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Skin and Soft Tissue Infection.pptx
- 1. OVERVIEW : Skin & Soft Tissue Infection Siti Hajar
- 2. OUTLINES Introduction Anatomy & Histology of Skin Anatomical Distribution Main Infectious Pathogens Most Common Types SSTI References 2
- 3. Introduction Include infections of skin, subcutaneous tissue, fascia, and muscle, encompass a wide spectrum of clinical presentations, ranging from simple cellulitis to rapidly progressive necrotizing fasciitis1. 3
- 4. 4
- 6. 6
- 8. Anatomical Distribution ANATOMY SYNDROME Epidermis Skin Erysipelas Impetigo Folliculitis Ecthyma Furunculosis Carbunculosis Dermis Cellulitis Superficial fascia Subcutaneous fat, nerves, arteries, veins Subcutaneous tissue Necrotizing fasciitis Deep fascia Muscle Myonecrosis 8
- 10. Main Infectious Pathogens 10 Viruses Bacteria Parasite s Fungi • Herpes simplex virus • Varicella-zoster virus • Human papillomavirus Herpes Labialis Herpes Genitalis Chickenpox / Shingles Kaposi Sarcoma • Staphylococcus aureus • Streptococcus pyogenes Impertigo Erysipelas Folliculitis Cellulitis • Dermatophytes (e.g., Microsporum, Epidermophyton species Trichophyton sp.) Tinea cruris (jock itch) Tinea pedis (athlete’s foot) Tinea capitis (fungal infection of the scalp) Onychophytosis (nail infection) • Sarcoptes scabiei Scabies Pediculosis
- 11. Most Common Types ssti
- 12. Impetigo 12 • A contagious superficial infection of the skin. • Staphylococci or β-haemolytic streptococci. • Common in children, but can occur at any age. • Usually involves the skin of the face, often around the mouth and nose. • Spread by direct contact. • Minor abrasions and other skin lesions predispose to infections. • Prevention is by good personal hygiene , particularly hand washing with soap.
- 13. 13
- 14. Non-bullous Impetigo Spongiosis of epidermis giving rise to vesicopustules in upper layers of epidermis. As lesions progress, epidermis may become eroded and covered with a thick layer of serous crust with neutrophilic debris and Gram positive cocci. Superficial dermis displays a moderately dense mixed inflammatory infiltrate. 14
- 16. • Cleavage plane is subcorneal or upper granular layer • Variable acantholysis • Pustule is filled with neutrophils, and bacterial clusters are evident with Gram stain • The underlying dermal infiltrate contains a mixed neutrophil and lymphocytes infiltrate; neutrophils may be seen in the spongiotic stratum spinosum 16 Bullous Impetigo
- 17. Erysipelas • Streptococcus pyogenes infections of dermis • Well demarcated, painful, erythematous • Erysipelas and Cellulitis often overlap • Indurated plaques, Blisters & Ulceration • Abrupt fever with chills • Face, legs • Common in very young, old, debilitated patients • Lymphoedematous 17
- 18. Erysipelas 18
- 19. Erysipelas
- 20. Folliculitis • Folliculitis is a superficial infection of hair follicles. • Assoc with areas of friction – neck, face, axillae, buttocks • The lesions are crops of red papules or pustules that are often pruritic. • Staphylococci, yeast, and occasionally, pseudomonas species are the responsible pathogens. 20
- 21. 21 Folliculitis
- 22. 22 Superficial folliculitis with neutrophils concentrated in the upper aspect of the follicle
- 23. Ecthyma • Ecthyma is a deeper form of impetigo with ulceration and scarring, commonly on the legs and associated with trauma or debility. • Ecthyma causes deeper erosions of the skin into the dermis. • Streptococcus pyogenes and Staphylococcus aureus are the bacteria responsible for ecthyma. 23
- 24. Ecthyma 24
- 25. • hyperkeratosis, cell vacuolization in the upper epidermis, spongiosis, pyknotic epidermal cells, and a dermoepidermal junction lymphohistiocytic infiltrate. (Hematoxylin- eosin stain; original magnification: ×40.) Ecthyma 25
