Skin Pathogens

Question 1

Immune defenses of Integument (skin)

Answer 1

• Keratinized skin: Tough, water resistant, continuous, sloughing of outer layers
• Sabaceous & sweat glands: High salt/Acidic
• Normal flora
• Resident macrophage in dermis ^{<strong>(basement)</strong>}
• Vascular supply/dermis (plasma proteins, Ig, complement, WBCs)
• Lesions:
• Vesicle=Raised filled w/clear fluid
• Bullae=Big Vesicle
• Pyoderma=infection w/Pus formation
  
  • Folliculitis, pustules
  • Abscess, furuncles(boils), carbuncles
• Impetigo=Vesicle w/honey colored crust
• empyema collection of pus w/in natural cavity (lung pleura)

Question 2

Staph Aureus (Properties)

Answer 2

• Gram(+) cocci=Cluster/grape arrangement
• Catalase (+) & Beta hemo
• Coagulase (+) also done as Latex slide agglutination
  
  • Called citrated plasma
• Mannitol salt agar(+)=color change
• Reservior: Human nose, skin, higher in hospital setting
• Transmission: Shedding from lesions or droplets.
• High risk: Broken skin (trauma), tampons, surgical packing, catheters
  
  • Diabetes IV drugs
  • Severe neutropenia or chronic granulomatous

Question 3

Staph Aureus (Virulence factors)

Answer 3

• Protein A-antiphagocytic,binds to Fc region of IgG.
• Cytolytic (membrane damaging toxins):
  
  • staphylolysin
  • leukotoxin
  • leukocidin **^{(P-V leukocidin)} **
• Staphylokinase/ Fibrinolysin:
• degrade fibrin clots=bacterial escape from clots
• Hyaluronidase: dissolves inter-cellular cement allowing bacterial spread
• Pyogenic infections-Direct organ invasion
• Toxin mediated disease-
• Scalded skin syndrome
• Toxic shock syndrome
• Food poisoning

Question 4

Staph Aureus (Skin)

Answer 4

• Impetigo (pyoderma)-Superficial infection, requires break in skin
  
  • Vesicular-crusts/dries
  • Young children (no FEVER)
• Folliculitis- infection of hair follicle
• On eyelid=Stye
• Furuncles-Extension of folliculitis (boils)
  
  • Draining in clusters
• Carbuncles-Big mass of Furuncles, deeper, more symptoms (chills, FEVER)
• Cellulites: Intense inflammtion w/systemic symptoms (skin/subcutaneous)
• Abscess-Wound infection after trauma/surgery ANY ORGAN
• Severe necrotizing fasciitis (skin/soft tissue) MRSA makes panton Valentine leukocidin=Kills macrophages/neutrophils RELEASE of toxic granules

Question 5

Staph Aureus (Pyogenic infections)

Answer 5

• Septicemia: Spread from IV drug user site-Found in blood
• Oseteomyelitis/Septic arthritis: Most common cause of osteomyelitis
• Pneumonia/Empyema: Acute/Typical
  
  • Post-viral
  • Post surgery
  • Aspiration or vent-assoc
  • Necrotizing pneumonia=CA-MRSA (+)
• Bacteremia/acute endocarditis (normal/prosthetic):
• Common among Injection drug users

Question 6

Staph Aureus (Toxin Med)

Answer 6

• Scalded skin syndrome(ritter’s): Exfoliating toxin
• Serine proteases cleave desmoglein 1 (cell adhesion protein)
• Leads to NO attraction of leukocytes=little/no inflammation
• Localized to nose–>spread to body
• Fever, Large bullae, skin desqaumation, electrolyte imbalance
• No scars after healing (children)
• Toxic shock syndrome:SuperAgs bind to MHC-TCR complex
• Massive release of IL-1, TNF-a, IL-6, IFN-y with systemic inflammation=Septic shock
• Rapid onset-fever, hypotension, diffuse macular/sun-burn rash, w/involvement of at least 3 organs
• Tampons, nose bleeds, or local wound can spread to TSS

Question 7

Staph Aureus (diagnosis)

Answer 7

• Microscope: Gram stain lesions/abscesses
  
  • Gram + cocci in clusters
• Culture:
  
