152: Gram-Positive Infections Associated with Toxin Production Flashcards
(145 cards)
1
Q
What is the likely diagnosis for a 5-year-old child with honey-colored crusts on an erythematous base?
A
The likely diagnosis is impetigo contagiosum, caused by S. aureus or S. pyogenes.
2
Q
What condition develops in a neonate with generalized erythema and large flaccid bullae?
A
The condition is called Ritter disease (generalized SSSS in neonates), caused by exfoliative toxins (ETB).
3
Q
What are the two forms of ET-mediated disease caused by Staphylococcus aureus?
A
- Localized bullous impetigo - caused by ETA
- Systemic SSSS - caused by ETB
4
Q
What is the clinical presentation of localized bullous impetigo?
A
- Infection of the epidermis by S. aureus or S. pyogenes
- Consists of honey-colored crusts on an erythematous base
- Early lesions are cloudy vesicles or bullae surrounded by an erythematous rim that can rupture, leading to superficial erosions.
5
Q
What are the risk factors associated with generalized Staphylococcal Scalded Skin Syndrome (SSSS)?
A
- Compromised immune response allowing for growth of S. aureus
- Impaired amounts of toxin-neutralizing antibodies
- Renal insufficiency decreasing the clearance of the toxin
6
Q
What is the pathophysiology of exfoliative toxins produced by Staphylococcus aureus?
A
- Exfoliative toxins (ETs) are serine proteases that bind to the cell-adhesion molecule desmoglein-1 and cleave it, resulting in a loss of cell-cell adhesion.
- This leads to epidermolysis between the stratum spinosum and granulosum, resulting in flaccid blisters that are easily disrupted, with a positive Nikolsky sign.
7
Q
What is the primary cause of localized bullous impetigo?
A
Infection of the epidermis by S. aureus or S. pyogenes.
8
Q
What is the characteristic appearance of early lesions in bullous impetigo?
A
Cloudy vesicles or bullae surrounded by an erythematous rim.
9
Q
What is the Nikolsky sign associated with in the context of exfoliative toxins?
A
It indicates the presence of a blister that is easily disrupted.
10
Q
What are the key factors that influence the development of toxin-mediated diseases caused by Staphylococcus aureus?
A
The development of toxin-mediated diseases is influenced by:
- Host Resistance: Intact skin and mucous membranes serve as barriers to infection.
- Defects in Barriers: Minor and major defects in skin and mucosal barriers increase the risk of infection.
- Immune Response: The types of immune cells activated play an important role in the host response, especially regarding superantigens.
11
Q
What are the clinical features and diagnostic criteria for localized bullous impetigo?
A
Clinical features of localized bullous impetigo include:
- Infection of the epidermis by S. aureus or S. pyogenes.
- Characterized by honey-colored crusts on an erythematous base.
- Early lesions present as cloudy vesicles or bullae surrounded by an erythematous rim, which can rupture leading to superficial erosions.
Diagnosis is primarily based on clinical appearance. Confirmation can be obtained by aspiration of blister fluid for Gram stain and cultures, which will reveal S. aureus.
12
Q
What are the risk factors and clinical progression of Staphylococcal Scalded Skin Syndrome (SSSS)?
A
Risk factors for Staphylococcal Scalded Skin Syndrome (SSSS) include:
- Compromised Immune Response: Allows for the growth of S. aureus.
- Impaired toxin-neutralizing antibodies or renal insufficiency, decreasing toxin clearance.
Clinical Progression: 1. Initial presentation: faint, orange-red macular exanthem sparing mucosal surfaces, often with conjunctivitis or otitis media. 2. Within 1-2 days, the rash progresses from an exanthematous scarlatiniform to a blistering eruption, leading to large flaccid bullae in flexural and periorificial surfaces.
13
Q
A patient with SSSS shows a positive Nikolsky sign. What does this indicate?
A
A positive Nikolsky sign indicates superficial blistering caused by exfoliative toxins.
14
Q
What does sterile cultures from an intact blister in a patient with SSSS suggest about the pathogenesis?
A
This suggests a hematogenously disseminated toxin originating from a distant focus of infection.
15
Q
What type of cells are visualized in the cleavage space of localized bullous impetigo?
