Unit 2: Staphylo And Streptococcus Flashcards
1
Q
An attenuated vaccine is composed of A. Killed Microorganisms B. Living microbes rendered a virulent or reduced in virulence C. Inactivated bacterial toxins D. Purified macromolecules
A
B. Living microbes rendered a virulent or reduced in virulence
2
Q
Which of the following is a type of vaccine?
A. Inactivated agent B. purified macromolecule C. Attenuated agent D. All of the above
A
D. All of the above
3
Q
Which o the following rxns is the result of a type 4 (delayed) hypersensitivity?
A. Sensitivity to pet dander
B. Runny nose triggered by pollen
C. Breathing difficulties after exposure to mold spores
D. Dermatitis in response to poison ivy
A
D. Dermatitis in response to poison ivy
4
Q
Anaphylactic shock from an insect venom causes an IgE mediated reaction. How much time would it take for clinical signs to appear?
A
Within a few minutes to few hours
5
Q
Rash on both arms after vacation in the woods, and then 12 cats days before that. What type of hypersensitivity?
A
Type 4
6
Q
29 yo woman w/ lethargic, jaundiced, anemic infant at birth. Enlarged liver and spleen. Mother is RhD negative and after is RhD positive. This their second child. Example of
A
Type 2 hypersensitivity
7
Q
Jane w/ hay fever and rashes after every soccer practice ( allergic to grass) why type of hypersensitivity? A. Atopic B. Cytotoxic C. Immune complex D. Delayed hypersensitivity
A
A. Atopic
8
Q
HIV infections typically cause
A
Secondary immunodeficiency
9
Q
Autoimmunity is always a reaction to…
A
Self antigen
10
Q
True or False: complement is responsible for some of the damage associated with hypersensitivity reaction
A
True
11
Q
Three types of infectious reservoirs
A
Human carriers: asymptomatic individuals that can transmit to others
Nonliving reservoirs: soil, food, water and objects (fomite)
Animal resevoirs: direct contact, eating animals, bloodsucking anthropods.
12
Q
Zoonoses
A
Diseases naturally spread from animal host to humans
13
Q
Pathogenicity
A
Ability of a microorganism to cause disease
14
Q
Virulence
A
Degree of pathogenicity: more virulent strains will only require a few cells to cause infection
15
Q
Virulence factors definition and 5 types
A
Cellular components that play role in the organism’s ability to cause disease
1. Adhesion factors, 2. Bio films 3. Extracellular 4. Toxins 5. Anti phagocytic factors
16
Q
Extracellular enzymes
A
Secreted by pathogens to dissolve structural chemicals- help pathogen maintain infection, and avoid defenses
17
Q
Toxins
A
Harm tissues or trigger host immune responses
18
Q
Toxemia
A
Presence of toxins in the bloodstream
19
Q
Anti phagocytic factors
A
Allows pathogens to remain in a host for longer time (bacterial capsule and chemicals)
20
Q
Direct contact transmission
A
Body contact, either between individuals or from different locations on one individual
21
Q
Indirect contact transmission
A
Pathogen are spread from host to host by fomites
22
Q
Droplet transmission
A
Spread of pathogen in droplets of mucus/ body fluids within one meter
23
Q
Biological vector transmission
A
Transmit pathogens and serve as host for some stage of the pathogen’s life cycle (mosquitos, ticks, lice)
24
Q
Mechanical vector transmission
A
Passively transmit pathogens present on their body to new hosts (flies, roaches and rats)
25
Airborn vehicle transmission
When pathogen travel more than 1 meter via an aerosol (sneezing, air- conditioning, coughing etc.)