  • Blood agar=Beta hemo
  • Mannitol salt agar=Yellow
• Biochemical: Coag/Catalase (+)
• Rapid hybridization: FISH-DNA probe=rapid ID:
  
  • Coagulase gene
  • rRNA sequence
• ID Resistant strains by ID of coding genes

Question 8

Staph Aureus (Treatment)

Answer 8

• 90% resistant to Pen G due beta-lactamases (plasmids)
• Beta-L resistant drugs:
• Methicillin/Nafcillin/Oxacillin
• some are Met/Naf resistant mutation on MecA gene = _{^{Penicillin binding proteins}}
• MRSA/NRSA=outbreaks in hospital
• MRSA use vancomycin ^{(cell wall inhibitor)}
• VRSA are vancomycin resistant
• VanA-Transposon gene on plasmid
• Quinupristin/Dalfopristin use in combo- (protein synthesis inhibitors)
• Toxic shock syndrome: Correction by fluid, removal of foreign body & treat with Antibio
• Prevention: Treat carries w/Mupirocin (bactroban) nasal spray-inhibits protein synthesis

Question 9

Staph Epidermis

Answer 9

• Coagulase (-) & Catalase (+)
• Non-Hemolytic & Non-mannitol fermenter
• Source=Normal skin flora
• Virulence: Surface slime layer & biofilm formation-Hides from immune response
  
  • Biofilm likes foreign implants
• Disease: Nosocomial infection
• Endocarditis: Bacteremia followed by deposition on heart valve
  
  • Prostatic valve
• Catheter/Prosthetic joint infection: Biofilm adhesion to catheter, prosthetic devices
  
  • Dialysis pts

Question 10

Strep Pyogenes (GAS)

Answer 10

• Gram (+) cocci-CHAINS
• Catalase (-)
• Beta hemolytic
• Bactiracin sensitive & PYR +
• Lancefield group A
• Structure-Capsule, M & F protein
• Streptolysin S & O=Hemolysins
• Streptokinase, Streptodornases, C5a peptidase, Pyrogenic exotoxins=SuperAgs
• Resevior: Oropharyngeal region/Skin
• High risk: all ages
• Pyogenic infection: Pharyngitis, Otitis media, pneumonia, Skin
• Toxin med:Scarlet fever, TSS, Fasciitis
• Immune med: Untreated pharyngitis/skin (NOT staph)=Rheumatic fever/Glomerulonephritis

Question 11

Strep Pyogenes (Pyogenic-skin)

Answer 11

• Impetigo: Like S. Aureus turns to pustules that rupture/crust
• Erysipelas(red skin): infection of skin, localized pain, inflammation, regional lymph swelling
• Skin raised w/demarcated margins
• Face/legs follows URT or skin infection
• Cellulitis: Inflammation of skin/subcutaneous tissue (border unclear)
• Necrotizing fasicitis: myonecrosis/streptococcal gangrene
• Deep tissue infection w/extensive destruction of muscle/fat
• “flesh eating strep”-Caused by exotoxin B (protease)

Question 12

Strep Pyogenes (Toxin med)

Answer 12

• Streptococcal TSS: Strep toxin A/C superAgs
• Follows soft tissue infections w/GAS
• Rapid demise due to septic shock
• High risk: Immunocompromised, cancer, diabetes, HIV
• Purpura w/ gangrenous changes
• Treatment:
• Pen G
• Severe systemic: IV Pen + protein inhibiting antiobios (clinadamycin)
• Surgical intervention maybe necessary

Question 13

Enterococcus Faecalis/Faecium (general)

Answer 13

• Gram (+) cocci-chains/pairs
• Catalase (-)
• Bacitracin/optochin resistant
• Bile & Nacl- resistance (GROW)
• PYR + = Group D (pink-red)
• Reservior: Colon, urethra, Female UT,
• Transmission: Autoinoculation, nosocomial infections, endogenous w/perforation of bowel
• High risk: Catheterization, surgery, broad spectrum antiboitics (vancomycin)
• Adhesion & production of biofilm
• Antibio resistance to common ones (oxacillin, cephalosporins)
• Aquire resistance genes-Plasmids & prove to be fatal

Question 14

Enterococcus faecalis/faecium (clinical)

