Infectious Diseases Dr. Ahmed Moyed Hussein INFECTIONS
Bacterial infections of the skin, soft tissues and bones

Most infections of the skin, soft tissues and bone are caused by either staphylococci (mainly Staph. aureus) or streptococci (mainly Strep. pyogenes).

Staphylococcal infections:

Staphylococci are usually found colonizing the anterior nares and skin. Traditionally, staphylococci were divided into two groups according to their ability to produce coagulase (an enzyme that converts fibrinogen to fibrin in rabbit plasma, causing it to clot) Staph. Aureus is coagulase-positive, and most other species are coagulase negative.
Staph. aureus is the main cause of staphylococcal infections. Staph. intermedius is another coagulase positive staphylococcus, which causes infection following dog bites. Among coagulase-negative organisms, Staph. epidermidis is the predominant commensal organism of the skin, and can cause severe infections in those with central venous catheters or implanted prosthetic materials.
Staphylococci are particularly dangerous if they gain access to the blood stream, having the potential to cause disease in many sites.

Skin infections:

Staphylococcal infections cause ecthyma, folliculitis, furuncles, carbuncles, bullous impetigo and the scalded skin syndrome. They may also be involved in necrotising infections of the skin and subcutaneous tissues.

Wound infections:

Many wound infections are caused by staphylococci, which may significantly prolong post-operative hospital stays. Prevention involves careful attention to hand hygiene, skin preparation and aseptic technique, and the use of topical and systemic antibiotic prophylaxis.
Treatment is by drainage of any abscesses plus adequate dosage of antistaphylococcal antibiotics(flucloxacillin or clindamycin) . These should be instituted early, particularly if prosthetic implants of any kind have been inserted.

Cannula-related infection:

Staphylococcal infection associated with cannula sepsis and thrombophlebitis is an important and, unfortunately, extremely common reason for morbidity following hospital admission. Staphylococci have a predilection for plastic, rapidly forming a biofilm which remains as a source of bacteraemia as long as the plastic is in situ. Local poultice application may relieve symptoms but cannula removal and antibiotic treatment with flucloxacillin (or a glycopeptide if MRSA is suspected) are necessary if there is any suggestion of spreading infection.

Meticillin-resistant Staph. Aureus (MRSA):

Resistance to meticillin, due to a penicillin-binding protein mutation, has been recognized in Staph. Aureus for more than 30 years. Meticillin-resistant Staph. Aureus (MRSA) is now a major worldwide health care-acquired pathogen, accounting for up to 40% of staphylococcal bacteraemia in developed countries.
Clinicians must be aware of the potential danger of these infections and be prepared to take whatever appropriate infection control measures are locally advised. Treatment options for MRSA are: Clindamycin, vancomycin, rifampicin (never used as monotherapy), linezolid, daptomycin, tetracyclines, tigecycline or co-trimoxazole. Treatment should always be based on the results of antimicrobial susceptibility testing.

Staphylococcal toxic shock syndrome:

Staphylococcal toxic shock syndrome (TSS) is a serious and life-threatening disease associated with infection by Staph. aureus, which produces a specific toxin (toxic shock syndrome toxin 1, TSST1). It was commonly seen in young women in association with the use of highly absorbent intravaginal tampons but can occur with any Staph. aureus infection involving a relevant toxin producing strain. The toxin acts as a ‘superantigen’, triggering significant T-helper cell activation and massive cytokine release.
TSS has an abrupt onset with high fever, generalized systemic upset (myalgia, headache, sore throat and vomiting), a generalized erythematous blanching rash resembling scarlet fever, and hypotension. It rapidly progresses over a matter of hours to multisystem involvement with cardiac, renal and hepatic compromise, leading to death in 10–20%. Recovery is accompanied at 7–10 days by desquamation. The diagnosis is clinical and may be confirmed in menstrual cases by vaginal examination, the finding of a retained tampon, and microbiological examination by Gram stain demonstrating typical staphylococci. Subsequent culture and demonstration of toxin production are confirmatory.
Treatment is with immediate and aggressive fluid resuscitation and an intravenous antistaphylococcal antibiotic (flucloxacillin or vancomycin), usually with the addition of a protein synthesis inhibitor (e.g. clindamycin) to inhibit toxin production. Intravenous immunoglobulin is occasionally added in the most severe cases on the basis of efficacy in streptococcal toxic shock.
Women who recover should be advised not to use tampons for at least 1 year and should also be warned that, due to an inadequate antibody response to TSST1, the condition can recur.

Streptococcal skin infections:

Streptococci are nasopharyngeal and gut commensals, which appear as Gram-positive cocci in chains. They are classified by the haemolysis they produce on blood agar.

Skin presentations of streptococcal infections:

Group A streptococci (GAS) are the major cause of cellulitis, erysipelas and impetigo. Groups C and G streptococci cause cellulitis, in elderly, diabetic or immunocompromised patients in particular. Group B streptococcal (GBS) infection is an increasing problem at the extremes of age.

Streptococcal scarlet fever:

Group A (or occasionally groups C and G) streptococci causing pharyngitis, tonsillitis or other infection may lead to scarlet fever, if the infecting strain produces a streptococcal pyrogenic exotoxin. Common in school age children, scarlet fever can occur in young adults who have contact with young children. A diffuse erythematous rash occurs, which blanches on pressure, classically with circumoral pallor. The tongue, initially coated, becomes red and swollen (‘strawberry tongue’). The disease lasts about 7 days, the rash disappearing in 7–10 days, followed by a fine desquamation. Residual petechial lesions in the antecubital fossa may be seen (‘Pastia’s sign’).
Treatment involves active therapy for the underlying infection (benzylpenicillin or orally available penicillin) plus symptomatic measures.

Streptococcal toxic shock syndrome:

This is associated with severe group A (or occasionally group C or G) streptococcal skin infections producing one of a variety of toxins, such as pyogenic exotoxin A. Like staphylococcal toxic shock syndrome toxin, these act as superantigens, stimulating a dramatic cytokine response. Initially, an influenza-like
illness occurs with, in 50% of cases, signs of localized infection, most often involving the skin and soft tissues. A faint erythematous rash, mainly on the chest, rapidly progresses to circulatory shock. Without aggressive management, multi-organ failure will develop.
Fluid resuscitation must be undertaken, with parenteral antistreptococcal antibiotic therapy, usually with benzylpenicillin and a protein inhibitor, such as
clindamycin, to inhibit toxin production. Intravenous immunoglobulin is usually administered in addition. If necrotising fasciitis is present, it should be treated with urgent débridement.

رفعت المحاضرة من قبل: Mohammed Khalil
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