Skin Infections PDF

The Structure of Human Skin Fatty acids contained in sebum show antimicrobial properties Salt from perspiration inhibits microbial growth Lysozyme hydrolyzes peptidoglycan wall of pathogens  Normal Microbiota of the Skin Gram-positive, salt-tolerant bacteria – Staphylo...

The Structure of Human Skin Fatty acids contained in sebum show antimicrobial properties Salt from perspiration inhibits microbial growth Lysozyme hydrolyzes peptidoglycan wall of pathogens  Normal Microbiota of the Skin Gram-positive, salt-tolerant bacteria – Staphylococci – Micrococci – Diphtheroids Skin Lesions Figure 21.2  Some Skin Diseases Caused by Microorganisms Acne Roseola Impetigo Warts Gas Gangrene Leishmaniasis Chickenpox Ringworm Measles Rubella  Acne Cutibacterium acnes –most common – Recently renamed (Formerly known as Propionibacterium acnes) Gram-positive rod Aerotolerant or anaerobic Nontoxigenic Common resident of pilosebaceous glands Sebum channels are blocked with skin cells 5  Mild Acne ▪ Few scattered pustules ▪ Minor pimples ▪ No inflammation ▪ No scarring – Treatment ▪ Topical agents ▪ Salicylic acid preparations  Inflammatory/ Moderate Acne – Many pustules (30-150 lesions) – Slight inflammation – May progress form face to other areas – Treatment ▪ Oral Accutane (Compound: Isotretinoin) ▪ Prevents sebum formation ▪ Topical antibiotics ▪ Topical Benzoyl peroxide to loosen clogged follicles ▪ Visible blue light (kills C. acnes)  Nodular Cystic / Severe Acne ▪ Hard, painful and deep lesions (including cystic nodules) ▪ High risk of scarring ▪ Significant inflammation ▪ Treatment ▪ Isotretinoin ▪ Oral antibiotics Figure 21.9  General Characteristics of Staphylococcus Common inhabitant of the skin and mucous membranes Spherical cells arranged in irregular clusters Gram-positive Lack spores and flagella May have capsules 9 Views of S. aureus shape and arrangements 10  Staphylococcus aureus Grows in large, round, golden-yellow colonies in agar Facultative anaerobe Withstands high salt, extremes in pH, and high temperatures Produces many virulence factors 11 Blood agar plate, S. aureus 12  Virulence factors of S. aureus Production of Enzymes: Coagulase – thickens blood Hyaluronidase – digests connective tissue Staphylokinase – digests blood clots Penicillinase – inactivates penicillin 13  Virulence factors of S. aureus Production of Toxins: Hemolysins (alpha toxin) – lyse RBC Leukocidins – lyses neutrophils and macrophages Enterotoxin – induce gastrointestinal distress Exfoliative toxin – separates epidermis from dermis Toxic shock syndrome toxin (TSST) – induces fever, vomiting, shock, systemic organ damage 14  Epidemiology S. aureus Present in most environments frequented by humans, everywhere! Can be isolated from fomites – Fomites: objects or materials which are likely to carry infection, such as clothes, utensils, and furniture. Carriage is mostly in anterior nares, skin, nasopharynx Predisposition to infection: poor hygiene and nutrition, tissue injury, immunodeficiency 15  Staphylococcal Infections Range from localized to systemic Localized infections – Folliculitis – superficial inflammation of hair follicle. Example: stye – Furuncle – boil; inflammation of hair follicle or sebaceous gland progresses into abscess – Carbuncle – larger and deeper lesion produced by a cluster of furuncles – Impetigo – bubble-like swellings that can break and peel away; most common in newborns 16 Stye Impetigo Figure 21.4 Furuncle vs Carbuncle  Gross Cyst Extraction HUGE CYST EXTRACTION (youtube.com)  Staphylococcal Infections Systemic infections – Osteomyelitis – infection is occurring inside the bone; abscess forms. Due to fractures or surgery – Bacteremia – infection starts on the skin, progresses, then S. aureus reaches bloodstream; endocarditis possible. 