Answer 14

• Soft tissue infections after colon issue-polymicrobal infection
  
  • Cystitis & pyelonephritis
  • Bacteremia & endocarditis
• Diagnosis-Culture & biochem test
  
  • Bile esculin=Hydrolysis of esculin/bile=Black
  • Used to diff from Streptococcus
  • Black=Iron
  • Catalase (-)
• Treat: Dual w/aminoglycosides & cell wall active antibios.
• Resistance increasing even vancomycin
• Prevention: Restricted use of Antibios

Question 15

Pseudomonas aeruginosa (general)

Answer 15

• Gram (-) rod
• Oxidase (+) aerobic
• Fruity grape like odor
• Virulence:
• Adhesion=Pili, LPS, Cap
• Exotoxin A: Inhibit protein
• Pigments: Pyocyanin, blue–>Attract WBC
• Phosopholipase: Digests lecithin (cell lysis)
• Cap/slime layer: Biofilm
• Reservoir: Everywhere, moist or wet sources, respirators, DISINFECTANT sol=Requires minimal nutrition
• Opputunistic pathogen
• High risk: Burn pts or healthy pt skin infection

Question 16

Pseudomonas aeruginosa (Clinical)

Answer 16

• Folliculitis: Associated w/Hot tubs & pools
  
  • Infects skin w/itchy rash
• Finger nail infection: Frequent exposure to water or NAIL SALONS
• Green due to microorganism secretion
• Proteases crumble nail over time
• Soft tissue infection: Burn wounds ^{(low blood supply to tissue)}
• Ecthyma gangrenosum: Severe invasive infection-among immunocomprimised pts
  
  • _{^{<em><strong>Round oval lesion w/nerotic center</strong></em>}}
• Primary Otitis media infection
• Pneumonia in previously infected pts
• Eye infection -trauma/Contact lenses
• UTI-Catheters

Question 17

Vidrio vulnificus (general)

Answer 17

• Motile & gram (-) curved rod
• Faculative anaerobe=Oxidase +
• Halophilic (requires salt)
• Reservoir: Warm seawater (gulf coast) seen in US
• Transmission: Direct contact w/contaminated salt water (break/scratch) or consumption of bad shellfish
• High risk: Wounds in warm water & septicemia in immunocomprimised pts (ingestion)
• Virulence: Capusle, cytolysin, w/numerous extracell enzymes

Question 18

Vidrio vulnificus (Clinical)

Answer 18

• Skin exposiure: Bullae & necrotizing fasciits
• 24-48 hours from exposure
• Erythema, edema, hemorrhagic bullae
• Rapid onset of necrotizing-Sepsis
• Ingestion: Septicemia (fatal 50%)
• Fever, chills, vomiting, diarrhea
• Blistering skin lesions
• Decrease in BP=Septic shock (Gram - rod)
• Diagnosis: Grow in blood agar (MacConkey)
• Thiosulfate citrate bile salts sucrose=Blue green colonies
• Treat: Doxyxycline & 3rd gen cephalosporin

Question 19

Clostridium Perfringes (general)

Answer 19

• Gram (+) rods & SPORES (not in-vivo)
• **Anaerobe **
• Resrvoir: Soil & human colon
• Transmission: Spores into wounds
• High risk:
• Trauma (war/car accidents)
• Septic abortions
• Diabetics due to poor circulation
• 12 toxins provide invasiveness:
• A toxin (lecithinase & a-phospholipase)
• Destroys cells membrane:
• Hemolytic/necrotic
• Kills RBC, platelets, WBCs, Endothelial
• Massive hemolysis w/increased permeability & tissue destruction

Question 20

Clostridium Perfringes (clinical)

Answer 20

• Soft Tissue: Myonecrosis=Gas gangrene
• Pain, edema w/cellulitis
• Rapid onset of fasiciits/myositis & myonecrosis
• Enzymes break glycosidic bonds in saccharide=necrosis
• Gas ++ under skin:
• Crepitant tissue (crumpling)
• Gas from microbial fermentation=Foul smell
• GI infection, diarrhea, necrotizing enteritis

Question 21

Clostridium perfringes (Diagnosis)

