Download Infection caused by S. auerus

Micrococcaeceae
the gram positive cocci is the most frequent isolated from the clinical specimens.
The family micrococcaeceae include the following genera:
1.
2.
3.
4.
Staphylococcus.
Micrococcus.
Planococcus.
Stomatococcus.
Genus staphylococcus:
The genus staphylococcus is composed of several spp. Many of them are a part of
the normal flora.
Staph are catalase positive gram positive cocci arranged in single pairs tetrads
and short chain predominantly in cluster. Non motile, non spore forming with
limited capsule formation aerobic or facultative anaerobe .
Staph is initially differentiated by coagulase into
1. Coagulase positive (Staph. aureus)
2. Coagulase negative (CoNS): more than 35 spp of CoNS is identified those of
clinical sigenificant are:
S. epidermidis, S. saprophyticus., S. haemolyticus.
.
1.
Coagulase positive Staph
Staphylococcus aureus:
It is the most important isolates it is responsible for infection from mild to a life
threatening infections. It is recovered from any clinical sample and an important
cause of hospital acquired infections. Increase drug resistance in the last decade is
an important concern. It can be found in the external environment and the anterior
naris in 20-50 % of adults.
Virulence factors:
i.
Peptidoglycan and tiechoic acid: it play an important role in adherence,
activation of complements and chemotaxises of PMN.
ii.
Protein A: has the ability to bind to the FC portion of all IgG .
iii.
Capsular polysaccharides: prevent the ingestion of the MO by the PMN
(polymophnuclear leucocyte).
iv.
Enzymes :
1. Catalase inactivate toxic H2O2 and free radicals formation in PMN.
2. Clumping factor: it is responsible of binding of staph to both fibrin and
fibrinogens.
3. Coagulase (staphylocoagulase) it is found free form in the medium or cell
bound it thrombin like molecule called coagulase-reacting factor (CRF) to form
coagulase- CRF complex the complex resemble thrombin and directly convert
fibrinogen to fibrin leading to clot formation.
4. Staphylokinase it causes fibrinolysis.
5. Hyaluronidase.
v.
Hemolysin and leukocidin:
vi Toxins:
1. Enterotoxin: Heat stable exotoxin (100C for 30min) it cause food poisoning.
2. TSST1(toxic shock syndrome toxin) it is called superantigen
3. Exfoliative toxin or epidermolysin Strains produce this toxin
cause
staphylococcus scaled skin syndrome.
Infection caused by S. auerus:
1. Skin and wound infection: S. aureus infection are suppurative. typically it
cause abscess. It causes folliculitis, furuncle, carbuncle and bullous impetigo &
post surgical wound infection.
2. Scalded skin syndrome (Ritter's disease) extensive exfoliative dermatitis
occur in new born baby. It occur in adult only in patients with renal failure.
3. Staphylococcal food poisoning caused by staph produce heat stable
enterotoxin, it cause vomiting abdominal pain with or without diarrhea NO fever.
4. Toxic shock syndrome : it is fatal multi systemic disease and could be
associated with menstruation or not associated with menstruation. Toxic shock
syndrome is manifested by an abrupt onset of high fever, vomiting, diarrhea,
myalgias, rash, and hypotension with cardiac and renal failure in the most severe
cases. It often occurs within 5 days after the onset of menses in young women
who use tampons, but it also occurs in children or in men with staphylococcal
wound infections.
5. S. aureus also cause bactermia,endocarditis, meningitis, osteomylitis and
pneumonia.
2.
Coagulase negative staph:
a. Staphylococcus epidermidis :
The role of this mo as an etiologic agent of diseases has become increasingly
evident. These mo is always isolated from the normal flora of skin. Infection is
predominantly hospital acquired. Most common hospital acquired infection
caused by S. epidermidis are UTIs, prosthetic valve endocarditis and intravascular
catheter and CSF shunt infection. Septicemia reported in immuncompromised
patient.
b. Staphylococcus saprophyticus :
It is associated with UTI in young sexually active female (true urinary pathogen)
but it is the commonest cause of UTI . It is rarely found on other mucous
membrane or skin surfaces. In urine culture it may be found in low concentration
but still considered pathogenic.
Laboratory diagnosis:
i.
Sample is taken from the site after proper cleansing of the area and transport
immediately without delay to avoid dryness of the sample.
ii.
Microscopical examination: Direct gram stain smear to see gram positive or
variable cocci arranged in single. Pairs tetrad or clusters inside and outside the
PMN.
iii.
