Download Bacteria Strain Disease Clinical Manifestations Mode of

Neisseria spp: Diplococci (aerobes), grows in a Thayer Martin agar (5% chocolate agar antibiotics for growth) and oxidase
posititve. (gram negative bacteria) Use attachment pilus (OPA), Porin protein (POR) and lipoligosaccharide to affect organism
Bacteria
Strain
Neisseria
Gonorroheae
Neisseria
Meningitidis
Disease
Clinical
Manifestations
Gonorrhea Males: ureteral
discharge and
dysuria (usually
colored thick
pus)
Females:
cervical
discharge and
dysuria and
severe pain.
Meningoco Initially mild
ccal
pharyngitis,
Meningitis sudden
headache, fever,
vomiting, stiff
neck(CNS fluid
build up) which
can cause rash
and then
necrosis
Mode of
Transmission
Sexual contact
Risk
Groups
South
east
African
America
n
14-24 y
Site of
Infections
Penis and
vagina
Mechanisms of
Disease
The damaged
mucosa allows for a
entry point and will
replicate here and
spread on this
epithelia tissue into a
bacteremia to the
skin and to the joints.
Contaminated
respiratory
droplets
<5years
CNS
Coughed out and
then breathed in and
replicates in the
nasopharyngeal
epithelium and
releases as a
bacteremia to the
lungs where you
become infectious (in
the lungs little
replication) then you
cough it out and
that’s where it can
affect the joints, CNS
and heart.
Gram Negative Bacteria coccobaccilus
Bacteria
Strain
Disease
Clinical
Manifestations
Catarhal (1-2 weeks):
mucoid rhinorrhea,
nasal congestion,
sneezing
Paroxysmal: intense
bouts of coughs
Convalescent:
persistent cough
Meningitis:
pharyngitis (first
symptom), headache,
stiff neck, fever.
Mode of
transmi
ssion
Resp.
droplets
Risk
groups
Site of
infectio
n
Lungs
Mechanism of Disease
Direct
contact;
contamin
ated
repertor
y
droplets
Unvaccinat
ed young
children
Lungs
joints,
brain,
skin
The bacteria colonize in the
nasopharynx and will replicate in the
lungs and the bacteremia will spread.
Hib capsule (ribose, ribitol,
phosphate PRP) and anti PRP
response for clearance.
*needs blood agar with hemin (x
factor) and NAD.
It goes into the mucosa or the skin
where it will begin to replicate in
these locations local macrophages
and dendritic cells. Then will go into
the lymph as a bacteremia and affect
other tissues. It enters through the M
cell and are directed to the ER and
replicate there
Enters through bite then replciates in
Macs/CD usually doesn’t spread.
Causes Macs to undergo apoptosis.
Bordetella
pertussis
Whooping
cough
Schools
homes
Haemophilus
(normal flora
not
encapsulated
)
Influenza
e
Meningitis
Epiglottiti
s
Celluaritis
and
Arthritis
Brucella
Spp
Brucellosi
s
Acute (1-2wks): flu
like
Undulant (disease):
fever, drenching
sweats and other
issues
Through
infected
animals
or
contamin
ated
foods
Farmers
Liver,
spleen,
bone,
heart
Fracisella
Tularensi
s
Tularemia
UGD: fever, headache,
chill, malaise, pain in
involved areas (bites)
lesion
ulceratesnecrotic
Ticks
and
rabbits
Hunters in
summer
(tick)
rabbit in
winter
Localize
d at bite
site
It attaches to the lungs and replicates
by FHA, P69 and PTX causing no
ciliary action and increase cAMP. Cell
debris + increase mucus +no ciliary
action= cough
Gram Positive anaerobes, faculatative or strictly anaerobic
Bacteria
Strain
Disease
Clinical
Manifestation
Mode of
Risk
Transmission group
Site of
infection
Mechanism of Disease
Actinomyces
(facilitative,
anaerobic)
spp
Actinomyc
osis
Endogenous
spread teeth
Teeth
Form delicate filaments
on the tooth and use
gialdiase onto attach and
invade on oral surfaces.
Clostridium
(anaerobe,
mobile,
spores)
botulinum
Botulism
Clostridium
(anaerobe,
spores) flora
difficile
Pseudome
mbranous
colitis
Boutulinum toxin A,B,E
block neurotransmitters
from binding and break
cleave snare proteins
which doesn’t allow
acetylcholine to be
released lack of muscle
contraction
Using A toxin to disrupt
tight junctions and B
toxin which is cytotoxic
and its detected in the
stool (ampicillin and
clindamycin)
Clostridium
(anaerobe,
motile,
spores)
Perfringens
Gas
gangrene
or
Clostridial
food
poisoning
Chronic
gramulomatous
lesions, colonies of
sulfur granules,
infections mostly
cervicofacial
18-36 hours:
weakenss, dizziness,
expressionless face
progressive: nausea,
vomiting, inability to
swallow, loss of
speech, respiratory
paralysis
Normal flora in % but
when they go wrong it
is in the hospital.
Associated with
antibiotics.
