Beruflich Dokumente
Kultur Dokumente
Cell
Features Features
Staph Aureus
Gram (+)
Cocci in
grape
cluster
1 u in
diameter
Staph.
Epidermis
Gram (+)
Cocci in
cluster
1 u in
diameter
Small, 28mm
Yellowgolden
opaque,
Beta
hemolytic
Colonies on
blood agar,
facultative
anaerobic,
37C
Small, 2-8
mm
White
(opaque),
Round,
Gamma
hemolytic
colonies on
blood agar
(No
hemolysis)
Staph.
Saprophyticus
Gram (+)
Cocci in
cluster
1 u in
diameter
Lab
Characteristics
Source &
Transmission
Virulence Factors
(disease causing)
Associated
Diseases
Host
Defenses /
Immunity
Treatment /
Prevention
Non-motile
- Catalase (+)
- Coagulase (+)
- Dnase (+)
-Mannitol (+)
- EXOTOXINS
- Cytoxins alpha, beta,
No long term
immunity
therefore
recurrent
infections
possible
Methicillin
Tellurite reduction +
(black colonies),
Localized Infections:
skin infections
- Folliculitis (plug hair)
- cellulites
- Impetigo (vesicular
lesion), Furuncle,
Scalded Skin Syndrome
(Ritters Disease), Toxic
epidermal necrolytic
TEN disease
Systemic Infections:
Food poisoning, TTSS,
Osteomyelitis, Infective
(septic) Arthritis, Acute
Bacterial Endocarditis,
Post-viral Lobar
Pneumonia (empyema),
Bactermia and Sepsis
Beta Hemolytic
Growth, presence of
7.5% NaCl
-Sens.Novabiocin
- Catalase (+)
- Coagulase (-)
- Dnase (-)
- Mannitol (-)
- Gamma
Hemolytic
Growth in presence
of 7.5% NaCl
-Sens.Novabiocin
Urease (+)
- Catalase (+)
- Coagulase (-)
- Dnase (-)
- Mannitol Var
Depending on
strain, Growth in
presence of 7.5%
NaCl
- Resistant to
Novabiocin,
- Urease (+)
- Enterotoxins
- toxin A (foodpoison)
- toxin B, entercolitis
(superinf)
- emesis (vomit)
- Toxic ShockS Toxin
- exfoliatin
- Colonize human
skin & mucus memb
- Normal Flora of the
skin
- May cause disease in
immunocompromised
patients following
trauma,also iatrogenic
intro, or by IV needles
Spreads by
hematogenous route
- COAGULASE
- Protein A (opsina. Attack
bacteria)
- Polysaccharide A
- Staph. Decomplementation
on antigen
- Var Enzym (Spread Fact)
- lipase, protease,
hyaluronidase, Nucldease,
DNase (staphylodornase),
staphylokinase (break fibrin)
Systemic Infection:
- Bacteremia & sepsis
- Subacute bacterial
endocarditis
Vancomycin (if
MRSA)
Bacitracin
(topically)
CD4+ T-cells
release
cytokines
Surgical
debridement
Opsonization
by IgG, etc
Drainage of
wound
- No
immunity
against
previous
infection
Vancomycin
(organism is
resistant to most
others)
- Intact skin is
important
defense
- CD4 + TCells release
cytokines
Exopolysaccharide
glycocalyx
(SLIME LAYER) sticks to
heart
Multiple drug resistance
Colonizes human
genitourinary, skin
(urogenitory) tract,
Penicillin resistance
Hemagglutinins & other cell
surface proteins may mediate
Mucous membranes
(lesser extent, GI)
Attachment to epithelial
cells
Opsonizat
IgG,
No immunity
against
previous
infection
CD4+ T-Cells
release
cytokines
Opsinization
by IgG
TrimethoprimSulfamethoxazole
(bactrim)
Strep
Pyogenes
Group A
Cell
Features
Colony
Features
Source &
Lab
Characteristics Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment
/
Prevention
Gram (+)
Non-motile
Human skin
* Hyaluronic acid
Mucous
membranes of
oropharynx (515%) & vaginal
tract
Intact skin is
defense
Catalase (-)
* Skin infection
* Impetigo (streptococcal
pyoderma)
Active
infection use
Penicillin G
or
erythromycin
Cocci in
chains
1 u in
diameter
Beta
hemolytic
Dnase (+)
Beta Hemolytic
No growth > 6.5%
NaCl
Sensitive
bacitracin
Transmitted by
respiratory
droplets from
contaminated food
Cross-reactive
AB ==> ARF.
Ag-ab
complexes ==>
AGN. Look
presence of
antibody to
Streptolysin O
and
streptodornase
Bacitracin
cream (GAS
susceptible,
other Strep
are not)
Strep
agalactiae
Group B
Cell
Features
Colony
Features
Lab
Source &
Characteristics Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Gram (+)
Small, graywhite,
round
Non-motile
Human skin
Beta
hemolytic
Mucous membranes
of vagina, male
urethra, throat, GI
tract
IgG to capsule
Catalase (-)
Capsule: polysaccharide
Type III capsule is composed
of sialic acid (serum
resistance)
Ampilicillin
plus
aminoglycosides
for infants
Cocci in
pairs
1 u in
diameter
Infects newborns
during birth
(Puerperal fever)
Hemolysin
Neonatal pneumonia in
utero infection
Post-partum endometriosis
(puerperal fever)
Immunocompromised leads
to pneumonia, septicemia,
prosthetic disease,
puerperal sepsis, skin
infection
Urinary tract infections
PMN attack
strep
Penicillin G for
adults (*
pregnant to
carry GBS)
Vancomycin for
Penicillin
sensitive
patients
Vaccine, Pen. G
develops
protective IgG
cross placenta &
protect fetus
Cell
Colony
Features Features
- Strep bovis
Gram (+)
- Enterococcus
faecalis
Pairs and
chains
Group D
1 u in
diameter
Lab
Source &
Characteristics Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Small, graywhite,
round
Non-motile
Bacteremia: S. bovis
invades blood via GI route.
Ab important
and PMN can
attack Strep.
variable
hemolytic
response
variable
hemolysis
Penicillin G for
S. bovis,
vancomycin
for Pen.
Sensitive
patiens.
Catalase (-)
bile-esculin
(black ppt)
Enterococcus
grows at 6.5%
NaCl (+, present)
Group D, S Bovis
Strep are (-, not
present)
Does not grow in
manitol!
Enterococci colonize
at the GI tract.
