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Species
Characteristics
Epidemiology
Diagnosis
Escherichia
(E. coli)
Facultative Anaerobe
Motile (peritrichous)
Fecal-Oral – leads to
gastroenteritis
Vigorous lactose
fermintation
Gram Negative
Bacilli
ROD SHAPED
Direct Contact - UTI
Reduces nitrate
Can form a coliform
2nd most common
cause of neonatal
meningitis
Enteropathogenic
E. Coli
EPEC
Gram Negative
Bacilli
Facultative Anaerobe
Motile (peritrichous)
Vigorous lactose
fermintation
Pathogenesis
Major Disease
Small Intestine
Gastroenteritis
- Infants < 1 year in developing
countries
EMB (EosinMethylene Blue)
Agar – Get’s a
metallic green
shape
EMB (EosinMethylene Blue)
Agar – Get’s a
metallic green
shape
Attachment:
Bundle-forming pili (BFP)
Afimbrial adhesions
Reduces nitrate
Can form a coliform
2nd most common
cause of neonatal
meningitis
ROD SHAPED
Locus of enterocyte effacement (LEE)
proteins
- Attaching & Effacing (A/E ) lesions
 T3SS – type 3 secretion system
 Tir/Intimin binding for firm
attachment
 SPATE (EspF, Tir, EspC) reorganizes
cell actin and cytoskeleton to make a
pedicle
- EspF a LEE protein that allows
interstitial fluid to leak out
Can bind to Monocytes and Macrophages
to block signaling & prevent phagocytosis
Watery diarrhea
Nausea & vomiting
Abdominal cramps
Enterohemorrhagic
E. Coli.
EHEC
STEC
VTEC
Facultative Anaerobe
Motile (peritrichous)
Gram Negative
Bacilli
Reduces nitrate
Can form a coliform
Vigorous lactose
fermintation
EMB (EosinMethylene Blue)
Agar – Get’s a
metallic green
shape
ROD SHAPED
Gram Negative
Bacilli
Facultative Anaerobe
Motile (peritrichous)
Vigorous lactose
fermintation
Reduces nitrate
Can form a coliform
2nd most common
cause of neonatal
meningitis
Attachment:
Plasmid-encoded pili & intimin-Tir
A/E mediated diarrhea that leads to
hemorrhagic colitis
Verotoxins:
- Shiga-like Toxin-1 (STX or STL)
- Shiga-like Toxin 2 (STX or STL)
 Binds to GB3 – expressed on
endothelial cells of kidneys, intestines
 produce microthrombi & Lifethreatening Illness (HUS)
= site that gets toxin dies and activates
coagulation
= coagulation leads to distal ischemic
necrosis
= and you get RBC fragmentation
=leads to Hemolytic Uremic Syndrome
2nd most common
cause of neonatal
meningitis
Diffusely Adherent
E. Coli
(DAEC)
Small & Large Intestine
EMB (EosinMethylene Blue)
Agar – Get’s a
metallic green
shape
Small Intestine
Afa-Dr adhesions
 binds to DAF
 activates the immune system and
recruits PMNs
diffuse
adherence
pattern on
cultured
epithelial cells
HeLa or HEp-2
Sat
 SPATE that disrupts tight junctions
can cause diarrhea
Type 1 Pili
 binds to PMNs to promote it’s action.
Gastroenteritis
All Ages – US
Hemorrhagic colitis
‘
Bloody diarrhea
Nausea & vomiting
Abdominal cramps
Gastroenteritis
Traveler’s diarrhea
Water diarrhea
Nausea & vomiting
Abdominal cramps
Enterotoxigenic
E. Coli
ETEC
Gram Negative
Bacilli
ROD SHAPED
cells
PMN’s produce DAF which enhances it’s
binding
Facultative Anaerobe
Motile (peritrichous)
EMB (EosinMethylene Blue)
Agar – Get’s a
metallic green
shape
Small Intestine
Vigorous lactose
fermintation
Reduces nitrate
Can form a coliform
Plasmid-encoded pili
Enterotoxins
- Heat-Stable Toxin (ST)
 activates cGMP
Gastroenteritis
All Ages – Travelers into US
Watery diarrhea
Nausea & vomiting
Abdominal cramps
- Heat-labile Toxin (LT)
 activates cAMP
2nd most common
cause of neonatal
meningitis
ROD SHAPED
Enteroinvasive
E. Coli
EIEC
Gram Negative
Bacilli
Facultative Anaerobe
Motile (peritrichous)
Vigorous lactose
fermintation
EMB (EosinMethylene Blue)
Agar – Get’s a
metallic green
shape
Small Intestine
 diarrhea
EIEC Dysentery
Infants & Children
Large Intestine
 Dysentery
Diarrhea
Watery diarrhea,
Cramps,
Reduces nitrate
Can form a coliform
Plasmid-encoded pili or
Macropinocytosis
2nd most common
cause of neonatal
meningitis
Invasion Plasmid Ags (IPA)
 lyse endosome so bacteria can escape
ROD SHAPED
mobilize actin for horizontal
transmission – lysing enterocyte and
causing bloody diarrhea
Dysentery
Mucoid diarrhea with blood
Fever
Abdominal pain
May lead to ulcerations
Enteroaggregative
E. Coli
EAEC)
Gram Negative
Bacilli
Facultative Anaerobe
Motile (peritrichous)
Vigorous lactose
fermintation
EMB (EosinMethylene Blue)
Agar – Get’s a
metallic green
shape
PMN infiltrate causing inflammation and
increasing mucus secretion
Large Intestine
Aggregative adherence fimbriae (AAF)
 forms a biofilm and you find on salad
leaves
Reduces nitrate
Can form a coliform
Dispersin
 neutralizes negative charge of LPS
2nd most common
cause of neonatal
meningitis
Pic
 induces mucus hypersecretion & # of
goblet cells
ROD SHAPED
Pet
 get endocytosed and cleaves
cytoskeleton protein – host cells round
and detach
Uropathogenic E.
