

Surrounded by extensive oedema

Painless and non-tender

71
Q

What are the minor features of cutaneous anthrax?

A

Development of black eschar
Progresses over 2-6 days through papular, vesicular and ulcerated stages before eschar appears
- hands, forearm, face and neck are most common
Discharge of serous fluid
Local erythema and induration
Local lymphadenopathy
Systemical malaise (headache, chills and sore throat -> afebrile)

72
Q

What are the specific risk factors for cutaneous anthrax?

A

Working with animals or animal hides
Making, owning or playing an animal hide drum
Drug use (particularly heroin)
Travel
Working in postal sorting office or handling large volumes of mail
Received threatening letter or package containing white powder

73
Q

What are the antibiotics used for cutaneous anthrax treatment?

A 
Penicillin
Flucloxacillin
Clindamycin
Ciprofloxacin
Metronidazole
74
Q

Describe PVL producing Staph aureus.

A

PVL is a toxin which destroys white blood cells
Carried by less than 2% of S.aureus isolates (normally MSSA)
Community isolates are more likely to carry the toxin that hospital

75
Q

What conditions are associated with PVL producing S.aureus?

A

Necrotising fasciitis
Pyogenic skin infections
Septic arthritis
Fulminant pneumonia

76
Q

When should PVL producing S.aureus be suspected?

A

Recurrent/multiple boils

- especially those in close contact situations

77
Q

What is the diagnosis and management plan for PVL producing S.aureus?

A

Screen nose, throat, axilla, perineum and skin lesions for carriage
PCR for toxin gene
Drainage and treatment according to sensitivity patterns
Decolonise using standard MRSA regimens

Microbiology (21 decks)

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