21 Staphylococcal osteomyelitis in a long bone 22  Staphylococcal Diseases Toxigenic diseases – Food intoxication – ingestion of heat stable enterotoxins; gastrointestinal distress---- upset stomach and the runs!! Heating food will not help after toxin production – Staphylococcal scalded skin syndrome – Exfoliative toxin induces bright red flush, blisters, then desquamation of the epidermis. (shedding of the skin) – Toxic shock syndrome – toxemia leading to shock and organ failure 23 Lesions of Skin Syndrome Figure 21.5  Effects of staphylococcal toxins on skin 25  Clinical Concerns and Treatment Resistance to antibiotics! 95% of infections involve strains that are resistant to penicillin – A strain is a subtype of a microorganism MRSA – Methicillin-Resistant S. aureus – this strain is resistant to all major drug groups except vancomycin or zyvox Treatment: – Abscesses must be surgically perforated and drained – Systemic infections require intensive lengthy therapy with antibiotics 26  HA-MRSA vs CA-MRSA Healthcare-associated (HA-MRSA): infections occur in people who have recently been in a hospital or health-care facility. Community-associated (CA-MRSA): infections occur among athletes who share equipment or personal items, and among children in daycare facilities. – Is more severe and shows higher incidence. 27  Prevention of Staphylococcal Infections Universal precautions by healthcare providers to prevent nosocomial infections Hygiene and cleansing 28  General Characteristics of Streptococcus Gram-positive spherical/ovoid cocci arranged in long chains; commonly in pairs Non-spore-forming, nonmotile Can form capsules and slime layers Facultative anaerobes Sensitive to drying, heat, and disinfectants 29 Freshly isolated Streptococcus 30  Streptococcus Classification Lancefield classification system is based on cell wall composition– 17 groups have been identified. (A, B, C etc.) Another classification system is based on hemolysis reactions (destruction of RBC). – β-hemolytic (clearing zone around colonies, complete lysis) – α hemolytic (green coloration, incomplete lysis) – γ hemolytic (no hemolysis) 31 Hemolysis patterns on blood agar 32  S. pyogenes Most serious streptococcal pathogen β-hemolytic Strict parasitic organism Inhabits skin, throat, nasopharynx. 33  Virulence Factors S. pyogenes Expresses surface antigens: – C substance (carbohydrate) – protection against lysozyme – Fimbriae – adherence to human cells – M-protein – contributes to resistance to phagocytosis – Capsule – helps with attachment and evasion of phagocytosis 34 View of group A Streptococcus 35  Virulence Factors S. pyogenes Production of extracellular toxins: Streptolysins – produce hemolysis; cause cell and tissue injury Erythrogenic toxin (pyrogenic) – induces fever and typical red rash Superantigens – strong monocyte and lymphocyte stimulants 36  Virulence Factors S. pyogenes Production of extracellular enzymes: Streptokinase – digests fibrin clots Hyaluronidase – breaks down connective tissue 37  Epidemiology and Pathogenesis Humans are the only reservoir Asymptomatic carriers Transmission – direct contact, droplets, food, fomites Portal of entry: skin or respiratory system Children are predominant group affected for cutaneous and throat infections Systemic infection and possible sequalae can happen if the infection is untreated 38  Scope of Clinical Disease Streptococcus Skin infections Impetigo (pyoderma) – superficial lesions that break and form highly contagious crust. – Common in school settings, it is associated with insect bites, poor hygiene, and crowded living conditions. Erysipelas – large red inflamed patches of skin with well-defined border, involving the dermis; pathogen enters through a break in the skin and eventually spreads to the dermis and subcutaneous tissues. – Infection can remain superficial or become systemic. 