26
Waterborne vehicle transmission
Fecal-oral infection, and cause of many GI diseases
27
Localized infection
Microbes enters body and reminds confined to a specific region or one or more anatomical areas (boil/ an acne pimple)
28
Focal infection
Spread from a local infection: exists within a circumscribed area (dental borne endocarditis)
29
Systemic infection
Infection spreads to several sites and tissue fluids usually in the bloodstream (throughout the body)
30
Secondary infection
Another infection by a different microbe occurring after a primary infection (primary weakens or breaks barriers, and secondary is opportunistic)
31
Fulminating infection
Multiplying with great intensity, acute with incredibly quick pathogenesis
32
Nosocomial infection
Hospital acquired
33
Overt infection
Symptomatic
34
Pyogenic infection
Pus producing
35
Zoonosis
Infection cause by pathogen normally found in animals but naturally transmissible to humans
36
Latent infection
A dormant state. Microbe can periodically become active and produce a recurrent disease
37
Four types of health-care associated infections
Exogenous, endogenous, iatrogenic, superinfections
38
Exogenous infection
Pathogenous acquired from the health care environment
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Endogenous
Pathogen arises from normal microbiota of patient introduced to new area
40
Iatrogenic infection
Infection resulting from modern medical procedure
41
Super infection
Use of antimicrobial drugs inhibit some resident microbiota allowing other microbes to thrive and overproduce
42
Staphylococcus aureus habitat
Human host normal flora, human carrier normal flora, fomite or environment
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Staphylococcus aureus disease state
Enters via barrier breach, pyogenic, either due to direct organism effect or toxin mediated
44
Predisposition to Staphylococcus aureus infection includes:
Poor hygiene/ nutrition, tissue injury, other primary infection, diabetes, immunodeficiency
45
Staphylococcus aureus pathogenic factors
1. Phagocytic avoidance structures
2. Production of enzymes
3. Production of toxins
46
Staphylococcus aureus protein A
Binds to IgG and inhibits opsonization and the complement cascade
47
Staphylococcus aureus bound coagulase
Converts fibrinogen into fibrin molecules, and clots hide the bacterial from phagocytic cells (vegetation in endocarditis)
48
Staphylococcus aureus polysaccharide slime layers
Inhibits chemotaxis of immune system, and facilitates staph attachment to surfaces
49
Staphylococcus aureus virulence factors- antiphagocytic
Protein A, bound coagulase/ cell-free coagulase, polysaccharide slime layers (capsules)
50
Staphylococcus aureus enzymatic virulence factors
Hylauronidase, staphylokinase, lipases, penicillinase (beta-lactamase)
51
Staphylococcus aureus hylarunoidase
Breaks down hyaluronic acid, enabling spread between cells
52
Staphylococcus aureus staphylokinasae
Dissolves fibrin threads in blood clots, allowing Staphylococcus aureus to free itself from clots and spread to other areas
53
Staphylococcus aureus lipases
Digests oils to remove protective layers and enhance colonization on skin and in cutaneous oil glands
54
5 Staphylococcus aureus toxins
1. Cytolytic toxins a, b and c
2. Leukocidin
3. Exfoliate or epidermolytic toxins
4. Toxic-shock syndrome toxin
5. Enterotoxins
55
Staphylococcus aureus cytolytic toxins
Disrupt the cytoplasmic membrane of cells
56
Staphylococcus aureus leukocidin (Panton-Valentine toxin)
Can lyse leukocytes specifically
57
Staphylococcus aureus toxic-shock syndrome toxin
Causes TSS, induces fever, vomiting, shock, systemic organ damage (superantigen)
58
Staphylococcus aureus Enterotoxin
Causes gastroenteritis; stimulating intestinal muscle contractions, nausea, intense/ violent vomiting and diarrhea
59
Localized cutaneous Staphylococcus aureus infections
Impetigo: bubble-like swelling that can break and peel away- much bumpier than strep A caused impetigo
2. Folliculitis: hair follicle
3. Furuncle: boil, follicle proceeded to abscess or pustule
4. Carbuncle- larger and deeper lesion created by aggregation and interconnection of a cluster furuncles
60
Staphylococcus aureus Dissemination
When the infection spreads throughout the body to case systemic disease
1. Bacteremia
2. Osteomyelitis (infection of bone growthplate)
3. Endocarditis
61
Staphylococcus aureus toxin mediated disease
1. Food intoxication- enterotoxin for GI distress
2. Staphylococcal scalded skin syndrome: toxin induces bright red rash, blisters, and desquamation of the epidermis (schluffing off)- no scarring
3. Toxic shock syndrome: toxemia of super-antigen leading to shock and organ failure
62
Treatment of Staphylococcus aureus
95% are beta-lactam resistant, and antimicrobial sensitivity testing is vital. Abscesses have to be surgically perforated (or irrigated and drained for deeper wounds- invasive and lengthy therapy)
63
Staphylococcus epidermis location and common diseases
Produces slime layer so commonly infects plastic/ artificial units (IV lines, catheters, prosthetic heart valves)
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Staphylococcus saprophyticus characteristic and diseases
Sensitive to a wide range of antibiotics, and common cause of urinary infection in sexually active young women
65
Gram stain of Staphylococcus aureus
Gram positive
66
Catalase activity of Staphylococcus aureus
Catalase positive
67
Staphylococcus aureus blood agar pattern
B-hemolysis
68
Staphylococcus aureus mannitol fermentation?
