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Updated: Jul 24, 2026

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat
Published on: October 29, 2014
Pyogenic cocci in infantile eczema throughout one year
Insights
Staphylococci causing sepsis in infantile eczema originate from persistent skin and nose colonization. Streptococci causing sepsis are new infections, often from external sources, and topical antibiotics are ineffective against these resistant bacteria.
Area of Science:
- Microbiology
- Dermatology
- Pediatrics
Background:
- Infantile eczema patients are susceptible to bacterial sepsis.
- Identifying the source of pyococci is crucial for preventing sepsis attacks.
Purpose of the Study:
- To determine the origin of staphylococci and streptococci causing sepsis in infantile eczema.
- To assess the effectiveness of topical antibiotics in preventing recurrent sepsis.
Main Methods:
- Longitudinal study of 20 infantile eczema patients over one year.
- Regular sampling of skin, nose, throat, and family contacts.
- Phage typing for staphylococci and serological typing for streptococci.
Main Results:
- Staphylococci causing sepsis originated from persistent colonization sites (skin, nose).
- Streptococci causing sepsis were new infections, sometimes from patient or contact throat infections.
- Antibiotic resistance (neomycin, sodium fusidate, gentamicin) was observed in both staphylococci and streptococci.
Conclusions:
- Staphylococcal sepsis in infantile eczema arises from endogenous reservoirs.
- Streptococcal sepsis is due to exogenous reinfection, highlighting the need for source control.
- Topical antibiotics have limited efficacy in preventing sepsis due to bacterial resistance.
Abstract:
To determine the source of pyococci causing attacks of sepsis in infantile eczema 20 patients with continuing eczema were followed up for one year, regular swabs being taken from the skin, nose, throat, and family contacts. The staphylococci were phage typed and the streptococci serologically typed. Staphylococci of the same phage type in most cases remained in reservoir sites on the skin and coincidently in the nose. Staphylococci causing attacks of clinical sepsis arose from these persistently colonized sites. Staphylococci of the same phage type were also common in family contacts. Streptococci of the same group in most cases did not remain on the skin. Streptococci causing attacks of clinical sepsis arose as new infections from external sources, sometimes from throat infections in the patient or family contacts. Strains of streptococci which are known to be associated with glomerulonephritis were isolated. It has been confirmed that staphylococci resistant to neomycin and sodium fusidate quickly emerge after the topical use of these antibiotics. Streptococci are highly resistant to neomycin and gentamicin, and moderately resistant to sodium fusidate, so the use of these antibiotics in topical steroid preparations will have little effect in preventing further attacks of clinical sepsis in these patients.
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