Commensals at the
genitourinary tract
Infection ==> blood
(GI to GU tracts)
S. Bovis found in GI
tract
E. faecalis: use
combination of
vancomycin &
aminoglycoside
Strep
pneumoniae
(pneumococcus
or diplococcus)
also part of S.
mitis
(No Group b/c
lack C cell
wall antigens
NO Lancefield
group)
Cell
Features
Colony
Features
Lab
Source &
Virulence Factors
Characteristics Transmission
Gram (+)
Non-motile
Pairs and
chains
(diplococci)
Lancet
shaped
1 u in
diameter
Grows better
in C02
(capnophilic)
Catalase (-)
alpha
hemolytic
Encapsulated
colonies
(smooth)
Nonencpasulated
are (rough)
Encapsulated
cell
alpha hemolytic*
(via pneumolysin
activity)
(+) for bile
solubility (10% Na
desoxycholate)
Sensitive for
optochin (ethyl
hydrocupreine)
induce lysis of S.
pneumoniae
(+) for inulin
fermentation
Autolysis
(amidase
activity)
Inf. Indicate
excess # of alpha
hemolytic
colonies on blood
agar plates w/
neomycin.
Naturally
competent
Quellung
Neufield Rxn
(swelling)
Colonizes
human upper
respiratory tract
(commensal)
People
susceptible to
viral infection,
allergy
malnutrition,
alcoholism,
debilitation,
ciliary motion
==> aspirate into
lungs
Sickle cell
anemia disease
Age related
Spread by
droplet nuclei
S. Pneumonoccus
Cell lyses
Cell lyses
Host
Defenses &
Immunity
Treatment /
Prevention
Lobar Pneumonia *: in
adults & sickle cell
anemia patients.
Symptoms:
- fever, productive cough,
dull chest percussion, Xray dxn. Maybe fatal
Diagnosis:
- Large # of strep & PMN
in sputm. Often sequela
to viral infection,
alcoholism, & smoking
(all disrupt fxn of cilia)
Antibodies
against capsule
offer typespecific
resistance
Multivalent, 23
most common
capsular ag
vaccine confers
immunity for a
few years
Pneumolysin
in high
concentration
leads to
activation of
complement
Meningitis *: in adults.
Results from bacterimia,
sinusitis, or otitis media,
skull fracture, other
injury.
Symptoms:
- fever, stiff neck,
headache, maybe fatal
Diagnosis:
-lumbar puncture,culture
Sinusitis *: Often sequela
of allergy, or viral infect
prevents drainage
Otitis media *: Often
sequela of allergy, viral
infection prevents
Eustachian clearance
Bacteremia (30% in
pneumonias) & 80% in
Menigitis
*common causative agent
* can be beta hemolytic if grown anaerobically but usually considered as alpha hemolytic
Viridans Strep.
Not sensitive (resistant)
Not sensitive (resistant)
Test
Bile soluble
Optochin
Associated Diseases
Penicillin G
(sulfonamides)
Vancomycin
for penicillin
sensitive indv,
but
vancomycin
NOT effective
for meningitis
b/c doesnt
penetrate the
BBB
(vancomysin
doesnt work
w/ meninges)
Viridans
Streptococci
Group
includes S.
Mutans, S.
Mitis, S.
Salivarius, S.
Sanguis
Cell
Features
Colony
Features
Lab
Source &
Virulence Factors
Characteristics Transmission
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Gram (+)
Non-motile
Subacute bacterial
endocarditis common
causative agent, from
dental work &
bacteremia. Infects heart
valves & prosthetic
devices
Bacteria killed
by host
immune system
(antibodies &
complement)
Penicillin G
and
aminoglycoside
before dental
surgery w/
patients w/
heart
conditions.
Vancomycin
for patients
allergic to
penicillin.
Pairs or
chains
1 u in
diameter
alpha
hemolytic
Organisms are
normal flora of
oropharynx
(commensal)
Infection caused
by bacteremia
following dental
work. Can be
present in GU
tract and can
lead to UTI
Dextran Glycocalyc
(exopolysaccharide):
adherence to defective heart
valves, block penetration of
antibiotics. Forms via
GLUCOSE metabolism
Lipoteichoic acid: mediates
adhesion to fibronectin in
blood clots on defective heart
valves
Glucan polysaccharide :
produced by S. Mutans from
SUCROSE in mouth thereby
allowing attachment of
bacteria to tooth enamel.
Acids (lactic acid)
Patients w/
heart
conditions are
at risk of
complications
Bacillus
Anthracis
Cell
Features
Colony
Features
Source &
Virulence Factors
Lab
Characteristics Transmission
Gram (+)
Catalase (+)
Rod, boxcar
shaped
Pairs or
chains
NONMOTILE
Aerobic
Endospores
(ex. from
soil)
Spores
resistant to
heat,
chemicals,
dryness, UV,
spore coat
contains
dipocolinic
acid & Ca++,
low water
content
10 x 3 u in
diameter
medusa head
colonies
rough w/
irregular
edges
NONHEMOLYTIC
Capsule
induced in
presence of
5% CO2 ==>
colonies
appear moist
Non-hemolytic,
NON-MOTILE
can stain
polypeptide
capsule w/
methylene blue
Associated
Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Ab against
polypeptide
capsule.
Vaccine for
humans confers
short-lived
immunity (require
annual boosting)
composed of
extract from a
virulent but NONENCAPSULATED
anthracis
Organism
(spores)
normally found
in soil.
Capsule: POLYPEPTIDE
composed of DGLUTAMATE (NOT
polysaccharide!)
Cutaneous Anthrax:
round necrotic black
ulcer (ESCHAR) on
skin, painless.
Reservoir for
spores are
herbivores,
contaminated
animal hides &
dust-laden,
spore-laden
articles.
Transmission
occurs when
host contacts
infected animals
/ products,
inhales or eats
spores. Spores
can also enter
via skin wounds
or abrasion.
Capsule is anti-phagocytic
ZOONOTIC
infection
associated w/
cattle
Septicemia: B.
Anthracis septicemia is
rare in humans
Respiratory anthrax
(Woolsorters Disease)
pneumonia following
inhalation of spores
from infected wool,
rare, but fatal. Has a
latent period > 2
months. Can hide in
lung macrophages
GI anthrax: ingest of
meat contaminated w/
spores. Mortality
~100%
Ab to PA
prevent
binding of LF
and EF to PA.
If no ab, no
time for
immune
response.
Antibiotics:
- penicillin G
- sulfonamides
(sensitive patients)
- erythromycin
- ciprofloxacin &
doxycycline
(PROMPT
treatment!)
Immunize all
uninfected animal
herds!
Bacillus Cereus
Cell
Features
Colony
Features
Source &
Virulence Factors
Lab
Characteristics Transmission
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Large
Gram (+)
rods in pairs
or chains
Large
granular
colonies on
nutrient agar
MOTILE
CHINESE
RESTAURANT
syndrome
Unknown
MOTILE
Mesophilic &
nutritionally
require
amino acid
supplements
Fluid &
electrolyte
replacement if
necessary. No
other
medication.
Aerobic
Endospores
centrally
located
(metacentric)
AEROBIC
Biotyping not
used
Vegetative cells
& spores
normally found
in soil, dust,
decaying
organic matter
also in rice,
meat products
Non-invase inf.
Occurs when
bacteria and/or
spores ingested.
