Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

27 Infections of skin, soft tissue, muscle Flashcards

(102 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which bacteria cause impetigo?

A

Can be staph aureus or/and strep pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

What is treatment?

A

Debridement

Penicillin + metronidazole

May progress to osteomyelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is incubation period of tetanus?

A

4-21 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is dose of IM-TIG if high risk injury in unvaccinated person?
250 IU usual dose 500 IU if >24 hours since injury, or severe contamination Dose same for adults/ children
26
What are four forms of tetanus presentation?
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
27
How to diagnose tetanus infection?
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
28
What is management of suspected tetanus case?
- 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)
29
Leprosy causes by Mycobacterium leprae. Also known as Hansen's disease How is it transmitted?
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
30
What is life cycle of M. leprae?
grows intracellulary within endothelial cells/ histiocytes/ Schwann cells of peripheral nerves After several years, disease presents - which depends on immune response
31
What are names of stages of M leprae infection?
Tuberculoid leprosy Borderline/ intermediate leprosy Lepromatous leprosy
32
What are clinical stages of these forms of leprosy? Tuberculoid leprosy Borderline/ intermediate leprosy Lepromatous leprosy
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
33
How does immune response effect clinical presentation of leprosy?
If vigorous cell-mediated immunity response, then can contain bacteria - tuberculoid leprosy with single lesion If poor CMI - organism multiplies unhindered
34
How to diagnose leprosy?
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
35
What is treatment for leprosy?
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
36
Mycobacterium TB can rarely infect skin when it is damaged. What condition does it cause?
Ulcerating lesion extends from skin to lymph node - scrofuloderma
37
What species of mycobacterium is associated with fish tanks/ swimming?
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
38
What is treatment of M marinum skin infection?
Clarithromycin + ethambutol 6-18 months treatment
39
What disease does M. ulcerans cause? What is its geographical spread?
Buruli ulcer - necrotic ulcers. Can spread over skin surface, and can invade and cause osteomyelitis Africa - primarily SEA SA Aus
40
What is M ulcerans route of infection?
Direct skin inoculation through traumatic wound Has been found in possums/ mosquitoes. Speculated may occur after infected mosquito bite
41
Fungal infectious can either be - superficial cutaneous or deep/ subcutaneous What are most common superficial fungal infection?
Pityriasis versicolor tinea species (other name is ringworm) white piedra black piedra
42
What is cause of pityriasis versicolor? How does it present?
M pityrosporum furfur common skin inhabitant, unclear why/ when becomes pathogenic Hypo- or hyperpigemtned macules form, which can coalesce into sclaing plaques
43
How to diagnose pityriasis versicolor? Treatment
Direct microscopy of scrapings - round yeas forms topical azole
44
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.
Causes of tinea include various Tinea species, and microsporum/ trichophyton. Tinea/ microsporum species have natural hosts in humans/ soil/ animals
45
Tinea infection (cutaneous dermatophyte) - what does lesion look like?
Annular patch with raised margin dry/ scaly itchy hair loss
46
How to diagnose cutaneous dermatophyte infection?
Skin scrapings to look for fungi - tinea/ microsporum/ trichophyton Culture - can take 2 weeks Fluorescence under UV light
47
What is treatment of cutaneous dermatophyte infection?
Skin - topical azole - ketoconazole/ clotrimazole/ miconazole Nails/ hair - oral terbinafine/ itraconazole
48
Why does candida grow in mouth/ groin?
Requires moist area for growth Can invade deeper if patient becomes immunosuppressed
49
What are causes of subcutaneous mycoses?
Rare Sporotrichosis Blastomycocsis Actinomyces if gram negative which can mimic appearance
50
sporotrichosis is fungi widespread in soil and rose bushes. Most common route of infection is via thorn What happens after initial inoculation?
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
How is sporotrichosis diagnosed? What is treatment?
Culture of drained/ aspirated material Itraconazole/ fluconazole
52
What parasites can cause skin lesions?
Leishmaniasis Schistosomiasis Cutaneous larva migrans - hookworm (ancylostoma/ necator) Guinea worm Onchocerciasis
53
How does hookwrom infections cause disease? Causes cutaneous larva migrans
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
What is treatment of scabies? Norweigan scabies is extensive thickening and crusting, which may occur in severely immunocompromised
Permethrin topical Oral ivermectin - if severe/ Norweigan scabies
55
What other tropical diseases can have rash? (maculopapular)
Dengue Marburg Hepatitis B Rickettsia - RMSF Typhus
56
Kawasaki syndrome can form part of differential diagnosis for skin rash. What is pathophysiology?
Children <4 acute vasculitis due to dysregulated T-cell activation to infectious trigger. Mortality 2% More common Asian population
57
What are symptoms of Kawasaki's disease?
Dryness/ redness of lips/ palms/ soles Desquamation of palms/ soles Oedema Arthralgia Myocarditis - 20% can develop coronary artery aneurysms
58
What is treatment of Kawasaki's?
Immunoglobulin Aspirin Both can prevent coronary artery damage
59
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?
Skin - chagoma/ Romanas sign 95% have cardiac defects - conduction/ heart failure due to myocardial invasion megaoesophagus megacolon
60
Parasitic worms are primarily intestinal parasites. Larval stages of non-human tape worms can invade muscle What species invade muscle?
