Microbiology bacteriology

DR HARITH ALAWADI LECTURES
G.S.M
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G.S.M MEDICAL EDUCATION

DR HARITH ALAWADI
LECTURES
G.S.M MEDICAL LECTURES /MICROBIOLOGY
G.S.M
MEDICAL EDUCATION
1G.S.M MEDICAL EDUCATION
Introduction tomicrobiology
Microbiology: isthesciencewhichstudies themicroorganisms.
And it is divided into:
1. bacteriology (bacteria),
2. virology (viruses),
3. mycology (fungi)
4. and parasitology.
*it studies the function, characteristics, virulence (the bacteria’s
weapons) andtreatment.

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1. Bacteriology:
1- General bacteriology
2- Clinical bacteriology
3- Antimicrobials (antibiotics)
Classification:
1. Morphology: the shape of the bacteria
2. Staining: special dies used to detect the bacteria
*stainingfirstdiscoveredbyHansChristiangram.
Gram+ (exotoxin) andgram- (endotoxin)
3. Bacterial composition
4. Toxins (virulencefactors)
5. Culturing
6. Environment (aerobic and anaerobic)

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Classification according to morphology:
A. Bacilli
• Clostridium
• Bacillus
• Salmonella
• Pseudomonas
• Yersinia
• Listeria
• Shigella
• Klebsiella
• E. coli
• Proteus
• Enterobacter

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B. Cocci
• Diplococci: Neisseria
• Streptococcus
• Staphylococcus
C.Coccobacilli
§ Haemophilus
§ Gardnerella
§ Coxiella
§ Bordetella
D.Spirilla:
• Borrelia
• Treponema
• Leptospira
• Spirillum

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E. Branching filaments:
• Nocardia
• Actinomyces
F. Additional (endospores)
• Bacillus antharcis
• Clostridium

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ThesimilaritiesanddifferencesbetweenGram+
and Gram – bacterial structures:

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Insidemostofthem,thereareplasmid (circularDNAwhich
contain informationaboutendoor(mostly)exotoxins)and
normalDNAwhichcontainsthewholeinformationofthecell.

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The structure:
1-cytoplasm inboth
2-cellular layer (cell membrane) (bilipid) in both.
3-peptidoglycans(cellwall):itisverybiginGram+andsmallin
Gram-,thislayerisveryimportant inGramstaining.
4-periplasm: it is a big space inGram – and very small in Gram
+, Beta-lactam antibiotics can attack the periplasm, but the
bacteria produce Beta-lactamase to attack the antibiotics.
5-lipidpolysaccharides (LPS): this is found in Gram – only.
6-capsule(inboth):protectionagainstphagocytosis,alsoitis
called(glycocalyx)--- thisislossynetworkofcapsulewhich
mediatesadherencetosurfaces,theencapsulatedbacteria
cannotberecognizedbythebody,buttheantibodiessurround

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it from all sides in a process called opsonization, so the
phagocyte can recognize it and kill it, then excrete it by spleen.
Patient with splenectomy cannot kill the encapsulated bacteria.
7-fembriae: cell to cell adhesion, found inboth.
8-pilus: conjunction for genetic material exchange by plasmid,
found inboth.
9-flagella: for movement, found in both.
- TheGram–:producesendotoxinsbytheLPSlayer:thelipid
partproducesTNF-alfa(mediatetosepticshockandalsosame
asIL-1)and thepolysaccharidepartproducesIL-1(enhances
endogenous pyrogens(fever), acute inflammation and
chemokines secretion for WBCs recruitments)

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-The Gram +: produces exotoxins by lipoteichoic acid (found
only inGram +) , the lipid part producesTNF-alfa and the
Teichoic acid part producesIL-190percent of the time.
Note: the capsule of the all bacteria contains polysaccharide
layer except the capsule of bacillus anthracis contains
(polydiglutamate).
Quelling reaction: is used to identify the bacteria is
encapsulatedornotbyaddinganticapsularserumtotheagar
which unknown contains the bacteria.

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ALAWADI LECTURES
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Encapsulated Bacteria:
Even Some Pretty Nasty Killers Have a Shiny Bodies
E. coli
Streptococcus pneumonia
Pseudomonasaeruginosa
Neisseria meningitis
Klebsella pneumonia
Hemophilus influenza
Salmonella typhi
B groupstreptococcus

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Classification according to staining
-thereareabout7stainingmethodsbutthemostused
one is Gram staining.
1_ Gramstaining:
*thepeptidoglycanlayerplaysanimportantrolein
gram staining.
Gram staining can be divided into three steps:
A_intheagarthatcontainthebacteriaweaddspecial
dyecalledcrystalviolet;whichcanenterthebacteria
cell and accumulate in them as crystal.

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B_in the second step we add tothe agar iodine which
bringsthecrystalsmoleculesinthecellstogetherto
form violetmass.
C_inthisstepweaddalcohol(acetone)totheagar,
whichmakesthecellstobedehydratedandshrink.
astheexotoxincells(gram+)havethickpeptidoglycan
layeritcanprotectthecellfromthealcoholeffectand
nottobeshrinksothosecellswellkeepthevioletor
purpledyeinsidethemandthosewellbegram+.
andtheendotoxin(gram-)havethinpeptidoglycan
layeritcan’tprotectthecellfromthealcoholeffectso
the cell well be dehydrated and dissolving of its
membraneandgiveusthepinkcolor,thosecellswellbe
gram (-).

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GRAM +
COCCI BRANCHING FILAMINTS
Aerobic
listeria
bacillus
Corynebacterium
Aerobic
Streptococcus Staphylococcus
Aerobic
nocardia
Anaerobic
actinomyces
Anaerobic
clostridium
BACILI

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*these microbes can’t be stained by gram staining.
These Microbes May Lack Real Color
Treponema,Leptospira too thin to visualized by microscope
Mycobacteria cell wall has high lipid membrane
Mycoplasma, ureaplasma no cellwall
Legionella
Reckttesia
Chlamydia , bartonella , ehrlichia ,anaplasma
Primary intracellular
microbes
+Chlamydia lack classic
peptidoglycan

STANINGS
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1
-thereareotherstains we mayuse to detectotherbacteria
As following:
1- GIEMSAstain
Certain Bugs Really Try my Patience
2- Periodic – acid – Schiff stain
Pass thesugar
• Itstainsthebacteria(trophermyawhipplei)whichcausewhipple
disease.
3- Ziehl – neelsen stain:
Chlamydia borellia Rikttesia trypanosoma plasmodium

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2
Carbol-fuchsinis the materialusedin this staininganditstains
the bacteria that have high acidin theirmembrane such as
*mycobacteria
*nocardia
*protozoa
• Anotherwayofstainingwemayuseinsteadofziehl–
neelsenstainisauramine- rhodaminestain.
It is inexpensive, more sensitive but less specific
4- INDIA INKstain
WeuseittostainCryptococcusneoformans(yeast),this
yeast in immune compromised patient grow in lung and
cause meningitis.
• Instead of it we may use mucicarmine stain.
5- SILVER stain
Fungi (pneumocystis jirovecii)
Legionella, h. pylori

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6- FLURSCENT ANTIBODYstain
Used for bacteria and viruses
*used for confirmation test like syphilis (FTA-Abs).

