150: Superficial Cutaneous Infections and Pyodermas Flashcards
(327 cards)
1
Q
What are the two major groups of Staphylococci and their characteristics?
A
- Coagulase-negative Staphylococci (e.g., S. epidermidis): Primarily harmless commensals, can cause superficial and invasive infections, especially on implanted foreign materials.
- Coagulase-positive Staphylococci (e.g., S. aureus): Can be harmless commensals but also aggressive pathogens, commonly associated with pyodermas and skin infections.
2
Q
What is the significance of S. aureus in pyodermas and skin infections?
A
S. aureus is the most common cause of primary pyodermas, SSTIs, and secondary infections on disease-altered skin.
It can be found colonizing the skin in up to 37% of patients with purulent community-acquired MRSA infections.
3
Q
What are the common sites of colonization for S. aureus?
A
Common sites of colonization include:
- Inguinal region: Moist area, prone to colonization.
- Axillae: Moist area, prone to colonization.
- Perirectal skin: Moist area, prone to colonization.
- Nasal mucosa: Permanent colonization in ~30% of population.
- Pharynx: Potential site of transient carriage.
- Rectal mucosa: Potential site of transient carriage.
4
Q
What conditions predispose individuals to S. aureus colonization?
A
Conditions predisposing to S. aureus colonization include:
1. Atopic dermatitis
2. Diabetes mellitus
3. Renal insufficiency (patients on dialysis)
4. Intravenous drug use
5. Liver dysfunction
6. Certain genetic or acquired immunosuppressive disorders, including HIV infection.
5
Q
What are the two clinical patterns of impetigo recognized?
A
- Nonbullous impetigo
- Bullous impetigo
6
Q
What is the primary cause of cutaneous pyodermas?
A
Staphylococcus aureus or group A Streptococcus (GAS).
7
Q
What is the role of S. epidermidis in human skin?
A
It is primarily a harmless commensal but can cause infections in certain conditions.
8
Q
How is S. aureus commonly transmitted?
A
By contact with skin of other persons or fomites rather than through the air.
9
Q
What percentage of the population has S. aureus colonized in their anterior nares?
A
Approximately 30%.
10
Q
What are the clinical implications of S. aureus being the most common cause of primary pyodermas and SSTIs?
A
The clinical implications include:
- Increased risk of infections: S. aureus is a leading cause of skin infections, necessitating prompt diagnosis and treatment to prevent complications.
- Need for effective infection control measures: Understanding its transmission routes (contact with skin or fomites) is crucial for preventing outbreaks, especially in healthcare settings.
- Consideration of antibiotic resistance: The prevalence of S. aureus, particularly MRSA strains, requires careful selection of antibiotics and monitoring for resistance patterns in treatment protocols.
11
Q
What is the most common cause of impetigo and how does it typically present?
A
Impetigo is most commonly caused by S. aureus (70% of cases), but can also be caused by GAS or both. It typically presents as erythematous papules that evolve into vesicles and pustules, leading to honey-colored crusted papules on an erythematous base, especially around the nares or on the face after trauma.
12
Q
What are the characteristics of bullous impetigo and its common demographic?
A
Bullous impetigo is caused by S. aureus strains that express exfoliative toxins, leading to clusters of thin-roofed bullae and vesicles. It occurs most commonly in newborns and older infants and is characterized by rapid progression from vesicles to flaccid bullae.
13
Q
What is ecthyma and how does it differ from impetigo?
A
Ecthyma is caused by S. aureus and/or GAS, evolving from untreated impetigo that is occluded by footwear and clothing. It produces ‘punched-out’ ulcers that extend deeply into the dermis, often healing with scarring, unlike impetigo which typically does not.
14
Q
What are the key elements in the pathogenesis of ecthyma?
A
Key elements in the pathogenesis of ecthyma include poor hygiene and neglect, often occurring in neglected elderly patients, children, and individuals with diabetes.
15
Q
How is folliculitis classified and what is its starting point?
A
Folliculitis begins within the hair follicle and is classified according to the depth of invasion (superficial and deep) and microbial etiology.
16
Q
A 5-year-old child presents with honey-colored crusted papules around the nares. What is the most likely diagnosis, and what is the causative organism?
A
The most likely diagnosis is nonbullous impetigo, commonly caused by Staphylococcus aureus or Group A Streptococcus (GAS).
17
Q
A newborn develops flaccid bullae that rupture to form thin, golden-yellow crusts. What is the diagnosis, and what toxin is responsible?
A
The diagnosis is bullous impetigo, caused by Staphylococcus aureus strains that express exfoliative toxins (ETA and ETB).
18
Q
A patient with diabetes presents with indurated, violaceous ulcers on the lower extremities. What is the diagnosis, and what are the key elements in its pathogenesis?
A
The diagnosis is ecthyma, caused by Staphylococcus aureus and/or GAS. Poor hygiene and neglect are key elements in its pathogenesis.
19
Q
What percentage of impetigo cases are caused by S. aureus or GAS?
A
70% of impetigo cases are caused by S. aureus or GAS, or both in combination.
20
Q
What is the typical progression of nonbullous impetigo lesions?
A
Nonbullous impetigo starts as erythematous papules that become vesicles and pustules, leading to honey-colored crusted papules on an erythematous base.
21
Q
What are the common areas where impetigo arises?
A
Impetigo often arises on the face, especially around the nares, or on extremities after trauma.
22
Q
What characterizes bullous impetigo?
A
Bullous impetigo is characterized by clusters of thin-roofed bullae, vesicles, and/or pustules that arise on normal skin and easily rupture.
23
Q
What is the typical appearance of bullae in bullous impetigo?
A
Bullae initially contain clear yellow fluid that becomes dark yellow and turbid, with sharply demarcated margins without an erythematous halo.
24
Q
What is ecthyma and how does it evolve?
A
Ecthyma is caused by S. aureus and/or GAS and evolves from untreated impetigo occluded by footwear and clothing, extending more deeply.
25
What are the characteristics of ulcers produced by ecthyma?
Ecthyma produces 'punched-out' ulcers that are indurated, raised, and violaceous, with a granulating base extending deeply into the dermis.
26
What are the common risk factors for developing ecthyma?
Ecthyma occurs most commonly on the lower extremities of children, neglected elderly patients, and individuals with diabetes, with poor hygiene and neglect being key elements in pathogenesis.
27
What is the classification of folliculitis based on?
Folliculitis is classified according to the depth of invasion (superficial and deep) and microbial etiology.
28
What are the clinical features and common causes of nonbullous impetigo, and how does it typically present on the skin?
**Nonbullous impetigo** is characterized by:
- **Etiology**: Primarily caused by **S. aureus** (most common) or **GAS**.
- **Demographics**: More prevalent in **children**, but can also occur in **adults**.
- **Presentation**: Begins as **erythematous papules** that evolve into **vesicles** and **pustules**. These rupture, leading to **honey-colored crusted papules** on an **erythematous base**.
- **Location**: Commonly arises on the **face** (especially around the **nares**) or **extremities** after trauma.
- **Symptoms**: Associated with **pruritus** or **soreness** in carriers of **S. aureus**.
29
Describe the pathogenesis and clinical presentation of bullous impetigo, including its common demographic and distinguishing features.
**Bullous impetigo** is characterized by:
- **Etiology**: Caused by **S. aureus** strains that produce **exfoliative toxins** cleaving **desmoglein 1** in the epidermis.
- **Demographics**: Most commonly occurs in **newborns** and **older infants**.
- **Presentation**: Features **clusters of thin-roofed bullae**, vesicles, and/or pustules on normal skin that easily rupture, leading to **crusted erosions**.
- **Fluid Characteristics**: Initially contains **clear yellow fluid** that becomes **dark yellow and turbid**.
- **Nikolsky Sign**: **Absent** in bullous impetigo.
- **Progression**: Rapid progression from vesicles to **flaccid bullae**; lesions may collapse within days, forming **light-brown to golden-yellow crusts**.
30
What are the key clinical features and complications associated with ecthyma, and how does it differ from impetigo?
**Ecthyma** is characterized by:
- **Etiology**: Caused by **S. aureus** and/or **GAS**.
- **Pathogenesis**: Evolves from untreated impetigo that is occluded by **footwear** and **clothing**, leading to deeper skin involvement.