Tapeworms - Echinococcus granulosus - sheep tapeworm Taneia solium - pork tapeworm. Can cause neurocysticercosis Roundworm (nematode) - Trichinella - pork roundworm
61
What are viral causes of arthritis?
HBV Rubella - post vaccination Mumps Parvovirus Togaviruses - Chikungunya, Ross River, Eastern Equine virus, Western Equine virus
62
What are causes of reactive arthritis? Associated with HLA B27 Due to immunogenic phenomena, as opposed to bacteria within joint
Campylobacter Salmonella Shigella Yersinia Chlamydia trachomatis - Reiter's syndrome urethritis, arthritis, conjunctivitis gonorrhoea streptococcal viral - many causes
63
What are causes of septic arthritis? Knees most commonly affected. Followed by hips, ankles, elbows. Occurs more commonly in damaged joints e.g RA
``` 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
What are symptoms of septic joint?
Fever joint pain swelling reduced movement
65
What is treatment of native joint septic arthritis?
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
What is treatment of prosthetic joint septic arthritis?
DAIR/ revision - see separate cards Vancomycin + rifampicin Duration 6 weeks at least
67
What are risk factors for septic joint?
Overlying skin infection recent surgery OA/ RA diabetes mellitus/ HIV immunosuppressive medication IVDU Soil exposure Animal bite
68
What is treatment of discitis/ vertebral osteomyelitis?
Ceftriaxone 2g OD or Vancomycin - aim higher level 15-20 Add metronidazole 400mg TDS if epidural abscess
69
Bone can become infected directly, or from haematogenous spread What bacteria are common causes of osteomyelitis?
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
What is treatment of osteomyelitis?
Flucloxacillin 2g QDS or Vancomycin + rifampicin 6 weeks therapy Minimum 2 weeks IV
71
How to diagnose osteomyelitis?
CRP/ ESR Blood cultures Imaging Bone biopsy
72
Which infective agents replicate in erythrocytes?
Plasmodium Babesia Bartonella Rickettsia Parvovirus Colorado tick fever All infections can cause anaemia
73
Why do EBV/ CMV cause thrombocytopenia?
Antibodies to virus cross-react and adhere to platelets
74
HTLV 1/2 infects T-cells in bone marrow. Which countries is it found in?
West Indies Japan Can have up to 15% population infected Rarer cases in SA/ Africa
75
How is HTLV primarily transmitted?
Maternal breast milk - most common sexual IVDU
76
What are symptoms of HTLV infection?
mild febrile illness lymphadenopathy pleural effusion/ aseptic meningitis can develop tropical spastic parapesis - myelopathy acute leukaemia PCP/ strongyloides and other opportunistic infection
77
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?
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
What are differential diagnosis of cellulitis?
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
Skin and soft tissue infection, with history of animal contact. What are possible organisms?
Cat bite - pasteurella dog bite - capnocytophaga bartonella Francisella tularensis bacillus anthracis yersinia pestis
80
Skin and soft tissue infection, with history of water contact. What are possible organisms?
vibrio vulnificus aeromonas hydrophilia mycobacterium marinum pseudomonas
81
Skin and soft tissue infection, with history of IVDU What are possible organisms?
MRSA C botulinum C tetani B anthracis
82
Skin and soft tissue infection, with history of foreign travel What are possibyle organisms?
cutaneous leishmaniasis cutaneous larva migrans myiasis
83
What are virulence factors of strep pyogenes in SSTI? Adherence factors Exotoxins Superantigen
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
What are virulence factors of staph aureus in SSTI? Adherence factors Exotoxins Superantigen
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
What is treatment duration for cellulitis?
7-14 days depending on severity prolonged course if underlying disease e.g PVD, lymphoedema
86
What scoring system is used to assess for probability of necrotising soft tissue infection?
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
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 ```
Itrazoncaole Sporotrichosis
88
Diabetic foot ulcer. What are indications of treatment for infection?
Inflammation cellulitis tissue loss ``` IDSA uses PEDIS to grade diabetic foot infections Perfusion Extent Depth Infection Sensation ```
89
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
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
What is differential diagnosis for septic arthritis?
Reactive arthritis bursitis gout lyme disease brucella whipples disease - mimic RA presentation
91
What is involved in two-stage revision of infected prosthetic joint?
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
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?
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
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
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
Why are rifampicin/ cipro useful in prosthetic infections?
Bactericidal Good joint penetration Prevent biofilm formation
95
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?
Nearly all caused by medication Antibiotics - co-trimoxazole Beta-lactam Fluroquinolones Anti-epileptics NSAIDs Allopurinol
96
Symptoms start between 1 week - 1 month after starting drug. What are symptoms of SJS/ TEN?
Prodromal flu-like illness - fever, coryza, myalgia Abrupt onset of rash which extends to maximal within 4 days - erythema - macules - blisters
97
How to diagnose SJS/ TEN?
Clinical diagnosis Skin biopsy
98
What is mortality risk of SJS/ TEN? What scoring systems can be used to predict mortality?
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
What is differential diagnosis of SJS/ TEN?
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
What is management of SJS/ TEN?
Stop offending drug Fluid support Temperature support Analgesia Antibiotics - only if infection develops Case reports - anti-TNF/ IVIG/ cyclophosphamide
101
IDSA use PEDIS is grade diabetic foot ulcers What constitutes the score?
``` 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
CUH guidelines Diabetic foot ulcer What is treatment? Mild Moderate Severe
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions