Midterms - L2 Microbiology and Parasitology PDF

MICROBIOLOGY AND PARASITOLOGY MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 DR. JOSEPHINE BANDALAN, MD | SEPTEMBER 18, 2024 When you collect specimens in the skin, you have to be...

MICROBIOLOGY AND PARASITOLOGY MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 DR. JOSEPHINE BANDALAN, MD | SEPTEMBER 18, 2024 When you collect specimens in the skin, you have to be OUTLINE careful and consider that they are under the normal flora which you might get instead of the pathogenic. I. Skin -Doc Bandalan Skin Normal Flora Manifestations of Skin Infections [TORTORA] Diphtheroids & M. furfur (p. 618) Diphtheroids - are pleomorphic rods which include II. Microbial Agents Causing Skin Infections Cutibacterium (Propionibacterium) acnes, that are Superficial Mycoses typically anaerobic and inhabit hair follicles. Cutaneous Mycoses Subcutaneous Mycoses Their growth is supported by secretions from oil III. Bacterial Agents of skin infection glands (sebum), which makes them a factor for acne. Staphylococcus spp. These bacteria produce propionic acid, which helps Streptococcus spp. maintain the low pH of skin (pH 3-5). Ricketssiae spp. Other diphtheroids, such as Corynebacterium xerosis are aerobic and occupy the skin surface. I. SKIN Malassezia furfur is associated with the scaling skin condition known as dandruff. Shampoos for treating dandruff contain the antibiotic ketoconazole or zinc pyrithione or selenium sulfide. All are active against this yeast. MANIFESTATIONS OF SKIN INFECTIONS 1. Macule 2. Papule 3. Nodule 4. Pustule 5. Vesicle/Bullae 6. Ulcer Doc Bandalan: These are the most commonly observed skin lesions and are objective findings in the skin for different infectious diseases. Macule Erythematous, circumscribed, flat discoloration The Structure of the Human Skin Starts as small Source: Tortora Microbiology lesion → coalesce Additional information: → become larger lesions There will be different areas of the skin that will be Usually involved depending on the type of etiologic agent. - associated with Dr. Bandalan papule Skin is the most exposed part of the body Viral exanthems and associated SKIN NORMAL FLORA with febrile Macules Staphylococcus conditions → Staphylococcus epidermidis Viral rashes Diphtheroids Syphilis - → Corynebacterium specifically in the → Propionibacterium secondary stage α-hemolytic Streptococci Gram(-) coliforms and Acinobacter Papules Candida Solid elevated lesions Cause benign Additional information: growths Opportunistic microorganisms can cause infection Can be as small rather than being part of normal flora as 0.5cm in Papules diameter Transcribed by: NMD 2027  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 Viral rashes, leading to blister warts, S. aureus formations infection Maculopapular Skin Skin Ulcer Rash Commonly seen in Combination of sexually macule and Maculopapular Skin Rash transmitted papule infections Measles, rubella, Excavation in the and other viral surface of the skin infections or in mucous membranes Skin Ulcer Nodule Not limited to Solid lesion genital areas Larger than a Primary Syphilis papule (very (chancre) obvious) ○ Trepone Subcutaneous Nodules ma mycosis pallidum Leprosy Chancroid (soft ○ Observe chancre) d in ○ Haemop Lepromat hilus ous ducreyi leprosy Petechiae Pustule → Abscess Pinpoint 1-3mm (when pustules become round reddish bigger) spots Collection of WBC Looks like a and pus mosquito bite Starts as Meningococcemia folliculitis In patients with (infection of the dengue Petechiae hair follicle) Purpura Layman’s term: Hemorrhagic Boil manifestations Pyogenic infection Larger than (Staphylococcus 4-10mm and Meningococcemia Streptococcus) ○ Specifical Also caused by Pustule and Abscess ly in coliforms and N.mening anaerobic itidis Purpura microorganisms when the patient Vesicle goes into Collection of fluid systemic 0.5 cm