Staphylococcus (Ch1) Flashcards
1
Q
What is the distinguishing characteristic of Staphylococcus bacteria?
A
Catalase-positive
2
Q
How is Staphylococcus aureus differentiated from other staphylococcus species?
A
S. aureus is coagulase-positive
3
Q
Are staphylococcus sp. gram positive or gram negative bacteria?
A
Gram positive
4
Q
How are staphylococcus sp. arranged?
A
In irregular clusters and tetrads
5
Q
Does staphylococcus sp. form spores?
A
No
6
Q
Staphylococcus sp is:
a) Obligate aerobe
b) Facultative anaerobic
c) Aerotolerant
A
b
7
Q
Staphylococcus sp. are motile.
a) True
b) False
A
b
8
Q
Are staphylococcus sp. capsulated?
A
Often unencapsulated (or limited capsule) or slime layer (serotype specific)
9
Q
What are the other staphylococcus species?
A
S. aureus
S. epidermitis
S. lugdenensis
S. saprophyticus
S. haemolyticus
10
Q
Which Staphylococcal species is most pathogenic?
A
S. aureus
11
Q
Function of teichoic acid as a virulence factor?
A
Bind to fibronectin and induce immune response
12
Q
How does the capsule aid as a virulence factor?
A
Inhibits chemotaxis and phagocytosis; inhibits proliferation of mononuclear cells
13
Q
How does the slime layer aid as a virulence factor?
A
Facilitates adherence to foreign bodies
14
Q
What is teichoic acid made of?
A
Teichoic acid: polymer of polyglycerol phosphate (Glc) or polyribitol phosphate covalently anchored to PG
15
Q
What is the mode of action of Protein A?
A
Protein A is a surface protein of S. aureus which binds IgG molecules by their Fc region. In serum, the bacteria will bind IgG molecules in the wrong orientation on their surface, which disrupts opsonization and phagocytosis.
16
Q
What are the adherence proteins of S. aureus? What do they bind to?
A
Clumping factor —> binds fibrinogen
Protein A —> binds IgG
Fibronectin-binding protein —> binds fibronectin and fibrinogen
Collagen-binding protein —> binds collagen
17
Q
Which adhesive protein on S. aureus is also an invasin?
A
Fibronectin binding protein
A Staphylococcus aureus cell surface-bound protein that binds to both fibronectin and fibrinogen—It is an adhesin which enables Staphylococcus aureus to adhere to host cells of another organism, and an invasin facilitating its internalisation into these cells.
18
Q
What are the enzymes released by Staphylococcal bacteria? List their functions.
A
» Coagulase : It binds fibrinogen and converts it to insoluble fibrin, causing the staphylococci to clump or aggregate
» Staphylokinase/Fibrnolysin: Dissolves fibrin clots (bacterial dissemination)
» Hyaluronidase: Hydrolyzes hyaluronic acids in connective tissue, promoting the spread of staphylococci in tissue
» Lipases: Hydrolyzes lipids (ensure the survival of Staphylococci in the sebaceous area)
» Nucleases (DNase): Hydrolyzes DNA (provide nutrient for the bacteria), unlikely to have a pathogenic effect
19
Q
Which enzyme is unlinkely to have a direct pathogenic effect?
A
Nuclease (DNase)
20
Q
In what form is Alpha toxin produced?
A
Alpha toxin is produced in a non-toxic soluble form.
21
Q
How does Alpha toxin affect eukaryotic membranes?
A
Alpha toxin multimerizes on eukaryotic membranes, forming lytic pores that cause osmotic swelling and cell lysis. It affects various cell types, including erythrocytes, leukocytes, hepatocytes, and platelets.
22
Q
What effect does Alpha toxin have on blood vessels?
A
Alpha toxin disrupts the smooth muscle in blood vessels.
23
Q
Which cells are affected by Beta toxin?
A
Beta toxin is toxic to a variety of cells, including erythrocytes, fibroblasts, leukocytes, and macrophages.