- **Presentation**: Produces **punched-out ulcers** with **grayish-yellow crust** and **purulent material**. Lesions are **indurated**, **raised**, and **violaceous** with surrounding **edema**.
- **Complications**: Untreated lesions can enlarge over weeks to months, often healing with **scarring**.
- **Demographics**: Commonly occurs on the **lower extremities** of **children**, **neglected elderly patients**, and individuals with **diabetes**.
- **Distinction**: Should be differentiated from **ecthyma gangrenosum**, which is caused by **Pseudomonas aeruginosa**.
31
How does folliculitis develop, and what factors influence its classification and microbial etiology?
**Folliculitis** develops as:
- **Origin**: Begins within the **hair follicle**.
- **Classification**: Classified according to the **depth of invasion** (superficial and deep) and **microbial etiology**.
- **Factors Influencing Development**:
- **Microbial agents**: Various bacteria, fungi, or viruses can cause folliculitis.
- **Skin conditions**: Conditions like **atopic dermatitis** or **abrasions** can predispose individuals to folliculitis.
- **Hygiene**: Poor hygiene practices can increase the risk of developing folliculitis.
32
What is the definition of superficial folliculitis and where is it commonly found?
Superficial folliculitis, also known as follicular or Bockhart impetigo, is often found on the scalps of children and in the beard area, as well as the axillae, extremities, and buttocks of adults.
33
What are the characteristics of furuncles?
Furuncles start as hard, tender, red folliculocentric nodules in hair-bearing skin that enlarge and become painful and fluctuant. They may rupture, discharging pus and necrotic material, and can occur as solitary or multiple lesions, particularly in areas subject to friction and perspiration.
34
What are some noninfectious and inflammatory differentials of folliculitis that are more common in black men?
1. Pseudofolliculitis barbae - occurs on the lower beard area.
2. Folliculitis keloidalis - occurs on the nape of the neck.
3. Perifolliculitis capitis - occurs on the scalp.
35
What systemic host factors are associated with furunculosis?
Systemic host factors associated with furunculosis include conditions that impair immune function, such as diabetes mellitus, obesity, and other chronic illnesses.
36
What are the characteristics of furuncles?
Furuncles start as a hard, tender, red folliculocentric nodule that enlarges and becomes painful and fluctuant.
37
What can complicate the occurrence of furuncles?
Preexisting lesions such as atopic dermatitis, excoriations, abrasions, scabies, or pediculosis.
38
What is the typical presentation of a furuncle?
A hard, tender, red nodule that may rupture and discharge pus.
39
What is superficial folliculitis also known as?
Follicular or Bockhart impetigo.
40
What areas are commonly affected by superficial folliculitis?
Scalps of children and the beard area, axillae, extremities, and buttocks of adults.
41
What is sycosis barbae?
A deep folliculitis with perifollicular inflammation occurring in the bearded areas of the face and upper lip.
42
What is a common cause of hot tub folliculitis?
Pseudomonas aeruginosa.
43
What are some noninfectious and inflammatory differentials of folliculitis that are more common in black men?
Pseudofolliculitis barbae, folliculitis keloidalis, and perifolliculitis capitis.
44
What are the systemic host factors associated with furunculosis?
Obesity, blood dyscrasias, defects in neutrophil function, and immunosuppression.
45
What are the clinical features and common sites of occurrence for furuncles?
Furuncles start as a hard, tender, red folliculocentric nodule in hair-bearing skin. They enlarge and become painful and fluctuant after several days, leading to abscess formation. They may occur as solitary lesions or multiple lesions, commonly found in areas such as the buttocks, neck, face, axillae, and buttocks.
46
What are the characteristics and clinical implications of carbuncles?
More extensive, deeper, and serious inflammatory lesions that develop when multiple closely set furuncles coalesce. Commonly occur on the nape of the neck, back, or thighs. Symptoms include fever and malaise, with the patient appearing quite ill.
47
What is botryomycosis and what are its predisposing factors?
Botryomycosis is a rare pyogenic disease presenting as a purulent, chronic, subcutaneous infection. Predisposing factors include trauma, immunosuppression, chronic alcoholism, and diabetes mellitus.
48
What are the clinical features of Staphylococcal paronychia?
Predisposition in individuals exposed to hand trauma or chronic moisture. Caused primarily by S. aureus, often around the fingernails, originating from a break in the skin.
49
What distinguishes Staphylococcal Whitlow from herpetic whitlow?
S. aureus - Red, hot, tender finger bulb with possible abscess formation
Herpes simplex virus - Grouped hemorrhagic vesicles that may become confluent
| Feature | Staphylococcal Whitlow | Herpetic Whitlow |
50
What systemic signs may indicate a serious infection requiring immediate antibiotic therapy?
Signs of systemic infection may include temperature higher than 38°C or lower than 36°C, tachypnea exceeding 24 breaths per minute, tachycardia exceeding 90 beats per minute, and abnormal white blood cell counts.
51
What complications can arise from S. aureus infections?
Can lead to cellulitis, lymphangitis, and bacteremia, which may result in life-threatening infections in various organs.
52
What is a carbuncle and how does it develop?
A carbuncle is a more extensive, deeper, and serious inflammatory lesion that develops when multiple closely set furuncles coalesce.
53
What are the common sites for abscess formation?
Abscesses occur at sites of trauma, foreign bodies, burns, or sites of insertion of intravenous catheters.
54
What is the major infectious cause of acute paronychia?
The major infectious cause of acute paronychia is Staphylococcus aureus.
55
What are the signs of systemic infection in skin infections?
Signs of systemic infection may include temperature higher than 38°C, tachypnea exceeding 24 breaths per minute, tachycardia exceeding 90 beats per minute, and abnormal white blood cell counts.
56
What are the potential complications of untreated staphylococcal infections?
Untreated staphylococcal infections can lead to serious complications, including cellulitis, lymphangitis, and bacteremia.
57
What are the risk factors for S. aureus skin and soft tissue infections?
Risk factors include colonization in mucosal sites and skin, preexisting tissue injury, immunodeficiency disorders, and conditions resulting in defective neutrophil function.
58
What are the virulence factors of S. aureus that promote colonization and infection?
Virulence factors include pore-forming toxins that lyse host cells, such as α-hemolysin.
59
What are the genetic or acquired deficiencies that affect neutrophil number or function?
Genetic disorders (e.g., chronic granulomatous disease) or acquired conditions (e.g., diabetes, cancer patients on chemotherapy).
60
What is a genetic or acquired deficiency of interleukin (IL)-17 responses?
Job’s syndrome.
61
What are the virulence factors of S. aureus that promote colonization and infection?
Virulence factors include pore-forming toxins, exfoliative toxins, superantigens/enterotoxins, inhibition of neutrophil function, and other factors like catalase and protein A.
62
How does S. aureus evade the immune system?
S. aureus evades the immune system through production of inhibitory proteins, pore-forming toxins, superantigens, catalase, and protein A.
63
What laboratory tests are recommended for diagnosing impetigo and ecthyma?
Gram stain and culture of pus or exudates to identify S. aureus (including MRSA) and/or GAS.
64
What is the role of antimicrobial peptides in the immune response to S. aureus?
Antimicrobial peptides are produced by keratinocytes and other immune cells, helping to kill bacteria and modulate the immune response.
65
What diagnostic tests are recommended to confirm the causative organism in a skin abscess?
Gram stain and culture of pus or exudates.
66
What virulence factor inhibits neutrophil chemotaxis?
The chemotaxis inhibitory protein of Staphylococcus aureus (CHIPS).
67
What virulence factor blocks antibody-mediated phagocytosis?
Protein A on the surface of Staphylococcus aureus.
68
What virulence factor degrades neutrophil extracellular traps (NETs)?
Staphylococcal nuclease (Nuc).
69
What virulence factor targets desmoglein 1?
Exfoliative toxins (ETA, ETB, and ETD).
70
What virulence factor is associated with toxic shock syndrome?
Toxic shock syndrome toxin-1 (TSST-1).
71
What virulence factor is responsible for the golden color of Staphylococcus aureus colonies?
Staphyloxanthin, a yellow carotenoid pigment.
72
What virulence factor targets ADAM10?
Alpha-toxin (α-toxin).
73
What virulence factor targets C5a receptors?
Panton-Valentine leukocidin (PVL).
