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Micro 2 class > Skin Bacteria > Flashcards

Skin Bacteria Flashcards

1
Q

What are the immunse defenses against skin infections?

A
  • Keratinization – skin tough, water resistant;
  • Sloughing of outer layers
  • Sebaceous and sweat gland secretions- high salt, acidic
  • Normal flora
  • Resident macrophage in dermis
  • Vascular supply in dermis (Plasma proteins, Ig, complement, WBCs)
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2
Q

A pateint come to your office with a skin lesion. This could be a manifestation of

A
  • systemic infections
  • localized infections
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3
Q

What are properties of the genus stapylococcus?

A
  • Gram positive cocci,
  • cluster/grape like arrangement,
  • catalase positive (deffininciate staph from strep)
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4
Q

What are the 3 species of staph? What are their distinguishing characteristics?

A
  • S. aureus
  • S. epidermidis
  • S. saprophyticus
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5
Q

What does the slide test detect?

A

Bound Coagulase

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6
Q

What does the tube test detect?

A

secreted coagulase enzyme

➢Coagulase producing bacteria clot plasma

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7
Q

What is the main point of a coagulase test?

A

Staphylococcus aureus is the only significant human pathogen that produces the enzyme coagulase.

Coagulase changes soluble fibrinogen into soluble fibrins

Plasma + bacteria = coagulation

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8
Q

What species grow on mannitol salt agar?

A

All staph grow BUT only S. Aureus ferments!

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9
Q

What are the general properties of S. aureus?

A
  • Gram positive cocci,
  • cluster/grape like arrangement,
  • catalase & coagulase positive.
  • Beta hemolytic,
  • Growth at 7.5% NaCl
  • Ferments mannitol
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10
Q

Where is S. aureus fonud?

A

Human Nose.

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11
Q

What populations are at risk for contracting a S.aureus inffections?

A
  • Broken skin –due to trauma/surgery
  • Presence of foreign body such as Tampons, Surgical packing, Sutures, Catheters
  • Diabetes, intravenous drug abuse, Severe neutropenia, chronic granulomatous disease
  • Post influenza infection
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12
Q

What is the purpose of protein A in S. Aureus?

A

Protects from phagocytosis. Binds to the FC region of the immunoglobulin.

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13
Q

What are the cytolytic toxins produced by S. aureus?

A
  • staphylolysin (hemolysin),
  • leukotoxin
  • leukocidin [Panton-Valentine (P-V) leukocidin]
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14
Q

What are the 2 super antigens produced by S. Auerus?

A

Toxic shock syndrome toxin-1

Enterotoxin

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15
Q

Which toxic enzymes does S. Aureus produce?

A
  • Staphylokinase/ Fibrinolysin : degrades fibrin clots, assists bacterial escape from clots
  • Coagulase: also known as clumping factor- form fibrin clots. It is secreted as well as expressed on the surface
  • Hyaluronidase dissolves inter-cellular cement allowing bacterial spread
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16
Q

What are the clinical categories of diseases caused by S. Aureus?

A
  • Pyogenic-direct organ invasion. Sevral organs
  • Toxin Mediated- SSS, TSS, Food poisioning
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17
Q

What clinical diseases are caused by S. Aureus?

A
  • endocarditis
  • Staph Scalded Skin (SSS)
  • Pneumonia
  • Staph Food poisioning
  • Catheter infections
  • TSS
  • Cutaneus (impetigo, folliculitis, cellulitis)
  • Septic Arthritis
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18
Q

What is the most common cause of folliculitis?

A

Staph Aureus

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19
Q

A young child presents with honey colored crust and pustules. What is the diagnosis? Cause?

A

Impetigo (pyoderma)

S.Aureus. Skin break is requied for infection

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20
Q

What is the most common bacterial cause of conjunctivitis?

A

S. Aureus

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21
Q

What are some cutaneus diseases caused by S. Aureus?