24
Q
What is the specificity of Beta toxin?
A
Beta toxin has a specificity for sphingomyelin and lysophosphatidylcholine.
25
How does Beta toxin damage membranes?
Beta toxin damages membranes by enzymatically altering their lipid contents.
26
Which cytolytic toxin acts like a surfactant?
Delta toxin
27
What is the cytolytic activity of Delta toxin?
Delta toxin has a wide spectrum of cytolytic activity and acts as a surfactant. It disrupts cellular membranes through a detergent-like action, affecting erythrocytes, many other mammalian cells, and intracellular membrane structures.
28
What is the name of the cytotoxin that lyses neutrophils and macrophages?
Gamma toxin
29
In what form is Gamma toxin produced?
Gamma toxin is produced in a non-toxic soluble form.
30
How does Gamma toxin affect eukaryotic membranes?
Gamma toxin multimerizes on eukaryotic membranes, forming lytic pores.
31
What type of cells does the Panton-Valentine (P-V) toxin target?
Panton-Valentine (P-V) toxin is leukotoxic but does not have hemolytic activity.
32
In which type of Staphylococcus strain is Panton-Valentine (P-V) toxin typically present?
Panton-Valentine (P-V) toxin is typically present in community-acquired methicillin-resistant Staphylococcus aureus (CA MRSA).
33
What types of infections are Panton-Valentine (P-V) toxin associated with?
Panton-Valentine (P-V) toxin is associated with skin and soft tissue infections and **severe pneumonia** in children and young adults.
34
What are exfoliative toxins?
Exfoliative toxins are esterases and proteases that split the intercellular bridges in the stratum granulosum of the epidermis.
35
What is the complication caused by exfoliative toxins?
Staphylococcal scalded skin syndrome (SSSS)
36
How do exfoliative toxins contribute to Staphylococcal scalded skin syndrome (SSSS)?
Exfoliative toxins lyse neutrophils, leading to the release of lysosomal enzymes that subsequently damage the surrounding tissues, resulting in the characteristic symptoms of SSSS.
37
What is TSST-1? What is its effect on the body?
TSST-1 is a superantigen that stimulates the release of cytokines. At low concentrations, it causes the leakage of endothelial cells, while at high concentrations, it has a cytotoxic effect on the cells.
TSST-1 causes generalized systemic inflammation, produces leakage or cellular destruction of endothelial cells, and can lead to increased intestinal peristalsis and fluid loss, as well as symptoms like nausea and vomiting.
38
What is the general effect of superantigens?
Superantigens stimulate the proliferation of T cells and the release of cytokines, leading to non-specific stimulation of the immune system.
39
What are the effects of TSST-1 on the body?
TSST-1 causes generalized systemic inflammation, produces leakage or cellular destruction of endothelial cells, and can lead to increased intestinal peristalsis and fluid loss, as well as symptoms like nausea and vomiting.
40
What are the most common Enterotoxins produced by Staphylococcus aureus?
Enterotoxins A, B, and C are the most common Enterotoxins produced by Staphylococcus aureus.
41
What are the effects of Enterotoxins on the body?
Severe vomiting, diarrhea, and abdominal pain or nausea are characteristic symptoms.
42
What are the characteristics of Enterotoxins?
Enterotoxins are heat-stable and have a short incubation period.
43
What is special about Enterotoxin B?
Enterotoxin B may cause staphylococcal enterocolitis by traversing
intestinal mucosa. They can act as a superantigen.
44
What specimen should be obtained from the patient to identify endocarditis?
Blood
45
What specimen should be obtained from the patient to identify SSSS?
Nasopharynx, skin, blood
46
What specimen should be obtained from the patient to identify pneumonia?
Sputum, blood
47
What specimen should be obtained from the patient to identify staphylococcal food poisoning?
Stool, food.
48
What specimen should be obtained from the patient to identify catheter infections?
