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25. 02.

2013
We have not passed that subtle line between
childhood and adulthood until we move from the
passive voice to the active voice that is,

until we have stopped saying It got lost

and say, I lost it.

Sydney J. Harris, journalist (1917-1986)


Modele

Anti-modele
Examen ... ... ... Sfaturi ... ... ...

Un caz ... Un student ... O situaie ...

A trecut semestrul I / ncepe semestrul al II-lea ...

Genul Staphylococcus

De trimis prin email


pentru tineri
VISA, VRSA
ndemn la a cuta / discuta / nu atepta ...
Student anul II la Facultatea de Medicin

Locuiete n cmin, Regie

ncepnd cu ora 21.00, joi 14 martie


Durere intens n zona flancului drept
Cu caracter colicativ
!?
mi cer scuze pentru faptul ca trimit intrebarile
multiple cu 2 zile inainte de examen, dar vi le trimit
acum pentru c redactarea lor m-a ajutat enorm n
procesul de invatare si recapitulare n aceasta
perioada ...

Scriindu-le am repetat intreaga materie si am inteles


anumite lucruri pe care nu le intelesesem.

Multumesc pentru nelegere!

Sper ca faptul ca le am trimis acum sa nu va supere.


Domnule profesor,

Vreau s v mulumesc pentru c ai insistat att


anul trecut s rezolvm cazurile clinice. Cutnd s le
rezolv temeinic, am trecut fr s vreau printr-un volum
consistent de informaii medicale.
Din tot ce am nvat n ultimii ani, acestea mi-au fost
cel mai mult de folos la examenele din sesiunea care
tocmai a trecut. i nu este numai cazul meu. Cazul
bieelului cu RAA i agenii etiologici ai pneumoniilor mi-
au adus multe puncte la examenul de semiologie.

M-am gndit s v scriu ca s nu v lsai descurajat


de dezinteresul sau protestele unor studeni de anul 2 cu
privire la cazuri. Sunt sigur c dac sunt de bun credin,
v vor mulumi i ei mai trziu.

O zi minunat v doresc!
Genul Staphylococcus
Stafilococii = coci gram-pozitivi aerobi, facultativ
anaerobi, imobili, nesporulai, catalazo-pozitivi.

Genul cuprinde mai multe grupe de microorganisme


de interes medical.
Unele dintre aceste grupuri includ mai multe specii.

Cele mai importante specii sunt reprezentate de:


- S. aureus;
- S. epidermidis (pigment alb);
- S. saprophyticus (pigment citrin).
S. aureus = specia cel mai frecvent implicat n clinic.

Celelalte dou specii sunt de obicei nepatogene.

n funcie de capacitatea de a elabora coagulaz,


toi stafilococii coagulazo-pozitivi sunt grupai ca
i Staphylococcus aureus.
Habitat

S. aureus se poate multiplica la nivelul tegumentelor


i mucoaselor (n special n zonele piloase i la
nivelul vestibulului nazal).

Stafilococii coaguloazo-negativi (SCN) formeaz


microcolonii la nivelul foliculilor piloi i la
nivelul glandelor sebacee.

i atunci, CE infecii pot produce ?


Patogenie
Staphylococcus aureus produce dou tipuri de
infecii, respectiv prin:
multiplicare + invazivitate i
multiplicare + toxigenez.
Manifestrile clinice ale TI
se datoreaz 1-n substane produse (toxine)
pot fi reproduse prin administrarea substanelor
respective (n lipsa infeciei).

Toxina poate fi produs:


in vivo (ex. TSS sau SSSS / staphylococcal scalded
skin syndrome) sau
n un vector prin intermediul cruia ajunge la
nivelul gazdei (ex. TIA stafilococic).
Patogenia TI stafilococice parcurge urmtoarele etape :

colonizare de ctre tulpina toxigen,

producerea toxinei,

absorbia toxinei i

fenomenele de intoxixaie.
Infeciile invazive implic:
aderena ... colonizarea
multiplicarea bacterian
invazie i distrugere tisular
rspuns inflamator local i / sau sistemic.
n acest scop, microorganismul produce o serie de
factori de virulen / patogenitate.
Colonizarea mucoasei nazale dup aderare la
componente celulare (ex. mucin-carbohidrai).
Pentru colonizarea altor mucoase, nu sunt
identificate structurile int.
Colonizarea poate fi:
tranzitorie
persistent ... i rezult procesul infecios.
Dar ce este inflamaia ?

i ce este procesul infecios ?


