Pyodermas.pptx

The skin is not only the largest organ of the body, but it also forms a living biological barrier with several functions.

Pyodermas are any pyogenic skin disease (has pus). Skin infections can be caused by bacteria (often Staphylococcal or Streptococcal) either invading normal skin, or affecting a compromised skin barrier
Some bacterial skin infections resolve without serious morbidity. However, skin infections can be severe and result in sepsis or death, particularly in vulnerable patient groups.

1. PYODERMAS Dr Samson Ojedokun MB;BS Ogbomoso Nigeria 1

2. Outline Introduction Prevalence Skin layers Risk factors Pathophysiology Descriptive Terms Classifications Management approach Conclusion References 2

3. Introduction The skin is not only the largest organ of the body, but it also forms a living biological barrier with several functions. Pyodermas are any pyogenic skin disease (has pus). Skin infections can be caused by bacteria (often Staphylococcal or Streptococcal) either invading normal skin, or affecting a compromised skin barrier Some bacterial skin infections resolve without serious morbidity. However, skin infections can be severe and result in sepsis or death, particularly in vulnerable patient groups. 3

4. Prevalence Infectious skin diseases are common in the tropics, but due to the paucity of epidemiologic surveys, not much is known about the prevalence and common types found in different sub-populations. Globally, all skin conditions combined were fourth leading cause of non-fatal disease burden. In 2005, the World Health Organisation (WHO) reported a high prevalence of skin disease in children from developing countries in sub-Saharan Africa BSD accounts for a prevalence rate of 7.38- 10.27% of the DALYs, an upward trend between 1990 to 2019. 4

5. 5 The highest burden was in the low-middle sociodemographic index (SDI) area and the lowest burden was recorded in the high-middle SDI area in 2019. Skin infections accounted for a large proportion of Years of healthy life lost due to disability YLD in tropical and resource-poor regions. The most common categories were infectious skin disease observed among schoolchildren in Ibadan( Ogunbiyi et al) and among dermatology clinic attendance in Lagos ( Ayanlowo et al)

6. 6 Skin Layers

7. Risk Factors Break in epidermal integrity Puncture or stab injury Immunosuppression Presence of systemic illnesses (DM, malignancy etc) Lesions; eczema, ulcers etc Low socioeconomic status Overcrowding 7

8. Pathophysiology A schematic view of bacterial skin infection, derived from a loss in epidermis integrity. 8

9. Descriptive Terms Primary skin lesions Macules Papules Nodules Vesicles Bullae Pustules Patches Wheal Erythema Purpura Burrows Telangiectasia 9

10. Primary lesions 10

11. Secondary lesions Crusts Erosions Scales Ulcers Scars Scabs Fissures Keloid Lichenifications Atrophy Excoriations Hyperpigmentation Hypopigmentation depigmentation 11

12. Secondary lesions Crust Scabs Excoriation 12

13. Classification Staphylococcal infections Streptococcal infection Overgrowth of diphtheroid Others Impetigo Ecthyma Furunculosis Folliculitis Pseudofolliculitis Carbuncle Scalded skin syndrome Erysipelas Cellulitis Necrotising fascitis Erythrasma Trichomycosis axillaris Pitted keratolysis Cat scratch disease Erysipeloid Hidradenitis suppurativa Acute bacterial paronychia 13

14. Impetigo Impetigo is a common, highly contagious, characterized by pustules/or bullae and honey-colored crusted erosions. It affects the superficial layers. Typically caused by Staphylococcus aureus and Streptococcus pyogenes (Group A beta – haemolytic streptococci (GABHS)). The staphylococcal exfoliative toxins (ETA, ETB, ETD) blister the superficial epidermis by hydrolyzing human desmoglein1, resulting in a subcorneal vesicle It can be classified into non-bullous (also known as ‘school sores’) and bullous impetigo. 14

15. Bullous impetigo Blisters or vesicle that ruptures easily and spreads distally due to autoinoculation. highly contagious Honey-coloured adherent crust with a finely cremated rim. Usually found on the face, trunk, extremities, buttocks, and perineal regions. Neonatal bullous impetigo can begin in the diaper area. Rupture of a bulla occurs easily, Systemic symptoms: malaise, fever, and lymphadenopathy. 15

16. Non-bullous impetigo Less crusting, less contagious; commoner in children. Commonly found on the face or extremities Begins with erythematous macule, evolves into a pustule or vesicle. Can spread rapidly with satellite lesions due to autoinoculation. Patients are typically otherwise well; they may experience some itching and regional lymphadenopathy. 16

17. 17 Treatment and Outcome Topical therapy with mupirocin 2%, and retapamulin 1% 2-3 times a day for 10-14 days for localized disease Application of antiseptic 2–3 times per day for 5–7 days (e.g. hydrogen peroxide 1% cream or povidone—iodine 10% ointment). Oral antibiotics are Recommended in bullous impetigo, widespread non-bullous impetigo (>3 lesions), when topical treatment fails or, in systemic manifestations. Cephalexin, 25-50 mg/kg/day in 3-4 divided doses for 7-10 days, is an excellent choice for initial therapy. If MRSA is suspected, clindamycin, doxycycline or sulfamethoxazole- trimethoprimis indicated.