Blood, catheter tip
49
What specimen should be obtained from the patient to identify TSS?
Vaginal swab, wound, blood
50
What specimen should be obtained from the patient to identify cutaneous infections?
Skin, blood
51
What specimen should be obtained from the patient to identify septic arithritis?
Synovial fluid, blood
52
What is impetigo?
- Infection of the *epidermis*.
- *Superficial* infection that mostly affects **young children, occurs primarily on the face and limbs**
53
What is folliculitis?
- Infection of *superficial dermis*. It is a *pyogenic infection* in the hair follicles
54
What is furuncles?
Infection of *deep dermis*. It is an **extension of folliculitis**, are large, painful, raised nodules that have an underlying collection of dead and necrotic tissue
55
What are carbuncles?
Infection of deep dermis. It occur when *furuncles coalesce* and *extend to the deeper* subcutaneous tissue
56
How does impetigo initially present?
Impetigo initially starts as a small macule (flattened red spot) that develops into a pus-filled vesicle (pustule) on an erythematous base. This is caused by the action of the epidermolytic toxin.
57
Which form of impetigo is most common in infants and children younger than 2 years?
The bullous form of impetigo
58
Which form of impetigo is most common in children aged 2 to 6 years?
The nonbullous form of impetigo
59
What is a characteristic feature of impetigo?
Multiple vesicles (>1cm) at different stages of development are common due to the secondary spread of the infection to adjacent skin sites.
60
How does impetigo present finally?
Crusting
61
Is impetigo easily spread from person to person?
Yes. Impetigo is highly contagious.
62
Who is more commonly affected by Staphylococcal Scalded Skin Syndrome (SSSS)?
Neonates
63
How does SSSS present in terms of its distribution?
SSSS can present as either generalized or localized. *Localized forms can resemble bullous impetigo*.
64
What is the initial characteristic feature of SSSS?
SSSS is characterized by the abrupt onset of a perioral erythema (redness and inflammation around the mouth) that rapidly spreads over the entire body within 2 days.
65
What is the main characteristic of SSSS?
SSSS is characterized by exfoliation of the skin, which is referred to as exfoliative dermatitis.
66
SSSS is commonly fatal. True or false?
False. The mortality rate of SSSS is low, usually less than 5%.
67
Bacteria is always present in SSSS. True or false?
False. Bacteria may or may not be present in cases of SSSS.
68
Which toxins are associated with Toxic Shock Syndrome (TSS)?
TSST-1 and enterotoxins (specifically, enterotoxin B and C) produced by certain strains of S. aureus.
69
How does localized growth of toxin-producing strains of S. aureus contribute to TSS?
In TSS, localized growth of toxin-producing strains of S. aureus in the vagina or a wound can occur, followed by the release of the toxins into the bloodstream. TSST-1 is particularly induced in the vaginal environment.
70
What are the clinical manifestations of TSS?
Clinical manifestations of TSS start abruptly and include fever, hypotension, and a diffuse, macular erythematous rash. Desquamation (skin peeling) occurs on the entire skin, including the palms and soles. Multiple organ systems, such as the central nervous, gastrointestinal, hematologic, hepatic, musculature, and renal systems, can also be involved.
71
What is purpura fulminans?
Purpura fulminans is a particularly virulent form of toxic shock syndrome. It is characterized by *large purpuric skin lesions* (purple discoloration due to bleeding under the skin), fever, hypotension, and **disseminated intravascular coagulation (DIC)**.
72
What is Erisepelas? What are its characteristics?
• Superficial cellulitis with prominent lymphatic involvement
*Characteristics:*.
• Soreness associated with skin infection
• Well demarcated than cellulitis
• Affects the skin rather than underlying tissue
• Peau d’orange appearance
• Clinical signs of sepsis and fever often present
73
What is cellulitis? What are its characteristics?
Cellulitis is a warm, tender, erythematous, and edematous plaque with *ill-defined borders* that **expands rapidly**.