in diameter stage of Blister-like infection Characteristic rash observed among: Source: Dr. Bandalan’s ppt Herpes simplex Varicella Herpes zoster Smallpox Monkey pox Bullae II. Microbial Agent Causing Skin Infection Larger than a vesicle Staphylococcus A. Fungal Agents and Streptococcus Vesicle and Bullae pyogenes Most widely accepted method of fungal classification is infections based on the major site of involvement in the body or Esp. organisms your clinical classification. that cause pyrogenic exotoxins causing exfoliative toxin 2 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 Table 1. Summary of Fungal Agents involved Superfici Cutaneous Subcutaneous al Mycoses Mycoses Mycoses Pityriasis Dermatophytoses Sporotrichosis (Tinea) or tineasis due to versicolor → Trichophyton → Epidermophyton → Microsporum Tinea Candidiasis Mycetoma nigra Piedras Chromomycosis Source: Dr. Bandalan’s PPT SUPERFICIAL MYCOSES Pytriasis or Tinea Versicolor Tinea nigra palmaris → Caused by Malassezia furfur Source: Doc Bandalan’s ppt → Layman’s term : Apap → May be endogenous infection Piedras → Predisposing conditions: ▪ Immune status of the patient → Nodular infection of the hair shaft ▪ Genetic factors ▪ Black piedra: Piedraia hortae ▪ Elevated temperature ▪ White piedra: Trichosporon beigelii ▪ Humidity → Hair of scalp, axilla, beard and genital may be infected → Treated with selenium sulfide and ketoconazole → Removal of infected hair and application of a topical → Implicated as the cause or contributor of dandruff antifungal agent → Diagnosis is confirmed by direct KOH microscopic exam of skin scrapings → Short unbranched hyphae and spherical yeast cells giving “spaghetti and meatballs” appearance → Cultivation require lipid in the culture medium for growth → SDA with olive oil: cream to yellowish, smooth to slightly wrinkled Black piedra Source: Doc Bandalan’s ppt Tinea Versicolor. Spaghetti and meatballs Source: Doc Bandalan’s ppt Doc Bandalan: Antifungal agents disinfects after several weeks May be considered as part of the normal flora of the skin. Tinea Nigra (Tinea nigra palmaris) → Caused by Hortea (Exophiala) werneckii, a dematiaceous fungi → Brown to black discoloration of the palm White piedra → Appears microscopically as branched septate hyphae Source: Doc Bandalan’s ppt and budding yeast cells with melanized cell walls 3 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 CUTANEOUS MYCOSES Cause superficial infections of the epidermis, hair and nails. All are considered chronic infections. Dermatophytosis characterized by erythema, itching and rashes. Ring-worm like formation → Tinea capitis- scalp → Tinea barbae- beard or mustache (Barber’s itch) → Tinea corporis-body → Tinea cruris- inguinal area or groin (Jock’s itch) → Tinea pedis-athlete’s foot → Tinea unguium- nail (onychomycosis) → Tinea manuum- hand Tinea infections Source: Doc Bandalan’s ppt Treatment of dermatophytosis → A thorough removal of infected and dead epithelial Dermatophytes structures should be done during treatment. Acquired through contaminated soil, infected animals or → Topical application of antifungal drug. humans. ▪ Miconazole, tolnaftate, clotrimazole, ketoconazole Identified by their colonial appearance and microscopic applied at least 2-4 weeks morphology → Scalp infections may require oral griseofulvin or terbinafine for several weeks → The hardest to treat are nail infections. Table 4. Microsporum infections Microsproum Colony Microscopic Table 2. Dermatophytes : Parts of the body affected morphology Hair Skin Nail M. canis White cottony Thick, rough cell Microsporum + + - surface and wall, multicellular Trichophyton + + + deep with curved tip Epidermophyto - + + yellow on n reverse Source: Doc Bandalan’s ppt M. gypseum Tan powdery Thin, rough-walled, colony multicellular Table 3. Subcutaneous infections Source: Doc Bandalan’s ppt Clinical Features Etiological