L.1 Staphylococcus Flashcards
1
Q
A
2
Q
What type of bacteria are Gram positive bacteria?
A
Small spherical cells (cocci, 1um) found in grapelike clusters
3
Q
What is a defining feature of Gram positive bacteria in terms of motility?
A
Nonmotile
4
Q
What do Gram positive bacteria produce that aids in their identification?
A
Catalase
5
Q
How many species and subspecies are included in the genus of Gram positive bacteria?
A
> 40 spp and subspecies
6
Q
What type of relationship is described as commensalistic?
A
Relationship where one organism benefits while the other is unaffected
7
Q
Which species of Staphylococcus has the greatest pathogenic potential?
A
S. aureus
8
Q
Which two species of Staphylococcus generally have limited pathogenic potential?
A
S. epidermidis & S. saprophyticus
9
Q
List the extracellular enzymes and exotoxins produced by Staphylococcus aureus
A
- Coagulase
- Alphatoxin
- Leukocidin
- Exfoliatins
- Enterotoxins
- Toxic shock toxin
10
Q
What percentage of healthy individuals are carriers of S. aureus?
A
30-40%
11
Q
Where is S. aureus commonly found in healthy individuals?
A
Nasal passages, skin, within skin glands, and on mucous membranes
12
Q
What is the prevalence of MRSA carriers in the population?
A
About 2 in every 100 people
13
Q
What range of clinical manifestations can S. aureus cause?
A
From mild to severe disease
14
Q
What is S. aureus’s role in nosocomial infections?
A
Frequent pathogen in nosocomial infections
15
Q
What is the most important prophylactic measure in hospitals to prevent S. aureus infections?
A
Hand washing by medical staff
16
Q
How long can S. aureus survive in the environment?
A
For long periods on dry, inanimate objects
17
Q
What conditions allow S. aureus to cause infections?
A
If it enters the bloodstream or internal tissues
18
Q
What risk is associated with S. aureus carriers?
A
Higher risk of infection and are an important source of spread
19
Q
What is the primary mode of transmission for S. aureus?
A
Direct contact, usually skin-to-skin contact
20
Q
What are high carrier rates of S. aureus typically found among?
A
Hospital patients and staff
21
Q
Where is the principal localization of S. aureus colonization in hospital patients?
A
Anterior nasal mucosa area
22
Q
What is the first step in the pathogenesis of S. aureus?
A
Colonization & Adhesion
This involves entry and transmission of S. aureus.
23
Q
Where is S. aureus commonly found in healthy individuals?
A
On the skin and mucous membranes, especially the nasal cavity
24
Q
How does S. aureus spread via direct contact?
A
Through contaminated hands and airborne droplets
25
What is an example of indirect contact transmission of S. aureus?
Contaminated surfaces, objects, or food
26
What are adhesins used for by S. aureus?
To bind to host tissue
27
Name a type of protein that S. aureus uses to bind to extracellular matrix components.
Fibronectin-binding proteins
28
What is the function of collagen-binding proteins in S. aureus?
They bind to collagen in connective tissues
29
What is one mechanism S. aureus uses to resist phagocytosis?
Capsule formation
30
What does Protein A (SpA) do in S. aureus?
Binds to the Fc region of antibodies (IgG) preventing opsonization
31
What enzyme does S. aureus produce to prevent phagocytosis?
Coagulase
32
How does coagulase function in the context of S. aureus?
Converts fibrinogen to fibrin, creating barriers against phagocytosis
33
What are leukocidins?
Substances that destroy neutrophils
34
What is the role of the Chemotaxis Inhibitory Protein in S. aureus?
Blocks neutrophil recruitment
35
What types of enzymes promote the spread of S. aureus?
Lipases & Proteases
36
What is the function of Staphylokinase?
Dissolves fibrin clots to aid bacterial dissemination
37
What does hyaluronidase do in the context of S. aureus?
Breaks down hyaluronic acid in connective tissue
38
What types of toxins does S. aureus produce?
Hemolysins, Leukocidin, PVL, TSST-1, Enterotoxins
39
What is the effect of hemolysins produced by S. aureus?
Destroy red blood cells (RBCs)
40
What is the function of Panton Valentine Leukocidin (PVL)?
Damages macrophages by degranulation
41
What is Toxic Shock Syndrome Toxin-1 (TSST-1)?
A superantigen that induces clonal expansion of T cell types
42
What symptoms are caused by enterotoxins produced by S. aureus?
Food poisoning symptoms
43
What is biofilm formation in relation to S. aureus?
Development of biofilms on medical devices
44
What does biofilm formation protect S. aureus from?