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Growth phases of bacteria during culturing:
1-Lag phase: the bacteria prepare itself for mitosis by
replicatingitsDNAandincreasing insize,andit’snotyetableto
divide, it needs from 0 to 5 hours.

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2-Logexponentialphase:(doublingperiod)mitosisoccurs,so
thebacteriaincreasesinnumber,itneeds5to10hours.
3-Stationaryphase,Depthpoint:thenumberoflivingand
death bacteria becomes equal at this point.
NOTE: THERE WAS SOME MISCONCEPTION IN THE VIDEO
REGARDING THIS PART DON’T WORRY JUST PUT IN MIND THAT
STATIONARY IS THE PHASE THAT COMES BEFORE DEATH PHASE
AND AFTER COMES DEATH PHASE.
4-deathphasedeclinephasewherebacteriastartdying
exponentially.
5-Viabecount:nolossofcellintegrity(maintainconstanttotal
count),thisistherealnumberofbacteriafordiagnosisand
treatment.

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Thestandardmedia:usedforalmostallbacteria
1-LB broth/Agar
2-Tryptic soybroth/Agar

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3-MH broth/Agar
-----------------------------------------------------
Media types:
1-Selective media:favorsthe growth of aparticularorganism
(we add to the media different materials like antibiotics and
otherstokilleverymicroorganisminthemedia,excepttheone
that we search about it.
2-Indicative(differential)media:inthismedia,thereisan
indicator, so whenwe add something suchaslactose, the color
changes,forexampleE.coli(itmakeslactosefermentation).
3-Indicative – selective media.

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Main 10agars
1-Chocolate agar: Factor V (NAD+) and X (hematin)
liquid mediacontainsblood of(horse orsheep) and chocolate
It is a selective media for Hemophilus influenza.
NAD+:(Nicotinamideadeninedinucleotide),coenzymefound
inalllivingcells,playsaroleinreductionandoxidationof
metabolism.
Hematin: blue to black particle taken from hemoglobin.
2-Thayer – Martin agar: contains blood and chocolate 5%, it is a
selective mediafor
Neisseria (gonorrhea and meningitis), (Gram-).
Becauseinthismedia cangrow gram (+,- and fungi), weuse:
1-Vancomycin to kill Gram +.

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2-TrimethoprimandcolistintokillGram–exceptNeisseria.
3-Nystatin to kill fungi.
(Very Typical Culture Neisseria)
Vancomycin
Trimethoprim
Colistin
Nystatin
3-Bodet– Gengouagar: (BodetforBordetella)
Contains potato
Regan-Lowemedium:contains(charcoal+blood+antibiotic)
or(potato+charcoal+blood+antibiotic),thisoneismore
specific and more useful.
They both are used for Bordetella Pertussis

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4-Telluriteagar:contains(mineral,beefexcrete+blood+
sodium …….), it is used as a first culture
Lofflermedium:contains(beefinfusion+hoursserum……),itis
used as a conformational culture for Corynebacterium
Diphtheria.
5-Lowenstein- Jensen agar: selective for M. Tuberculosis
6-Eaton agar: selective for M. pneumonia
7-MacConkeyagar:indicativeforEntericbacteriasuchas(E.
coli)
Theyaddlactose +bile acid inthisagar, the colorchangesfrom
green topink.
8-Eosin – methylene – blue (EMB) agar: selective for E. coli
9-CHarcolYeastextractagarbufferedwithcysteineandIron:
selective forLegionella.

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10- Sabouraund agar: for fungi

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G.S.M MEDICAL LECTURES /MICROBIOLOGY DR HARITH ALAWADI
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Further investigation
GRAM +
- +
Bacilli
Aerobic
listeria
bacillus
Corynebacterium
Anaerobic
clostridium
Branching
filaments
Anaerobic
actinomyces
not acid fast
Aerobic
nocardia
acid fast
Cocci
Aerobic
Catalase
Streptococcus staphylococcus
Hemolysis
α (partial) β (complete) γ (no hemolysis)
Optochin senst
&bile soluble
(-)
viridians st
s. mutans
s.mitis
pneumonia
encapsulated
Bacitracin senst
(-) GB
agalactiae
(+)GA
s.pyrogens
Coagulase
(+) s. aureus(-)
Novobiocin senst
(-) s. saprophyticus (+) s. epidermidis

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Acid fast bacteria: this bacterium contain mycolic acid (waxy material)
in their membrane, such bacteria not easy to discover it by gram
staining and called indeterminate bacteria and they need further
investigation.
• When we add to the agar that contain the branching filaments
carbofuchsin, the bacteria will react with it and it will increase the
acidity and the color of the agar will be red.
• Then we add alcohol to the agars, the not acid-fast bacteria will
loss its color and become colorless while the acid-fast bacteria
agar will keep its red color.
• Then we add methylene blue, the acid fast will keep its red color
and the not acid-fast bacteria will become blue.
6.5 % nacl
(-) non-
enterococcus
s. bovis
(+) enterococcus
e. faecium
e. faecalis

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• To distinguish between staphylococcus and streptococcus
we have to use catalase test
*catalase is an enzyme secreted by staphylococcus
bacteria.
We bring the agar that contain both staph. And sterp.
Bacteria and add to it H2O2, the bacteria which have the
ability to lyse it will be (+) and will appear gas bubbles and
the which can’t will be (-).
*to distinguish between staphylococcus bacteria types, we
use coagulase test
To the blood agar we add staph Bacteria, the bacteria
which have the ability to coagulase the blood will be (+) as
this bacterium makes the fibrinogen become fibrin around
this bacterium will see blood clot
If the agar stays without any coagulation this bacterium
will be staph. (-) . and for these bacteria we use antibiotic

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test (novobiocin sensitivity test), the bacteria which will be
killed by this antibiotic will be (+) and the other bacteria
nothing happen to it will be (-).
*catalase (-) streptococcus we use to distinguish its types
hemolysis test
α (partial) react only with the ferrus in the hemoglobin and
these bacteria will give black dots on the agar, so it
partially harm the blood cells.
β _complete hemolysis to the blood around the bacteria
γ_no hemolysis, we add to the agar that contain it 6.5 % of
nacl and that’s give us (+) enterococcus and (-) non-
enterococcus

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Gram (-)
Diplococcic
aerobic
Maltose
utilization
(+) Meningitides (-) gonorrhea
Comma shaped
rods
Oxidase (+)
Coccobacilli
H. influenza (requires
factors v and x)
Pasteurella
Brucella
Bordetella pertussis
francisella tularensis
Produce
urease
H. pylori
Grows in
alkaline media
vibrio cholerae
Grows in 42c
campylobacter
jejuni
Bacilli
Lactose fermentation
+
Fast
klebsiella
E.coli
Enterobacter
Slow
Citrobacter
Serratia
-
Oxidase

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We use maltose utilization to distinguish between N. meningitides which utilize
maltose (+) and N. gonorrhoeae which is not (-).
For comma shaped rods we use oxidase (+) test
*in the agar we have the rods we add to it phenylene diamine which have the
ability to accept an (e) and produce dark substance.
Then we start to change the circumstances of the agar:
1- We heat the agar till 42c all rods will die except campylobacter jejuni.
2- Change the media to alkaline media also all rods will die except vibrio
cholera
(+) pseudomonas(-) H2S production on TSI
agar
(-) shigella, Yersinia(+) salmonella, porteus

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3- We add urea to the agar and water this will produce ammonia and carbon
dioxide this bacterium is H. pylori.
For the bacilli in the lactose fermentation test will give us (+) and (-),
For the (-) one we use oxidase test if it is (+) this pseudomonas and if it is (-) we
use another agar called (TSI) agar and f the bacteria release h2s this will be (+)
and if not, this will be (-).