Coli
UPEC
Gram Negative
Bacilli
Facultative Anaerobe
Motile (peritrichous)
2nd most common
cause of neonatal
meningitis
Reduces nitrate
MOST COMMON
CAUSE OF UTI
2nd most common
cause of neonatal
meningitis
ROD SHAPED
Vigorous lactose
fermintation
Can form a coliform
EMB (EosinMethylene Blue)
Agar – Get’s a
metallic green
shape
EAST-1
 activates cGMP
Bladder
Attachment:
 Type 1 pili
- the key to virulence. It recruits PMNs to
come and kill bacteria. Releases it’s
compounds which destroy cells and
exfoliate, but bacteria travels and escapes
Gastroenteritis
Infants & children in developing
countries
Fever
Watery to mucoid diarrhea
Nasuea & vomiting
Abdominal cramps
MOST COMMON CAUSE OF UTI
Urethral Infection & Cystitis
 polyuria
 dysuria
 cloudy urine
Pyelonephritis (upper ureter to
kidney)
 fever
 polyuria
 hematuria
Salmonella enterica
Facultative Anaerobe
Salmonellosis:
Fecal-oral –
contaminated food
(eggs, poultry, dairy)
Culture:
SalmonellaShigella
Agar (SS-Agar)
Small & Large Intestine
Attaches to enterocyte surface
Gram Negative
Bacilli
Motile (peritrichous)
No lactose or sucrose
fermentation
Food-borne
Taken up by DC sampling the gut
Reduces sulfate to
hydrogen sulfide
Colonizes GI tract of
animals
Hektoen Enteric
Agar
(HEK) – look for
fish eye
VACCINE FOR TYPHOID
FEVER
Shigella
Facultative Anaerobe
Gram Negative
Bacilli
Nonmotile
All species produce
Shiga toxin
S. dysenteriae is most
potent
Typhoid Fever:
Fecal-oral – contact
with contaminated
fomites
Fecal-oral –
contaminated food
and water
DOES NOT
Ferment lactose
DOES reduce
sulfur
NO lactose
fermentation
No sulfate
reduction
Greatest risk group
in US are children <
15 years – 70% of
cases
Attaches to M cell surface
S. enterica enteritidis:
Salmonellosis
Low-grade fever
Water diarrhea
 can be bloody diarrhea if severe
Nausea & vomiting
Abdominal cramps
Can reside in M cells via S-CV using SPI-2
In Macrophage or DC, it can disseminate
to bone marrow, lymphatics, spleen, liver
Small and Large Intestine
Bacteria enter M cells
Apoptose macrophages
Invade basolateral side of enterocytes
using IPS
S. enterica typhimurium
Typhoid Fever
Fever
Headache
Bloody diarrhea
Lethargy
Delirium
Abdominal cramps
Rose spots on abdomen
Shigellosis
Fever
Tiredness
Water diarrhea
Abdominal pain
Tenesmus
Enterocyte invasion
 activate cAMP
Shiga Toxin
Inhibits protein synthesis
Cytotoxic
Klebsiella
pneumonia
Facultative Anaerobe
Agar plate
Stringy? Has
Polysaccharide capsule is most
important virulence factor
Pneumonia
 thick blood with sputum
Nonmotile
Gram Negative
Bacilli
capsule
Puffy and shiny?
Has a capsule
Has a mucoid capsule
 lung necrosis and abscess
 Most common in ventilator
associated pneumonia
Opportunistic
Wound and soft tissue infections
HIGH RESISTANCE TO
MICROBIALS
Second leading cause of UTI
Septicemia – bacteria in blood
Yersinia
Facultative Anaerobe
Fecal-oral
Blood agar has
robust growth
Not pestis
T3SS
Y. pestis
Bubonic Plague
Gram Negative
Bacilli
Nonmotile
Encapsulated
Three species:
Pestis  bubonic &
Pneumonic Plague
Pestis  flea bite
Pestis 
contaminated
respiratory droplets
Pestis  person to
person
Psuedotuberculosis &
enterocolitica 
gastroenteritis
Spiked RBCs –
there are lipid
problems
Bipolar staining
with Giemsa
staining looks
like a hairpin
apparently
Can grow at 4 celcius –
loves growth on blood
agars
Yersinia outer membrane proteins –
YOPS
YPM = super antigen
Pestis
Phospholipase
Protein capsule
Ymt – bacteria can survive in flea
Forms clots in GI tract so it’s hungry and
it feeds
Intestines, Skin, Lungs
Macrophages engulf bacteria (YOPS)
allows them to live and replicate inside –
and move them to lymphatics
Have a capsule that allows them to
escapde phagocytosis
T cells produce IFN-y and promote killing
of enterolitica but no pestis
Proteus mirabilis
Facultative Anaerobe
Gram Negative
Bacilli
Motile (peritrichous)
Rapid Urease
production
Swarming motility - form clusters of
flagellated cells.
Sulfur reduction
Fever
Chills
Myalgia
Nausea
Sore Throat
Headache
Painful bubo (groin or axella) –
lesions due to lymphadenopathy
Septic shock – 50-75% of cases
Pneumonic Plague
When it disseminates to the lungs
High fever
Shortness of breath
Coughing
Hemoptysis
Lethargy
Respiratory failure
Septicemia
- High fever, hypotension and
shock, delirium, organ damage
UTI infections transmitted from
contaminated catheters
Bladder and kidney infections
Swarming motility
Urease activity can raise pH
which precipitates kidney
stones
Pseudomonas
aeurginosa
Strict Aerobe
Find it in soil, and it
can survive high
Oxidase positive
(Along with
Has many virulence factors
Respiratory Infections
Motile (Monotrichous)
Gram Negative
Bacilli
Oxidase-positive
Notable antimicrobial
resistance
temperatures and
in all environments
10% of hospital
acquired infections
Brucella and
cholera) and
antimicrobial
resistance
Produces lots of
ATP and has a
fruit smell
Opportunistic bacteria
Biofilms on soil and
water
Has a turquoise
colored agar
Eye and ear infections
Elastases – degrade ECM
IgG proteases
C3b proteases
Exotoxin A – Inactivates EFII
Phospholipase – cell membrane
damage
Pyocyanin – kills leukocytes
Exoenzyme S – for adhesion
Can lead to endocarditis
Small Intestine
Cholera
Voluminous watery diarrhea
 no blood
 large loss of electrolytes
- dehydration, metabolic acidosis
(bicarbonate loss), hypokalemia (K
loss), hypovolemia (cardiac
arrhythmia and renal failure)
Open wound and soft-tissue
infections
Adapts to nearly all
environments
Adapts to nearly all
environments
#1 Disease in CF
patients
Vibrio Cholerae
Facultative Anaerobe
Fecal-Oral
Gram Negative
Bacilli
Motile (Monotrichous)
Multiples freely in
water and found in
waters worldwide
Oxidase positive
Can get from
chitinous shellfish
Thiosulfate
Citrate Bile Salts
Agar (TCBS) –
grows well in
high salinity
Cholera Toxin
- Activates cAMP
Oxidase positive
(Along with
Brucella and
Pseudomonas)
Rice water stool
Low bp
Vomiting
Rapid heart rate and feeble pulse
GramNegative,
GramNegative,
GramNegative,
GramGram-Negative,
Negative, Fastidious Bacteria
Gram-Negative,
Fastidious
Fastidiou Fastidious
s Bacteria Bacteria
Fastidious Fastidiou
Bacteria
sBacteria
Neisseria
Aerobe
GRAM NEGATIVE
DIPPLOCOCCI
Nonmotile
Sexual Contact
(gonococcus)
 replicates in GU,
rectum, eyes, throat
 bacteremia
spreads to skin and
joints of knees,
ankles, and wrists
(arthralgia)
Diplococcus
#1 CAUSE OF
MENINGITIS
Bordatella
pertussis
DOES NOT ferment carbs
Aerobe
Nonmotile
GRAM NEGATIVE
Coccobacillus
Ferments glucose &
lactose
Contaminated
respiratory
droplets
(Meningococcus)
 replicates in
epithelial tissue of
nasopharynx
 bacteremia
spreads to lungs,
then joints, brain and
heart
100% respiratory
droplets
 replicates in the
lungs
 cilia become
immobilized,
destroyed, get
patches of no ciliated
cells which causes
irritation
Bacteria
Thayer-Martin
agar
5% chocolate
agar+antibiotics
Mucosa
1. Bacteria attach to epithelial cells
N. gonorrhoeae
N. meningitides
3. LOS (lipooligosaccharide) stimulates
cytokine production (can function as an
endotoxin)
Catalase positive
2. Porin I (POR) induces endocytosis
4. PMNs get active, destroy tissue
Gonorrhea
Males
 THICK urethral discharge
Dysuria
Females
 cervical discharge
dysuria
severe pain
Meningococcal Meningitis
Initially – mild pharyngitis
Sudden onset headache
Fever
Vomiting
Stiff neck
Petechial rash (DIC)
 necrotic lesions, loss of limbs,
brain covered with exudate, 100%
mortality
Bordet-Gengou
media, or
potato-bloodglycerol
Requires
nicotinamide and
charcoal
Respiratory mucosa
 Attach via FHA, P69, and Pertussis
toxin (PTX)
 PTX impairs ciliary action and
activates cAMP which causes mucus
secretion
 causes tracheal cytotoxin to kill cilia
Cell debris + mucus + impaired ciliary
action = severe, persistent cough
Whooping Cough
Catarrhal (1-2 wks)
 mucoid rhinorrhea
 nasal congestion
 sneezing
Paroxysmal (1-6 wks)
Intense bouts of cough
Convalescent (3 wks – months)
Persistent cough
Secondary infections
Haemophilus
influenza
Facultative anaerobe
Nonmotile
Direct contact OR
Contaminated
respiratory droplets
GRAM NEGATIVE
Number 2 cause of
meningitis
Coccobacillus
Normal flora H.
