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Flashcards in skin infections 1 Deck (47):
1

host defense

*intact epidermis*, acid pH, dryness, salty sweat, low surface temp

cidal props of skin: excreted chem compounds: sebum (FAs) and urea

phagocytosis by WBC

NF: Propionibacterium acnes, diphtheroids, staphylococci (coag-negative)

2

etiology of skin infections

non-infectious: allergic rxns, cancer, etc.

parasites and arthropods

bac, viruses, fungi


3

pathogenic patters of skin disease caused by bac, viruses, fungi:

systemic: blood-brn dis w. skin rash: (i.e. RMSF: rocky mountain spotted fever (Rickettia))

exotoxin mediated: TSS

*primary skin infection: bac, fungi, viruses (i.e. HSV most common viral agent)

4

exanthematous disease approach: progression and chronology are important:

where did it first appear?
chronology: how long has it been there and how has it changed?
Does it appear first on the limbs and then on the trunk or vice versa? Head first then spread down? Cheeks and torso?
did it always look like how it does now?
is there an enanthem or s/s of such?
is the enanthem present concurrently with the exanthem?

5

exanthematous disease approach: symmetry and anatomical distribution:

localized or regional or generalized?
where concentrated? (limbs, torso, head, face, etc)

6

exanthematous disease approach: description ?

ulcerative, pustular, petechial, macular, papular, vesicular?
pruritic? painful?
blanching? (fever + non-blanching rash: meningicoccal meningitis)
size
confluent or sparse?
color

7

exanthematous disease approach: associated s/s

concurrent fever? If not, when? before or after rash appeared? how long did it last?
is there a prodrome?
If so, does it occur with all age groups?
Is agent present in the lesions? IMPORTANT - Relates to transmission, is person
infectious?

8

Propionibacterium acnes: Acne Vulgaris

most common skin disease (not necessarily infectious disease)

initially caused by alteration in physiologic processes of sebaceous glands and hair follicle

If the sebaceous glands become colonized by P. acnes, an inflammatory, a self- limiting form of the disease occurs.

9

P. acnes

G+
non-motile
diphtheroid/pleomorphic rod
obligate anaerobe

virulence factor: extracellular Lipase

10

P. acnes epidemiology

predominant anaerobic member of NF of skin
most common contaminate in clinical specimen: blood and urine (is it causing the disease/infection or just there?)
Age - Teenagers (85% have acne) --> adults (persons [esp. women] in their 30s-40s). Direct cost $1 billion/yr.
Female>male but more scarring in males

11

pathogenic mechs: absence of P. acnes

increased sebum production occurs after puberty: follicular canal becomes plugged due to altered physiology
In absence of P. acnes: Get comedones

closed comedones "white heads": Surface pore of the follicular canal is closed
Open comedones "black heads.": Surface pore of the follicular canal is open, so air can enter in to oxidize material. Lesion with a central follicular impaction of lipid, keratin, melanin (which causes the easily observed brown or black appearance).

12

NFLAMMATORY LESIONS

- COLONIZED by P. acnes: (papules, pustules, nodules, cysts)
Proinflammatory mediators are FAs cleaved from sebum by lipase produced by P. acnes breaking down sebaceous gland secretions

first progress to *papules* then to *pustules* and *nodules* (cysts/cystic acne). Cystic acne associated with most of the scarring seen in acne.