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AEROBIC AND NON-AEROBIC

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AEROBIC vs ANAEROBIC
Aerobic
Requires o2 for living Doesn’t requires o2 for living
Capnophilic aerobic bacteria requires very high amount of
o2 for living such as Neisseria
Microaerophile requires low amount of o2 to survive
such as:
Strept. Pyogen, H. pylori, campylobacter, borrelia
Obligates this bacteria survive in any level of o2 :
Nocardia , pseudomonas , M.tuberculosis , bacillus
Moody
bacteria

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Anaerobic
Obligates: these bacteria survive only when o2 is absent 100% such as
Clostridium, Bacteroides, actinomyces, treponema.
*in the presence of o2 it will die
Aerotolerant : this bacteria can live if there is o2 but it
doesn’t use it
Facultative (smart)
bacteria
Utilize o2
staphylococcus
E-coli
listeria
vibrio cholera
salmonella
shigella
Fermentation
(can’t use o2)
Lack catalase
enzyme

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Aerobic bacteria are the bacteria that requires O2 for living.
*aerobic bacteria may cause respiratory infections, infection
due trauma and infection during burns.
Anaerobic bacteria may die in the presence of the O2.
Aerobic bacteria divided into three types, those are:
1-capnophilic bacteria: these bacteria require high level of
oxygen to live like Neisseria.
2- microaerophile: this requires low concentration like
streptococcus pyogenes, H. pylori, campylobacter and borrelia
(cause Lyme disease).
Those two types are moody bacteria which requires
special environments to survive.

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3-obligate bacteria: survive in any concentration of O2 like:
nocardia (cause ncardiosis systemic infection), pseudomonas
(burns, trauma, intubation and CF), M. tuberculosis and bacillus
(anthrax ).
Anaerobic bacteria (lack catalase enzyme): doesn’t require O2
to survive and it also has three types:
1- Obligate bacteria: it lives only in the absence of O2 100%
like clostridium, Bacteroides , actinomyces (endocarditis) ,
and treponema (syphilis ) .
2- Aerotolerant: can live the presence of O2 but it not utilizes
it.
3- Facultative (smart): these bacteria can use O2 (utilization)
and can use fermentation. like staphylococcus, E-coli,
listeria, vibrio cholera, salmonella and shigella.

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ENDOTOXINS AND EXOTOXINS

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Endotoxins
Endotoxins: are produced by Gram – bacteria from the outer
membrane (LPS), (found only in Gram –).
The LSP: produces a lipid particle called Lipid A.
The body recognizes the lipid A and activate the following
mechanisms:
1- Macrophage: it activates IL-1, IL- 6 (cause fever)
TNF alfa (causes fever and hypotension, because it causes
dilation in the blood vessels).
NO {also causes dilation of the vessels, which lead to
hypotension and Tachycardia (increasing heart rate) occurs as a
compensatory mechanism}.

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2- complement system:
- C3A: produces Histamine (causes very big dilation, then leads
to stretching of the vessels, then it makes pores in the walls, so
the liquid goes from intra to extra vascular.
histamine causes hypotension and edema
-C5A: produces neutrophil chemotaxis, which leads to migration
of WBCs to the inflamed area.
3- Tissue factor: the endothelial cells of blood vessels become very weak
and damaged easily, and bleeding occurs which lead to the formation of
multiple thrombi and causes DCI (palpable purpura).

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E N D O T O X I N S (summary according to each later)
E= Edema
N=NO
D=DIC or death
O=Outer membrane (LPS)
T=TNF alfa
O=O antigen (on the capsule of the bacteria)
E=extremely heat staple
I=IL – 1 and IL – 6
N=Neutrophils chemotaxis
S=Shock

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Exotoxins Endotoxins
1- Gram + and some of
gram –
Only gram -
2- Secreted from cell Not
3- Poly peptides LPS (lipid A)
4- Location of gene on
plasmid or bacteriophage
On chromosome
5- Adverse effect high low
6- Low heat stable 60 c High heat stable 100 c
7- Clinical effect,
mechanism
Fever, shock (hypotension),
DIC
8- Induce high titer
antibodies called
antitoxin
Poorly antigenic
9- Toxoid used as vaccine no
10- Tetanus, diphtheria Meningococcemia, sepsis by (-
)

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• Endotoxins secreted only from gram (-) bacteria
• Exotoxins secreted from gram (+) and some of gram (-)
*gram (-) bacteria should be lysed and the membrane
destroyed to release the endotoxin because it is part of the
LPS (lipid A).
*gram (+) bacteria secrete the exotoxins through the LTA
directly.
• The exotoxin is a poly peptide or it is amino acid chain,
have high effect on the body and it has direct effect on the
cells.
• The endotoxin is a lipid poly saccharide and its effect are
not direct but by induction of the immune system.

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*the endotoxin is poorly antigenic not like the exotoxin
which induce high titer antibodies called antitoxins.
• The body can produce antibody against the antigens of the
exotoxin those are toxoids which use in production of
vaccine.
EXOTOXINS:
1- Inhibit protein synthesis
2- Increased fluid secretion
3- Inhibit phagocytic ability
4- Inhibit release of neurotransmitters
5- Lyse cell membrane
6- Super antigen causing shock

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Super antigens causing shock toxin:
Antigen: is the information that transmit from antigen
presenting cell (APC) to T cell which by its effect induce
immune reaction.
*the information that is transmit from APC through the
MHC II to naive T cell through the T cell receptor.
Naive cell: is the pure cell which haven’t been identified
any antigen and those cells start to secrete: IL1, IL2, TNF α,
INF gamma.
IL1, IL6 cause fever. IL2, invoice for other T cells.
*the exotoxin is like a “clip” when it attaches to the MHCII
and TCR it makes them connect for long time and that’s

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cause the T cell to secrete high amount of IL1, IL2, TNF α,
INF gamma eventually this lead to shock.
Shock: low perfusion to one specific organ.
TNF α, INF gamma they cause vasodilation and cause
systemic shock or fast shock for one organ.
*there are two types of super antigen shock bacteria those
are: staphylococcus aureus and streptococcus pyogenes.
Staphylococcus aureus toxins:
1- α-toxin
2- β-toxin
3- γ-toxin
4- Panton- valentine leukocidin toxin
5- enterotoxin
6- TSST-1
7- Exfoliative toxin

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α-toxin: damage the endothelium, epithelium and
erythrocyte.
Epithelium: attack the cell and damage it.
Endothelium: attack the blood vessels and make gaps
between the cells
Erythrocyte: damage it and deform its structure.
Β-toxin: the role in human body is not known.
γ-toxin: it attacks all the leukocyte and weaken the
immunity.
Panton- valentine leukocidin toxin: is the toxin of MRSA bacteria
which is resistant to beta lactam antibiotics.