Inflamaia =
proces fiziopatologic complex care include
fenomene alterative,
fenomene de tip reactiv (vasculo-exudative i
proliferative) i
fenomene reparatorii
cu scopul limitrii i / sau neutralizrii agresorului
(indiferent de natura acestuia).
Inflamaia poate interesa
esuturi,
organe,
sisteme sau
chiar ntregul organismul
Inflamaia cuprinde n mod clasic
tumor (edem),

rubor (eritem, nroire local),

calor (temperatur crescut n zona inflamat),

dolor (durere), nsoite sau nu de

functio laesa (tulburri funcionale ... pn la


impoten funcional)
Inflamaia / etiologie
ageni determinani diveri
microorganisme (prioni, virusuri, bacterii,
fungi, parazii)
ageni fizici (radiaii, frig, cldur, curent
electric, traume etc)
ageni chimici
exogeni (ulei de croton, terebentin, caolin,
dextran etc) i / sau
endogeni (uree, acizi biliari etc)
Modificrile fiziopatologice
apar independent de cauza inflamaiei ...
se traduc prin sinteza i eliberarea reactanilor de
faz acut (RFA)

Particulariti structurale ale


organismului
esutului lezat
ar putea explica n parte varietatea fenomenelor.

ex. Mycobacterium tuberculosis produce


inflamaii alterative (la nivel pulmonar),
exsudative (la nivel pleural) sau
inflamaii proliferative (la nivel dermic).
Consecine ale activrii inflamaiei
apariia unui tip particular de inflamaie
cu mai multe forme clinice evolutive
acut
subacut
cronic
i mai multe forme anatomoclinice
Evoluia spre vindecare presupune:
- asanarea focarului inflamator
constituirea barierei fibrino-leucocitare
ndeprtarea resturilor celulare
i a eventualelor microorganisme
devine maxim dup acumularea de PMN
i macrofage.
- vindecarea propriu-zis
se intersecteaz cu fenomenele lezionale
pe care ncepe s le substituie
Vindecarea propriu-zis
a). vindecarea anatomic
b). Cicatrizarea
fenomene lezionale ntinse
pierdere de esuturi i / sau
infecii i supuraii supraadugate
Aspecte anatomo-clinice
- inflamaii alterative
predomin procesele distrofice i
necrobiotice
ex. n miocardita difteric, miozita cu
clostridii

- inflamaii proliferative
form particular granulomul
ex. dup infecii cu M. tuberculosis,
T. pallidum, prezena unui corp strin
Aspecte anatomo-clinice
- inflamaii exsudative
predomin proceselor exsudative
a). seroase (3-5 % proteine), ex. n
pleurezia tuberculoas;
b). fibroase, de obicei infecioase
(pneumococic, dizenteric, difteric etc),
cu acumulare de fibrinogen i aderene,
care se organizeaz;
c). purulente, produse de exemplu de
coci piogeni (abcese etc);
d). hemoragice, de exemplu n cium.
Procesul infecios = ansamblul relaiilor dintre
microorganism i gazd, aprute dup infecie.

Condiii ?
Starea de boal (clinic sau subclinic)
datorat interaciunii microorganism-gazd
urmat de
leziuni manifeste i
reacii funcionale din partea gazdei.

