Cl inical i nfectio ns

Th e S taph yl ococci
 Th e S taph yl ococci

• The ma in role in the etiology of

infl ama tory, pyogeni c sept ical
infecti ons plays facul tive pa th ogeni c
ba cter ia .
• The grea test signi fi cance has
staphy loc occi , St rept oc occ i, gr am-
nega tive ba cteri a from th e famil y
Ent eroba cteri acea e.
 Sta phyl ococci
• St aphylo cocci are among the common of
the pyogenic or pus-producing bacteria.
St aphylo cocci causes more frequent and
more varied diseases than perhaps any
other human pathogen, includes infection of
the skin, an abscess in deep tissue, more
serious infections such as pneumonia,
mastitis, phlebitis, endocarditis, central
nervus system infections (meningitis, brain
abscess),pulmonary infections (embolic,
aspiration).
 Sta phyl ococci

• Special strains also produce toxins, that

cause different types of disease: namaly
• foo d poi soni ng , to xi c s ho ck
syndro me
• (TSS), and disease, mainly of children,
called sc alded skin sy ndrom e.
 Taxonomically, the genus
Sta ph yloc occu s
• Bacteria l f amil y Sta phyloco cca ceae
• genu s St ap hylococ cus
• St aphyl oc occ us aur eus caus es a
va ri ety of pus -f orming ) in fe ct ions and
toxinos es i n huma ns
• S. epi dermidi s may be a pathog en in
the hosp ita l envi ronment.
• S.s aproph yti cus caus es a uri na ry tr act
• infecti on.
 Char ac te risti cs o f
Sta ph yloc occu s a ur eus
• Gr am- posi ti ve, cl ust er-formi ng coc cus
nonmot ile, n onsporef ormin g fa cult at ive
ana erobe
ferme nt ati on of glu cose prod uc es ma inly
lactic aci d
ferme nt s ma nni tol ( di st in gui shes fr om S.
epi dermi di s)
ca ta las e pos it ive
coag ul as e p osit ive
golden ye llow col ony on aga r
nor mal fl ora of huma ns f ound on na sa l
passa ges, skin and muco us me mb ra nes
 Sta phylo cocci
• St aphylo coccus aureu s forms a large
yellow colony on rich medium, S.
ep ide rmi dis has a relatively small white
colony. S. aureu s is often hemolytic on
blood agar; S. epi de rm idis is non
hemolytic. Staphyloc occi are facultative
anaerobes that grow by aerobic respiration
or by fermentation that yields principally
lactic acid. The bacteria are catalase-positive
and oxidase-negative. S. aureus can grow
at a temperature range of 15 to 45 degrees
and at NaCl concentrations as high as 15
percent.
 Sta phyl ococci
• Near ly all st rains of S. aureus
pr oduc e the enz ym e coa gula se:
ne arly all stra ins of S. epiderm idi s
lac k thi s enz ym e. S. aureus should
alw ays be co ns ide red a po tenti al
pa thoge n; mo st stra ins of S.
epide rmidis are nonpat ho ge nic and
may even pla y a pro tective ro le in
the ir hos t as nor mal fl or a.
St ap hyl oc occus epide rmidis may be a
pa thoge n in the ho spi tal
en vi ro nm ent.
Gram stain of Staphylococcus
aureus in pustular exudate
Sta phyl ococci
Sta phyl ococci
 Sta phyl ococci