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*pneumonia due to MRSA cause necrotizing syndrome (necrosis
inside the lung) this leads to decrease the function of the lung.
*the antibiotic which works on these bacteria: linezolid,
Bactrim and clindamycin.
*methicillin used only in labs.
Enterotoxin: cause gastroenteritis by food poisoning, but the
symptoms in this toxin appear fast (4-6 hours).
Exfoliative toxin: this toxin attaches the dismoglein between the
dermatocytes which give the skin its integrity, so when this
dismoglein is damaged the skin become scaly and leads to
scalded skin syndrome.
TSST-1: toxic shock syndrome toxin-1

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This toxin has same effect as super antigen toxin and cause
(fever, rash, hypotension, skin damage, mucosal damage and
shock).
Streptococcus pyogenes toxins
It has three toxin those are:
1- Streptolysin O: it lyses the RBC. This toxin cause
pharyngitis and on clinical examination we may find
hemorrhagic spots on the posterior wall of the throat
they are called(petechiae). This toxin has antibody titer
ASO titer we can detect through blood test.
2- Streptolysin S: this toxin like streptolysin O but this
doesn’t have antibody titer.
3- Pyogenic endotoxin A: this toxin has two results, the
first one is like the TSST-1 toxin effect, and the second

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one is scarlet fever which can be manifested by: fever,
rash (sand paper rash), and strawberry tongue.

MUTHANNA
ALLAMI
G.S.M
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BILAL
HUSSEIN

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Exotoxins: increase fluid secretion
This toxin forces the cells to lose fluids
Such bacteria cause diarrhea, they are (E. coli, Bacillus anthracis
and vibrio cholera)
They produce sugar toxin (ST) or sugar like toxin (SLT)
E. coli (Gram -): produces 2 types of exotoxins
1- Heat labile (SLT): activation of CAMP
The toxin contains A and B parts , they come together to the
receptor on the cell , B part opens the receptor and allows A
part to enter inside the cell , where it joins the ADP ( Adenosine
Diphosphate) , and makes ribosylation to activate GS receptor (
it affects a molecule contains alfa , beta and gamma) that make
activation and leading to increase Adenylate cyclase ( converts
ATB into CAMP + ppi) , the CAMB goes to the intestines and
causes secretion of iron and forces the cell to produce chloride {

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(where chloride goes , sodium goes), (where sodium goes ,
water goes) } so diarrhea occurs , then dehydration , then
hypovolemia ( decrease in the total volume of blood) , the
decrease blood perfusion to 1 or more organs and this is shock.
This is the mechanism of (Travelling diarrhea)
This E. coli is called (Enterotoxigenic)
2- Heat stable (ST): activation of CGMP
The same mechanism occurs here, except the following
differences:
- A part activates Guanylate Cyclase (converts GTP to CGMP +
ppi).
- this causes inhibition of reabsorption of sodium chloride
(NaCl), so the cells do not reabsorb H2O and diarrhea will occur.

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2- Bacillus Anthracis: activates CAMP and the toxin is called
(edema toxin), because the fluids accumulate between the
cellular tissues and causes bleeding called (Eschar).
3- Vibrio Cholera: activates CGMP and the toxin is called cholera
toxin
It causes (Rice watery diarrhea).

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Note: some sources are talking about Yersinia Entrocolitica
with exotoxin bacteria that increase fluid secretion, so we will
mention it here
Yersinia Entrocolitica: causes enterocolitis, the toxin is called
Yersinia stable toxin (causes the same mechanism of Guanylate
cyclase).
This toxin attacks the internal layers of the colon, so it causes a
bloody diarrhea.
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Exotoxins: inhibit protein synthesis
Protein synthesis is done by rRNA or mRNA, if any of these 2
processes, stops the protein synthesis will stop
In the process of rRNA, the protein synthesis depends on 60s
ribosome, which depends on (Adenine), but the toxin causes

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inhibition of adenine particle or prevent the connection of
adenine to 60s ribosome, so rRNA becomes inactive.
2 types of bacteria have such toxin:
1- shigella: shiga toxin
-It causes damage in the GI mucosa; high production of
cytokines and the disease is called(shigellosis)
-dysentery: due to mucosal damage, diarrhea with blood
And the cytokines attack RBCs and cause (hemolytic uremic
syndrome), then it causes systemic shock.
2- E. coli: shiga like toxin
-unlike shiga toxin, it does not invade the mucosa layer of the
intestines.
---------------------------------

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During mRNA in the protein synthesis, the elongation process
occurs by EF-2 (Elongation factor), this process stops if, 1- the
(NAD+): is prevented by diphtheria toxin.
2-ADP: is prevented by pseudomonas toxin (pseudomonas A(a)),
so they cause inhibition of mRNA, so they cause inhibition of
mRNA, so the protein synthesis stops.
Diphtheria causes: pseudomembranous pharyngitis and
lymphadenopathy.
Exotoxins that inhibit release of neurotransmitters:
-there are two types of neurotransmitters: excitatory(acetylcholine)
which is responsible for muscle contraction and inhibitory (GABA,
GLYCINE) which is responsible for muscle relaxation.
The neurotransmitters are kept in vesicles which attach with fusion
section molecule to help them to be released in the synaptic cleft.

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*the toxin which effect the inhibitory neurotransmitters called tetanus
spasm in which secreted by the bacteria clostridium tetani. This toxin by
its effect prevent the vesicle from the attaching to the presynaptic
neurons and this leads to lack of GABA transmitters and the effect of
acetylcholine will stay dominant and cause spastic paralysis.
The bacteria found in soil and patient may catch the disease through
the wound by rusted nail for an example.
Symptoms: spastic paralysis, locked jaw and risus sardonicus (sad face).
*the toxin which effect the vesicles that contain the excitatory
(acetylcholine) split the fusion section from the vesicle and it will not be
able to attach to presynaptic membrane and that’s why there will be
only the effect of the inhibitory neurotransmitters and patient will
develop flaccid paralysis.
This toxin is called botulinum toxin and secreted be the bacteria
clostridium botulinum.

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Exotoxins that lyse cell membrane:
There are two bacteria in this part:
Clostridium perfingens(αtoxin), this bacterium secrete enzyme called
phospholipase or lecithinase. This enzyme attacks the cell membrane
phospholipids and destroy it especially phosphate C. this led to
destruction of the cell membrane and lyse of the cell.
*it causes myonecrosis (gas gangrene) as the gas accumulate under the
skin and can be felt in examination.
In the blood agar this toxin has special appearance called double zone
hemolysis agar.
Streptococcus pyogenes (streptolysin O) this bacteria cause destruction
to the membrane of the RBC.
This toxin causes rheumatic fever and can be detected by the ASO test.

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Exotoxins that inhibit phagocytic ability
Bordetella pertussis this bacterium has the pertussis toxin which have
two ways to affect the cells:
First one by damaging the Gi protein which responsible for the inhibition
of adynlate cyclase effect this led to high production of CAMP and the
high level of CAMP increase the production of the insulin and eventually
cause hypoglycemia.
The second way that the pertussis toxin attacks the phagocyte and
impairing phagocytosis to permit the surviving of the bacteria.
The symptoms are like, child having during inspiration whooping and
during expiration cough this leads to whooping cough.
In adults called 100-day cough.