features Tinea Circular bald Trichophyton Table 5. Trichophyton infections capitis patches with broken mentagrophyte, Trichophyto Colony Microscopic hair Trichophyton n morphology tonsurans, T. tonsurans Flat to powdery to Microconidia mostly Microsporum canis velvety colonies elongate T. Cottony to Grape-like Tinea Circular patches with Trichophyton rubrum, mentagrophyt granular microconidia; coiled corporis advancing red Epidermophyton e spiral hyphae border floccosum T. rubrum White cottony Small pear-shaped Tinea pedis Interdigital spaces of T. rubrum, T. surface with deep microconidia feet mentagrophyte, red on Epidermophyton Source: Doc Bandalan’s ppt floccosum Tinea Nails thickened, T. rubrum, T. ungium discolored and mentagrophyte, Table 6. Epidermophyton infection deformed Epidermophyton Epidermo Colony Microscopic floccosum Source: Doc Bandalan’s ppt phyton morphology E. Flat and velvety, Smooth-walled, Dermatophytid floccosum tan to olive green club-shaped, → hypersensitivity to products of fungi (vesicles) multi celled macroconidia in clusters Source: Doc Bandalan’s ppt Candidiasis Most frequently encountered fungal infection. Etiologic agents- Opportunistic pathogens → Candida albicans – most frequent → → C. tropicalis → C. parapsilosis → C. glabrata 4 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 Candida albicans and other species are part of the normal Direct microscopic examination of clinical specimens. flora, seen in the oropharynx, GIT, GUT, skin Observe the following: Infections are believed to be endogenous in origin. → Budding yeast cells (blastoconidia 2-4 u) Clinical infections → Pseudohyphae structures → Cutaneous and mucocutaneous → Strongly Gram (+) → Systemic candidiasis Candida albicans → Chronic mucocutaneous candidiasis → identified microscopically by production of germ tubes. Candida Infections In Normal And ▪ Germ tube Immunocompromised Hosts − hypha-like extension of the yeast cells with no → Intertriginous candidiasis (skin folds) constrictions at the point of origin. → Onychomycosis and paronychia ▪ Onychomycosis- infection of the nail unit. ▪ Paronychia- infection in the proximal and lateral fingernails and toenail folds. → Mucocutaneous junction of lips → Oral thrush → Vulvovaginitis → Pulmonary infection → Eye infections → Endocarditis → Meningitis → Fungemia and disseminated infection ▪ Most commonly seen in immunocompromised patients ▪ Onychomycosis and esophagitis caused by Candida Candida albicans microscopic specimen Source: Doc Bandalan’s ppt albicans are very common in AIDS patients. Predisposing Factors For Candidiasis Germ tube test Procedure → Alteration in the normal skin and mucous membrane → Pipette 0.5 ml sterile serum into a test tube barriers → Inoculate the tube with a small amount of organisms to → Prolonged antibiotic administration be tested. → Use of immunosuppressive drugs → Incubate at 37 C for 1-3 hours → Diseases of the immune system → Place a drop of the suspension on a slide, apply a Candidiasis coverslip, examine microscopically In infants → Highly predisposed if skin microbial flora has not developed and the mother is infected. → Begins with perianal and genital infections, prolonged and painful diaper rash. In adults → Normal skin is unaffected by candida growth. → Excessive skin moisture and warmth and trauma (friction, abrasion) leads to infection. → Intertriginous infections occur in skin folds, toe webs, groin or under the breasts, especially in the obese. → Common among dishwashers, fruit pickers, bartenders, etc. → May precede underlying endocrine problems like Positive Germ tube test diabetes mellitus, hypoparathyroidism and Addison’s Source: Doc Bandalan’s ppt disease. Treatment of Candidiasis → Topical nystatin or oral ketoconazole → Eliminate contributory factors SUBCUTANEOUS MYCOSES involves the hypodermis and subcutaneous tissue origin: from the outside acquired through traumatic inoculation Candidiasis clinical symptoms Sporotrichosis Source: Doc Bandalan’s ppt Candida Macroscopic → Candida species cannot be differentiated based on colonial appearance. → Colonies are produced within 24-48 hours → Raised, cream-colored, opaque, 1-2 mm; after several days on agar medium hyphae may be observed. 