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Microbial Diseases of the Skin and Eyes
Skin Salt inhibits microbes. Lysozyme hydrolyzes peptidoglycan. Fatty acids inhibit some pathogens. Defensins are antimicrobial peptides. Figure 21.1
Mucous Membranes Line body cavities. The epithelial cells are attached to an extracellular matrix. Cells secrete mucus. Some cells have cilia.
Normal Microbiota of the Skin Gram-positive, salt-tolerant bacteria Staphylococci Micrococci Diphtheroids Malasseziafurfur Figure 14.1a
Microbial Diseases of the Skin Exanthem: Skin rash arising from another focus of the infection. Enanthem: Mucous membrane rash arising from another focus of the infection.
Microbial Diseases of the Skin Figure 21.2
Staphylococcal Skin Infections
Streptococcus Staphylococcus
Staphylococcal Biofilms Figure 21.3
S. aureus Differential Characteristics Coagulase Fibrinogen  Fibrin
Mannitol Salts Agar (MSA) Staphylococcus aureus
Staphylococcal Skin Infections
Clinical Manifestations/Disease SKIN   folliculitis   boils (furuncles)   carbuncles
Folliculitis
Furuncles (boil)
Staphylococcal Skin Infections
Clinical Manifestations/Disease ,[object Object]
scalded skin syndrome
Neonates and     children under 2years
Impetigo
Staphylococcal Skin Infections Scalded skin syndrome Bright red lesionsthat easily peels off in sheets Exfoliative toxin Antibiotic tx Part  of  Toxic Shock Syndrome  TSS Figure 21.4
Staphylococcal scalded skin syndrom (SSSS) ,[object Object]
Bullous exfoliative dermatitis,[object Object]
Toxic shock syndrome ,[object Object]
Super antigen
Produced by 5-25% isolates
Tampon or infected wound
Fever
Rash
Exfoliation of skin
Shock (death rate 3%),[object Object]
Metastatic Infections ,[object Object]
Osteomyelitisdisease of growing bone Pulmonary and cardiovascular infection
Streptococcal Skin Infections Streptococcus pyogenes Group A beta-hemolytic streptococci M proteins Figure 21.5
Streptococcus pyogenes Local infections Impetigo Erysipelas Cellulitis Necrotizing fasciitis (flesh-eating bacterium) Systemic effect Streptococcal toxic shock-like syndrome (STSS) Spe (similar to TSS by S. aureus) Scarlet fever (pyrogenic toxin by lysogenized ) Post-infection Rheumatic fever (associated with pharyngitis) Glomerulonephritis
Invasive Group A Streptococcal Infections M protein Streptokinases Hyaluronidase Exotoxin A,  superantigen Cellulitis Necrotizing       fasciitis Figure 21.8
Virulence factors Adhesins M protein (fibrillar Ag) Fibronectin binding proteins (Protein F) Lipoteichoic acid (LTA) Hyaluronic acid capsule Invasins Streptolysins (S & O) Hyaluronidase Streptokinases  activates blood clot dissolving protein-plasminogen (human specific) Dnase Exotoxins Pyrogenic (erythrogenic) toxin - Spe Scarlet fever Toxic shock syndrome
Streptococcal Infections
S. pyogenes Necrotizing  fasciitis Scarlet Fever
Streptococcal Infections
Streptococcal Skin Infections Erysipelas Impetigo Figures 21.6, 21.7
Erysipelas NOTE: ,[object Object]
bullae,[object Object]
Cellulitis
Pseudomonas Infections
Infections by Pseudomonads Pseudomonas aeruginosa Gram-negative, aerobic rod Pyocyanin produces a blue-green pus Pseudomonas dermatitis Otitis externa Post-burn infections
Pseudomonas Infections
Acne Comedonal acne occurs when sebum channels are blocked with shed cells. Inflammatory acne Propionibacterium acnes Gram-positive, anaerobic rod Treatment Preventing sebum formation (isotretinoin) Antibiotics Benzoyl peroxide to loosen clogged follicles Visible (blue) light (kills P. acnes)
Propionibacterium Infections
Acne Inflammatory acne (continued) Nodular cystic acne Treatment: isotretinoin
Skin and other infections ,[object Object]
Skin, food poisoning, osteomyelitis, kidney abscess, endocarditis
Streptococcus pyogenes
Skin, pharyngitis and blood stream
Botulinum
Wound, food & infant
C. perfringens
Skin and diarrhea
Anthrax
Cutaneous, respiratory & GI,[object Object]
ClostridialCellulitis
NOTE:Large rectangular       gram-positive bacilli NOTE:Double zone of hemolysis Inner beta-hemolysis = θ toxin Outer alpha-hemolysis = α toxin Micro & Macroscopic C. perfringens
Alpha toxin Treatment Debridement and excision Antibiotics (prevent further spreading) Hyperbaric oxygen therapy Inhibit or kill the anaerobic bacteria
Epidemiology of Bacillus anthracis ,[object Object]
Enzootic in certain foreign countries (e.g., Turkey, Iran, Pakistan,and Sudan)
Anthrax spores infectious for decades
Biologic warfare experiments (annual tests for 20 years)