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Nocardia and Actinomyces
Nocardia Actinomyces
Aerobic Anaerobic / facultative
Acid fast Not acid fast
Found in the soil Normal (oral, reproductive and GI)
flora
Causes pulmonary infection in
immunocompromised (can mimic TB
but with – PPD) , cutaneous infection
after trauma in immunocompetent
Causes oral / facial abscess that drain
through sinus tract, forms yellow
“sulfur granules” , can also cause PID
with IUDs
Treat with sulfonamides ( TMP – SMX)
or the combination ( ceftriaxone +
Amikacin)
Treat with pencillin , if allergy
(doxycycline)
Alternatively (sulfonamides)
Nocardia: causes systemic disease called nocardiotic, it causes pulmonary
infection ( mostly in the alveoli ) with abscess formation , so it may case
pneumonia .
The abscess should be drained by thoracentesis.
PPD: cutaneous test for TB
It can be stained by ziehl – neelsen stain.

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--------------------------------------------------
Actinomyces: causes actinomycosis, mostly in post-operative patients or during
dental procedures.
It causes abscess between the layers of facial muscles, so it causes lock jaw as a
sign, also leukocytosis, high CRP and high ESR.
The abscess should be drained.
Bacillus Cereus
1-cause food poisoning
2-spor- former/entrotoxic(cerealid)
3- reheated rice syndrome (in the first heating , the bacteria stay inside the spor
but after reheating , the bacteria get germination and go out of the spor, os they
cause infections.
B. cereus can be different types according what they cause:
1-nausea and vomiting type
-cerealid a performed toxin
-(1-5 h) after eating

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- mostly after reheated rice and pasta.
2-diarrhea type
- watery non-bloody diarrhea
-(8 – 18 h) after eating
-mostly after unheated rice.
Bacillus anthracis
- Gram +, spore forming, aerobic
- Produce anthrax toxin(edema toxin and lethal toxin)
- It is the only bacterium with a polypeptide capsule (contains
D_Glutamate)
- It causes two type of infections:
- Cutaneous anthrax: increase the CAMP and cause neutrophils
dysfunction.

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*in the cutaneous type it transmits from the goats to the shepherd
through the direct contact with the skin. The symptoms start with
painless papules sounded by vesicles then it develops to painless
ulcers, these ulcers develop necrotic ulcers(eschars). As the disease
is progressive the ulcers go deeper and reach blood vessels
causing bacteremia eventually cause septic shock.
*the pulmonary type (lethal toxin), way of transmission is when
the patient inhales the bacteria spores.
The most related symptoms:
As it effects the mediastinum it causes mediastinitis and infection
of the other organs of the mediastinum.
If It effects the lung it effects the alveoli and can spread up to the
other structures.
Signs and symptoms: flue like symptoms
Fever after hemorrhage and then mediastinitis.

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*as the bacteria cause necrosis and hemorrhage lead to effusion
and exudates eventually mediastinitis.
*all symptoms can be gathered in wool sorter’s disease.
- Infection may start with mediastinum and not causing
hemorrhage.
- Anthrax may develop in GI (not common).
- During physical examination we may find crackles in auscultation,
dull sound during percussion, chest pain and leukocytosis.
Treatment can be single or doubled:
Ciprofloxacin or doxycycline.
*biological treatment with raxibacumab.
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Corynebacterium diphtheria
1- Gram + bacilli grows on tellurite agar (black colonies).
2- Exotoxin encoded by β-phages(bacteriophages).
*a virus which parasitizes a bacterium by infecting it
and reproducing inside it, THEN a new genetic
material will be produced.
the toxin is toxgene. Exotoxin that inhibit protein synthesis.
As the exotoxin composed of A and B portions they have two
effects.
- Toxin part A cause ADP ribosylation to the EF2.
- Toxin part B effects heparin-binding epidermal growth
factor which found in heart(myocarditis) and in nerves
(cranial nerve deficit).

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- it effects children less than 12 years.
- Vaccine DPT (as the toxin in bacteriophage)
*DPT for diphtheria, pertussis and tetanus.
- Symptoms: fever, sore throat, pseudomembranous
pharyngitis (white grayish or yellowish plaques) at the end of
the mouth spots composed of leukocytes and necrotized
membrane.
- Cervical lymphadenopathy (bulk neck).
- Dysphagia (due to inflammation), cough (as at the end of the
mouth there is the point of gag reflex).
- DX: fever, history and age of the patient.
*+ positive throat sinus culture.
*metachromatic(blue-red) granules in the culture.
*alanine is the pigment that added to the culture.
*ELEK test for diphtheria toxin.
*leukocytosis and proteinuria.
TX: erythromycin, penicillin and DPT.

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Listeria monocytogenes
- Gram (+), Aerobic and bacilli
- (The only Gram(+) bacterium that produces endotoxin).
- The infection can be got by consuming of dairy (milk and
cheese) and from deli meat.
- It affects the immunocompromised patients (cancer and
chemotherapy and chronic diseases that are treated with
corticosteroids), such as children and elderly.
- vaginal and transplacental transmission for children, (it may
cause spontaneous abortion, due to amnionitis or
chorioamnionitis)
- it also causes (granulomatosis infantiseptica) and meningitis
due to septicemia.

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-the general disease, which is caused by the bacterium is
called(listeriosis).
-this bacterium is dangerous in immunocompromised patients
because it makes rockt-tail (makes it able to move from cell to
cell to protect itself from the immunoglobulins), but it is self-
limited in immunocompetent people because it is targeted by
CD4 (T-killers).
Treatment: Ampicillin
And in elderly, the empiric treatment of meningitis can be used.

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Clostridium
- Gram (+), anaerobic, bacilli
1- Clostridium Tetani: tetani toxin
- Inhibit the release of neurotransmitters
- Causes spastic paralysis (lock jaw, risus sardonicus,
opisthontonus)
- Inhibit the inhibitory neurotransmitters (GABA and glycin)
Treatment:
1-debridement of the necrotic cell with antiseptic
2-vaccine DPT
3-antitoxin + diazepam.
2-clostridium botulinum: botulinum toxin

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- Inhibit the release of neurotransmitters (inhibit the excitatory
neurotransmitters, Acetylcholine)
- It occurs in infants after eating honey
- It causes floppy baby syndrome (flaccid paralysis)
Treatment: Antitoxin
3-clostridium perferinges(perforation): alfa toxin
- Lysis the cell membrane
- Causes myonecrosis (gas gangrene), foul smell and hemolysis, also it causes food
poisoning and gangrenous leg
- It can be got by eating not properly cooked meat.

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4-clostridium difficile:(clostridium diarrhea)
- Produces 2 toxins (A and B)
- Toxin A: binds the brush border of the gut(enterotoxin)
- Toxin B:it is a cytotoxin and causes cytoskeletal disruption of
the cells, so it causes diarrhea and pseudomembranous colitis
- One of the main reasons to get such infection is abnormal use
of antibiotics (Ampicillin and clindamycin) and PPI (omeprazole)
Diagnosis: PCR from the stool
Treatment: Vancomycin(oral)
Metronidazole (IV)
- In recurrent cases, (Fidaxomicin)can be used
- if antibiotics don’t help the patient, microbiota transplant can
be used.

