1. Staphylococcal and Streptococcal infections
For Fourth- Year Medical Students
Dr : Hussein Mohammed Jumaah
CABM
Mosul College of Medicine
Monday , October 16 , 2017

2. Catalyzing 2 H2O2 → 2 H2O + O2

3. Most infections of the skin, soft tissues and bone are caused by either staphylococci (mainly Aureus). or streptococci (mainly Pyogenes(.

4. 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 converts fibrinogen to fibrin in rabbit plasma, causing it to clot.

5. Infections caused by Staph. aureus.

6. prolong hospital stays
Skin infections
folliculitis, furuncles, carbuncles, impetigo and the scalded skin syndrome
Mid-facial cellulitis, which can result in cavernous sinus thrombophlebitis.
Wound infections
prolong hospital stays
Treatment drainage of abscesses plus antistaphylococcal antibiotics.
Prevention hand hygiene, aspetic technique, topical and systemic antibiotic prophylaxis.
carbuncle
folliculitis
impetigo

7. * MRSA= Meticillin-resistant Staph. Aureus
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.
* MRSA= Meticillin-resistant Staph. Aureus

8. How to assess an intravenous cannula
using the Visual Infusion Phlebitis score (VIP)

9. Endocarditis Staphylococci are particularly dangerous if they gain access to the blood stream . In any patient with staphylococcal bacteraemia, especially injection drug users, the possibility of endocarditis must be considered.

10. Meticillin-resistant Staph. Aureus (MRSA)
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.
* Polymorphonucleocytes

11. MRSA
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(

12. 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.

13. 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.

14. 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.

15. Staphylococcal toxic shock syndrome
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.

16. Staphylococcal toxic shock syndrome
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.

17. 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.

18. Scarlet fever
Group A (occasionally C and G) causing pharyngitis, tonsillitis may lead to scarlet fever, if the infecting strain produces a streptococcal pyrogenic exotoxin A, B, 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 disappear in 7-10 days , followed by a fine desquamation. Residual petechial lesions in the antecubital fossa may be seen (Pastia’s sign).
Treatment :benzylpenicillin or oral penicillin plus symptomatic measures .

19. Streptococcal and related infections

20. 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.

21. 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.

22. Treatment of Streptococcal toxic shock syndrome
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.

23. 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.