Download Staphylococcal toxic shock syndrome

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Staphylococcal and Streptococcal infections
catalyzing2 H2O2
→ 2 H2O + O2
Most infections of the skin, soft tissues and bone are caused by either
staphylococci (mainly Aureus.)
or
streptococci (mainly Pyogenes.(
Staphylococcal infections
 Gram-positive form grapelike clusters
 Catalase-positive nonmotile, aerobic, and
facultatively anaerobic.
 Colonising the anterior nares and skin .
 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 .
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
Infections caused by Staphylococcus aureus
Skin infections
 folliculitis, furuncles, carbuncles, impetigo and the scalded
skin syndrome
 Mid-facial cellulitis, which can result in cavernous sinus
thrombophlebitis .
Folliculitis
carbuncle
Wound infections
prolong hospital stays
Treatment drainage of abscesses plus
.antistaphylococcal antibiotics
Prevention hand hygiene, aspetic technique,
topical and systemic antibiotic prophylaxis.
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Cannula-related infection
 Extremely common.
 Visual Infusion Phlebitis (VIP) score is a useful way of monitoring
cannulae .
 Treatment Cannula removal and antibiotic treatment with
flucloxacillin
 or a glycopeptide if MRSA* is suspected.
Endocarditis
 Staphylococci are particularly dangerous if they gain access to the
blood stream
 )injection drug-users.(
 The possibility of endocarditis must always be considered .
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Meticillin-resistant Staph. Aureus
 Due to a penicillin-binding protein mutation.
 MRSA is now accounting for up to 40% of staphylococcal
bacteraemia in developed countries .
 Also acquired other virulence factors such as Panton-Valentine
leukocidin (PVL) , cytolytic to PMNs, macrophages, and
monocytes.
 S. aureus can survive within PMNs* and may use these cells to
spread to other tissue.
Meticillin-resistant Staph. Aureus Treatment
based on the results of susceptibility testing .
 Milder infections ,treated with clindamycin, tetracyclines or cotrimoxazole .
 Severe infections. Glycopeptides, linezolid and daptomycin
 PVL-producing Staph. infections should be treated with proteininhibiting antibiotics (clindamycin, linezolid(
Quinupristin/dalfopristin :Used successfully to treat serious MRSA
infections .
Oritavancin: Anew parenteral bactericidal agent recently approved for
the treatment of complicated skin infections .
Toxin-Mediated Illnesses
 Toxic shock syndrome
 Food poisoning
 Staphylococcal scalded-skin syndrome
Food poisoning
Inoculation of toxin-producing S. aureus into food by
colonized food handlers. Even if the bacteria are killed by
warming, the heat-stable toxin is not destroyed .
The onset is explosive, within 1 to 6 h of ingestion,nausea
and vomiting, although diarrhea, hypotension, and
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dehydration may also occur. Symptoms generally resolve
within 8 to 10 h .
The diagnosis can be established by the demonstration of
bacteria or the documentation of enterotoxin in the implicated
food .
Treatment is entirely supportive.
Staphylococcal toxic shock syndrome
 life-threatening disease is associated with infection by Staph.
Aureus which produces a specific toxin
)toxic shock syndrome toxin 1 (TSST1 .(
 It was commonly seen in young women associated with the use of
highly absorbent intravaginal tampons. The toxin acts as a 'superantigen', triggering significant T-helper cell activation and massive
cytokine release .
Staphylococcal toxic shock syndrome
 Abrupt onset with high fever, myalgia, headache, sore throat and
vomiting, a generalised erythematous blanching rash resembling
scarlet fever, and hypotension. 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.
culture and demonstration of toxin production are confirmatory .
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Treatment
 Immediate and aggressive fluid resuscitation and an intravenous
antistaphylococcal antibiotic (flucloxacillin or vancomycin), 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 .
 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 .
PREVENTION S. aureus infections
Prevention of the spread of S. aureus infections in the
hospital setting involves
1. Hand washing
2. Appropriate isolation procedures..
3. The use of topical antimicrobial agents (e.g., mupirocin) to
eliminate nasal colonization with S. aureus .
The ability of a capsular polysaccharide–protein conjugate
vaccine to prevent staphylococcal infections in
hemodialysis patients was studied.
4. Are nasopharyngeal and gut commensals, Gram-positive spherical
to ovoid form chains when grown .
Streptococcal infections
 Are nasopharyngeal and gut commensals, Grampositive spherical to ovoid form chains when grown .
 Most are facultative anaerobes.
 Classified by the haemolysis they produce on blood
agar and by their serotypes .
 In the medical setting, the most important groups are
the:
1. alpha-hemolytic :S. pneumoniae and Streptococcus Viridans.
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2. beta-hemolytic streptococci of Lancefield groups A and B.
)β-haemolytic group A (Strep. pyogenes
),Skin and soft tissue infection (erysipelas, impetigo
Streptococcal toxic shock syndrome
Puerperal sepsis ,Scarlet fever , Tonsillitis , Bone and joint infection
Glomerulonephritis
Rheumatic fever
)β-haemolytic group B (Strep. agalactiae
Neonatal infections, including meningitis.Female pelvic
infections.Cellulitis
Septicaemia
α-haemolytic viridans group
Septicaemia in immunosuppressed .Endocarditis
)α-haemolytic optochin-sensitive (Strep. pneumoniae
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Pneumonia. Meningitis. Endocarditis. Otitis media. Spontaneous bacterial
peritonitis . Septicaemia
).Anaerobic streptococci (Peptostreptococcus spp
Peritonitis. Dental infections . Liver abscess. Pelvic inflammatory disease
Scarlet fever
 Group A (or occasionally C and G) causing pharyngitis, tonsillitis
may lead to scarlet fever, if the infecting strain produces a
streptococcal pyrogenic exotoxin A, B, and C.
 Common in school-age children,diffuse erythematous rash occurs,
blanches on pressure with circumoral pallor. The tongue becomes
red and swollen ('strawberry tongue) . The rash disappea in 7-10
days.
 Treatment :benzylpenicillin or oral penicillin plus symptomatic
measures .
Streptococcal toxic shock syndrome
 Associated with severe group A (occasionally 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 T-helper cells and a dramatic
cytokine response.
Streptococcal toxic shock syndrome
 Initially, an influenza-like illness occurs signs of localised
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.
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Treatment
 Fluid resuscitation, with parenteral antistreptococcal
antibiotic, usually with benzylpenicillin and a protein
inhibitor such as clindamycin to inhibit toxin production .
 Intravenous immunoglobulin.
 If necrotising fasciitis is present, it should be treated as
with urgent débridement .
Remote complications of streptococcal sore throat
1. Rheumatic fever
2. Acute post-streptococcal glomerulonephritis
These occur 2-3 weeks after strept.sore
throat, and they are immunological reaction
to strept. Antigens.
ERYSIPELAS
It is an acute streptococcal infection, affect the skin most commonly the
face but may occur at other areas like leg. Usually occurs in elderly and
immune comprised. Local pain and hotness at involved are. Rapid
.spreading red patch, oedema of subcutaneous tissue with palpable edge
R: Penicillin
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