• St ap hyl oc occi are sphe ric al cells

abo ut 1 mic rom eter in diam eter.
The y gr ow in clus ters be cause
stap hyl oc occi divi de in two pl anes .
The confi gu rati on of the cocci helps
to dis tinguis h staphylo cocci fro m
strepto cocci, which are slight ly
oblo ng cells tha t usua ll y grow in
cha ins (bec aus e they di vide in one
pl ane only) .
 Sta phyl ococci
• The catal as e test is impo rt ant in
dis tinguis hi ng stre pt ococ ci
(catal as e-n egat ive ) fro m
staphylo cocci , whi ch are vi gor ous
cata la se-produc ers . T he tes t is
pe rform ed by addi ng 3% hyd roge n
pe roxide to a colo ny on an agar
pla te or sla nt . Cata la se-po sit ive
cult ures pr oduc e O 2 and bu bb le at
once. The test should not be do ne
on bl oo d aga r be cause blo od its elf
contains cat ala se
 Sta phyl ococci
• Wit hin a spa cie s of St aph yloc occus
can be iden tifi ed in resis tanc e to
di ff erent ant ibi ot ics or more
commo nly, by a pro cedure col led
pha ge typing. Its usefulness in
epide miol ogy.
• Hum an ar e the ma jor re servo ir for
S.a ureu s.
• S.a ureu s fr eque nt ly col oni ze the
ext ernal nares and are found in
abo ut 30 % of no rm al indi vidual .
 Sta phyl ococci
• The y can al so be fo und t rans ien tly on
the skin, in the ora pharynx, and in
feces. S.a ureus are well equi ppe d to
colo nize the skin be cause they gro w
at high salt and lip id conc enrat ion.
• S.a ureu s spre ad fro m pe rson to
pers on us uall y via hand cont act.
The y can als o spr ead by aero sol s
pr odus ed by pa tie nt s wit h
pne um onia.
 Sta phyl ococci
• Babies colo nize d short ly after bi rt h , a
pr esent fro m peopl e in the ir
surro unding,
• includ ing ph ys icia ns, nu rses, and
hos pi ta l
• worke rs.
• Cert ain pat ients ( compromi sed
imm une syst em ) inc ludi ng di abet ic
pa tie nt s, chro nic int ra ve no us dr ug,
have a higher carr ia ge ra te the n the
ge nera l po pu lati on.
 Adh eren ce to Ho st C ell
Pro tein s
• S. aureus cel ls ex pr ess on their surf ace
prot eins tha t pr omot e att achme nt to host
prot eins such as fi br onecti n tha t for m the
ex tra cel lul ar ma tri x of epit heli al sur fa ce s.
Most stra ins ex pr ess a fi brin /fi br in ogen
bind ing pr otein ( cl umpi ng fact or ) whi ch
promotes atta chme nt to bl ood clots and
tra uma tize d tiss ue. An adhesi n tha t
promotes att achme nt to coll ag en has been
found in st ra ins th at caus e ost eomyeli tis
and sep ti c art hri ti s.
 Adh eren ce to Ho st Cel l
Pro tein s
• Teic ho ic acids –ar e spec ies sp ecif ic ,
phos pha te-c onta inig po lym ers that
are bound cova le nt ly to the
pe pti dogl yc an la ye r or thr ough
lipo phi lic linka ge to the cyt opla smi c
membra ne ( lipo teic ho ic acids ).
• Teic ho ic ac ids media te the
att ec hmen t of sta phylo cocci to
muc os al surf ac es thr ough the ir
spe cifi c binding to fibronec ti n.
 Extr ac el lular e nzymes
Inva si on

• Spreading Factors" is a term for a

family of bacterial enzymes that affect
the physical properties of tissue
matrices and intercellular spaces,
thereby promoting the spread of the
pathogen. Hyaluronidase. is the
original spreading factor It is
produced by staphylococci. The
enzyme attacks the interstitial cement
("ground substance") of connective
tissue by depolymerizing hyaluronic
acid.
 Extr ac el lular e nz ymes
Inva si on
• Staphylokinase are produced by
staphylococci. Kinase enzymes convert
inactive plasminogen to plasmin which
digests fibrin and prevents clotting of
the blood. The relative absence of fibrin
in spreading bacterial lesions allows
more rapid diffusion of the infectious
bacteria.
 Extr ac el lular e nz ymes
Inva si on

• Coa gula se and clumpi ng fa ctor

• Coa gula se is an ext rac ellul ar
pr ot ein which binds to
pr ot hro mbin in the hos t to fo rm a
comple x called staphyl ot hro mbin
and convert s fibri nogen to fi bri n .
Coa gula se is a tra dit io nal mar ke r
for ide nt if ying S aureus i n the
clinic al mic robi ol ogy labo ra tor y .
 Extr ac ellula r enz ym es
In vas ion
• These enzyme s a ct on the ani ma l ce ll
membr ane by in sert ion int o t he
membr ane (f ormin g a por e th at resul ts
in cell lys is ), or b y enz ymat ic at tack
on phos pholi pid s, whi ch d esta bil ize s
the membr ane. They ma y be ref err ed
to as lecit hina ses or
phos pho lip as es
• DNA-a za, wh ich thi ns out pus ma de
vi sco us by the DNA r eleased f rom
dea d whit e bl ood cel ls.
 Avoidance of Host Defenses
• Caps ula r Poly sa cchar ide
• Thi s ha s bee n ca ll ed a microca psu le
beca use it can be vi sua lize d only by
elec tron micr oscop y. S. aur eus s tr ai ns
isol at ed from inf ect ions ex pr ess hi gh levels
of the polys acchar id e but rapi dl y los e the
abi lit y when cult ur ed in the la bora tory. The
fu ncti on of the cap sul e in vi rul enc e is not
clea r. Can preve nt pha goc yt osis ,inhi bit
he motaxi s. Als o fas il it ates the
adhe rence of ba cteri a to cat he ters .
 Avoidance of Host Defenses

