Staphylococci Flashcards
Self-review for board exams (167 cards)
1
Q
What are the general characteristics of staphylococci?
A
Catalase-producing, gram-positive cocci, appearing singly, in pairs, or in clusters; nonmotile; non–spore-forming; aerobic or facultatively anaerobic (except S. saccharolyticus).
2
Q
Where does the name Staphylococcus come from?
A
From the Greek word staphyle, meaning “bunches of grapes,” referring to their clustered appearance.
3
Q
Can staphylococci be differentiated from other gram-positive cocci by microscopy alone?
A
No, microscopy alone cannot definitively differentiate staphylococci from other gram-positive cocci.
4
Q
What family do staphylococci belong to?
A
The family Staphylococcaceae.
5
Q
How are staphylococci similar to micrococci?
A
Both are catalase-producing, coagulase-negative, gram-positive cocci, and part of the skin’s normal flora.
6
Q
How can micrococci be differentiated from coagulase-negative staphylococci (CoNS)?
A
Through distinct characteristics such as yellow pigment production and biochemical testing.
7
Q
Name some other gram-positive cocci recovered with staphylococci.
A
Rothia mucilaginosa, Aerococcus, and Alloiococcus otitis.
8
Q
Describe the colony appearance of staphylococci after 18-24 hours of incubation.
A
Medium-sized (4–8 mm), cream-colored, white, or rarely light gold, with a “buttery-looking” appearance.
9
Q
What are small colony variants of staphylococci?
A
Rare, fastidious strains requiring special growth factors, forming colonies 1/10 the size of wild-type after ≥48 hours.
10
Q
What test is used to differentiate staphylococcal species?
A
The coagulase test – positive results in clot formation due to staphylocoagulase.
11
Q
Which species are coagulase-positive?
A
S. aureus, S. intermedius, S. delphini, S. lutrae, and some strains of S. hyicus.
12
Q
What is clumping factor and which species may cause confusion in coagulase testing?
A
Clumping factor causes agglutination in plasma; S. lugdunensis and S. schleiferi may be mistaken for coagulase-positive staphylococci.
13
Q
What is the most clinically significant staphylococcal species?
A
Staphylococcus aureus.
14
Q
What are coagulase-negative staphylococci (CoNS)?
A
Staphylococcal species that do not produce coagulase; includes species like S. epidermidis, S. saprophyticus, S. haemolyticus, and S. lugdunensis.
14
Q
What diseases are associated with S. aureus?
A
Cutaneous infections, abscesses, bacteremia, septicemia, food poisoning, scalded skin syndrome (SSS), and toxic shock syndrome (TSS).
15
Q
Which CoNS species is most associated with UTIs in young women?
A
Staphylococcus saprophyticus.
16
Q
Which CoNS species is a common cause of nosocomial infections?
A
Staphylococcus epidermidis.
17
Q
Why can S. lugdunensis be mistaken for S. aureus?
A
It may give a positive result in traditional slide coagulase tests due to clumping factor.
18
Q
What infections can S. lugdunensis cause?
A
Catheter-related bacteremia and endocarditis; it can be aggressively infective.
19
Q
How many recognized species of CoNS are there?
A
More than 40 recognized species.
20
Q
Where are CoNS species commonly found?
A
On the skin and mucous membranes of humans
21
Q
some species have site specificity
A
e.g., S. capitis – head, S. auricularis – ear
21
Q
Which Staphylococcus species is found in the ear?
A
S. auricularis
22
Q
Which Staphylococcus species is found on the head?
A
S. capitis
23
What factor causes agglutination in slide coagulase tests?
Clumping factor
24
What hemolysis pattern is seen in some staphylococci?
Beta-hemolysis
25
What is the texture of typical staphylococcal colonies?
Buttery-looking colonies
26
What is the only obligate anaerobic staphylococcus?
A: S. saccharolyticus
27
What is the oxygen requirement of most staphylococci?
A: Facultative
28
What CoNS species mimics S. aureus in slide tests?
A: S. lugdunensis
29
What pigment do some micrococci produce?
A: Yellow
30
Which CoNS is linked to nosocomial infections?
A: S. epidermidis
31
Which coagulase-negative species causes UTIs?
A: Saprophyticus
32
What test differentiates S. aureus from CoNS?
A: Coagulase
33
What is the cellular arrangement of staphylococci?
A: Clusters
34
Why is Staphylococcus aureus considered the most clinically significant species among staphylococci?
Because it causes a wide range of infections from mild to life-threatening, can be isolated from nearly all clinical specimens, and is a major cause of both community-acquired and nosocomial infections.
35
How is S. aureus increasingly relevant in public health today?
Due to its growing role as a community-acquired pathogen and rising antimicrobial resistance.
