GRAM NEGATIVE BACTERIA
ENTEROBACTERIACEAE- catalase-positive and oxidase-negative; they all share same LPS core structures (common Ag); aerobic and anaerobic; can be nitrate or
sulfate reducing.
BACTERIA
(STRAIN)
DISEASE
CLINICAL
MANIFESTATIONS
MODE OF
TRANSMISSION
RISK
GROUPS
SITES OF
INFECTION
MECHANISMS OF DISEASE
Escherichia
EIEC
Dysentery
Fever, bloody
dysentery, n/v, abd
cramps
Fecal-oral;
consumption of
contaminated
foods and water;
direct contact
(UTI)
Infants and
kids
Large
intestine
All ages
(travelers
into US)
Small
intestine
* plasmid- encoded pili or
micropinocytosis for attachment
*Invasion: invasion plasmid Ags
(IPA)- lyse endosome- bacteria
escape; mobilize actin for
horizontal transmission of bacteria;
PMN infiltrate and incr mucus
secretion; enterocytes lysed.
*Escape immune function
*Plasmid-encoded pili.
*Enterotoxins: Heat-stable toxin
(ST) and Heat-Labile toxin (LT).
*DIARRHEA CAUSED
BY INVASION
*Facultative
anaerobe;
motile; K1
strain- very
severe
(second most
common
cause of
neonatal
meningitis
*Most
infections are
endogenous
in nature.
*Can also
replicate
w/in tissues
of plants and
water
(coliform)
ETEC
Gastroenteritis
Watery diarrhea,
n/v, abd cramps
-Toxin causes the
diarrhea
DAEC
Gastroenteritis
-Mild infection
Traveler’s diarrhea,
watery, n/v, abd
cramps
“LABILE in the Air, STABLE on the
Ground” (heat-labile, incr cAMP;
heat-stable, incr cGMP)
travelers
Small
intestinesurface of
cells
*Targets chloride channelsinfluences electrolyte balance so
fluids move toward lumen
*Afa-Dr adhesions- bind to DAF
IL-8, TNFa, IL-1B
*Sat- taken up by cell. SPATE that
disrupts tight junctions.
*Type 1 pili- upon bacteria binding
to PMN. Induces PMN IL-8, decr
phagocytosis & promotes
apoptosis.
**bacteria wants PMN to come
b/c it activates DAF which incr
binding ability to cell surface.
BACTERIA
(STRAIN)
DISEASE
EPEC
Gastroenteritis
EHEC
Gastroenteritis
HUS- hemolytic
Uremic
Syndrome (life
threatening
illness)
SITES OF
INFECTION
MECHANISMS OF DISEASE
Watery diarrhea,
n/v, abd cramps
Infants <1
yr. in
developing
countries
Attaches to
small
intestine
*Bundle-forming pili (BFP)encoded by plasmid, initial
attachment.
*Afrimbrial adhesions
*Locus of enterocyte effacement
(LEE)- plasmid encoding genes; Tir
and EspFu recognize host cell actin
and cytoskeleton. Weakens tight
junctions- fluids flow out. Clchannels manipulated causing
higher conc of solute in lumen.
*Apoptosis regulated by bacteriabind to Mф & block signalingextends symptoms
Hemorrhagic colitisbloody diarrhea,
n/v, abd cramps
All ages70,000
cases/yr.
(USA)
Small and
large
intestines
*Plasmid-encoded pili & intimin-Tir
for attachment
*Verotoxins- lysogenic phageshiga-like toxin-1 and 2: binds to
GB3 which allows disruption of BV.
A subunit binds to rRNA  Dec
protein synthesis
-no toxin
produced, just
prevents
absorption
*VIGOROUS
LACTOSE
FERMENTATI
ON;
REDUCES
NITRATE
EPEC & EHEC
GRAM NEGATIVE BACTERIA
CLINICAL
MODE OF
RISK
MANIFESTATIONS
TRANSMISSION
GROUPS
-Tight junctions
disrupted, BV
effected, so blood
able to leak into
lumen.
*HUS- Shiga-like toxin produce
microthrombi which limits flow of
blood to organ (particularly the
kidney). Causes necrosis, PLT
consumption, and RBC
fragmentation. Kidneys become
essentially non-functioning.
