العدد : 5 1 lec :
د. حسين باطنية الاربعاء 2/10/2013
العدد : 5 1 lec :
د. حسين باطنية الاربعاء 2/10/2013
catalyzing2 H2O2 → 2 H2O + O2
catalyzing2 H2O2 → 2 H2O + O2
Staphylococcal and Streptococcal infections
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.
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.
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 .
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 co-trimoxazole.
Severe infections. Glycopeptides, linezolid and daptomycin
PVL-producing Staph. infections should be treated with protein-inhibiting 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 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 'super-antigen', 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.
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
Hand washing
Appropriate isolation procedures..
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.
Are nasopharyngeal and gut commensals, Gram-positive spherical to ovoid form chains when grown.
Streptococcal infections
Are nasopharyngeal and gut commensals, Gram-positive 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 :
alpha-hemolytic :S. pneumoniae and Streptococcus Viridans.
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)
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.
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
Rheumatic fever
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