5 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3. Sporotrichosis infection Source: Dr. Bandalan’s ppt Source: Doc Bandalan’s ppt Mycetoma Chronic infection of the subcutaneous tissues and lymphatics → other names: Madura foot or Maduromycosis Acquired through trauma (thorns or splinters) → Traumatic inoculation with several saprophytic fungi usually to the hand, arm or leg ▪ commonly involving the lower extremities but may Starts from the fingers if left untreated, then spreads occur in any part of the body on the hand Occupational hazard for farmers, miners, gardeners, florists “Rose gardener’s disease” Sporothrix schenckii (etiologic agent) → dimorphic fungi ▪ fungi growing into 2 different forms if exposed to different thermal environment ▪ at room temp: MOLDS ▪ at body temp: YEASTS − recovered from the infected patients → specimens for diagnosis Madura foot ▪ aspirated pus from nodules Source: Doc Bandalan’s ppt ▪ swabs ▪ scrapings → extreme lesions with sinus tracts and discharges ▪ biopsy tissue present → it starts small and becomes bigger because it is left Table 7. Macroscopic vs. Microscopic appearance of untreated or misdiagnosed S. schenckii Table 8. 2 TYPES OF MYCETOMA MACROSCOPIC rapidly growing (3-5 days) ACTINOMYCOTIC Etiologic agents: white (bacterial) Actinomycetes group pasty ○ Actinomyces moist colony that ○ Streptomyces later becomes ○ Nocardia brown black EUMYCOTIC Pseudallesheria boydii wrinkled or (fungal) (most common/major leathery etiologic agent) Exophialla jaenselmi MICROSCOPIC 1. Mycelial form (room Source: Dr. Bandalan’s ppt temperature) narrow, septate Chromoblastomycosis hyphae with pyriform conidia arranged singly or in a flowerette 2. Yeast form (37℃) small, elliptoid, budding, cigar-shaped yeasts recovered from infected patients. Warty lesions of chromoblastomycosis Source: Doc Bandalan’s ppt 6 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 → (Chromomycosis) → Traumatic inoculation into the subcutaneous tissue → Chronic infection produce warty or cauliflower-like or tumor-like lesions mostly in the lower extremities → not common in the Philippines → Etiologic agents: ▪ Cladosporium (Cladosporium carrionii) ▪ Phialophora (Philaphora verrucosa) ▪ Fonsecaea (Fonsecaea pedrosoi) S. aureus: COAGULASE TEST Microscopic view of C. carrionii, P. verrucosa, and F. pedrosoi from left to right respectively The best test that differentiates S. aureus from other Source: Doc Bandalan’s ppt Staphylococcal spp. Two types of Coagulase test: Free and Bound (clumping factor) COAGULASE TEST Coagulase-positive Staphylococci → Staphylococcus aureus ▪ Most virulent spp Figure 23. Sclerotic Bodies ▪ Produce coagulase (clots plasma) Source: Doc Bandalan’s ppt Coagulase-negative Staphylococci ▪ low virulence histologic hallmark of chromoblastomycosis in → S. epidermidis: used to be non-infectious but now tissues associated with prosthetic implant infections copper-colored, septate cells that appear to be (biofilms); predominant normal flora of skin dividing → S. saprophyticus: urinary tract infections (cystitis in sexually-active young females) III. BACTERIAL AGENTS OF SKIN INFECTION - Staphylococcus aureus - Streptococcus pyogenes - Pseudomonas aeruginosa - Mycobacterium leprae - Rickettsiae Slide Coagulase test detects bound coagulase clumping factor Reagent: Plasma (+) clumping STAPHYLOCOCCUS SPP. Gram-positive cocci in clusters/groups Colonies on Blood Agar Plate (BAP): ○ Round, smooth, raised, glistening, white to gray to deep yellow pigments There are some spp. that may produce a