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110 Cards in this Set
- Front
- Back
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Gram-stain and shape/arrangement of the members of the Staphylococcus genus |
Gram-positive cocci arranged in "grape-like" clusters |
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Do the staphylococci have flagella? |
No |
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To which metabolic class do the staphylococci belong? |
Facultative anaerobes |
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Staphylococci grow best (aerobically or anaerobically?) |
Aerobically |
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Unlike streptococci, staphylococci produce _____ |
Catalase |
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What is the most virulent species of staphylococci? |
Staphylococcus aureus |
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What separates S. aureus from the other, less virulent species of staphylococci? |
The ability to form coagulase |
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Staphylococci other than S. aureus are called... |
Coagulase-negative staphylococci (CoNS) |
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Describe the appearance of S. aureus in growing cultures |
Regular in size
Fit together in clusters |
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Describe the appearance of S. aureus in older cultures, in resolving lesions, or in the presence of some antibiotics |
Variable in size
Many lose their Gram-positivity |
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Examples of surface proteins found on S. aureus |
Clumping factor (Clf)
Fibronectin-binding proteins (FnBPs)
Protein A |
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What does clumping factor (Clf) bind? |
Fibrinogen |
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What is the purpose of clumping factor (Clf) and fibronectin-binding proteins (FnBPs)? |
They likely play a role in the early stages of infection |
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What is the role of protein A? |
Binds the Fc portion of IgG molecules (leaving the Fab portion directed externally)
Stimulates cytokines (TNF-α), platelets, and B cells
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Describe the appearance of S. aureus colonies on blood agar |
White or golden colonies with a rim of clear β-hemolysis |
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What is the role of coagulase? |
It binds and activates prothrombin, leading to the formation of a fibrin clot |
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What cytolytic toxins are produced by S. aureus? |
α-toxin, β-toxin, δ-toxin, and γ-toxin |
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What is the most important toxin produced by S. aureus? |
α-toxin |
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What is another name for α-toxin? |
α-hemolysin |
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Do CoNS secrete α-toxin? |
No |
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What is the function of α-toxin? |
It lyses cells by the formation of transmembrane pores |
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What type of cell is not affected by α-toxin? |
Neutrophils |
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Example of a cell type affected by α-toxin |
Keratinocytes |
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What pore-forming toxin is active against neutrophils and causes tissue necrosis? |
Panton-Valentine leukocidin (PVL) |
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What percentage of S. aureus clinical isolates produces PVL? |
<10% |
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What is exfoliatin? |
A protease produced by a small number of S. aureus strains that binds to a specific cell membrane ganglioside found only in the stratum granulosum of the keratinized epithelium of the skin |
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What does exfoliatin do? |
It causes intercellular splitting of the epidermis between the stratum spinosum and stratum granulosum by acting on desmosomes |
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How can the body prevent the effects of exfoliatin? |
Circulating antibodies |
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What are the most important staphylococcal superantigen toxins (StaphSAgs) in human disease? |
Staphylococcal enterotoxins (SEA, SEB, etc.)
Toxic shock syndrome toxin (TSST-1) |
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What percentage of S. aureus strains produces any StaphSAgs? |
<20% |
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What is the result of superantigen release? |
Massive cytokine release |
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What is the primary symptom of the S. aureus enterotoxins? |
Vomiting |
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How do the S. aureus enterotoxins cause vomiting? |
By stimulating reflexes in the abdominal viscera, which are transmitted to medullary emitic centers via the vagus nerve |
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Can boiling or digestive enzymes destroy S. aureus enterotoxins? |
No |
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Infections produced by S. aureus are typified by... |
Acute, aggressive, locally destructive purulent (pus-producing) lesions (e.g. boil) |
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What is the basic human habitat of S. aureus? |
The anterior nares |
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What percentage of the population carries S. aureus in the anterior nares at any give time? |
10-30% |
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How is S. aureus spread from the anterior nares to exposed skin or clothing? |
Face touching
Nose picking |
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How can the spread of S. aureus be blocked? |
Handwashing |
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How can S. aureus gain deeper access once present on the skin? |
Skin appendages (hairs, sebaceous glands, sweat glands, etc.)