39  Streptococcal Skin Infections Impetigo  Streptococcal Skin Infections Erysipelas Figure 21.7  Streptococcal Infections Scarlet Fever – Group A Streptococcus – Erythrogenic toxin (pyrogenic) – induces fever and typical red rash  Identification Cultivation and diagnosis ensure proper treatment to prevent possible complications Rapid diagnostic tests based on monoclonal antibodies that react with C-carbohydrates 43  General Characteristics of the Genus Bacillus Gram-positive rods Endospore-forming, motile Mostly saprobic Aerobic and catalase positive Digest complex macromolecules Source of antibiotics Primary habitat is soil 2 species of medical importance: – Bacillus anthracis – Bacillus cereus 44  Bacillus anthracis Large, block-shaped rod It produces central spores under extreme conditions Virulence factors – Polypeptide capsule – Production of exotoxins Causative agent of anthrax 45 Bacillus anthracis 46  Types of Anthrax Cutaneous anthrax – A lesion that begins as a raised bump that turns into a blister, then a painless ulcer with a black center. – High incidence -90% of cases – Endospores enter through minor cut on the skin – Low mortality rate Figure 23.7 Cutaneous anthrax 48  Types of Anthrax Gastrointestinal anthrax – Ingestion of undercooked or contaminated food with toxins – Causes mortality in 50% of cases Inhalational (pulmonary) anthrax – Inhalation of endospores – Causes mortality in 100% of cases  Control and Treatment Anthrax occurs naturally cattle, sheep, goats, camels and antelopes Cattle are routinely vaccinated Preparation of vaccines – For livestock: spores – For high-risk occupations and military personnel: toxoid; it involves 6 doses over 1.5 years, annual boosters Treatment: – Ciprofloxacin or doxycycline 50  Gangrene Clostridium perfringens Ischemia: Loss of blood supply to tissue Necrosis: Death of tissue Gangrene: Death of soft tissue Gas gangrene – Infection characterized by rapidly progressive gangrene of the injured tissue along with the production of foul-smelling gas. Caused by: – Clostridium perfringens: gram-positive, endospore-forming anaerobic rod, grows in necrotic tissue  Gas Gangrene Predisposing factors – surgical incisions, compound fractures, diabetic ulcers, septic abortions, puncture wounds, gunshot wounds 52  Virulence Factors Clostridium perfringens – Production of toxins Alpha toxin – causes RBC rupture, edema, and tissue destruction – Production of enzymes Collagenase Hyaluronidase 53  Pathology Clostridium perfringens requires damaged and dead tissue with anaerobic conditions These conditions stimulate spore germination and release of exotoxins, and destructive enzymes Virulence factors will cause fermentation of carbohydrates in muscle cells which results in the formation of gas and further destruction of tissue 54  Myonecrosis Clostridium perfringens 55  Treatment and Prevention Immediate cleansing of dirty wounds, deep wounds, compound fractures, and infected incisions Removal of damaged tissue Large doses of cephalosporin or penicillin Hyperbaric oxygen therapy No vaccines available 56  Mycobacteria: Acid-Fast Bacilli Gram-neutral irregular bacilli Acid-fast staining Expresses mycolic acids in cell wall Strict aerobe Catalase positive Does not form capsules, flagella, or spores Grows slowly 2 Species of medical importance: – Mycobacterium tuberculosis – Mycobacterium leprae 57 Microscopic morphology of mycobacteria 58  Mycobacterium leprae: Leprosy Bacillus Strict parasite – feeds from carbon sources in the host It has not been grown on artificial media or tissue culture Slowest growing of all Mycobacterium species Multiplies inside host cells in large packets called globi Causes leprosy (Hansen’s Disease) a chronic disease that begins in the skin and mucous membranes and the progresses into nerves 59 Mycobacterium Leprae: Leprosy Bacillus 60  Epidemiology and Transmission of Leprosy Not highly virulent Risk factors involve poor health and crowded living conditions Mechanism of transmission: droplets Infection requires prolonged direct skin to skin contact with an infected person (months) It is rare but still exists today Endemic in Asia and Africa 61 Course of Infection and Disease Pathogen will live in nasal membranes and skin Macrophages ingest the bacilli, but it will survive phagocytosis Incubation period of 2-5 years If untreated, bacilli grow slowly in the skin and then migrate to Schwann cells of peripheral nerves 62 Course of Infection and Disease 2 Types of skin lesions: Tuberculoid – asymmetrical, shallow lesions which damage the nerves – this results in local loss of pain reception Lepromatous – deep and nodular lesions that cause severe