Antibiotics and immune responses
45
What chronic infections can S. aureus cause due to persistent biofilms?
Chronic osteomyelitis, endocarditis, and prosthetic joint infections
46
What is required for the diagnosis of S. aureus?
Microscopic + culture-based pathogen identification.
47
What is the purpose of detecting plasma coagulase and/or clumping factor?
To differentiate S. aureus from coagulase negative species.
48
How is plasma coagulase detected?
Suspend several colonies in 0.5ml of rabbit plasma, incubate for 1, 4, and 24 hours, and record levels of coagulation.
49
What methods are used to detect enterotoxins and TSST-1?
Immunological and molecular biological methods, e.g., ELISA.
50
What types of infections is S. aureus implicated in?
* Suppurative infections
* Systemic infections
* Toxin-associated infections
51
What are examples of suppurative infections caused by S. aureus?
Skin & soft tissue infections.
52
What are examples of systemic infections caused by S. aureus?
* Bloodstream infection
* Endocarditis
* Pneumonia
* Osteomyelitis
53
What are some toxin-associated infections caused by S. aureus?
* Toxic shock syndrome
* Scalded skin syndrome
* Gastroenteritis
* Foodborne illness
54
What types of infections can be due to S. aureus invasion?
* Boils
* Cellulitis
* Ulcers
* Wound infections
* Bloodstream infections
55
What causes foodborne illness related to S. aureus?
Intoxication (toxin production).
56
What conditions lead to scalded skin syndrome and toxic shock syndrome?
Invasion + intoxication.
57
How does the state of the skin affect S. aureus infection?
Intact skin = colonization; skin trauma = infection.
58
What are uncomplicated skin and soft tissue infections?
Superficial infections such as hair follicles, skin, cellulitis, impetigo, and mastitis
## Footnote
These infections are typically localized and do not require surgical intervention.
59
What defines complicated skin and soft tissue infections?
Deep seated infections or those requiring surgical intervention
## Footnote
Examples include wound infections and deep abscesses.
60
What is folliculitis?
Localized infection of hair follicles, also known as a pimple
## Footnote
It is a pus-forming infection of hair follicles.
61
What is a sty?
An infection of an eyelash hair follicle
## Footnote
It is a type of folliculitis.
62
What are furuncles?
Extension of an infected hair follicle, commonly known as a boil
## Footnote
Often form around foreign bodies like splinters.
63
What are carbuncles?
Deep-seated infections of several hair follicles
## Footnote
Can spread to subcutaneous tissues and lead to bloodstream infections.
64
What is impetigo?
Superficial skin infection involving exposed areas such as face and legs
## Footnote
It can be either pustular or bullous.
65
What characterizes pustular impetigo?
Small blisters that rupture and are covered by honey-coloured crust
## Footnote
May also be caused by streptococci.
66
What are the features of bullous impetigo?
Large, fragile blisters leaving a bright red, inflamed area
## Footnote
Nearly always caused by S. aureus.
67
What is cellulitis?
Infection of connective tissue underlying the skin, primarily in arms and legs
## Footnote
Can spread to lymph nodes and bloodstream.
68
What type of infection are burn patients susceptible to?
All S. aureus skin infections, including burn impetigo and cellulitis
## Footnote
This is due to their compromised skin barrier.
69
What is mastitis?
Blockage of the milk ducts in a lactating mother
## Footnote
Babies can transmit S. aureus to their mothers.
70
What defines a surgical wound infection?
Infection of a surgical wound within 30 days of operation or within 1 year after implant
## Footnote
Occurs in 1-3% of surgeries.
71
What are common signs of surgical wound infection?
Redness, swelling, pain, and pus production
## Footnote
Significant risk of bloodstream infection is associated.
72
What are abscesses?
Pus-filled areas under the skin
## Footnote
Can be single or multiple and are often associated with S. aureus.
73
What percentage of nursing mothers may experience breast abscesses?
1-3%
## Footnote
Very uncommon in non-lactating women.
74
What are the common sources of system infections?
Spread from skin infections or other focal infection points to bones, joints, deep organs or may result from trauma
## Footnote
Can occur during surgery or dental work, necessitating prophylaxis.
75
What does bacteremia mean?
Bacteria in the blood
## Footnote
Bacteraemia can lead to widespread immune reactions.
76
What are the consequences of widespread immune reactions in system infections?
Expansion of blood vessels, falls in blood pressure, hypotension, and poor perfusion
## Footnote
This can lead to critical conditions if not addressed.
77
Name the types of infections associated with system infections.