A
  • Furuncles (boils)
  • Carbuncles
  • Impetigo
  • Folliculitis
  • Cellulitis
  • Abscess
  • Sever Necrotizing Fasciitis
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22
Q

What is cellulitis?

A

intense inflammation around an infected site, with systemic symptoms,

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23
Q

What is the most common cause of post surgical infection?

A

Abscess caused by S. Aureus

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24
Q

What are the key characteristics of sever necrotizing fasciitis?

A
  • Caused by MRSA that produce Panton Valentine leukocidin (P-V leukocidin), the gene of which is located in lysogenic phage
  • This toxin kills phagocytic cells – releasing their toxic contents.
  • Usually community acquired, thus known as CA-MRSA
  • Infected by bacterio phage.
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25
Q

What are non cutaneus pyogenic diseases caused by S. Aureus?

A
  • Septicemia
  • Osteomyelitis and septic arthritis (most common cause)
  • Pneumonia/ Empyema
  • Acute endocarditis
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26
Q

Acute endocarditis caused by S. aureus is common in which patients?

A

IV Drug abusers

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27
Q

What is the cause of necrotizing pneumonia?

A
  • CA-MRSA strains, P-V leukocidin positive
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28
Q

Who is at risk for scaled skin syndrome?

A

neonates and young children

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29
Q

How is scalded skin syndrome caused?

A
  • Exfoliative toxin
    • serine protease that cleaves desmoglein 1
    • a cell adhesion protein
  • Follows Localized infection, mostly nasopharynx
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30
Q

What is the cause of toxic shock syndrome?

A

Toxic Shock Syndrome Toxins (TSST) which are superantigens, bind to MHC—TCR complex with massive release of IL-1, IL-6, TNFα and IFNγ

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31
Q

What are the risk factors for toxic shock syndrome?

A

Tampon use

Nasal Packing

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32
Q

What are the 6 major symptoms of TSS?

A
  • Fever,
  • hypotension,
  • a diffuse, macular, sunburn-like rash which later desquamate,
  • involvement of at least three organs
  • oragn failure
  • septic shock
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33
Q

How is S. aureus diagnosed?

A
  • Microscopy: Gram + cocci in clusters

Culture:

  • Blood agar- beta hemolytic
  • Mannitol– fermentation(yellow)
  • Biochemical: Coagulase test +, catalase test +
  • FISH- identification of coagulase gene or rRNA genes
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34
Q

What is the treatment of S.aureus?

A
  • Beta lactamase resistant drugs
  • MRSA Strains:
    • vancomycin is the drug of choice
  • Vancomycin resistant strains have emerged (VRSA), coded by VanA
    • Quinupristin/dalfopristin (protein synthesis inhibitors)
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35
Q

What is the treatment for TSS?

A

Correction of shock-by fluid, removal of foreign body.

Antibiotics (Vancomycin)

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36
Q

What is the prevention of S. Aureus?

A

Carriers: nasal spray with Mupirocin (Bactroban)

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37
Q

What are the properties of S. epidermidis?

A
  • Coagulase negative,
  • catalase positive,
  • non-hemolytic,
  • Mannitol non fermenter
  • lacks the classic virulence properties of S. aureus
  • Novobiocin sensitive
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38
Q

What are the virulence factors of S.aureus?

A
  • Surface slime layer and biofilm formation
  • Surface of foreign implants
  • makes treatment difficult, hide from immune response
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39
Q

Which diseases are caused by S. epidermidis?

A
  • Endocarditis: prosthetic heart valve or damaged native valve
  • Catheter and prosthetic joint infections (prosthetic devices such as in dialysis patients)

Are almost always Nosocomial infection

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40
Q

What are the general characteristics of S. Pyogenes (GAS)?

A
  • Gram positive cocci in chains,
  • catalase negative,
  • beta hemolytic on blood agar plate,
  • bacitracin sensitive,
  • Lancefield group A, PYR +.
  • Over 150 different strains – M types
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41
Q

What are the virulence factors of S. pyogenes? Which is the most important?

