Pimples and Boils!! Dr Nathan Harvey Anatomical Pathology, PathWest

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1 Pimples and Boils!! Dr Nathan Harvey Anatomical Pathology, PathWest

2 Overview & Learning Objectives Review the cardinal signs/symptoms of acute inflammation Review the histological features of acute inflammation Overview of the possible outcomes of acute inflammation Understand the clinical signs/symptoms, pathological mechanisms and histological features of common acute inflammatory disorders of the skin: Impetigo Acne vulgaris Folliculitis Furuncle Erysipelas/cellulitis

3

4

5 Neutrophils

6 What is Pus? A protein-rich fluid produced as a product of inflammation It comprises: Leukocytes (white blood cells) Debris from dead cells Tissue elements which have been liquified by the action of neutrophil enzymes Bacteria that cause pus formation are called suppurative, pyogenic or purulent

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8 Microscopic Structure of the Skin Stratum Corneum

9 Hair follicle Epidermis Dermis Arrector pili muscle Eccrine sweat gland Subcutaneous adipose tissue

10 Papillary dermis Hair follicle (note the solar elastosis : not technically normal, but almost ubiquitous in WA!) Sebaceous gland Reticular dermis Arrector pili muscle Blood vessels Eccrine sweat gland

11 Cornified layer (stratum corneum) Granular layer (stratum granulosum) Prickle layer (stratum spinosum) Basal layer (stratum basalis) Melanin pigment Melanocyte Solar elastosis

12 Cutaneous Bacterial Infections Pyogenic infections Staphylococcus aureus Streptococcus Corynebacteria Neisseria Mycobacteria Chlamydia Rickettsia

13 Impetigo Acute superficial infection of the skin Most common bacterial skin infection of childhood Adults can also be affected Athletes Military Institutions Predisposing factors Minor trauma Poor hygiene Warm, humid climate

14 Impetigo Organism is often Staphylococcus aureus (esp in bullous subtype) Also Streptococcus, anaerobes Staphylococcus aureus may produce exfoliative toxins

15 Common Impetigo School sores Impetigo Thin walled vesicles or pustules Rupture to form a thick golden crust Solitary or clustered, face or extremities Bullous Impetigo Erosions and flaccid bullae Caused by an exotoxin which results in keratinocytes falling apart and blister formation

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17 Histopathology Subcorneal (ie under the stratum corneum) collection of neutrophils Can see more neutrophils migrating upwards through the epidermis Surface crust of serum and dying neutrophils May see bacterial colonies

18 Neutrophils

19 Staphylococcal Scalded Skin Syndrome Another blistering disorder caused by Staphylococcus aureus, but with a different mechanism Occurs in infants Widespread blisters that rupture easily No bacteria in the blisters Caused by an endotoxin that is made by the bacteria elsewhere and is transported via the bloodstream

20 Acne Vulgaris Pimples! An inflammatory disorder of the pilosebaceous unit ie the hair follicle and attached sebaceous gland Common Affects a large proportion of teenagers Usually improves spontaneously after adolescence

21 Clinical Appearances The lesions that make up acne are variable and include: Comedones Papules Pustules Cysts Sinuses Scars

22 Clinical Appearances Comedones are widened hair follicles which are filled with keratin, other debris, bacteria and sebum Closed : whiteheads Open: blackheads

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24 Scars Inflamed papule Open comedones

25 Pathogenesis Four inter-related factors Abnormal follicular keratinisation, with retention of keratin within the follicle This process is the precursor to comedone formation May be aided by a bacterial biofilm Increased sebum production Androgens Presence of bacteria: Propionibacterium acnes Inflammation

26 Pathogenesis Ongoing dilation of comedo leads to the wall of the follicle becoming very thin Eventually it ruptures The keratin, sebum and bacteria incite an acute inflammatory response Predominantly neutrophils at first pustule formation Followed by granulomatous inflammation and fibrosis (scarring) The acute inflammatory focus can enlarge into an abscess. Sinus tracts result when the epidermis grows down in an attempt to wall off the inflammation

27 Neutrophils Plugged and dilated follicle

28 Superficial Folliculitis Typically affects the superficial part of the hair follicle, called the infundibulum Thus, perhaps more correctly should be called infundibulitis May be related to bacterial infection (eg Staphylococcus aureus) Neutrophils under the statum corneum and around the infundibulum pseudofolliculitis is a term used to describe a foreign body response to hair shafts that have ruptured out of the follicle into the surrounding dermis

29 Small pustules around hair follicles

30 Neutrophils

31 Furuncle Boils A deeper infectious inflammatory process centred on the pilosebaceous unit Typical locations include the back of the neck, buttocks and thighs Sites of friction with clothing Begins as a painful papule with surrounding erythema (redness) and swelling The centre becomes soft, yellow and may discharge pus A carbuncle is a coalescence of several furuncles

32 Histological features A deep dermal abscess (ie neutrophils again!) centred around a hair follicle The follicle may be destroyed although residual hair shafts may be seen The surrounding inflammation may extend into the deeper tissues The surface oftens shows a crust of serum and dying neutrophils

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34 Acute inflammation (ie neutrophils) in the deeper parts of the follicle

35 Furuncle - Causes Often bacterial, usually Staphyloccocus aureus Pseudomonas aeruginosa is associated with hot tub folliculitis Develops 8-48 hours after recreational exposure to the organisms, which is found in contaminated spas Viral eg herpes simplex Fungal

36 Erysipelas/Cellulitis Erysipelas is an acute inflammatory process within the dermis which is usually caused by Streptococcus pyogenes Oedematous, tender, hot, well demarcated red plaques Often accompanied by a fever Face, feet, hands and lower limbs are most affected

37 Erysipelas/Cellulitis Cellulitis is a similar processs which involves slightly deeper tissues More often occurs on the legs Expanding area of erythema S pyogenes is again usually the causative organism

38 Predisposing Factors Minor trauma Peripheral vascular disease Diabetes Lymphoedema Alcohol abuse

39 Histology Dermal oedema and lymphatic dilatation Diffuse infiltrate of neutrophils

40 Erysipelas

41 Neutrophils Oedema

42 Summary Remember: the cardinal signs & symptoms of acute inflammation The histological features The possible sequelae By applying the above to different anatomical components of the skin: Impetigo Acne vulgaris Folliculitis Furuncle Erysipelas/cellulitis

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