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Staphylococcus epidermidis
- Gram +, cocci, aerobic, catalase+, coagulase+, and Novobiocin
sensitivity test positive +.
- Part of normal flora of the skin.
- Cause inflammation to the heart valves (by biofilm bacterium
through pacemaker device, IV catheterization).
- It can cause prosthetic device infection.
- If it enters the blood stream may cause septicemia.
staphylococcus saprophyticus
- Gram +, cocci, aerobic, catalase+, coagulase+, and Novobiocin
sensitivity test negative –
- normal flora of the female genital and perineum (area
between anus and scrotum).
- 10 to 20 % of female infections after E. coli and it cause UTI.
Staphylococcus aureus
- Gram+, cocci, aerobic, catalase+, coagulase+ and β hemolytic.

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- Super antigen shock causing exotoxin.
- It produces the following toxins:
1- α toxin: which affects the erythrocytes.
2- β toxin unknown role in human.
3- γ toxin affects leukocytes.
4- Panton-valentaine leukocidin: cause MARSA(nosocomial
infection) hospital acquired pneumonia.
5- Exfoliative toxin
6- TSST-1: polyclonal naive t cell activation and cause sever
inflammation.
7- Enterotoxin: 2-6 or 4-6 hours after eating
8- TSS: toxic shock like syndrome it causes elevation in ALT,
AST and bilirubin.

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*these microbes make colonization in nares. So, anything
the patient might do in the nares may lead to the infection
by this bacterium.
*it has protein virulence (materials that are produced by the
microorganism to help them to infect the body), prevents
the opsonization of the bacteria, so it is dangerous in
*patient who lost their spleen because they can’t excrete it
out of the body.
*It preens the antibody from recognizing the bacteria and
inhibits the complement activation and phagocyte.
• Infection with this bacterium most common in case of
Nasal tampons (in case of bleeding) and vaginal tampons
(during menstruation) can cause the infection.

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• Summary:
1- Lung(pneumonia)
2- Eyes (blepharitis): the inflammation in the eye lid.
3- Skin: wound infection, furuncles, carbuncle and
impetigo (honey eating children).
4- Heart: endocarditis.
5- Brain: meningitis.
6- Bone: osteomyelitis
7- GI: food poisoning.

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The Gram (+) cocci and alfa-hemolytic streptococcus
Aerobic bacteria, can be differentiated as staphylococcus or
streptococcus by catalase test.
Catalase + are staphylococcus and – are streptococcus (we
differentiate between them by the hemolysis test.
- by hemolysis, the streptococcus bacteria can be:
1- alfa – partial hemolysis: in the blood agar, a green structure
is seen around the bacteria, due to the lysis of RBCs, the
hemoglobin is divided into globin (goes back to the blood) and
heme{ which is transferred into biliverdin( the green structure is
formed by it) by heme oxygenase}, then by biliverdin reductase,
the biliverdin is transferred into bilirubin.
- here the process of hemolysis is incomplete, that is why the
green structure is formed.

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2- beta – complete hemolysis: in the blood agar, the blood
around the bacteria disappear.
3- gamma – hemolysis: no hemolysis
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Alfa – hemolysis: we can differentiate between them by
optochin sensitivity + bile acid
(+) is S. pneumonia and (-) are the viridans
Streptococcus pneumonia
- Encapsulated bacteria: the body can’t recognize it and it is
dangerous in aspleenic patients, because they can’t excrete
them out of the body after the opsonization.
- It is optochin sensitive bacteria (+)
- Lancet shape diplococcus and has a pneumolysin toxin.
- It causes:

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1- pneumonia: cough (rusty sputum), fever, chest pain
2- meningitis: neck stiffness, high grad fever, headache
3- sinusitis: fever, tenderness (like pain)
4- otitis media: fever, pain, tinnitus
The viridans
- They include: S.mutant, S.mitis and S.sanguinis
- Resistant to optochin(-)
- They are part of normal of the oropharynx.
- the infection occurs when there is dental caries and it causes
(subacute endocarditis), and damage of heart valves by(S .
sanguinis)

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- S .sanguinis: produces dextrans(polysaccharides), which join
the fibrins and platelets and accumulate in the heart valves,
that is how this bacterium causes damage of the valves.
Beta–hemolysis streptococcus
We can differentiate between them by bacitracin sensitivity:
The (+) is GA and it is S. pyogenes
The (-) is GB and it is S. agalactia
Streptococcus pyogenes (pus formation)
- Gram (+), Aerobic, cocci, catalase (-), beta – hemolysis,
bacitracin sensitive (+) and GA
- It produces 4 toxins:
1- Streptolysin O, 2-Streptolysin S, 3- Exotoxin A

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4- Erythrogenic toxin: causes erythema on the skin.
- It causes super antigen shock exotoxins
- It causes the following:
1-Toxogenic: TSST, TSS, necrotizing fasciitis can be internal (in
the mouth) or external on the skin
2- Pyogenic: us formation, Impetigo, pharyngitis, erysipelas,
cellulitis
3- Immunogenic: Rheumatic fever and Glomerulonephritis.

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The immunogenic affect during Rheumatic fever (R.H.D):
-The bacterium contains antigen presenting cells, which after
lysis are joined by macrophages and call all other cytokines, in
the heart the normal tissues mimic the bacterial antigens, so
the antibodies recognize them us abnormal antigens, this is
called (Biological Mimicry ) and the process of the attack is
called(Cross Reactivity).
The immunogenic affect during Glomerulonephritis:
-The bacterium is surrounded by antibodies, when it comes in
bowmen capsule between the endothelium and the basement
membrane, it causes damage in the basement membrane, so
the RBCs go out with the urine and resulting in hematuria (Tea
or Cola colored urine),
It usually occurs 1 – 2 weeks post streptococcal pharyngitis, and
usually Impetigo before the glomerulonephritis.

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Diagnosis:
1- ASO titer
2- Major J NES criteria
J –joints(polyarthritis), - (carditis), N – (nodules), E –
(erythema marginatum),
S – (Sydenham chorea)
3- minor criteria: high CRP, high ESR, fever, arthralgia,
sometimes leukocytosis,
peaked P – R interval in the ECG.

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Streptococcus agalactiae
Gram+, aerobic, cocci, catalase-, bacitracin- resistant, β-
hemolytic.
- Colonization in vagina: it’s found in the vagina, so the
infant may get the infection during the pregnancy and may
lead to congenital infection.
- Screening to the pregnant woman (35-37) weeks.
It causes:
1- Pneumonia in the infant due to aspiration of infected
amniotic fluid. (easily immunocompromised)
2- Meningitis in the infant, if the fluid goes to the NS
3- Sepsis.

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DX:
1- CAMP factor (mainly in babies): causes enlargement in the
area of the hemolysis in the agar.
2- PYR (pyrrolidonyl arylamidase): it’s – in this bacterium.
3- Hippurate test: it’s +, causes hydrolysis to the Hippurate and
can be used for:
- Campylobacter jejuni.
- Gardnerella vaginalis.
- Listeria manocytogenes.
- G B streptococcus.
TX: intrapartum penicillin prophylaxis to the mother or the fetus or
both.
*intrapartum: period from the onset of labor to the expulsion of
the placenta.