74
What virulence factor targets CCR5, CXCR1, and CXCR2?
Leukocidin ED (LukED).
75
What virulence factor blocks P-selectin and ICAM-1?
Staphylococcal superantigen-like proteins (SSL5 and SSL11) and extracellular adherence protein (Eap).
76
What virulence factor nonspecifically activates T cells?
Superantigens interact with human leukocyte antigen-DR molecules.
77
What virulence factor inhibits reactive oxygen-mediated killing?
Catalase, alkyl hydroperoxide reductase, and staphyloxanthin.
78
What virulence factor is associated with increased severity of atopic dermatitis?
Staphylococcus aureus superantigens, especially SEB.
79
What virulence factor is associated with community-acquired MRSA?
Alpha-toxin (α-toxin) and Panton-Valentine leukocidin (PVL).
80
What virulence factor correlates with protection against recurrent infections?
High serum antibody titers against alpha-toxin (α-toxin).
81
What virulence factor is located in Staphylococcus aureus bacteriophages?
Exfoliative toxins ETA and ETB.
82
What virulence factor is located in the bacterial chromosome?
Exfoliative toxin ETD.
83
What virulence factor blocks complement and formyl peptide receptors?
Chemotaxis inhibitory protein of Staphylococcus aureus (CHIPS).
84
What virulence factor blocks CXCR2 neutrophil-attracting chemokines?
Staphopain A (ScpA).
85
What virulence factor prevents NETosis-mediated killing?
Adenosine synthase A (AdsA) and staphylococcal nuclease (Nuc).
86
What virulence factor is responsible for staphylococcal scalded-skin syndrome?
Exfoliative toxins (ETA and ETB).
87
What virulence factor is responsible for toxic shock syndrome?
Toxic shock syndrome toxin-1 (TSST-1).
88
What are the risk factors for S. aureus skin and soft tissue infection?
Colonization in mucosal sites and skin, preexisting tissue injury or inflammation, immunodeficiency disorders, and genetic or acquired deficiency of interleukin (IL)-17 responses.
89
What are pore-forming toxins associated with S. aureus?
Single-component α-hemolysin and biocomponent leukotoxins like Panton-Valentine leukocidin (PVL).
90
What is the role of exfoliative toxins in S. aureus infections?
They are serine proteases that target desmoglein 1.
91
How do superantigens affect T cells in S. aureus infections?
They nonspecifically activate T cells by interacting with human leukocyte antigen-DR molecules.
92
What is the significance of IL-1β in S. aureus infections?
IL-1β induces neutrophil recruitment and abscess formation.
93
What laboratory tests are recommended for diagnosing impetigo and ecthyma?
Gram stain and culture of pus or exudates to identify S. aureus or GAS.
94
What is the recommended approach for large furuncles, carbuncles, and abscesses?
Culture of pus following incision and drainage is strongly recommended.
95
What is the purpose of biopsy or aspiration in patients with extensive furuncles or abscesses?
To perform histologic evaluation and microbiology cultures.
96
What are the risk factors associated with S. aureus skin and soft tissue infections?
Colonization, preexisting tissue injury, immunodeficiency disorders, defective neutrophil function, and genetic deficiency of IL-17 responses (Job syndrome).
97
How do pore-forming toxins contribute to the virulence of S. aureus?
Pore-forming toxins like α-hemolysin and PVL lyse host immune cells, impairing the immune response.
98
What role do superantigens play in S. aureus infections?
Superantigens nonspecifically activate T cells, leading to increased cytokine release and severe inflammatory responses.
99
How does the activation of the inflammasome contribute to the immune response against S. aureus infections?
Pore-forming toxins induce phagosomal rupture, activating caspase-1 and promoting IL-1β release.
100
What histological findings are characteristic of a furuncle?
A dense polymorphonuclear inflammatory process in the dermis and subcutaneous fat.
101
What are the clinical implications of untreated S. aureus skin infections?
Untreated infections can lead to invasive spread, cellulitis, lymphangitis, and bacteremia.
102
What is the recommended treatment for localized impetigo?
Mupirocin 2% topical ointment or retapamulin 1% ointment twice daily for 5 to 7 days.
103
What should be considered when imaging is indicated in cases of furuncles or carbuncles?
Imaging is indicated in febrile neutropenic patients with extensive lesions.
104
What is the first-line oral antibiotic treatment for impetigo caused by methicillin-sensitive S. aureus?
Dicloxacillin or cephalexin.
105
What are the recommended initial empiric antibiotics for suspected CA-MRSA?
Doxycycline, clindamycin, or TMP-SMX.
106
What is a suitable substitute for treating impetigo in a patient with a penicillin allergy?
Erythromycin is suitable, but resistance is common.
107
What does histologic examination of a furuncle reveal?
A dense polymorphonuclear inflammatory process.
108
What is the typical imaging indication for furuncles and carbuncles?
Imaging is not typically indicated except in febrile neutropenic patients.
109
What is the potential consequence of untreated S. aureus infections?
Invasive spread of the infection.
110
What is the recommended topical treatment for impetigo?
Mupirocin 2% topical ointment or retapamulin 1% ointment.
111
What is the typical imaging indication for furuncles and carbuncles?
Imaging is not typically indicated except in febrile neutropenic patients with extensive furuncles, carbuncles, or abscesses.
112
What is the potential consequence of untreated S. aureus infections?
There is a potential for invasive spread of the infection, resulting in cellulitis, lymphangitis, and bacteremia.
113
What is the recommended topical treatment for impetigo?
Mupirocin 2% topical ointment or retapamulin 1% ointment twice daily for 5 to 7 days.
114
What oral antibiotic is commonly recommended for methicillin-sensitive S. aureus infections?
Dicloxacillin or cephalexin.
115
What should be done if CA-MRSA is suspected in a patient?
Doxycycline, clindamycin, or TMP-SMX are recommended for initial empiric therapy.
116
What is the importance of continuing oral antibiotic treatment for skin infections?
Oral antibiotic treatment should be continued for 7 days (10 days if streptococci are isolated).
117
What are the side effects of fusidic acid when used for localized impetigo?
Fusidic acid has few adverse side effects.
118
What is the clinical significance of S. aureus in skin infections?
S. aureus can disseminate and cause infections of many organs and tissues, such as osteomyelitis and pneumonia.
119
What histological findings are characteristic of a furuncle and carbuncle caused by Staphylococcus aureus?
A furuncle shows a dense polymorphonuclear inflammatory process in the dermis and subcutaneous fat. In carbuncles, there are multiple abscesses separated by connective-tissue trabeculae present in the dermis, especially along the edges of hair follicles, reaching the skin surface through openings in the undermined epidermis.
120
What are the potential complications of untreated Staphylococcus aureus skin infections?
If untreated, Staphylococcus aureus skin infections can lead to invasive spread resulting in: 1. Cellulitis 2. Lymphangitis 3. Bacteremia 4. Infections of various organs such as osteomyelitis, septic arthritis, endocarditis, pneumonia, and sepsis.
121
What is the recommended management for impetigo caused by Staphylococcus aureus?
The management for impetigo includes: 1. Topical treatment: Mupirocin 2% ointment or retapamulin 1% ointment twice daily for 5 to 7 days. 2. Physical removal: Gentle cleansing of the affected area with soap and water. 3. Oral antibiotics: Dicloxacillin or cephalexin for adults; for children, appropriate dosing based on weight is recommended. 4. Alternative options: For penicillin-allergic patients, erythromycin can be used, but resistance is common. Other options include amoxicillin with clavulanic acid or clindamycin for children.
122
What imaging considerations should be taken into account for patients with extensive furuncles or carbuncles?
Imaging is not typically indicated except in cases of febrile neutropenic patients with extensive furuncles, carbuncles, or abscesses. It is important if there is a concern for underlying osteomyelitis or if there is an indolent pulmonary site of Staphylococcus aureus infection, which can spread to the overlying skin and soft tissues.
123
What are the first-line oral antibiotics for treating folliculitis caused by Staphylococcus aureus?
The first-line oral antibiotics for treating folliculitis include: 1. Dicloxacillin: 250 to 500 mg orally 4 times a day for adults. 2. Cephalexin: 500 mg orally 4 times a day for adults; for children, 50 to 100 mg/kg/day divided 3 to 4 times per day. 3. Erythromycin: Can be used for patients allergic to penicillin, but resistance is common.