A
Neutrophils are visualized in the cleavage space of localized bullous impetigo.
16
Q
What is the major complication of SSSS?
A
The major complication of SSSS is serious fluid and electrolyte disturbances.
17
Q
Where does the splitting occur in a patient with SSSS?
A
Splitting occurs beneath and within the stratum granulosum.
18
Q
What is the Positive Nikolsky sign and its significance in diagnosing SSSS?
A
The Positive Nikolsky sign is elicited by stroking the skin, resulting in a superficial blister. It indicates superficial epidermal detachment and is significant in diagnosing Staphylococcal Scalded Skin Syndrome (SSSS) as it reveals large sheets of epidermal surface typically shed, exposing a moist underlying erythematous base.
19
Q
What are the characteristics of intermediate (abortive) forms of SSSS?
A
Intermediate (abortive) forms of SSSS may present as localized bullous impetigo, producing regionally limited bullae and denuded areas that may or may not harbor S. aureus.
20
Q
What are the major complications associated with SSSS?
A
Major complications of Staphylococcal Scalded Skin Syndrome (SSSS) include: 1. Serious fluid and electrolyte disturbances 2. Mortality in uncomplicated pediatric SSSS is very low (2%) and not usually associated with sepsis. 3. Adult mortality is higher (approximately 10%) due to concomitant morbidity factors and increased likelihood of sepsis.
21
Q
How do superantigens differ from conventional peptide antigens?
A
Superantigens are a group of microbial and viral proteins that differ from conventional peptide antigens in several ways: They exert their effects as globular extracellular intact proteins. They primarily recognize and bind to the variable region of the T-cell receptor β chain (Vβ). The responding frequency of a superantigen for resting T cells is significantly greater (up to 30%) compared to conventional peptide antigens (0.01% to 0.1%). They activate T cells by binding directly to MHC class II molecules and crosslinking T cells, leading to potent immune stimulation.
22
Q
What is the clinical significance of superantigens in relation to cytokine release?
A
Superantigens lead to a massive release of cytokines, including tumor necrosis factor α, interleukin-1, and interleukin-6. This release is responsible for a capillary leak syndrome and accounts for the majority of clinical manifestations seen in superantigen-mediated diseases, such as toxic shock syndrome (TSS).
23
Q
What is the clinical significance of the Positive Nikolsky sign in the context of SSSS?
A
The Positive Nikolsky sign indicates superficial blistering of the skin, which is a hallmark of Staphylococcal Scalded Skin Syndrome (SSSS). This sign suggests the presence of epidermal detachment and is associated with the hemagglutinating toxin that disseminates from a distant focus of infection, leading to the characteristic desquamation and healing within 5 to 7 days with appropriate antibiotic treatment.
24
Q
What distinguishes generalized SSSS from toxic epidermal necrolysis (TEN) in terms of diagnosis?
A
The principal diagnostic challenge is distinguishing generalized SSSS, characterized by superficial subgranular epidermolysis, from toxic epidermal necrolysis (TEN), which involves full-thickness epidermal necrosis and dermal-epidermal separation. Accurate diagnosis is crucial for appropriate management and treatment strategies.
25
What role do superantigens play in the pathogenesis of toxic shock syndrome (TSS)?
Superantigens, such as those produced by staphylococcal or streptococcal toxins, lead to toxic shock syndrome (TSS) by activating a large number of T cells, resulting in a massive release of cytokines. This cytokine storm is responsible for the clinical manifestations of TSS, including capillary leak syndrome and systemic toxicity, which can be life-threatening.
26
What is the most likely diagnosis for a patient presenting with fever, hypotension, and a diffuse macular erythema?
The most likely diagnosis is staphylococcal toxic shock syndrome (TSS), commonly associated with TSST-1 in menstrual cases.
27
What is the likely diagnosis for a patient with a history of tampon use who develops fever, rash, and hypotension?
The likely diagnosis is staphylococcal TSS. The tampon serves as a nidus for infection, with blood neutralizing the normally bactericidal acidic vaginal pH.
28
What is the likely diagnosis for a patient with necrotizing fasciitis who develops hypotension and multiorgan failure?
