Staphylococci are normal commensals of human skin and anterior nares, but they can disseminate widely if they gain access to the blood through a cannula, a surgical incision or a primary skin condition such as eczema.
Ecthyma, folliculitis, furuncles and carbuncles represent superficial skin infections with this ubiquitous organism (p. 749).
Wound- and cannula- related infections caused by S. aureus are important causes of inpatient morbidity. Their incidence may be lessened by good infection control techniques. If there is evidence of spreading infection such as a surround- ing cellulitis, antistaphylococcal antimicrobial therapy, for example, flucloxacillin, should be instituted. IV drug users who are susceptible to skin and subcutane- ous tissue infections may also develop thrombosis in the affected limb. If staphy- lococcal infection reaches the blood stream (staphylococcal bacteraemia), this may cause severe sepsis and complications (e.g. endocarditis or cavernous sinus thrombosis), and must be treated aggressively. Growth of S. aureus in blood cultures should never be dismissed as a ‘contaminant’ unless all possible underlying causes have been excluded and repeat cultures are negative.
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S. aureus can also cause severe systemic disease by production of tox- ins at superficial sites, in the absence of tissue invasion by bacteria.
MRSA
Resistance to meticillin is attributed to a penicillin- binding protein muta- tion in S. aureus. Resistance to vancomycin/teicoplanin (glycopeptides) in either glycopeptide- intermediate S. aureus or, rarely, vancomycin- resistant strains threatens the ability to manage serious infections with such organ- isms. MRSA now accounts for up to 40% of staphylococcal bacteraemias in developed countries, requiring care in both control and specific therapy of these infections. Clinicians must prescribe according to sensitivity testing and take whatever infection control measures are advised locally.
Staphylococcal TSS
This serious and life- threatening disease is associated with infection by S.
aureus that produces toxic shock syndrome toxin 1. Staphylococcal TSS is seen in women using tampons, but can also complicate any staphylococcal infection with a relevant toxin- producing strain. The toxin acts as a ‘super- antigen’, triggering significant T cell activation and massive cytokine release.
TSS has an abrupt onset with high fever, generalised systemic upset (myal- gia, headache, sore throat and vomiting), a widespread erythematous blanch- ing rash resembling scarlet fever and hypotension. It rapidly progresses over a few hours to multiorgan failure, leading to death in 10% to 20% of patients.
The diagnosis is clinical, supported by Gram stain of menstrual fluid dem- onstrating typical staphylococci. Treatment is with IV fluid resuscitation and antistaphylococcal antibiotics such as flucloxacillin or vancomycin. Recovery is accompanied at 7 to 10 days by desquamation (Fig. 5.7).
Fig. 5.7 Full- thickness desquamation after toxic shock syndrome.
Streptococcal infections
Streptococci are Gram- positive oropharyngeal and gut commensals that cause a range of human infections (Box 5.15).
Streptococcal scarlet fever
Group A (or occasionally group C and G) streptococci causing pharyngitis or tonsillitis may lead to scarlet fever if the organism produces pyogenic
exotoxin. Common in school- age children, scarlet fever can occur in young adults in contact with young children.
A diffuse erythematous rash occurs, which blanches on pressure (Fig. 5.8), classically with circumoral pallor. The tongue, initially coated, becomes red and swollen (‘strawberry tongue’). The disease lasts around 7 days; the rash disappears in 7 to 10 days, followed by a fine desqua- mation. Residual petechial lesions in the antecubital fossa may be seen.
Treatment involves IV benzylpenicillin or oral penicillin, plus symptomatic measures.
Streptococcal TSS
Group A (or occasionally C or G) streptococci can produce toxins such as pyogenic exotoxin A. Initially, an influenza- like illness occurs with signs of localised skin or soft tissue infection in 50% of cases. A faint erythematous rash, mainly on the chest, progresses rapidly to circulatory shock, then multi- organ failure.
Fluid resuscitation is essential, along with parenteral antistreptococcal antibiotics, usually benzylpenicillin with clindamycin. If necrotising fasciitis is present (p. 105), urgent debridement is required.
Cellulitis, erysipelas and impetigo See p. 749 and 747.
5.15 Streptococcal and related infections Group A (Streptococcus pyogenes)
• Skin/tissue infection (erysipelas, impetigo, necrotising fasciitis) • Puerperal sepsis
• Glomerulonephritis • Bone and joint infection
• Streptococcal toxic shock syndrome • Scarlet fever
• Rheumatic fever • Tonsillitis
Group B streptococci (S. agalactiae) • Neonatal infections, including meningitis • Septicaemia
• Female pelvic infections • Cellulitis
Group D enterococci (Enterococcus faecalis) • Endocarditis
• Urinary tract infection
α- Haemolytic viridans streptococci (S. mitis, sanguinis, mutans, salivarius) • Endocarditis
• Septicaemia in immunosuppressed
α- Haemolytic optochin- sensitive (S. pneumoniae) • Pneumonia
• Meningitis • Endocarditis • Septicaemia • Bacterial peritonitis • Otitis media
Anaerobic streptococci (Peptostreptococcus spp.) • Peritonitis
• Liver abscess • Dental infections • Pelvic inflammatory disease
Note: All streptococci can cause septicaemia.
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exotoxin. Common in school- age children, scarlet fever can occur in young adults in contact with young children.
A diffuse erythematous rash occurs, which blanches on pressure (Fig. 5.8), classically with circumoral pallor. The tongue, initially coated, becomes red and swollen (‘strawberry tongue’). The disease lasts around 7 days; the rash disappears in 7 to 10 days, followed by a fine desqua- mation. Residual petechial lesions in the antecubital fossa may be seen.
Treatment involves IV benzylpenicillin or oral penicillin, plus symptomatic measures.
Streptococcal TSS
Group A (or occasionally C or G) streptococci can produce toxins such as pyogenic exotoxin A. Initially, an influenza- like illness occurs with signs of localised skin or soft tissue infection in 50% of cases. A faint erythematous rash, mainly on the chest, progresses rapidly to circulatory shock, then multi- organ failure.
Fluid resuscitation is essential, along with parenteral antistreptococcal antibiotics, usually benzylpenicillin with clindamycin. If necrotising fasciitis is present (p. 105), urgent debridement is required.
Cellulitis, erysipelas and impetigo See p. 749 and 747.
Fig. 5.8 Scarlet fever. Note blanching on pressure.
Treponematoses Syphilis
This disease is described on p. 173.
Endemic treponematoses
Yaws: This granulomatous disease is caused by Treponema pertenue, which is morphologically and serologically indistinguishable from the causative organisms of syphilis and pinta. Organisms are transmitted through minor skin abrasions by bodily contact with a patient with infectious yaws. After 3 to 4 weeks, a granulomatous primary lesion develops at the site of infection. This is followed by secondary eruptions and hypertrophic periosteal bone lesions and, in late yaws, osteitis and gummas resembling tertiary syphilis.
Pinta and bejel:These two treponemal infections occur in poor rural populations with low standards of domestic hygiene but are found in sepa- rate parts of the world (pinta: South and Central America; bejel: Middle East, Central Asia). Pinta is a skin disease transmitted by contact, and bejel is a nonvenereal form of syphilis transmitted by contact and through com- mon eating and drinking utensils.
For yaws, pinta and bejel, diagnosis is by microscopic detection of spirochaetes and serology; treatment involves a single IM dose of long- acting (e.g. benzathine) benzylpenicillin. Improvements in domestic hygiene greatly reduce these diseases.