Ferments mannitol
69
Staphylococcus aureus coagulase activity?
Coagulase positive
70
Staphylococcus aureus DNAase activity?
DNAase positive
71
Staphylococcus aureus: novobiocin sensitivity?
Yes, novobiocin sensitive
72
Staphylococcus epidermidis gram stain
Gram positive cocci
73
Staphylococcus epidermidis catalase activity?
Catalase positive
74
Staphylococcus epidermidis Blood agar pattern
Non-hemolytic
75
Staphylococcus epidermidis mannitol fermentation?
Does not ferment mannitol
76
Staphylococcus epidermidis coagulase activity?
Coagulase negative
77
Staphylococcus epidermidis novobiocin sensitivity
Novobiocin sensitive
78
Staphylococcus saprophyticus gram stain
Gram positive cocci
79
Staphylococcus saprophyticus catalase activity
Catalase positive
80
Staphylococcus saprophyticus blood agar pattern
Non-hemolytic
81
Staphylococcus saprophyticus mannitol fermentation
Does not ferment mannitol
82
Staphylococcus saprophyticus coagulase activity
Coagulase negative
83
Staphylococcus saprophyticus DNAase activity
DNAase negative
84
Staphylococcus saprophyticus Novobiocin sensitivity
Novobiocin RESISTANT
85
Streptococcus pyogenic virulence factors
M protein, streptokinase, hyaluronidase, streptolysins, Erythrogenic toxin
86
Streptococcus pyogenes M protein
Destabilizes complement and evade phagocytosis
87
Streptococcus pyogenes streptokinase
Lysis of fibrin- blood clots. Aids in spreading
88
Streptococcus pyogenes hyaluronidase
Facilitates the spread of streptococcus through tissue by breaking down hyaluronic acid
89
Streptococcus pyogenes streptolysins
Lyse red blood cells, leukocyte, platelets, other cells (cytolysins) causing cell and tissue injury
90
Streptolysins S
Alters membrane permeability and lysis RBC, leukocytes and other cells
91
Streptolysins O
Forms membrane penetrating channels (porin) leading to membrane defects and cell lysis (losing cytoplasmic content)
— Cardiotoxic
— Antigenic during strep throat infections, but not during skin infections.
92
Erythrogenic toxin (Streptococcus pyogenes)
Act as super antigen- cardiotoxic, can suppress antibody response: results in rash seen in scarlet fever
93
Streptococcus pyogenes impetigo
Crusted, flatter and flakey, school-age epidemics; highly contagious
94
Streptococcus pyogenes erysipelas
Pathogen (through skin) that enters through a break in the skin and eventually spreads through dermis and subcutaneous tissues: can remain superficial or become systemic (VERY red and inflamed)
95
Streptococcal pharyngitis
Inflammation and white spots. If untreated can create severe sequelae
96
Rheumatic fever (Streptococcus pyogenes)
—Follows overt or subclinical pharyngitis
— Carditis, joints, blood vessels and subcutaneous tissues
— chronic progressive damage to heart valves/ muscles
— autoimmune response against heart antigen
97
Streptococcus pyogenes scarlet fever
Streptococcus pyogenes strain carrying a prophage, coding for Erythrogenic toxin: chest rash across whole body; typically due to untreated pharyngitis
98
Streptococcus pyogenes acute glomerulonephritis
Follows either cutaneous or pharyngeal infections (common in children)antigen-antibody complexes deposit in the glomerulus- impairs kidney filtration
99
Streptococcal Toxic Shock Syndrome
Bacteria: multisystem, system to StrepTSS. Organ failure, shock, death. Usually due to wound infection instead of tampon over exposure
100
Necrotizing Fasciitis (Streptococcus pyogenes)
Life-threatening, sepsis, edema, erythema and pain. Streptococcal myositis resembles clostridial gangrene. Toxin mediated so will not be able to cure with antibiotics
101
Streptococcus pyogenes treatment
Penicillin IS effective. Catalase negative, bacitracin susceptible, slide agglutination (clumping)
102
Streptococcus agalactiae-
Group B streptococcus
103
Streptococcus agalactiae most common infection
Colonizes urogenital tract of pregnant woman and mother fails to pass protective antibodies to fetus. Invasive disease in newborns.