The likely diagnosis is streptococcal TSS, commonly caused by streptococcal pyrogenic exotoxin A (SPEA).
29
What is the likely explanation for a patient with staphylococcal TSS having no signs of localized infection?
In nonmenstrual cases, classic signs of localized infection such as erythema, pain, and purulence can be absent.
30
When does desquamation typically occur in a patient with staphylococcal TSS?
Desquamation typically occurs within 1 to 2 weeks after the onset of the rash.
31
How does lack of neutralizing antibodies against TSST-1 affect susceptibility in a patient with staphylococcal TSS?
Lack of neutralizing antibodies increases susceptibility to staphylococcal TSS.
32
What does orthostatic dizziness indicate in a patient with staphylococcal TSS?
This indicates symptoms of hypotension.
33
How do blood cultures differ in streptococcal TSS compared to staphylococcal TSS?
Blood cultures are positive in more than half of streptococcal TSS cases, compared to only 10% in staphylococcal TSS.
34
Does lack of neutralizing antibodies affect susceptibility?
Lack of neutralizing antibodies increases susceptibility to staphylococcal TSS.
35
What is the progression of symptoms in a patient with streptococcal TSS who develops cellulitis?
Symptoms progress from localized skin pain to erythema and edema, then cellulitis, necrotizing fasciitis, and myositis.
36
What characterizes Toxic Shock Syndrome (TSS)?
TSS is characterized by fever, rash, hypotension, and multiorgan involvement.
37
What is the most common staphylococcal toxin associated with TSS?
The most common staphylococcal toxin associated with TSS is TSS toxin-1 (TSST-1).
38
What are the common types of infections associated with Streptococcal Toxic Shock Syndrome?
The most common types of infections associated with Streptococcal Toxic Shock Syndrome appear to be wounds, and it has been described as a complication of varicella and influenza A.
39
What is the initial presentation of Streptococcal TSS?
The initial presentation of Streptococcal TSS is skin pain often localized to an extremity, which progresses to localized erythema and edema.
40
What is the recommended treatment for TSS?
The treatment of TSS is supportive and usually in the intensive care setting, along with antibiotics such as vancomycin and clindamycin.
41
How does Kawasaki syndrome differ from TSS?
Kawasaki syndrome differs from TSS in that the course of fever is prolonged and diarrhea and hypotension are absent.
42
What are the common symptoms of TSS?
Acute onset of fever, sore throat, myalgia, diarrhea, and vomiting.
43
What is the most common cause of streptococcal TSS?
Streptococcal pyrogenic exotoxin A (SPEA).
44
How does the incidence of nonmenstrual TSS compare to menstrual TSS?
The incidence of nonmenstrual TSS exceeds that of menstrual-associated cases.
45
What is a critical factor in the development of TSS?
The host response and the presence of neutralizing antibodies against TSST-1.
46
What differentiates streptococcal TSS from staphylococcal TSS in terms of blood cultures?
Blood cultures are positive in more than half of patients with streptococcal TSS, compared to only 10% with staphylococcal TSS.
47
What are the key clinical features of Staphylococcal Toxic Shock Syndrome (TSS)?
Staphylococcal TSS is caused primarily by TSST-1, with symptoms including fever, sore throat, myalgia, and a macular erythema rash.
48
What are the key clinical features of Streptococcal Toxic Shock Syndrome (TSS)?
Streptococcal TSS is most commonly caused by streptococcal pyrogenic exotoxin A (SPEA) with initial skin pain localized to an extremity.
49
What is the significance of the host response in TSS?
The host response influences susceptibility, with patients lacking neutralizing antibodies at higher risk.
50
What are the treatment options for Toxic Shock Syndrome (TSS)?
Treatment typically involves supportive care, antibiotics like nafcillin, clindamycin, and vancomycin, and IVIG.
51
What differentiates Staphylococcal TSS from Streptococcal TSS in terms of infection sources?
Staphylococcal TSS is often associated with menstrual-related cases, while streptococcal TSS is more commonly associated with wounds.
52
What is the likely diagnosis for a child with a scarlatiniform rash that spares the palms and soles?