BACTERIA
(STRAIN)
DISEASE
EAEC
Gastroenteritis
UPEC
GRAM NEGATIVE BACTERIA
CLINICAL
MODE OF
RISK
MANIFESTATIONS
TRANSMISSION
GROUPS
Fever, watery-tomucoid diarrhea,
n/v, abd cramps
UTI- E. Coli is the
most common
cause.
UTI- Polyuria,
dysuria, cloudy
urine.
Pyelonephritis
(upper ureter to
kidney).
Pyelonephritis
(upper ureter to
kidney)- fever,
polyuria, hematuria,
malaise.
*inflammation from
being taken up by
cell.
SITES OF
INFECTION
MECHANISMS OF DISEASE
Infants and
kids in
developing
countries
Large
intestine
Anyonemore
prevalent in
sexually
active
adults,
females, and
older
patients
Bladder
Attachment-*Aggregative
adherence fimbriae (AAF)encoded on a virulence plasmid
(pAA). Attach to salad leaves,
enterocytes & other EAEC. Biofilm
formation (stacking)  lead to
malabsorption (decr fluid
absorption)
*Dispersin- neutralizes negative
charge of LPS allows AAF to
extend from cell.
SPATES & toxin*Pic- digests mucin. Induce mucus
hypersecretion & # goblet cells.
Impair leukocyte migration.
*Pet- endocytosed; cleaves
spectrin  host cells round and
detach.
*EAST-1: Encoded on pAA. Incr
cGMP.
*Type 1 pili for attachment.
Internalized.
*Cytokines induced by bacteria
presencerecruits PMN & Mф.
*Phagocytes release compounds to
kill infected cells cells die or
exfoliate (bacteria can escape).
-“Stacked
bricks”
--Pili used to
climb up
urethra.
--Exfoliation cause of some
cloudiness of urine. That and pus
from PMN.
BACTERIA
(STRAIN)
DISEASE
Salmonella
S. enterica
Enteritidis
&
s.enterica
typhimuriu
m
Salmonellosismild
S- low-grade fever,
water diarrhea, n/v,
abd cramps.
T- Fever, headache,
bloody diarrhea,
lethargy, delirium,
abd cramps, “rose
spots” on abd.
Foodborne
illness- fecal oral;
contaminated
food (eggs,
poultry, diary)
Errybody
--For s.
enterica
Typhicontact with
-Colonizes GI tract contaminate
of animals. Can
fomites can
be found on
cause
eggshell.
infection
SITES OF
INFECTION
MECHANISMS OF DISEASE
Both start in
small and
large
intestines.
*attaches to enterocyte surface
attaches to M cell surface.
*if attached to enterocyte- SPI1/T3SS induced. Mediates bacteria
uptake by enterocyte.
*Mucosal DC- take up bacteria.
Reside in DC through SPI-2.
Bacteria disseminated to bone
marrow, spleen, liver, lymphs.
*Bacteria taken up can remain in a
Salmonella-containing vacuole
(SCV) via SPI-2- that brings food to
and from SCV- causes incr cAMP,
diarrhea starts.
* Some bacteria exit by
transcytosis.
*Mф engulf bacteria (via M cell or
surrounding enterocytes)disseminated to lymphs and
surrounding enterocytes.
S-localized
T-Systemic
Typhoid Fever(VACCINE)
growth on
Hektoen Agar
Shigella
GRAM NEGATIVE BACTERIA
CLINICAL
MODE OF
RISK
MANIFESTATIONS
TRANSMISSION
GROUPS
S. sonnei
(USA) &
S. flexneri
(3rd world)
-Facultative
anaerobes;
nonmotile
Shigellosis
Fever, tiredness,
water diarrhea, abd
pain, tenesmus
(painful straining to
pass small volume
stool)
*Facultative
anaerobes;
Motile;
encapsulated. NO
LACTOSE OR
SURCROSE
FERMENTATION.
REDUCESOLFATE
TO HYDROGEN
SULFIDE
Fecal-oral;
contaminated
food and water.