* Meningitis
* Pneumonia
* Endocarditis
* Pyelonephritis
## Footnote
Each type has specific causes and implications.
78
What is a biofilm?
A layer of 'slime' within which Staph aureus lives
## Footnote
It forms on medical implants like catheters and prosthetic valves.
79
How does Staphylococcus aureus create a biofilm?
A cluster of Staph aureus adheres to a surface and produces ECM made of exopolysaccharides (EPS)
## Footnote
Over time, the cells get completely surrounded by it.
80
What are the consequences of biofilm formation?
* Chronic and persistent infections
* Increased tolerance to disinfectants and antibiotics
* Difficulty in eradication
## Footnote
Removal of the source or surface is essential to combat biofilms.
81
What is Toxic Shock Syndrome (TSST-1)?
A superantigen produced by 20% of S.aureus isolates that acts on the vascular system
## Footnote
It causes inflammation, fever, and shock.
82
How does TSST-1 affect the immune system?
Binds to MHC2 on APCs and TCRs on CD4+ T cells, bypassing normal immune regulation
## Footnote
This leads to a cytokine storm.
83
What are the physiological changes induced by TSST-1?
* Fever
* Rash
* Low blood pressure
* Poor end-organ perfusion
## Footnote
These changes can lead to critical health issues.
84
What can prolonged tampon use lead to?
Toxic Shock Syndrome (TSST-1)
## Footnote
TSST-1 can also occur from infections at wounds, burns, surgical sites, and postpartum infections.
85
Fill in the blank: S. aureus can create biofilm on medical implants like _______.
[indwelling intravenous catheters, prosthetic heart valves, artificial joints]
86
True or False: The toxin TSST-1 is produced by bacteria growing in the blood.
False
## Footnote
The toxin is produced at the local site of infection.
87
What cytokines are stimulated by TSST-1?
* IL-1
* IL-2
* TNF
## Footnote
These cytokines contribute to the cytokine storm and its effects.
88
What is TSS and when was it first reported?
Toxic Shock Syndrome (TSS) was first reported in 1978 in women with vaginal colonisation with S. aureus that produce TSS toxin (TSST).
89
What is the association of TSS with menstrual practices?
TSS is associated with menstruating women using super absorbent tampons.
90
What is the current incidence rate of TSS in women of menstrual age?
The incidence of TSS in women of menstrual age has been reduced to 1 in 100,000.
91
How is TSS now more frequently recognized in the medical field?
TSS is now more frequently recognized as a complication of S. aureus surgical wound infections in all patient populations.
92
What are the symptoms and mortality rate associated with TSST?
Symptoms include fever, hypotension, multi-system shutdown, and organ failure with an 8% mortality rate.
93
What is Panton-Valentine Leukocidin (PVL)?
PVL is a pore-forming exotoxin that lyses host cells resulting in membrane damage.
94
What is the impact of PVL on leukocytes?
PVL targets leukocytes, leading to tissue destruction and a strong inflammatory response.
95
In what type of infections is PVL commonly found?
PVL is common in community-associated infections, e.g., necrotizing pneumonia, which has a high mortality rate (~50% despite aggressive treatment).
96
What are hemolysins?
Hemolysins are membrane-damaging exotoxins that lyse host cells and produce pores in RBCs.
97
What is the significance of Fe2+ in the context of hemolysins?
Fe2+ is used by S. aureus as part of its metabolism.
98
What are exfoliatins/exfoliative toxins?
Exfoliatins are serine proteases that cause epidermal damage by cleaving proteins that hold skin cells together in a process termed desquamation.
99
What specific protein do exfoliatins attack?
Exfoliatins specifically attack desmoglein-1.
100
What conditions are associated with exfoliative toxins?
Exfoliative toxins lead to blistering and peeling, seen in Staphylococcal Scalded Skin Syndrome (SSSS) and bullous impetigo.
101
What percentage of S. aureus isolates produce exfoliative toxin?
Exfoliative toxin is produced by approximately 5% of S. aureus isolates.
102
What populations are primarily affected by Stapylococcal Scalded Skin Syndrome?
Neonates, infants, and immunocompromised individuals
## Footnote
Particularly infants due to higher levels of desmoglein-1 in their skin
103
What is a key characteristic of the skin condition caused by Stapylococcal Scalded Skin Syndrome?
Widespread skin peeling resembling burns
104
What forms in Stapylococcal Scalded Skin Syndrome followed by epidermal separation?
Large bullae or cutaneous blisters
105
How can the toxin from Stapylococcal Scalded Skin Syndrome affect the body?
