Bacterial Skin Infections Flashcards

1
Q

What is impetigo and what are the types?

A

-Common, superficial, contagious infection of skin
-More common in younger children aged under 6
=Most common bacterial infection worldwide in this group

  1. Bullous (less common)
  2. Non-bullous (most common)
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2
Q

How does impetigo arise?

A

-Self-inoculation of pathogenic bacteria elsewhere on skin or in the nasopharynx; or sometimes following an insect bite or atopic dermatitis induced scratching, for example
=Staph aureus most common cause for both types
=Beta haemolytic strep cause of non-bullous

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3
Q

Clinical features of impetigo

A

-Most commonly seen in children on the face, around the nose, and mouth
-Early lesions are characterised by the presence of small vesicles which may be clear, and rupture. Subsequently blisters (>1cm), which are pus filled may then be seen (local toxin production against desmoglein 1 only)
-There are usually surrounding scabs and a characteristic golden / honey coloured exudate or crust
-Lesions may itch, and scratching results in further inoculation of surrounding areas
-Leucocytosis is common, as is lymphadenopathy

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4
Q

Treatment of impetigo

A

-Contents of a blister should be sampled, or failing that a swab taken from the skin surface.
=Treatment should be started before the results are available.
-The crusts should be removed with wet dressings, and the wounds cleaned.
-If the disease is particularly localised, then topical antibiotics such as mupirocin or fusidic acid may be used.
-Antiseptics such as chlorhexidine are often added in.

-Treatment will usually be with a systemic anti-staphylococcal agent (e.g flucloxacillin or cephalosporin) before waiting for the culture and sensitivity results from microbiology.
-Take advice on local patterns of resistance.
-Infection is easily spread in a household and individuals should use their own towels and face flannels.
-Small epidemics may occur amongst health care staff.
-In some parts of the world, streptococcal impetigo is a major precipitating cause of glomerulonephritis

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5
Q

What is folliculitis?

A

-Inflammation centred around the hair follicle, an obvious opening within the skin, and an area rich in bacteria.
-May be infective – more commonly bacterial, or fungal – or non-infective.
-Most folliculitis is bacterial in origin, self-limiting, and rarely requires medical attention

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6
Q

Clinical features of folliculitis

A

-Most easily noticed around terminal hairs, but may occur around vellus hairs (which are harder to see) and is characterised by a pustule and surrounding erythema.
-There may be pain or itch.
-A boil (furuncle) refers to a deeper, larger, and more painful focus of infective folliculitis. I
-f the follicle is particularly large (carbuncle) there may be multiple openings from the lesion to the skin’s surface.

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7
Q

Common causes of folliculitis

A
  • Staphylococcal infection
  • Candida folliculitis
  • Herpes simplex folliculitis
  • Gram-negative folliculitis (something seen occasionally in patients who have been treated with tetracyclines, or other antibiotics, for acne)
  • In dermatology patients, a non-infective folliculitis due to emollients or tar therapy
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8
Q

Predisposing factors to folliculitis

A

-Excess sweating
-Occlusion and maceration (blue jeans/ truck drivers= secondary to friction and maceration from wearing tight clothes against skin or plastic car seats)
-Obesity and diabetes
-Topical or systemic corticosteroids (as in Cushing’s syndrome)
-Oily skin care preparations (make-up etc), greasy emollients or tars applied to the skin
-Hot-tub (pseudomonas)

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9
Q

Treatment of folliculitis

A

-Most folliculitis resolves spontaneously.
-Topical antiseptics (such as chlorhexidine) or topical chemotherapeutic agents, such as fusidic acid or mupirocin may be used.
-For boils that cause systemic symptoms, or are particularly large or multiple, then systemic antibiotics may be required.
=Start with an anti-staph agent and be guided by microbiology.
=There is an unresolved debate about whether large boils are better managed by surgical treatment (‘if there is pus about, let it out’) or whether conservative measures are more appropriate in most instances.
-If there are particular risk factors, see if they can be altered (obesity, diabetes, occlusion etc)

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10
Q

Cellulitis vs erysipelas

A

-Cellulitis: inflammation of the deep dermis and subcutaneous tissues, usually due to infection.
-Erysipelas: inflammation usually due to streptococcal infection of the deep dermis. =more commonly it affects the face than cellulitis, and the ‘edge’ is sharper and palpable.