124
What is the recommended treatment for simple furuncles, carbuncles, and abscesses?
Incision and drainage (I&D) is often performed and is likely adequate, but additional antibiotic coverage has a better cure rate.
125
What adjunctive therapy should be considered for patients with severe or extensive disease after I&D?
Adjunctive antibiotic therapy should be added if there is severe or extensive disease with multiple sites of infection, surrounding cellulitis, or signs of systemic infection or inflammation.
126
What should be done for severe infections or infections in dangerous areas?
Maximal antibiotic dosage should be employed by the parenteral route.
127
What is the role of vancomycin in treating serious purulent infections?
Vancomycin or other systemic parenteral agents with anti-CA-MRSA activity are indicated for patients with serious purulent infections.
128
What is the recommended duration for antibiotic treatment in cases of furuncles, carbuncles, and abscesses?
Antibiotic treatment should be continued for at least 7 to 14 days and until all evidence of inflammation has regressed.
129
What preventive measures should be taken to avoid reinfection of draining wounds?
Draining wounds should be kept clean and covered with clean and dry bandages, and frequent hand cleansing is important after contacting infected skin.
130
What should be done to decolonize patients with recurrent S. aureus SSTIs?
Nasal decolonization can be achieved with mupirocin ointment administered to the nares twice daily for 5 to 10 days, along with body decolonization using chlorhexidine or bleach baths.
131
What is the importance of cleaning fomites in the environment?
Fomites can serve as a reinfection source and should be routinely cleaned with antimicrobial commercial cleansers and detergents.
132
What should be considered for recurrent furuncles, carbuncles, and abscesses at the same site of prior infection?
A source for other etiologies should be considered, such as hidradenitis suppurativa, a pilonidal cyst, or a foreign body.
133
What is the significance of evaluating children or adults with recurrent abscesses that began in childhood?
They should be evaluated for neutrophil disorders or other primary immunodeficiency syndromes.
134
A patient presents with recurrent skin abscesses. What underlying conditions should be evaluated?
Evaluate for neutrophil disorders or other primary immunodeficiency syndromes.
135
What is the initial treatment for simple furuncles, carbuncles, and abscesses?
Incision and drainage (I&D) is often performed and is likely adequate, but additional antibiotic coverage has a better cure rate.
136
What is the recommended duration for antibiotic treatment in cases of furuncles, carbuncles, and abscesses?
Antibiotic treatment should be continued for at least 7 to 14 days until all evidence of inflammation has regressed.
137
What hygiene measures should be taken to prevent reinfection of furuncles and carbuncles?
Draining wounds should be kept clean and covered with clean and dry bandages, and hands should be frequently cleansed with soap and water or alcohol-based hand gels.
138
What should be considered for recurrent furuncles, carbuncles, and abscesses at the same site?
A source for other etiologies should be considered, such as hidradenitis suppurativa, a pilonidal cyst, or a foreign body.
139
What is the role of mupirocin ointment in the management of S. aureus infections?
Nasal decolonization of S. aureus can be achieved with mupirocin ointment administered to the nares twice daily for 5 to 10 days.
140
What should be done if decolonization measures are ineffective?
Oral antibiotic treatment according to the treatment regimens could be used in conjunction with rifampin.
141
Why is rifampin used in combination with other antibiotics?
Rifampin can only be used in combination with other systemic antibiotics because rapid antibiotic resistance develops if rifampin is used as a single agent.
142
What should be done for children or adults with recurrent abscesses that began in childhood?
They should be evaluated for neutrophil disorders or other primary immunodeficiency syndromes.
143
What is the importance of cleaning fomites in the environment?
Fomites can serve as a reinfection source and should be routinely and repeatedly cleaned with antimicrobial commercial cleansers and detergents.
144
What adjunctive therapy should be considered for patients with severe or extensive furuncles, carbuncles, or abscesses who have failed prior treatment with incision and drainage alone?
Adjunctive antibiotic therapy should be added for patients with severe or extensive disease, especially if there are multiple sites of infection, surrounding cellulitis, or signs of systemic infection or inflammation.
145
What is the recommended duration for antibiotic treatment in cases of furuncles, carbuncles, and abscesses, and when should it be continued?
Antibiotic treatment should be continued for at least 7 to 14 days and should be maintained until all evidence of inflammation has regressed.
146
What measures should be taken to prevent autoinoculation in patients with draining lesions from furuncles, carbuncles, or abscesses?
Draining lesions should be covered with dry bandages to prevent autoinoculation, and diligent hand-washing should be performed.
147
In cases of recurrent S. aureus SSTIs, what decolonization regimen can be attempted?
Nasal decolonization of S. aureus can be achieved with mupirocin ointment administered to the nares twice daily for 5 to 10 days, along with body decolonization using chlorhexidine cleansing solution or bleach baths.
148
What is the significance of using rifampin in the treatment of recurrent infections, and how should it be used?
Rifampin can only be used in combination with other systemic antibiotics to prevent rapid antibiotic resistance; it should not be used as a single agent.
149
What are the key steps in the diagnostic and management algorithm for Staphylococcus aureus infections?
1. History: Gather patient history including symptoms and previous infections. 2. Clinical Examination: Assess the patient for signs of infection. 3. Classify Infection and Assess Severity: Determine the type and severity of the infection. 4. Laboratory Testing: Conduct necessary tests to confirm the diagnosis. 5. Treatment: Based on classification and severity, initiate appropriate treatment.
150
What factors are considered when classifying the severity of Staphylococcus aureus infections?
Clinical Features: Presence of systemic symptoms, local signs of infection. Patient History: Previous infections, underlying health conditions. Laboratory Results: Culture results, sensitivity to antibiotics. Response to Treatment: Monitoring the patient's response to initial treatment.
151
What are the management strategies for Staphylococcus aureus skin infections?
| Management Strategy | Description |
|---------------------|-------------|
| Antibiotic Therapy | Use appropriate antibiotics based on culture and sensitivity results. |
| Surgical Intervention | Drainage of abscesses or infected areas if necessary. |
| Supportive Care | Pain management, wound care, and monitoring for complications. |
| Follow-up | Regular follow-up to assess treatment efficacy and prevent recurrence.
152
What is the first step in the diagnostic algorithm for Staphylococcus aureus infections?
Obtain a thorough history and clinical examination.
153
What factors are considered when classifying the severity of a Staphylococcus aureus infection?
Clinical examination findings and patient history.
154
What is the management approach for mild Staphylococcus aureus skin infections?
Oral antibiotics may be prescribed based on susceptibility.
155
What is a key consideration in the treatment of severe Staphylococcus aureus infections?
Intravenous antibiotics may be necessary, and cultures should guide therapy.
156
What role does laboratory testing play in managing Staphylococcus aureus infections?
It helps in identifying the organism and determining antibiotic susceptibility.
157
What is the significance of assessing the patient's clinical history in Staphylococcus aureus infections?
It aids in understanding the context and potential risk factors for infection.
158
What are common clinical features to look for in Staphylococcus aureus infections?
Signs of infection such as redness, swelling, and pus formation.
159
What is the importance of classifying the infection severity in Staphylococcus aureus cases?
It guides the treatment approach and management decisions.
160
What are the key steps in the diagnostic and management algorithm for Staphylococcus aureus infections?
1. History: Gather patient history including symptoms and previous infections. 2. Clinical Examination: Assess the patient for signs of infection, such as fever, skin lesions, and lymphadenopathy. 3. Classification of Infection: Determine the type of infection (e.g., skin, soft tissue, systemic). 4. Assess Severity: Evaluate the severity of the infection based on clinical findings and laboratory tests. 5. Management: Implement appropriate treatment based on the classification and severity, including antibiotics and possible surgical intervention.
161
How should a clinician classify and assess the severity of a Staphylococcus aureus infection based on clinical examination?
- Classification: Identify the type of infection (e.g., impetigo, cellulitis, abscess).
- Assessment of Severity:
- Check for systemic symptoms (fever, chills).
- Evaluate local signs (swelling, redness, pain).
- Consider risk factors (immunocompromised status, presence of foreign bodies).
- Use laboratory tests (CBC, cultures) to support the assessment.