Inflammation on
mucosal surface
Severe pain at
woundedema
discoloration stinky
Incubation 8-24
nausea diarrhea (no
fever)
Spore
ingestion from
contaminated
foods or direct
contact
Infants or
foodborne
Intestines
and
travels to
CNS
Spores
Hospital
Intestines
Direct contact
with spores
(open wound)
or ingestion
(replicates in
intestine/skin
(deep tissue)
Soil
Open
wounds
intestines
Enterotoxin attaches and
increase Ca2+, theta
toxin forms pores (heart)
and alpha phospholipase
dissolves cell membranes
of RBC,WBC/muscle
Gram positive (clostridium) Gram negative anaerobic bacteria (bacteriodes) weak to no gram stain
Bacteria
Strain
Disease
Clinical
Mode of
Risk
Site of
Manifestation
Transmissio group
infection
n
Clostridium
(last gram
positive)
tetani
Tetanus
Bacteroides
(gram
negative,
anaerobic,
LPS w/o
activity)
fragilis
Chlamydia
(does not
gram stain
needs host
ATP)
Trachomatis
Trachoma
urogenital
infection
Legionella
(Gimenez&
Dieterle
silver stain)
Pneumophila
Ligionnaires
disease
Early (4-5d)painful
spasms then
lockjaw.
Progressive
violent spams and
respiratory causing
death.
Abscess formation
causing
intraabdominal
infections
Direct
contact with
spore into a
wound
People of
soil
Skin
(endospore
replicate
and
produce
toxin)
Via capsule
binding on
surfaces
Sterile
sites
usually
(wrong
place at
wrong
time)
Skin
Follicular
conjunctivitis,
corneal scarring,
blindness
Urtheritis or
cervictisi, dysuria,
thin urethral
discharge
Fever, chills,
headache, cough
(75%) non
productive
Direct
contact with
contaminated
secretions
Inhalation of
airborne
microbes
Epithelia of
eye vagina
or penis
Travelers
Lungs
Mechanism of Disease
Tetanospasmin binds &
degrades synaptobrevin
(docking site) which
causes continuous
muscle contract by
blocking GABA and
glycine release.
Adhesions, short chain
fatty acids (inhibit phag)
enzymes (catalase, SOD
tolerate o2, cytotoxic for
tissue destruction).
Toxin is heat labile zinc
metalloprotease damages
epithelium
EB (metab inactive but
infectious) enter host
and prevent lysosome
fusion. EBRB and
these are meta active and
will replicate and
explode.
Uses virulence (peptide
toxin inhibits resp. burst,
catalase and exotoxins)
attacks Macs in summer.
Bacteria
Strain
Disease
Clinical
Manifestation
Mode of
Risk
Transmission group
Site of
infection
Mechanism of Disease
Mycobacteri
um (aerobe,
acid fast
weak gram
stain)
Leprae
(form
tuberculoid
Th1)
Tuberculosis
Th1 : granulomas
primary tb
(clinical) fever,
night sweats etc or
secondary 10%
latent immunosup.
Shows up again
Contaminated
respiratory
droplets
(viable for
hours)
People
of soil
Intracellular persistence
it evades lysosome fusion
and catabolizes NO and
ROS. Activates macs
IL1/TNF,IL12 forms
granuloma
Mycobacteri
um
Leprae (Th2
lepromatous)
Respiratory
droplets
People
Rickettsia
Rickettsia
(rocky
mountain
spotted fever)
Rocky
mountain
spotted
fever
Tick bite
Reservoir:
dog/roden
Skin
Rickettsia
(aerobic,
gram –
coccobacilli)
prowazekii
Epidemic
typhus
Erythematous
macules, papules
or nodules,
extensive tissue
destruction and
foamy
macrophages.
Abrupt onset of
fever, chills
headache myalgia
(2-12) rash from
heads and to trunk
Sudden fever,
chills, headache,
myaligai
maculopapular
rash
(trunklimbs)
Lungs
reactivates
in the CT,
epithelial,
muscle,
nervous
(bacteremi
a)
Skin/lungs
Bite from
louse the
reservoir is
humans
Skin
Ahderance by Omp A
binding to endothelial
cells then pathogenesis
due to destruction of
infected cells by bacteria.
Ahderance by opma A
binding to endothelial
cells (destruction of
cellsdisease)
Inhibit TLR expression
enhance phag, bacterial
growth and instruct
adapative humoral
response (IL-4/IL-10)
(weak cell response)
Spirochetes
Bacteria
Strain
Disease
Clinical
Manifestation
Mode of
Risk
Transmission group
Site of
infection
Mechanism of Disease
Treponema
(spirilla,
gram -,
cannot be
gown in
vitro)
manifestatio
n due to host
inflame
response.
pallidum
Syphilis
Sexual contact,
or congenital
(in utero)
Fetuses,
sexually
active
Geneitals
CNS
Little Ag exposed (little
response) outer
membrane proteins have
minimal expression and
adhere to all body tissues
and coated to avoid
phagocytosis. Use
hyalurodiase to break
down cells
Borrelia
(Giemsa or
Wright stain,
large many
flagella no
either – or +
burgdorferi
Lyme
Disease
Primary: 2-6 wk
incubation/dur.
Painless
2 (6wk-6mo inc. 2
wk dur.): rash
(trunk palms soles)
flu
Teritary (5-20 yrs)
multiple orangs
develop gummas,
arteritis,
menintgitis
Erythema migransannular lesion with
clear or necrotic
center and raised
red border,
neurologic and
cardiac symptoms,
arthritis.
Third ticks
from
mice/deer
Humans
Whole body
Capable of antigen
variation, antigenic
modulation. The cell all
contains a toxic LPS
different form other
bacteria endotoxin and
the peptidoglycan has
other inflammatory
properties.