Early onset: neonatal bacteremia, meningitis, and pneumonia
Late-onset disease: meningitis
104
Viridans group streptococci characteristics and diseases
— mostly a-hemolytic, some non hemolytic, lack group-specific carbohydrates, most common cause of dental carries, gingivitis and subacute bacterial endocarditis. Can also cause meningitis
105
5 groups of Viridans streptococci
```
Boris
Anginosus
Mitis
Mutant
Salivarius
```
106
Pneumococcal pneumonia
Most common disease caused by Streptococcus pneumoniae, usually requiring some predisposing condition or age factor
107
Streptococcus pneumoniae sinusitis and otitis media
Ear and sinus infection. Sometimes occur following viral infection due to wet congested areas and compromised mucosa. Most common cause of otitis media in children under the age of 3
108
Streptococcus pneumoniae bacteremia and endocarditis
Streptococcus pneumoniae can enter the blood through lacerations or tissue damage
109
Pneumococcal meningitis
Incredibly severe form of meningitis, with much higher mortality rate than other causes. Partially due to damaging treatment, where additional toxins are released upon attack by antimicrobials, further progressing the disease state and irritating the brain and spinal fluid
110
Streptococcus pneumoniae vs Enterococcus
Enterococcus distinguished by its sensitivity to bile
111
Streptococcus pyogenes hemolytic pattern
large zone of beta-hemolysis
112
Streptococcus pyogenes external components
C5a protease, 5-protein antigen, C-carbohydrate, capsule and fimbriae
113
Streptococcus pyogenes penicillin resistant?
No, B-lactams are largely effective. Uncommon but possible resistant strains
114
Streptococcus pyogenes bacitracin sensitivity?
Sensitive to bacitracin
115
Group B Streptococcus (agalactiae) B-hemolytic pattern
Smaller zone of B-hemolysis
116
Group B Streptococcus (agalactiae) bacitracin sensitivity?
Resistant to bacitracin
117
Group B Streptococcus (agalactiae) pathogenicity?
Most often infects newborns (and sometimes the mother) who lacks specific antibodies
118
Group B Streptococcus (agalactiae) catalase activity
Catalase negative
119
Group B Streptococcus (agalactiae) bile esculin?
Bile esculin negative
120
Group B Streptococcus (agalactiae) B-lactam usage?
penicillin, ampicillin (B-lactams) are effective (often used as a prophylactic during birth to reduce cases of newborn infections
121
Streptococcus Pneumoniae B-hemolytic pattern
Alpha-hemolytic in aerobic conditions, B-hemolytic in anaerobic conditions! Crazy...
122
Streptococcus Pneumoniae external characteristics
Diplococci, with capsule required for pathogenicity, bile sensitive
123
Streptococcus Pneumoniae Quellung rxn
Confirmed with positive quellung reaction, testing for the capsule
124
Enterococcus B-hemolytic pattern
None (gamma hemolytic)
125
Enterococcus external characteristics
Diplococci, or in short chains, no capsule, bile insenstive
126
Two species of Enterococcus that cause diseases in humans
Enterococcus faecalis and Enterococcus faecium. Normally found in human colon and rarely pathogenic there, but if introduced to a different body cavity.
127
Enterococcus infections
Often healthcare-associated; wound infections, endocarditis, urinary tract infections.
128
Enterococcus treatment
Difficult to treat, as often resistant to antimicrobials (susceptibility studies are important)