A
  • Structural components: Capsule, M protein and F protein
  • Toxins: Streptolysin S & Streptolysin O (Hemolysins), Pyrogenic exotoxins (Superantigens)
  • Enzymes: Streptokinase, Streptodornases (DNase), Hyaluronidase, C5a peptidase
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42
Q

What skin infections are caused by S. pyogenes?

A
  • Impetigo (clinical similar to S. Aureus)
  • Erysipeias
  • Cellulitis
  • Endometritis (puerperal fever)
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43
Q

What is the differnece between erysipelas and cellulitis?

A

Erysipelas- affected skin is typically raised and has demarcated margins.

Cellulitis: No distinction of affected skin

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44
Q

What is endometritis (puerperal fever?

A

fever caused by uterine infection following childbirth.

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45
Q

What are the toxin mediated diseases caused by S. pyogenes?

A
  • Necotizing fasciitis
  • Streptococcal toxic shock syndrome
46
Q

What is nectrotizing fasciitis?

A
  • bacteria entering through break in skin
  • Myonecrosis/Streptococcal gangrene
  • Caused by Streptococcal exotoxin B (SpeB),
    • a protease that destroys tissue
  • “ flesh eating streptococci”
47
Q

What is steptococcal toxix shock syndrome?

A
  • Caused by Streptoccal pyrogenic exotoxin SpeA and SpeC (super antigens).
  • Mostly due to GAS serotype M1 and M3
  • Abrupt pain, fever, chills, malaise, N &V, diarrhoea
  • multi-organ failure
48
Q

How is a S. Pyogenes infection diagnosed?

A
  1. Culture on blood agar- B hemolytic colonies; can also use a bacitracin disk.
  2. Rapid test for throat infection
49
Q

What is the treatment used for S. Pyogenes?

A
  • Penicillin G
  • Severe: Intravenous penicillin + protein synthesis inhibitors (clindamycin)
  • Drainage and aggressive surgical debridement for soft tissue
50
Q

What are the general properties of E. Faecalis (faecium)?

A
  • Gram positive cocci in chains/pairs,
  • catalase negative
  • bacitracin and optochin resistant,
  • varied hemolysis
  • grow in 6.5% NaCl and 40% bile (can infect GI tract)
  • hydrolyze esculin
  • PYR + (pyrolidonyl arylamidase)
51
Q

What populations are at risk for enterococcus?

A
  • Hospitalization,
  • catheterization,
  • surgery,
  • broad spectrum antibiotic use,
  • treatment with vancomycin
52
Q

What is the pathogenesis of enterococcus faecalis?

A
  • biofilm
  • Antibiotic resistance
    • common (oxacillin cephalosporins)-inherently
    • aminoglycosides and vancomycin- aquired
53
Q

What are the clinical diseases caused by E. faecalis?

A
  • Soft tissue infections/peritonitis after colon surgery- trauma
  • UTI-Cystitis and Pyelonephritis.
  • Bacteremia; and endocarditis
  • Biliary tract infection
54
Q

What is the treatment for E. faecalis?

A
  • Dual treatment with aminoglycosides + cell wall inhibitors.
  • Resistance is increasing, plasmid gene( vancomycin)
  • Resistant strain can be very deadly (VRE)
55
Q

What is the lab diagnosis for Enterococcus?

A
  • Capable of growing in the presence of 40% bile
  • Hydrolyzing esculin to glucose and esculetin (turn meadia black)
56
Q

What are the general properties of Clostridium perfinges?

A
  • Gram positive rod (rectangular)
  • Anaerobe,
  • spore former
  • several types: A-E.
  • Most human infections due to type A.
57
Q

What populations are at risk for clostridium perfingens?