- 26. Furuncle • A small subcutaneous staphylococcal abscess • Develops in deeper parts of hair follicle • Solitary or multiple • Staphylococcal furuncle better known commonly as a “ Boil” 26
- 27. Carbuncle • Cluster of boils that form a connected area of infection (Multiloculated abscess) • Spread to the dermis and subcutaneous tissue 27
- 29. Furuncle
- 30. Carbuncle 30
- 31. Cellulitis • Deep skin or subcutaneous layer infection of normal skin flora or exogenous bacteria (S. aureus and ß- haemolytic streptococci) • History of Trauma and Ulceration • Organisms enter through breach in skin • Infection can spread to blood stream (bacteremia /septicemia) • Lower leg , hand ,nose ,periorbital 31
- 32. Cellulitis 32
- 33. Cellulitis 33
- 34. Cellulitis
- 35. Necrotizing fasciitis NF • Necrotizing fasciitis is a severe infection of the subcutaneous tissue that results in destruction of fascia and fat. • The most common primary site is the extremities. • The first cutaneous clue to fasciitis is diffuse swelling of an arm or leg, the skin may appear normal or have a red or dusky hue, followed by the appearance of bullae filled with clear fluid, which rapidly takes on a maroon or violaceous color. • In some instances crepitus may be present. • Type I = polymicrobial infection, • Type II = monomicrobial infection. Presentation title 35
- 39. Pyomyositis • S. aureus & Streptococcus infection of the skeletal muscles • Pus-filled abscess • Most common in tropical areas- “ myositis tropicans” • Can affect any skeletal muscle • Most often infects the large muscle groups e.g.- quadriceps or gluteal muscles. Presentation title 39
- 40. Pyomyositis 40
- 41. Pyomyositis
- 42. Clostridial Myonecrosis • Myonecrosis or infarction of skeletal muscle occurs when the blood supply is inadequate to maintain muscle viability. • Clostridial myonecrosis (gas gangrene) is a life-threatening muscle infection Extensive tissue destruction and gas production by fermentative action of bacteria. • Principally C. perfringens but C. novyi and C. septicum also seen. Presentation title 42
- 45. Summary At Contoso, we believe in giving 110%. By using our next-generation data architecture, we help organizations virtually manage agile workflows. We thrive because of our market knowledge and great team behind our product. As our CEO says, "Efficiencies will come from proactively transforming how we do business." Presentation title 45
- 46. References 1. https://emedicine.medscape.com/article/1830144-overview 2. https://www.pathologyoutlines.com/topic/skinnontumorerysipelas.htm 3. https://emedicine.medscape.com/article/784690-overview#a4l 4. https://www.researchgate.net/figure/Histology-report-of-the-muscle-biopsy-which-shows-destruction-of- the-muscle-architecture_fig1_273338710 Presentation title 46
- 47. Thank You
- 48. Thank you
Editor's Notes
- The epidermis: a thin outer portion, that is the keratinised stratified squamous epithelium of skin. The epidermis is important for the protective function of skin. The basal layers of this epithelium are folded to form dermal papillae. The dermis: a thicker inner portion. This is the connective tissue layer of skin. It is important for sensation, protection and thermoregulation. It contains nerves, the blood supply, fibroblasts, etc, as well as sweat glands, which open out onto the surface of the skin, and in some regions, hair. The apical layers of the dermis are folded, to form dermal papillae, which are particularly prominent in thick skin. The hypodermis. This layer is underneath the dermis, and merges with it. It mainly contains adipose tissue and sweat glands. The adipose tissue has metabolic functions: it is responsible for production of vitamin D, and triglycerides.