• Pept ido glyc an

• The pe pt id ogl yc anla ue r stim ulat es
the pr oduc tio n of endogenous
pyr ogen s, act ivat es the
pr oduc tio n of interleu ki n-I, fro m
monocyt es, and at tra cts,
po lym or phonuc lear leukoc yt es,
can ac tiva ted comple ment .
 Avoidance of Host Defenses

• Pr ot ein A
• Pr ot ein A is a surf ac e pro tein of S.
aureus whic h binds IgG mole cul es by
the ir Fc regio n. In serum, the
ba cteri a will bind IgG mole cules
pr eve nt ops oniza tio n and f
 Avoidance of Host Defenses
• Leu ko cidi n
• Leukoc idi n forms a tra nsmem bra ne pore
co mp osed of f our LukF a nd four LukS
su buni ts, thereb y for ming a n oc tame ric
por e in t he a ff ect ed membr an e. Le ukoci din
is he mol yti c , but l ess so tha n alp ha
hemolys in.
• S. aureus can ex pr ess a t ox in t ha t
sp ec ifi cally acts on p olymor phonucl ear
leuk ocytes. Pha goc yt osi s is a n import ant
def ens e aga in st s ta ph yloco ccal inf ect ion so
leuk ocid in s houl d be a v ir ulence fa ctor.
 Exotoxins
• Membr ane -da mag ing tox ins
• a-t oxin (a-h emol ysi n) . It is express ed a s a
monomer t ha t bin ds to th e membra ne of
su sce pti bl e ce lls. Subu nit s the n
oli gomeri ze t o f orm hept ameri c ring s wi th
a centr al por e th rough whi ch cel lu la r
co ntent s lea k.
• In huma ns, pl atelet s an d mo noc yt es a re
pa rti cula rl y sensi ti ve t o a-t oxin.
Sus cept ibl e cel ls have a sp eci fi c rec ept or
for a -t ox in w hi ch a llows the tox in to bind
cau si ng sma ll pores throug h whi ch
monova lent ca ti ons can pa ss. The mode of
action of alpha h emol ysi n i s likely by
 Exotoxins

• ß-t oxi n is a sphi ngom ye lina se

whic h da ma ge s membra ne s ri ch in
this li pid. The cla ssic al test fo r ß-
toxin is lys is of she ep
eryt hrocytes . The maj orit y of
hum an is ola tes of S. aure us do no t
express ß-t oxi n. A lys oge ni c
ba cteri opha ge is kno wn to enc ode
the toxin.
 Exot ox in s

• d-tox in i s a v ery s mall

pepti de to xin produc ed by
mo st s tra ins o f S. aure us . It
is also produc ed by S.
epid ermi di s . Th e r ole o f d-
tox in i n di sea se i s un kn own.
 Exot ox in s
• The ex folia tin t ox in – caus es t he
sca ld ed s kin s yndr ome in
neona tes .Ther e ar e two anti geni cally
di st inc t forms of the toxin, ET A and
ET B. T he tox ins ha ve est era se a nd
pr otea se acti vi ty and a pp ar entl y t arg et
a prot ein ( st ra tum g ra nul osum) ,
int ra cell ul ar bri dge s, whi ch i s inv ol ved
in m ai nt aini ng the integ rit y of t he
epi dermi s. The t ox in s ar e not
ass oc iat ed wi th cytol ysi s or
infl amma ti on.
 Super anti gen s: e nte ro toxins
an d to xic sh ock syn drom e to xin
• S. au reu s se cre tes two typ es of toxi n wit h
su pe ran tig en act ivi ty , ente ro to xi ns, of whi ch
the re ar e s ix an tig en ic type s (n amed SE- A, B,
C, D, E an d G ), and toxi c shock sy nd rome
toxi n (TSS T-1) . Sup er ant ige ns st imu lat e T
cells non-sp eci ficall y wi tho ut norma l ant ige nic
reco gni tio n. Cyt oki ne s are rel eas ed in lar ge
amo unts, ca us in g the symp toms of TSS.
( feve r, ski n rash , hyp oten si on).Su pe ran tig en s
bi nd dire ctly to cl ass II ma jor
hist oco mp at ibi li ty co mp le xes of ant ige n-
pr esen tin g cel ls outsi de the co nve nt ional
an tig en -bin din g gr ove.
 Superantigens and the non-
specific stimulation of T cells.
 Path oge ni c Staph yl oco ccu s
epi de rmi dis