Trauma |
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Are we able to distinguish strains of S. aureus with increased virulence? |
No |
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Most S. aureus infections acquired in the community are... |
Autoinfections with strains that the subject carries in the anterior nares, on the skin, or both |
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Community outbreaks are usually associated with... |
Poor hygiene
Fomite transmission |
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Can S. aureus survive drying? |
Yes |
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What is the significance of S. aureus' ability to survive drying? |
Clothing contaminated with pus can cause recurrent skin infections |
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How is S. aureus spread in hospitals? |
On the hands of hospital personnel |
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What are some potential sources for a hospital outbreak of S. aureus infection? |
A patient with an overt or unapparent staphylococcal infection that has undergone surgical or other invasive procedures
A nasal or perineal carrier among medical, nursing, or other hospital personnel
A medical attendant with a staphylococcal lesion (e.g. a boil) |
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What kinds of foods are often contaminated with S. aureus enterotoxins? |
Moist and rich foods (e.g. red meat, poultry, creamy dishes) |
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How might a dish become contaminated with S. aureus enterotoxin? |
The dish is prepared by a nasal carrier or someone with a staphylococcal lesion and is then left unrefrigerated for hours between preparation and serving |
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Can a dish be rid of S. aureus enterotoxins by cooking? |
No |
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What are the steps involved in the formation of a primary infection by S. aureus? |
1) Fibronectin-binding proteins (FnBPs) bind to fibronectin on cell surfaces
2) α-Toxin destroys keratinocytes and other cells, allowing the lesion to expand
3) Coagulase, clumping factor (Clf), protein A, and PV leukocidin compromise host defenses |
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How is a boil formed? |
Inflammatory cells, fibrin, and other tissue components form a walled-off compartment of pus |
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What is a carbuncle? |
A red, swollen, and painful cluster of boils connected under the skin |
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What determines the fate of a S. aureus lesion? |
The ability of the host to localize the process, which differs depending on the tissue involved |
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How are S. aureus lesions resolved in the skin? |
Granulation and fibrosis |
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What are common outcomes of S. aureus lesions in the lung, kidney, bone, and other organs? |
Tissue destruction (cavities and massive necrosis)
Spread with satellite foci |
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What happens when staphylococci spread to the bloodstream? |
Spread to distant organs
Shedding of cell wall peptidoglycans, producing massive complement activation, leukopenia, thrombocytopenia, and septic shock |
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Is there an infection in staphylococcal food poisoning? |
No |
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After ingestion, preformed enterotoxin exerts its effects within... |
Hours |
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After a primary infection is established, when does the in vivo production of exfoliative toxin begin? |
At least a few days after the primary infection is established |
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What are two diseases caused by exfoliative toxin? |
Scalded skin syndrome
Bullous impetigo |
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In general, how do toxins produced by S. aureus reach the circulation? |
Absorption at the primary infection site |
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In terms of absorption across mucosal membranes, how does TSST-1 compare to other StaphSAgs? |
It is more readily absorbed |
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Is TSST-1 the only StapSAg that causes toxic shock syndrome? |
No |
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What causes menstruation-associated toxic shock syndrome? |
The relatively high pH in the vagina during menstruation and the composition of high-absorbency tampons provide conditions that enhance both the growth of staphylococci and the production of TSST-1 |
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Why is menstruation-associated toxic shock syndrome improbable? |
<15% of women carry S. aureus in their vaginal flora, and <20% of these have the potential to produce TSST-1 |
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What evidence points to poor immunity against staphylococcal infection? |
Relapsing infections |
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Why do women suffering from menstruation-associated TSS often have low or absent antibody levels to TSST-1? |
SAgs stimulate Th1 responses with minimal Th2 component |
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Where does a boil usually develop? |
In a hair follicle, sebaceous gland, or sweat gland |
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How does a boil usually resolve? |
By spontaneous drainage of pus |
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Where do carbuncles usually form? |
On the back of the neck |
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Why are carbuncles more serious than boils? |
They may result in bloodstream invasion (bacteremia) |
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What is chronic furunculosis? |
Repeated attacks of boils caused by the same strain of S. aureus |
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Is chronic furunculosis associated with immune dysfunction? |