 Three well-defined cycles
  Survival of spores in the soil
  Animal infection
  Infection in humans,[object Object]
Most commonly transmitted to humans by direct contact with animal products (e.g., wool and hair)
Also acquired via inhalation & ingestion
Increased mortality with these portals of entry,[object Object]
Importing materials contaminated with spores from these countries (e.g., bones, hides, and other materials)
Usually encountered as an occupational disease
Veterinarians, agricultural workers,[object Object]
Cutaneous Anthrax Bacilllusanthracis G+ and spore forming Farm animals are major reservoir 	Inhalation, GI, cutaneous Virulence factors: 	Capsules 	Edema factor 	Lethal factor Vaccine Toxoid (protective antigen) 	Effective in short term but not long term Day 4 Day 5 Day 7 Day 12
Clinical Presentation of Anthrax ,[object Object]
1 to 5 days after contact –
 Small, pruritic, non-painful papule
hemorrhagic vesicle & ruptures
Slow-healing painless ulcer with black escharsurrounded by edema
Infection may spread -- Septicemia -- 20% mortality,[object Object]
Other Skin and Mucus Membrane Infections Staphylococcus epidermidis Catheters and prostheses Vibriovulnificus From shellfish and salt water Obligate anaerobes (usually polymicrobic and foul smelling) Puncture wounds Deep wounds Impaired blood supply Gram negative bacteria Decubitus ulcer (bed sores)  After intestinal “spill” Pseudomonas aeruginosa Catheters and prostheses Burns   and Surgical wounds
VIRAL SKIN INFECTION
Warts Papillomaviruses Treatment Removal Imiquimod (stimulates interferon production) Interferon
WART
HPV and skin warts (From Fields Virology, 4th ed, Knipe & Howley, eds, Lippincott Williams & Wilkins, 2001, Table 66-3.)
Poxviruses Smallpox (variola) Smallpox virus (orthopox virus) Variola major has 20% mortality Variola minor has <1% mortality Monkeypox Prevention by smallpox vaccination Figure 21.9
SMALLPOX
Distinguishing features of Smallpox from other rashes Note in this slide that the density of the rash is greater on the face than on the body.  Pocks are usually present on the palms of the hands and on the soles of the feet.
Monkeypox an emerging disease
Monkeypox – an indigenous virus of equatorial Africa Although not a virus of humans, the clinical symptoms are indistinguishable from smallpox.   Lethality is only slightly less than smallpox. Although not as efficient as smallpox, Human to human transmission has been well documented Monkeypox should perhaps be considered a bioterrorist agent
In smallpox, fever is present for 2 to 4 days before the rash begins, while with chickenpox, fever and rash develop at the same time.All the pocks of the smallpox rash are in the same stage of development on any given part of the body and develop slowly. In chickenpox, the rash develops more rapidly, and vesicles, pustules, and scabs may be seen at the same time.
Herpesviruses ,[object Object]
Varicella zoster (chicken pox, shingles)
Cytomegalovirus (microcephaly, infectious mono)
Epstein-Barr virus (mononucleosis,Burkitt’slymphoma)
Human herpesvirus 6 & 7 (Roseola)
Human herpesvirus 8 (Kaposi’s sarcoma),[object Object]
CHICKENPOX  (VARICELLA)
Zoster
Neonatal Varicella
Varicella Vaccine ,[object Object]
Greatly reduces the severity in the rest
Attenuated virus
Can still establish latency and reactivate,[object Object]
Shingles Reactivation of latent HHV-3 releases viruses that move along peripheral nerves to skin. Figure 21.10b
Zoster
Human Herpesviruses Virus		    Subfamily	     Disease	       Site of Latency Herpes Simplex Virus Ia	  Orofacial lesions           Sensory Nerve Ganglia Herpes Simplex Virus IIa	  Genital lesions	       Sensory Nerve Ganglia Varicella Zoster Virusa	  Chicken Pox	       Sensory Nerve Ganglia Recurs as Shingles Cytomegalovirusb	  Microcephaly/Mono       Lymphocytes Human Herpesvirus 6b	  Roseola Infantum	        CD4 T cells Human Herpesvirus 7b	  Roseola Infantum	        CD4T  cells Epstein-Barr Virus	g	  Infectious Mono	        B lymphocytes, salivary Human Herpesvirus 8g	  Kaposi’s Sarcoma          Kaposi’s Sarcoma Tissue
Herpes Simplex 1 and Herpes Simplex 2 Human herpes virus 1 and HHV-2 Cold sores or fever blisters (vesicles on lips) Herpes gladiatorum (vesicles on skin) Herpes whitlow (vesicles on fingers) Herpes encephalitis (HHV-2 has up to a 70% fatality rate)
Herpes Simplex 1 and Herpes Simplex 2 HHV-1 can remain latent in trigeminal nerve ganglia. HHV-2 can remain latent in sacral nerve ganglia. Acyclovir may lessen symptoms.