influenza are NOT
encapsulated
Hib vaccine
Gets into
nasopharynx,
replicates in
epithelial cells, and
bacteremia gets in
lungs, then to joints,
skin and brain
Hemin (X
Factor) &
Nicotinamide
adenine
dinucleotide
(NAD, V factor)
Look for shiny,
smooth, thick
growth
Respiratory mucosa
 bacteria colonize nasopharynx
 Hib capsule responsible for virulence
- composed of ribose, ribitol, phosphate
(PRP) –
 impairs ciliary action
 protects bacteria from phagocytosis
 anti-PRP response important for
bacterial clearance
Meningitis (Type B capsular
form)
 pharyngitis
headache
stiff neck
fever
lethargy
irritability
vomiting
Epiglottitis
Inflamed epiglottis & surrounding
tissue
Airway obstruction
Cellulitis & arthritis
 Tender red swelling
 Pain in large joints
Brucella spp.
Strict aerobe
Nonmotile
GRAM NEGATIVE
Coccobacillus
Replication occurs in
DC and Macs
Direct contact with
infected animal
(feces, urine, tissues)
Ingestion of
contaminated foods
(unpasteurized
dairy)
Oxidase,
catalase, urease
positive (Oxidase
positive along
with
Pseudomonas and
Cholerae)
 Gets in skin or
mucosa
 Replicates in
Reduces sulfur
and nitrate
Skin, Oral, Respiratory
OMP allows to bind
Variable bacteria are directed to ER and
develop ER vacuole and replicate
Activation of the macrophage by the
bacteria can generate granulomas
Brucellosis
 Acute
Flue-like illness (fever, sweats,
malaise, headache,
joint/muscle/back pain, fatigue)
 Undulant
Fever during the day
Drenching sweats at night
Can form arthritis, endocarditis,
Francisella
tularensis
Strict aerobe
Nonmotile
GRAM NEGATIVE
Coccobacillus
Macs, DCs
 cell bacteremia in
spleen, heart, bone,
lymph nodes
Chocolate agar
Bite Tick
Dog tick, wood tick,
lone star tick
Direct contact with
infected animal
Medias added
with cysteine
Skin, Oral, Respiratory mucosa
OMP to bind
Oxidase negative
Pathogenicity island allows to escape
phagosome and replicate in cytosol
Two groups:
Type A
 occurs only in N.
America (Most lethal)
Type B
 Occurs in Europe, Asia,
N. America
(Not as lethal)
Gets in skin or
mucosa and
replicates in DC and
Macs
Replication occurs in
DC and Macs
Rabbits are the
main resovoirs
Anaerob Anaerobic
ic &
& Atypical
Atypical Bacteria
Bacteria
Actinomyces
Gram positive
Gram positive
Facultative or strictly
Cell bacteremia in
spleen, heart, bone,
lymph nodes
Anaerobi
c&
Atypical
Bacteria
hepatomegaly
splenomegaly
Mac undergoes apoptosis release it to
infect another mac
It can go through lemphatics and cause
lymphadenopathy
It can disseminate and cause granulomas
Tularemia
Ulceroglandular Disease (UGD)
 fever, headache, chills, malaise
 pain in bite areas
 lesion ulcerates (necrotic death
of Macs)
Oculoglandular Disease
 sames as above but with
conjunctivitis
Oropharyngeal or Typhoidal
Disease
 same as above but ulcers are in
oral cavity or in intestine
Pneumonic Disease
Same as above but you get
respiratory ulcerations
Sepsis
Anaero Anaerobic &
bic &
Atypical Bacteria
Atypical
Bacteria
REALLY ONLY PRESENT AFTER SOME
SORT OF TRAUMA TO SURGERY
Anaerobic &
Atypical
Bacteria
Actinomycosis
 chronic granulomatous lesions
cervicofacial-most common
anaerobic
thoracic
abdominal
pelvic
CNS
 colonies called sulfur granules
Found in mouth, gut,
and GI
Clostridium
botulinum
Anaerobe
Motile
Gram positive
Spore-forming
Ingestion of toxincontaminated foods
(Canned foods) –
TOXINS ARE
PREFORMED
Or
Direct contact with
spores (in a wound)
– SPORES DON’T
HAVE PREFORMED
TOXIN
Botulism Toxin A, B, & E
1. binds to receptors on
presynaptic membranes of
motor neurons
2. Botulism toxin cleaves SNARE
proteins to inhibit Ach from
binding to it’s receptor
3. Botulism neurotoxin enters
4. Can’t contract muscles and you
get paralysis
Foodborne Botulism
18-36 hours
 Weakness, dizziness,
expressionless face
Two main toxins:
 A toxin – disrupts tight junctions
and gives diarrhea
Pseudo
membranous colitis:
 get from intense inflammation
that forms the pseudomembrane
Often seen in
infants who don’t
have an established
flora in their gut
Clostridium
difficile
Anaerobe
Spore-forming
Gram positive
Normal flora of 5% of
INFECTION
ENDOGENOUS
 ampicillin and
clindamycin
treatment
CAUSES THIS
SINCE IT’S AN
 B Toxin – Cytotoxic
Progressively: IN MUSCLE
 Nausea and vomiting
 Blurred vision
 inability to swallow
 Difficulty in speech
 weakness of skeletal muscles
 respiratory panalysis
the population
Clostridium
perfringens
Gram positive
Anaerobe
Nonmotile
Spore-forming
OPPORTUNISTIC
BACTERIA
Direct contact with
Spores in open
wound
OR
Ingestion of
spores/bacteria
Endospores get into
intestines and skin
- Replicates and
makes the 3 toxins
- Grows into deep
muscle tissue and
toxins induce
edema and necrosis
(SHOCK)
Clostridium tetani
GRAM POSITIVE ROD
Gram positive
Strict anaerobe
Motile
Spore-forming
Direct contact with
spores
Look for zone of
hemolysis
Antibiotics allows the bacteria to take
over
Alpha Toxin
 Phospholipase dissolves RBC,
leukocyte and muscle cell membranes
Theta Toxin
 Pore-forming toxin that alters
capillary permeability and is toxic to the
heart muscles
Gas Gangrene
 Severe pain at the site of wound
 Edema, tenderness,
discoloration, hemorrhage bullae
(Large, red blisters)
 CO2 and hydrogen released at
wound as a gas and it smells
terrible
Enterotoxin
 Activates Calcium levels and you lose
fluids and macromolecules
Clostridial Food Poisoning
 Nausea, abdominal pain,
diarrhea
Tetanospasmin – toxin
 Degrades synaptobrevin required to
dock on presynaptic membrane
 blocks glycine and GABA, motor
neurons are not inhibited and you get
continues voluntary muscle contraction
Tetanus
Early:
 Severe painful spasms,
Rigidity of voluntary muscles,
Lockjaw
Progressively
Rigidity and violent spasms of
trunk and limb muscles
Spasms of pharyngeal muscles,
difficulty swallowing
Respiratory spasms which leads
to death
Bacteroides
fragilis
Gram NEGATIVE
Enzymes –
catalase and SOD
helper tolerate
ROS
Anaerobic
Gram Negative
Major cause of
intrabdominal infections
Virulence Factors
 Adhesions
 Enzymes – catalase and SOD helper
tolerate ROS
 Toxins – Heat labile zinc