LIPOCHROME (yellow colonies) pigment on BAP ○ Beta-hemolytic Ubiquitous; part of human normal flora Tube Coagulase test Able to acquire antibiotic more reliable Resistance detects both bound and free coagulase ○ Relatively resistant to heat and drying (+) after 4-24 hours incubation is clotting or ○ Can persist for long periods in fomites coagulation 7 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 Cell wall factors of S. aureus Teichoic acid: antigenic Cell wall virulence factors ○ Peptidoglycan: stimulate production of IL-1 (endogenous pyrogens) and opsonic antibodies: chemoattractant for polymorphonuclears; endotoxin-like activity and activate complement ○ Protein A: binds to Fc of IgG (anti-opsonin, anti-phagocytic); adhesion Enzymes of S. aureus Plasma is utilized in this test d/t to its component Hyaluronidase COAGULASE-REACTING FACTOR that would ○ destroy the hyaluronic acid present in the react with COAGULASE produced by the organism, ground substance of our ECM to break producing a THROMBIN-like substance which will barriers in the connective tissue → this transform FIBRINOGEN to FIBRIN would facilitate the spread of the organism Staphylokinase Lipase Beta-lactamase ○ destroy the beta lactam ring of penicillin → penicillin-resistant organism Staphylococcus aureus vs Streptococcus spp. Staphylococcus spp. needs to be differentiated from Cytolytic exotoxins of S. aureus Streptococcus spp. Alpha, beta, gamma and delta toxins Using CATALASE TEST Hemolysins: polymerizes into tubes that pierce ○ Reagent: Hydrogen peroxide membranes resulting in osmotic lysis of host cells ○ (+) Bubbles/Effervescence due to the hydrolyzation of Panton-Valentine Leukocidin of S. aureus hydrogen peroxide into water and Destroy cell membranes and kill white blood cells oxygen by the Staphylococcus organism Superantigen exotoxins of S. aureus ○ (+) Staphylococci - since Staphylococci Stimulate enhanced T cell response (toxic shock) produce catalase enzyme ○ Toxic shock syndrome toxin (TSST) Exfoliative toxin Scalded skin syndrome in children Enterotoxins 15 enterotoxins (A-E; G-P) Heat stable Stimulates vomiting center of brain Carbohydrate-rich food ○ associated with food poisoning S. aureus: INFECTIONS INVOLVING HAIR How does coagulase production by S. aureus relate to FOLLICLES the virulence of the organism? Precipitated by blockage with sebum or minor The clot that is produced following the reaction S. trauma (e.g. clothes rubbing on skin) aureus and CRF will act like a capsule resulting to the S. aureus is the most common etiologic agent resistance to phagocytosis Less common causes are members of the The clot that is produced will also surround the abscess Enterobacteriaceae (Coliforms) that is produced by the Staphylococcal organism INFECTION CHARACTERISTICS making that abscess inaccessible to immune cells and Folliculitis: Papules or pustules pierced by a hair even to the antibiotic material used for treatment minor infection and surrounded with redness → That is why whenever you have an abscess, the of hair follicles treatment modality that you have is to INCISE AND Furuncle (boil) Abscess that begins as a red nodule in DRAIN to remove the pyogenic abscess so that the a hair follicle that ultimately becomes lesion can be accessed by the antibiotics that you are painful and full of pus using Carbuncle Furuncles that spread more deeply to the dermis and beyond; associated with fever and malaise Pathogenesis of S. aureus FOLLICULITIS FURUNCLE Pathogenesis of Staphylococcus aureus is the combined effect of: ○ Extracellular factors ○ Toxins ○ Invasive property 8 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 Papules or pustules pierced Abscess that begins as a by a hair and surrounded red nodule in a hair follicle S. aureus: Laboratory Identification with redness that ultimately becomes Gram staining, Catalase test painful and full of pus Coagulase