• A cha ra cteri st ic of ma ny pa thogenic

st rai ns of S. epid ermi dis is t he
pr oduct ion of a sl ime resul ting i n
bi ofi lm f orma ti on. T he sl ime i s
pr edomin ant ly a sec reted teichoic aci d,
nor mal ly f ound in t he ce ll w all of t he
st aphy loc occi. Thi s ab il ity to form a
bi ofi lm on th e sur fa ce of a pr osth etic
devi ce is pr oba bl y a si gni fican t
det ermin an t of viru lence for t hese
ba cter ia .
 Ho st D efen se aga ins t
Sta phylo cocca l Infecti ons
• Pha gocy tosi s is th e ma jor mecha nis m for
co mba tt ing stap hylococ ca l inf ect ion. The
ba cter ia l caps ul e and protei n A ma y
int erfere wi th phag oc yt osi s . Biof il m
gr owt h on imp la nt s is als o im pe rvi ous to
ph agoc yt osi s. Sta phyl ococ ci ma y be
di fficul t to kil l after pha gocyti c engul fment
beca use the y pr oduce carot enoids and
cat alas e whi ch neut ra lize si ngl et ox ygen
and su pe rox id e wh ich are pri mar y
ph agoc yt ic kil ling me cha ni sms withi n the
ph agolys osome .
 Tre atmen t

• Infection is often caused by antibiotic

resis ta nt st ra ins (MRSA ) and can only be
treated with va nc omycin or an
alt erna tive. Many of the community
acquired (CA) Staphylococcal infections are
now methici ll in resi st an t. These
organisms are uni for mly resi st ant to
penicillins and cephalosporins. The infections
have been treated with combination therapy
using sulfa drugs and minocycline or rifampin.
 Vaccines

