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)
2
Q
A pateint come to your office with a skin lesion. This could be a manifestation of
A
- systemic infections
- localized infections
3
Q
What are properties of the genus stapylococcus?
A
- Gram positive cocci,
- cluster/grape like arrangement,
- catalase positive (deffininciate staph from strep)
4
Q
What are the 3 species of staph? What are their distinguishing characteristics?
A
- S. aureus
- S. epidermidis
- S. saprophyticus
5
Q
What does the slide test detect?
A
Bound Coagulase
6
Q
What does the tube test detect?
A
secreted coagulase enzyme
➢Coagulase producing bacteria clot plasma
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
8
Q
What species grow on mannitol salt agar?
A
All staph grow BUT only S. Aureus ferments!
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
10
Q
Where is S. aureus fonud?
A
Human Nose.
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
12
Q
What is the purpose of protein A in S. Aureus?
A
Protects from phagocytosis. Binds to the FC region of the immunoglobulin.
13
Q
What are the cytolytic toxins produced by S. aureus?
A
- staphylolysin (hemolysin),
- leukotoxin
- leukocidin [Panton-Valentine (P-V) leukocidin]
14
Q
What are the 2 super antigens produced by S. Auerus?
A
Toxic shock syndrome toxin-1
Enterotoxin
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
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
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
18
Q
What is the most common cause of folliculitis?
A
Staph Aureus
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
20
Q
What is the most common bacterial cause of conjunctivitis?
A
S. Aureus
21
Q
What are some cutaneus diseases caused by S. Aureus?
A
- Furuncles (boils)
- Carbuncles
- Impetigo
- Folliculitis
- Cellulitis
- Abscess
- Sever Necrotizing Fasciitis
22
Q
What is cellulitis?
A
intense inflammation around an infected site, with systemic symptoms,
23
Q
What is the most common cause of post surgical infection?
A
Abscess caused by S. Aureus
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.
25
What are non cutaneus pyogenic diseases caused by S. Aureus?
* Septicemia
* Osteomyelitis and septic arthritis (most common cause)
* Pneumonia/ Empyema
* Acute endocarditis
26
Acute endocarditis caused by S. aureus is common in which patients?
IV Drug abusers
27
What is the cause of necrotizing pneumonia?
* CA-MRSA strains, P-V leukocidin positive
28
Who is at risk for scaled skin syndrome?
neonates and young children
29
How is scalded skin syndrome caused?
* Exfoliative toxin
* serine protease that cleaves desmoglein 1
* a cell adhesion protein
* Follows Localized infection, mostly nasopharynx
30
What is the cause of toxic shock syndrome?
Toxic Shock Syndrome Toxins (TSST) which are superantigens, bind to MHC---TCR complex with **massive release of IL-1, IL-6, TNFα and IFNγ**
31
What are the risk factors for toxic shock syndrome?
Tampon use
Nasal Packing
32
What are the 6 major symptoms of TSS?
* Fever,
* hypotension,
* a diffuse, macular, sunburn-like rash which later desquamate,
* involvement of at least three organs
* oragn failure
* septic shock
33
How is S. aureus diagnosed?
* 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
34
What is the treatment of S.aureus?
* 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)
35
What is the treatment for TSS?
Correction of shock-by fluid, removal of foreign body.
Antibiotics (Vancomycin)
36
What is the prevention of S. Aureus?
Carriers: nasal spray with Mupirocin (Bactroban)
37
What are the properties of S. epidermidis?
* Coagulase negative,
* catalase positive,
* non-hemolytic,
* **Mannitol non fermenter**
* lacks the classic virulence properties of S. aureus
* **Novobiocin sensitive**
38
What are the virulence factors of S.aureus?
* Surface slime layer and biofilm formation
* Surface of foreign implants
* makes treatment difficult, hide from immune response
39
Which diseases are caused by S. epidermidis?
* 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**
40
What are the general characteristics of S. Pyogenes (GAS)?
* 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
41
What are the virulence factors of S. pyogenes? Which is the most important?
* Structural components: Capsule, **M protein** and F protein
* Toxins: Streptolysin S & Streptolysin O (Hemolysins), _Pyrogenic exotoxins (Superantigens)_
* Enzymes: Streptokinase, Streptodornases (DNase), Hyaluronidase, C5a peptidase
42
What skin infections are caused by S. pyogenes?
* Impetigo (clinical similar to S. Aureus)
* Erysipeias
* Cellulitis
* Endometritis (puerperal fever)
43
What is the differnece between erysipelas and cellulitis?
Erysipelas- affected skin is typically raised and has demarcated margins.
Cellulitis: No distinction of affected skin
44
What is endometritis (puerperal fever?
fever caused by uterine infection following childbirth.