test, Culture, Biochemical, Drug CARBUNCLE sensitivity test Species Coagulase Color of Mannitol Novobiocin colonies fermentation resistance S. aureus + Golden yellow + _ S. epidermidis _ White to gray _ _ Furuncles that spread more S. saprophyticus _ White to gray _ + deeply to the dermis and beyond; associated with fever and malaise Doc Bandalan: Impetigo Catalase test is positive on the following Staphylococcal Clinical infections: organisms: Localized skin infections: folliculitis, furuncles, - S. aureus carbuncles, impetigo (generally seen in children) - S. epidermidis Deep localized infections: osteomyelitis, arthritis - S. saprophyticus Acute endocarditis ○ intravenous drug abuse Septicemia S.aureus beta-hemolytic: presence of HEMOLYSIS Scalded skin syndrome How can one determine whether Beta-hemolysis Clinical infections: is present? The colonies are surrounded by a clear Pneumonia: severe, necrotizing zone. Nosocomial infections: wounds, catheters Implication: COMPLETE HEMOLYSIS Toxinoses: toxic shock syndrome, gastroenteritis ○ Complete destruction of RBCs around (food poisoning), scalded skin syndrome colonies S. aureus: Epidemiology Nasal carriage of S aureus in 20-50% of humans Chief sources of infection: shedding from human lesions, fomites, human respiratory tract and skin Nurseries, ICU, operating rooms, immunocompromised patients S. aureus: Drug for Treatment 95% resistance to Penicillin G Cephalosporins S. aureus: Antimicrobial Drug Resistance Nafcillin, Methicillin B-lactamase production Vancomycin ○ many penicilines, plasmid mediates via ○ For terminally-ill patients,(patients with conjugation systemic infections & patients with Altered access to PBPs immunosuppression) ○ against nafcillin, methicillin and oxacillin Increased cell wall synthesis ○ against vancomycin (VISA) STREPTOCOCCUS SPP. VanA gene from enterococci Streptococcus pyogenes ○ VRSA Doc Bandalan: Doc Bandalan: Streptococcal organisms are classified based on the One of the causes of Penicillin resistance in numerous following: Staphylococcal organisms is the production of - Hemolysis on blood agar plate (Brown’s B-lactamases. Classification) 9 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 - Presence of cell wall group specific antigen S. pyogenes: Exotoxins and Exoenzymes (Lancefield Classification) Promotes rapid spread of infection Streptokinase (fibrinolysin) Streptococcus spp.: Brown’s Classification ○ allows entry into blood despite presence of based on hemolytic activity on blood agar plate clot (BAP) Hyaluronidase ○ Alpha: incomplete hemolysis; seen as ○ destroys hyaluronic acid of connective brownish or greenish discoloration around tissue ground substance colony Pyrogenic exotoxins ○ Beta: complete hemolysis; clear zone ○ superantigen; associated with around colony streptococcal toxic shock syndrome and ○ Gamma: nonhemolytic scarlet fever S. pyogenes: Hemolysins (Streptolysins) Streptolysin O ○ Active in reduced state In low oxygen tension, hemolysis of red blood cells is typically the result. Hemolysis is most effectively demonstrated when the Streptococcus spp.: Lancefield Classification inoculation is placed beneath the (cell wall group specific antigen) agar layer with reduced oxygen. Lancefield group ○ Antigenic producing antistreptolysin O (ASO) Group A (Streptococcus pyogenes) Stimulates antibody production Group B (Streptococcus agalactiae) Antibody: Antistreptolysin O ○ A urogenital organism is typically present (ASO) in approximately 5-30% of women. ○ ASO titer in excess of 160-200 units is ○ Show early clinical manifestation (e.g., significant septicemia, neonatal meningitis) Group D (Streptococcus faecalis or Enterococcus) Doc Bandalan: Non-Lancefield group The ASO Titer is a critical factor in the determination of a Streptococcus pneumoniae prior streptococcal infection. It is also crucial for the Viridans Streptococci diagnosis of