162
What are the treatment options for Staphylococcus aureus skin infections based on severity?
| Severity Level | Treatment Options |
|----------------|------------------|
| Mild | Oral antibiotics (e.g., cephalexin, dicloxacillin) |
| Moderate | Oral or IV antibiotics (e.g., clindamycin, TMP-SMX) |
| Severe | IV antibiotics (e.g., vancomycin, daptomycin) and possible surgical intervention |
| Complicated | Consult infectious disease specialist for tailored therapy and management |
163
Is Nikolski sign present in bullous impetigo?
Absent
164
Do endotoxins that cause bullous impetigo target the same cadherin protein that affects pemphigus vulgaris?
Yes (dsg-1)
165
Is non-bullous impetigo mostly seen in children?
True
166
Is ecthyma frequently seen on the lower extremities of children, neglected elderly patients, and individuals with diabetes?
Yes
167
Are broken or loosened hair, suppurative or granulomatous nodules rather than pustules and painless hair when plucked seen in staphylococcal folliculitis?
No. It is seen in dermatophytic folliculitis.
168
Is staphylococcal paronychia an infection of the space created by separation of the proximal dorsal nail plate and the undersurface of the proximal nailfold?
No - candidal paronychia
169
For simple furuncles, carbuncles, and abscesses, is incision and drainage (I&D) alone often performed and likely to be adequate but additional antibiotic coverage has a better cure rate?
True
170
Are surveillance cultures of nares or body sites following decolonization regimens typically necessary even in the absence of recurrent infections?
True
171
Can rifampin only be used in combination with other systemic antibiotics because rapid antibiotic resistance develops if rifampin is used as a single agent?
True
172
Is vancomycin available as an oral agent and has excellent (100%) bioavailability when given orally or intravenously?
True
173
Which of the following is not a feature of systemic inflammatory response syndrome?
a. Temperature higher than 38°C (100.4°F) or lower than 36°C (96.8°F)
174
Which of the following is a pore-forming toxin?
a. Panton-Valentin leucocidin
175
Is rifampin used as a single agent?
True
176
Lesions about the lips and nose can spread via which two routes to the cavernous sinus?
Facial veins and cavernous sinus
177
What has a gross appearance of a ruptured epidermal inclusion cyst or prurigo nodularis?
An erythematous circumscribed tender nodule
178
What is the substitute and dosage of the medication used in patients with penicillin or B-lactam antibiotic allergy?
Clindamycin or macrolides, dosage varies based on infection type
179
What are 3 medications used if there is a suspected CA-MRSA infection?
1. Trimethoprim-sulfamethoxazole
2. Clindamycin
3. Doxycycline
180
What is the regimen for nasal decolonization?
1. Mupirocin nasal ointment applied twice daily for 5 days
2. Chlorhexidine body wash
3. Daily nasal saline rinses
181
What is the regimen for bleach bath?
1. Add 1/2 cup of household bleach to a full bathtub of water
2. Soak for 10-15 minutes
3. Rinse off thoroughly with water
182
Is Nikolski sign present in bullous impetigo?
True
183
What is the clinical significance of Nikolski sign in relation to bullous impetigo?
Nikolski sign is typically present in **bullous impetigo**, indicating the fragility of the skin and the presence of **blistering** lesions. This sign helps differentiate bullous impetigo from other skin conditions such as **pemphigus vulgaris**.
184
How does the presence of endotoxins in bullous impetigo relate to pemphigus vulgaris?
Endotoxins in bullous impetigo target the same **cadherin protein** that is affected in **pemphigus vulgaris**, leading to similar blistering skin manifestations. This relationship highlights the **pathophysiological similarities** between the two conditions.
185
What demographic is most affected by non-bullous impetigo and what are its common characteristics?
**Non-bullous impetigo** is mostly seen in **children** and is characterized by **crusted lesions** that are often **painless** and can appear on the face and extremities. It is important to recognize this form for appropriate management.
186
What are the common sites for ecthyma and which populations are most at risk?
**Ecthyma** is frequently seen on the **lower extremities** of children, neglected elderly patients, and individuals with **diabetes**. This condition is characterized by **ulcerative lesions** that can lead to complications if not treated promptly.
187
What is the clinical implication of staphylococcal paronychia?
**Staphylococcal paronychia** is an infection that occurs in the space created by the separation of the **proximal dorsal nail plate** and the undersurface of the proximal nailfold. It can lead to **painful swelling** and requires appropriate management to prevent further complications.
188
What is the recommended management for simple furuncles and carbuncles?
For simple **furuncles**, **carbuncles**, and **abscesses**, incision and drainage (I&D) alone is often performed and is likely to be adequate. However, additional **antibiotic coverage** may improve the **cure rate** and prevent recurrence.
189
What is the importance of surveillance cultures in decolonization regimens?
**Surveillance cultures** of nares or body sites following decolonization regimens are typically necessary even in the absence of recurrent infections. This practice helps to monitor for **persistent colonization** and guides further management strategies.
190
Why is rifampin used in combination with other systemic antibiotics?
**Rifampin** can only be used in combination with other systemic antibiotics because **rapid antibiotic resistance** develops if rifampin is used as a single agent. This combination is crucial for effective treatment of certain infections, particularly those caused by **Staphylococcus aureus**.
191
What is the significance of vancomycin's bioavailability when treating infections?
**Vancomycin** is available as an oral agent and has excellent (100%) **bioavailability** when given orally or intravenously. This characteristic is significant for treating **serious infections** caused by resistant bacteria, ensuring effective therapeutic levels are achieved.
192
What is the primary cause of superficial skin infections known as pyodermas?
Group A Streptococcus (Streptococcus pyogenes) is the primary cause of superficial skin infections, also known as pyodermas, which include conditions like impetigo, ecthyma, and blistering distal dactylitis.
193
What are the common clinical features of GAS impetigo?
GAS impetigo presents as a crusted superficial infection of the skin, characterized by honey-colored crusted papules, often painless, with potential pruritus and burning.
194
What are the epidemiological factors associated with GAS infections?
GAS infections are primarily transmitted through respiratory droplets. They affect 15% of school-age children and 4% to 10% of adults in industrialized countries.
195
What are the severe infections caused by Group A Streptococcus?
Severe infections caused by Group A Streptococcus include necrotizing fasciitis, cellulitis, erysipelas, lymphangitis, bacteremia, septic arthritis, osteomyelitis, pneumonia, meningitis, and streptococcal toxic shock syndrome.
196
What are the characteristics of blistering distal dactylitis caused by GAS?
Blistering distal dactylitis, also known as bulla repens, is primarily caused by GAS and S. aureus, usually occurring in children and adolescents. It is characterized by the formation of blisters on the distal phalanges.
197
What factors contribute to the spread of GAS impetigo?
Crowding, poor hygiene, and neglected minor skin trauma.
198
What is the peak seasonal incidence for GAS impetigo?
Late summer and early fall.
199
What is the significance of the M protein in Group A Streptococcus?
It is a key virulence factor used for serotyping GAS isolates.
200
What is the typical age group affected by GAS impetigo?
Predominantly preschool age children.
201
What is the clinical appearance of ecthyma caused by GAS?
It is indistinguishable from S. aureus ecthyma.
202
What are the common sites for intertriginous streptococcal infections?
Perineum, vulva, axillae, and web spaces of the feet.
203
What are the potential complications of untreated perianal streptococcal cellulitis in children?
Intense perianal erythema, pain on defecation, and chronicity.
204
What is the likely diagnosis for a patient with a crusted superficial skin infection?
The most likely diagnosis is nonbullous impetigo caused by GAS. Predisposing factors include preexisting lesions (e.g., scabies, varicella, eczema), crowding, poor hygiene, and neglected minor skin trauma.
205
What is the likely diagnosis for a child with intense perianal erythema and blood-streaked stools?
The likely diagnosis is perianal (group A) streptococcal cellulitis. It might be confused with psoriasis, candidiasis, seborrheic dermatitis, inflammatory bowel disease, pinworm infection, or a behavioral problem.
206
What is the likely diagnosis for a patient with a superficial skin infection involving the perineum and axillae?
The likely diagnosis is intertriginous streptococcal infection caused by GAS.
207
What is the diagnosis for a patient with a history of GAS pharyngitis who develops a morbilliform rash?
The diagnosis is scarlet fever, caused by streptococcal pyrogenic exotoxins.
