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Dermatology > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Name five virulence factors

A
  • adhesin
  • invasin
  • impedin
  • aggressin
  • modulin
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2
Q

What does adhesin do?

A

Enables binding of the organism to host tissue

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3
Q

What does invasin do?

A

Enables the organism to invade a host cell/tissue

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4
Q

What does impedin do?

A

Enables the organism to avoid host defence mechanisms

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5
Q

What does aggressin do?

A

Causes damage to the host directly

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6
Q

What does modulin do?

A

Induces damage to the host indirectly

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7
Q

State the name for hospital acquired

A

Nosocomial

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8
Q

What skin conditions can staph aureus cause?

A
  • folliculitis
  • carbuncle (boils)
  • abscess
  • impetigo
  • scalded skin syndrome
  • toxic shock syndrome
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9
Q

State the virulence factors of staph aureus

A
  • adhesin (collagen & fibrinogen binding protein)
  • coagulase positive (clots plasma)
  • PVL (leukocidin - kills leukocytes)
  • TSST-1 (shock, rash, desquamation)
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10
Q

Describe how toxic shock syndrome arises

A

Superantigen TSST1 activates 1 in 5 T cells causing a massive release of cytokines & inappropriate immune response

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11
Q

What are the signs and symptoms of toxic shock syndrome?

A

Diffuse macular erythroderma
Hypotension
>/= three organ systems involved
Also includes high fever, vomiting, diarrhoea, sore throat, muscle pain

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12
Q

How does scaled skin syndrome arise?

A

Toxins produced by specific types of staph aureus cause disruption of epidermal keratinocyte adhesion causing blistering, desquamation and re-epithelialisation

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13
Q

What are the signs and symptoms of SSS?

A

Pyrexia, tender erythema, superficial blisters that are easy to burst, bulls impetigo (skin looks burnt).

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14
Q

Why are young children mainly affected by SSS?

A

As they have underdeveloped immune systems & kidneys

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15
Q

How is SSS diagnosed?

A

Swab

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16
Q

What does PVL stand for?

A

Panton Valentine Leukocidin

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17
Q

Describe the mechanism of action of PVL

A

Toxin that can kill white blood cells & cause damage to skin and deeper tissue

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18
Q

What are the five C’s of PVL?

A 
Close contact 
Contaminated items 
Crowding 
Cleanliness
Cuts
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19
Q

How can PVL present?

A

Recurrent and painful boils/red areas of skin that don’t get better with antibiotics

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20
Q

How is PVL diagnosed?

A

Swab

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21
Q

What happens if PVL is combined with other toxins e.g MRSA or alpha toxin?

A

Necrotising pneumonia

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22
Q

What is the most common type of group A strep?

A

Strep pyogenes - most GAS come under this name however there are some other GAS strains

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23
Q

How can strep pyogenes be identified?

A

Beta haemolysis & by lancefield system

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24
Q

What is the lancefield system?

A

Serotyping cell wall carbohydrate of change in M protein

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25
Q

What conditions can GAS cause?

A
  • impetigo
  • cellulitis
  • erysipelas
  • necrotising fascitis
  • infected eczema
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26
Q

Describe the presentation of impetigo

A

Red, sore, itchy skin with pus filled blisters on hands and face which pop to leave brown crusty patches

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27
Q

What is cellulitis?

A

Infection of the dermis that is not associated with necrosis

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28
Q

What is erysipelas?

A

Infection of the upper dermis & superficial lymphatics

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29
Q

How will cellulitis and erysipelas present?

A

Cellulitis - lower leg (ill defined edge)
Erysipelas - legs and face (sharp edge)
Pyrexia, shivers, sore, swollen, erythema, blisters, enlarged lymph nodes.

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30
Q

What causes necrotising fasciitis?

A

invasive GAS

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31
Q

Describe necrotising fasciitis

A

Penetration of mucous membrane causes a lesion and bacteria rapidly destroys the connective tissue

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32
Q

Name the symptoms of necrotising fasciitis

A

Severe pain, fever, purple coloured skin, abscess, vomiting
Necrosis - bullae, bleeding into the skin, reduced sensation, shock. Spreads along facial planes - life threatening disease

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33
Q

State four virulence factors of invasive GAS responsible for necrotising fasciitis

A
  • haemolysin
  • superantigen
  • streptolysin
  • capsule
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34
Q

How is intact skin able to fight infection?

A
  • dry (desiccation of micro-organisms)
  • sebum (inhibit bacterial growth)
  • competitive flora
35
Q

How do you treat staph aureus & MRSA?

A

Flucloxacillin

MRSA - doxycycline, co-trimoxazole, clindamycin, vancomycin

36
Q

What are the three strains of strep with examples?

A

alpha - pneumonia and viridian’s
beta - GAS & GBS (meningitis in neonates)
none - enterococcus (bowel commensal & UTIs)

37
Q

How do you treat streptococcus infections?

A

Penicillin but flucloxacillin will kill both staph and strep

38
Q

What in ringworm commonly known as?

39
Q

Where can tinea occur and what is it called in each place?

A 
scalp - capitis
beard - barbae
body - corporis 
hand - manuum 
nails - unguinm
groin - cruris
foot - pedis
40
Q

What is tinea pedis commonly known as?

