_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 leukocidi n=Kills macrophages/neutrophils RELEASE of toxic granules

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

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

Skin Pathogens Flashcards by Pedro Ramirez

Immune defenses of Integument (skin)

Keratinized skin: Tough, water resistant, continuous, sloughing of outer layers
Sabaceous & sweat glands: High salt/Acidic
Normal flora
Resident macrophage in dermis ^{(basement)}
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)

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Staph Aureus (Properties)

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

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Staph Aureus (Virulence factors)

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

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Staph Aureus (Skin)

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

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Staph Aureus (Pyogenic infections)

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

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Staph Aureus (Toxin Med)

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

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Staph Aureus (diagnosis)

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

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Staph Aureus (Treatment)

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

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Staph Epidermis

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

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Strep Pyogenes (GAS)

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

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Strep Pyogenes (Pyogenic-skin)

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)

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Strep Pyogenes (Toxin med)

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

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Enterococcus Faecalis/Faecium (general)

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

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Enterococcus faecalis/faecium (clinical)

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

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Pseudomonas aeruginosa (general)

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

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Pseudomonas aeruginosa (Clinical)

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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
- _{^{Round oval lesion w/nerotic center}}
Primary Otitis media infection
Pneumonia in previously infected pts
Eye infection -trauma/Contact lenses
UTI-Catheters

Vidrio vulnificus (general)

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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

Vidrio vulnificus (Clinical)

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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

Clostridium Perfringes (general)

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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

Clostridium Perfringes (clinical)

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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

Clostridium perfringes (Diagnosis)

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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

Propionibacterium Spp

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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

Actinomyces Israelli (general)

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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

Actinomyces Israelli (Diagnosis)

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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

Bacteroides fragilis (general)

* 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***^{(_{prevents phago/intracellular killing)}}@ anaerobic growth * Capsule=Purified toxin ***induce abscess (PAMP)*** * Catalase/superoxidase (+)=***Resists O2 radicals=Resist to killing***

Bacteroides fragilis (Clinical)

* 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***

Nocardia Spp (general)

* 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

Nocardia Spp (diagnosis)

* **_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

Mycobacterium Leprae (general)

* ***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)***

Mycobacterium Leprae (Clinical)

* 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*** _{^{(fine touch, pain, temp)}} * ***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 (-)***

Mycobacterium Leprae (diagnosis)

* **_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)***

MOTTS-Mycobacterium Marium

* 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***

MOTTS-Mycobacterium Ulcerans

* **_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

MOTTS-Mycobacterium Chelonae

* **_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

Skin Pathogens Flashcards

(34 cards)