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11
Q

Clinical features of cellulitis

A
  • Elderly
  • Have a unilateral area of erythema on the lower leg, with oedema, pain, and local warmth. Rarely there may be blisters, with or without haemorrhage
  • Pyrexia with general malaise,
    -Elevated white count
    -Blood cultures usually negative. Signs of severe sepsis may be present.
  • Occasionally, there may be an ascending painful lymphangitis and lymphadenopathy
  • There is sometimes an obvious focus that has allowed bacterial entry: a local wound; dermatophyte infection; or skin fissures
  • The causative agent is usually a streptococcus, but staphylococci may also be implicated
  • Any region can be affected: face, neck, torso, perianal area.
    =In the presence of immunosuppression or local surgery, broaden your perspective for causative organisms, and consider tissue sampling
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12
Q

Diagnosis of cellulitis

A

-Clinical, but cellulitis is frequently over-diagnosed.
-If there is a typical raised edge as you see in erysipelas, the diagnosis should not be in doubt.
-Skin swabs of intact skin are unhelpful and aspirates of the affected areas have a low yield in uncomplicated cases, and are not indicated.

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13
Q

Treatment of cellulitis

A

-IV antibiotics focussed on strep, or strep and staph (e.g. benzylpenicillin and flucloxacillin).
=Starting with flucloxacillin only is reasonable.
-Oral antibiotics may be an alternative in some cases, obviating the need for hospitalisation iv therapy.
-Treatment regimens differ between countries and regions. Topical therapies usually play no meaningful role
-Cellulitis often causes damage to lymphatic drainage system so predisposes to further episodes of cellulitis

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14
Q

Differential diagnosis for cellulitis

A

-Contact allergic eczema, often on the background of venous disease
-The deeper and much more serious necrotising fasciitis (rapidly advancing erythema, severe malaise or collapse, crepitation etc). Rare, but fatal unless treated surgically early.
-Pseudocellulitis: also known as hypodermitis, but representing an early stage of lipodermatosclerosis secondary to venous insufficiency. This is usually bilateral, with erythema, skin thickening and tightness, without systemic features or a history of sudden change in the limb.
- Panniculitis (e.g. erythema nodosum)
- Carcinomatous infiltration (especially breast), is rare

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15
Q

What is syphilis?

A

-Sexually transmitted infection caused by the spirochaete Treponema pallidum. –The incubation period is between 9-90 days

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16
Q

Presentation of syphilis

A

-Primary features
=chancre - painless ulcer at the site of sexual contact
=local non-tender lymphadenopathy
=often not seen in women (the lesion may be on the cervix)

-Secondary features - occurs 6-10 weeks after primary infection
=systemic symptoms: fevers, lymphadenopathy
=rash on trunk, palms and soles
=buccal ‘snail track’ ulcers (30%)
=condylomata lata (painless, warty lesions on the genitalia )

-Tertiary features
=gummas (granulomatous lesions of the skin and bones)
=ascending aortic aneurysms
=general paralysis of the insane
=tabes dorsalis
=Argyll-Robertson pupil

-Features of congenital syphilis
=blunted upper incisor teeth (Hutchinson’s teeth), ‘mulberry’ molars
=rhagades (linear scars at the angle of the mouth)
=keratitis
=saber shins
=saddle nose
=deafness

17
Q

Investigation of syphilis

A

-Very sensitive organism and cannot be grown on artificial media. The diagnosis is therefore usually based on clinical features, serology and microscopic examination of infected tissue.

Serological tests can be divided into:
-Non-treponemal tests
=not specific for syphilis, therefore may result in false positives (see below)
=based upon the reactivity of serum from infected patients to a cardiolipin-cholesterol-lecithin antigen
=assesses the quantity of antibodies being produced
=becomes negative after treatment
=examples include: rapid plasma reagin (RPR) and Venereal Disease Research Laboratory (VDRL)

-Treponemal-specific tests
=generally more complex and expensive but specific for syphilis
=qualitative only and are reported as ‘reactive’ or ‘non-reactive’
=examples include: TP-EIA (T. pallidum enzyme immunoassay), TPHA (T. pallidum HaemAgglutination test)
=the TP-EIA test has become increasingly popular in recent years

-The testing algorithms for syphilis are complicated but typically involve a combination of a non-treponemal test with a treponemal-specific test.
-Causes of false positive non-treponemal (cardiolipin) tests:
=pregnancy
=SLE, anti-phospholipid syndrome
=tuberculosis
=leprosy
=malaria
=HIV

18
Q

Management of syphilis

A

-Intramuscular benzathine penicillin is the first-line management
-Alternatives: doxycycline
-Nontreponemal (rapid plasma regain [RPR] or Venereal Disease Research Laboratory [VDRL]) titres should be monitored after treatment to assess the response

-The Jarisch-Herxheimer reaction is sometimes seen following treatment
=fever, rash, tachycardia after the first dose of antibiotic
=in contrast to anaphylaxis, there is no wheeze or hypotension
=it is thought to be due to the release of endotoxins following bacterial death and typically occurs within a few hours of treatment
=no treatment is needed other than antipyretics if required