A
  • Trauma (war, automobile accidents),
  • septic abortions,
  • Diabetics or others with poor peripheral circulation
58
Q

What is a septic abortion?

A

Is serious uterine infection during or shortly before or after an abortion. Septic abortions usually result from induced abortions done by untrained practitioners using nonsterile techniques

59
Q

What are the toxins of clostridium perfingens?

A

More than 12 toxins- lyse blood cells and destroy tissues.

  • α toxin (Lecithinase - a Phospholipase)
    • Destroys cell membrane: hemolytic/necrotic
    • Kills RBC, platelets, white blood cells, endothelial cells,
60
Q

What is a complication of the clostrridium perfringens toxins?

A

Necrosis and destruction of blood vessels and the surrounding tissue, especially muscle, anaerobic environment in adjacent tissue and the organism spreads systemically.

Death can occur within 2 days.

61
Q

What are the clinical diseases caused by clostridium perfingens?

A
  • Cellulitis
  • Suppurative myositis
  • Myonecrosis = Gas Gangrene
62
Q

What is gas gangrene?

A
  • Painful rapid destruction of muscle tissue
  • Gas accumulation under the skin results in crepitation in the tissue
  • Microbial fermentation of host tissue – gives foul smelling
  • Systemic spread
  • Mortality 30% treated 100% not
63
Q

What Gi disease is caused by clostridium perfrinhens?

A

Necrotizing enteritis knows as pigbel.

64
Q

What is crepitus?

A

crackling or popping sounds and sensations experienced under the skin and joints

65
Q

How is clostridium perfringens diagnosed?

A
  • Microscopy: Gram positive rods, no inflammatory cells
  • Culture: blood agar -anaerobic culture, double zone of hemolysis
  • Nagler reaction-alpha toxin in egg yolk agar produce opacity
66
Q

How is clostridium perfingens treated?

prevented?

A
  • Treatment: Surgical debridement and high dose penicillin, Hyperbaric oxygen
  • Prevention: Proper wound care and judicious use of prophylactic antibiotics
67
Q

What are the two organisms under the propionibacterium spp?

A
  • Propionibacterium acnes
  • Propionibacterium propionicum
68
Q

What are the general properties of propionibacterium spp?

A
  • Short, small,
  • Gram positive rods,
  • non-spore forming anaerobe,
  • produce propionic acid from sugars
69
Q

What clinical diseases are caused by propionibacterium ssp?

A
  • Acne vulgaris: metabolic by-products of the bacteria induce inflammatory response in sebaceous glands
  • Opportunistic infections in patients with prosthetic devices or IV lines
70
Q

How is Propionibacterium treated?

A

Benzoyl peroxide has a bactericidal effect and does not induce antibiotic resistance

71
Q

What are the general properties of actinomyces israelii?

A
  • Filamentous –resemble fungi but are bacteria
  • Gram positive anaerobe
  • non acid fast.
  • Forms sulfur granules – yellow/orange color
72
Q

What is are the risk factors for actinomyces israelli?

A
  • Trauma,
  • dental work
  • surgery,
  • intrauterine device
73
Q

What is the pathogenesis of actinomyces israelii?

A
  • Chronic granulomatous lesions that form abscesses in connective tissue
  • Sinus tract formation
74
Q

What is the main clinical disease caused by actinomyces israelii?

What pateints are at risk for this?

A

Cervicofacial actinomycosis

History of dental manipulation or trauma to the mouth, poor oral hygiene, dental caries, or periodontal disease

75
Q

A 41 yr old male present to the clinid with a submaxilary nodule. History reveals a recent visit to the dentist for a molar removal.

The nodule has a woddy feel and is draining yellow pus. What is the organism repopnsible for these symptoms?

A

Acintomyces Israelii.

Pus- Sulfur granules

76
Q

How is actinomyces israelii treates?

A
  • Sulfur granules (crush granules, Gram stain)
  • Culture: Starch casein agar- irregular, rough, colonies, white to yellow pigment, molar tooth appearance
77
Q

What are sulfur granules?