208
What additional interventions might be necessary for a patient with necrotizing fasciitis caused by GAS?
Additional interventions include surgical debridement and supportive care for sepsis and multiorgan failure.
209
What are the key diagnostic features for a patient with suspected GAS infection and necrotizing fasciitis?
Key diagnostic features include rapid progression of soft tissue necrosis, systemic toxicity, and severe pain disproportionate to physical findings.
210
What are the distinguishing features of erysipelas?
Erysipelas is characterized by infection of the superficial layers of the skin and lymphatics, with well-demarcated erythema.
211
What are the common clinical features of GAS impetigo?
GAS impetigo presents as a crusted superficial infection of the skin, characterized by honey-colored crusted papules.
212
What factors contribute to the spread of GAS impetigo in communities?
Factors contributing to the spread of GAS impetigo include crowding, poor hygiene practices, neglected minor skin trauma, preexisting skin conditions, and contact sports.
213
What are the potential complications associated with untreated GAS infections?
Untreated GAS infections can lead to serious complications, including necrotizing fasciitis, acute rheumatic fever, glomerulonephritis, and severe invasive infections.
214
How does the clinical presentation of ecthyma caused by GAS compare to that caused by S. aureus?
Ecthyma caused by GAS is clinically indistinguishable from that caused by S. aureus, presenting similarly as a deeply seated ulcerative skin infection.
215
What is the significance of the M protein in the classification and virulence of GAS infections?
The M protein is significant because it is a key virulence factor for GAS infections, influencing the severity and type of disease.
216
What is acute lymphangitis and what are its common causes?
Acute lymphangitis is an inflammatory process involving the subcutaneous lymphatic channels, usually caused by Group A Streptococcus (GAS).
217
What are the clinical manifestations of acute lymphangitis?
Acute lymphangitis presents as the rapid onset of red linear streaks extending from the local portal of entry toward the regional lymph nodes.
218
What complications can arise from GAS skin infections?
Complications from GAS skin infections can include GAS erysipelas, cellulitis, streptococcal gangrene, necrotizing fasciitis, and poststreptococcal glomerulonephritis.
219
What are the risk factors for GAS skin infections?
Risk factors for GAS skin infections include colonization by GAS in the nasopharynx and skin, crowding, poor hygiene, poverty, and preexisting tissue injury or inflammation.
220
How does poststreptococcal glomerulonephritis typically present and when does it occur?
Poststreptococcal glomerulonephritis typically occurs 1 to 3 weeks following GAS pharyngitis and 3 to 6 weeks following GAS impetigo.
221
What are the common portals of entry for infections leading to acute lymphangitis?
Common portals of entry include wounds on an extremity, infected blisters, or paronychia.
222
What are the clinical features of acute lymphangitis caused by Group A Streptococcus (GAS)?
Acute lymphangitis typically presents with rapid onset of red linear streaks extending from the portal of entry toward regional lymph nodes.
223
What is poststreptococcal glomerulonephritis and when does it typically occur?
Poststreptococcal glomerulonephritis typically occurs 1 to 3 weeks following GAS pharyngitis and 3 to 6 weeks following GAS impetigo.
224
What is the frequency of occurrence of poststreptococcal glomerulonephritis after GAS infections?
The frequency of occurrence is higher following a GAS skin infection (25%) than following GAS pharyngitis (approximately 5%).
225
What is the significance of the absence of a portal of entry in diagnosing acute lymphangitis?
The absence of a portal of entry and tender regional adenopathy helps distinguish superficial thrombophlebitis from acute lymphangitis.
226
What is the relationship between GAS infections and rheumatic fever?
Acute rheumatic fever occurs in less than 1% of patients with a GAS infection, typically 2 weeks following a GAS pharyngitis infection.
227
What are the major manifestations of rheumatic fever according to Jones criteria?
Major manifestations include arthritis, endocarditis, chorea, erythema marginatum, and subcutaneous nodules.
228
What is the diagnosis for a patient with red linear streaks extending from a wound on the hand?
The diagnosis is acute lymphangitis, commonly caused by GAS. Complications to monitor include subpectoral abscesses, pleural effusion, and systemic infection.
229
What is the likely diagnosis for a patient with edema, hematuria, and hypertension following GAS pharyngitis?
The likely diagnosis is poststreptococcal glomerulonephritis, which typically occurs 1 to 3 weeks following GAS pharyngitis.
230
What is the diagnosis for a patient with a large blister filled with seropurulent fluid on the distal finger?
The diagnosis is blistering distal dactylitis, commonly caused by GAS or S. aureus. Treatment includes systemic antibiotics and incision and drainage (I&D) to release subungual pus.
231
What condition might indicate a history of GAS infection with choreoathetosis and obsessive-compulsive disorder?
This might indicate Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS).
232
What is the likely diagnosis for a patient with erythema marginatum and arthritis after a GAS infection?
The likely diagnosis is acute rheumatic fever. Diagnosis is based on the Jones criteria.
233
What is the underlying mechanism for erythema nodosum following a GAS infection?
Erythema nodosum is a cutaneous sequela of GAS infection, likely mediated by an immunologic response.
234
What is the timeline for Sydenham chorea after a GAS infection?
Sydenham chorea can appear with acute rheumatic fever or up to 6 months after the preceding GAS infection.
235
What is the likely trigger for guttate psoriasis following a GAS infection?
The likely trigger is an immunologic response following a GAS infection.
236
What are the complications of untreated GAS infections?
Untreated GAS infections can lead to serious complications, including:
- Erysipelas
- Cellulitis
- Lymphangitis
- Bacteremia
- Necrotizing fasciitis
## Footnote
The clinical significance of these complications is that they can result in invasive spread of the infection, which may require aggressive treatment and can lead to severe systemic illness or even death if not managed promptly.
237
What are the risk factors for GAS skin infections?
Risk factors for GAS skin infections include:
1. Colonization by GAS in the nasopharynx and skin.
2. Crowding.
3. Poor hygiene.
4. Poverty.
5. Preexisting tissue injury or inflammation.
238
How does poststreptococcal glomerulonephritis typically present?
Poststreptococcal glomerulonephritis typically presents with:
- Edema
- Hematuria
- Hypertension
## Footnote
It usually resolves without specific treatment, but renal failure can occur in some cases.
239
What is the significance of the absence of a portal of entry in diagnosing acute lymphangitis?
The absence of a portal of entry and tender regional adenopathy is crucial in distinguishing acute lymphangitis from superficial thrombophlebitis, as it indicates that the infection is not due to a superficial vein inflammation but rather a deeper lymphatic infection.
240
What are the chromosomal patterns of the emm gene associated with different infections caused by GAS?
The emm gene can be classified into patterns A to E:
| Pattern | Associated Infection |
|---------|---------------------|
| A, B, C | Pharyngitis |
| D | Skin infections |
| E | Both pharyngitis and skin infections |
241
How does the M protein of GAS contribute to its virulence?
The M protein is a multifunctional virulence factor that:
- Binds to regulators of the complement system, inhibiting activation of classic and alternative pathways.
- Interacts with the Fc region of IgG, inhibiting antibody-mediated phagocytosis.
- Induces inflammation by interacting with TLR2 on monocytes, leading to proinflammatory cytokine production.
- Facilitates invasion of host cells by binding to extracellular matrix components and CD46 on keratinocytes.
242
What role do neutrophils play in the immune response against GAS infections?
Neutrophils are crucial in host defense against GAS infections. They:
- Produce reactive oxygen species to kill pathogens.
- Are targeted by GAS mechanisms to evade immune function, including the production of enzymes that inhibit reactive oxygen-mediated killing.
- Are recruited to the site of infection, which is mediated by pattern recognition receptors like TLR2, NOD2, and TLR9.
243
What laboratory tests are recommended for diagnosing GAS infections?
For diagnosing GAS infections, the following laboratory tests are recommended:
- Gram stain: Typically reveals Gram-positive cocci in chains (GAS) or clusters (S. aureus).
- Bacterial culture and sensitivity: Important for determining the cause of infection and guiding treatment.
- Blood cultures: Obtained in cases of lymphangitis or suspected bacteremia.
- Antibody titers: Antistreptolysin O and anti-deoxyribonuclease B titers help determine antecedent GAS infections.
244
What challenges exist in developing an effective vaccine against GAS?
