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Medical Microbiology and Virology > 27 Infections of skin, soft tissue, muscle > Flashcards

27 Infections of skin, soft tissue, muscle Flashcards

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1
Q

How does skin control its own flora and prevent growth of pathogens?

A

acid pH - fatty acids, sebum

salty sweat

competition between flora/ pathogens

surface temperature is too low for many pathogens

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2
Q

How can infection (of any site) cause skin disease?

A

Direct damage/ infection of skin

Skin manifestations of systemic infections from blood e.g draining sinus from actinomycotic lesion

Toxin-mediate skin damage due to microbial toxin at another site in body e.g Scarlet fever (strep pyogenes, toxic shock syndrome (staph aureus)

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3
Q

Which layers of skin are affected?

Ringworm
Impetigo
Erysipelas
Folliculitis
Cellulitis
Necrotising fasciitis
A

Ringworm - epithelium

Impetigo - epidermis

Erysipelas - dermis

Folliculitis - hair follicles

Cellulitis - dermis/ subcutaneous fat

Necrotising fasciitis - fascia

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4
Q

What sign can be produced by pseudomonas sepsis?

A

Ecythma gangrenosum - bloody pustule evolves into black ulcer at any site of body

Perivascular bacterial invasion, with associated ischaemic necrosis

Usually immunocompromised or severely unwell

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5
Q

Staph aureus is most common cause of skin infection

Can cause minor or serious infection.

How does boil form?

A

Infection around hair follicle

organism multiples rapidly

Inflamation with neutrophils

Fibrin produced walls off infection. Neutrophils create pus, which expands

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6
Q

What is scalded skin syndrome?

A

Staph aureus can infect small lesion, and release toxin knwon as exfoliatin.

This causes destruction of intercellular connections, and separation of top layer of epidermis.

Large blisters form. In 2 days they rupture, leaving normal skin underneath.

Baby is usually irritable, but rarely severely ill.

Treat with antibiotics, and fluid replacement

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7
Q

What is toxic shock syndrome, and what are clinical manifestations?

A

Multi-organ failure with fever, hypotension and macular rash. Which then begins desquamation - particularly soles/ palms

Due to TSST1 exotoxin

Seen in tampon use, but can occur in any skin wounds

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8
Q

Which bacteria cause impetigo?

A

Can be staph aureus or/and strep pyogenes

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9
Q

Strep pyogenes can cause infection in respiratory tract, but also skin infections.

Species have different M/ T proteins which specialise it to each site

What toxins can strep pyogenes produce?

A

hyaluronidase - helps organism spread in tissue

Strep pyogenes exotoxin (SPE)

Toxins are super-antigens and stimulate massive immune response e.g diffuse erythematous rash of scarlet fever

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10
Q

Streptococcal infections cause immune complex deposition on various organs.

What complications can it produce?

A

Glomerulonephritis

Rheumatic fever

reactive arthritis

erythema nodosum

PANDAS

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11
Q

Cellulitis involves infection of subcutaneous tissue/ fat

Why should it be treated?
Decision to treat clinically

A

Risk of bacteria seeding into bloodstream causing sepsis

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12
Q

SSTI is usually due to staph/ strep.

What infections can develop in damaged/ devascularised tissue?

A

Anaerobic infection

Surgical/ traumatic wound
Diabetic feet

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13
Q

Cellulitis with possible anaerobic cause (e.g diabetic foot/ surgical wound)

What is treatment?

A

Debridement

Penicillin + metronidazole

May progress to osteomyelitis

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14
Q

Staph/ strep are common causes of necrotising fasciitis

Infection spreads along fascia, and rash far outgrows the size of initial infection site. If affects scrotum/ perineum called Fournier’s gangrene

What is treatment?

A

Radical debridement

antibiotics

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15
Q

Human bite/ animal bite

what infections to be concerned about?

A

HBV
HCV
HIV

bacterial infection - oral flora

cat - pasteurella

dog - capnocytophagia

Tetanus

rabies

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16
Q

Which organism causes gas gangrene?