• The vaccine called St aphVA X is

composed of S. aureu s type 5 and 8
capsular polysaccharides conjugated to
nontoxic recombinant Pseudom onas
aerugi nos a exo toxi n A.
 Str eptoco ccu s py ogenes
• St rept oc occ us p yogenes (Group A
st reptoco cc us) i s a Gr am- posi ti ve ,
nonmot il e, nons poreformi ng coc cus tha t
oc cur s in cha in s or i n pa irs of cel ls.
St rept oc occ i di vid e in one p la ne and t hus
oc cur i n pa irs or (esp ecia lly in l iqui d me dia
or cli ni cal ma teria l) in chai ns of va ryi ng
leng ths. The meta boli sm of S. py ogenes i s
fer me nt ati ve ; th e orga nism is a catala se-
nega tive aerot olera nt a na erobe (fa cul ta ti ve
ana erobe), and requi res enri che d medi um
co nta ini ng bl ood i n order to gr ow.
 Streptoco ccu s pyog ene s
• St repto coc cus pyo ge ne s is one of
the mos t fre quent pa thogen s of
hum ans . It is estim ated that
be twee n 5- 15% of nor ma l
indi vidua ls har bor the bac terium ,
us ually in the res pir at or y tra ct,
wit ho ut signs of di sease. As no rm al
flo ra , S. pyo ge nes can infec t whe n
de fens es are com pr om is ed or when
the orga nis ms are abl e to pene tra te
the const itut ive de fens es.
 Streptoco ccu s pyog ene s
• Acute Str eptoco ccus pyogenes infections may
present as pha ryngi tis (s trep throa t) , sca rl et
fever (rash), impet igo (infection of the superficial
layers of the skin) or ce lluli tis (infection of the deep
layers of the skin). Invasive, toxigenic infections can
result in nec rot izin g fa scii ti s, myosi ti s and
st reptoco cc al tox ic sho ck synd rome . Patients
may also develop immune-mediated post-
st reptoco cc al sequela e , such as acute
rhe um at ic feve r and acute gl om eru lonephr iti s,
following acute infections caused by St rept ococ cus
py ogenes .
Cl ass ifica ti on of Str epto cocc i
– Hemolys is on blood agar The type
of hemo lyti c reac tio n dis pla ye d on
bl oo d aga r. Beta -he molys is is
asso cia ted with comple te lys is of
red cells surro unding the col ony,
where as al ph a-hemo lys is is a
pa rt ial o r " gree n " he molys is
asso cia ted with reduc tio n of red
cell hem ogl obi n. Nonhe molyt ic
colo nies ha ve be en term ed
ga mma-he molyt ic .
Hem olys is o n b lood a ga r
 Cl ass ifica ti on of Str epto cocc i
• An ti genic typ es
• Hist orica ll y , the defi ni ti ve id ent if ication of
st reptoco cc i ha s rest ed on the serol ogic
reactivit y of "cell wall " polys accha ri de
ant ig ens as ori gi na ll y descri bed by Re bec ca
La nce fiel d. Ei ght een gr oup- specifi c ant ig ens
(Lancefi eld groups ) were est ab lish ed. The
Gr oup A polys accha rid e is a pol ymer of N-
acet ylg lucosa mi ne an d rha mnose. Some
gr oup ant ig ens ar e sha red by more tha n one
sp ec ies. Thi s polys accha ri de is also cal led
the C su bst ance or gr oup carb ohydr at e
ant ig en.
 Str eptoco ccu s py ogenes
• Acut e dis eases associated with Streptococcus
pyogenes occur in the resp ir atory tra ct ,
bl oodst ream, or the ski n. Streptococcal disease
is most often a respiratory infection (pharyngitis or
tonsillitis) or a skin infection (pyoderma).
• S. pyogenes is the leading cause of uncomplicated
bacterial ph ar yngi tis and tonsi ll iti s commonly
referred to a st rep throa t. Other respiratory
infections include si nusi tis , otiti s, and
pn eumo nia .
Streptococcus pyogenes occur in the
res pira tor y tr act /
 Str eptoco ccu s py ogenes
• Infec ti ons of th e sk in ca n be
su per fici al ( impeti go ) or deep
(ce llulitis). I nva si ve str epto cocc i
cau se joi nt o r bo ne i nfec ti ons,
des tructi ve w oun d i nfectio ns
(n ec ro tizi ng fasc iiti s) an d
myo siti s, men ingitis and
en do car di ti s.
 Str eptoco ccu s py ogenes
• Sc ar let feve r and st rept oc occal
toxic shoc k syndro me are systemic
responses to circulating bacterial toxins.
• Sc ar let feve r and st rept oc occal
toxic shoc k syndro me are systemic
responses to circulating bacterial toxins.
 Adh esin s

• Prod uces mult iple a dhe sins wit h

va ri ed spe cifi cit ie s. Str ept ococ cus
pyo ge ne s ut il ize s li pot eic hoi c
acids (LTA ), M pro tein , and
mult ipl e fibro ne ctin-bi nding
pr ot eins in it s re pert oire of
adhe sins .
 Adh esin s
• Teic ho ic acids mediate the attechment of
Streptococcus to mucosal surfaces through
their specific binding to fibronectin. Both the M
pr ot eins and lipo teic ho ic acid are
supported externally to the cell wall on fimbriae
and appear to mediate bacterial adherence to
host epithelial cells.
• The M pr ot eins are clearly virulence factors
associated with bot h colo niza ti on and
res is tanc e to pha goc yt osi s and blo cks
the binding of complement to the
peptidoglycan.
M pr ot ein a nd fim bria e of Gro up A
strept oc occi
 Adh esins

• The str ept oco ccal M p ro tein ,

contain anti ge nic epit ope s that
mim ic those of mamm ali an musc le
and co nne ctive tis sue.
• The M pr ot eins of cert ain M-t ypes
are co ns ide red rhe um at oge nic
sinc e t hey cont ai n ant igen ic
ep itopes re lat ed to he art musc le,
and the y there for e may lead to
autoim mun e rhe um ati c cardit is
(rhe uma tic fever) follo wing an
 Adh es in s

• Th e fib ronec ti n- bindi ng

protei n, Protei n F , has also
bee n show n to mediate
str epto cocc al adh ere nce to
th e ami no ter minus of
fi brone cti n on mucosa l
su rfa ce s.
 Th e Hyalur onic Acid Ca psul e

