BMI10 - Staphylococci

What biochemical trait distinguishes Staphylococci from Streptococci?

Staphylococci are catalase-positive, while Streptococci are catalase-negative.

What is the Gram stain morphology of Staphylococcus aureus?

Staphylococcus aureus is a Gram-positive coccus that forms clusters.

Is Staphylococcus aureus coagulase-positive or coagulase-negative?

Staphylococcus aureus is coagulase-positive.

What does the coagulase enzyme do in Staphylococcus aureus?

Coagulase converts fibrinogen to fibrin, coating the bacterial surface with fibrin to help camouflage the bacteria from the immune system.

What type of oxygen requirements does Staphylococcus aureus have?

Staphylococcus aureus is a facultative anaerobe that grows best aerobically.

Where is Staphylococcus aureus commonly found in humans?

Staphylococcus aureus commonly colonizes the skin and anterior nares.

What types of infections are commonly caused by Staphylococcus aureus?

Staphylococcus aureus commonly causes pyogenic infections that produce pus.

What are the major epidemiologic settings for Staphylococcus aureus infections?

Staphylococcus aureus infections can be hospital-acquired or community-acquired.

What percentage of adults may have continual nasal colonization with Staphylococcus aureus for a year or more?

Approximately 20% of adults have continually positive nasal cultures for a year or more.

What percentage of people become colonized with Staphylococcus aureus at some point during a year?

Approximately 60% of people become colonized during a given year.

How is Staphylococcus aureus commonly spread?

Staphylococcus aureus spreads by hands, auto-infection, fomites, and environmental contamination.

Why are healthcare workers at increased risk for Staphylococcus aureus colonization?

Healthcare workers have higher exposure to colonized patients and contaminated environments, leading to carriage rates of 50–70%.

Why is Staphylococcus aureus a major problem in healthcare facilities?

Staphylococcus aureus survives well in the environment and spreads through hands, fomites, and invasive medical procedures.

Why should people with boils avoid working with food or surgical patients?

Boils shed large amounts of Staphylococcus aureus that can contaminate food or infect vulnerable patients.

What is the role of the capsule in Staphylococcus aureus virulence?

The capsule inhibits chemotaxis and phagocytosis, helping the bacteria evade immune defenses.

What is the function of fibronectin-binding protein (Fbp) in Staphylococcus aureus?

Fibronectin-binding protein allows Staphylococcus aureus to adhere to fibrin, fibrinogen, wounds, and fibronectin-coated plastic medical devices.

Which virulence factors of Staphylococcus aureus are classified as exotoxins?

Hemolysins, leukocidins, enterotoxins, TSST-1, and exfoliatin are exotoxins.

What is the function of alpha-toxin in Staphylococcus aureus?

Alpha-toxin damages many types of host cells and is produced by most strains causing human disease.

Which Staphylococcus aureus toxin acts as a superantigen?

Toxic Shock Syndrome Toxin-1 (TSST-1) acts as a superantigen.

How do superantigens such as TSST-1 cause disease?

Superantigens activate massive numbers of T cells, causing excessive cytokine release, hypotension, and multi-organ failure.

Approximately how many T cells can TSST-1 stimulate?

TSST-1 can stimulate approximately 1 in 5 T cells.

Which Staphylococcus aureus toxin causes food poisoning?

Staphylococcal enterotoxin causes food poisoning.

What is the role of catalase in Staphylococcus aureus?

Catalase breaks down hydrogen peroxide, protecting the bacteria from oxidative killing.

How does hyaluronidase contribute to Staphylococcus aureus virulence?

Hyaluronidase cleaves hyaluronic acid in the extracellular matrix, allowing bacterial spread through tissues.

Why is hyaluronidase called a “spreading factor”?

Hyaluronidase breaks down extracellular matrix material, allowing bacteria to invade deeper tissues.

What does fibrinolysin (staphylokinase) do?

Fibrinolysin dissolves fibrin clots, helping Staphylococcus aureus spread through tissues.

What is the role of lipases in Staphylococcus aureus infections?

Lipases break down oils and fats in skin secretions, providing nutrients in hair follicles.

What are beta-lactamases in Staphylococcus aureus?

Beta-lactamases, also called penicillinases, are enzymes that break down beta-lactam antibiotics.

What is folliculitis?

Folliculitis is inflammation of a hair follicle characterized by red bumps or pus-filled pimples.

What is a furuncle?

A furuncle, or boil, is a painful infection extending from a hair follicle into adjacent tissues with pus drainage.

What is a carbuncle?

A carbuncle is a cluster of furuncles that forms the most severe type of hair follicle infection.

Which hair follicle infection caused by Staphylococcus aureus is the most severe?