18. Ecthyma Ulcerative pyoderma of the skin caused by Grp A Beta streptococci, Staphylococci or both Vesicle or pustule deepens to produce a punchout ulceration of about 4cm in diameter with an overlying crust. The dermal ulcer has a raised and indurated surrounding margin. Heals slowly and commonly produces a scar Common among malnourished children and older people 18

19. 19 Treatment Soak crusted areas with wet pads to remove crust. Topical antibiotics ointment such as fusidic acid or mupirocin are used. Topical antiseptic such as povidone iodine, superoxidised solution, or hydrogen peroxide cream may be used instead after removing crusts. Oral antibiotics are recommended if the infection is extensive or failed topical treatment. The antibiotic of choice is a penicillin (dicloxacillin or flucloxacillin)

20. Folliculitis Folliculitis means an inflamed hair follicle due to infection, occlusion of hair opening, or irritation. result in tender red spot, often with a surface pustule. commonly due to Staph aureus. Systemic symptoms are uncommon. 20

21. 21 Treatment Warm compresses to relieve itch and pain Analgesics and anti-inflammatories to relieve pain Antiseptic cleansers ( eg , hydrogen peroxide, chlorhexidine, triclosan) Topical antibiotic therapy (e.g., clindamycin 1% lotion or solution twice a day) is usually all that is needed for mild cases. Systemic antibiotic in severe case such as dicloxacillin or cephalexin. Bacterial culture should be performed in treatment resistant cases. In chronic recurrent folliculitis, daily application of benzoyl peroxide 5% gel or wash may facilitate resolution.

22. Furunculosis and Carbunculosis A furuncle is a deep form of bacterial folliculitis Deep seated infection around the hair bulb. tender red spots, lumps or pustules. Round or dome-shaped tense and tender nodule with central necrosis and suppuration. Involvement of several follicles and tracking between fibrous tissue septa results in carbuncles Collection of abscesses became boggy indurated painful and tender mass. Ultimately suppurate and discharge through multiple sinuses 22

23. 23 Treatment Antiseptic or antibacterial soap 70% isopropyl alcohol in water (this will make the skin dry) for cleaning. topical antiseptic such as povidone iodine or chlorhexidine cream to the boils and cover with gauze. If oral antibiotics are needed, those with coverage against MRSA are recommended and commonly include oral trimethoprim-sulfamethoxazole (8-12 mg trimethoprim/kg/day in divided doses every 12 hr ) or clindamycin (10-20 mg/kg/day in divided doses 3 times daily). To reduce colonization and reinfection, bleach baths for patients, and mupirocin intranasally in patients and in family members has been recommended.

24. Cellulitis Acute inflammation of dermis and subcut (deeper layers) not contagious. Commonly caused by Streptococcus pyogenes and Staphylococcus aureus.  start with feeling of unwell, fever with chills and rigors due to bacteraemia . followed by localised inflammatory features. Warmth, Blistering, Erosions and ulceration, Abscess formation Purpura: petechiae, ecchymoses, or haemorrhagic bullae 24

25. 25 Treatment In mild cellulitis, oral antibiotics for a minimum of 5–10 days or until all signs of infection have cleared, analgesia and fluid intake. More severe cellulitis with systemic symptoms: fluids, intravenous antibiotics and oxygen. Amoxicillin and clavulanic acid provide broad-spectrum cover till culture reports is available. Cephalosporins are also commonly used ( eg ceftriaxone, cefotaxime or cefazolin) I&D Treatment may be switched to oral antibiotics with clinical improvements

26. Erysipelas (St. Anthony's fire) Erysipelas is a superficial form of cellulitis, affects the upper dermis and extends into the superficial cutaneous lymphatics. often affects infants and older people but can affect any age group. Unlike cellulitis, mostly caused by Group A beta- haemolytic  streptococci 26

27. 27 Treatment Cold packs and analgesics to relieve local discomfort Elevation, compression stockings, Wound care with saline dressings Antibiotics Oral or intravenous penicillin is the antibiotic of first choice. (Erythromycin, may be used in patients with penicillin allergy or Vancomycin is used for facial erysipelas caused by MRSA) Treatment is usually for 10–14 days While signs of general illness resolve within a day or two, the skin changes may take some weeks to resolve completely. No scarring occurs.

