A: Impetigo is a
superficial cutaneous
infection usually due to
group A beta-hemolytic
streptococci.

Staphylococcus aureus
is the sole cause in
about 10% of cases.

Streptococcal Infections of Skin and
Soft Tissues. Bisno, Alan L. et. al.
N Engl J Med. 1996 Jan 25; 334(4):
240-5.
Where does Impetigo Occur?
Impetigo is a bacterial skin infection. It causes red sores that can break open, ooze
fluid, and develop a yellow-brown crust. These sores can occur anywhere on the
body but most often appear around the mouth and nose.

Impetigo and Kids
Impetigo is one of the most common skin infections in children. It can occur in adults
but is seen far more often in children. Impetigo is contagious and can be spread to
others through close contact or by sharing towels, sheets, clothing, toys, or other
items. Scratching can also spread the sores to other parts of the body.

Treatment of Impetigo
Antibiotic ointment that is applied directly to the infected areas of skin usually cures
impetigo. Sometimes antibiotic pills are needed.

Causes of Impetigo
Impetigo is caused by one of two kinds of bacteria-strep (streptococcus) or staph
(staphylococcus). Often these bacteria enter the body when the skin has already
been irritated or injured because of other skin problems such as eczema, poison ivy,
insect bites, chickenpox, burns, or cuts. Children may get impetigo after they have
had a cold or allergies that have made the skin under the nose raw. However,
impetigo can also develop in completely healthy skin.

Impetigo is treated with antibiotics. For cases of mild impetigo, a doctor will prescribe
an antibiotic ointment to put on the sores. For cases of more serious impetigo, a
doctor may also prescribe antibiotic pills.

Duration of Impetigo
After 3 days of treatment, you or your child should begin to get better. A child can
usually return to school or daycare after 48 hours of treatment. If you apply the
ointment or take the pills exactly as prescribed, most sores will be completely healed
in 1 week.
http://www.webmd.com/a-to-z-guides/Impetigo-Overview

Necrotizing fasciitis Infection (flesh-eating bacteria)
Since the 1980s there has been a marked increase in the recognition and reporting
of highly invasive group A streptococcal infections with or without necrotizing fasciitis
associated with shock and organ failure. Such dramatic cases have been defined as
streptococcal toxic-shock syndrome. Strains of group A streptococci isolated from
patients with invasive disease have been predominantly M types 1 and 3 that
produce pyrogenic exotoxin A or B or both.

An emerging pathogen can be
  • one that is totally new (e.g., human immunodeficiency virus),
  • one that was known but has only recently been identified (e.g., Helicobacter
    pylori), or
  • one that is old but has learned new tricks.

The last type is, as Dr. Stanley Falkow contends, merely trying to "make a living" in a
changing environment. Regardless of environmental pressures, many old pathogens
have become major clinical problems because of increased virulence or antibiotic
resistance for example:
  • penicillin-resistant pneumococcus,
  • multidrug-resistant Mycobacterium tuberculosis,
  • methicillin-resistant Staphylococcus aureus, and
  • vancomycin-resistant Enterococcus faecium).

Group A Streptococcus
Arguably, group A Streptococcus (GAS) is the quintessence of an old organism that
has become more virulent.

Clearly, epidemics of streptococcal infections, including impetigo, pharyngitis, scarlet
fever, and rheumatic fever have occurred in the past. However, in the last decade,
subsequent to early reports of streptococcal TSS, we have observed that the
incidence has remained relatively low. I hypothesize that large outbreaks have not
occurred because:
  1. most of the population probably has immunity to one or more streptococcal
    virulence factors  
  2. predisposing conditions (e.g., varicella, and use of NSAIDs) are required in a
    given patient; and
  3. only a small percentage of the population may have an inherent predisposition
    to severe streptococcal infection because of constitutional factors such as
    HLA Class II antigen type, B-cell, or specific Vb regions on lymphocytes.
http://www.cdc.gov/ncidod/EID/vol1no3/stevens.htm
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