A carbuncle is the most severe form of hair follicle infection.

What systemic signs are commonly associated with carbuncles?

Carbuncles are commonly associated with fever and other systemic signs of infection.

What is impetigo?

Impetigo is a localized cutaneous infection characterized by pus-filled vesicles on an erythematous base.

Which other bacterium commonly causes impetigo besides Staphylococcus aureus?

Group A Streptococcus can also cause impetigo.

Why may antibiotic selection for impetigo need to cover Staphylococcus aureus?

Because Staphylococcus aureus may produce beta-lactamase and may be involved in mixed infections.

What is the tissue manifestation of pyogenic Staphylococcus aureus infections?

The tissue manifestation is suppuration, which is the formation of pus.

What is Staphylococcal Scalded Skin Syndrome (SSSS)?

Staphylococcal Scalded Skin Syndrome is a toxin-mediated disease characterized by blistering and peeling of the skin.

Which toxin causes Staphylococcal Scalded Skin Syndrome?

Exfoliatin causes Staphylococcal Scalded Skin Syndrome.

How does exfoliatin cause skin peeling in Staphylococcal Scalded Skin Syndrome?

Exfoliatin disrupts binding between epidermal cells, causing blistering and peeling of the outer epidermis.

Which age group is most commonly affected by Staphylococcal Scalded Skin Syndrome?

Newborns and children younger than 5 years old are most commonly affected.

How does Staphylococcal Scalded Skin Syndrome typically begin?

It usually begins with localized perioral erythema.

Why does Staphylococcal Scalded Skin Syndrome resemble burns?

The skin becomes red, wrinkled, blistered, tender, and peels easily due to exfoliatin activity.

Why does Staphylococcal Scalded Skin Syndrome usually not cause scarring?

Only the superficial epidermal layer is shed, leaving deeper skin layers intact.

What contributes to mortality in Staphylococcal Scalded Skin Syndrome?

Fluid loss and secondary infections contribute to mortality.

How is Staphylococcal Scalded Skin Syndrome treated?

Treatment includes fluid replacement and antibiotics.

What usually happens with prompt treatment of Staphylococcal Scalded Skin Syndrome?

Quick treatment usually results in full recovery.

How do Staphylococcus aureus wound infections commonly occur?

Wound infections occur when skin flora are introduced into wounds during trauma or surgery.

Why do foreign materials promote Staphylococcus aureus wound infections?

Foreign materials such as splinters or stitches provide surfaces that help bacteria survive and persist.

Why can Staphylococcus aureus wound infections become difficult to treat?

They may progress into chronic anaerobic mixed infections.

How can Staphylococcus aureus wound infections be prevented?

Thorough wound cleansing and aseptic technique help prevent infection.

What was the original major association with Staphylococcal Toxic Shock Syndrome?

It was originally associated with highly absorbent tampon use.

What other setting can lead to Staphylococcal Toxic Shock Syndrome?

Post-operative wound infections can also lead to Toxic Shock Syndrome.

Which toxin causes Staphylococcal Toxic Shock Syndrome?

TSST-1 causes Staphylococcal Toxic Shock Syndrome.

What are common symptoms of Staphylococcal Toxic Shock Syndrome?

Symptoms include fever, rash, desquamation, hypotension, and multi-organ failure.

What can happen if Staphylococcal Toxic Shock Syndrome is untreated?

Untreated disease can progress to coma and death.

How is Staphylococcal Toxic Shock Syndrome treated?

Treatment includes penicillinase-resistant antibiotics and supportive care.

What is Staphylococcal food poisoning?

Staphylococcal food poisoning is an intoxication caused by ingestion of preformed enterotoxin in food.

Why is Staphylococcal food poisoning considered an intoxication rather than an infection?

Disease symptoms result from ingestion of toxin rather than bacterial growth in the body.

What conditions favor production of Staphylococcal enterotoxin in food?

Enterotoxin is commonly produced in unrefrigerated or undercooked food.

Why is Staphylococcal enterotoxin dangerous even after reheating food?

The enterotoxin is heat-stable and resistant to digestive enzymes.

What is the incubation period for Staphylococcal food poisoning?

Symptoms typically begin 30 minutes to 6 hours after ingestion.

What are the symptoms of Staphylococcal food poisoning?

Symptoms include sudden nausea, vomiting, abdominal cramps, and diarrhea.

How long do symptoms of Staphylococcal food poisoning usually last?

Symptoms usually resolve within one day.

Which foods are at highest risk for Staphylococcal food poisoning?

Foods handled extensively after cooking and not reheated are highest risk.

Why are antibiotics not used to treat Staphylococcal food poisoning?