A

bacterial colonies-consisting of thin Gram positive filaments surrounded by antigen-antibody complexes (gives sunray appearance)

78
Q

How is actinomyces treated?

A
  • Drainage or surgical debridement
  • Penicillin G-drug of choice. (TREATMENT MUST BE SUSTAINED FOR WEEKS TO MONTHS)
79
Q

What are the general properties of bacteroides fragillis?

A
  • Gram negative bacilli,
  • Capsule,
  • pleomorphic in size and shape;
  • obligate anaerobe,
  • 20% bile salt enhances growth,
  • hydrolyzes esculin
80
Q

How is B. fragillig transmitted? What populations are at risk?

A
  • break of the mucosal surfaces (due to surgery or perforation)
  • Bowel surgery, penetrating abdominal wounds (reservoir: colon)
81
Q

What is the most important virulence factor of B. fragilis?

A

Capsule

  1. adhesion factors
  2. antiphagocytic
  3. abscess formation

LPS lacks phosphate group in lipid A - has little/no endotoxicity

82
Q

What clinical diseases are caused by B. fragilis?

A
  • Intra-abdominal Abscess, peritonitis, appendicitis
  • Genital infections and pelvic inflammatory disease (PID)
  • Necrotizing fasciitis/Myonecrosis
  • Bacteremia
  • Metastatic abscesses by hematogenous spread to distant organs (eg. Brain abscess)
83
Q

Patient presents with the following physical finding. What is the culture used to grow the culprit?

A

Patient has myonecrosis caused by B. fragilis.

  • Culture: Anaerobic culture, special media with 20% bile salt, Esculin and gentamicin Bacteroides Bile Esculin agar (BBE)
  • Weakly stains gram negative
84
Q

How is bacteroides fragilis treated?

A

Metronidazole

85
Q

What are the acid fast bacteria of skin lesions?

A
  • Nocardia spp.
  • Mycobacterium leprae
  • MOTTS: Mycobacteria Other Than Tuberculosis
86
Q

What are the organisms under the nocardia spp?

A
  • Nocardia asteroides
  • Nocardia brasiliensis
87
Q

What are the general properties of Nocardia spp?

A
  • Gram positive,
  • strictly aerobic,
  • non spore former,
  • branching rods
  • Aerial hyphae on culture
  • Weakly acid fast
88
Q

What are the virulence factors for nocardia spp?

A
  • Cord factor prevents phagosome-lysosome formation
  • Catalase and superoxide-dismutase-avoid phagocytic killing
89
Q

What are the clinical diseases caused by nocardia spp?

A
  • Pulmonary: N. asteroides
  • Cutaneous nocardiosis: N. brasiliensis
  • Mycetoma
  • CNS: brain abscesses and chronic meningitis
90
Q

What is a mycetoma?

A

Painless, chronic infection, primarily of the feet, characterized by localized subcutaneous swelling with involvement of the underlying tissues, muscle and bone, suppuration and the formation of multiple sinus tracts

91
Q

How is nocardia spp diagnosed?

A
  • Acid-fast staining: weakly acid fast, not uniform i.e beaded appearance
  • Culture: Selective media-BCYE agar
  • waxy, aerial hyphae on colonies
92
Q

What is the treatment of Nocardia spp?

A

trimethoprim sulfamethoxazole

93
Q

What organisms are under the mycobacterium spp?

A
  • Mycobacterium leprae
  • MOTTS; Mycobacteria Other Than Tuberculosis
94
Q

What are the properties of M. leprae?

A
  • An acid-fast rod
  • resist decolorisation- upto 5% H2SO4
  • cannot be grown in culture
95
Q

How is m. leprae transmitted?

A

Inhalation and prolonged close contact

96
Q

Where is M. leprae endemic?