Spores survive
cooking &
germinate ==>
produce toxin &
ingest preformed toxin
(food
intoxication)
Two Enterotoxins:
- Necrotic toxin: heat-labile
toxin (LT) that stimulates cells
adenylate cyclase. Causes
diarrhea
- Heat-stable enterotoxin (ST)
acts by diff. mechanism than
LT, leads to vomiting but
not to diarrhea
Endospore formation:
surivival in harsh conditions.
Germination requires oxygen
Lecithinase (phospholipase C)
enzymes active on cell
membranes (associated w/
ocular infection)
Cereolysin (potent hemolysin)
& Necrotic toxin (associated
w/ ocular infection)
Vancomycin
for eye
infections.
Multiple drug
resistance
Corynebacterium
Diphtheriae
Cell
Features
Colony
Features
Source &
Virulence Factors
Lab
Characteristics Transmission
Associated
Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Slender
Pleomorphic on
SERUMTELLURITE
Agar (blackgray colonies
indicate
tellurite
reduction), the
differences are
NOT correlated
w/
pathogenicity
Loefflers
coagulated blood
serum medium,
stain w/
methylene blue
or toluidine blue
to look for
metachromatic
granules,
Respiratory diphtheria
Non-invasive therefore
non-systemic (localized)
infection => intoxicat
==> pseudomembrane
in throat due to inflame.
Response.
Peptide B may
develop in
patient, but
development
maybe slow
Vaccine consist
of formalininactivated
(TOXOID) is
given as part of
DPT vaccine to
children.
Gram (+)
Club shaped
pleomorphic
rods
1.6 u long x 0.5
u wide usually
in L or V
shaped
Chinese letter
clumps
(palisades)
Cells contain
metachromatic
phosphatecontaining,
inclusion
body for
energy storage
VOLUTIN
granules
which are lost
when cultured
in vitro.
Non-motile,
aerobic
C. Diphtheriae
- gravis: large
black colonies
- mitis: small
black colonies
- intermedius:
large gray
colonies
C. Diphtheriae
is very
sensitive to
sunlight, soaps,
desiccation, &
antibiotics
Catalase (+)
Tellurite
reduction
Iron requirement
In vitro test is
ELEK test, test for
TOXIN ex.
CardioToxin
(+) test indicates
ab-ag ppt toxin
(form precipitin
line as in double
diffusion /
Ouchterlongy
assays)
In vivo test use
guinea pig skin
test ==> (-) then
no redness
Humans are
only reservoir
for C.
diphtheriae.
They maybe
considered
normal skin &
upper
respiratory tract
flora
Horizontal
transmission
occurs by
respiratory
droplets or via
contaminated
skin lesions in
cutaneous form
Pseudomembrane can
occur regardless of
whether strain is
toxigenic or not
Intoxication: systemic
effects of toxin ==> heart
toxicity ==> myocarditis,
arrhythmias, kidney
damage, neurological
toxicity
Diagnosis must be fast
and is based on clinical
symptoms. Toxin-cell
interaction irreversible
& antibodies are
ineffective once toxin is
bound
Start to see endocarditis
w/ non-toxigenic strains
Cutaneous diphtheria
infects open wounds
Gray pseudomembrane
on non-healing wounds
Schick skin test test for
protective antibodies
(-) test: when diluate
toxin is injected , no
redness on skin
(+) test: redness lack
immunity
DT toxin too
small in
amount to be
antigenic in
natural
infection
Booster to
confer longterm protection
10 years
Serum sickness
used to test
hypersensitivity
, too many
doses
Penicillin G
used to kill
organism.
Erythromycin is
a substitute
Diphtheroids
refers to all
NONpathogenic
Corynebacteria.
Facultative
anaerobes.
They are
opportunistic
Elek test to diff.
diphtheroids
from toxinproducing C.
diphtheriae
Anerobic
Corynebacteria
(propionbacterium)
Description
Treatment / Prevention
Coryne-bacterium
Minutissimum
Organism grows on skin areas with high moisture (ex. skin folds)
(Foot Associated
diphtheroid!)
Superificial infection w/ this organism ==> ex. Athletes Foot w/ scaly plaques especially
btw toes. Not pus forming and is called ERYTHRASMA
Listeria
monocytogenes
Cell
Features
Colony
Features
Lab
Characteristics
Source &
Virulence Factors
Transmission
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
- Gram (+)
Pleomorphic
& translucent
on blood
agar
Catalase (+)
Organism found
in dust, soil,
water, sewage,
unpasteurized
milk, poultry, &
vegetables
Abortions: pregnant
women (due to cell
mediated immunity) are
prone to listeriosis.
(Spont. Abortions!)
T Cellmediated
immunity
combats
intracellular
listeria.
Listeria induces
infected
macrophages
to secrete IL-12
which
promotes T
Cells to
differentiate to
TH-1. TH-1
cells produce
IL-2 & gamma
interferon.
Keep pregnant
females away
from listeriosis
patients.
Tetracycline is
a drug of
choice, or
erythromycin
Pen G or
ampicillin kills
organism
- coccobcilli
or short rod
(pleomorphic)
usually in
clumps or
short chains
Aerobic
Tumbling
motility 22C
& non-motile
@ 37C
Facultative
INTRACELLULAR!
No spores!
Small zone
of beta
hemolysis
Cold storage
4C on bloodcontaining
media helps
to enrich for
Listeria
B hemolysis (+)
Tumbling
motility 22C
Widespread
among animals
& humans in GI
tract, female
genital tract &
throat.
Vertical
transmission:
transplacental or
during birth
Zoonotic
transmission:
animal contact
or ingestion of
contaminated
foods
Activation in
carriers who
become
immunocompromised
Listeria infects
macrophages &
epithelial cells
Listeriolysin O (LLO)!!!!!!:
mediates escape of organism
from phagosome. Found in S.
Pneumonia
Membranolytic activity is
enhanced by low pH & low
iron (phagosome bacteria)
Toxin is hemolytic (leads to
hemolysis) Similar to
Streptolysin O (pneumolysin
& tetanolysin) Lyse vacuole
membranes of macrophage,
monocyte and epithelial cells
Actin tail: acquires a tail
made of actin filaments
directs the bacteria ==> cell
surface to infect
neighborhood cells.
Ability to remove iron from
hosts transferrin
Produce zinc-dependent
phospholipase C used to lyse
membranes (works w/ LLO)
Neonatal listeriosis:
cross in utero to fetus
prior to birth. Early
onset: 1-2 days after
birth, most common form
is pneumonia & sepsis
==> lead to
granulomatosis
infantiseptica: neonatal
granulomas and
abscesses of skin, eyes,
brain. Inf. Occur in utero
maybe fatal if not treated
Late onset: 5-90 days
post-partum, meningitis
/ meningoencephalitis
similar to S. agalactiae
Immuno-compromised
meningitis: elderly,
cancer patients, & renal
transplant patients (on
systemic steroid
treatments). Leading
cause of meningitis
among this population.
CSF PMN
Glucose, cloudy
culture
Food poisoning
unpasteurized milk,
turkey
Gamma IFN
may activate
listericidal fxn
in macrophage.