Four F’s: Fingers,
Flies, Food, Feces
* NO
FERMENTATION
OF LACTOSE; NO
REDUCTION OF
SULFATE
In US, kids
<15 yrs
greatest risk
Small and
large
intestines
-generally
starts in
small
intestine
*Bacteria enter M cellstranscytosis of bacteria to
phagocytes.
*Mф undergo apoptosis- releasing
bacteria. Invade from basolateral
side (IPA)infect adj. enterocytes
(leads to incr cAMP).
*infected enterocytes/Mф produce
chemokines to recruit PMNs
(which destroy infected cells).
*Shiga toxin inhibits protein
synthesis; cytotoxic
BACTERIA
(STRAIN)
Klebsiella
Yersinia
Y. pestis
DISEASE
Pneumonia
(most common);
wound and soft
tissue infections;
UTI (second to E.
Coli); septicemia
Usually no diarrhea.
Bubonic Plague
B- General sx like
f/c/n, sore throat,
myalgia, headache.
Painful bubo (groin
or axilla)- lesions
due to
lymphadenopathy.
Septic shock (5075% of cases)
*3
pandemics
so far
Looks like a
“safety
pin”
GRAM NEGATIVE BACTERIA
CLINICAL
MODE OF
RISK
MANIFESTATIONS
TRANSMISSION
GROUPS
and Pneumonic
Plague
*Destruction of
lungs basically
Normal gut flora!
Errybody
SITES OF
INFECTION
Commonly
colon and
urinary tract
(opportunist
ic)
MECHANISMS OF DISEASE
-usually a “solid” fever since IL-1
produced.
*Highly resistant to microbes.
*Polysaccharide capsule is the
most important virulence factorreally thick.
* facultative anaerobes;
nonmotile; Mucoid capsule
P- Respiratory
failure (2-3 days).
High fever,
coughing, SOB,
hemoptysis,
lethargy.
Septicemia.
Bite of a flea (rat
flea);
contaminated
respiratory
droplets..personto-person
*can grow at 39F
with preferential
growth on blood
agars
SW US,
Europe
Intestines,
skin, lungs
*Bacteria
enter: M
cells (food &
water),
Dermis
(flea), Lung
(inhalation).
*Bacteria taken up by flea, controls
the flea, or kills it off- regurgitation
of the microbe by the flea at bite
site is how it gets into humans.
*Bacteria makes a change in lipid
Anormally cause an immune
response but now in the humans it
elicits a very weak signal.
*Mф engulf bacteria- bacteria
induce uptake – YOPS (suppress
innate immunity) allow bacteria to
replicate w/in phagosomes.
*Other bacteria remain
extracellular- protein capsule
prevents phagocytosis.
*Mф engulf bacteria- can lyse Mф
as well. Spread bacteria to
lymphatics (& other organs)
BACTERIA
(STRAIN)
Proteus
DISEASE
UTI- main
disease.
Bladder and
kidney infections
GRAM NEGATIVE BACTERIA
CLINICAL
MODE OF
RISK
MANIFESTATIONS
TRANSMISSION
GROUPS
Urease activity(urea ammonia)
raises pH which if
sustained can lead
to kidney stones.
Transmitted by
contaminated
catheters.
SITES OF
INFECTION
Can colonize
skin and oral
mucosa.
MECHANISMS OF DISEASE
*Can spread from lymphatics
through blood to lungs
*Facultative anaerobes; nonmotile;
Y. pestis is encapsulated
*Facultative anaerobes; motile
(peritrichous)
*Swarming motility- differentiate
into clusters of joined, flagellated
cells. Move together over solid
surfaces at high rates.
*Rapid urease production; Sulfur
reducer.
Pseudomona
s
Aeruginosa
- aerobic
-OXIDASEPOSITIVE
Respiratory
infections main
one (especially
in cystic fibrosis
pts)
Fruity smelling.
Adapts to nearly
all environmentssinks, mops,
water, food,
surfaces, etc.
PSEUDDOmonas
: pneumonia,
sepsis, otitis
externa, UTIs,
drug use,
diabetes,
osteomyelitis
Vibrio
V. cholerae
Cholera
Ubiquitous in soil
and water
(usually in
biofilms).