In some cases, but not most |
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What is responsible for much of the inflammation and necrosis that develops with chronic furunculosis? |
Delayed-type hypersensitivity to staphylococcal products |
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How does S. aureus spread to deep tissues (bones, joints, deep organs, etc.)? |
Bacteremic spread from a skin lesion |
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What percentage of acute osteomyelitis cases in children are caused by S. aureus? |
90% |
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What are predisposing factors for S. aureus infection of deep tissues? |
Diabetes
Leukocyte defects
General reduction of host defenses by alcoholism, malignancy, old age, or steroid or cytotoxic therapy |
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What subgroup of patients is particularly vulnerable to bacteremic spread and severe S. aureus infections, such as endocarditis? |
IV drug users |
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In patients with scalded skin syndrome, is S. aureus isolated from sites with erythema and intraepidermal desquamation? |
No |
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Scalded skin syndrome is most common among what age groups? |
Neonates and children <5 years of age |
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What areas tend to be affected first in scalded skin syndrome? |
Face
Axilla
Groin |
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What two diseases are considered milder versions of scalded skin syndrome? |
Staphylococcal scarlet fever
Bullous impetigo |
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What are some early symptoms of toxic shock syndrome? |
High fever
Vomiting
Diarrhea
Sore throat
Muscle pain |
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What are the late symptoms of toxic shock syndrome? |
Severe shock
Renal and hepatic damage
Skin rash and desquamation |
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Does staphylococcal food poisoning cause a fever? |
No |
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What are the primary diagnostic methods for S. aureus infection? |
Gram stain
Culture on blood agar
Catalase and coagulase tests |
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How are deep S. aureus infections, such as osteomyelitis, diagnosed? |
Aspirates and blood cultures |
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Why are antibiotic susceptibility tests used when diagnosing S. aureus infections? |
The emerging resistance to multiple antimicrobials (e.g. methicillin-resistant S. aureus or MRSA) |
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How are superficial S. aureus lesions treated? |
They resolve spontaneously |
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How are deep S. aureus infections treated? |
A combination of surgical drainage and antimicrobials |
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What antibiotics are used to treat S. aureus infections? Why? |
Penicillinase-resistant penicillins (β-lactams) and first-generation cephalosporins (methicillin) because of the high-frequency of penicillin resistance |
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What percentage of S. aureus strains is resistant to penicillin? |
>80% |
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How is MRSA treated? |
Vancomycin, clindamycin, or erythromycin |
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Why are most strains of S. aureus penicillin-resistant? |
Selection of penicillinase-positve strains |
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Where is the penicillinase gene located? |
On a plasmid |
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Why are some strains of S. aureus resistant to methicillin? |
Alterations in the β-lactam target, the peptidoglycan transpeptidases (penicillin-binding proteins or PBPs) |
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Acquisition of which gene results in methicillin resistance? |
mecA |
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What clone of community-acquired MRSA produces PV leukocidin? |
USA 300 |
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How might the spread of S. aureus be prevented? |
Washing clothes and bedding at 70° C or higher
The use of antistaphylococcal soaps that increased the bactericidal activity of the skin
Nasal creams containing topical antimicrobials and oral therapy with antimicrobials that are concentrated within phagocytes and nasal secretions |
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How is S. aureus infection prevented during high-risk surgery? |
Chemoprophylaxis with methicillin or vancomycin |
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Do the CoNS produce α-toxin, exfoliatin, or any of the StaphSAgs? |
No |
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What is the most common CoNS species isolated from human infections? |
S. epidermidis |
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What CoNS species is a significant cause of UTIs, and how can it be distinguished from other urinary isolates? |
S. saprophyticus
Novobiocin resistance test |
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S. epidermidis is a normal ____ of the skin, anterior nares, and ear canals |
Commensal |
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How does S. epidermidis cause infection? |
By colonizing implanted medical devices |
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Why is S. epidermidis able to colonize implanted medical devices? |
It forms biofilms |
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What is the most commonly colonized implanted medical device? |
The IV catheter |
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What is the usual habitat of S. saphrophyticus? |
GI tract |
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Is S. saphrophyticus the most common cause of actute UTI among sexually active women? |
No, it is second (E. coli is first) |