28. Staphylococcal Scalded Skin Syndrome The blistering of large areas of skin gives the appearance of a burn or scalding, hence the name staphylococcal scalded skin syndrome. Predominantly seen in infants and children <5 years These toxins then spread to the skin via the circulating blood and target the desmoglein-1 protein in the epidermis leading to the blistering and sloughing 28

29. Treatment Systemic therapy, with a semisynthetic penicillinase-resistant penicillin or vancomycin if MRSA is considered. Clindamycin is added to inhibit bacterial protein (toxin) synthesis. The skin should be gently moistened and cleansed. Application of an emollient provides lubrication and decreases discomfort. In neonates, or infants or children with severe infection, hospitalization is mandatory, with attention to fluid and electrolyte management, infection control measures, pain management, and meticulous wound care with contact isolation. 29

30. Necrotising fasciitis Potentially life-threatening medical emergencies encompass devastating and rapidly spreading destruction of soft tissue with associated systemic toxicity . The infection is usually polymicrobial. Implicated orgs include S. aureus, streptococcal species, Klebsiella species, E. coli, and anaerobic bacteria. The rest of the cases and the most fulminant infections, associated with toxic shock syndrome and a high case fatality rate, are usually caused by S. pyogenes (group A streptococcus) Streptococcal necrotizing fasciitis may occur in the absence of toxic shock–like syndrome; potentially fatal and associated with substantial morbidity. 30

31. Features 31

32. 32 Treatment Early supportive care, surgical debridement, repeated within 24-36 hr to confirm that no necrotic tissue remains. Meticulous daily wound care is also paramount. Parenteral antibiotic therapy with broad-spectrum agents Initial empirical therapy should be instituted with vancomycin, linezolid, daptomycin, or quinupristin to cover Gram-positive and piperacillin tazobactam to cover Gram-negative organisms. An alternative is to add ceftriaxone with metronidazole to cover mixed aerobic–anaerobic organisms. Penicillin with clindamycin is indicated for documented group A streptococcal necrotizing fasciitis.

33. Management Approach General history/lesion history When? Where? How? Progression Aggravating/relieving factors (Heat, cold, sun) Other symptoms like pruritus Contact history Allergy General relevant medical history Care so far Examination Treatment 33

34. Complications Wider spread infection; cellulitis, lymphangitis, and bacteraemia . Streptococcal toxic shock syndrome Post inflammatory pigmentation. Scarring, particularly with ecthyma, Secondary infections Infection of other organs, eg osteomyelitis, meningitis, Endocarditis  etc Disability Death 34

35. Preventions Health education Improved general living conditions Early presentation Proactive treatment Prevention of complications Rehabilitation 35

36. Conclusions The skin is a complex and dynamic ecosystem that is inhabited by microorganisms. Interactions between skin microbes and the host can fall anywhere along the continuum between mutualism and pathogenicity. Skin infections should be managed proactively to limit damage or prevent further spread. 36

37. References Nelson textbook of pediatrics, twentieth edition Hutchison's Clinical Methods An Integrated Approach to Clinical Practice 24th Edition - 2017 Bacterial skin infections Nataki Duncan MPH, MHS, Meharry Medical College, USA; Dr Libby Whittaker, DermNet Staff Writer, New Zealand (2023) Previous contributors: Dr Amanda Oakley, Dermatologist (2002) Reviewing dermatologist: Dr Ian Coulson Yi Xue ,  Wu Bao ,  Jie Zhou ,  Qing-Liang Zhao ,  Su-Zhuang Hong ,  Jun Ren ,  Bai-Cheng Yang , Peng Wang,  Bin Yin ,  Cheng-Chao Chu ,  Gang Liu  and  Chi-Yu Jia Global Burden, Incidence and Disability-Adjusted Life-Years for Dermatitis: A Systematic Analysis Combined With Socioeconomic Development Status, 1990–2019 Ogunbiyi AO, Owoaje E, Ndahi A. Prevalence of skin disorders in school children in Ibadan, Nigeria. Pediatr Dermatol. 2005;22(1):6-10. doi:10.1111/j.1525-1470.2005.22101. 37

38. Nigwekar SU, Kroshinsky D, Nazarian RM, Goverman J, Malhotra R, Jackson VA, Calciphylaxis: Risk factors, diagnosis, and treatment, Am J Kidney Dis 2015;66(1):133-46. Auriemma M, Carbone A, Liberato DL, Cupaiolo A, Caponio C, De Simone C, et al, Treatment of cutaneous calciphylaxis with sodium thiosulfate: two case reports and a review of the literature. Am J Clin Dermatol. 2011;12(5):339-46 Olusola Ayanlowo et al. Pattern of skin diseases amongst children attending a dermatology clinic in Lagos, Nigeria. Pan African Medical Journal. 2018;29:162. [ doi : 10.11604/pamj.2018.29.162.14503] 38

39. Thank you 39