A

Clostridium perfringens

Found in soil and human/ animal faeces. Causes infection by wound contamination

Organism multiplies in subcutaneous tissue, causing gas formation, which may be clinically detectable.

alpha toxin produced causes massive cell lysis

Progresses rapidly

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17
Q

What is management of gas gangrene due to Clostridium perfringens?

A

surgical debridement is mainstay. Remove dead tissue which anaerobes use for growth

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18
Q

How do blackheads form?

Which bacteria are implicated?

A

Increase responsiveness to androgenic hormones increases sebum production.

Proprionibacterium/ staph/ microccoi act on sebum to form fatty acids. In combination with neutrophils, this causes inflmamation of skin

keratin/ neutrophil/ bacteria and layer of melanin form plug which blocks pilosebaceous duct

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19
Q

Clostridium tetani itself does not cause a problem, but infection with toxin causes rigidity and lockjaw which can progress to death

Lives in soil, can never be eliminated

Most people vaccinated against it

when is routine vaccination given?

A
  • 3 doses - at 2/3/4 months of age as part of routine immunisation.
  • 1st booster dose aged approximately 4 years
  • 2nd booster dose 10 years after 1st booster
  • Not vaccinated in childhood - give adult 3 doses, each a month apart
  • always give a booster dose if any doubt about immunisation status
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20
Q

Which injuries are considered to be at risk of tetanus?

Clean cuts are not at risk e.g knife in kitchen. As superficial injury, and unlikely to be contaminated with spores

A

Tetanus- prone wounds

  • puncture in garden
  • IVDU at risk
  • wound foreign body
  • compound fracture
  • burns with systemic sepsis
  • animal bites - certain ones

High risk tetanus-prone wounds

  • heavy wound contamination with soil
  • wounds requiring surgery which is delayed >6 hours
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21
Q

What is management of tetanus-prone wound?

A

Wound cleaning

Previously vaccinated (within past 10 years)
no action required

Previously vaccinated (last dose >10 years ago) -
tetanus booster vaccine
Tetanus immunoglobulin only if very high risk - e.g >6 hours, soil exposure

Unvaccinated -
tetanus vaccine
Tetanus immunoglobulin if medium or high risk - e.g >6 hours, soil exposure

see green book table

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22
Q

what is incubation period of tetanus?

A

4-21 days

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23
Q

What is tetanus treatment in following cases following injury?

Fully tetanus vaccinated (3 doses) (in past 10 years)

Fully tetanus vaccinated (3 doses) (last does >10 years ago)

A

Fully tetanus vaccinated (3 doses) (in past 10 years)
- No further vaccine or IM-TIG required

Fully tetanus vaccinated (3 doses) (last does >10 years ago)

  • vaccine booster
  • IM-TIG if high risk tetanus prone injury
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24
Q

What is tetanus treatment in following cases following injury?

Not completed initial tetanus immunisation (3 doses) or uncertain immunisation status

A
  • give booster vaccine

- give IM-TIG

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25
Q

What is dose of IM-TIG if high risk injury in unvaccinated person?

A

250 IU usual dose

500 IU if >24 hours since injury, or severe contamination

Dose same for adults/ children

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26
Q

What are four forms of tetanus presentation?

A

Generalised muscle spasms

Cephalic tetanus is localised tetanus after a head or neck injury, involving primarily the musculature supplied by the cranial nerves

Localised tetanus is rigidity and spasms confined to the area around the site of the infection and may be more common in partially immunised individuals. Localised symptoms can continue for weeks or may develop into generalised tetanus

Neonatal - umbilical stump infection from use of manure. Muscle rigidity, unable to feet, 70-100% mortality

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27
Q

How to diagnose tetanus infection?

A

Mostly a clinical diagnosis - muscle rigidity/ spasms/ trismus. Can lead on to autonomic dysfunction, and respiratory difficulties

Wound sample - clostridium tetani PCR

Serology - check toxin in serum

Serology - check antibody status. Although cases of patients with sufficient antibody developing infection. So reasonable antibody level cannot exclude tetanus infection

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28
Q

What is management of suspected tetanus case?