The likely diagnosis is scarlet fever, most commonly caused by pyrogenic exotoxin-producing group A Streptococcus.
53
What is the likely diagnosis for a patient with a white strawberry tongue followed by a red strawberry tongue?
The likely diagnosis is scarlet fever, with progression due to desquamation of the white coat on the tongue.
54
What is the likely diagnosis for a patient with a sandpaper-like rash and circumoral pallor?
The likely diagnosis is scarlet fever, caused by pyrogenic exotoxin-producing group A Streptococcus.
55
What does the Pastia sign indicate in a patient with a history of pharyngitis?
The Pastia sign indicates confluent petechiae in skinfolds due to increased capillary fragility.
56
What should a clinician investigate in a patient with staphylococcal scarlet fever who lacks pharyngitis?
The clinician should look for a localized nidus of infection in the skin.
57
When does peeling typically occur in a patient with scarlet fever?
Peeling typically occurs a week after the generalized exanthem and can last for up to a month.
58
Where are Forchheimer spots located in a patient with scarlet fever?
Forchheimer spots are located on the soft palate and uvula.
59
What does a flushed face with circumoral pallor indicate in a patient with scarlet fever?
This is a characteristic finding of scarlet fever.
60
What happens after a patient with staphylococcal scarlet fever develops thick flakes?
The entire skin desquamates over the next week.
61
What does a white strawberry tongue indicate in a patient with scarlet fever?
This indicates the first 2 days of the disease, where the tongue has a white coat with red papillae.
62
What causes the change from a white strawberry tongue to a red strawberry tongue in scarlet fever?
The white coat on the tongue desquamates, revealing the red tongue with prominent papillae.
63
What is the texture of the rash in a patient with scarlet fever?
The texture is due to the fine-grade sandpaper-like erythema.
64
What is the Pastia sign in scarlet fever?
This is called the Pastia sign, indicating petechiae in skinfolds.
65
When does the desquamative phase begin in a patient with scarlet fever?
The desquamative phase begins 3 to 4 days after the onset of the generalized exanthem.
66
What other oral findings are common in a patient with scarlet fever who has erythematous tonsils with exudate?
Other findings include petechiae and punctuate red macules on the soft palate and uvula.
67
What does a rash that blanches with pressure indicate in a patient with scarlet fever?
This indicates the erythema is blanchable, a characteristic of scarlet fever.
68
What does a rash that spares the palms and soles suggest in a patient with scarlet fever?
This is a characteristic distribution of the rash in scarlet fever.
69
What is the mortality rate of staphylococcal Toxic Shock Syndrome (TSS)?
The mortality rate of staphylococcal TSS is approximately 5%.
70
What are the clinical findings associated with Recalcitrant Erythematous Desquamating Disorder?
The clinical findings include fever, hypotension, diffuse macular erythema with delayed desquamation, ocular and oral mucosal injection, and strawberry tongue.
71
What are the key characteristics of Scarlet Fever?
Scarlet Fever is characterized by exudative pharyngitis, fever, and scarlatiniform rash, most commonly caused by pyrogenic exotoxin-producing group A Streptococcus.
72
What are the initial symptoms of Scarlet Fever after exposure?
Pharyngitis, headache, vomiting, abdominal pain, and fever.
73
What is the characteristic rash appearance in Scarlet Fever?
Rash appears first on the neck and then extends to the trunk and extremities, sparing the palms and soles.
74
What distinguishes Staphylococcal Scarlet Fever from Streptococcal Scarlet Fever?
Staphylococcal Scarlet Fever lacks pharyngitis and has a more tender exanthem.
75
What is the significance of the Pastia sign in Scarlet Fever?
It indicates increased capillary fragility, resulting in confluent petechiae.
76
What is the differential diagnosis for Scarlet Fever?
Diagnosis is made upon clinical grounds with supporting positive bacterial cultures.
77
What are the key clinical features that differentiate Staphylococcal Scarlet Fever from Streptococcal Scarlet Fever?
Staphylococcal Scarlet Fever has a rough rash texture, absent pharyngitis, and thick flakes of desquamation, while Streptococcal Scarlet Fever has a coarse rash, present pharyngitis, and peeling from palms and fingers.