Infecia
nu este urmat obligatoriu de starea de
boal
Rezultatele infeciei
cuprind manifestri foarte variate
pot aprea sau nu
n funcie de:

agentul infecios
organismul gazd
mediul extern (factori geografici,
climatici, sociali, economici etc).
Manifestri subclinice

a) Infecia inaparent
b) Boala subclinic
c) Infecia latent
d) Starea de purttor
Infecia inaparent
asimptomatic
decelat prin examene de laborator
este limitat n timp
contribuie la crearea unei stri de imunitate

Boala subclinic
apar unele tulburri funcionale
chiar i unele leziuni organice
uneori fr simptomatologie distinct
Infecia latent
asimptomatic
agenii patogeni persist timp ndelungat
poate deveni evident clinic
ex. infecia cu M tuberculosis

Starea de purttor de germeni


bolnav
convalescent
persoanele aparent sntoase
(ex. Salmonella typhi la nivelul veziculei
biliare, dup febr tifoid)
Manifestri clinice

a) Infecia local
b) Infecia de focar
c) Infecia regional
d) Infecie generalizat (sepsis)
Bacteriemie =
prezena pasager de germeni n snge.

Bacteriemia
nu duce la apariia de metastaze septice
poate aprea dup
extracii dentare
intervenii chirurgicale pe focare
septice

precum i n multe dintre bolile infecioase (ex. n


pneumonia pneumococic).
Starea de sepsis reunete
infecia i
rspunsul inflamator sistemic

Include 2 sau mai multe din urmtoarele:


febr (peste 38C) i frisoane / sau
hipotermie (sub 36C),
tahicardie,
polipnee (peste 20 respiraii / minut) cu
hiperventilaie sau Pa CO2 sub 32 mmHg,
leucocitoz peste 12.000 / mm3 sau
leucopenie sub 4.000 / mm3, cu forme
tinere n circulaia periferic (peste 10%).
Revenind la stafilococi
De regul invazia NU este posibil atunci cnd barierele
naturale sunt intacte.

Invazia este facilitat de agresiuni mecanice la nivel


epidelial, glandular sau la nivelul unui folicul pilos.
Dac este realizat depirea barierelor mecanice,
colonizarea devine posibil prin aderarea S. aureus la
diferite molecule (unele precizate, altele presupuse) situate la
nivel tisular.

Dintre adezine menionm proteinele de suprafa (ex.


proteina A) care ader la:
fibrinogen,
fibronectin,
colagen,
elastin etc.
Dintre substanele produse de ctre S. aureus care altereaz
structuri la nivelul gazdei, permind colonizarea:

- Coagulaza
- Lipazele
- Hialuronidaza etc, precum i diferite
- Toxine
Filtratele culturilor de S. aureus coaguleaz plasma
recoltat de la o serie de specii animale sub aciunea
coagulazei, care este cel mai important marker
pentru S. aureus.

Exist totui i tulpini de stafilococ implicate


patogenic care sunt coagulazo-negative.
Coagularea necesit prezena unui factor coagulazo-
reactant (FCR), care este probabil un derivat de
protrombin.

Complexul coagulazei realizat cu FCR convertete


fibrinogenul n fibrin.

Procesul difer de coagularea normal = nu sunt


necesari o serie de factori (ex. Ca2+) iar cheagul care
se formeaz este mai friabil i nu se retract.
S. aureus produce diferite lipaze evideniabile prin
opacifierea agarului cu glbenu de ou
scindarea Tween 80.

Contribuie la supravieuirea stafilococului la nivel dermic.


Hialuronidaza hydrolizeaz acidul hialuronic
(mucopolizaharid prezent extracelular).

Faciliteaz invazia microorganismelor.


Stafilokinazele, termonucleaza i proteazele serice = produse
de tip enzimatic cu posibil rol n patogenez.
S. aureus produce i o serie de toxine active la nivel
membranar, cu rol probabil (dar neprecizat) n patogenez.

Dintre aceste toxine ar fi de amintit:


-, - i -hemolizinele,
alte produse cu caracter toxic
-hemolizina i
leucocidina / Panton-Valentine.
-Hemolizina ( -toxin) prototip de toxin productoare
de pori. Se inser la nivel membranar, creaz canale ionice i
integritatea membranei este distrus.