• The caps ule of S. pyo ge nes is non

antigenic since it is composed of hyal uroni c
acid , which is chem ic ally sim il ar to that of
host conne cti ve tis sue . This allows the
bacterium to hide its own antigens and to go
unrec ognized as antigenic by its host. The
Hyaluronic acid ca ps ule also pr eve nt s
opso nize d phago cyto sis by neutrophils or
mancrophages.
 Ex tr ac el lular produc ts:
inv asins an d exo to xins

• Three strept oc occal pyr oge nic exot oxins

(SPE), formerly known as Eryt hr oge ni c
toxin , are recognized: types A, B, C. These
toxins act as supera ntige ns . They
stim ula te T cells by bi nding clas s II MHC
mole cul es di re ctly and nonspecifically. With
superantigens about 20% of T cells may be
stimulated resulting in massive detrimental
cyt okine releas e . SPE A and SPE C are
encoded by lysoge ni c pha ge s ; the gene for
SPE B is located on the bacterial chromosome.
 Extra ce llular prod ucts : inv as ins
an d ex oto xins
• Streptol ysi n S is an oxygen-
sta bl e leukoci di n; Str epto lysi n
O is an oxyge n-labi le
leukoci din , res po ns ibl e fo r the
hae mol ysi s see n on bl ood
agar. Str epto lysi n O bi nds to
ch oleste rol in the cel l
memb ran e, ina cti ved
 Post str epto cocc al sequ el ae

• Infec ti on wit h Str ept oco ccus

pyo ge ne s can give ri se to seri ous
no nsuppura tive seque lae: acute
rheuma tic fever and acute
gl om erulo neph rit is . These
patho lo gic al ev ent s begin 1-3 wee ks
aft er an acute str ept ococ cal ill nes s,
a la tent pe ri od cons is tent wit h an
imm une -m edia ted eti ol ogy.
 Host defe nse s
• S. pyo ge nes is usua lly an exogen ous
secondar y invader . In the nor mal
hum an the skin is an effective
ba rri er aga ins t invas ive
strepto coc ci.
• The hos t pha go cyti c sys tem is a
second line of de fens e aga ins t
strepto coc cal invas io n. Org anis ms
can be opso nize d by ac tivatio n of
the cla ssic al or alt ernate
• IgG ant ibo dies r eactive wit h M
pr ot ein pr om ote pha goc yt os is which
res ult s in kill ing of the orga nis m
 Tre atmen t an d pre ven ti on
• Penic il li n is stil l unif orm ly effect ive in
treat ment of Group A strept oc occal
di seas e.
• No effec ti ve va ccine h as bee n
pr oduc ed, but spe cif ic M-pr otein
va ccine s are be ing tested.
•M pro tein types cro ss- re act
antige nic all y wit h the hear t and
the mselves ma y be respons ible for
rheuma tic carditis . This ris k of
autoim mun ity ha s preve nt ed the use of
Group A st rept oc occal va ccine s
 Pseu do mo nas
infe cti ons
• Gram -ne ga tive , Ro d-s hape d,

St ric tly aero bic ;

Mot il e by po la r fl agell a; som e stra ins
als o prod uce la tera l fla ge lla
Oxid at ive, che moor gano tr ophi c
metabol is m
Cat ala se-po sit ive
oxida se-po sit ive
No orga nic gr ow th fa ctor s are
required
Diff us ible and/o r insoluble pigm ent s
Ps eudom ona s Gr am-n ega tive
Rod-sh aped
Pse udom onas
Pse udom onas aer ugi nosa
on bl ood a gar
Pseu domo nas ae ru ginosa
col onies o n a gar
Pseu domo nas ae ru ginosa
col onies o n a gar
 Pseu domo nas ae ru ginosa

• P. a er ugi nosa is c apa bl e of

produc ing s eve ral pi gm ents,
of which th e mo st
cha ra cter istic i s pyo cy an in,
th is bl ue pig men t is an
abso lute diagnosti c ch arac ter ,
sinc e n o othe r s peci es h as
bee n foun d to produ ce it.
 Pseu domo nas ae ru ginosa

• P. aerugino sa ha s long be en
kno wn as an oppor tuni st ic
pa thoge n , es pe ciall y dreaded in
the ho spi tal enviro nm ent .
• Se vera l ext rac ell ula r pro duc ts
( pr ot eas es, ela stas e, etc .) he lp
the inva sio n and dis semina tio n of
P. aerugino sa.
 Pseu dom ona s a er ugi nosa
• Most of the species produce exotox in
A. The target of this toxin is one of the
elo ngati on fac to rs in translation
during protein synthesis. Strains
incapable of producing exoto xin A
have reduced virulence.