metalloprotease toxin – damages
epithelium, causes fluid loss and PMN
recruitment
Abscess formation in normally
sterile sites
Bacteremia
Intra-abdominal Infections
(80%)
Gynecological infections
Chlaymdia
Trachomatis
NO GRAM STAIN
NO GRAM STAIN
Direct contact with
contaminated
secretions
ACID FAST STAIN
Chlamydia gets into
genitals, replicates,
Th1 response leads
to acute
inflammation and
chronic infection
IFN-y can halt
replication, but RB
can resist it.
Legionella
pneumophila
NO GRAM STAIN
COCOO-BACILLI
Flagellated
Inhalation of
airborne, aerosolized
microbes – it lives in
water supplies in
Gimenez and
Dieterle silver
stain
EB (Elemenarty Bodies)
 enters conjunctiva or urogenital tracts
and infects epithelium.
 EB = metabolically inactive, but
infectious
 Enters lysosome but doesn’t die – it
then becomes a RB (Reticulate Bodies)
 RB is metabolically active, but NONinfectious
 TSS3 allow for nutrient uptake. Once
there are a lot, RB  EB and infectious
part bursts from cell
Virulence Factors
 Peptide toxin inhibits respiratory
burst
 Catalse detoxifies residual H2O2
Skin and soft-tissue infections
Follicular Conjunctivitis
 person to person
Leading cause of blindness in the
world
Corneal Scarring
 Eyelid turns inward
 eyelashes abrasive to cornea
 corneal ulcerations
Urogentical Infection
 Dysuria
 THIN, urethral discharge
Legionnaire’s Disease – a type of
pneumonia
Fever, chills, headache, NONPRODUCTIVE COUGH
buildings
Mycobacterium
leprae
Tuberculoid  Th1
response
NO GRAM STAIN
Lepromatous  Th2
response
Survives in macs.
contaminated
respiratory droplets
Need cysteine
for growth
 exotoxins
DETECT with an
ACID-FAST
STAIN
Tuberculosis
Intracellular Persistence
 Evades lysosomal fusion with
phagosome
 Catabolizes NO and ROS
 Activates Macs to produce IL-1, TNF,
IL-12 to form a granuloma
Tuberculosis
Primary TB
 Fever, night sweats, anorexia,
weakness, bloody cough
Secondary TB
Immunosupression triggers
reactivation, granulomas dissolve,
get TB again
Lepromatous
Rickettsia
NO GRAM STAIN
Obligate, intracellular,
aerobic,
GRAM NEGATIVE
COCCOBACILLI
Arthropod vector
Rickettsia rickettsia –
vector – tick
Resovoir – dog or
rodent
Virulence Factors
 Adherance: OMP A binds to
endothelial cells
Pathogenesis: due to destruction of
infected cells (endothelial) by bacteria
Rickettsia
prowazekii
Vector – louse
Resovoir – Human
Endemic Typhus (Prowazekii)
 Sudden fever, chills, headache,
myalgia, arthralgia, maculopapular
rash (trunk then to extremities)
 Myocarditis, stupor, delirium
Rickettsia typhi
Vector – flea
Resovoir - rodent
Treponema
pallidum
SYPHILIS
Gram-negative
Person-to-person
Sexual contact (STD)
Congenital (in utero)
Rocky Mountain Spotted Fever
(Rickettsii)
 Sudden Fever, then Chills,
headache, myalgia
 Rash on hands and feet and
spreads toward trunk
 widespread vasculitis – GI,
respiratory and renal failure, coma
and seizures
Outer Membrane Proteins
 minimal expression (100-fold less
than gram-negative bacteria)
 adherence to nearly all body tissues
Primary
 Painless, ulcerative lesion at site
of entry (chancre)
Gram-negative
 coat with fibrin to avoid phagocytosis
 also shown to bind Ig and complement
proteins as a “disguise”
Little ag exposure on
bacterial surface
(limited if any host
response initially)
Hyaluronidase
Gets into your
genitals, replicates
in epithelium
(PRIMARY
SYPHILIS)
Tertiary (5-20 years later – due
to a hypersensitivity reaction)
 Multiple organs develop
inflammatory lesions
Arteritis
Meningitis (with hallucinations
and psychosis)
- Gummas
Bacteremia to
lymphatics and
bloodstream
Spreads to heart,
brain, liver, bone
(SECONDARY AND
TERTIARY
SYPHILIS)
Borrelia
burgdorferi
SPIROCHETES
SPIROCHETES
7-20 periplastic flagella
VECTOR: Hard tick
Secondary
 Rash (trunk, palms of hands,
soles of feet), and flu-likesymptoms
 hepatitis
 arthritis
 nephropathy
 GI disease
Giemsa or
Wright stain
LPS is toxic
Peptidoglycan is inflammatory
Antigen can change, making for a
prolonged immune response
Lyme Disease
 Erythema migrans-annular
lesion with a clear or necrotic
center and a raised order
 neurologic and cardiac
symptoms
 arthiritis
CAN CAUSE CARDIAC SYMPTOMS
GRAM
+++++++
+++++++
BACTERI
A
GRAM
+++++++++
+++++BACT
ERIA
GRAM
+++++++
+++++++
BACTERI
A
GRAM
GRAM
++++++ ++++++++++++++
++++++ BACTERIA
++BACT
ERIA
GRAM
++++++++++++
++BACTERIA
Staphylococcus
Facultative anaerobe
Coagulase positive
– autoinfection,
direct contact,
contaminated food,
fomite
Catalase positive
Adhesion
 techoic acid binds to nasal epithelial
 Protein A binds to Fc portion to
prevent opsonization
S. aureus
 Furuncle (Boils) & Carbuncles
Lesions of hair follicles, sebaceous
glands, sweat glands
Mannitol Salt
Agar (MSA)
- it contains a
7.5% NaCL
which inhibits
growth of other
normal flora
Pyrogenic toxins
Enterotoxins
 Heat-stable superantigens resistant to
gut enzymes
- Micro dilution
or Disk diffusion
susceptibility
test – add
antibiotics and
see if it’s
susceptible
Beta, delta, gamma hemolysins
 Beta = degrades sphingomyelin
 Gamma = Combine with PV proteins
that lyse WBC
 Delta = disrupts cell membranes
 Impetigo
Forms large blisters and rupture
and crust
 Scalded Skin Syndrome (SSS)
– Ritters Disease
Causes erythema and epidermal
desquamation at remote sites from
staph infections
You see this in babies usually
Nonmotile
Irregular clusters
Bacteria gets into
mucus and skin,
replicates, and gets into
different types of tissue
causing necrosis of
tissue
S. epidermidis
(Opportunistic, from
indwelling equipment)
S. aureus (most
virulent)
S. saprophyticus (agent
of UTI)
Coagulase negative
– autinfection
LOOKS LIKE
GRAPES
Catalse positive
= STAPH
Toxic Shock Syndrome Toxin (TSST-1)
Superantigen – cytotoxic
Leukocidins
 Toxin that lyses WBC by forming pore
Exfoliatin – SUPER ANTIGEN
 A = heat stable, B = heat-labile
 Toxic Shock Syndrome
High fever, vomiting, diarrhea,
sore throat and myalgia – you get
this crazy rash everywhere
 Food poisoning
You ingest one of the enterotoxins,
NOT THE BACTERIA, and you get
BOTH cause desquamation of skin
Coagulase
positive = S.