Ampicilin &
gentamycin for
neonatal
meningitis
Pasterurized
milk
Clostridium
botulinum
Cell
Features
Colony
Features
Source &
Virulence Factors
Lab
Characteristics Transmission
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Large
Gram(+) rod
Not usually
cultured
Organism not
usually grown
b/c dangerous.
Botulunum food
poisoning
(INTOXICATION)
Immunity to
reinfection is
type specific &
permanent
Anti-toxin
needs to be
given early
enough to
neutralize
toxin monitor
hypersensitivity rxn
Pairs or
chains
Endospores
formed (subterminal
location)
under poor
growth
conditions
Found in soil,
not in
patients
Spores
resistant to
boiling for
several hr
Obligate
anaerobic
Non-motile
Spores normally
found in soil,
dust and in
decaying
organic matter.
Vacuum-packed
canned goods,
the spores may
germinate &
produce toxin.
Food
intoxication
* Inadequate
canning, pH < 7,
smoked fish,
canned tuna
Infant botulism
associated w/
honey loaded
w/ spores &
wound infection
==> subsequent
toxin poisoning
Early symptoms:
vomiting, nausea but no
fever. Diplopia (double
vision), dysphagia
(difficult swallowing), &
dysphonia (thickness
speech)
Late symptoms: flaccid
paralysis, respiratory
distress ==> can be fatal
Infant botulism
(INFECTION): infects
infants GI tract &
produce toxin. Toxin is
most common source of
spores. Symptoms:
weakness, feeble cry,
paralysis, respiratory
distress. Maybe fatal,
could be cause of SIDS.
FLOPPY BABY
SYNDROME (limp baby
syndrome) Honey may
contain spores!
Wound Botulism:
entrance of endospores
into wounds ==>
germinate ==> toxin
Respiratory
support
Surgical
debridement
of wounds &
metronidazole
for infection
Guanidine HCl
treatment
stimulates
acetylcholine
release
Clostridium
difficile
Cell
Features
Colony
Features
Lab
Characteristics
Source &
Virulence Factors
Transmission
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Large
Gram(+) rod
Not usually
cultured
C. difficile is
part of normal
flora of 10%
humans ( in
hospitalized)
ANTIBIOTIC
ASSOCIATED COLITIS
(AAC), ULCERATIVE
COLITIS Most common
agent; occurs in GI tract
Commensal, no
strong host
response
Toxin detected by
a) Latex
agglutination
b) ELISA kit
detect toxins A&B
75% of neonates
colonized &
serve as
reservoirs to
others in
hospital & at
home
NEONATES are
asymptomatic
Discontinue
current antibiotic
treatment &
substitute
quinolone,
sulfonamide or
aminoglycosides
TMP-SMZ.
Obligate
anaerobic
Sporeformers
motile
Anaerobic
Nosocomial
spread in adults
is activation in
carrier via
changed
bacterial
balance
associated w/
antibiotic use
pseudomembranous
colitis, arises few days
after antibiotic treatment
(clindamycin, ampicillin
& cephalosporins)
* Explosive, bloody
diarrhea, fever &
pseudomembrane in
colon (detected by
endoscopy)
Need to restore
normal flora
Vancomycin
best!
Metronidazole
less effective
Clostridium
perfringens
Cell
Features
Colony
Features
Lab
Characterist
ics
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Large
Gram(+) rod
Double beta
hemolysis on
blood agar
Obligate
anaerobic
Spores normally
found in soil, dust
& in feces
Antibodies &
other host
defenses
ineffective.
Respiratory
support
Anaerobic
Sub-terminal
spores
(spores in
soil, not in
patients)
Non-motile
Thioglycolate
medium
Double beta
hemolysis (1
ring beta / 1
ring partial)
Lecithinase (+)
form ppt rings
of insoluble
diglycerides
Need to
confirm A & C
serotypes Gas
gangrene have
different causes
Wound
contamination
with dirt leads to
infection.
C. perfringens
similar to c. novyi,
c. septicum, c.
histolyticum, c.
bifermentans
Large amount of
C02 produced w/
necrosis. Spores
growth. Restricted
blood flow ==> gas
gangrene /
myonecrosis
Organism can also
colonize GI tract &
female genital tract
(leads to septicemia
& organ abscess) in
immunocompromised by
drug &/or other
disease
Food poisioning
(beta toxin)
Exotoxins
- Alpha toxin ==> lecithinase
= phospholipase C (converts
lecithin in cell membrane to
diglyceride &
phosphorylcholine) ==> RBC
lysis, destroys membranes &
mitochondria
- beta, epsilon & iota toxins
leads to necrosis & lethality
(beta toxin ==> w/ pig bel)
Spreading factors:
- kappa toxin = collagenase
(collagen digestion &
liquefication, destroy bone,
cartilage, & skin, found in
extracellular matrix)
- mu toxin = hyaluronidase
- nu toxin = DNase
- delta toxin = hemolysin
- lambda toxin = proteinase
(degrades gelatin &
hemoglobin)
- Enterotoxin (heat liable)
inhibit fluid absportion from
gut associated w/ serotype A
food infection.
- Neuraminidase
- fibrinolysin
- theta toxin: heat & O2 labile
(sensitive) hemolysin;
membranolytic
Myonecrosis by alpha
toxin, gas production
due to fermentation of
muscle carbohydrates
(saccharolytic activity)
Anaerobic cellulites
similar to gas green
limited to fascia (no
muscle invasion)
Myositos (muscle
infection)
Food poisoning
Enteritis Necroticans
(Pig-bel) associated w/
serotype C producing
alpha & beta toxin
Septicemia & organ
abscesses:
Antitoxin to
alpha toxin is
ineffective &
leads to
hypersensitivity.
No immunity to
reinforcement
Surgical
debridement
of wounds &
metronidazole
for infection
Refrigerate
meats after
cooking
Maintain
sterility of
surgical
instruments
Hyperbaric O2
environment
Penicillin &
other broad
spectrum
antibiotics
Penicillin G
antibiotics (pg
128)
Clostridia
Tetani
Cell
Features
Colony
Features
Lab
Characteristics
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Large
Gram(+) rod
In pairs or
chains
Forms
transparent
colonies on
serum agar
cultured
ANAEROBICAL
LY
(O2 sensitive)
Culture C. tetani
from wound site
(anaerobic) but also
culture aerobically
to check 2ndary
bacterial invaders
Staph, Strep
Spores are
normally found
in soil, dust &
may be
introduced into
host via
puncture
wounds,
gunshots, &
burns
Exotoxins:
a) tetanus toxin
(tetanospasmin): coded for
on plasmid, produced after
germination of spores,
released (during cell
autolysis) as pretoxin &
activated by bacterial
protease.
Deep wound
infection ==>
TETANUS. Spores
enter deep wound
Ab against
toxin develop
in host but too
late to stop
tetanus &
death.