Answer 21

• Micro: Gram stain of tissues & exudate (spores not seen in tissue)
• Culture: Blood agar anaerobic, hemolysis
• Detect alpha toxin-egg yolk agar-produce **OPACITY **
• diffusable lecithinase acts w/yolk = Lipase inhibition
• Treatment: Surgical amputation & HIgh dose pen
• Hyperbaric O2
• Prevention: proper wound care & use of prophylatic antibiotics

Question 22

Propionibacterium Spp

Answer 22

• Short/Small Gram (+) rods
• Non-spore make propionic acid (sugars)
• Reservoir: Skin, conjunctiva. external ear, oropharynx & femal genitals
• Endogenous transmission
• Oppurtunistic pathogen
• Acne vulgaris: Metabolic products of pathogen=inflammation in sebaceous gland
• Post surgical would infection or Prostetic device
• White head=Closed comedo
• Black head=Open comedo

Question 23

Actinomyces Israelli (general)

Answer 23

• Filamentous (fungi-like) bacteria
• Gram (+) anaerobe & non acid fast
• Forms sulfur granules (yellow-orange)
• Reservoir: normal flora-oral, gut, female genital tract
• Endogenous & oppurtunitic pathogen
• High risk: Disruption to mucosal surface (trauma, dental work, surgery)
• Chronic granulomatos lesions form=abscesses in connective tissue
• Cervicofacial-Lumpy Jaw=Nodule on cheek or submax region
• Hard woody feel-Progress to Abscess
• Abscess drains into sinus tract
• PUS orange/yellow (sulfur)
• Thoracic/Abdominal form after swallowing-Presents in lung
• Pelvic-Benign vaginitis w/tissue destruction,tubo-ovarian abscesses or ureteral obstruction

Question 24

Actinomyces Israelli (Diagnosis)

Answer 24

• Microscope: Uneven distrubution in affected tissue-Found in sulfur granules
• Collect granules smash between slides-GRAM STAIN
• Culture: Anaerobic-2 weeks until irregular rough
• White-yellow pigment w/molar tooth look
• Treatment: Drainage/surgery w/Pen G for Weeks to months
• Prevention: Good dental hygiene, antibio before surgery

Question 25

Bacteroides fragilis (general)

Answer 25

• Gram (-) bacteria rods
• Pleomorphic=vary in size/shape
• Obligate anaerobe
• 20% bile salt enchances growth
• Reservoir: GI (colon), vagina, feces
• Endogenous due to break of mucosal surfaces-ex surgery/perforation (appendicitis)
• _Virulence: _
• LPS (no endotoxins) lacks lipid A
• Adhesion factors-capsule (polysac) & pili
• Antiphago-capsule, succinic acid production^{(_{<strong><u>prevents phago/intracellular killing)</u></strong>}}@ anaerobic growth
• Capsule=Purified toxin induce abscess (PAMP)
• Catalase/superoxidase (+)=Resists O2 radicals=Resist to killing

Question 26

Bacteroides fragilis (Clinical)

Answer 26

• Intra-abdominal abscess
• Peritonitis
• Genital infections w/inflammatory disease in females
• Necrotizing fasciitis
• Bacteremia w/polymicrobal infection
• _Diagnosis: _
• Gram stain-abscess fluid WEAK stain
• Culture-Anaerobic=culture w/20% bile salt (esculin & gentamycin)
  
  • _{^{Hydrolized esculin turns black}}
• bacterorides bile esculin agar (BBE)
• Gas chromatography-ID FAs made by B.fragilis
• Treat: Metronidazole due to betalactamases
• Anaetobic infection=polymicrobial=1+ antibios used w/wound drainage
• RESISTANT to gentamycin

Question 27

Nocardia Spp (general)

Answer 27

• Gram (+) aerobic, NON-spore former
• Branching rods _{^{(like actinomycetes)}}
• Form aerial hyphae in culture
• Weak acid fast-cell wall has mycolic acid BUT shorter fatty acids compared to MTB
• Cell wall=trehalose dimycolate ^{_{(Cord factor)}}
• Resevoir: Anything rich in organic material
• Virulence: Avoids phagocytic killing
• Catalase & superoxide (+)
• **Cord factors stop phago-lysosome **
• Pulmonary presentations-Bronchitis, pneumonia & lung abcess (cavity)
• Cutaneous nocardiosis:
• Mycetoma-resemebles actinomycosis (NO Face)-**Presents in feet **
• Lymph infection-Cellulitis w/chornic ulcerative abscess
• CNS: brain abscesses/chronic meningitis