aeureus
Novobicin
sensitive = S.
epidermidis
Novobicin
resistant = S.
saprophyticus
GAS (S. pyogenes)
Bacteria gets into
skin and mucus
membranes,
replicates, enters
lymphatics, and
release toxins and
enzymes which
causes necrosis in
tissues – possibly
SHOCK
GAS = Direct contact,
fomites, or
contaminated
respiratory droplets
MRSA –
MethicillinResistant S.
Aureus is on the
rise
Ag Detection
 Rapid
detection kit for
Group A Carbs
Culture
 Beta Hemolysis
 Bacitracin
sensitive
Enzymes
Coagulase
 Protects from phagocytosis
 binds to fibrinogen and fibrin
nausea, vomiting, and diarrhea.
Toxins are heat-stable so reheating
food does no inactive toxins.
SALTED MEATS< CUSTARD< ICE
CREAM< SALAD BARS
It’s explosive and fast
Hyaluronidase/staphylokinase
 Permits invasion of tissues
 dissolves fibrin clots
M protein/ Lipoteichoic Acids /
Protein F
 Adherance to nasopharynx and skin
epithelia
Streptodornase / Streptokinase
 DNase and Fibrinolysin to break up
PMS’s NET
Pyrogenic Exotoxin A, B, C
 Superantigens
 TSS and Scarlet fever are produced by
these
Diphopyridine Nucleotidase
 Lyse WBC
Streptolysin O & S – only need a little
Strepococcal Pharyngitis (Strep
Throat)
 Sore throat, fever, headache
 Tonsil, soft palate, and uvula are
red, swollen, and covered with
yellow exudate
Impetigo
 Small vesicle surrounded by
erythema on face or lower
extremities
 Enlarges, develops into a
pustule, and breaks into a form
crusted lesion
Erysipelas
 Spreading area of erythema /
edema (face), pain, fever,
bit
 O = Anaerobic Hemolysin
 S = aerobic hemolysin induces upon
bacteria exposure to serum
 BOTH DAMAGE TISSUE AND LYSE
PHAGOCYTES
lymphadenopathy
Strep TSS
 myalgia, severe pain,
necrotizing fasciitis, myonecrosis,
nausea, vomiting, diarrhea
Scarlet fever
 Buccal mucosa, temples, cheeks
are deep red
 STRAWBERRY TONGUE and
SANDPAPER RASH on chest
Acute Rheumatic Fever (ARF)
 3 weeks after strep throat – due
to recurrent infections Fever,
carditis, chorea, arthritis
GBS (S.
agalactiae)
LEADING CAUSE OF
SEPSIS AND MININGITIS
IN THE 1st FEW DAYS
OF LIFE
Bacteria gets into the
mucus membrane
and quickly spreads
to the lungs and CNS
Normal resident of GI
tract
GBS = Direct contact
with nasal secretions
or contaminated
respiratory droplets
Detect Group B
Ag in blood agar
Capsule can bind Serum Factor H to
inhibit alternative pathway for
complement
Beta Hemolysis
Bacitrant
resistent
Acute Glomerulonephritis (AGN)
 6 wks after strep throat –
lesions of glomerulii
Onset in first few days leads to:
Respiratory distress
Fever
Lethargy
Irritability
Hypotension
Pneumonia
Meningitis (5 – 10%)
If it gets into the CNS, there is a
20% mortality rate and a 20-30%
brain damage rate
S. Pneumoniae
Treat with PCV13
Bacteria get into
Gram-positive
Choline Binding Protein
Pneumococcal Pmeumonia
3RD LEADING
CAUSE OF
MENINGITIS
Gram-positive
diplococcic
vaccine –
Pneumococcal
conjugate vaccine
 Do this in children –
it’s conjugated to a
protein and it generates a
stronger immune
response
Pneemococcal
Polysaccharide Vaccine
(PPSV23)
 Do this in adults over
65. It’s only a
polysaccharide vaccine
so it only generates an
IgM response and isn’t as
strong
Bacillus anthracis
Aerobic or facultative
anaerobe
GRAM POSITIVE
Nonmotile
Spore-forming
Protein capsule
PREVENTION:
Anthrax Vaccine
Absorbed (AVA,
Biothrax)
 vaccine requires an
aluminum hydroxide
adjuvant
your lungs because
of impaired host
defense – smoking,
pollution, drugs,
alcohol. It
replicates, the
pneumolysin toxin
is released and it
causes DIC so you
die
B. anthracis
Direct contact with
spores through
spores
B. cereus and B.
subtilis
Cause infections of
the eye, soft-tissue
and lung associated
with
immunosuppression,
trauma, indwelling
catheters or
contaminated
medical equipment
diplococcic
Susceptible to
Optochin
 Binds phosphocholines of bacteria
with Carbs of nasopharynx
Capsule
 Prevents C3b opsoniation
 Blocks phagocytosis
Pneumolysin
 Directly cytotoxic to endothelial cells
(so it can disseminate into the
bloodstream)
 Impairs ciliary action
 Suppresses phagocytic activity
 Increases anti-inflammatory cytokines
(Like IL-10 and TGF-beta)
 Triggers platelet activation (Can cause
DIC)
Take skin lesion,
sputum, CSF or
blood specimen
and inoculate
onto blood agar
 get nonhemolytic growth,
gram positive
stain
Add penicillin and
you get a stringof-pearls kind of
look.