rheumatic fever. Streptococcus pyogenes Streptolysin S Group A beta-hemolytic Streptococci ○ Hemolysis on the surface Gram (+) cocci in chain ○ Nonantigenic Resides in the skin and mucous membranes ○ Can invade apparently intact skin or S. pyogenes: Clinical importance mucous membranes Impetigo ○ spreading crusty lesion usually in children Erysipelas ○ fiery red advancing erythema on face or lower limbs affecting all age groups Invasive disease ○ cellulitis, necrotizing fasciitis/myositis (flesh-eating bacteria) Pharyngitis (bacterial sore throat) and tonsillitis Transmission: direct contact with exudates Capsule: made of hyaluronic acid identical to that of humans Cell wall ○ M protein (hair-like structure) major virulence factor; resist phagocytosis ○ Virulence factor ○ 150 types Doc Bandalan: The M protein is an antigen that is employed for serotyping Postreptococcal diseases: develop 1-4 weeks and to classify streptococcus into 150 serotypes. after S. pyogenes infection ○ Acute glomerulonephritis: follow skin infection and sore throat ○ Rheumatic fever: follow sore throat only 10 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 Piperacillin + Aminoglycoside S. pyogenes: Laboratory identification Aztreonam Gram staining Carbapenems Beta-hemolytic on BA Fluoroquinolones Catalase-negative Ceftazidime, Cefoperazone, Cefepime Bacitracin sensitive: presumptive identification for group A streptococci Mycobacterium leprae Antistreptolysin O (ASO) Cause Hansen’s disease (Leprosy) ○ The titer of which is measured Acid-fast, long, slender, non-motile bacilli serologically to prove recent streptococcal Cell walls: contain long chain β-hydroxylated fatty infection acids (mycolic acids) complexed with carbohydrates and proteins creating a waxy Doc Bandalan: hydrophobic surface The term "Group A beta-hemolytic streptococci" will Obligate intracellular organisms consistently denote Streptococcus pyogenes. ○ Do not grow in ordinary culture media ○ The optimal temperature for growth is one that is lower than the body's temperature. ○ The mouse foot soles are a suitable environment for the growth of Mycobacterium leprae. Doc Bandalan: The presence of long-chain Mycolic Acid in the cell wall is the cause of the acid-fast reaction of Mycobacterium leprae. M. leprae: Pathogenesis Transmitted from human to human: respiratory, exudates of skin lesions, abrasions S. pyogenes: Drugs for treatment Low infectivity, long incubation period (years) Penicillin G Genetic predisposition ○ Penicillin G is typically administered intramuscularly to patients who exhibit M. leprae: Clinical infection rheumatic fever for a period of several weeks. Chronic granulomatous condition of peripheral Erythromycin and Clindamycin for patients with nerves and mucocutaneous tissue allergy to Penicillin Tuberculoid leprosy: large macule in cooler body parts (nose, ear lobes, testicles), neuritis (anesthesia) Pseudomonas aeruginosa ○ Manifests earlier than lepromatous leprosy Widely distributed in nature and is characterized by a hypopigmented Gram (-) coccobacilli macule that is typically neglected due to its Opportunistic bacteria; nosocomial infection resemblance to a fungal infection, (hospital acquired infection) specifically a ringworm infection. Outbreaks from swimming pool and hot tubs Lepromatous leprosy: multiple skin lesions, Non-fermentative classic leonine facies, deformities ○ Pseudomonas aeruginosa will not undergo ○ manifests as the end of the spectrum fermentation on sugars; however, it will Tuberculoid Lepromatous induce oxidation on sugars. Produced pigments Leprosy Leprosy ○ Bluish pigment called Pyocyanin Lesions Macules or Multiple lesions, ○ Fluorescent pigment called Pyoverdin hypopigmented nodular, leonine Ecthyma gangrenosum lesions facies ○ Hemorrhagic necrosis of the skin often Bacillus from Scarce Abundant seen in patients with sepsis lesions Granuloma Present