Recovery does
not confer
immunity to
reinfection
Vaccination with
tetanus toxoid (@
1st, formalininactivated toxin
as part of DPT
with boosters give
long lasting
protection)
Tennis
racket or
drumstick
appearance
Endospores
located
terminally
Obligate
Anaerobic
Motile
Risus sardonicus
==> fascial grimace
Tetanolysin: is a hemolysin
serologically related to
Streptolysin O (&
listeriolysin &
pneumolysin). Also these
are found S. Pyogenes, S.
Pneumoniiae, Listeria Lyses
RBC, PMN, macrophages,
platelets & fibroblasts.
Respiratory distress:
due to tetanus of
diaphragm. Resp.
arrest
Endospore formation:
survives harsh conditions
Localized tetanus
Neonatal tetanus
==> infection of
umbilical stump.
Infant weak
Cephalic tetanus
DPT involves 3
injections
beginning of 3
months. Once
immunity, booster
every 5-10 years.
Tetanus antitoxinhuman derived ab
to the toxin;
respiratory
support;
hyperbaric oxygen
Surgical
debridement of
wounds &
metronidazole
(kills bacteria)
Antibiotics: inhibit
bacterial growth
toxin production
C. tetani is
sensitive to
pencillin. Pen.
Inhibits normal
GABA.
Propionibact
erium acnes
Cell
Features
Colony
Features
Lab
Characteristics
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Cultured
anaerobically
Propionic acid
production
part of normal
flora of skin,
mouth & eyes
Acne vulgaris
(common acne)
PMN attracted
to bacterial
substances
Benzyoyl peroxide
topical
bacteriostatic
effect by oxidation
of area
Anaerobic
(anaerobic
diphtheroid)
Non-motile
Indole (+)
Contaiminates
blood cultures, b/c
its on skin
Not spore!
grows in acne
lesions
metabolize skindervived lipids,
blocks sebaceous
glands cuase
acne & other
pustular rxn.
May enter via
wounds.
Chronic
inflammatory
infection of hair
follicles. Papules,
comedones
(blackheads),
pustules or cysts on
face
Bacteremia: ==>
endocarditis
(opportunistic!)
Complement
activiation
occurs
Trimethoprim for
systemic treatment
Retinoids (Vit A)
for cystic acne
Actinomyces
Israelii
Cell
Features
Colony
Features
Source &
Lab
Characteristics Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Gram (+)
Cultured
anaerobically
Actinomycosis is caused
by obligate anaerobes
such as A. israelii.
Local, acute
inflammatory
response
Oral actinomycosis
(cervical-facial):
overgrowth of normal
oral flora or soft tissue
mass along the jaw.
(no pain in
actinomycosis)
Rods
Long chain
branch &
filamentous
Anaerobic
(microaerophilic
Non-motile
Produce
exospores
(looks like
fungus but
its a
bacteria!)
Mold like
structures
Colony
resembles
molar like
tooth
Lesions:
forms
sulfur
granules b/c
of yellow
color
(CaPO4)
Staining of
sulfur granules
from pus,
sputum, tissue
biopsy w/
hematoxilin-eosin
(H&E)
Normal dental
flora (in & around
teeth & gum
margin) & vaginal
flora of women
Due to poor
hygiene, trauma, or
bacterial infection.
Endogenous
activation
(immunocompromised host)
Immunofluorescence
No nucleus
Prevention:
- Amoxicillin 812 months
- tetracycline
- preg. Women
(erythromycin)
- good oral
hygiene
Chronic, suppurative,
granulamatous disease
(described as punched
out mandible bone
lesions)
Treatment:
- Surgical
debridgement
- Penicillin G
Swallowed ==>
abdominal disease.
Infection ==> appendix,
trauma, or performated
ulcer
Treatment /
Prevention
Pelvic Actinomycosis:
serious infection, caused
by chronic IUD
(intravenous used drug)
use / inflammation
associated w/ STD
A. bovis: lumpy jaw
Actino: dental plaques
- drainage
Nocardia
asteroides
Nocardia
brasiliensis
Cell
Features
Colony
Features
Source &
Lab
Characteristics Transmission
Gram (+)
Cultured
aerobically
on blood
agar
Short rods
Long chains
Branch &
filamentous
Aerobic
Non-motile
Stained w/
modified
(nonalochol)
acid-fast
b/c of
mycolic acid
6%
Smells
musty
Grows slow
Rough
surface (may
have aerial
filaments)
Use modified
acid-stain
(sulfuric acid) .
Considered
paritial/weak
acid fast
Catalase (+)
Superoxide
dismutase (+)
In vivo:
INTRACELLULAR!
Nocardia asteroides
pulmonary infections (from environment) and/or
actinomycetoma infections of foot
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Nocardiosis (not
contagious, but lethal, &
may relapse after
treatment)
Caught early:
Sulfonamide
Pulmonary abscesses:
cavitating lesions in lungs
==> TB, Crhonic lobar
pneumonia
Host generates
acute
inflammatory
(pyogenic)
response due to
PMN
phagocytosis.
Ab needed for
phagocytosis
(require
cytokine
production).
Activated CD8+
T cells are toxic
to N. asteroides
Mycolic acid
Nocardia brasiliensis
major cause of actinomycetoma infections of foot
Or else:
80% fatality
TMP-SMZ for
propylaxis
Mycobacterium
tuberculos
(Kochs
bacillus)
Cell
Features
Colony
Features
Lab Test
Character.
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Gram (+)
TB is a pulmonary disease,
dissemination occurs by blood
STEPS in disease process:
Combination of
drugs, lasts up to
12 months.
T Cell
mediated
delayed
type hypersensitivity
(TDTH)
2. Alveolar macrophages
ingest TB ==> TB multiply
intracellularly ==> tubercle
formation w/ minor inflam
(tubercle undetect by X-ray)
==> hypersens response
TDTH. Tubercle is granuloma
composed of inf macrophages,
epithelioid cells, multincleatd
Antibodies
ineffective
b/c intracellular in
macrophage.
Macrophage
fuse to form
Langhans
giant cells.
Granulomas
form w/
epithelioid
cells
surround
central
necrosis.
Prevention!!
Vents, UV
lamps,
masks &
respirators
Primary infections:
- heal by fibrosis, calcification
----------------------------------------Ghon complexes, calcified
legions visible by X-rays
Vaccine:
Intradermal,
w/ Live
attenuated
isolate of M.
bovis
(Bacile of
Calmette
Guerin
strain or
BCG stain)
Slender rods
in long chains
& branches
Use Acid-Fast
stain
Waxy surface
(lipid
composed
*mycolic acid
fatty acid, very
long chain) if
waxy layer
removed can
stain
Obligate
Aerobe
Looks beaded
or granular
Non-motile
Cell wall:
N-glycolym.
Acid/base
resistant
* Catalase (+)
* INH (+)
TB INTRACELLULAR
Grown w/
MuellerHinton agar,
JensenLowenstein
agar (egg type)
or
Middelbrook
7H10 serum
agar. Simple
medium w/
inorganic salts,
asparagines &
glycerol.