Toxina este:
dermonecrotic (la injectarea s.c),
induce modificri proinflamatorii n celulele mamiferelor
i n cazul modelelor animale
induce multe din semnele ntlnite n sepsis, ex.
hipotensiune i
trombocitopenie.
Leukocidina (Panton-Valentine)
activ fa de PMN, monocite, macrofage.
este dermonecrotic (i.d. la iepure)
tulpinile care produc L sunt asociate semnificativ statistic
cu apariia furunculozei la om.
i atunci ?
Abces / Furuncul
Endocardit
Sindromul de piele oprit SSS-S
Diagnostic
clinic
bacteriologic
Tratament
etiologic
conform ANTIBIOGRAMEI !
patogenic
Elemente eseniale n tratament:
drenajul coleciei purulente,
eliminarea esuturilor necrotice,
eliminarea corpilor strini i
administrarea medicamentelor antimicrobiene.
Importana drenajului este extrem de mare !!!

Chiar i n cazul celei mai mici colecii


purulente TREBUIE fcut drenajul.
Apariia i extinderea rezistenei la antibiotice =
preocupare important n ultimii 15 - 20 ani.

n doar 4 ani de la introducerea penicilinei, a fost


identificat producerea de -lactamaz i respectiv
rezistena la penicilin.

Rezistena la diferite alte antibiotice s-a dezvoltat n


special dup 1950.
Antibioticele lactamice se leag penicillin-
binding proteins (PBPs), transpeptidazele care
catalizeaz ultima etap n formarea peretelui
bacterian.
S. aureus poate produce patru PBPs.
Rezistena la penicilin a S. aureus este datorat i
producerii de -lactamaz, care degradeaz inelul -
lactamic inactivnd medicamentul.

n majoritatea studiilor cunoscute, 70-90% dintre tulpinile


de S. aureus produc lactamaz ...
Meticilina, prima penicilin sintetic, stabil la
lactamaz, a fost introdus n practic n anul 1960; n doar
1 an, au aprut tulpinile de MRSA.

MRSA rezist la toate antibioticele cu nucleu -lactam


(peniciline, cefalosporine, carbapeneme etc).

Din 1980, apare rezistena i la antibiotice i chimioterapice


(cloramphenicol, tetracicline, gentamicin, macrolide etc,
prin alte mecanisme de rezisten).
Pn relativ recent, tulpinile MRSA erau nc susceptibile la
vancomicin medicament de elecie n infeciile cu MRSA.

Din pcate
eficacitatea Vancomicinei n infeciile grave produse
de S. aureus nu este maxim
a aprut fenomenul de rezisten

NB. S nu uitm totui, penicilina.


Antibiograma: Se face testul coagulazei (G-ral
Medical Pantelimon)

Stafilococ auriu
sensibil doar la Vancomicin, Linezolid;

intermediar la Teicoplanin i

rezistent la Oxa, Cipro, Genta, Meropenem,


Imipenem, Cefuroxim, Ceftazidin, Levofloxacin.
What is Staphylococcus aureus?

Staphylococcus aureus, often simply referred to simply as staph,


are bacteria commonly found on the skin and in the noses of
healthy people. Occasionally, staph can cause infection; staph
bacteria are one of the most common causes of skin infections in
the United States. Most of these infections are minor (such as
pimples, boils, and other skin conditions) and most can be treated
without antimicrobial agents (also known as antibiotics or
antibacterial agents). However, staph bacteria can also cause
serious and sometimes fatal infections (such as bloodstream
infections, surgical wound infections, and pneumonia). In the past,
most serious staph bacterial infections were treated with a type of
antimicrobial agent related to penicillin. Over the past 50 years,
treatment of these infections has become more difficult because
staph bacteria have become resistant to various antimicrobial
agents, including the commonly used penicillin-related antibiotics.
What are VISA and VRSA?

VISA and VRSA are specific types of antimicrobial-resistant staph


bacteria. While most staph bacteria are susceptible to the
antimicrobial agent vancomycin some have developed resistance.
VISA and VRSA cannot be successfully treated with vancomycin
because these organisms are no longer susceptibile to vancomycin.
However, to date, all VISA and VRSA isolates have been susceptible
to other Food and Drug Administration (FDA) approved drugs.
How do VISA and VRSA get their names?