A
  • wound debridement
  • antimicrobials including agents reliably active against anaerobes such as intravenous benzylpenicillin, metronidazole can used
  • IM-TIG or intravenous Immunoglobulin (IVIG) given IM
  • vaccination with tetanus toxoid following recovery
  • supportive care (benzodiazepines for muscle spasms, treatment of autonomic dysfunction, maintenance of ventilation, nursing in a quiet room etc)
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29
Q

Leprosy causes by Mycobacterium leprae. Also known as Hansen’s disease

How is it transmitted?

A

Direct contact skin lesion - particularly overcrowding. Requires prolonged contact as not very contagious

Aerosol - nasal secretions contain bacteria

Infects armadillos, chimpanzee, mangabey monkeys, but little evidence of transmission

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30
Q

What is life cycle of M. leprae?

A

grows intracellulary within endothelial cells/ histiocytes/ Schwann cells of peripheral nerves

After several years, disease presents - which depends on immune response

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31
Q

What are names of stages of M leprae infection?

A

Tuberculoid leprosy

Borderline/ intermediate leprosy

Lepromatous leprosy

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32
Q

What are clinical stages of these forms of leprosy?

Tuberculoid leprosy

Borderline/ intermediate leprosy

Lepromatous leprosy

A

Tuberculoid leprosy - hypopigmented skin, anaesthesia, thickening of nerves

Borderline/ intermediate leprosy - numerous tuberculoid lesions

Lepromatous leprosy - generalised involvement of the skin/ nerves with evidence of nodules. Enlargement of nostrils/ ears/ cheeks - Lion like appearance

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33
Q

How does immune response effect clinical presentation of leprosy?

A

If vigorous cell-mediated immunity response, then can contain bacteria - tuberculoid leprosy with single lesion

If poor CMI - organism multiplies unhindered

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34
Q

How to diagnose leprosy?

A

Skin biopsy - stain Ziel-Neelsen or auramine to see acid-fast rods

does not grow in culture, as compared to M Tb which does grow in culture

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35
Q

What is treatment for leprosy?

A

Dapsone, rifampicin and clofazimine given between 6 months- 2 year depending on stage

Repeat skin biopsies to confirm clearance

BCG vaccine has some protection against leprosy

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36
Q

Mycobacterium TB can rarely infect skin when it is damaged. What condition does it cause?

A

Ulcerating lesion extends from skin to lymph node - scrofuloderma

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37
Q

What species of mycobacterium is associated with fish tanks/ swimming?

A

M marinum

At risk -
aquarium owners
marine biologist
fishermen
swimmer

Injury allows mycobacteria to enter wound. Incubates for 2-8 weeks, then small papule appears. May ulcerate

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38
Q

What is treatment of M marinum skin infection?

A

Clarithromycin + ethambutol

6-18 months treatment

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39
Q

What disease does M. ulcerans cause?

What is its geographical spread?

A

Buruli ulcer - necrotic ulcers. Can spread over skin surface, and can invade and cause osteomyelitis

Africa - primarily
SEA
SA
Aus

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40
Q

What is M ulcerans route of infection?

A

Direct skin inoculation through traumatic wound

Has been found in possums/ mosquitoes. Speculated may occur after infected mosquito bite

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41
Q

Fungal infectious can either be -
superficial
cutaneous or
deep/ subcutaneous

What are most common superficial fungal infection?

A

Pityriasis versicolor
tinea species (other name is ringworm)
white piedra
black piedra

42
Q

What is cause of pityriasis versicolor?

How does it present?

A

M pityrosporum furfur

common skin inhabitant, unclear why/ when becomes pathogenic

Hypo- or hyperpigemtned macules form, which can coalesce into sclaing plaques

43
Q

How to diagnose pityriasis versicolor?

Treatment

A

Direct microscopy of scrapings - round yeas forms

topical azole

44
Q

What are causes of cutaneous fungal infections?