78
What is the significance of IVIG in the treatment of Staphylococcal Toxic Shock Syndrome (TSS)?
IVIG helps neutralize toxins and supports the immune response, decreasing the mortality rate.
79
How does the clinical presentation of Scarlet Fever evolve over time after exposure?
Initial symptoms appear 12 hours to 5 days after exposure, followed by rash onset 1 to 2 days later, intensifying around skinfolds, and a desquamative phase starting 3 to 4 days after onset.
80
What are the potential complications associated with Scarlet Fever, particularly in children?
Complications can include rheumatic fever and post-streptococcal glomerulonephritis.
81
What are the potential complications associated with Scarlet Fever, particularly in children?
Complications of Scarlet Fever can include:
- Rheumatic Fever: An autoimmune response that can affect the heart, joints, and nervous system.
- Post-streptococcal Glomerulonephritis: A kidney condition that can occur after infection.
- Severe Skin Infections: Due to the rash and skin breakdown.
- Otitis Media: Ear infections can develop as a complication of pharyngitis.
82
What is the likely diagnosis for a patient with a history of pharyngitis who develops diffuse macular perineal erythema within 48 hours?
The likely diagnosis is toxin-mediated erythema caused by a toxin-producing group A Streptococcus or S. aureus.
83
What bacterial infection is commonly associated with flare-ups in atopic dermatitis?
Secondary infection with S. aureus or group A Streptococcus is commonly associated due to decreased levels of antimicrobial proteins in atopic skin.
84
What is the likely mechanism for psoriasis flare-ups after a streptococcal infection?
The mechanism involves superantigen-mediated systemic activation of T cells and MHC II-expressing accessory cells.
85
What is the likely role of S. aureus in cutaneous T-cell lymphoma (CTCL)?
S. aureus colonization correlates with CTCL severity, and its eradication improves disease activity.
86
What should be investigated in patients with psoriasis experiencing menstrual-associated flares?
Investigate for superantigen-secreting microbes, such as S. aureus, associated with tampon use.
87
What is the likely diagnosis for a patient with a history of pharyngitis who develops palmoplantar desquamation?
The likely diagnosis is toxin-mediated erythema.
88
What are the clinical findings associated with toxin-mediated erythema after pharyngitis caused by a toxin-producing group A Streptococcus or S. aureus?
Clinical findings include:
- Striking diffuse macular perineal erythema occurring within 24 to 48 hours after pharyngitis.
- Strawberry tongue, erythema, edema, and later palmoplantar desquamation.
- Systemic signs of scarlet fever or TSS are characteristically absent, although diarrhea is common.
- Recurrences are more frequent, often associated with preceding bacterial pharyngitis.
89
How do superantigens contribute to the exacerbation of psoriasis?
Superantigens are implicated in psoriasis in two settings:
1. Guttate form: Rapid onset of small erythematous papules, often following a group A streptococcal infection, particularly in children and young adults.
2. Worsening of psoriasis: A localized infection with a superantigen-secreting microbe can trigger worsening of psoriasis.
90
What is the role of superantigens in the autoeczematization response?
Superantigens can stimulate high numbers of T cells expressing CLA, leading to an autoeczematization response characterized by:
- Acute, generalized skin reaction to various stimuli.
- Erythematous and papular pruritic rash developing at distant sites, often symmetric.
- Localized bacterial infection with superantigen-producing S. aureus or group A Streptococcus may trigger this response without systemic toxicities.
91
What is the significance of S. aureus infection in atopic dermatitis?
S. aureus infection is a well-known trigger for atopic dermatitis due to:
- Decreased levels of antimicrobial proteins in the skin of affected individuals, which may explain the frequent bacterial infections during flares.
- Many patients have immunoglobulin E antibodies that recognize globular proteins, contributing to allergic reactions.
- Lytic toxin staphylococcal delta-toxin can trigger mast cell degranulation, exacerbating the condition.
92
How do staphylococcal toxins relate to cutaneous T-cell lymphoma (CTCL)?
Staphylococcal toxins may play a role in the progression of CTCL through:
- High levels of S. aureus colonization in CTCL patients, which is a source of local and systemic infections.
- Correlation of S. aureus infection with CTCL disease severity.