Tissue tropism of HSV-1 and HSV-2 HSV-1: ,[object Object]
Causes 10 - 30% of primary genital herpes (but seldom recurs there)HSV-2: ,[object Object]
May cause primary oral herpes but, like HSV-1 in genital area, it seldom recurs there ,[object Object]
Cold Sores
Eczema/Herpes
Herpes Simplex Virus type 2 ,[object Object]
Is sexually transmitted
Complicates childbirth,[object Object]
ROSEOLA
Roseola
Measles (Rubeola) Measles virus Transmitted by respiratory route. Macular rash and Koplik's spots. Prevented by vaccination. Encephalitis in 1 in 1,000 cases. Subacute sclerosing panencephalitis in 1 in 1,000,000 cases. Figure 21.14
MEASLES (RUBEOLA)
Measles induced syncytia Formation of giant cells (syncytia) in measles pneumonia. Notice the eosinophilic inclusions in both the cytoplasm and nuclei.  (From Schaechter’s Mechanisms of Microbial Disease; 4th ed.; Engleberg, DiRita & Dermody; Lippincott, Williams & Wilkins; 2007; Fig.  34-3)
Measles pathogenesis Mechanisms of spread of the measles virus within the body and the pathogenesis of measles. CMI, Cell-mediated immunity; CNS, central nervous system.  (From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 59-3.)
Measles time course Time course of measles virus infection. Characteristic prodrome symptoms are cough, conjunctivitis, coryza, and photophobia (CCC and P), followed by the appearance of Koplik's spots and rash. SSPE, Subacute sclerosing panencephalitis. (From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 59-4.)
Koplik’s spots Koplik's spots in the mouth and exanthem. Koplik's spots usually precede the measles rash and may be seen for the first day or two after the rash appears. (Courtesy Dr. J.I. Pugh, St. Albans; from Emond RTD, Rowland HAK: A color atlas of infectious diseases, ed 3, London, 1995, Mosby.) (From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 59-5.)
Measles rash Measles rash. (From Habif TP: Clinical dermatology: Color guide to diagnosis and therapy, St Louis, 1985, Mosby.) (From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 59-6.)
Rubella (German Measles) Rubella virus Macular rash and fever Congenital rubella syndrome causes severe fetal damage. Prevented by vaccination Figure 21.15
GERMAN MEASLES (RUBELLA)
Rubella virus Pathogenesis ,[object Object]
replication in cytoplasm; budding
Viremia
Mild rash in adults; congenital rubella syndrome (CRS) after infection in first trimester when virus passes the placenta and infects fetus
CRS- deafness, blindness, mental retardation,[object Object]
RUBELLACLINICAL MANIFESTATIONS Malaise Headache Myalgias and arthralgias Post-auricular adenopathy Conjunctivitis NON-PRURITIC, ERYTHEMATOUS, MACULOPAPULAR RASH
RUBELLACLINICAL MANIFESTATIONS
RUBELLACLINICAL MANIFESTATIONS
A 1905 list of skin rashes included (1)measles, (2)scarlet fever, (3)rubella, (4)Filatow-Dukes (mild scarlet fever), and (5)Fifth Disease: Erythema infectiosum Human parvovirus B19 produces milk flu-like symptoms and facial rash. Roseola Human herpesvirus 6 causes a high fever and rash, lasting for 1-2 days.