A

California, Hawaii, Louisiana, Texas and Puerto Rico

97
Q

What are the virulence factors of M. Leprae?

A
  • Infects histiocytes, endothelial cells and Schwann cells
  • PGL-1 (phenolic glycolipid 1) present in cell wall – resists macrophage killing
  • Lipoarabinomannan and Trehalose dimycolate
  • Preferes Lower temp (skin)
98
Q

what is the incubation period for m.laprae?

A

Average 5-7 yrs (vary between 2-40 yrs )

99
Q

What are the two forms of M. laprae infection?

A
  • Tuberculoid: strong cellular; weak humoral, few bacteria in tissue
  • Lepromatous: weak cellular, strong humoral, heavy bacterial burden
  • There are interbediate manifestations as well
100
Q

What are the features of tuberculoid leprosy?

A
  • Cutaneous macular rash with erythematous borders
  • and pigment loss in center;
  • sensory loss (fine touch, pain, temperature)
  • Lepromin skin test positive
101
Q

What are the features of lepromatous leprosy?

A
  • Cutaneous nodular lesions- sensory loss
  • concurrent upper respiratory congestion
  • Widespread dissemination
  • Involvement of the nasal mucosa(epistaxis)
  • Ocular involvement leads to iritis and keratitis
  • Lepromin skin test negative
102
Q

Lepromarous vs Tuberculoid leprosy

A

Tub has granulomas and local inflammation. Peripheral nerve damage

Lep has a disseminated infection. Bone cartilage and diffuse damage.

103
Q

How is m. bacterium leprae diagnosed?

A
  • Slit skin Smear- collecting tissue pulp. (taken from ear lobe, infected skin and healthy skin)
  • Acid Fast (weakly)
  • Serology: IgM against phenolic glycolipid-1 (not for tuberculoid)
  • Lepromin test (Intradermal injection)-Useless in lepromatous
104
Q

How is M. Leprae treated?

A
  • Dapsone + rifampin for tuberculoid;
  • Clofazimine added for lepromatous
105
Q

How do we prevent M. Leprae?

A
  • Isolation of lepromatous patients
  • chemoprophylaxis with dapsone for exposed children
106
Q

What is erythema nodosum lerprosum?

A
  • After therapy, patients with lepromatous can develop Erythema nodosum leprosum (ENL),
  • Sign that cell mediated immunity is being restored.
  • Characterized by painful nodules, especially along the extensor surfaces of the tibia and ulna, neurtitis and uveitis.
107
Q

What is the microscopic apperance of m. leprea?

A
  • Densely clustered acid fast bacilli
  • cytoplasmic vacuoles of foamy histiocytes
  • bacilli masses known as globi (cigar bundle appearance)
108
Q

Which are the MOTTs organisms?

A
  • Mycobacterium avium-intracellulare (lung)
  • Mycobacterium kansasii (lung)
  • Mycobacterium marinum
  • Mycobacterium ulcerans
  • Mycobacterium chelonae
109
Q

What disease is caused by Mycobacterium marinum?

A
  • Fish tank granulomas (can evolve into an ascending lymphangitis)
  • in people with recreational or occupational exposure to contaminated freshwater or saltwater
110
Q

What disease is caused by mycobacterium ulcerans?

A
  • Buruli ulcer (3rd most common mycobacterial infection)
  • Mycolactone toxin
  • IP: 1-2 weeks: Solitary, painless and sometimes itchy nodule of 1-2 cm
  • In 1-2 months, the nodule form a shallow ulcer that spreads rapidly
111
Q

What are the risk factors for m. ulcerans?

A
  • Tropical and subtropical countries (Africa, Australia and Asia)
  • broken skin
112
Q

What diseases is caused by mycobacterium chelonae?

A
  • non-healing wound, subcutaneous nodule or abscess
  • associated with tattoing (contaminated water in the ink)
  • medical procedures: laser eye surgery

Micro 2 class (6 decks)

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