Colorless or
cream-colored
Dry
Wrinkled
Colonies
develop in 4-8
weeks
Cord factor
(serpentine
cords )
Surface
Pellicle in
liquid culture
Culture sputum
(egg agar)
Chest X-ray:
Chk calcification
of lesion (Ghon
complex)
PPD: {cell wall}
(Purified Protein
Derivative)
Skin test (Tine or
Mantoux), chk in
2-3 days. Chks
for delayed
hypersensitivity
response.
----------------------< 5 mm = (-) resp
or
< 5 mm = T_s
----------------------5-9mm=try again
> 10mm =(+)resp
Severe TB can
CD4 T-Cell
(AIDS)
TB colonies
prod. large
amnts NIACIN
only M.
tuberculosis!!!!!
Nitriate Red. (+)
Bactec sys: chks
release of 14CO2
Horizontal transfer
via respiratory
droplets from
infected patients.
(secondary TB ex.
reactivated
infection)
Infect via fomites
Healthy patients
contain TB
organisms to
tubercles (mini
lesions in lung w/
macrophages w/
TB organism
intracellularly)
Resolves into
chronic, quiescent
infection
Spreads through
out body if
unhealthy patient
b/c reactivation of
quiescent infection
(secondary TB)
Cells can airbone
M. Bovis can
spread TB-like
infection in
humans
Antibiotic resist.
isolates arise in
non-compliant
Drug therapies:
Isoniazid (INH).
INH requires
catalase activity
of TB to be
effective. In
PPD+ HIV+
INH, liver toxic
1st line drugs:
INH,
ethambutol,
streptomycin,
rifampin, paraaminosalicyclic
pyrazinamide
combinations, 6
months, Vit B6
Alternative:
Kanamycin,
cycloserine, INH,
& Rifampin==
MDR TB is
difficult to
manage.
Immunosuppressive
drugs reactive
primary TB
Secondary
Extrapulmonary TB: Potts Disease (vertibal osteomyelitis)
- involvement of cervical lympth one is copying AIDS patients are s
- SCROFULA = 10% of as AIDS also bC
Non-Runyons mycobacteria
- M. tuberculosis
- M. bovis
- M leprae
Runyons classification of atypical mycobacteria
== > Pigament Formation in <==
Group
Growth Rate
Light
Dark
Species
I
II
III
IV
MOTTS
Slow
Slow
Slow
Rapid
+
+
-
+
-
M. kansasii, M. marinum
M. scrofulaceum
M. avium-intracellulare complex
M. fortuitum-chelonei complex
Cell
Features
Colony
Features
Lab
Source &
Characteristics Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
g(+)
Runyon
Groups I-III
are cultured
aerobically
& grow very
slowly
Acid-fast stain
Group I
- M. kansasii, pulmon. Inf.
- M. marinum, swim pool
granuloma
T cell mediated
DTHR
Group I
- Kansaii: multidrug + INH
- Marinum:
rifampin &
ethambutol
slender rods
long chains,
branching
waxy
surface
mycolic acid
non-motile
aerobic
visualize w/
acid-fast
Produce no niacin
Group II
- M. scrofulaceum, cause
scrofula
Group III
- M. Avium Intracellulare
(MAC)
Group IV
- less mycolic acid
- M. smegmatis (foreskin)
AB ineffective
b/c bacteria are
intracellular
Granulomas
may form w/
MOTT
infection
Group II
- Scrofulaceum:
rifampin
Group III
- MAC:
ethambutol,
streptomycin,
rifampin
Group IV
- Smegmatis,
amikacin
Mycobacterium
Bovis
Cell
Features
Colony
Features
Source &
Lab
Characteristics Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Gram (+)
Grows very
slowly
Colonies
develop in 48 weeks
Causes pulmonary
infection, similar to TB
Chest X-ray
T Cell Mediated
delayed
hypersensitivity
(TDTH)
Decontaminate
w/ concentrated
NaOH
Grown on
MuellerHinton agar,
JensenLowenstein
agar or
Middlebrook
7H10 serum
agar
Colonies, colorless
Infection occurs by
ingestion of Raw
Milk obtained from
infected animals.
Slender rods
in long
chainsbranching
Waxy
surface
(mycolic
acid)
Obligate
aerobe
Non-motile
Acid-fast
Catalase (-)
Cord factor
(trehalsoe
dimycolate)
produce
pathogenic
strains leads
serpentine
cords&
surface
pellicle in
liquid
culture.
NO NIACIN
Catalase (-),
resistant to
isoniazid, INH
(differs from TB)
Detected by
Bactec within 10
days cultivation
Human to human
transmission can
occur via respiratory
droplets from
individuals with
secondary TB
Infections:
- GI tract
- scrofuloderm (skin inf)
- osteoarticular TB (joints)
Use of immunosuppressive drugs
(steroids) re-activate
primary M. Bovis.
PPD + indicate exposure to
M. Tuberculosis or M. Bovis
AB are
ineffective b/c
intracellular in
macrophage
Macrophage
fuse to form
Langhans giant
cells.
Granulomas
form w/
epitheliod
surrounding
central necrosis
Prevent
development of
drug-resistance,
use combo of
drugs.
Mycobacterium
aviumintracellulare
MAC
complex
Runyon
Group III
& MOTT
Cell
Features
Colony
Features
Source &
Lab
Characteristics Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Gram (+)
Grows very
slowly
Grown on
MuellerHinton agar
Catalase (-)
T cell mediated
(DTHR). Antibody ineffective
b/c bacteria are
intracellular
Multi-drug
therapy b/c
most are multidrug resistant
(MDR)
Slender,
rods, in long
chains
Aerobic
Waxy surf=
mycolic acid
Non-motile
Middlebrook
7H10 serum
agar (w/o
pigment
production)
Acid-fast
Catalase (-)
Colonies are
colorless & do
not produce
niacin
Nitrate Red. (-)
Chest X-ray
Bactec test: test for
C02 production
Catalase (-)
Catalase (+)
M. Bovis
M. Leprae
M. Avium Intracellulare (MAC)
Acinetobacter
M. Tuberculosis
Norcadia
Mycobacterium
Leprae
Hansens
Disease
Cell
Features
Colony
Features
Lab
Characteristics
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Gram (+)
CAN NOT
BE
CULTURED
IN VITRO
Humans &
armadillos are the
only reservoirs
Multi-drug
therapy dapson
w/ rifampin
T cell
mediated
(delayed type
hypersensitivity
response)
Slender,
rods, long
chains, &
branching
Waxy
surface
mycolic
acid
Non-motile
Aerobe
acid-fast
stain
Catalase (-)
But inside
ARMADILL
OS
& Foot pads
of mice.