Tinea -

  • capitis (head)
  • corporis (body)
  • cruris (crotch)
  • manuum (hands)
  • unguium (nails)
  • pedis (feet)

Tinea means maggot, and is uses interchangeable with ringworm to describe cutaneous fungal infection of different sites.

A

Causes of tinea include various Tinea species, and microsporum/ trichophyton.

Tinea/ microsporum species have natural hosts in humans/ soil/ animals

45
Q

Tinea infection (cutaneous dermatophyte) - what does lesion look like?

A

Annular patch with raised margin

dry/ scaly

itchy

hair loss

46
Q

How to diagnose cutaneous dermatophyte infection?

A

Skin scrapings to look for fungi - tinea/ microsporum/ trichophyton

Culture - can take 2 weeks
Fluorescence under UV light

47
Q

What is treatment of cutaneous dermatophyte infection?

A

Skin - topical azole - ketoconazole/ clotrimazole/ miconazole

Nails/ hair - oral terbinafine/ itraconazole

48
Q

Why does candida grow in mouth/ groin?

A

Requires moist area for growth

Can invade deeper if patient becomes immunosuppressed

49
Q

What are causes of subcutaneous mycoses?

A

Rare

Sporotrichosis

Blastomycocsis

Actinomyces if gram negative which can mimic appearance

50
Q

sporotrichosis is fungi widespread in soil and rose bushes. Most common route of infection is via thorn

What happens after initial inoculation?

A

Small papule/ nodule forms at site 1 week - 6 months after inoculation

Infection spreads along lymphatics, producing a series of nodules

Can cause disseminated disease and pulmonary infection. More common if immunocompromised, but can occur in immunocompetent. Prognosis poor

51
Q

How is sporotrichosis diagnosed?

What is treatment?

A

Culture of drained/ aspirated material

Itraconazole/ fluconazole

52
Q

What parasites can cause skin lesions?

A

Leishmaniasis

Schistosomiasis

Cutaneous larva migrans - hookworm (ancylostoma/ necator)

Guinea worm

Onchocerciasis

53
Q

How does hookwrom infections cause disease?

Causes cutaneous larva migrans

A

Hookwrom ivnades via skin after contact with soil

Life cycle takes it through blood to intestine

As humans are not natural hosts, larva fail to escape via skin. So can creep along parallel to skin, leaving intensely itchy rash

54
Q

What is treatment of scabies?

Norweigan scabies is extensive thickening and crusting, which may occur in severely immunocompromised

A

Permethrin topical

Oral ivermectin - if severe/ Norweigan scabies

55
Q

What other tropical diseases can have rash? (maculopapular)

A

Dengue

Marburg

Hepatitis B

Rickettsia - RMSF

Typhus

56
Q

Kawasaki syndrome can form part of differential diagnosis for skin rash.

What is pathophysiology?

A

Children <4

acute vasculitis due to dysregulated T-cell activation to infectious trigger.

Mortality 2%

More common Asian population

57
Q

What are symptoms of Kawasaki’s disease?

A

Dryness/ redness of lips/ palms/ soles

Desquamation of palms/ soles

Oedema

Arthralgia

Myocarditis - 20% can develop coronary artery aneurysms

58
Q

What is treatment of Kawasaki’s?

A

Immunoglobulin

Aspirin

Both can prevent coronary artery damage

59
Q

Trypanosoma cruzi invades via skin. Reduviid bug deposits parasite on skin during feeding. This is then rubbed into wound/ mucus membrane. Can invade muscle

What are common symptoms?

A

Skin - chagoma/ Romanas sign

95% have cardiac defects - conduction/ heart failure due to myocardial invasion

megaoesophagus

megacolon

60
Q

Parasitic worms are primarily intestinal parasites. Larval stages of non-human tape worms can invade muscle

What species invade muscle?

A

Tapeworms -
Echinococcus granulosus - sheep tapeworm

Taneia solium - pork tapeworm. Can cause neurocysticercosis

Roundworm (nematode) -
Trichinella - pork roundworm

61
Q

What are viral causes of arthritis?

