Family medicine #3 – MEHLMANMEDICAL

HY lecture notes (double-posting this lecture as Internal medicine #15 because it’s exceedingly HY for both shelf exams):

Impetigo (“school sores”), which is divided into bullous and non-bullous types.¹ When “impetigo” is stated alone, the implication is non-bullous.

Impetigo is largely pediatric and presents as erythematous plaques with a yellow crust caused by Staph and/or Strep. The lesions may be itchy or painful and are highly contagious.¹

Staph aureus now exceeds Strep pyogenes (Group A Strep) as the most likely causal organism of non-bullous impetigo.

Regarding non-bullous (i.e., “normal” impetigo)

2019 source: “Nonbullous impetigo is most commonly caused by S aureus which is responsible for 80% of cases. Group A beta-hemolytic Strep (GABHS) accounts for 10% of cases and the causative agent is a combination of S. aureus and GABHS 10% of the time.”¹
2019 source: “Impetigo is a skin infection caused by bacteria. It is usually caused by staphylococcal (staph) bacteria, but it can also be caused by streptococcal (strep) bacteria. It is most common in children between the ages of two and six. It usually starts when bacteria get into a break in the skin, such as a cut, scratch, or insect bite.”²
2016 source: “Although bullous impetigo remains almost exclusively caused by staphylococcus, the bacteriology of non-bullous impetigo has changed. S. aureus, either alone or in combination with S. pyogenes, is now the predominant causative agent.”³
2014 source: “S. aureus, alone or in combination with group A beta hemolytic streptococci, is responsible for about 80% of the cases, being the most frequently recovered isolated agent.”⁴
2001 source: “In the 1960s, streptococci were the predominant isolates in impetigo. Even when S. aureus grew, S. pyogenes was usually also present. The microbiology, however, has changed: In the 1980s and 1990s, streptococci alone grew in about 5% to 10% of cases, staphylococci alone in 50% to 60%, and both in 20% to 45%.”⁵

Staph aureus has always been the most implicated causal organism in bullous impetigo.

“Bullous impetigo is more common in infants. Children younger than two account for 90% of cases of bullous impetigo. Bullous impetigo is caused almost exclusively by S aureus. Sometimes a deep ulcerated infection may occur known as ecthyma, which is a complication of bullous impetigo.”¹
“Bullous impetigo is almost universally caused by a single organism, S. aureus. Bullous impetigo starts with smaller vesicles, which become flaccid blisters, measuring up to 2 cm in diameter, initially with clear content that later becomes purulent.”³
“Impetigo is a common, superficial, bacterial infection of the skin characterized by an inflamed and infected epidermis. The rarer variant, bullous impetigo, is characterized by fragile fluid-filled vesicles and flaccid blisters and is invariably caused by pathogenic strains of Staphylococcus aureus.”⁶
“Bullous impetigo is an acute blistering infection caused by Staphylococcus aureus group II, typically phage 71 infection. This strain of S. aureus carries exfoliative toxin A, which specifically targets and disrupts the intraepidermal keratinocyte connection desmoglein 1 (DSG1).”⁷

Treatment⁸

Topical
- Mupirocin, retapamulin, and fusidic acid.
- For the USMLE, they are obsessed with topical mupirocin as a treatment for impetigo.
Oral
- Dicloxacillin
- Cephalexin
- Amoxicillin/clavulanate
- You must know that you these oral agents cover S. aureus.
- If you give penicillin or amoxicillin alone, they will NOT cover Staph due to its beta-lactamase production.

1) https://www.ncbi.nlm.nih.gov/books/NBK430974/

2) https://medlineplus.gov/impetigo.html

3) https://www.ncbi.nlm.nih.gov/books/NBK333408/

4) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4008061/

5) https://www.jwatch.org/jd200108140000006/2001/08/14/

6) https://www.ncbi.nlm.nih.gov/pubmed/15482208

7) https://www.sciencedirect.com/science/article/pii/B9780323401814000700

8) https://www.aafp.org/afp/2014/0815/p229.html

Erysipelas, which is a bacterial skin infection involving the upper dermis with characteristic extension to the superficial cutaneous lymphatics.¹

Group A strep (S. pyogenes) is widely accepted to be the most common culprit, although S. aureus is an important, albeit less frequent cause.^{1, 2}

Erysipelas is characterized by the abrupt onset of a fiery red, tender, intensely erythematous, indurated plaque with a sharply demarcated border.^{3, 4}Its rapid progression, intense pain, and well-defined margins, particularly when involving the nasolabial fold, help differentiate it from cellulitis.²

Cellulitis extends into the subcutaneous tissues, which may explain its more diffuse margins and lighter, pinkish color.⁴

70% to 80% of erysipelas lesions involve the lower extremities; 5% to 20% are facial.⁵

Treatment^{6, 7}

Oral dicloxacillin, cephalexin, or clindamycin.
If severe or systemic features, give IV flucloxacillin or cephazolin
Although Group A strep is the most common cause of erysipelas, these above agents effectively cover strep AND staph.
Penicillin is frequently cited across the literature as an additional first-line option^{8, 9, 10}, but be aware that it does not cover S. aureus; it will only account for Strep.
Many clinicians will use penicillin if the presentation is subjectively “classic” erysipelas (as seen with this patient) and will choose a staph-covering agent if:
- The diagnosis is more subjectively equivocal (i.e., one believes it may or may not potentially be cellulitis).
- There are characteristic features of staph infection (i.e., bullae or purulence).
- Systemic features or underlying trauma.
- There is no improvement with penicillin.¹¹
“Coverage for Staphylococcus aureus is not usually necessary for typical infections, but it should be considered in patients who do not improve with penicillin or who present with atypical forms of erysipelas, including bullous erysipelas.”¹¹
In about half of cases, an antibiotic effective against S. aureus is chosen instead of penicillin.¹

In other words, if penicillin is used and the causal organism is indeed Group A strep (most common cause), the patient is in the clear. But if the less common S. aureus turns out to be the culprit, the patient will not respond to the penicillin.

Although penicillin is discussed thoroughly in the literature as one of the first-line choices for erysipelas, the treating practitioner should be aware that a percentage of his or her patients will not respond to it, and therefore should consider using dicloxacillin or cephalexin over penicillin.

It is exceedingly HY for the USMLE that you know dicloxacillin and cephalexin can treat community Staph (methicillin-sensitive S. aureus; MSSA), whereas penicillin does not.¹²

In contrast to erysipelas, S. aureus exceeds S. pyogenes as the culprit for cellulitis.^{13, 14} Treatment therefore must certainly cover staph, and penicillin is considered incorrect treatment.¹⁵

Both non-bullous and bullous impetigo are most commonly caused by S. aureus. Group A Strep is no longer the most common causal organism for the non-bullous variant.¹⁶^{, 17, 18, 19, 20}

1) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4590694/

2) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5079789/

3) https://emedicine.medscape.com/article/1052445-overview

4) https://www.sciencedirect.com/science/article/pii/B9781437701265000197

5) https://www.sciencedirect.com/science/article/pii/B9781455748013000953

6) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5079789/

7) https://academic.oup.com/cid/article/59/2/147/442347

8) https://www.ebm-guidelines.com/ebmg/ltk.free?p_artikkeli=ebm00275

9) https://www.ncbi.nlm.nih.gov/books/NBK532247/

10) https://link.springer.com/article/10.2165/00042310-200319120-00004

11) https://emedicine.medscape.com/article/1052445-treatment

12) https://www.ncbi.nlm.nih.gov/pubmed/16271060