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G.S.M
MEDICAL EDUCATION
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LECTURES
1
G.S.M
MEDICAL EDUCATION
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LECTURES
2
G.S.M
MEDICAL EDUCATION
γ hemolytic streptococcus
- No hemolysis, also called group D streptococcus.
- They grow in the bile and NACL 6.5 %.
- They are divided into: - or non enterococcus and + or
enterococcus.
Non-enterococcus: bovis (s. gallolyticus).
- Colonies in the gut
- It’s called streptococcus bovis serotype I
- It causes:1-bacteremia, 2-sub acute endocarditis
*they are associated with colon cancer
(bovis in blood= cancer in colon).

LECTURES
3
G.S.M
MEDICAL EDUCATION
Enterococcus: they are E.faecium and E.faecalis
*both cases the same infection but with different severity.
- part of normal flora of colon
- penicillin G resistant
-it causes:
1-sub acute endocarditis (following GI and GU procedures
for diagnosis or treatment)
2-biliary tract infection
*they are harder than non-enterococcal bacteria
*enterococcal bacteria are VRE (vancomycin resistant
enterococcus) in case of nosocomial infection.

LECTURES
4
G.S.M
MEDICAL EDUCATION
Helicobacter pylori
Gram (-), rod shaped, urease(+), catalase(+)
-Causes: gastritis and peptic ulcer (90 % duodenal and 10 %
gastric)
-It is a risk factor for: gastric adenocarcinoma and lymphoma
(MALT)
-Symptoms: depend on the location of the ulcer
-Diagnosis: urea breath test (C 14 urea)
The patient should not take any PPI or antibiotics in the day
before the test and he is given (C 14 urea) also 1 day before the
test, so the Pylori can be diagnosed
-Virulence factors: {flagellum, mucinase (causes lysis of the
mucosal membrane), catalase, urease, and oxidase (+)}

LECTURES
5
G.S.M
MEDICAL EDUCATION
-Treatment: PPI (omeprazole)+ (clarithromycin, amoxicillin,
metronidazole)+Bismuth salisylate
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LECTURES
6
G.S.M
MEDICAL EDUCATION
Vibrio
1-Cholera:
*Halophilic (salt lover), Gram (-) {but exotoxin}, comma shaped
rod, oxidase (+)
*Causes: cholera epidemic (in poor sanitation in developing
countries)
-It requires high accumulation of the bacteria to cause the
infection, unless the level of gastric acid is very low.
*Symptoms: rice water stool, very perfuse watery diarrhea.
Diarrhea – dehydration – oliguriacollapse.
Vomiting.
*Properties: mobileoxidase (+),non – lactose fermenting O1
serotype

LECTURES
7
G.S.M
MEDICAL EDUCATION
*Virulence factors:
1-pilus, 2- mucinase, 3- cholera AB toxin(exotoxin)
*Treatment:1- rehydration, 2- DX5(dextrans), 3-IV fluid
---------------------------------------
2- Parahaemolyticus
-Associated with shellfish
-Causes:1- self-limited diarrhea+GI symptoms for 3 days
2-wound infection while fishing
-Culture: 3% of NaCl
-Virulence: hemolysine
-Treatment: Rehydration if needed.

LECTURES
8
G.S.M
MEDICAL EDUCATION
Campylobacter jejuni
- Gram -, comma-shaped(s), oxidase +, micro aerophilic.
- Sources: fecal oral route of transmission via foods(poultry,
meat, unpasteurized milk, from animals pigs, dogs, cats).
- Causes: invasive gastroenteritis, ulcers, crypt abscess,
hemorrhagic necrosis, bloody diarrhea(children).
- Culture: campy agar (42c) heat label.
- Virulence:
1- Antigenic diversity (H and O antigens)
2- Flagellum
3- Entrotoxin –increase CAMP
4- Cytotoxin injuries for enterocytes

LECTURES
9
G.S.M
MEDICAL EDUCATION
*associated with: reactive arthritis and GUILLIAN BARRE
syndrome
*before these diseases always there is an infection, but if there
is an infection those diseases not develop always.
- GUILLIAN BARRE SYNDROME: autoimmune degenerative
disease of the nerves with unknown etiology, it affects the
peripheral nerves and cause(numbness, tangling and
paralysis of the limb).
- REACTIVE ARTHRITIS:HLA_B27(human leukocyte antigen
b27) binds to the leukocytes so it makes confusion to them,
so the leukocytes don’t recognize between the normal and
effected cells and cause autoimmune reaction, known as
post infectious arthritis.

LECTURES
10
G.S.M
MEDICAL EDUCATION
*can be detected by HLA_B27 test.
Treatment:the treatment is controversial, but most patients
how have been treated with erythromycin shows good results.
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LECTURES
11
G.S.M
MEDICAL EDUCATION
yersinia enterocolitica
- Gram -, rod
- sources:pet feces, milk and pork.
- Causes:acute diarrhea in less than 5 years children, acute
mesenteric adenitis(5-15 years), acute terminal ileitis and
adult diarrhea.
*acute mesenteric adenitis and acute terminal ileitis cause
pseudo appendicitis.
*associated with:HLA_B27 gene
- Identifying:pet feces, joint fluid(HLA-B27)
- Culturing:28c enrichment broth
- Virulence:
1- YAD-A
2- Arthritogenic factor:HLA-B27
3- Enterotoxin:increase CGMP and eventually diarrhea

LECTURES
12
G.S.M
MEDICAL EDUCATION
Treatment:aminoglycosides + doxycycline
Or trimethoprime, ceftriaxone,
sulfomethoxasole.
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LECTURES
13
G.S.M
MEDICAL EDUCATION
Salmonella
-Gram(-), Bacilli, lactose fermenting(-), oxidase(-), H2S(+)
-Common cause of:bloody diarrhea
-Sources:beef, poultry, eggs, fruits, vegetables, shellfish, dairy
products
-Types:self limited in USA, high morbidity in other countries,
because it causes bacteremia, so it can be fatal, it can be 1-
Typhoidal(S.Typhi, S.Paratyphi), they cause infection in humans
only.{S. Typhi : incubation period (8-14 days), S.Paratyphi:
incubation period (1-10 days)
2-Non-typhoidal:S.newport, it causes infection in humans and
animals, incubation period(6-72h)and symptoms(2-7 days)

LECTURES
14
G.S.M
MEDICAL EDUCATION
-Symptoms:fever, abdominal pain, vomiting, headache, large
volume watery diarrhea, dehydration, mylgia, rose spots on
chestabdomen(Typhoid fever only)
-Labs:bone marrow aspiration culture, urine culture,
pancytopenia, stool culture
*It needs large inculum of bacteria to cause the infection
-Treatment:supportive treatment(rehydration fluids + proteins)
Life attenuated vaccine for S.Typhi
Antibiotics:ciftriaxon, fluroquinolone.
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LECTURES
15
G.S.M
MEDICAL EDUCATION
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LECTURES
16
G.S.M
MEDICAL EDUCATION
Shigella
-Gram(-), bacilli, lactose fermentation(-), oxidase(-), H2S(-)
-Common cause of:bloody diarrhea
-Endotoxin, shiga toxin(low inculum is enough to cause the
infection)
-Facal-oral transmission(food, water), 4F(Finger, Food, Feces,
Flies)
-4serotypes according to the severity:
A-S. dysenteria
B-S. flexeneri
C-S. bodyii
D-S. sonnei
*It is self limited in USA