13

P. acnes dx is usually obvious, but a number of disorders can be mistaken for acne: this ?? is helpful to rule out ??
and ?? can rule out ??

bacterial culture can be helpful to diagnose bacterial folliculitis (or Malazzia furfur)

skin biopsy will confirm or rule out granulomatous and neoplastic conditions

14

When signs of androgen excess are present in female patients, measurement of levels of ?? may be helpful

total and free testosterone, dehydroepiandrosterone sulfate, leutinizing hormone, and follicle- stimulating hormone

15

if PCOS is suspected, ?? can assist in confirming the diagnosis.

fasting glucose and insulin levels and pelvic ultrasonography

16

acne ddx

Malassezia folliculitis
G- folliculitis
Milia
Perioral dermatitis
Chloracne
Favre-Racouchot disease
Rosacea
Herpes gladiatorum
Tinea barbae
CA-Staph aureus

17

Malassezia folliculitis

not limited to the usual acne sites (face, back, and
chest). It does not respond to typical acne therapies. Gram stain of pus from the lesions reveals gram-positive budding yeast

18

G- folliculitis

In patients on long-term antibiotics, superficial pustules or nodules can develop at the anterior nares and spread outward on the face; responds quickly to oral ampicillin.

19

Milia

white pinpoint cysts that resemble closed comedones. They frequently occur around the eyes but can develop anywhere on the face. If untreated, they last for months or years. Milia can be opened with a small surgical blade and their contents easily drained.

20

Perioral dermatitis

Long-term use of topical corticosteroids on the face can result in acneiform, erythematous, inflamed papules on the chin and cheeks. Despite the name, the area immediately around the mouth is typically spared in perioral dermatitis.

21

Chloracne

Cysts and closed comedones that resemble acne lesions can be caused by exposure to halogenated hydrocarbons.

22

Favre-Racouchot disease

Numerous open and closed comedones can appear around the eyes of elderly patients, especially men who have worked out of doors for much of their lives. This condition has been attributed to a lifetime of sun exposure.

23

Rosacea

(acne rosacea): A common condition that usually begins after 30 years of age. Facial flushing is a common feature. In patients with a predominance of inflamed papules and pustules, differentiation from acne can be difficult. Presence of telangiectasia and the occurrence of flushing help distinguish this common condition from acne.

24

acne: acute or chronic?

A chronic disease; may require intermittent treatment for months or years.

25

acne Purpose/Goal of treatment

Inhibition of physiologic processes: antikeratinizing; sebum production
inhibition (Salicylic acid, retinoic acid, Azelaic acid [dicarboxylic acid])

anti-P. acnes. (Antibiotics, Benzoyl peroxide, Salicylic acid (cheap), retinoic acid,
Azelaic acid)

anti-inflammatory. Corticosteroids-oral or local injection

26

treatments that are ineffective and/or may be harmful (increase severity of acne)

Frequent, non-medicated, vigorous scrubbing: harmful
use of abrasive cleansing: harmful
A restricted diet: ineffective
Squeezing pimples – otherwise known as popping zits: harmful

27

peroxide will kill P. acne because?

it is an oxide and P. acne is anaerobic

28

The physician must recognize 3 important issues:

Acne patients report levels of social, psychological and emotional problems
as great as those with chronic disabling asthma, epilepsy, diabetes, back pain, or arthritis.

The impact on the quality of life does not correlate with the severity of acne.

Patients are frequently miss-informed; e.g., @ 1/2 of all acne patients (all ages) think acne is curable and that treatment duration of is less than 6 months
*Neither is true!*

29

Staph aureus

G+ cocci, pairs, short chains, grape-like clusters
EC enzymes: coagulase +, catalase +
not fastidious
yellow on McConkey agar

*common agent of community AND hospital-acquired infections*

30

Staph exotoxins

Exfoliatin exotoxins (ET; ETA and ETB)
Panton-Valentine Leukocidin
TSST-1

31

Exfoliatin exotoxins (ET; ETA and ETB).

causes an epidermal desquamation of superficial intraepidermal layers of skin (*cleavage in epidermis*)
Produces Nikolsky sign and/or bullae; No inflammation or necrosis, no scarring unless 2o infection occurs
Exfoliatins are glutamate- specific serine proteases highly specific to the *cadherin desmoglein I*, an adhesion protein in the desmosomes of the stratum granulosum that facilitates intracelluar adhesion between keratinocytes. The resulting vesicles are an intraepidermal clefts between the stratum corneum and stratum spinosum and is located above the basal cells (supra basal)

32

very similar non-infectious condition (looks like S. aureus infection) is seen in the autoimmune skin disorder ??

pemphigus vulgaris in which there is an IgG antibody against the cadherin desmoglein 3.