45
What are the toxin mediated diseases caused by S. pyogenes?
* Necotizing fasciitis
* Streptococcal toxic shock syndrome
46
What is nectrotizing fasciitis?
* bacteria entering through break in skin
* Myonecrosis/Streptococcal gangrene
* Caused by **Streptococcal exotoxin B (SpeB),**
* a protease that destroys tissue
* “ flesh eating streptococci”
47
What is steptococcal toxix shock syndrome?
* 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
How is a S. Pyogenes infection diagnosed?
1. Culture on blood agar- B hemolytic colonies; can also use a bacitracin disk.
2. Rapid test for throat infection
49
What is the treatment used for S. Pyogenes?
* Penicillin G
* Severe: Intravenous penicillin + protein synthesis inhibitors (clindamycin)
* Drainage and aggressive surgical debridement for soft tissue
50
What are the general properties of E. Faecalis (faecium)?
* 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
What populations are at risk for enterococcus?
* Hospitalization,
* catheterization,
* surgery,
* broad spectrum antibiotic use,
* treatment with vancomycin
52
What is the pathogenesis of enterococcus faecalis?
* biofilm
* Antibiotic resistance
* common (oxacillin cephalosporins)-inherently
* aminoglycosides and vancomycin- aquired
53
What are the clinical diseases caused by E. faecalis?
* Soft tissue infections/peritonitis after colon surgery- trauma
* **UTI-**Cystitis and Pyelonephritis.
* Bacteremia; and endocarditis
* Biliary tract infection
54
What is the treatment for E. faecalis?
* Dual treatment with aminoglycosides + cell wall inhibitors.
* Resistance is increasing, plasmid gene( vancomycin)
* Resistant strain can be very deadly (VRE)
55
What is the lab diagnosis for Enterococcus?
* Capable of growing in the presence of 40% bile
* Hydrolyzing esculin to glucose and esculetin (turn meadia black)
56
What are the general properties of Clostridium perfinges?
* Gram positive rod (rectangular)
* Anaerobe,
* spore former
* several types: A-E.
* Most human infections due to type A.
57
What populations are at risk for clostridium perfingens?
* Trauma (war, automobile accidents),
* septic abortions,
* Diabetics or others with poor peripheral circulation
58
What is a septic abortion?
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
What are the toxins of clostridium perfingens?
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
What is a complication of the clostrridium perfringens toxins?
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
What are the clinical diseases caused by clostridium perfingens?
* Cellulitis
* Suppurative myositis
* **Myonecrosis = Gas Gangrene**
62
What is gas gangrene?
* 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
What Gi disease is caused by clostridium perfrinhens?
Necrotizing enteritis knows as pigbel.
64
What is crepitus?
crackling or popping sounds and sensations experienced under the skin and joints
65
How is clostridium perfringens diagnosed?
* 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
How is clostridium perfingens treated?
prevented?
* **Treatment:** Surgical debridement and high dose penicillin, Hyperbaric oxygen
* **Prevention:** Proper wound care and judicious use of prophylactic antibiotics
67
What are the two organisms under the propionibacterium spp?
* Propionibacterium acnes
* Propionibacterium propionicum
68
What are the general properties of propionibacterium spp?
* Short, small,
* Gram positive rods,
* non-spore forming anaerobe,
* produce propionic acid from sugars
69
What clinical diseases are caused by propionibacterium ssp?
* **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
How is Propionibacterium treated?
**Benzoyl peroxide** has a bactericidal effect and does not induce antibiotic resistance
71
What are the general properties of actinomyces israelii?
* Filamentous –resemble fungi but are bacteria
* Gram positive anaerobe
* non acid fast.
* Forms sulfur granules – yellow/orange color
72
What is are the risk factors for actinomyces israelli?
* Trauma,
* **dental work**
* surgery,
* intrauterine device
73
What is the pathogenesis of actinomyces israelii?
* Chronic granulomatous lesions that form abscesses in connective tissue
* Sinus tract formation
74
What is the main clinical disease caused by actinomyces israelii?
What pateints are at risk for this?
Cervicofacial actinomycosis
History of dental manipulation or trauma to the mouth, poor oral hygiene, dental caries, or periodontal disease
75
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?
Acintomyces Israelii.
Pus- Sulfur granules
76
How is actinomyces israelii treates?
* Sulfur granules (crush granules, Gram stain)
* Culture: Starch casein agar- irregular, rough, colonies, white to yellow pigment, **molar tooth appearance**
77
What are sulfur granules?
bacterial colonies-consisting of thin Gram positive filaments surrounded by antigen-antibody complexes (gives sunray appearance)
78
How is actinomyces treated?
* Drainage or surgical debridement
* Penicillin G-drug of choice. (TREATMENT MUST BE SUSTAINED FOR WEEKS TO MONTHS)
79
What are the general properties of bacteroides fragillis?