Protein capsule
 allows for adherence
Anthrax Toxin
PA (Protective Antigen) clusters ATR on
a lipid raft which then binds either to EF
(Edema Factor) which activates cAMP or
LEF (Lethal Factor) which cleaves
MAPKK pathway and leads to
macrophage and endothelial cell death
(Necrosis)
Endospore into lungs, intestine or skin,
replicates then spreads via macrophages
and lymphatics, spreads to different
tissues and causes necrosis
 A leading cause of pneumonia in
the world
 5 million children die each year
 Shaking chills, high fever, cough,
chest pain
Pneumococcal Meningitis
 One of the leading causes of
bacterial meningitis
 H. Influenza and N. Meningitidis
are the others
 Headache, stiff neck,
photophobia, irritability
Other infections
 Otitis Media
 sinusitis
 bacteremia
Cutaneous Anthrax
 Erythematous papule 
vesicular lesion  Ulcerative
lesion  Scab (Black Eschar)
Pulmonary Anthrax
Mild fever, nonproductive cough
which leads to respiratory distress,
causing cyanosis (alveoli die)
 Bacteremia can occur, it seeds
to every organ and you die.
Coryanebacteriu
m diphtheria
Facultative anaerobe
Club-shaped bacillus
GRAM POSITIVE
B. Cereus
Causes diarrhea
(cAMP)
Contaminated
respiratory
droplets
PREVENTION
DTaP vaccine
Anitmicrobials and
Diphtheria antitoxin
Swabs of nose or
throat
inoculated onto
Blood agar
(eliminate
Strep) and
Cystin-Tellurite
agar – should
form a black
colony
PCR for DTX
Listeria
monoctogenes
GRAM POSITIVE
Diptheria Toxin (DTX)
 encoded by a lysogenic phage
 B subunit serves as ligand for host
receptor
Inactivates EF-II and kills the cells
Bacteria in pharynx, larynx, or tonsils.
Replicates and resides in
pseudomembrane providing DTX.
Toxemia develops with necrosis of
heart muscle (MYOCARDITIS), liver,
kidneys, adrenals, neuronal and
endothelia (hemorrhaging)
Contaminated food
(unpasteurized
milk, ice cream,
raw vegetables,
cold cuts)
PALCAM agar
with a food
source
Internalin
Actin reorganization allows to move to
another cell.
Or
Double-Membraned Vacuole
Babies can get it
during
labor/delivery
Mueller-Hinton
Agar
- Gram +
- Catalase +
- Small zone of
hemolysis
Listeriolysin O
Degrades
endosome/phagosome/vacuole so it can
escape into cytosol and avoid being fused
with a lysosome
Diphtheria:
First, as an exudative pharyngitis
- Sore throat, low-grade fever,
malaise
Second, exudate on tonsils,
pharynx, and larynx evolves into a
pseudomembrane (necrotic
epithelia embedded in fibrin, RBC
and WBC, - active bacteria
Lymphodenopathy
Breathing obstruction
Myocarditis
Cardiac arrhythmia
Coma
Listeriosis
Nausea,
abdominal pain,
watery diarrhea,
fever
Can disseminate to CNS and
cause meningitis
Characteristic
S. aereus
S. epidermidis
S. saprophyticus
Color of Colonies
Often yellow
White
White to pale grey
Hemolysis
Most isolates
A few isolates
Non-hemolytic
Coagulase production
Yes
No
No
Mannitol fermentation
Yes
No
Yes
Novobiocin
Sensitive
Sensitive
Resistant
Characteristics
• Facultative Anaerobes; Nonmotile
• Blood agar is preferred because satisfies growth requirements and can differentiate groups based upon hemolysis patterns
• Catalase-negative (Staphylococcus catalase-positive)
• Classification by Group-Specific Surface Carbohydrate (which C-protein):
− Group A
(S. pyogenes) – Beta Hemolysis
− Group B
(S. agalactiae) – Beta Hemolyis
− Group C
(S. dysgalactiae)
− Group D
(S. bovis, Enterococcus)
− Non-Groupable
(S. pneumoniae, Viridans) – Non-hemolytic (S. pneumoniae is alpha-hemolytics)
• Classification by Hemolysis Pattern:
− Alpha
(Group D and Non-groupable)
− Beta – most destructive (Groups A, B, C, F, G)
− Non-hemolytic
(Some Group D and Non-Groupable)
Epidemiology
• Transmission – Direct contact, Fomites or Contaminated respiratory droplets (GAS); In utero or during birth (GBS); Direct contact with nasal
secretions or Contaminated respiratory droplets (S. pneumoniae or Pneumococcus)
•
Lancefield’s
Groups
•
Species
•
Sub-Types
•
Characteristics
•
Group A
•
S. pyrogenes
•
>80 subtypes based on M
protein
•
•
Beta-hemolytic
Highly pathogenic
•
Group B
•
S. agalactiae
•
5 sub-groups
•
•
Beta-hemolytic
Pathogenic for neonates
•
Group D
•
Enterococci, including E.
faecalis and E. faecium
•
•
Ungroupable
•
Viridans streptococci
•
•
Ungroupable
•
S. pneumoniae
•
•
•
•
Alpha, beta, or gamma hemolytic
Grow in 6.5% NaCl
Opportunistic
S. mutans, S. sanguis, S.
salivarius, etc
•
Alpha-hemolytic; often associated
with dental cavities and endocarditis
Smooth (capsulated) and
rough
•
•
•
Mostly alpha-hemolytic
Bile soluble, optochin sensitive
Highly pathogenic
Optochin
sensitive
Characteristic
bactitracent
Group A
Streptococcus
Group B
Viridans
Streptococcus
Enterococci
Streptococcus
pneumoniae
Streptococcus
Hemolysis in
agar
b
b
a
a, o, r, g
a
Growth in
6.5% NaCl
-
-
-
+
-
Bacitracin
sensitivity
+
-
-
-
-
Bile solubility
-
-
-
-
+
Optochin
sensitivity
-
-
-
1. 2nd most common cause of neonatal meningitis
a. E. Coli
2. Most common cause of UTI
a. E. Coli, mainly UPEC
nd
3. 2 most common cause of UTI
a. Klebsiella pneumonia
4. Most common cause of UTI from a catheter
a. Proteus mirabilis
5. #1 disease along with cystic fibrosis
a. Pseudomonas aeuroginosa
6. #1 most common cause of meningitis
a. Neisseria
7. #2 most common cause of meningitis
a. H. influenza
8. #3 most common cause of meningitis
a. Strep. Pneumonia
9. #1 most common cause of neonatal meningitis and sepsis in the first few days of life