- HSV-1 is the cause of herpetic vesicles on the lips (herpes labialis), also known as cold sores. HSV-2 is the cause of genital vesicles (herpes genitalis). Varicella-zoster virus is the cause of chickenpox in children. Reactivation of the same virus causes shingles (herpes zoster) in adults. HSV-8 is the cause of Kaposi sarcoma in AIDS patients
- It has two forms: 1. Non-bullous Streptococcus pyogenes "honey-crust" lesions The initial lesions are small vesicles or pustules (< 2 cm) that rupture and become a honey-colored crust with a moist erythematous base. Early lesions: easily ruptured vesicopustules on an erythematous base Later lesions: ruptured lesions are replaced by thick, adherent, distinct golden yellow (honey colored) crust Satellite lesions due to self inoculation are common 2. Bullous rupture of the bullae "varnish-like" crust Due to Staphylococcus aureus which produces exfoliative toxins (exfoliatins A and B). Exfoliative toxins target intracellular adhesion molecules (desmoglein – 1) present in the epidermal granular layer. Results in dissociation of epidermal cells which causes blister formation. The initial lesions are fragile thin-roofed, flaccid, and transparent bullae (< 3 cm) with a clear, yellow fluid that turns cloudy and dark yellow. Once the bullae rupture, they leave behind a rim of scale around an erythematous moist base but no crust, followed by a brown-lacquered or scalded-skin appearance, with a collarette of scale or a peripheral tubelike rim.
- As lesions progress, epidermis may become eroded and covered with a thick layer of serous crust with neutrophilic debris and Gram positive cocci. Superficial dermis displays a moderately dense mixed inflammatory infiltrate.
- Acantholysis = loss of coherence between keratinocytes of epidermal cells due to breakdown of intercellular bridges formation of rounded, detached cells within the blister
- Erysipelas is a superficial form of cellulitis Is an acute infection of the upper dermis and superficial lymphatics, usually caused by streptococcus bacteria. Erysipelas is more superficial than cellulitis, and is typically more raised and demarcated. Bacterial inoculation into an area of skin trauma is the initial event in developing erysipelas. The patient may be febrile and have a leucocytosis. The infection rapidly invades and spreads through the lymphatic vessels. This can produce overlying skin "streaking" and regional lymph node swelling and tenderness.
- Lesions predominantly appear on lower limbs, but when it involves the face, it gives rise to a characteristic butterfly distribution on the cheeks and bridge of the nose Usually abrupt onset; can be distinguished from other forms of cellulitis by a sharply demarcated, raised border Causes upper dermal edema with blockage of the superficial lymphatics, causing the clinical orange peel or peau dorange appearance of the affected skin and localized lymphadenopathy
- Marked dermal edema, vascular dilatation (vascular ectasia) and streptococcal invasion of lymphatics and tissues Dermal inflammatory infiltrate consist of neutrophils and mononuclear cells
- The most common yeast to cause a folliculitis is Pityrosporum ovale, also known as Malassezia. Malassezia folliculitis (pityrosporum folliculitis) is an itchy acne-like condition usually affecting the upper trunk of a young adult. Folliculitis may be caused by the herpes simplex virus. Herpes zoster (the cause of shingles) may present as folliculitis with painful pustules and crusted spots within a dermatome (an area of skin supplied by a single nerve).
- multiple small papules and pustules on an erythematous base that are pierced by a central hair, The lesions are seen in the bearded area, often on the upper lip near the nose, as erythematous follicular-based papules or pustules that occur in crops and may rupture leaving a yellow crust.
- Ecthyma is an ulcerative form of impetigo. Ulcer forms under a crusted surface of the infection Heals with scarring
- Lesion: small, purulent, shallow, punched-out ulcers with thick, brown-black crusts, and surrounding erythema. Ecthyma lesion usually begins as a vesicle (small blister) or a pustule on an inflamed area of skin. A hard crust soon covers the blister. With difficulty, the crust can be removed to reveal an indurated ulcer that may be red, swollen and oozing with pus. Lesions may stay fixed in size and sometimes resolve spontaneously without treatment, or they may gradually enlarge to a sore of 0.5–3 cm in diameter. They resolve slowly leaving a scar.