There is no active infection, only toxin-mediated illness.

What is the primary treatment for Staphylococcal food poisoning?

Fluid replacement is the primary treatment.

What bacterial process is targeted by beta-lactam antibiotics?

Beta-lactam antibiotics target bacterial cell wall synthesis.

How do beta-lactam antibiotics inhibit bacterial cell wall synthesis?

They inhibit penicillin-binding proteins that crosslink peptidoglycan.

Why are beta-lactam antibiotics only bactericidal against growing bacteria?

Only actively growing bacteria are synthesizing new peptidoglycan cell wall.

What are the major antibacterial drug targets in bacteria?

Major targets include cell wall synthesis, protein synthesis, nucleic acid synthesis, metabolic pathways, and cell membranes.

How did penicillin resistance arise in Staphylococcus aureus?

Staphylococcus aureus acquired beta-lactamase enzymes that destroy penicillin.

What percentage of hospital Staphylococcus aureus strains remain sensitive to penicillin?

Fewer than 10–20% of hospital strains remain sensitive to penicillin.

What is another name for beta-lactamase?

Beta-lactamase is also called penicillinase.

How does beta-lactamase inactivate penicillin?

Beta-lactamase cleaves the beta-lactam ring of penicillin.

Why are beta-lactamase-resistant antibiotics needed for Staphylococcus aureus infections?

Most Staphylococcus aureus strains produce beta-lactamase enzymes that destroy standard penicillins.

What are examples of beta-lactamase-resistant antibiotics?

Methicillin, nafcillin, oxacillin, and dicloxacillin are beta-lactamase-resistant antibiotics.

What is Augmentin?

Augmentin is a combination of amoxicillin and clavulanic acid, a beta-lactamase inhibitor.

How does clavulanic acid improve antibiotic effectiveness?

Clavulanic acid inhibits beta-lactamase enzymes, protecting the antibiotic from degradation.

What is MRSA?

MRSA is methicillin-resistant Staphylococcus aureus that is resistant to methicillin and many other antibiotics.

What protein mediates methicillin resistance in MRSA?

Methicillin resistance is mediated by MecA, also called PBP2a.

How does MecA cause methicillin resistance?

MecA alters the penicillin-binding protein target so methicillin can no longer bind effectively.

What are the two antibiotic resistance mechanisms emphasized for Staphylococcus aureus?

Antibiotic inactivation by beta-lactamase and altered binding targets such as modified PBPs.

Where is hospital-acquired MRSA most commonly encountered?

Hospital-acquired MRSA is commonly encountered in hospitals and nursing homes.

How is community-acquired MRSA usually transmitted?

Community-acquired MRSA spreads through skin-to-skin contact, cuts, fomites, crowded living conditions, and poor hygiene.

How does community-acquired MRSA most commonly present clinically?

Community-acquired MRSA usually presents as boils or abscesses.

What are common features of CA-MRSA skin infections?

CA-MRSA infections are red, swollen, painful, warm, and may drain pus.

What serious complications can develop from CA-MRSA infections?

CA-MRSA can spread into the bloodstream or cause pneumonia.

How are MRSA infections diagnosed?

MRSA infections are diagnosed by bacterial culture.

What procedure is often necessary for MRSA abscess treatment?

Incision and drainage are often required.

What intravenous antibiotic is commonly used for hospitalized MRSA patients?

Intravenous vancomycin is commonly used.

What oral antibiotics may be used for outpatient MRSA infections?

Clindamycin, trimethoprim-sulfamethoxazole, and doxycycline may be used.

What is VRSA?

VRSA is vancomycin-resistant Staphylococcus aureus.

Where was the first United States case of VRSA identified?

The first US VRSA case was identified in Michigan in 2002.

What underlying conditions did the first US VRSA patient have?

The patient had diabetes, peripheral vascular disease, and chronic renal failure.

What organism besides VRSA was isolated from the patient’s chronic foot ulcer in the first US VRSA case?

Vancomycin-resistant Enterococcus (VRE) and Klebsiella oxytoca were also isolated.

How was the first US VRSA case treated?

The patient was treated with aggressive wound care and trimethoprim-sulfamethoxazole.

How is Staphylococcus epidermidis differentiated biochemically from Staphylococcus aureus?

Staphylococcus epidermidis is coagulase-negative, unlike Staphylococcus aureus which is coagulase-positive.

When is Staphylococcus epidermidis particularly problematic clinically?

Staphylococcus epidermidis is problematic in patients with implanted medical devices.

What virulence property makes Staphylococcus epidermidis difficult to eradicate from medical devices?

Staphylococcus epidermidis forms biofilms on medical devices.