36
What are the major classes of virulence factors produced by S. aureus?
Enterotoxins, cytolytic toxins, exfoliative toxins, enzymes (like coagulase and hyaluronidase), and cell wall components (like Protein A).
37
Despite its virulence factors, why is S. aureus still considered opportunistic?
Because healthy immune systems generally provide strong innate resistance against it.
38
Which enterotoxins are most commonly implicated in staphylococcal food poisoning?
Enterotoxins A, B, and D.
39
Why does reheating food contaminated with S. aureus enterotoxins fail to prevent illness?
Because enterotoxins are heat-stable and remain active even after heating to 100°C for 30 minutes.
40
Which enterotoxins are associated with toxic shock syndrome (TSS)?
Enterotoxins B, C, and sometimes G and I.
41
How do enterotoxins act as superantigens?
They nonspecifically activate T cells, triggering an excessive immune response and cytokine release.
42
Which toxin is the major cause of menstruation-associated TSS?
TSST-1.
43
What is the mechanism of action of TSST-1?
Acts as a superantigen, stimulates massive T-cell proliferation, and leads to high cytokine levels, vascular leakage, and cytotoxicity.
44
How is TSST-1 absorbed and disseminated in tampon-related TSS?
Absorbed through the vaginal mucosa, causing systemic effects.
45
What skin condition in children is also linked to exfoliative toxin?
Bullous impetigo.
45
What disease is caused by the exfoliative toxin of S. aureus?
Staphylococcal Scalded Skin Syndrome (SSSS), also called Ritter disease.
46
List the four hemolysins produced by S. aureus.
Alpha (α), Beta (β), Gamma (γ), and Delta (δ) hemolysins.
47
What is the role of α-hemolysin?
Lyses erythrocytes, damages platelets and macrophages, and causes severe tissue damage.
48
What unique characteristic does β-hemolysin (sphingomyelinase C) exhibit?
"Hot-cold" lysis — activity increases after incubation at 37°C followed by exposure to 4°C.
49
Which test in the lab exploits the “hot-cold” effect of β-hemolysin?
CAMP test used for identifying Group B streptococci.
50
What is Panton-Valentine leukocidin (PVL), and why is it important?
A leukocidin lethal to PMNs, associated with necrotizing pneumonia and severe skin infections in community-acquired S. aureus strains.
51
Which enzyme is considered a virulence marker for S. aureus?
Staphylocoagulase (coagulase).
52
What does hyaluronidase do?
Breaks down hyaluronic acid in connective tissues, helping the bacteria spread.
53
How do lipases contribute to skin infections by S. aureus?
They degrade lipids and oils secreted by sebaceous glands, allowing bacterial colonization and spread.
54
Which three enzymes are tissue-damaging and facilitate local spread of infection?
Protease, lipase, and hyaluronidase.
55
What is the function of Protein A in S. aureus pathogenicity?
Binds the Fc portion of IgG, blocking opsonization and phagocytosis.
56
Why is Protein A considered an immune evasion tool?
It inhibits the protective functions of IgG, particularly phagocyte recruitment.
57
How can TSST-1 and staphylococcal enterotoxins contribute to systemic immune dysregulation?
As superantigens, they bypass normal antigen presentation and stimulate a large fraction of T cells, leading to a cytokine storm.
58
What makes PVL-positive S. aureus strains more dangerous in community outbreaks?
Their ability to lyse neutrophils reduces host defense and promotes tissue necrosis, often resulting in aggressive infections.
59
Why might coagulase-negative staphylococci (CoNS) also be pathogenic despite lacking coagulase?
They may still produce tissue-destroying enzymes like lipase and hyaluronidase, especially in immunocompromised individuals.
60
Heat-stable exotoxins causing food poisoning
Enterotoxins
61
Toxins stable at 100°C for 30 minutes
Enterotoxins
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Enterotoxins linked to TSS
B, C, G, I
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Enterotoxin linked to pseudomembranous enterocolitis
Enterotoxin B
64
Superantigen toxin causing TSS
TSST-1
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Former name of TSST-1
Enterotoxin F
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% of nonmenstrual TSS linked to TSST-1
~50 percent
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Toxin absorbed through vaginal mucosa
TSST-1
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Toxin causing Ritter disease
Exfoliative toxin
69
Another name for exfoliative toxin
A: Epidermolytic toxin
70
Q: Disease with epidermal sloughing in infants
SSS (Scalded Skin Syndrome)
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Blistering skin infection from exfoliative toxin
Bullous impetigo
72
Toxin damaging RBCs and tissues
Alpha-hemolysin
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Hemolysin with “hot-cold” activity
Beta-hemolysin
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Hemolysin with lowest toxicity
A: Delta-hemolysin
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Hemolysin often paired with PVL
Gamma-hemolysin
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PVL-linked serious pneumonia
Necrotizing pneumonia
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Leukocidin damaging neutrophils
Panton-Valentine leukocidin (PVL)
77
Enzyme that clots plasma
Coagulase
78
Enzyme that degrades connective tissue
Hyaluronidase
79
Enzyme acting on skin oils
Lipase
80
Enzyme that breaks down proteins
PROTEASE
81
Cell wall protein blocking phagocytosis
Protein A
82
Protein A binds this antibody part
Fc of IgG
83
General term for toxins destroying cells
Cytolytic toxins
84
Cellular lipid targeted by beta-hemolysin
Sphingomyelin
85
What is the primary reservoir of Staphylococcus aureus in humans?