Parvovirus Structure Small (5 kb) linear ssDNA genome, naked capsid Pathogenesis respiratory transmission replication in nucleus, very host dependent, needs S phase cells or helper virus viremia antibody important in immunity targets erythroid lineage cells; fifth disease (symptoms immunological); transient aplastic crisis; hydropsfetalis Diagnosis serology, viral nucleic acid Treatment/prevention none
FIFTH DISEASE(ERYTHEMA INFECTIOSUM)
Parvovirus pathogenesis From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 56-3.
Parvovirus pathogenesis A "slapped-cheek" appearance is typical of the rash for erythema infectiosum.(From Medical Microbiology, 5th ed., Murray, Rosenthal & Pfaller, Mosby Inc., 2005, Fig. 56-5.)
PARVOVIRUSERYTHEMA INFECTIOSUM
Coxsakie Viral infection
Hand and mouth disease
FUNGAL SKIN INFECTION
Cutaneous Mycoses Dermatomycoses: Tineas or ringworm Metabolize keratin  Trichophyton:Infects hair, skin, and nails Epidermophyton: Infects skin and nails Microsporum: Infects hair and skin Treatment Oral griseofulvin Topical miconazole
Tinea Ringworm (moth)
RINGWORM (TINEA)
Tinea corporis(the body)
Tinea pedis(feet)
Tinea unguium(nails)
Tinea capitis(scalp)
Tinea cruris(jock itch)
Tinea barbae(bearded area)
Tinea versicolor (Spaghetti and meatballs)
Ecology of Dermatophytes To determine the source of infection Anthropophilic Zoophilic Geophilic
Anthropophilic Associated with humans only.  Person -to-person transmission through contaminated objects (comb, hat, etc.)
Zoophilic Associated with animals. Direct transmission to humans by close contact with animals.
Geophilic Usually found in soil. Transmitted to humans by direct exposure.
Geographic Distribution Worldwide
Dermatophytes3 Genera Trichophyton Microsporum Epidermophyton
Trichophyton(19 species) Hair  Skin Nails
Trichophyton species Large, smooth, thin wall, septate, pencil-shaped
Trichophytonrubrum Causes a chronic infection in patients with a cell-mediated immune defect. (most common in SC blacks)
Microsporum(13 species) Skin Hair
Microsporum species Thick wall, spindle shape, multicellular
Microsporum canis . Most common etiologic agent of tinea in SC whites
Epidermophytonfloccosum Skin Nails
Epidermophyton floccosum Bifurcated hyphae with multiple, smooth, club shaped macroconidia (2-4 cells)
Therapy Griseofulvin Tinactin Clotrimazole Miconazole Ketoconazole Itraconazole Terbinafine
Dermatophytid Reaction(ID) Dermatophyte infection on feet           (not clinically evident)    Ringworm Lesion on hand          (usually the dominant side)
Dermatophytid Reaction(ID) Culture skin scrapings from feet Treat the tineapedis The hand lesion (ID phenomenon) will respond to therapy of the foot.
Dermatophyte Culture
Cutaneous Mycoses Figure 21.16
Subcutaneous Mycoses Sporotrichosis Sporothrix schenckii enters puncture wound Treated with KI
SPOROTRICHOSIS Primarily a disease of the cutaneous tissue and lymph nodes.  Recently, pulmonary disease.
SPOROTRICHOSIS
PORTALS OF ENTRY           Inhalation           Inoculation
ECOLOGICAL ASSOCIATIONS    Rose thorns    Sphagnum moss    Timbers    Soil
SPOROTRICHOSIS
Subcutaneous mycoses Tineacorporis Subcutaneous infections - produce chronic inflammatory disease of subcutaneous tissues and lymphatics.  sporotrichosis - ulcerated lesions at site of inoculation followed by multiple nodules -  caused by a dimorphic fungus: Sporotrixschenckii.
Daisies
DRUGS OF CHOICE CUTANEOUS  OR SYSTEMIC FORM  Itraconazole
Candidiasis Candida albicans (yeast) Candidiasis may result from suppression of competing bacteria by antibiotics. Occurs in skin; mucous membranes of genitourinary tract and mouth. Thrush is an infection of mucous membranes of mouth. Topical treatment with miconazole or nystatin.
CANDIDIASIS
Candidiasis Figure 21.17
Candidiasis Thrush Risk factors for candidiasis 	Post-operative status Cytotoxic cancer 	Chemotherapy 	Antibiotic therapy 	Burns 	Drug abuse 	Gastrointestinal damage. Cutaneous
Chronic mucocutaneous candidiasis ,[object Object]
These infections affect the skin, nails and mucous membranes. ,[object Object]
Scabies Sarcoptes scabiei burrows in the skin to lay eggs Treatment with topical insecticides Figure 21.18

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