a. GBS
10. Leading cause of pneumonia in the world
-
+
a. Step. Pneumonia
11. Most common cause of intra-abdominal infections
a. Bacterioides Fragilis
12. Most ubiquitous bacteria in hospitals
a. Pseudomonas Auerginosa
13. Oxidase Positive?
a. Vibrio, Brucella, Neisseria, Pseudomonas
14. Acid Fast Stain
a. Chlamydia
b. Mycobacterium
15. Forms spores?
a. Bacillus, Anthracis, Clostridium
16. Gram (+) Coccus
a. Staph
b. Strep
17. Gram (+) Bacillus
a. Bacillus anthracis
b. Clostridium
c. Corneybacterium diphtheria
d. Listeria
e. Mycobacterium tuberculosis
18. Gram (+) Anaerobes
a. Actinomyces
b. Clostridium
19. Gram (-) Anaerobes
a. Bacteriodes fragilis
20. Gram (-) Enterobacteriaceae NON-FASTIDIOUS
a. E. Coli – Facultative Anaerobe
b. Salmonella – Facultative Anaerobe
c. Shigella – Facultative Anaerobe
d. Klebsiella – Facultative Anaerobe
e. Yersinia – Facultative Anaerobe
f. Proteus – Facultative Anaerobe
g. Pseudomonas – Obligate Aerobe
h. Vibrio - – Facultative Anaerobe
21. Gram (-) Bacteria FASTIDIOUS
a. Coccus
i. Neisseria
1. Thayer-Martin
b. Coccobacillus
1. Bordatella
a. Bordet-Gengou
2. Haemophilus
a. Factor V and X (NAD and Hemin)
b. Chocolate Agar
3. Brucella
a. Reduces sulfur, nitrate
b. Chocolate Agar
4. Francisella Tularensis
a. Agars that contain cysteine
22. Gram negative has what for virulence?
a. Capsule
23. Where are E. Coli normally found?
a. Digestive tract
24. Where is Staph. Aeurus normally found?
a. The nose
25. What are obligate pathogens
a. Organisms always associated with disease
26. Are skin flora more gram + or gram -?
a. Gram +
27. Are internal flora more gram – or gram +?
a. Gram –
28. Anaerobes outnumber anaerobes by how much?
a. 100:1
29. What is an example of mutualistic relationship?
a. E. Coli synthesize Vitamin K and complex B vitamins. In return, we provide a warm, moist, nutrient rich
environment for E. coli
30. How can E. Coli be an opportunistic infection?
a. It can leave it’s normal home of the digestive tract and gets into the urinary tract and cause UTI infections
31. How Can S. aureus be an opportunistic infection?
a. S. aureus is commonly found in the upper respiratory tract, but if it gets into a wound it can cause problems
32. Which type of bacteria normally colonize the skin?
a. Gram positive bacteria
33. Which type of bacteria normally colonize the internal flora?
a. Gram negative bacteria
34. What is the ratio of anaerobes to aerobes?
a. 100:1
35. What are some beneficial roles of bacteria?
a. Stimulate the host immune response
b. Prevent adherence and colonization of pathogens
c. Produce vitamins
d. Produce substances which kill other bacteria
e. Stimulate the lymphatic tissue of GI tract
36. What are specific mechanisms of commensal bacteria that aid us?
a. Outcompete for space and nutrients
b. Secrete mucins that prevent attachment
c. Secrete metabolic products that inhibit pathogens
d. Produce antibiotic substances
37. What are the characteristics of Lactobacillus?
a. Gram (+), anaerobic
b. Found in mouth, stomach, intestines and GU
c. Used as probiotics
38. What are the factors that affect microflora location and composition?
a. Nutrients
b. Physical and chemical factors
c. Mechanical factors
d. Variation in age, diet, hygiene, stress
39. Major flora of the skin?
a. S. epidermidis
b. Propionibacterium acnes
40. What two species are important pathogens in implant-related infections
a. P. acnes and P. granulosum
41. Major flora of the anterior nares?
a. S. epidermidis
b. S. aureus
c. P. acnes
42. Major flora of the posterior nares?
a. Corynebacterium species
b. Strep. pneumonia
c. Haemophilus influence
43. Major flora of the saliva and oral mucosa?
a. Bacteria:
i. S. epidermidis
ii. S. aureus
iii. S. salivarius
iv. H. influenza
v. Lactobacillus
b. Yeast:
i. Candida albicans
c. Protozoa
i. Trichomonas tenax
ii. Entamoeba gingivalis
44. Major flora of the teeth
a. Streptococcus mitis, mutans, and sanguis
45. How do S. mutans stick to the surface of you teeth?
a. They convert sucrose to a polysaccharide and stick to the dental pellicle
46. What do S. mutans and Lactobacillus do to damage your teeth?
a. They metabolize sugars to lactic acid and cause cavities
47. What is the pathogenicity of S. sanguis?
a. They can enter the bloodstream from minor trauma and adhere to the heart causing endocarditis
48. Significant cause of peptic ulcers and gastritis?
a. Helicobactor pylori
49. What two categories of phyla compose most of the large intestine flora?
a. Bacteroidetes (Gram -)
i. Bacteroides (fragilis)
ii. Proteobacteria
b. Fermicutes (Gram +)
i. Bacilli
1. Peptostreptococci
2. Enterococci
3. Lactobacilli
4. Clostridia
50. What ratio of large intestinal flora determined obesity in mice?
a. Fermicutes/bacteroidetes ratio.
i. A higher bacteroidetes vs. fermicutes lead to weight loss
51. What is the normal vaginal flora ratio of anaerobes:aerobe?
a. 4:1
52. What is the most common cause of meningitis and sepsis in new newborns?
a. Women infected with Group B. Streptococcus
53. Full-term pregnancy, vaginal delivery, breastfeed
a. Bifidiobacterium
54. Full-term pregnancy, vaginal delivery, bottle-feed
a. Facultative and obligate anaerobes
55. C-section?
a. Coliforms
56. Premi?
a. BAD STUFF
57. Post-menopause?
a. Gram (-) increase and decrease in lactobacillus
58. Old?
a. Candida albicans
59. 4 Steps to a Gram stain
a. Stain with crystal violet
b. Precipitate
c. Decolorize with an alcohol
d. Counterstain with safranin
e. Purple = positive
f. Red = Negative
60. Coccus example
a. Staph (diplococcus)
61. Bacillus example
a. E. Coli
62. Spirillum example
a. Borrelia Burgoderfi
63. Vibrio example
a. Cholera
64. Coccobacillus example
a. Chlamydia
65. What is a plasmid that has integrated into the DNA?
a. Episome
66. What is conjugative plasmid
a. F plasmid
b. Encodes for genetics transfer enzymes and sex-pilis gene
c. This kind can be transferrable to other similar bacteria
67. What are non-conjugative plasmids?
a. Don’t code for transfer enzymes
b. Can be transferred to other similar bacteria only if the other bacteria already has an F-plasmid
68. What’s significant about plasmids?
a. They transfer antibiotic resistance, virulence factors, and can alter key antigens