Isolation
1. staph grows readily on routine culture medium particularly SBA (sheep
blood agar) within 24 hr. On SBA after 18-24 hr of incubation at 35-37 C Staph
aureus produce round smooth colony with hemolytic zone with golden yellow
pigment.
S epidermidis produce non hemolytic white colony .
S. saprophyticus produce larger colonies only 50% produce yellow colonies.
2. MSA (mannitol salt agar) is good selective culture media for isolation of S.
auerus. It diagnosed by mannitol fermentation .
iv.
1.
On Identification :
Catalase differentiated staph from Streptococci.
Staph differentiated from micrococci (Micrococcus is a saprotrophic or commensal
organism, though it can be an opportunistic pathogen, particularly in hosts with
compromised immune systems, such as HIV patients.) on basis of
a. oxidative fermentation reaction. Staph ferment glucose while micrococci fail to
form acid under anaerobic condition.
b. modified oxidase test staph –ve, micrococci +ve.
3. Identification of staph auerus :
a.
Slide coagulase :Clumping factor formerly referred to as cell bound
coagulase it causes agglutination in human and rabbit serum detected by slide
method.
b.
Tube coagulase: strain of Staph aureus does not produce clumping factor
should be investigated for stapyhlocoagulase production by tube method.
c.
Isolates do not produce clumping factor or staphylocoagulase are reported as
CoNS.
v.
Antimicrobial susceptibility :
Broth microdilution or disk diffusion susceptibility testing should be done
routinely on Staph aureus isolates from clinically significant infections.
Resistance to penicillin G can be predicted by a positive test for β-lactamase;
approximately 90% of S aureus produce β- lactamase. Increasing resistance to
alternative antibiotics is of major concern. Testing of CoNS is dependent on
source and determination if the isolate is a likely pathogen. Resistance to nafcillin
(and oxacillin and methicillin) occurs in about 35% of S aureus and approximately
75% of S epidermidis isolates.
Methicillin resistant Staphylococci:
Isolates resistant to penicillinase resistant penicillin called methicillin resistance
staph. (MRSA =S.aureus, MRSE=epidermidis).
In the past MRSA was associated with hospital acquired infection since the late
1990s, however, MRSA has been found to be associated with community acquired
infections.
Oxacillin and other penicillinase- resistant penicillin such as methicillin , naficillin
cloxacillin , constitutes the drug class of choice for treating staphylococcal
infection . Staphylococcal resistance to the penicillinase- resistant penicillin is due
to the presence of a unique penicillin binding protein (PBP2a or PBP2'). The
penicillin binding protein , which has a low affinity for binding all β-lactam drugs,
is encoded by mec a gene.
Identification of MRSA
1.
Disk diffusion method: If disk diffusion is used the edge of the inhibition
should be examined closely. The border is sharp and clear when oxacillin is
susceptible organism are tested. Growth of oxacillin resistant organism " feather "
or trails as the disk approach.
2. If disk susceptibility is not clear using oxacillin salt agar screening test ,
use Mueller hinton agar with 4% NaCl and 6µg/ml oxacillin.
3. Gold standard is by detecting the mec gene by PCR.
4. Detection of PBP2a using latex, fluorescence technology.
All oxacillin resistant staph should be considered resistant to all β lactam drug
regardless the in vitro test results.
Vancomycin remain the DOC for MRSA, but increase resistance to glycopeptides
call for restrictive use of these drugs.
Vancomycin resistant staphylococci:
Vancomycin is the drug of choice and sometimes the only drug available for
serious staphylococcus infection. And thus the development of vancomycin
resistance has been a serious concern.
The most accurate susceptibility is done by nonautomated method. Detection of
these strain should be reported to the CDC.
Treatment of Staph infection:
Minor skin infections are usually treated with an antibiotic ointment such as a
nonprescription triple-antibiotic mixture. In some cases, oral antibiotics may be
given for skin infections. Additionally, if abscesses are present, they are surgically
drained. More serious and life-threatening infections are treated with intravenous
antibiotics.
Several different types of antibiotics have been used to treat staph infections. The
choice of antibiotic depends on the type and severity of the infection as well as
drug-resistance patterns of the particular bacterial type. Some of the antibiotics
that have been used to treat staph infections are cephalosporines nafcillin
,oxacillin, rifampin and clinamycin. Combinations of antibiotics and other
antibiotics can also be used. MRSA treated with vancomycin.
Treatment of vancomycin resistant staph is by the use of daptomycin