A

HBV

Rubella - post vaccination

Mumps

Parvovirus

Togaviruses - Chikungunya, Ross River, Eastern Equine virus, Western Equine virus

62
Q

What are causes of reactive arthritis?

Associated with HLA B27

Due to immunogenic phenomena, as opposed to bacteria within joint

A

Campylobacter
Salmonella
Shigella
Yersinia

Chlamydia trachomatis - Reiter’s syndrome urethritis, arthritis, conjunctivitis
gonorrhoea

streptococcal

viral - many causes

63
Q

What are causes of septic arthritis?

Knees most commonly affected. Followed by hips, ankles, elbows. Occurs more commonly in damaged joints e.g RA

A 
Staphylococcus - most common
Streptococci - A/B
Haemophilus influenzae - children
Kingella - age <4
Neisseria gonorrhoea
E. Coli
Rarer -
Salmonella - disseminated infection
Mycobacterium TB
Borrelia burgdorferi
Sporotrichosis - fungal
64
Q

What are symptoms of septic joint?

A

Fever

joint pain

swelling

reduced movement

65
Q

What is treatment of native joint septic arthritis?

A

Flucloxacillin 2g QDS or
Vancomycin or
Clindamicin or
ceftriaxone

Oral options (depending on sensitivities) -
flucloxacillin
ciprofloxacin
linezolid
clindamicin

6 weeks therapy
Minimum 2 weeks IV

66
Q

What is treatment of prosthetic joint septic arthritis?

A

DAIR/ revision - see separate cards

Vancomycin + rifampicin

Duration 6 weeks at least

67
Q

What are risk factors for septic joint?

A

Overlying skin infection

recent surgery

OA/ RA

diabetes mellitus/ HIV

immunosuppressive medication

IVDU

Soil exposure

Animal bite

68
Q

What is treatment of discitis/ vertebral osteomyelitis?

A

Ceftriaxone 2g OD or
Vancomycin - aim higher level 15-20

Add metronidazole 400mg TDS if epidural abscess

69
Q

Bone can become infected directly, or from haematogenous spread

What bacteria are common causes of osteomyelitis?

A

Staph aureus

Staph epidermidis

GroupB strep - neonates

Neisseria gonorrhoea

Pseudomonas - diabetic

Enterococci

Enterobacter

Rarer -
salmonella - sickle cell
TB - Potts disease
pasteurella - cat bite
serratia
70
Q

What is treatment of osteomyelitis?

A

Flucloxacillin 2g QDS or
Vancomycin + rifampicin

6 weeks therapy
Minimum 2 weeks IV

71
Q

How to diagnose osteomyelitis?

A

CRP/ ESR
Blood cultures
Imaging
Bone biopsy

72
Q

Which infective agents replicate in erythrocytes?

A

Plasmodium
Babesia

Bartonella
Rickettsia

Parvovirus
Colorado tick fever

All infections can cause anaemia

73
Q

Why do EBV/ CMV cause thrombocytopenia?

A

Antibodies to virus cross-react and adhere to platelets

74
Q

HTLV 1/2 infects T-cells in bone marrow.

Which countries is it found in?

A

West Indies

Japan

Can have up to 15% population infected

Rarer cases in SA/ Africa

75
Q

How is HTLV primarily transmitted?

A

Maternal breast milk - most common

sexual

IVDU

76
Q

What are symptoms of HTLV infection?

A

mild febrile illness

lymphadenopathy

pleural effusion/ aseptic meningitis can develop

tropical spastic parapesis - myelopathy

acute leukaemia

PCP/ strongyloides and other opportunistic infection

77
Q

Cellulitis is erythema of skin, with pain, swelling, fever. Can have systemic features

What grading system can be used to help decide about treatment/ admission?

A

Eron grading

Class I - no systemic signs

Class II - systemically unwell, but reasonably stable

Class III - significant systemic upset - confusion/ tachycardia/ hypotension

Class IV - septic/ life-threatening

Class I - oral
Class II - I 48 hours, then oral or OPAT
Class III/ IV - IV

78
Q

What are differential diagnosis of cellulitis?