It can spread through the bloodstream and affect distant skin areas
106
What type of infection is Bullous Impetigo?
Localized skin infection with fluid-filled blisters
107
How does Bullous Impetigo differ from Stapylococcal Scalded Skin Syndrome?
It remains localized
108
What role do enterotoxins play in foodborne illness caused by S.aureus?
They act as superantigens, stimulating an excessive immune response and affecting the GI system
109
What is the stability of enterotoxins produced by S.aureus?
Heat stable, withstand cooking and boiling up to 100C
110
What percentage of S.aureus strains produce enterotoxins?
30-50%
111
What is the required concentration of S.aureus for enterotoxin production?
10^5 organisms/gram gives 1ug enterotoxin and symptoms
112
When do symptoms typically onset after ingesting food contaminated with S.aureus enterotoxins?
2-6 hours after ingestion
113
What symptoms are triggered by S.aureus enterotoxins?
* Severe nausea
* Vomiting
* Abdominal pain
* Diarrhea
114
What is the nature of the illness caused by S.aureus enterotoxins?
Self-limiting and resolves within 8-24 hours
115
What can occur if S.aureus enterotoxins disseminate to the blood?
Can cause Toxic Shock Syndrome (TSS) similar to TSST-1
116
What are common causes of foodborne illness related to S.aureus?
* Contaminated food (improperly stored)
* Dairy
* Processed meats
* Mayonnaise-based salads
* Pastries/cream-filled baked goods
* Sandwiches
117
How can food handlers contribute to S.aureus contamination?
By touching food without proper hygiene while infected
118
What is the resistance status of virtually all strains of S.aureus?
Virtually all strains of S.aureus are penicillin resistant
## Footnote
This resistance has significant implications for treatment options.
119
What drug became the drug of choice for S.aureus until the emergence of MRSA in the 1970s?
Methicillin
## Footnote
Methicillin is a stable form of penicillin.
120
What is MRSA resistant to besides methicillin?
Other B-lactam antibiotics and other classes of antibiotics such as Fluoroquinolones
## Footnote
MRSA is classified as multi-drug resistant (MDR).
121
What type of infections was MRSA initially confined to?
Healthcare-associated infections (HCAI)
## Footnote
HCAI is also known as nosocomial infections.
122
What has happened to HA-MRSA in recent years?
HA-MRSA has decreased
## Footnote
Despite its decrease, MRSA remains a concern in healthcare settings.
123
When did community-acquired MRSA (CA-MRSA) emerge?
1990s
## Footnote
CA-MRSA occurs in individuals with no previous risk factors for MRSA.
124
What characterizes CA-MRSA compared to HA-MRSA?
CA-MRSA is often more virulent but does not display broad spectrum antibiotic resistance
## Footnote
CA-MRSA is often PVL positive.
125
What gene is responsible for methicillin resistance in S.aureus?
mecA gene
## Footnote
The mecA gene encodes penicillin-binding protein 2a (PBP2a).
126
What serious infections does HA-MRSA cause?
Serious infections in hospitalized patients
## Footnote
HA-MRSA is multi-drug resistant.
127
How is HA-MRSA transmitted?
Via contaminated hospital surfaces, equipment, and healthcare workers
## Footnote
This highlights the importance of infection control measures.
128
What is one of the characteristics of CA-MRSA?
It is more virulent due to PVL toxin
## Footnote
CA-MRSA typically causes skin infections in healthy individuals.
129
How is CA-MRSA transmitted?
Via direct skin-to-skin contact and contaminated objects
## Footnote
This method of transmission emphasizes the importance of hygiene.
130
What is one major cause of antibiotic resistance?
Overuse of antibiotics
## Footnote
There is a common misconception that antibiotics help with viral infections.
131
What role does agriculture play in antibiotic resistance?
Extensive use of antibiotics as growth supplements and to prevent livestock infection
## Footnote
This widespread use contributes to resistance patterns.
132
Why is there a lack of new antibiotics?
Lack of economical appeal for pharmaceutical companies
## Footnote
Many companies have exited the antibiotic field due to low profitability.
133
What is one strategy for preventing antibiotic resistance in hospitals?
Infection control measures such as hand hygiene and contact precautions
## Footnote
These practices are essential in healthcare settings.
134
What is the purpose of antibiotic stewardship?
To avoid overuse of antibiotics to prevent resistance
## Footnote
Effective stewardship is crucial in managing antibiotic use.
135
What do surveillance programs aim to achieve?
Track resistance patterns and implement policies accordingly
## Footnote
Surveillance is vital for understanding and combating antibiotic resistance.