- Antibiotic treatment of S. aureus improving CTCL disease activity.
- Superantigens activating specific B patterns that support the role of toxins in CTCL.
93
What is the nidus of infection in streptococcal scarlet fever?
It is from a pharyngitis.
94
What are the clinical findings in scarlet fever?
Strawberry tongue, erythema, edema, and palmoplantar desquamation.
95
What is a common feature of recurrent toxin-mediated perineal erythema?
Striking diffuse macular perineal erythema occurring within 24 to 48 hours after pharyngitis.
96
What systemic signs are characteristically absent in recurrent toxin-mediated perineal erythema?
Systemic signs of scarlet fever or TSS.
97
What role do superantigens play in psoriasis?
They have been implicated in both the guttate form and in flares of psoriasis due to secondary infections.
98
What triggers the acute guttate form of psoriasis?
It develops during or right after a group A streptococcal infection.
99
What is the relationship between atopic dermatitis and S. aureus?
Secondary infection with S. aureus is a well-known trigger for atopic dermatitis.
100
What is the significance of lytic toxin staphylococcal delta-toxin in atopic dermatitis?
It triggers mast cell degranulation.
101
How does S. aureus infection relate to cutaneous T-cell lymphoma (CTCL)?
S. aureus infection is reported to correlate with CTCL disease severity.
102
What is the effect of antibiotic treatment of S. aureus in CTCL patients?
It is reported to improve CTCL disease activity.
103
What are the clinical findings associated with toxin-mediated erythema following a pharyngitis caused by a toxin-producing group A Streptococcus or S. aureus?
Clinical findings include:
- Striking diffuse macular perineal erythema occurring within 24 to 48 hours after pharyngitis.
- Symptoms such as strawberry tongue, erythema, edema, and later palmoplantar desquamation.
- Systemic signs of scarlet fever or TSS are typically absent, although diarrhea may be present.
104
How do superantigens contribute to the exacerbation of psoriasis, particularly in the acute guttate form?
Superantigens contribute to psoriasis by:
1. Triggering rapid onset of small erythematous psoriasiform papules, often following a group A streptococcal infection.
2. Being implicated in up to 20% of psoriasis cases, especially in children and young adults.
3. Inducing systemic activation of T cells and MHC II-expressing accessory cells, which may initiate this form of psoriasis.
105
What role do superantigens play in the autoeczematization response observed in patients with atopic dermatitis?
Superantigens can:
- Stimulate high numbers of T cells expressing CLA, leading to a generalized skin reaction.
- Cause erythematous and papular pruritic rashes that develop symmetrically at distant sites.
- Result in localized bacterial infections with superantigen-producing S. aureus or group A Streptococcus, contributing to the autoeczematization response.
106
What is the significance of S. aureus colonization in patients with cutaneous T-cell lymphoma (CTCL)?
S. aureus colonization in CTCL patients is significant because:
- It is a major source of local and systemic infections.
- Infection with S. aureus correlates with CTCL disease severity.
- Antibiotic treatment of S. aureus has been reported to improve CTCL disease activity, indicating a potential role of bacterial toxins in disease progression.
107
What are the toxins produced by Staphylococcus aureus and their associated clinical diseases?
| Bacteria | Toxin | Toxin Type | Clinical Disease |
|-----------------------|--------------------------------|--------------|---------------------------------------------------|
| Staphylococcus aureus | Exfoliation type A (ETA) | Epidermolytic | Bullous impetigo |
| | Exfoliation type B (ETB) | Epidermolytic | Staphylococcal scalded skin syndrome (SSSS) |
| | Toxic shock syndrome toxin 1 (TSST-1) | Superantigen | Toxic shock syndrome (TSS) (menstrual, food poisoning) |
| | Staphylococcal enterotoxins A to C (SEA, SEB, SEC) | Superantigen | TSS (nonmenstrual > menstrual), food poisoning |
| Streptococcus pyogenes| Streptococcal pyrogenic exotoxins A and C (SPEA, SPEC) | Superantigen | TSS (nonmenstrual), scarlet fever |
108
What are the major criteria for diagnosing Staphylococcal Toxic Shock Syndrome?