A: The human anterior nares (nostrils).
86
Besides the nares, name at least three other sites where S. aureus colonization commonly occurs.
A: Axillae, vagina, pharynx, and other skin surfaces.
87
Why is nasal carriage of S. aureus significant in hospitalized patients?
A: Because it facilitates the spread among patients and healthcare workers, leading to increased colonization and hospital outbreaks.
88
How is S. aureus transmitted in hospitals?
A: Through direct contact with contaminated hands or contact with fomites (inanimate objects).
89
Which hospital units are especially vulnerable to S. aureus outbreaks?
A: Nurseries, burn units, and surgical wards.
90
Why is MRSA considered a major healthcare concern?
A: It is resistant to methicillin and causes both healthcare-associated and community-acquired infections.
91
What are the two major types of S. aureus infections?
A: Suppurative and toxin-mediated infections.
92
What determines the development of a staphylococcal infection?
A: Strain virulence, inoculum size, and host immune status.
93
What host defense response is triggered after S. aureus breaches the barrier?
A: Acute inflammation with activation of polymorphonuclear leukocytes (neutrophils).
94
How does S. aureus resist the action of inflammatory cells?
A: By producing toxins and enzymes that neutralize immune defenses and promote tissue damage.
95
What is a hallmark feature of suppurative infections by S. aureus?
A: Formation of pus-filled abscesses surrounded by necrotic tissue and damaged leukocytes.
96
What is folliculitis?
A: Mild inflammation of a hair follicle or oil gland, characterized by raised, red lesions.
97
Compare bullous impetigo caused by S. aureus and nonbullous impetigo caused by streptococci.
A: Bullous impetigo features larger pustules with erythema; it is highly contagious and spread via direct contact or fomites.
97
How does a furuncle differ from folliculitis?
A: A furuncle (boil) is a larger, superficial abscess that may develop from folliculitis.
98
What is a carbuncle, and how does it differ from a furuncle?
A: A carbuncle is a deeper, more invasive lesion from multiple furuncles; may cause fever and chills due to systemic spread.
99
Compare bullous impetigo caused by S. aureus and nonbullous impetigo caused by streptococci.
A: Bullous impetigo features larger pustules with erythema; it is highly contagious and spread via direct contact or fomites.
99
What predisposing factors increase the risk of staphylococcal skin infections?
Dry skin, poor hygiene, immunocompromised state, presence of foreign devices, and underlying skin disease.
100
Which superficial S. aureus infections are often misdiagnosed as spider bites?
A: Furuncles or localized skin abscesses.
101
What causes Scalded Skin Syndrome in S. aureus infections?
A: Exfoliative (epidermolytic) toxin produced at a distant lesion site.
102
Who are most commonly affected by SSS?
A: Newborns and young children, but it can also occur in immunocompromised adults.
103
What is the mortality rate of SSS in children vs. adults?
A: 0–7% in children; up to 50% in adults.
104
What is the localized form of SSS called?
A: Pemphigus neonatorum (a few blisters).
105
What is Ritter disease?
A: A severe, generalized form of SSS affecting up to 90% of the body with erythema and epidermal peeling.
106
toxin-mediated by S. aureus, but causes widespread desquamation and is Nikolsky-positive
SSSS
107
Describe the typical progression of SSS skin lesions.
A: Erythema starts on face, neck, axillae, and groin, then spreads to trunk and limbs, followed by skin peeling.
108
Why is SSS more common in children under 5 and in adults with renal failure?
A: The exfoliative toxin is metabolized and excreted by the kidneys—these populations have decreased renal clearance.
109
How long does SSS typically last?
A: Around 2 to 4 days.