- Ecthyma lesions show dermal necrosis and inflammation. A deep and superficial granulomatous perivascular infiltrate occurs along with endothelial edema. A heavy crust covers the surface of the ecthyma ulcer.
- Reddish or purplish pus-filled bump that forms under the skin when bacteria infect and inflame one or more of hair follicles.
- It is formed by a cluster of interconnected furuncles, pus-filled, inflamed hair follicles.
- Acute folliculitis accompanying intradermal abscess (HE). Intradermal abscess is caused by destructive proliferation of S. aureus.
- Inflammatory cells, predominantly neutrophils, within the wall and ostia of the hair follicle, creating a follicular-based pustule Inflammation can be either limited to the superficial follicle, primarily involving the infundibulum, or can affect both the superficial and deep aspects of the follicle Deep folliculitis can arise from the chronic lesions of superficial folliculitis or from lesions that are manipulated or scratched; may cause scarring
- Aetiology: • S. pyogenes • S. aureus • Enteric gram negative bacilli • Clostridia • Anaerobes
- Non-raised skin lesions with indistinct margin, sometimes with lymphangitis (unlike superficial form Erysipelas which is typically more raised and demarcated) There is usually no localization of the infection or pus formation
- (Hematoxylin and eosin stain, original magnification ×200) - Perivascular chronic inflammatory infiltrates with eosinophils and some phagocytic histiocytes were seen
- Hematoxylin and eosin (H&E) stain, high power. This image shows deeper subcutaneous tissue involved in a case of cellulitis, with acute inflammatory cells and fat necrosis. Histologically, cellulitides contain suppurative neutrophilic infiltrate involving dermis &/or subcutaneous tissue ± associated necrotizing vasculitis, vascular ectasia, subepidermal edema, and sometimes bacteria
- Fournier gangrene (when localized to the scrotum and perineal area) Aetiology • S. aureus • Streptococci – Group A and Strep milleri • Anaerobes • Clostridia spp • Vibrio vulnificus • Aeromonas hydrophila
- Common initial findings include swelling, pain, and erythema, present in 70%-80% of patients. [35, 8, 29] Findings in more advanced necrotizing fasciitis include dusky skin and yellowish to red-black fluid-filled bullae that rapidly progresses to a demarcated area of necrosis resembling a third-degree burn, evolving to frank cutaneous gangrene with penetration along deep fascial planes and myonecrosis. Other manifestations include thrombophlebitis in the lower extremities, bacteremia, septic shock, and hypotension with rapid death.
- Necrosis of fascia - key feature. PMNs and necrotic debris (amorphous grey or pink material). +/-Vascular thrombosis.[6] Note: Fat lobules between septae may be normal.
- Necrosis of fascia - key feature. PMNs and necrotic debris (amorphous grey or pink material). +/-Vascular thrombosis.[6] Note: Fat lobules between septae may be normal.
- Pyomyositis, also known as tropical pyomyositis or myositis tropicans, is a bacterial infection of the skeletal muscles which results in a pus-filled abscess
- Insidious onset of dull, cramping pain, a low-grade fever, muscle ache upon exertion or palpation, general malaise, and anorexia. There is localized edema, sometimes described as indurated or woody, with little or no tenderness. Not much skin discoloration as compared to cellulitis
- destruction of the muscle architecture and thrombosis in the vessels (pyomyositis) Pathologic findings on biopsy show edematous muscle fibers, lymphocytic infiltration, and suppuration as the muscle belly is replaced by pus. The involved muscle is usually tender and the overlying skin may be normal or mild eruptive.
- Myonecrosis causes: infection, diabetic myonecrosis, trauma-induced myonecrosis, etc Clostridial myonecrosis (gas gangrene) is a life-threatening muscle infection that develops either contiguously from an area of trauma or hematogenously from the gastrointestinal tract with muscle seeding.
- Severe pain out of proportion to clinical findings and loss of motor function – Erythema and cutaneous blisters – Gangrene – Crepitus – Brown foul smelling discharge