33

Panton-Valentine Leukocidin:

Community-acquired methicillin-resistant strains (MRSA)
Single strain is responsible for nearly all cases word-wide.
*Strain that causes skin infections*
Strain that can cause severe necrotizing pneumonia and scarlet fever

pick up by lysogenic conversion

34

Strain identification is based on ??

phage typing; Group II strains are most frequently associated with skin infections.

35

CA-MRSA skin/soft tissue infection risk factors

IDU, previous MRSA infection and colonization, prescriptions for antibiotics in previous 8 weeks and admission to hospital in the preceding 12 months

accounts for >50% of community-acquired skin and soft tissue infections presenting to the hospital for treatment

36

Children with staphylococcal scarlet fever caused by Panton-Valentine leukocidin–positive Staphylococcus aureus strains had more exacerbated ??

skin manifestations and greater systemic inflammatory responses compared with children who had strains that were negative for the cytotoxin.

37

Staph predisposing factors

Defects in PMN chemotaxis and/or opsonization.
Immunosuppression (e.g. unregulated diabetes, corticosteroid treatment).
Foreign bodies (infectious dose decreases if a foreign body is present).
Age – neonates (SSSS).
Poor hygiene (failure of HCW to wash hands)

38

Staph transmission/reservoirs

-Inhalation resulting in colonization of nares.
-Direct contact - entry of organism through breaks in skin

Reservoirs:
a. *Mostly humans* (by far #1): NF of nasal nares (10-40% carriage rate).
b. Fomites - clothes, bedding, towels, etc.

39

S. aureusage and seasonality

all ages
no seasonality exp. GIT disease

40

Pathogenicity and Clinical Manifestations of Pyodermic Infections

All are contagious; contact with lesions will result in colonization with a virulent
strain; disease development – host, condition dependent.

41

Pyodermic infections include:

folliculitis
furuncles
carbuncles
epidemic impetigo
bullous impetigo
staphylococcal scalded skin syndrome.

42

folliculitis

Superficial infection of individual hair follicle and apocrine regions. A. Lesions are:
small (2-5 mm),
erythematous,
sometimes pruritic
papule often topped by a central pustule
can occur on any hair-bearing site on body.

43

Etiologic Agents of folliculitis

Most common agent is Staphylococcus aureus (Coagulase positive staphylococci).
If hot tub then: Pseudomonas aeurginosa
If refractory to treatment think: Malazzia furfur

44

furuncles and carbuncles develop from ??
occur most commonly in what age group ??
what are they??

staphylococcal folliculitis

children 3-15 y-o-age

Recurrent boils occur in predisposed individuals (see above)
Infection of hair follicle and subcutaneous tissue, tend to occur on: neck, face, axillae, back, buttocks, thighs

45

furuncles are ?? from infection of INDIVIDUAL hair follicle and adjacent underlying tissue
characteristics of lesions??

boils/deep folliculitis

lesions are necrotic, pyogenic abscesses in the dermis:
firm, painful - tender, discrete, red nodule (~1 cm) with purulent
drainage. **Skin around furuncle is hot but NO systemic signs**

46

carbuncles involve ??
lesions compared to furuncles ??

several hair follicles

lesions are larger, deeper, indurated lesions than that seen in furuncles
Lesions are erythematous, edematous, painful, with a central, necrotic crater that
coalesce-->spreading, drain to the surface along hair follicles
**Systemic signs of fever and malaise MUST be present!**

47

tx of furuncles and carbuncles

Moist heat to promote drainage.
More severe furuncles and localized carbuncles require judicious incision and drainage plus antibiotics.
If there is recurrence, screen family members for carriage and treat if appropriate

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