The major findings are local *erythema and tenderness, frequently with lymphangitis and regional lymphadenopathy*
74
Which cutaneous infection is frequently associated with lymphangitis and regional lymphadenopathy?
Cellulitis
75
What are the differences between cellulitis and erisepelas?
- Cellulitis is the infection of the dermis (inner skin) while erisepelas affects the skin rather than underlying tissue.
- Cellulitis have ill-defined borders while erisepelas manifests well demarcated borders
76
What is Fasciitis? What are its common clinical manifestations?
Fascitis:
Necrotizing fasciitis, while rare, is the most aggressive manifestation of skin and soft
tissue infections and can cause significant morbidity and mortality
» Patients often reportedly complain of aches, chills, and feverishness
77
Which staphylococcal intoxication is usually self-limiting?
Gastroenteritis
78
Can adding salt to a potato salad prevent gastroenteritis? What about heating the food?
No. S. aureus is halophilic, meaning it can tolerate high salt concentrations. Its toxins are also heat-stable.
79
Which heat-stable enterotoxins are commonly associated with food poisoning caused by S. aureus?
Enterotoxin A, B, and C are the most common heat-stable enterotoxins associated with S. aureus-related food poisoning.
80
How quickly does the disease onset occur in S. aureus-related food poisoning?
The onset of disease is abrupt and rapid, with a mean incubation period of around 4 hours.
81
What is the recommended treatment for staphylococcal food poisoning?
Treatment for staphylococcal food poisoning primarily focuses on the relief of abdominal cramping and diarrhea and the replacement of fluids. Antibiotic therapy is generally not indicated.
82
What are some common sources of bacteremia caused by Staphylococcus aureus?
Intravenous devices, surgical treatment, dialysis, or as a complication of a previous infection, such as a skin infection.
83
How can bacteremia lead to endocarditis?
The bacteria can enter the bloodstream and attach to damaged or abnormal heart valves.
84
What are the symptoms of endocarditis?
Fever, chills, pleural chest pain due to pulmonary embolism (blockage of blood vessels in the lungs), and potential spread to other organs.
85
What percentage of endocarditis cases are parenteral (related to operations and/or catheterization)?
Approximately 50% of endocarditis cases are related to parenteral routes.
86
Who is at higher risk of developing endocarditis?
People with a history of heart valve problems
87
What is the prognosis for endocarditis without intervention?
Poor
88
How does staph. aureus infect the heart through a damaged heart valve (and cause endocarditis)?
When there is damage or inflammation to the heart valve, platelets in the blood can become activated and form a clot or thrombus. Bacteria can take advantage of this process by *adhering to the platelet-fibrin matrix* that forms on the damaged valve surface.
89
What are some complications that can occur as a result of embolization of vegetation particles and systemic hematogenous spreading of pathogens in endocarditis?
1. Ischemic stroke: Blockage of blood vessels in the brain leading to reduced blood flow and tissue damage.
2. Cerebral hemorrhage: Bleeding in the brain due to the rupture of blood vessels.
3. Meningitis or meningeal reaction: Inflammation of the membranes surrounding the brain and spinal cord.
4. Brain abscess: A localized collection of pus in the brain tissue.
5. Mycotic aneurysm: An aneurysm (ballooning of a blood vessel) caused by infection, which can lead to rupture and bleeding.
90
In which setting is S. aureus a more significant cause of pneumonia?
In the hospital setting. S. aureus accounts for 30% of HAP and less than 10% of CAP.
91
Which group of individuals is particularly prone to aspiration pneumonia?
Aspiration pneumonia is more common in the very young, the elderly, and patients with conditions such as cystic fibrosis, influenza, and chronic obstructive pulmonary disease (COPD).
92
What can aspiration pneumonia lead to?
Aspiration pneumonia can lead to the formation of lung abscesses.
93
Which type of toxin causes aspiration pneumonia?
Panton-Valentine leukocidin (PVL)
94
How does pneumonia occur in patients with bacteremia or endocarditis? What type of pneumonia is this.