Absent Lepromin test Positive Negative P. aeruginosa: Treatment M. leprae: Laboratory identification Combination antimicrobial therapy especially for Cannot be grown in artificial medium serious infections Animal inoculation 11 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 ○ Footpads of mice ○ Armadillo Doc Bandalan: PCR The Scrub Typhus group of Rickettsiae is the sole group that Biopsy is commonly seen in the Philippines, as Rickettsiae are not ○ Lepra cells: infected Schwann cells and commonly found in the country. macrophages (“packets of cigar”) ○ Tuberculoid leprosy: organisms are extremely rare, lesions are heavily Rickettsial Infections infiltrated with lymphocytes and giant Common clinical manifestations: epithelioid cells - Fever ○ Lepromatous leprosy: numerous - Headache organisms in lesions - Myalgia - Skin rash (usually maculopapular) Scrub Typhus Orientia tsutsugamushi (Old Name: Rickettsia M. leprae: Drugs for treatment tsutsugamushi) Dapsone: first-line therapy Rodents are reservoir Rifampin and/or Clofazimine are generally included Chigger (larva) of mite in the initial treatment Treatment prolonged for years Other drugs ○ Minocycline ○ Clarithromycin ○ Fluoroquinolones RICKETTSIAE Obligate intracellular parasites Transmitted by bite of arthropod vector Tropism for endothelial cells, lysis occurs upon release of organisms Hallmark of the infection is vasculitis ○ Rickettsiae targets endothelial cells, resulting in vasculitis and ultimately Fever, headache skin rashes and in 50% an eschar thrombosis subsequent to infection. at the site of bite Eschar puncheout ulcer covered by blackened Rickettsiae: Morphology scab Pleomorphic (coccoid to rod-shaped), poor Gram Illness can be severe associated with cardiac and staining reaction, stain better with Giemsa stain cerebral involvement leading to death in about 30% (Red Stain) of patients Cell envelope is same for Gram-negatives Rickettsiae: Pathology Multiply within endothelial cells of small blood vessels and produce vasculitis; occur in the skin and many other organs There is thrombosis of the vessel leading to rupture and necrosis Spotted fever group Rickettsiae: Laboratory Diagnosis ○ Rocky Mountain Spotted Fever (RMSF) Cultivation (R. rickettsii, tick-bite) ○ Hazardous and must be done inside a ○ Rickettsialpox (R. akari, mites) biological safety cabinet Typhus group ○ Grow in yolk sacs of embryonated egg ○ Epidemic typhus (R. prowazekii, lice) ○ Cell cultures have replaced animal Brill-Zinsser disease (R. inoculation and yolk sac inoculation prowazekii, no vector because it Skin biopsy is a recrudescence) ○ Immunohistochemical stains ○ Murine typhus (R. typhi, flea-bite) PCR Scrub typhus group ○ Earlier results than serology ○ Orientia tsutsugamushi Serology ○ Bite of chigger mite 12 of 13  MICROBIAL AGENTS OF SKIN INFECTIONS 1-3 ○ Main method available in clinical laboratories ○ Most widely used are indirect IF and enzyme immunoassays Weil-Felix reaction ○ An old serologic test that utilize Proteus OX19 strain that is similar to rickettsial antigens ○ No longer in use Rickettsiae: Treatment Tetracyclines preferably Doxycycline are effective Chloramphenicol can be effective Sulfonamides can enhance the disease and are contraindicated Coxiella burnetii Small obligate intracellular organism Poorly stained with Gram stain best stained with Gimenez stain Endospore-like structures are formed ○ Resistant to drying and pasteurization Found in ticks which transmit to goats, sheeps, and cattles Phase I are the infectious forms to humans Cause Q fever C. burnetii: Q fever Human transmission handling of infected animals; inhalation of infected dusts Acute: influenza-like, atypical pneumonia, hepatitis; no skin rash Chronic: last > 6 months; infective endocarditis is the most common form Serology is the diagnostic method of choice: Indirect IF PCR Doxycycline FREEDOM WALL 13 of 13