Developing an effective vaccine against GAS is challenging due to:
- The substantial genetic diversity among clinical isolates, with over 200 different emm types identified.
- The need for a vaccine to target multiple M protein types to provide broad protection against various strains.
245
What are the key pore-forming toxins produced by GAS?
Streptolysin O and streptolysin S.
246
What is the significance of GAS superantigens?
They nonspecifically activate T cells and contribute to the pathogenesis of infections like streptococcal toxic shock syndrome and scarlet fever.
247
What is the importance of neutrophils in host defense against GAS?
Neutrophils are crucial for immune defense, but GAS has mechanisms to evade their function.
248
What is the role of TLR9 in host defense against GAS?
TLR9 recognizes hypomethylated DNA from bacteria and GAS DNA, promoting an immune response.
249
What do high antistreptolysin O titers indicate?
They are more common after GAS pharyngitis.
250
Why are biopsies recommended in immunocompromised patients with suspected GAS infections?
For histologic evaluation and to help direct appropriate antibiotic therapy.
251
What are the key virulence factors of GAS involved in necrotizing fasciitis?
Key virulence factors include M protein, streptolysin O, streptolysin S, and streptococcal pyrogenic exotoxins.
252
What laboratory tests should be performed for a patient with GAS infection and systemic inflammatory response syndrome (SIRS)?
Tests include body temperature, respiratory rate, peripheral blood counts, and blood cultures to evaluate for systemic infection or inflammation.
253
What findings would confirm a diagnosis of GAS infection from Gram staining?
Gram staining would reveal Gram-positive cocci in chains, characteristic of GAS.
254
What alternative diagnostic methods can be used if a patient with acute lymphangitis has negative skin cultures?
Alternative methods include cultures from aspirated fluid, biopsy of the portal of entry, or a suppurative lymph node.
255
What does high antideoxyribonuclease B titers indicate?
High antideoxyribonuclease B titers are more common following GAS skin infections and indicate a recent or past GAS infection.
256
What findings would confirm the diagnosis of a suspected GAS infection from a biopsy?
Findings include Gram-positive cocci in chains, seen on Gram, periodic acid–Schiff, or methenamine silver stains.
257
How does the M protein affect host immune defenses?
The M protein inhibits host immune defenses by:
1. Binding to regulators of the complement system, decreasing activation of classic and alternative pathways.
2. Inhibiting antibody-mediated phagocytosis by interacting with the Fc region of IgG.
3. Inducing inflammation by interacting with TLR2 on monocytes, leading to proinflammatory cytokine production.
4. Facilitating invasion of host cells by binding to extracellular matrix components and CD46 on keratinocytes.
258
How do the superantigens produced by GAS contribute to its pathogenicity?
GAS produces superantigens, including streptococcal pyrogenic exotoxins, which:
- Nonspecifically activate T cells, leading to a robust immune response.
- Are responsible for conditions such as streptococcal toxic shock syndrome and scarlet fever.
- Contribute to the pathogenesis of more invasive infections like erysipelas.
259
What is the recommended topical therapy for GAS impetigo?
Topical therapy for GAS impetigo includes:
- Mupirocin 2% topical ointment or Retapamulin 1% ointment applied twice daily for 5 days.
- Cleanse the area with soap and water to remove superficial crusts.
260
What is the first-line systemic antibiotic treatment for superficial pyodermas caused by GAS?
The first-line systemic antibiotic treatment for superficial pyodermas caused by GAS is penicillin. Treatment should be continued for 10 days using:
- Oral penicillin V potassium (penicillin VK):
- Adults: 250 to 500 mg QID
- Children: 250 to 500 mg BID/TID or 25 to 45 mg/kg/day
## Footnote
Alternatively, Amoxicillin-clavulanic acid can be used in place of oral penicillin V for young children.
261
What is the clinical significance of asymptomatic carriers of GAS?
Asymptomatic carriers of GAS can serve as common sources for GAS transmission and potential recurrent infection, with GAS persisting in approximately 20% to 30% of individuals.
262
What should be done for patients showing signs of systemic infection or inflammation due to GAS?
Patients showing signs of systemic infection or inflammation (systemic inflammatory response syndrome) should be admitted to the hospital and treated aggressively with intravenous antibiotics as required for complicated erysipelas or cellulitis.
263
What is the typical indication for imaging in cases of acute lymphangitis?
Imaging is indicated when there is evidence of spread into the axillary nodes, raising suspicion of subpectoral abscesses and pleural effusion.
264
What is the recommended treatment duration for oral penicillin in cases of GAS impetigo?
Treatment should be continued for 10 days.
265
What is the alternative treatment for patients with penicillin allergy when treating GAS infections?
Erythromycin can be used as an alternative.
266
What is the clinical course of untreated GAS impetigo?
It may persist and new lesions may develop over several weeks, potentially resolving spontaneously unless there is an underlying disorder.
267
What is the recommended management for blistering distal dactylitis?
It can be treated the same way as GAS pyodermas, but incision and drainage (I&D) may be required to release subungual pus.
268
What is the diagnosis and first-line topical treatment for a honey-colored crusted papule near a hair follicle?
The diagnosis is nonbullous impetigo caused by GAS. The first-line topical treatment is mupirocin 2% ointment or retapamulin 1% ointment applied twice daily for 5 days.
269
What alternative antibiotics can be used for a patient with GAS impetigo who develops a rash from oral penicillin?
Alternative antibiotics include erythromycin (250-500 mg QID for adults, 30-50 mg/kg/day QID for children) or clindamycin (300-450 mg TID for adults, 20-30 mg/kg/day TID-QID for children).
270
What is the empirical treatment for a superficial skin infection that cannot be clinically distinguished between GAS and S. aureus?
Empirical treatment includes dicloxacillin or cephalexin to cover S. aureus, as most cases of nonbullous impetigo are caused by this organism.
271
What imaging might be indicated for a patient with suspected GAS infection and systemic symptoms?
Imaging such as chest X-ray or CT imaging might be indicated to evaluate for complications like subpectoral abscesses or pleural effusion.
272
What is the management for a patient with suspected GAS infection and a history of systemic inflammatory response syndrome (SIRS)?
Management includes hospitalization and aggressive treatment with intravenous antibiotics.
273
What is the recommended treatment duration for GAS impetigo in adults and children?
The recommended treatment duration for GAS impetigo is 10 days. The first-line antibiotics used are:
- Oral Penicillin V potassium (penicillin VK):
- Adults: 250 to 500 mg QID
- Children: 250 to 500 mg BID/TID or 25 to 45 mg/kg/day
- Amoxicillin-clavulanic acid can be used in place of oral penicillin V for young children.
274
What imaging studies are indicated in cases of acute lymphangitis?
Radiographic imaging (such as chest X-ray or CT imaging) is indicated to determine the extent of chest infection, especially if there is suspicion of subpectoral abscesses or pleural effusion.
275
What is the management approach for patients with signs of systemic infection due to GAS infections?
Patients should be admitted to the hospital and treated aggressively with intravenous antibiotics as required for complicated erysipelas or cellulitis.
276
What are the differential diagnoses for impetigo and ecthyma?
The differential diagnoses include intertrigo, blistering distal dactylitis, and acute lymphangitis.
277
What is the recommended treatment for patients hospitalized with GAS infections?
Patients should be isolated until the organisms have been eradicated by antibiotic treatment.
278
What are the clinical features of pitted keratolysis?
Pitted keratolysis presents as superficial erosion of the stratum corneum with numerous small crateriform pits coalescing to form a large discrete defect with serpiginous borders on the plantar surface of the foot.
279
What are the prophylactic measures recommended for managing pitted keratolysis?
Prophylactic measures include keeping the feet as dry as possible, wearing well-fitted and nonocclusive shoes, changing socks and shoes often, using inert antiseptic foot powders, and applying aluminum chloride 20% solution.
280
What is the epidemiology of pitted keratolysis?
Pitted keratolysis is more common in adult males with a male-to-female ratio of approximately 8:1 and is much more prevalent in tropical climates.
281
What are the differential diagnoses for pitted keratolysis?
Differential diagnoses include interdigital tinea pedis and erythrasma.
282
What is the typical antibiotic treatment for individuals with recurrent episodes of GAS infections?
A 10-day course of clindamycin or amoxicillin-clavulanic acid.