*Pneumonia is common in patients with bacteremia or endocarditis.* In these cases, pneumonia may be **caused by MRSA (methicillin-resistant Staphylococcus aureus)** present in the blood. This type of pneumonia is hematogenous pneumonia (meaning the bacteria was carried to the lungs via the bloodstream).
95
What is common for patients with endocarditis or bacteremia?
Pneumonia (Hematogenous)
96
What are the side effects of hematogenous pneumonia.
Necrotizing pneumonia → Hemoptysis → Septic shock → Death
97
How does methicillin susceptible S. aureus (MSSA) get converted to methicillin resistant S. aureus (MRSA) and **produce PVL toxin**?
1. A PVL phage infects MSSA integrating its DNA
2. The prophage containing PVL genes is now capable of encoding PVL toxins
3. Methicillin resistant cassette (SCCmec IV or V) enters cell and integrates into chromosome
4. MSSA becomes MRSA and produced PVL toxins
98
What are common consequences of osteomyelitis after trauma or surgery?
Osteomyelitis can occur after trauma or surgery. In these cases, it is often accompanied by inflammation and **purulent (pus) drainage from the wound or sinus tract overlying the infected bone.**
99
How does hematogenous spread occur in children with osteomyelitis?
Hematogenous spread of osteomyelitis in children is usually the result of a cutaneous staphylococcal infection. It typically affects the *metaphyseal area* of long bones, which is a highly vascularized area of bony growth.
100
What are some symptoms of osteomyelitis?
Symptoms of osteomyelitis include chills, high fever, malaise (general discomfort or unease), bone pain, and swelling.
101
Where do coagulase-negative staphylococci (CoNS) commonly reside in the human body?
Coagulase-negative staphylococci (CoNS) can be found as commensal bacteria on the human skin, mucous membranes (such as S. hominis and S. epidermidis), and the vaginal tract (such as S. saprophyticus).
102
How do coagulase-negative Staphylococcus species compare to coagulase-positive S. aureus in terms of virulence?
Coagulase-negative Staphylococcus species are generally less virulent than coagulase-positive S. aureus. They are almost never pathogenic in healthy individuals.
103
Why have CoNS infections become a significant medical concern?
CoNS infections have become a major medical problem due to the common use of long-dwelling catheters and shunts for the medical management of critically ill patients. CoNS species can form biofilms on these medical devices, leading to persistent infections that are often challenging to treat.
104
In which areas of the body can Staphylococcus lugdunensis cause infections?
Staphylococcus lugdunensis can cause infections in various areas of the body, including:
- Cardiovascular infections
- Osteomyelitis and prosthetic joint infections
- Bloodstream infections
- Skin and soft-tissue infections
- Central nervous system infections
- Peritonitis
- Endophthalmitis (inflammation of the inner eye) and urinary tract infections.
105
What type of endocarditis can Staphylococcus lugdunensis cause?
Staphylococcus lugdunensis can cause endocarditis, which can affect both prosthetic heart valves and native heart valves. Staphylococcus epidermidis is another species that can cause endocarditis, particularly in cases involving native heart valves.
106
How is endocarditis caused by Staphylococcus lugdunensis typically acquired?
Endocarditis caused by Staphylococcus lugdunensis is usually acquired parenterally, such as during valve replacement therapy. It is considered a hospital-acquired infection.
107
What type of infection is a person with a prosthetic joint at risk of?
Prosthetic joint infection caused by Staphylococcus lugdunensis.
108
Which species of Staphylococcus is frequently associated with urinary tract infections (UTIs) in young, sexually active women?
S. saprophyticus
109
What are some common symptoms of urinary tract infections caused by Staphylococcus saprophyticus?
Common symptoms of urinary tract infections caused by Staphylococcus saprophyticus include dysuria (painful urination), pyuria (presence of pus in urine), and bacteriuria (presence of bacteria in urine).