110
Primary reservoir of S. aureus
A: Anterior nares
111
Common hospital-acquired resistant strain
MRSA
111
Type of infection that forms pus
SUPPURATIVE
112
Toxin-mediated skin syndrome
A: Scalded skin syndrome
113
Localized SSS in neonates
A: Pemphigus neonatorum
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Severe generalized form of SSS
Ritter Disease
115
SSS mortality in adults
50%
115
Skin lesion misdiagnosed as spider bite
furuncles
116
Common superficial infection
folliculitis
117
Highly contagious pustular skin infection
A: Bullous impetigo
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SSS mortality in children
A: 0–7%
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SSS toxin is excreted by what organ
kidney
120
Q: What public health measures contributed to the reduction of TSS cases over the years?
A: Use of minimum absorbency tampons and FDA-required warning labels on tampon products.
120
Signs of systemic spread in carbuncles
fever and chills
121
Q: What organism causes Toxic Shock Syndrome and what systemic toxin is involved?
A: Staphylococcus aureus causes TSS; the systemic toxin is TSST-1 (Toxic Shock Syndrome Toxin-1).
122
Q: What are the hallmark clinical symptoms of TSS?
A: Sudden high fever, chills, vomiting, diarrhea, muscle aches, rash, hypotension, and possible shock.
123
Q: What are the two categories of TSS, and what differentiates them?
A: Menstruating-associated and nonmenstruating-associated; the former is linked to tampon use, the latter to infections such as postsurgical or secondary to influenza.
124
Q: Why might TSS be underreported in clinical settings?
A: Due to misdiagnosis or failure to meet CDC case criteria.
125
Q: Can S. aureus be absent from blood cultures in TSS? Why or why not?
A: Yes; TSS is toxin-mediated, and the toxin can be systemic even if S. aureus remains localized.
126
Q: Which lab findings support a clinical diagnosis of TSS?
A: Elevated leukocyte count with increased band forms/metamyelocytes (left shift), decreased platelets, elevated serum creatinine and urea.
126
Q: What is the immediate management step upon diagnosing TEN?
A: Discontinue the suspected offending drug.
127
Q: What is the cornerstone of treatment for TSS?
A: Supportive therapy (volume replacement) and appropriate antibiotics.
128
Q: What are the most common causes of Toxic Epidermal Necrolysis?
A: Drug reactions, though it can also be triggered by infections and vaccines.
128
Q: How can you differentiate TEN from Staphylococcal Scalded Skin Syndrome (SSS) in terms of treatment?
A: TEN improves with early steroid administration; steroids worsen SSS.
128
Q: What is the underlying mechanism believed to cause TEN?
A: A hypersensitivity reaction.
129
Q: What is the prognosis of TEN, and what factor influences outcome?
A: TEN has a high mortality rate; early withdrawal of the causative drug improves survival.
130
Q: Why is early differentiation between TEN and SSS critical in clinical settings?
A: Because treatments differ: steroids are beneficial in TEN but contraindicated in SSS.
131
Skin manifestation often seen in TSS
Truncal rash
132
Electrolyte/fluid-related complication in TSS
dehydration
133
Hematologic finding in TSS with no bleeding
thrombocytopenia
134
Systemic complication due to vascular collapse
Hypotension
135
Site where S. aureus is often found in TSS
focsl lesions
136
Lab marker elevated due to kidney injury in TSS
serum creatinine and urea
137
Year TSS was first described
1978
138
Pathogenesis mechanism of TEN
hypersensitivity
138
Most common cause of Toxic Epidermal Necrolysis
drugs
139
Drug class used early in TEN
steroids
139
Diagnostic clue differentiating TEN from SSS
steroid response
139
Serious outcome if TEN is untreated
death
140
Blood culture result in most TSS cases
negative
141
Type of immunity involved in TEN
delayed hypersensitivity
142
What type of disease is staphylococcal food poisoning, intoxication or infection?
Intoxication — caused by ingestion of preformed enterotoxins, not by bacterial infection within the body.
143
Which S. aureus enterotoxins are most commonly associated with food poisoning?
Enterotoxins A (78%), D (38%), and B (10%).
143
What is the usual source of contamination in staphylococcal food poisoning?
infected food handler
144
What storage condition promotes toxin production in contaminated food?
Improper storage at room temperature.
144
Why can staphylococcal food poisoning be difficult to detect before ingestion?
The enterotoxins cause no detectable odor, taste, or appearance change in the food.
145
List foods commonly implicated in staphylococcal food poisoning.
Salads (especially with mayonnaise and eggs), meat and poultry, egg products, bakery products with cream fillings, sandwich fillings, and dairy products.
146
How soon do symptoms of staphylococcal food poisoning typically appear?
Within 2 to 8 hours after ingestion.
147
How long do symptoms of staphylococcal food poisoning usually last?
Symptoms resolve within 24 to 48 hours.
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148
What are the most common symptoms of staphylococcal food poisoning?
Nausea, vomiting, abdominal pain, and severe cramping. Diarrhea and headaches can also occur.
149