* Gram negative bacilli,
* **Capsule,**
* pleomorphic in size and shape;
* obligate anaerobe,
* **20% bile salt enhances growth,**
* **hydrolyzes esculin**
80
How is B. fragillig transmitted? What populations are at risk?
* break of the mucosal surfaces (due to surgery or perforation)
* Bowel surgery, penetrating abdominal wounds (reservoir: colon)
81
What is the most important virulence factor of B. fragilis?
Capsule
1. adhesion factors
2. antiphagocytic
3. abscess formation
LPS lacks phosphate group in lipid A - has little/no endotoxicity
82
What clinical diseases are caused by B. fragilis?
* 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
Patient presents with the following physical finding. What is the culture used to grow the culprit?
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
How is bacteroides fragilis treated?
Metronidazole
85
What are the acid fast bacteria of skin lesions?
* Nocardia spp.
* Mycobacterium leprae
* MOTTS: Mycobacteria Other Than Tuberculosis
86
What are the organisms under the nocardia spp?
* Nocardia asteroides
* Nocardia brasiliensis
87
What are the general properties of Nocardia spp?
* Gram positive,
* **strictly aerobic**,
* non spore former,
* branching rods
* **Aerial hyphae on culture**
* **Weakly acid fast**
88
What are the virulence factors for nocardia spp?
* Cord factor prevents phagosome-lysosome formation
* Catalase and superoxide-dismutase-avoid phagocytic killing
89
What are the clinical diseases caused by nocardia spp?
* Pulmonary: N. asteroides
* Cutaneous nocardiosis: N. brasiliensis
* Mycetoma
* CNS: brain abscesses and chronic meningitis
90
What is a mycetoma?
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
How is nocardia spp diagnosed?
* Acid-fast staining: weakly acid fast, not uniform i.e beaded appearance
* Culture: Selective media-BCYE agar
* waxy, aerial hyphae on colonies
92
What is the treatment of Nocardia spp?
trimethoprim sulfamethoxazole
93
What organisms are under the mycobacterium spp?
* Mycobacterium leprae
* MOTTS; Mycobacteria Other Than Tuberculosis
94
What are the properties of M. leprae?
* An acid-fast rod
* resist decolorisation- upto 5% H2SO4
* cannot be grown in culture
95
How is m. leprae transmitted?
Inhalation and prolonged close contact
96
Where is M. leprae endemic?
California, Hawaii, Louisiana, Texas and Puerto Rico
97
What are the virulence factors of M. Leprae?
* 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
what is the incubation period for m.laprae?
Average 5-7 yrs (vary between 2-40 yrs )
99
What are the two forms of M. laprae infection?
* Tuberculoid: strong cellular; weak humoral, few bacteria in tissue
* Lepromatous: weak cellular, strong humoral, heavy bacterial burden
* There are interbediate manifestations as well
100
What are the features of tuberculoid leprosy?
* Cutaneous **macular rash** with erythematous borders
* and pigment loss in center;
* sensory loss (fine touch, pain, temperature)
* **Lepromin skin test positive**
101
What are the features of lepromatous leprosy?
* 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
Lepromarous vs Tuberculoid leprosy
Tub has granulomas and local inflammation. Peripheral nerve damage
Lep has a disseminated infection. Bone cartilage and diffuse damage.
103
How is m. bacterium leprae diagnosed?
* 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
How is M. Leprae treated?
* Dapsone + rifampin for tuberculoid;
* Clofazimine added for lepromatous
105
How do we prevent M. Leprae?
* Isolation of lepromatous patients
* chemoprophylaxis with dapsone for exposed children
106
What is erythema nodosum lerprosum?
* 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
What is the microscopic apperance of m. leprea?
* Densely clustered acid fast bacilli
* cytoplasmic vacuoles of foamy histiocytes
* bacilli masses known as globi (cigar bundle appearance)
108
Which are the MOTTs organisms?
* Mycobacterium avium-intracellulare (lung)
* Mycobacterium kansasii (lung)
* Mycobacterium marinum
* Mycobacterium ulcerans
* Mycobacterium chelonae
109
What disease is caused by Mycobacterium marinum?
* Fish tank granulomas (can evolve into an ascending lymphangitis)
* in people with recreational or occupational exposure to contaminated freshwater or saltwater
110
What disease is caused by mycobacterium ulcerans?
* 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
What are the risk factors for m. ulcerans?
* Tropical and subtropical countries (Africa, Australia and Asia)
* broken skin
112
What diseases is caused by mycobacterium chelonae?
* non-healing wound, subcutaneous nodule or abscess
* associated with tattoing (contaminated water in the ink)
* medical procedures: laser eye surgery