Lepromin test:
similar to PPD
Catalase (-)
PCR and rRNA
probes
Lepromatous form:
skin lesion biopsies
& nasal secretions,
look for acid fast
bacilli in
macrophage (foam
cells) globi
Tuberculoid form:
difficult to observe
bacteria
Horizontal transfer
occurs via
respiratory
droplets
Skin contact
(ulcerative lesions)
Leprae likes to
grow at lower
temp. extremities
ex. skin
Depends on intensity of
CMI (cellular Mediated
Immunity) response
- Strong CMI: tuberculoid
- Impair CMI: lepromatous
a) Tuberculoid leprosy:
strong CMI, tuberculoid
leprosy develop w/o
neurological involvement.
Disfigured (Lions face)
scars
Biopsy shows few bacilli
b/c few bacteria are in
lesions Activated
macrophages kill leprae. T
cells is detected by lepromin
test (+) Lepromatous form
not infect
b) Intermediary Leprosy
c) Lepromatous leprosy:
disfigured due to nodules
(lepromas), sense loss, pain,
& temp. Weak CMI. No
TDTH. Biopsy w/ large #
of bacilli. Respiratory
congestion immune anergy
(no activation of
macrophages) Numerous
T_s cells observed but giant
cells & epitheliods are rare.
Patient w/o hypers
lempromin(-). HIGHLY
INFECTIOUS
In
tuberculoid
form (strong
CMI)
Granulomas
form w/
epithelioid
cells
surrounding
central
necrosis.
Lepromatous
form: strong
AB response
but weak
cytokine
response.
or
dapson w/
clofazimine (for
lepromatous
leprosy))
Neisseria
gonorrheae
Cell
Features
Colony
Features
Lab
Characteristics
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
G(-)
Chocolate
agar
Catalase (+)
Humans ONLY
reservoir
Lipooligosaccharide (LOS)
similar to LPS (+attract PMN
to primary inf site)
N. gonorrhea
infection
leads to local
acute
inflammation
due to PMN
activity &
complement
activation.
Ceftriaxone
(expensive)
Diplococci
Aerobe capnophilic
as well
Non-motile
Lipooligosaccharide
(LOS)
T1-T2: pili
T3-T5: no
pili
OXIDASE (+)
Contains enyme
cytochrome C,
turns black, due to
oxidation
ONLY glucose (+)
Maltose (-)
Sucrose (-)
Lactose (-)
Ferments under
glucose, NOT (-)
Superoxol (+) test
(30% H202)
Use Thayer-Martin
(TM) or (NYC)
agar for 48 hrs. TM
==> contains
vancomycin inhibt
g(+)
Colistin inhibit:
g(-) rods
Nystatin inhibit:
yeasts
Trimethroprim
inhibit: Proteus
Horizontal transfer
occurs via sexual
contact.
Complement
deficiency (C5-C8)
leads to meningitis,
predisposes patient
to coccemia.
No immunity
to reinfection
possibly b/c
of antigenic
variation
Alternative:
- Spectinomycin
- doxycycline
Neisseria
meningitides
Cell
Features
Colony
Features
Source &
Virulence Factors
Lab
Characteristics Transmission
G(-)
Grows on
chocolate
agar,
produce
transparent
colonies
Catalase (+)
Diplococci
Aerobe
Capnophilic
Non-motile
Lipooligosacharide
(LOS)
similar LPS
Naturally
competent
OXIDASE (+),
only glucose &
maltose are used
by this species
Glucose (+)
Maltose (+)
Sucrose (-)
Lactose (-)
Needs & uses Fe
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Epidemic meningitis:
youngsters & military
personnel. * Symptoms:
fever, neck pain (stiffness),
headache.
Treat as early as
possible
Penicillin G
B = poorly immunogenic +
resembles uropathogenic E.
colis. K1 capsule (neonatal
meningitis) E. coli ass. w/
neonatal meningitis B capsule
rich sialic acid resid.
Pili available
may get
activation to
complement,
results
inflammation
and pus
formation.
Meningococcemia: upper
respiratory infection, result
in meningitis. Sepsis is
diagnosed by skin rash.
Disseminated
Intracellular Collapse
(DIC) ==> rapidly fatal.
Waterhouse-Friderichsen
Syndrome!!!: rapid DIC,
vascular collapse, shock &
death w/in 6-8 hr &
adrenal bilateral
hemorrhage. FATAL.
Meningococcal
pneumonia: w/ carriers,
pneumonia after viral
infection.
Alternative:
Chloramphenicol
Rifampin, given
prophylactically
VACCINE:
polyvalent
capsular antigen
New vaccine
Menactra with
capsule
conjugated to
vaccine.
Not on
final!!!
Cell
Features
Colony
Features
Source &
Virulence Factors
Lab
Characteristics Transmission
Eikenella
corrodens
G(-)
Grows on
blood agar
that shows
pitting of
the agar
Catalase (-)
Oxidase (+)
Slender rods
Faculatative
anaerobe
Capnophilic
LPS
Twitching
motility
Bleach like
odor on
agar
No sugar is used
(lack oxidative &
fermentative)
Aerobic growth
requires hemin
supplementation
Lysine
decarboxylase (+)
Urease (-)
Gelatinase (-)
Indole (-)
Nitrate reduction
to nitrite only
Yellow pigment
production
Human mucous
membranes
(mouth & upper
respiratory tract)
are reservoirs
Normal flora
1. LPS (endotoxin)
2. Pili: attach to epithelial cell
3. Type IV pili: adhesion to host
cell surface, twitching
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
1. Human BITE
WOUND!!! Could also be
mixed infections (staph &
strep) Clenched fist.
Associated w/ lower
extremity infections by
stepping something
contaminated to break the
skin.
NA
Augmentin
(clavulanic &
amoxicillin)
2. post-surgical infections:
soft tissues w/ abscesses &
arthritis, empyema often
seen. Spreads throughout
body. Associated w/
meningitis, endocarditis,
osteomyelitis & soft tissue
abscesses
Alternative:
Tetracycline or
quinolones
Acinetobacter
Baumannii
Cell
Features
Colony
Features
Source &
Lab
Characteristics Transmission
G(-)
Grows on
blood agar
Oxidase (-)
Coccobacilli
Obligate
aerobe
Non-motile
Oxidase (-)
Nonhemolytic
Glucosa
oxidized
Produce
colonies that
are nonhemolytic
Widely distributed in
nature (free living
saprophyte)
Often associated w/
hospitals
Organism is able to
survive on moist
surfaces & skin
Acinetobacter is only
2nd to the nonfermenting
Pseudomonas
aeruginosa in causing
nosocomial infections
maybe associated w/
hospital outbreak
Ex. Acinetobacter,
Xanthomonas,
pseudomonas, can
colonize mechnical
ventilator ==>
introduce into
respiratory tract of
patient undergoing
assisted ventilation
Host
Defenses &
Immunity
Treatment /
Prevention
NA
TMP-SMA
(Bactrim) similar
S. Saprophyticus
Alternative:
- Kanamycin,
- Colistin,
- Tetracycline
---------------------Resistant to
Penicillin b/c of
beta-lactamase
G (-) bacilli
Cell
Features
Colony Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
G(-)
Phase I most
virulent grows on
Bordet-Gengou
(contains potatoe
starch, glycerol, &
50% blood) has a
pili & O-antigen are
expressed
Nasopharyngeal
swab ==>
incubate 10 days
Humans, the
only reservoirs!!!