Staph bacteria are classified as VISA or VRSA based on laboratory


tests. Laboratories perform tests to determine if staph bacteria are
resistant to antimicrobial agents that might be used for treatment of
infections. For vancomycin and other antimicrobial agents,
laboratories determine how much of the agent it requires to inhibit the
growth of the organism in a test tube. The result of the test is usually
expressed as a minimum inhibitory concentration (MIC) or the
minimum amount of antimicrobial agent that inhibits bacterial growth
in the test tube. Therefore, staph bacteria are classified as VISA if the
MIC for vancomycin is 8-16 g/ml, and classified as VRSA if the
vancomycin MIC is >32 g/ml.
How common are VISA and VRSA infections?

VISA and VRSA infections are rare. Only eight cases of infection
caused by VISA (Michigan 1997, New Jersey 1997, New York 1998,
Illinois 1999, Minnesota 2000, Nevada 2000, Maryland 2000, and
Ohio 2001) and two cases of infection caused by VRSA (Michigan
2002 and Pennsylvania 2002) have been reported in the United
States.
Who gets VISA and VRSA infections?

Persons that developed VISA and VRSA infections had several


underlying health conditions (such as diabetes and kidney
disease), previous infections with methicillin-resistant Staphylococcus
aureus (MRSA), tubes going into their bodies (such as intravenous
[IV] catheters), recent hospitalizations, and recent exposure to
vancomycin and other antimicrobial agents.
What should I do if I think I have a Staph, MRSA, VISA, or VRSA
infection?

See your healthcare provider.


Are VISA and VRSA infections treatable?

Yes. To date, all VISA and VRSA isolates have been susceptible to
several Food and Drug Administration (FDA) approved drugs.
How can the spread of VISA and VRSA be prevented?

Use of appropriate infection control practices (such as wearing


gloves before and after contact with infectious body substances and
adherence to hand hygiene) by healthcare personnel can reduce the
spread of VISA and VRSA.
Because VISA and VRSA are only part of the larger problem of
antimicrobial resistance in healthcare settings, CDC has started a
Campaign to Prevent Antimicrobial Resistance. The campaign centers
around four strategies that clinicians can use to prevent antimicrobial
resistance: prevent infections; diagnose and treat infections
effectively; use antimicrobials wisely; and prevent transmission. A
series of evidence-based steps are described that can reduce the
development and spread of resistant organisms such as VISA and
VRSA.
What should I do if a family member or close friend has VISA or
VRSA?

VISA and VRSA are types of antibiotic-resistant staph bacteria.


Therefore, as with all staph bacteria, spread occurs among people
having close physical contact with infected patients or contaminated
material like bandages. Therefore, persons having close physical
contact with infected patients while they are outside of the healthcare
setting should: (1) keep their hands clean by washing thoroughly with
soap and water, (2) avoid contact with other peoples wounds or
material contaminated from wounds. If you visit a friend or family
member who is infected with VISA or VRSA while they are
hospitalized, follow the hospitals recommended precautions.
What is CDC doing to address VISA and VRSA?

CDC has established several programs to promote appropriate use of


antimicrobial agents because inappropriate antibiotic use is a major cause of
antimicrobial resistance. One program that focuses on patients in healthcare
facilities is the Campaign to Prevent Antimicrobial Resistance. The campaign
centers around four strategies that clinicians can use to prevent antimicrobial
resistance: prevent infections; diagnose and treat infections effectively; use
antimicrobials wisely; and prevent transmission of infections. A series of evidence-
based steps are described that can reduce the development and spread of resistant
organisms, such as VISA and VRSA. CDC also has published guidance to prevent
the spread of vancomycin resistance in healthcare settings.
In addition to providing guidance for clinicians and infection control personnel, CDC
is also working with state and local health agencies, healthcare facilities and clinical
microbiology laboratories to ensure that laboratories are using proper methods to
detect VISA and VRSA (S.E.A.R.C.H.). Recently CDC developed a training tool for
laboratorians to enhance their understanding and improve their proficiency in
performing antimicrobial susceptibility testing (M.A.S.T.E.R.). Accurate antimicrobial
susceptibility test results not only help physicians choose the best therapy for their
patients, but guide infection control efforts to the most serious infections.
www.cdc.gov