Voluminous watery
diarrhea (explosive
diarrhea), loss of
Wide
temperature
range.
Fecal-oral;
contaminated
food/water
Errybody
Variable.
*Cystic
Fibrosis pts
more
susceptible
to
respiratory
*Opportunistic; strict aerobe;
motile.
*Virulence factors:
-IgG protease
-Pyocyanin directly toxic to
leukocytes
-Exoenzyme S adhesion and
cleavage of inflammatory cytokines
*NOTABLE ANTIMICROBIAL
RESISTANCE
Small
intestine
*bacteria attach to enterocytes by
pilusphage-infected bacteria
produce cholera toxin (activates G
BACTERIA
(STRAIN)
DISEASE
GRAM NEGATIVE BACTERIA
CLINICAL
MODE OF
RISK
MANIFESTATIONS
TRANSMISSION
GROUPS
electrolytes, rice
water stool, low BP,
rapid HR, vomiting
SITES OF
INFECTION
MECHANISMS OF DISEASE
proteins to promote cAMP
production).
*bacteria produces other
enterotoxins to enhance secretion
of electrolytes.
-MULTIPLIES
FREELY IN WATER
(levels incr during
warm months)
*Facultative anaerobes; Motile;
curved bacillus
*Oxidase-positive and tolerates
incr salinity
THIOSULFATE CITRATE BILE SALTS
(TCBS) AGAR
Neisseria
N. gonorrhoeae
&
N. meningitidis
(incapsulat
ed)
Gonorrhea
Meningooccal
Meningitis
(VACCINE)
G- males- urethra
discharge (usually
thicker and
yellow/green color),
dysuria.
Females- cervical
discharge (may not
always be
noticeable), dysuria.
M- Initially mild
pharyngitis. Sudden
onset headache,
f/v, stiff neck
--discharge on brain
G- sexually
transmitted
M- Respiratory
(common in dry,
cold months)
G- Greatest
risk to SE
African
Americans
15-24 yrs.
M- greatest
risk to kids
G- GU,
rectum,
eyes, throat
*Aerobes; nonmotile; Diplococci
*Oxidase-positive
*DOES NOT FERMENT MOST
CARBS- GROWTH ON THAYERMMARTIN AGAR (5% chocolate agar
nasopharynx + antibiotics)
/oropharynx
*Mucosa- Exudate generation:
1. bacteria attach to epi cells- pilus,
opacity proteins (OPA)
2. Porin I (POR) protein induces
endocytosis
3. LOS, peptidoglycan, lipoproteins
stimulate cytokine production by
epith and Mфrecruits and
activates PMN—LOS can function
as an endotoxin
4. activated PMN phagocytize
bacteria and destroy infected cells
(infectious exudate)
BACTERIA
(STRAIN)
DISEASE
Bordetella
B. pertussis
Whooping cough
(VACCINE)
Haemophilus
FERMENTS
GLUCOSE
AND
LACTOSE
*HIGH
CONTAGIOUS
H.
influenza
type b (Hib)
Meningitis and
others
(VACCINE)
*Type B most
virulent!
GRAM NEGATIVE BACTERIA
CLINICAL
MODE OF
RISK
MANIFESTATIONS
TRANSMISSION
GROUPS
3 phases*catarrhal- mucoid
rhinorrhea, nasal
congestion,
sneezing
*paroxysmalintense bough of
cough, vomiting
(usually end of
infection: coughing
due to damage)
*Convalescentpersistent cough,
secondary
infections
Contaminated
respiratory
droplets
M- Always starts as
a sore throat.
Headache, stiff
neck, fever
Direct contact;
contaminated
respiratory
droplets
Infantsworldwide
cases
however
Worldwide
SITES OF
INFECTION
MECHANISMS OF DISEASE
Lungs
*Aerobe; nonmotile; Coccobacillus
*Susceptible to environmental
changes
REQUIRES
NICOTINAM
IDE AND
CHARCOAL
IN MEDIA
(BORDETGENGOU
MEDIA,
POTATOBLOODGLYCEROL)
Nasopharyn
x,
oropharynx,
laryngophar
ynx
*Respiratory mucosa- bacteria
attach to ciliated epith cells—FHA,
P69, PTX bind to host cell
glycolipids
*PTX- impairs ciliary action ADP
ribosylation of g inhibitory
proteins, incr cAMP= incr mucus
secretion. Also disrupts cell
signaling in phagocytes to prevent
phagocytosis.