LECTURES
17
G.S.M
MEDICAL EDUCATION
*It affects human only
-Symptoms:fever, abdominal pain, vomiting, large volume
watery diarrhea, dehydration
-Labs:stool with facal blood, leukocyte, shigella organism
-Treatment:*Do not give anti diarrheal agents
*antibiotics prolong bacterial secretion, but they
shorten the duration of infection.
*Zink

LECTURES
18
G.S.M
MEDICAL EDUCATION
Neisseria gonorrhea
Characteristics:gram -, diplococci, no polysaccharide capsule,
catalase+, oxidase+, glucose fermenter.
Disease:gonorrhea in males causes painful urethritis, dysuria.
And in females cause UTI, VD which leads to vaginitis 80% and
this may cause PID eventually sterility.
*it’s sexually transmitted disease or from mother to
infants while delivery.
Culture:Thayer martin agar.
Causes:
1- Pharyngitis(oral sex) and usually it is asymptomatic.
2- Fitz- Hugh Curtis syndrome (acute gonococcal
perihepatitis).

LECTURES
19
G.S.M
MEDICAL EDUCATION
3- Septic arthritis
4- Neonatal conjunctivitis
Virulence:pili, LPS, sometimes IgA protease(makes
cleavage into IgA)
Treatments:ceftriaxone + azithromycin(Chlamydia) or
doxycycline.
Ointment(silver nitrate in neonatal age).
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LECTURES
20
G.S.M
MEDICAL EDUCATION
NEISSERIA MENINGITIDIS
Characteristics:gram -, diplococci, catalase+, oxidase+, glucose
+ maltose fermenter, thick polysaccharide capsule.
Transmissio:inhaled droplets, oral secretions.
Diseases:meningitis (fever, stiff neck and headache),
meningococcemia(water, friderichsen syndrome) and
hemorrhagic adrenalitis and in this case will develop: septic
shock, organ failure, coma, DIC purpura and adrenal
insufficiency.
*in case of hemorrhagic adrenalitis if we give the patient
norepinephrine or epinephrine during resuscitation and there is
no improvements in his BP this means that the patient have
adrenalin insufficiency and we give(hydrocortisone).

LECTURES
21
G.S.M
MEDICAL EDUCATION
* quelling reaction +
Serotypes:A, B(most virulence, not immunogenic), C, D, 24E, W,
35, X,Y, Z
Virulence:thick polysaccharide, IgA protease.
Vaccine:(after the age of 2 years) all serotypes except B
serotype.
Treatment:ceftriaxone, penicillin G. for
prophylaxis(ciprofloxacine, rifampin, ceftriaxone.

LECTURES
22
G.S.M
MEDICAL EDUCATION
Bordetella pertussis
Gram (-), obligate aerobic, occcibacillus, pleumorphic
-Virulence factor:
1-pertussis toxin
2-trachial cytotoxic
3-capsule
-Stages :
1-incubation period:7-10 days
2-catarrhal stage:1-2 weeks
3-paroxysmal stage:2-4 weeks(lymphocytosis and vomiting)
*After increasing CAMP:IgE switching occurs, which cause
lymphocytosis and vomiting
4-Convalescent stage:2-4 weeks(pneumonia, convulsion)

LECTURES
23
G.S.M
MEDICAL EDUCATION
-Culture:Bordet- Gengue agar
-Staining:Toluidine Blue
-Causes:
1-whooping cough(high histamine sensitization)
2-lymphocytosis
3-connjectavial hemorrhage
4-hypoglycemia
5-hemolysis
-treatment:DTP Vaccine and DTaP(a=boosting shots)
Erythromycin
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LECTURES
24
G.S.M
MEDICAL EDUCATION
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LECTURES
25
G.S.M
MEDICAL EDUCATION
Klebsiella pneumoniae
*Gram(-), rod, encapsulated, facultative anaerobic, glucose
fermenter
*Normal flora of GI
*Virulence factors:capsule, beta lactamase(beta lactam
resistant)
*4A klebsiellA
Aspiration pneumonia + UTI
Alcoholic
Abscess in lung and liver
diAbetes(diabetic patients are at high risk to get this infection)
*The pneumonia is lobar and causes dark-red jelly sputum
*Culture:in macConkey agar, it is very mucoid colonies

LECTURES
26
G.S.M
MEDICAL EDUCATION
*Treatment:cephalosporins
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LECTURES
27
G.S.M
MEDICAL EDUCATION
Legionella pneumophila
Gram -, rod, catalase +.
Transmissio:contaminated water system, aerosolized mist,
associated with AC(air conditioner).
*no person to person transmission
Causes:legionnaires disease(sever pneumonia) and GI
symptoms, CNS symptoms, fever, often unilateral lobar
pneumonia.
Pantiac fever- mild form(flu like symptoms)
Culture:transtracheal aspiration(broncho-alveolar lavage)
Staining:silver stain, charcoal yeast extract stain with cysteine
and iron.

LECTURES
28
G.S.M
MEDICAL EDUCATION
Virulence factors:1-β lactamase.
2- metalloprotease(IL2) *breaks the antigenic bonds between
the antigen presenting cells and antibodies.
3- catalase.
4- intracellular.
Treatments:macrolids(azithromycin)and
quinolones(ciprofloxacin).
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LECTURES
29
G.S.M
MEDICAL EDUCATION
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LECTURES
30
G.S.M
MEDICAL EDUCATION
Pseudomonas aeruginosa
Gram -, aerobic rod, motile, non lactose fermenting, oxidase+.
Produce pyocyanin(grape like odor and generates reactive
oxygen species).
Virulence factors:endotoxin, exotoxin A, phospholipase,
pyocyanin, capsule.
PSEUDOMONAS (associations)
Pneumonia(patients with CF), pyocyanin.
Sepsis
Ecthyma gangrenosum (hot tub folliculitis)
UTI

LECTURES
31
G.S.M
MEDICAL EDUCATION
Diabetes, drug use
Osteomyelitis
Mucoid polysaccharides capsule
Otitis externa
Nosocomial infection
Exotoxin A
Skin infection
Treatments: campfire
Carbapenems, aminoglycosids, monobactams,
polymyxins(ploymyxin B, colistin), floroquinolones(levofloxacin),
third and fourth generation cephalosporins(seftazidine,
cefepime), extended spectrum penicillin(pepracillin, ticarcillin).
Escherichia coli

LECTURES
32
G.S.M
MEDICAL EDUCATION
*Gram(-), rod, fast lactose ferment(+)
*Virulence factors:fembria(cystitis), pili(pyelonephritis), K
capsule(pneumonia, neonatal meningitis), LPS endotoxin(septic
shock)
***E 3PHIT E.C
1-E 3P EC:Pathogenic, Pediatric diarrhea, losse stool, vomiting,
tenesmus
No toxin
There is adherence to the villi, so it causes flattened of the villi
and the absorption area decreases and that leads to diarrhea
2-E 3T EC:Toxogenic, Travelers diarrhea
Heat labile and heat stable toxins, it affects small
intestine mostly
3-E 3I EC:Invasive, Innocent(No toxin)

Microbiology bacteriology

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