283
What is the male-to-female ratio of susceptibility for pitted keratolysis?
Approximately 8:1.
284
Which bacterial species are implicated in pitted keratolysis?
Kytococcus sedentarius, Dermatophilus congolensis, and Corynebacterium spp.
285
What is the significance of the web spaces between the toes in pitted keratolysis?
They are commonly involved sites and may be the only manifestation of the disease.
286
What is the role of systemic antibiotics during outbreaks of poststreptococcal glomerulonephritis?
They should be used to help eliminate nephritogenic strains of GAS from the community.
287
What is the clinical diagnosis of pitted keratolysis based on?
The diagnosis is made clinically, often with the presence of malodor and sliminess of the skin.
288
What are the predisposing factors for pitted keratolysis?
Warm, moist skin, occlusive footwear, and hyperhidrosis.
289
What are the options for prophylactic antibiotics for recurrent GAS infections?
Options include a 10-day course of clindamycin or amoxicillin-clavulanic acid, or prophylactic penicillin for close family contacts.
290
What are the options for topical therapy in pitted keratolysis?
Options include benzoyl peroxide cleanser, clindamycin, erythromycin, and imidazole derivatives.
291
What is erythrasma and how is it characterized?
Erythrasma is a superficial bacterial infection characterized by well-defined but irregular reddish-brown patches in intertriginous areas.
292
What is the etiologic agent of erythrasma?
The etiologic agent is Corynebacterium minutissimum, a short, Gram-positive rod.
293
What diagnostic methods are used for erythrasma?
Diagnosis can be confirmed by culture of Corynebacterium, Gram-stained imprints, or Wood’s lamp examination.
294
What are the management options for localized erythrasma?
Management options include benzoyl peroxide cleanser, clindamycin, or erythromycin.
295
What is trichobacteriosis and how is it characterized?
Trichobacteriosis is a bacterial infection of the hair shaft characterized by nodular thickenings composed of colonies of aerobic Corynebacterium spp.
296
What are the clinical features of trichobacteriosis?
Clinical features include nodular thickenings on the hair shaft and various pigments giving nodules a range of colors.
297
What is the significance of C. minutissimum in erythrasma?
C. minutissimum can lead to severe complications in immunocompromised patients, highlighting the importance of early diagnosis and treatment.
298
What management strategies are recommended for localized and widespread erythrasma?
Localized management includes benzoyl peroxide cleanser and topical antibiotics, while widespread management may require oral antibiotics.
299
How does the clinical course of erythrasma typically progress?
Erythrasma may remain asymptomatic for years or undergo periodic exacerbations, indicating the need for ongoing monitoring.
300
What are the predisposing factors for the development of trichobacteriosis?
Warm, moist environment, poor hygiene, and disturbances in sweat production.
301
What diagnostic methods are used to visualize concretions in trichobacteriosis?
Potassium hydroxide preparation and Wood’s lamp examination.
302
What are the predisposing factors for the development of trichobacteriosis?
Warm, moist environment; Poor hygiene; Disturbances in sweat production and bacterial proliferation.
303
What diagnostic methods are used to visualize concretions in trichobacteriosis?
Potassium hydroxide preparation; Wood’s lamp examination reveals a pale yellowish fluorescence; Ultraviolet light enhanced visualization highlights the presence of corynebacteria biofilms on the hair shaft.
304
What management strategies are effective for trichobacteriosis?
1. Removal of involved hair by shaving. 2. Use of benzoyl peroxide cleansers and gels/creams. 3. Topical clindamycin or erythromycin solutions. 4. Improved hygiene and regular use of antiperspirants like aluminum chloride.
305
What is the clinical significance of acute rheumatic fever in relation to GAS pharyngitis?
Acute rheumatic fever occurs 2 to 3 weeks following a GAS pharyngitis infection, indicating a serious complication that can affect the heart and other organs.
306
What is the role of Wood’s lamp examination in diagnosing erythrasma and trichobacteriosis?
Wood’s lamp examination of erythrasma reveals a coral-red fluorescence; Wood’s lamp examination of trichobacteriosis reveals a pale yellowish fluorescence, indicating the presence of corynebacteria.
307
What are the common risk factors for developing GAS skin infections?
1. Poor hygiene 2. Close contact with infected individuals 3. Skin breaks or wounds 4. Chronic skin conditions 5. Immunocompromised status.
308
What are the matching types for the conditions and their associated streptococci?
| Condition | Associated Streptococci |
|-----------|------------------------|
| Impetigo | Group B and D streptococci |
| Cellulitis | Group B streptococci |
| Mixed infections with enteric bacteria or S. aureus | Group L streptococci |
| Otitis | Group B and L streptococci |
| Paronychias in meat handlers | Group B streptococci |
309
What factors are likely needed for the development of trichobacteriosis?
Disturbances in sweat production and bacterial proliferation, along with a warm moist environment and poor hygiene.
310
What is the role of Wood's lamp in diagnosing skin conditions?
It can reveal a pale yellowish fluorescence in certain skin conditions.
311
What is a common treatment for trichobacteriosis?
Benzoyl peroxide cleansers and gels/creams are effective for treatment and prevention.
312
What is the significance of potassium hydroxide preparation in diagnosis?
It is used to visualize concretions in the diagnosis of certain skin conditions.
313
What is the clinical finding that helps distinguish superficial thrombophlebitis from acute lymphangitis?
Clinical findings and diagnostic modalities such as Wood's lamp examination.
314
What is the typical time frame for acute rheumatic fever to occur after GAS pharyngitis?
It occurs 2 to 3 weeks following a GAS pharyngitis infection.
315
What is the recommended management for patients with trichobacteriosis?
Improved hygiene, cleansing practices, and regular use of antiperspirants.
316
What is the importance of isolating patients with GAS infections?
Patients should be isolated until the organisms have been eradicated by antibiotic treatment.
317
What does a Gram stain typically reveal in cases of GAS infections?
It typically reveals Gram-positive cocci in chains.
318
What is the relationship between high antistreptolysin O titers and GAS infections?
High antistreptolysin O titers are more common after GAS skin infections.
319
A patient presents with nodular thickenings on axillary hair shafts that fluoresce pale yellow under Wood’s lamp. What is the diagnosis, and what is the management?
The diagnosis is trichobacteriosis. Management includes shaving the involved hair, using benzoyl peroxide cleansers, and improving hygiene.
320
A patient with trichobacteriosis is concerned about recurrence. What preventive measures can be recommended?
Preventive measures include improved hygiene, regular use of antiperspirants (e.g., aluminum chloride), and benzoyl peroxide cleansers.
321
What are the key factors contributing to the development of trichobacteriosis?
- **Disturbances in sweat production**
- **Bacterial proliferation**
- **Warm, moist environment**
- **Poor hygiene**
322
What diagnostic methods can be used to identify trichobacteriosis?
- **Clinical findings**
- **Potassium hydroxide preparation** to visualize concretions
- **Wood’s lamp** to reveal pale yellowish fluorescence
- **Ultraviolet light** to highlight corynebacteria biofilms on the hair shaft
323
What management strategies are effective for treating trichobacteriosis?
1. **Shaving** the involved hair
2. Use of **benzoyl peroxide** cleansers and gels/creams
3. Application of **topical clindamycin** or **erythromycin solutions**
4. Improved hygiene and regular use of **antiperspirants** like aluminum chloride
324
What is the clinical significance of acute rheumatic fever in relation to GAS pharyngitis?
Acute rheumatic fever typically occurs **2 to 4 weeks** following a GAS pharyngitis infection, highlighting the importance of timely diagnosis and treatment of GAS infections to prevent this complication.
325
How can Wood’s lamp examination assist in diagnosing erythrasma and trichobacteriosis?
- **Erythrasma**: Reveals a **coral-red fluorescence**
- **Trichobacteriosis**: Reveals a **pale yellowish fluorescence**
326
What are the risk factors for developing GAS skin infections?
1. **Poor hygiene**
2. **Close contact** with infected individuals
3. **Skin breaks or wounds**
4. **Chronic skin conditions**
5. **Immunocompromised state**
327
What is the relationship between high antistreptolysin O titers and GAS infections?
High antistreptolysin O titers are more common after **GAS skin infections**, while high antideoxyribonuclease B titers are more common following **GAS pharyngitis**, indicating different immune responses based on the type of infection.