A

DVT

Ruptured Baker’s cyst

Septic arthritis

gout

superficial thrombophlebitis

varicose eczema

lymphoedema

lipdoermatosclerosis - subcutaneous panniculitis in lower limbs of obese women with venous insufficiency

79
Q

Skin and soft tissue infection, with history of animal contact.

What are possible organisms?

A

Cat bite - pasteurella

dog bite - capnocytophaga

bartonella

Francisella tularensis

bacillus anthracis

yersinia pestis

80
Q

Skin and soft tissue infection, with history of water contact.

What are possible organisms?

A

vibrio vulnificus

aeromonas hydrophilia

mycobacterium marinum

pseudomonas

81
Q

Skin and soft tissue infection, with history of IVDU

What are possible organisms?

A

MRSA

C botulinum

C tetani

B anthracis

82
Q

Skin and soft tissue infection, with history of foreign travel

What are possibyle organisms?

A

cutaneous leishmaniasis

cutaneous larva migrans

myiasis

83
Q

What are virulence factors of strep pyogenes in SSTI?

Adherence factors
Exotoxins
Superantigen

A

Adherence factors -
fimbrillae - binds host epithelial cells
M protein - binds fibrinogen and blocks complement binding
Protein F - allows invasion into epithelial cells

Exotoxins -
Haemolysin (Streptolysin O) - tissue damage
Hyaluronidase - digest host tisse

Superantigens -
streptococcal pyrogenic exotoxins (SPEs) - bind to T cells causing mass cytokine release - toxic shock

84
Q

What are virulence factors of staph aureus in SSTI?

Adherence factors
Exotoxins
Superantigen

A

Adherence factors -
clumping factor - bind host epithelial cells
Protein A - prevents opsonisation

Exotoxin -
PVL (5% of isolates) - causes membrane pore formation in neutrophils, leading to skin lysis/ necrosis

Superantigen -
Enterotoxin, TSST, Exfoliative toxin A/B - bind to T cells causing massive cytokine activation

85
Q

What is treatment duration for cellulitis?

A

7-14 days depending on severity

prolonged course if underlying disease e.g PVD, lymphoedema

86
Q

What scoring system is used to assess for probability of necrotising soft tissue infection?

A

If high clinical suspicion, then do not check score, proceed to debridement

Laboratory Risk Indicator for Necrotising Fasciitis - LRINEC

CRP
WCC
Hb
Na+
Cr
Glucose
87
Q

Gardener presents with lump over left leg. Was ulcer, but now hard red nodule. Nodules in distribution of lymphatics

What is treatment?

Dapsone
Doxycycline
Cidofovir
Itraconazole
Peg-IFN
A

Itrazoncaole

Sporotrichosis

88
Q

Diabetic foot ulcer.

What are indications of treatment for infection?

A

Inflammation
cellulitis
tissue loss

IDSA uses PEDIS to grade diabetic foot infections
Perfusion
Extent
Depth
Infection
Sensation
89
Q

HCA has skin abscess. Swab shows PVL staph which is treated. What is advice about returning to work?

Repeat screen one week after treatment, and return to work once lesion healed

Repeat screen on last day treatment, return to work if negative

Repeat screen one week post-decolonisation, return to work if three negative screens

Return to work after completing antibiotics

A

PVL is notifiable disease

Repeat screen one week after treatment, and return to work once lesion healed

If unwell/ cellulitis/ boils - treat with antibiotics
If well - chlorhexidine decolonisation wash

If repeat screen positive, then for further decolonisation.
May be positive due to persistent infection, or re-infection from close contact in community

If repeatedly positive, can still return to work if no active skin lesions

90
Q

What is differential diagnosis for septic arthritis?

A

Reactive arthritis

bursitis

gout

lyme disease

brucella

whipples disease - mimic RA presentation

91
Q

What is involved in two-stage revision of infected prosthetic joint?

A

Infected tissue/ implant removed

4-6 samples of deep tissue taken with new set of instruments (not wound swabs)

6 weeks antibiotics given

Repeat sampling and insertion of prothesis to ensure clearance of infection

92
Q

48 year old with ESRF, has right hip fracture and surgery. Now has discharging sinus.