*Tracheal cytotoxin released which
kills the ciliated epith cells.
*Cell debris + incr mucus +
impaired ciliary action severe,
persistent cough.
*Facultative anaerobe; nonmotile;
Coccobacillus
*Requires hemin (Xf factor) and
nicotinamide adenine dinucleotide
(NAD, V factor) for growth – X & V
found in RBCs.
*Normal flora Haemophilus are
NOT encapsulated.
*Bacteria colonize nasopharynx w/i
first few months of life—pilus
allows attachment to epith
*Hib capsule responsible for
virulence—composed of ribose,
ribitol, phosphate (polyribitol
phosphate or PRP); adheres
bacteria to ciliated epith; impairs
BACTERIA
Brucella
Francisella
(STRAIN)
DISEASE
REDUCES
SULFUR
AND
NITRATEGROWS
WELL ON
CHOCOLAT
E AGAR
Brucellosis
F.
tularensis
Tularemia- AKA
Rabbit Fever
-Two major
groups:
A-only N.
America;
lethal
GRAM NEGATIVE BACTERIA
CLINICAL
MODE OF
RISK
MANIFESTATIONS
TRANSMISSION
GROUPS
Acute- flu-like
illness
Worldwide
Chronic-undulantFever, drenching
sweats, etch
Greatest risk
hunters in
summer
(ticks) and
winter
(rabbits)
Bite of tick
(transferred
Primary
replication
occurs in DC
and Mф
-skin, oral
(main route)
and
respiratory
Picked up mostly
by farmers- direct
contact with
infected animal
(feces, urine,
tissues); ingestion
of contaminate
foods
Ulceroglandular
disease (UGD)- f/c,
headache, malaise,
pain in involved
area, lesion
ulcerates 
necrotic (death of
Mф)
SITES OF
INFECTION
Primary
replication
occurs in DC
and Mф
-skin, oral,
respiratory
mucosa
MECHANISMS OF DISEASE
ciliary action; protects from
phagocytosis; anti-PRP response
important for bacterial clearance
(IgA protease can protect from Ab
response)
*Strict aerobe; nonmotile;
Coccobacillus
*Oxidase, catalase, and ureasepositive
*Bacteria captured by receptors
for outer membrane proteins
(OMP)—bacteria transcytose to
underlying Mф or are taken up by
sampling DCs.
*Regulatory proteins BvR/S, LPS
and beta glucans directs
phagosome to endocytic
compartment- majority encounter
lysosomes & are digested. Few
bacteria are resistant to lysosomal
enzymes
*Viable bacteria are directed to ER
and develop ER vacuole and
replicateactivation of the Mф by
bacteria can generate granulomas
*Strict aerobe; nonmotile;
Coccobacillus
*Grows well on medias with added
cysteine; OXIDASE-NEGATIVE
*Bacteria captured by receptors
for OMP—can also infected endoth
cells and hepatocytes
*Francisella pathogenicity island
genes allow bacteria to escape
BACTERIA
(STRAIN)
infections
in rabbits;
severe
illness in
humans
DISEASE
GRAM NEGATIVE BACTERIA
CLINICAL
MODE OF
RISK
MANIFESTATIONS
TRANSMISSION
GROUPS
through feces);
direct contact
with infected
animal (minor
abrasion)
B-Europe,
Asia, & N.
Americamild
disease in
humans;
NOT lethal
in rabbits
Inhalation and
ingestion also
shown to
transmit
*can survive for a
week at low temp
in water, moist
soil, hay, straw, or
decaying animal
carcasses
SITES OF
INFECTION
MECHANISMS OF DISEASE
phagosome and replicate in the
cytosol.
*Mф undergo apoptosis releasing
bacteria to infection other Mф 
leads to lymphadenopathy; may
disseminate (if persists in tissues it
can form granulomas)