disfigurement of the face and extremities Leprosy Lesions Figure 22.9a Leprosy Lesions Figure 22.9b  Diagnosis Combination of symptomology, microscopic examination of lesions, and patient’s medical history Symptoms: – Numbness in hands and feet, loss of sensitivity, muscle weakness, thickened earlobes, chronic stuffy nose Feather test Detection of acid-fast bacilli in samples from skin lesions and nasal discharges 66 Feather test for leprosy 67  Treatment and Prevention Treatment involves a long-term therapy with steroids and antibiotics Prevention: – Constant surveillance of high-risk populations – Vaccine – clinical development stage 68  Human Papillomavirus Disease characterized by papillomas or warts – squamous epithelial growth Caused by 100 different strains of HPV Transmission: direct contact with lesions or contaminated fomites Incubation period of 2 weeks to a year Location of warts: – Common seed warts – small, painless, elevated, rough growth warts on fingers – Plantar warts – deep, painful warts on soles of feet – Genital warts – most common STD in U.S.; morphology ranges from tiny, flat bumps to extensive, branching, cauliflower-like masses 69  Treatment: Removal of warts using: –Cryotherapy (liquid Nitrogen) –Electrodesiccation –Salicylic acid Imiquimod (topical drug that stimulates interferon proteins production) Bleomycin (anti-tumor drug) Prevention: – Vaccination against HPV strains Human papilloma 71  Herpes Simplex Virus Belongs to Herpesviridae family All strains show prolonged latency and cause recurrent infections Complications occur on hosts of advanced age, chemotherapy, or immunodeficiency Common among AIDS patients Source of many diseases: – Chickenpox – Shingles – Mononucleosis – Cold sores – Genital herpes We all get infected by HSV at some point in life 72  Chickenpox Disease caused by varicella-zoster virus (Herpesvirus 3) Transmitted by the respiratory route (droplets) and direct contact with rash Causes pus-filled papules on skin Virus may remain dormant in dorsal root ganglia (spinal nerves) Prevention: Live attenuated vaccine  Shingles Disease caused by the reactivation of latent HV3 in which viral agents are released from peripheral nerves back to skin Rash usually appears on chest, abdomen or back but it can also show on face and genitals Postherpetic neuralgia – burning pain on skin that lasts long after the rash disappears Prevention: Live attenuated vaccine Treatment: – Acyclovir (antiviral) may lessen symptoms Figure 21.11b  Rubeola (Measles) Disease caused by the Measles virus Transmitted by respiratory route Virus will live in nose and throat Causes a macular rash on skin and Koplik's spots in throat and mouth Symptoms can last up to 10 days Prevented by vaccination No treatment, it goes away by itself Koplik's spots  Rubella (German Measles) Disease caused by the Rubella virus It causes macular rash on skin and fever Rash dissolves in 5 days In pregnant women it causes: – Congenital Rubella Syndrome causes severe fetal damage Prevented by vaccination No treatment  Fungal Infections on skin Dermatomycosis Ringworm (it is a disease not a worm!) – Caused by any of these fungal organisms: Trichophyton Microsporum Epidermophyton – They are called “Dermatophytes” They produce enzymes that digest keratin on the skin – They produce a rash on various body parts  Ringworm Infection Locations Tinea Corporis - itchy circular rash in body Tinea Pedis - athlete’s foot Tinea Capatis - scalp Tinea Barbae - beard Tinea Unguium - nails Tinea Cruris - groin Tinea Capatis - scalp Tinea Unguium - nails  Dermatomycoses Treatment: Topical antifungals –Tolnaftate- Figure 21.16  Scabies Disease caused a mite -Sarcoptes scabiei- This arachnid burrows in the skin to lay eggs causing a rash with intense itching Transmission involves direct contact with rash or fomites Treatment: – Topical insecticides Figure 21.18  Pediculosis Disease caused by lice (head louse) It affects mostly the scalp and skin Feed on blood from host Lay eggs on hair Transmission involves direct contact (head-to-head) or by sharing belongings – Treatment: Topical insecticides