  • Wound swab grows enterobacter and coagulase-negative staph.
  • Deep wound culture grows enterobacter.

Plan for 2 stage revision. He has hip washout, with spacer inserted.

What is plan for antibiotics?

A

Ignore coagulase negative staph in wound swab. Deep wound swab more indicative of actual infection

Given six weeks therapy (minimum 2 IV), in between first and second stage revision arthroplasty

93
Q

79 THR 2015. Presents 8 month history pain on weight bearing. Has discharing sinus.

Has single stage revision surgery. Then has teicoplanin IV, and rifampicin oral for 6 weeks via OPAT.

Returns to clinic for 6 week post-operative assessment. Doing well, and pain free. What is plan with antibiotics?

continue antibiotics further 6 weeks
stop teicoplanin, continue rifampicin further 6 weeks
give cipro and rifampicin further 6 weeks
stop all antibiotics

A

give cipro and rifampicin further 6 weeks

Single stage considered if no co-morbidities, good soft tissue health, and sensitive organism

Total three months therapy, which includes initial 6 weeks therapy

Extend to six months total for knee infection

94
Q

Why are rifampicin/ cipro useful in prosthetic infections?

A

Bactericidal

Good joint penetration

Prevent biofilm formation

95
Q

SJS/ TEN are part of same spectrum of disease, in which there is mucosal loss. Nearly always caused by drugs. CD8 T cells directed towards drug, and cytokines produced cause damage and skin shedding.

What are causes?

A

Nearly all caused by medication

Antibiotics -
co-trimoxazole
Beta-lactam
Fluroquinolones

Anti-epileptics

NSAIDs

Allopurinol

96
Q

Symptoms start between 1 week - 1 month after starting drug.

What are symptoms of SJS/ TEN?

A

Prodromal flu-like illness - fever, coryza, myalgia

Abrupt onset of rash which extends to maximal within 4 days

  • erythema
  • macules
  • blisters
97
Q

How to diagnose SJS/ TEN?

A

Clinical diagnosis

Skin biopsy

98
Q

What is mortality risk of SJS/ TEN?

What scoring systems can be used to predict mortality?

A

Mortality 10% SJS/ 30% TEN

SCORTEN score -
Age > 40 years
Presence of malignancy (cancer)
Heart rate > 120
Initial percentage of epidermal detachment > 10%
Serum urea level > 10 mmol/L
Serum glucose level > 14 mmol/L
Serum bicarbonate level < 20 mmol/L.
99
Q

What is differential diagnosis of SJS/ TEN?

A

Other severe cutaneous adverse reactions (SCARs) to drugs (eg, drug hypersensitivity syndrome)

Staphylococcal scalded skin syndrome and toxic shock syndrome

Erythema multiforme

Mycoplasma infections

Bullous systemic lupus erythematosus

Paraneoplastic pemphigus

100
Q

What is management of SJS/ TEN?

A

Stop offending drug

Fluid support

Temperature support

Analgesia

Antibiotics - only if infection develops

Case reports - anti-TNF/ IVIG/ cyclophosphamide

101
Q

IDSA use PEDIS is grade diabetic foot ulcers

What constitutes the score?

A 
Perfusion
Extent
Depth
Infection
Sensation

Uninfected 1
Mild 2 - cellulitis >2cm
Moderate 3 - deep involving muscle/ bone
Severe 4 - sepsis

diagnosis of infection is clinical. Microbiology cannot diagnose infection, but can be used to identify infecting organism

102
Q

CUH guidelines

Diabetic foot ulcer

What is treatment?

Mild
Moderate
Severe

A

Mild
- flucloxacillin/ co-amoxicalv

Moderate

  • co-amoxiclav
  • doxycycline + metro

Severe

  • co-amoxiclav IV
  • tazocin
  • MRSA - vancomycin + tazocin

duration minimum 2 weeks

Medical Microbiology and Virology (60 decks)

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