1. Temperature: ≥38.9°C (102°F)
2. Rash: Diffuse macular erythroderma
3. Desquamation: 1 to 2 weeks after onset of illness, particularly on palms/soles
4. Hypotension: Systolic blood pressure <95 mm Hg for adults, or less than 5th percentile by age for children <16 years of age, or orthostatic syncope.
109
What are the differential diagnoses for Toxic Shock Syndrome?
| Differential Diagnosis |
|-------------------------------------------|
| Septic shock |
| Staphylococcal exfoliative syndromes |
| Rocky Mountain spotted fever |
| Viral hemorrhagic shock |
| Measles |
| Leptospirosis |
| Stevens-Johnson syndrome |
| Kawasaki syndrome |
110
What are the toxins produced by Staphylococcus aureus and their types?
Exfoliation type A (ETA) and B (ETB) are epidermolytic toxins; Toxic shock syndrome toxin 1 (TSST-1) and Staphylococcal enterotoxins A to C (SEA, SEB, SEC) are superantigens.
111
What clinical diseases are associated with Staphylococcus aureus toxins?
Bullous impetigo, Staphylococcal scalded skin syndrome (SSSS), and toxic shock syndrome (TSS).
112
What are the major criteria for diagnosing Staphylococcal Toxic Shock Syndrome?
Fever, rash, desquamation, hypotension, and involvement of multiple organ systems.
113
What is the role of superantigens in Staphylococcus aureus infections?
Superantigens like TSST-1 activate T-cells non-specifically, leading to a strong immune response and potential toxic shock syndrome.
114
What are some differential diagnoses for Toxic Shock Syndrome?
Septic shock, Staphylococcal exfoliative syndromes, Rocky Mountain spotted fever, viral hemorrhagic shock, and measles.
115
What are the clinical diseases associated with Staphylococcus aureus toxins, and how do they differ in terms of their toxin types?
| Toxin | Toxin Type | Clinical Disease |
|--------|------------|-----------------|
| Exfoliation type A (ETA) | Epidermolytic | Bullous impetigo |
| Exfoliation type B (ETB) | Epidermolytic | Staphylococcal scalded skin syndrome (SSSS) |
| Toxic shock syndrome toxin 1 (TSST-1) | Superantigen | Toxic shock syndrome (TSS) (menstrual and nonmenstrual) |
| Staphylococcal enterotoxins A to C (SEA, SEB, SEC) | Superantigen | TSS (nonmenstrual), food poisoning |
116
What are the major criteria for diagnosing Staphylococcal Toxic Shock Syndrome according to the CDC 2011 case definition?
1. Fever: Temperature ≥38.9°C (102°F)
2. Rash: Diffuse macular erythroderma
3. Desquamation: 1 to 2 weeks after onset of illness, particularly on palms/soles
4. Hypotension: Systolic blood pressure <95 mm Hg for adults, or less than 5th percentile by age for children <16 years of age, or orthostatic syncope.
117
What are the differential diagnoses for Toxic Shock Syndrome and how do they relate to Staphylococcal and Streptococcal infections?
| Differential Diagnosis | Relation to TSS |
|-----------------------|-----------------|
| Septic shock | Can present similarly to TSS |
| Staphylococcal exfoliative syndromes | Directly related to Staphylococcus aureus toxins |
| Rocky Mountain spotted fever | Can mimic TSS symptoms |
| Viral hemorrhagic shock | Differential diagnosis due to similar presentation |
| Measles | Can present with fever and rash |
| Leptospirosis | Similar systemic symptoms |
| Stevens-Johnson syndrome | Can present with rash and systemic symptoms |
| Kawasaki syndrome | Can present with fever and rash, especially in children |
118
What is the cell-adhesion molecule that exfoliative toxins bind to?
Exfoliative toxins are serine proteases that bind to the desmoglein cell-adhesion molecule.
119
What layers of the skin are involved in epidermolysis due to exfoliative toxins?
Epidermolysis takes place between the stratum granulosum and the stratum corneum.
120
What disease is characterized by honey-colored crusts on an erythematous base?
The disease characterized by honey-colored crusts on an erythematous base is Impetigo.