Question 28

Nocardia Spp (diagnosis)

Answer 28

• Microscope: Drainage or sputum gram & acid fast stain
• Acid stain NOT uniform-beaded
• Culture: Grow on MOST medias-SLOW
• Colonies are waxy & aerial hyphae
  
  • Sabourand dextrose agar
• Treat: Trimethoprim-sulfa w/1 year
• Prevention: Wound cleaning & drainage

Question 29

Mycobacterium Leprae (general)

Answer 29

• Leprosy/Hansen’s disease
• Acid-fast rod & CANNOT be grown in culture
• Reservoir: Humans & armadillos in LS/TX
• Can be transmitted BUT through PROLONGED close contact
• High risk: Pts with cases over long periods of time, Children in houshold with infected pts
• Cases seen in CA, HI, PR, LS, TX
• Virulence:
• PGL-1 ^{_{(phenolic glycolipid)}}-resist macrophages
• Acid fast cell wall-Lipoarabinomannan/Trehalose dimycolate
• Intracellular survival in skin histocytes & schwann cells
• Prefers lower temps (nasopharynx/Skin)

Question 30

Mycobacterium Leprae (Clinical)

Answer 30

• Progressive disfiguring disease
• Chronic bacterial infections of skin, Peripheral nerves & Upper airway
• Tuberculoid-Strong humoral (T-cells), WEAK cellular, few bacteria in tissues
• Few Cutaneous macular rash w/pigment loss center w/Loss of sensory _{<u>^{(fine touch, pain, temp)}</u>}
  
  • Lepromin skin test (+)
• Lepromatous-Strong humoral, WEAK cellular, Heavy bacteria buden
• Many Cutaneous nodular lesion assoc w/sensory loss & counter current upper resp congestion
• Involvement of nasal (destruction)
• mucosa=Crusting=Troubled breathing
• Occular involvement
  
  • Lepromin skin test (-)

Question 31

Mycobacterium Leprae (diagnosis)

Answer 31

• Microscopy-Acid fast bacilli present in dermal macrophages in Lepromatous form (nasal scrapings)
• NO CULTURE
• Skin test: Lepromin (_{^{intradermal injection}}) Only Tuberuloid form
• Treat:
• Dapsone w/wo rifampin=Tuberculoid
  
  • inhibits bacterial synthesis of dihydrofolic acid
• + Clofazimine=Lepromatous
  
  • Binds to guanine in DNA=Block of bacteria prolif
• Tuberculoid = IL-2, IFN-y, TNF-B (TH1)
• Lepromatous = IL-4, IL-5, IL-10 (TH2)

Question 32

MOTTS-Mycobacterium Marium

Answer 32

• Mycobacteria other than than TB
• Reservoir: Cold/warm fresh/Salt water
• High risk: Pts w/recrational or occupational exposure to contanminated water
• Disease=Fish tank granulomas
• Localized but can progress w/ascending lymphangitis
• Resembles sporotrichosis & norcardia
• Commonly affects elbows, knees, feet, knuckles or fingers

Question 33

MOTTS-Mycobacterium Ulcerans

Answer 33

• Reservoir: Bodies of water-slow flowing rivers, ponds, swamps, lakes
• High risk: Tropical/subtropical (africa, australia, Asia) enters through broken skin
• Disease-Buruli Ulcer
• 7-14 days=Painless w/itchy nodule
• 1-2 months=Nodule BREAKS to form shallow ulcer spreads rapidly
  
  • ^{Could involve 15% of pts skin}
• Severe infections destroy BVs, nerves, & Bone

Question 34

MOTTS-Mycobacterium Chelonae

Answer 34

• Reservoir: Tap water
• High risk: Grows in soft tissue
• Infection related to medical procedures
• Cosmetic practices or Tattoo (INK)
• _Disease: _
• Non-healing wound, subcutaneous nodule or abscess
• Can cause lung disease, joint infection, eye disease
• Systemic organ infections