69. What are 3 ways the plasmid can replicate?
a. On it’s own and get passed to a daughter cell
b. By fusing with the DNA and replicating that way
c. Replication for conjugation to pass on it’s plasmid to another bacteria
70. What’s important about the operon?
a. It’s essential for regulating the coding all the necessary genes for a given function
71. Pathogenicity island
a. A group of genes that coordinate their own control (Francisella tularensis)
b. They often are surrounded by transposon-like elements that encode for virulence properties
72. Inducible operons – positive or negative control?
a. Positive control – it’s silenced until the activator binds
73. Repressor operons – positive or negative control?
a. Negative control – It’s active until the repressor binds
74. How do you get genetic variability?
a. DNA mutations
b. Transposons
75. What is transduction?
a. The transfer of DNA between bacterial cells using a bacteriophage
76. What is Generalized transduction
a. Involves the lytic cycle, no integration, and there is no control over transferrable elements
77. What is Specialized transduction
a. Involves the lysogenic stage
b. There is an integration step
c. More control over where it’s inserted
78. What is transformation?
a. Bacteria eat dead bacteria DNA and the DNA incorporates into their DNA
79. Bacteria who can do transformation has what ability>
a. Competence
80. What are the four stages of bacterial growth
a. Lag phase
i. Cells are adapting to the environment and are no dividing
b. Log phase
i. Cells divide quicker than they die
c. Stationary phase
i. Cells die and duplicate at an equal rate
d. Decline phase
i. Cells die quicker than they duplicate
81. Bacteria that undergo aerobic respiration remove toxic oxygen byproducts by what enzymes
a. Catalase, peroxidase, SOD
82. Obligate aerobes
a. Require oxygen
b. Has catalase and SOD
83. Obligate anaerobes
a. Cannot grow in the presence of oxygen
b. Does not have catalase or SOD
84. Facultative anaerobes
a. Can grow with or without oxygen, but like oxygen
b. Has catalase and SOD
85. Microaerophiles
a. Can grow in little oxygen concentrations
b. Does not have Catalase or SOD
86. Aerotolerant Anaerobes
a. Oxygen doesn’t affect this organism
b. Does not have catalase, but does have SOD
87. Bacteria need iron for growth How do they get free iron?
a. Cytotoxins cause cells to release ferritin, and then hemolysins break up RBCs to release hemoglobin
88. How do PMN’s respond to the above question
a. They release lactoferrin to sequester iron again
89. Temperature and pH can affect bacterial growth, T/F
a. T
90. What are the five steps to bacterial suvivial
a. Colonization
b. Spreading Factors (Invasins)
c. Accessing nutrient sources
d. Production of endo and exotoxins
e. Escaping the host defense
91. How do bacteria spread – what three enzymes
a. Hyaluronidase
b. Collagenase
c. Streptokinase / Staphylokinase
92. What does Hyaluronidase do?
a. Attacks connective tissue and opens the extracllular matrix
93. What bacteria use this?
a. Strep, Staph, Clost
94. What does collagenase do?
a. Breaks collagen, especially muscle tissue
95. What bacteria uses this?
a. Clost. Perf
96. What do Licthinases do?
a. They degrade phosphotidylcholine in membranes
97. What kind of enzyme cleaves immunoglobulins
a. Proteases
98. What kinds of enzymes are used to escape PMN’s NETs
a. Nucleases and Catalases
99. Endotoxins are a part of Gram (-) cell wall that are released when a bacteria dies
100.
Exotoxins are a part of Gram (+) bacteria that are released and secreted
101.
Penicillin
a. Beta-lactam drugs
b. Interfere with peptidoglycan synthesis by preventing cross-bridge formations – blocks PBP (penicillin binding
protein) or transpeptidases
c. Penicillin G and V
d. Used for:
i. S. pyogenes (GAS), (Neiserria) meningococcus, pneumococcus
e. Disadvantages
i. Most bacteria now have Beta-lactamases
ii. Allergies
102.
Cephalosporins
a. Beta-lactam drugs
b. Does the same as penicillin, but it has a longer half-life and is more resistant to Beta-lactamases
c. Used for:
i. Gram (+) bacteria and bacteria resistant to penicillins
d. Disadvantages
i. Bacteria still have beta-lactamases
ii. Allergies
103.
Glycopeptide (VANCOMYCIN)
a. Complex glycopeptide that disrupts synthesis of peptidoglycan synthesis of Gram (+)
b. Binds to D-alanine of the pentapeptide side chain
c. Used for:
i. Super Beta-lactam resistant Gram (+) bacteria
d. Disadvantages:
104.
a.
b.
c.
105.
106.
a.
b.
a.
b.
c.
d.
107.
a.
b.
108.
c.
a.
i. S. Aeureus are beginning to have a plasmid to resist this.
ii. It’s damaging to the kidneys
Bacitracin
It interferes with bactoprenol for peptidoglycan synthesis
Used for:
i. Skin infections by Gram (+) bacteria, usually Staph and GAS
You find this in Neosporin
Polymyxins
Cyclic polypeptides that insert into membranes and dissociate LPS and phospholipids in Gram (-) bacteria
Used for:
i. External ear, eye, and skin infections
Tetracyclines
Reversibly bind to 16S of 30S ribosomal subunit
Bacteriostatic
Used for:
i. UTI, eye and respiratory infections caused by Chlamydia, mycoplasma (pneumonia), rickettsia
(fever)
ii. Spirochetes infections (Borrelia and Treponema), Yersinia, brucellosis, and tularemia
Tetracycline and Doxycycline
i. Better GI absorption and longer half-life
ii.
Amingoglycosides
Irreversibly binds to 30S subunit by inserting incorrect amino acids
i. Bacteriocidal
Treats severe Gram +/- bacteria
i. Strep, E. Coli,
Streptomycin, Kanamycin, Gentamicin
Macrolides
Reversibly binds to peptidyl transferase of 50S subunit and inhibits protein elongation
i. Bacteriostatic
109.
110.
111.
112.
b. Used for:
i. Staph, strep, chlamydia, corynebacterium (diphtheria), Treponema, Borrelia
ii. DOC for mycoplasma, Legionella, Bordatella,
iii. Erythromycin, Azithromycin, Clarithomycin, Roxithromycin
Clindamycin
a. Binds reversibly to peptidyl transferase and can bind to charged tRNA to block elongation
i. Bacteriostatic
b. Used for:
i. Staph and Strep, Anaerobic Gram (-) bacteria
Quinolones (Fluoroquinnolones)
a. Inhibits the action of bacterial DNA topoisomerase (DNA Gyrase)
b. Used for:
i. Broad spectrum of Gram +/- bacteria
ii. DOC for UTI cause by E. Coli and enterobacteria
c. Ciprofloxacin, Levofloxacin, Moxifloxacin
Sulfonamide
a. Antimetabolite drug
b. Competes with PABA to block synthesis of folic acid
c. Mammals do not synthesize folic acid so low sideeffects
d. Used for:
i. UTI of gram-negative
ii. Otitis media (pneumococcus)
iii. Chronic bronchitis (pneumococcus)
iv. Shigellosis
v. Traveler’s diarrhea
e. Sulfamethoxazole, sulfanilamide
Trimethoprim
a. Inhibits DHRP to block synthesis of folic acid
b. Combined with Sulfamethoxazole
CIPRO for UTI (Quinolone)
Erythromycin (MACROLIDE) for A-typical pneumonia for mycoplasma