121
What term defines generalized SSSS in neonates?
The term that defines generalized SSSS in neonates is Staphylococcal Scalded Skin Syndrome (SSSS).
122
What is a possibly abortive form of SSSS with minimal blister formation?
A possibly abortive form of SSSS with features of early erythrodermic and final desquamative stages yet very little blister formation is known as Staphylococcal Scalded Skin Syndrome (SSSS) in its milder form.
123
What is a major complication of SSSS?
A major complication of SSSS is secondary bacterial infection due to skin barrier disruption.
124
What is the most common staphylococcal toxin associated with TSS?
The most common staphylococcal toxin associated with TSS is toxic shock syndrome toxin-1 (TSST-1).
125
What syndrome is characterized by exudative pharyngitis, fever, and scarlatiniform rash?
The syndrome characterized by exudative pharyngitis, fever, and scarlatiniform rash is Streptococcal Toxic Shock Syndrome.
126
What is the most common cause of the syndrome characterized by exudative pharyngitis, fever, and scarlatiniform rash?
The most common cause of this syndrome is Group A Streptococcus (Streptococcus pyogenes).
127
What is the striking diffuse macular perineal erythema that occurs after pharyngitis associated with?
The striking diffuse macular perineal erythema that occurs within 24 to 48 hours after pharyngitis is associated with a toxin-producing group A Streptococcus or S. aureus.
128
What are exfoliative toxins and what do they bind to?
Exfoliative toxins are serine proteases that bind to the cell-adhesion molecule.
129
What causes epidermolysis to take place between the stratum corneum and what?
Epidermolysis takes place between the stratum corneum and the stratum granulosum.
130
What occurs after pharyngitis associated with?
The striking diffuse macular perineal erythema that occurs within 24 to 48 hours after pharyngitis is associated with a toxin-producing group A Streptococcus or S. aureus.
131
What are exfoliative toxins and what do they bind to?
Exfoliative toxins are serine proteases that bind to the cell-adhesion molecule.
## Footnote
Exfoliative toxins bind to the desmoglein cell-adhesion molecule.
132
What disease consists of honey-colored crusts on an erythematous base?
Bullous impetigo.
133
What is the term to define generalized SSSS in neonates?
Generalized Staphylococcal Scalded Skin Syndrome (SSSS).
134
What is a possibly abortive form of SSSS with very little blister formation?
A form of SSSS that features early erythrodermic and final desquamative stages.
135
What is a major complication of SSSS?
Secondary bacterial infection.
136
What is the most common staphylococcal toxin associated with TSS?
Toxic Shock Syndrome Toxin-1 (TSST-1).
137
What syndrome is characterized by exudative pharyngitis, fever, and scarlatiniform rash?
Streptococcal Toxic Shock Syndrome.
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What is the most common cause of the syndrome characterized by exudative pharyngitis, fever, and scarlatiniform rash?
Group A Streptococcus (S. pyogenes).
139
What is the striking diffuse macular perineal erythema that occurs after pharyngitis associated with?
A toxin-producing group A Streptococcus or S. aureus.
140
What layers of the skin are affected by epidermolysis due to exfoliative toxins?
Epidermolysis occurs between the stratum granulosum and the stratum corneum.
141
What term is used to define generalized SSSS in neonates?
The term used to define generalized SSSS in neonates is Staphylococcal Scalded Skin Syndrome (SSSS).
142
What is a possibly abortive form of SSSS with minimal blister formation?
A possibly abortive form of SSSS with minimal blister formation is known as Staphylococcal Scalded Skin Syndrome (SSSS) without significant blistering.
143
What is the most common staphylococcal toxin associated with Toxic Shock Syndrome (TSS)?
The most common staphylococcal toxin associated with TSS is toxic shock syndrome toxin-1 (TSST-1).
144
What syndrome is characterized by exudative pharyngitis, fever, and scarlatiniform rash?
The syndrome characterized by exudative pharyngitis, fever, and scarlatiniform rash is Scarlet Fever.
145
What condition is described as striking diffuse macular perineal erythema occurring after pharyngitis?
This condition is known as toxic shock syndrome associated with a toxin-producing group A Streptococcus or S. aureus.