A

Athletes Foot

41
Q

What is the name of fungi that require keratin to grow?`

A

Dermatophyte

42
Q

Describe the pathogenesis of ringworm

A
  1. Fungus enters abraded/soggy skin
  2. Hyphae spread in stratum corneum
  3. Infects keratinised tissue
  4. Increases epidermal turnover (scaling)
  5. Inflammatory response
  6. Invades hair follicles & shafts
  7. Lesion grows outwards but heals in the centre
43
Q

How is tinea transmitted?

A

Infected humans, animals, soil

44
Q

How is tinea diagnosed?

A

Appearance, woods light, skin scrapings around edge of lesion

45
Q

What is the treatment for tinea?

A

Small areas/nails - clotrimazole cream or amorolfine nail pain
Extensive skin/nail/scalp - oral terbinafine or itraconazole

46
Q

How is candida treated?

A

Clotrimazole (cream or pessary)

Fluconazole (oral)

47
Q

What parasites can cause skin conditions?

A

Scabies

Lice

48
Q

Describe scabies

A

Highly infectious, mites spread through skin to skin contact - main symptom is an itch (worse at night) and they may develop a rash (similar to eczema)

49
Q

How is scabies treated?

A 
Malathion lotion 
Benzyl benzoate (not in children)
50
Q

Where can lice be found?

A

Head, body, pubic hair - present with severe itch and visible lice and eggs

51
Q

How is head lice commonly treated?

A

Malathion lotion

52
Q

What causes chickenpox and shingles?

A

Varicella Zoster virus

53
Q

Describe chickenpox

A

Primary infection typically occurs in childhood effects sensory nerve roots and causes generalised rash and fever

54
Q

What is the pathway of a chickenpox rash?

A

macule - papule - vesicle - scab - recovery

55
Q

What are the complications of chickenpox?

A

secondary bacterial pneumonitis, scarring, encephalitis, haemorrhagic rash

56
Q

Which groups of patients are at increased risk if they catch chickenpox?

A

Immunocompromised

Pregnant women

57
Q

Why are pregnant women at increased risk?

A

Neonatal VZV is secondary to chickenpox in a mother in late pregnancy

58
Q

How is VZV prevented in pregnant women?

A

Immune globulin or aciclovir

59
Q

Describe shingles

A

Caused by zoster/herpes zoster it presents with dermatomal distribution due to reactivation of the virus. Increased incidence in elderly & immunocompromised
tingling - erythema - vesicles - crusts

60
Q

What is a serious type of shingles?

A

Ophthalmic zoster - need urgent ophthalmology referral - can happen in children due to chicken pox in utero

61
Q

What is Ramsay Hunt Syndrome Type 2?

A

Reactivation of heres zoster in the geniculate ganglion (sensory fascial nerves)- also known as herpes zoster otic

62
Q

How does Ramsay Hunt Type 2 present?

A

Vesicles & pain in the auditory canal & throat, fascial palsy (7th nerve palsy) & irritation of 8th cranial nerve (deafness, vertigo, tinnitus)

63
Q

What is the treatment for Ramsay Hunt Syndrome Type 2?

A

Prednisolone & aciclovir

64
Q

Describe Herpes Simplex virus

A

Gingivostomatitis common in pre school children - extensive ulceration in and around the mouth - heals without scarring

65
Q

When does herpes simplex become an emergency?

A

If it spreads to eczema

66
Q

What is the difference between type 1 and type 2 herpes simplex virus?

A

Type 1 - mainly oral lesions, 50% genital

Type 2 - rarely oral lesions, encephalitis/disseminated infection can occur in neonates

67
Q

What can herpes simplex virus provoke?

A

Erythema multiforme

68
Q

How can recurrent herpes simplex virus be treated if recurrent?

A

3-6 months of aciclovir

69
Q

Describer molluscum contagiosum

A

Fleshy firm umbilicate pearlescent nodules usually asymptomatic but can be itchy. They are fairly self limiting and may take months to go away.

70
Q

What causes warts?

71
Q

How can warts be treated?

A

Topical salicylic acid

72
Q

What is herpangina?

A

Blistering rash on back of mouth caused by enterovirus

73
Q

What are the three causes of herpangina?

A
  • Hand/Foot/Mouth Disease
  • Coxsackie virus
  • Echovirus
74
Q

Who usually presents with hand/foot/mouth disease?

A

Children, often family outbreaks

75
Q

How is herpangina diagnosed/treated?

A

Swab/stool sample is required, condition is self limiting

76
Q

What is erythema infectiosum?

A

Contagious viral infection that causes a blotchy or raised red rash with mild illness

77
Q

What causes erythema infectiosum?

A

Parvovirus B19 (slap cheek disease)

78
Q

How does parvovirus B19 present?

A

Bright red rash on cheeks, mild systemic illness, acute polyarthritis of the small joints may be more common in adult patients

79
Q

What are the complications of parvovirus B19?

A
  • spontaneous abortion
  • aplastic crises (sudden drop in haemoglobin)
  • chronic anaemia
80
Q

Describe Orf

A

Virus of sheep - nodules found on farmers hand, Self limiting

81
Q

Describe the difference between primary, secondary and tertiary syphilis

A

Primary - chancre (painless ulcer at site of entry)
Secondary - red rash on soles of feet & palms, snail track ulcers on mucous membrane
Tertiary - CNS, cardiovascular, gummatous necrosis

82
Q

What causes syphilis?

A

STI - treponema pallidum bacteria

83
Q

How is syphilis diagnosed and treated?

A

Blood test or swab for diagnosis

Treated using injections of penicillin

Dermatology (13 decks)

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