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
3 stages of
whooping cough or
pertussis (intense
cough)
Ab made
against
capsule.
Infection is
non-invasive
w/ bacteria
remaining in
respiratory
tract.
Erythromycin
1. Catarrhal stage:
Most infectious,
most bacteria.
Most contagious.
RRHEA
2. Paroxymal stage:
violent cough,
vomit. CNS
damage. Less
contagious.
VIOLENT stage
3. Convalescent
stage: gradual
reduction in cough,
may last 1-6months
Alternative:
Tetracycline
chloramphenicol
Paroxymal stage:
oxygen therapy
may be effective
& steroids
severity.
Vaccination:
Kills phase I
bacteria, DPT
vaccine w/
boosters 4,6, 18
months.
This vaccine has
been replaced by
ACELLULAR
vaccine w/
reduced side
effects. PT,
FHA, pertactin,
& pili are
commonly used.
G (-) bacilli
Cell
Features
Colony Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Haemophilus
influenze
G(-)
Grows on chocolate
agar producing
small colonies that
are non-hemolytic
contrast to
Catalase (+)
Humans are
only reservoir
for H.
influenzae.
Tryptophanase (+)
Nasopharyngitis:
H. influenzae
infections (include
non-typable or
non-encapsulated
strains) Infection
may become
sinusitis, otitis
media or cellulites
also pneumonia,
chronic bronchitis,
epiglottitis.
Neonate got
ab from
mother &
was
protected for
first few
months of
life.
Eventually,
reproduce
its own.
Ceftriaxone or
cefotaxime
Beta-Hemolytic:
- H. Ducreyi
- H. hemolyticus
Coccobacilli
bipolar stain
chains/filam
ents
facultative
anaerobic
Capnophilic
CO2
Non-motile
Naturally
competent!!!
Capsule: Quellung
Rxn, destroyed by
autolysis by
endogenous enzyme
Requires: (hexe, navy)
- Factor X: HEME
- Factor V: NAD
grows on chocolate
agar
H. influenzae
recovered during
primary isolation on
standard blood
agar. Also grows in
close proximity to S.
Aureus (beta
hemolytic)
Satellite
phenomenon: test
for nutritional req.
Fermentation rxn
are variable
(glucose only)
Nitrates used as
terminal electron
acceptors
Vancomycin
sensitive
Requires X & V
factors and CO2
Specimens: CSF,
blood & carry out
antigenic typing of
capsule (Quellung
rxn)
Nonencapsulated
variants are
considered to be
normal flora of
the pharynx &
conjuctiva.
Carrier rate is
~30%
Hortizontal
transmission
primarily
respiratory
droplets
Individuals had
protective ab to
type b capsule by
age 5-6
Carriage is
mostly by nonencapsulated
strains, maybe
non-typable
encapsulated
strains. Lead to
localized
infections, w/o
dissemination
May lead to
bacteremia & septic
arthritis
Epiglottitis:
inflamed epiglotis
swollen, red,
edematous tissue
leads to airway
obstruction
Meningitis: H.
influenzae (type b)
#1 cause of
meningitis in
young children - 6
Purulent
conjunctivitis
(pink eye): caused
by H. aegypticus
(Kochs Weeks
bacillus)
Combination of:
Cefotaxime w/
ampicillin
Alternative:
(sensitive Pen.)
chloramphenicol
Vaccine:
Composed of
polyribitol
phosphate (PRP)
conjugated to
protein. Used as
a booster
G (-) bacilli
Cell
Features
Colony Features
Lab
Characteristic
Source &
Transmission
Virulence
Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Haemophilus
ducreyi
G(-)
Grows on blood
agar produce small
colonies that are
hemolytic
Catalase (+)
1. LPS
(endotoxin)
na
Erythromycin
Requires Factor X
(heme)
Coccobacilli
bipolar stain
facultative
anaerobic
Non-motile
Glucose is
fermented
Hortizontal
transmission
occurs via sexual
contact
Vancomycin
resistant
Alternative:
Sulfa drugs
(sulfonamide) or
streptomycin
G (-) bacilli
Cell
Features
Colony Features
Lab
Characteristic
Source &
Transmission
Virulence
Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Klebsiella
pneumoniae
G(-)
Grows on blood
agar produce slimy
mucoid colonies
b/c of capsule, nonhemolytic.
Spreading
Oxidase (-)
Widely distributed
in nature (soil,
vegetables)
Capsule: resist
phagocytosis,
attracts
macrophages
to area
Ab made
against
capsule
Cefotaxime &
gentamycin
(Friedlanders
bacillus)
Slow fermentation
of glucose, lactose
& sucrose (pink
colonies on
MacConkey
lactose agar)
Bile salt selectin
Indole (-)
Methyl red (-)
Voges-Proskauer
(+)
Citrate (+)
Urease (+)
H2S (-)
Capsule: Quellng
Rxn
Often associated
w/ nosocomial
infections:
K. pneumoniae is
normal flora of
human colon.
Nosocomial
infections:
organism is
transmitted by
dwelling catheters
& endotracheal
tubes
Mostly in immunocompromised,
hospital patients
Diabetics risk
Urease:
develop UTI
R plasmid:
codes for Pen.
&
aminoglycosid
e resistance
LPS, endotoxin
ST & LT
enterotoxin
Sensitive Pen:
TMP-SMZ
(Bactrim)
G (-) bacilli
Cell
Features
Colony Features
Lab
Characteristic
Source &
Transmission
Virulence
Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Legionella
Pneumophila
G(-)
Catalase (+)
NO horizontal
transmission btw
humans to humans
(not infectious)
LPS (endotoxin)
1. Legionnaires Disease:
Atypical pneumonia.
Non-productive cough,
classic shallow sound
when pertuss lungs in
back.
Ab are
ineffective
against
intracellular
bacterium.
Erythomycin or
other macrolide
antibiotic
Catalase (+)
Thin rods
Seen w/ Ag
impregnatio
n w/ StarryWarthin
procedure
Motile
Aerobic
Grow w/
CO2
Colonies have
brown pigmentation
BCYE +Cysteine +
Fe gets L.
pneumophila to
grow
Superoxide
dismutase (+)
Produces brown
pigment in vitro
Gelatinase (+)
Oxidase (+)
No fermentation of
sugars.
Bastards can hide
in amoeba difficult
to kill, even w/
Chlorine
Air conditioning
tanks, whirlpool
baths, humidifiers,
hot water systems,
shower heads, &
contaminated
water supply
systems
Can be found in
hospitals &
community settings
Survives
intracellularly in
amoebae
Transmission
occurs by
inhalation of
aerosols &
aspiration of
contaminated
water
* patient w/
immunosuppressive drugs,
smoking, or had
surgery are at high
risk.
Inhibition of fusion
of phagosome &
lysosome in
macrophages &
monocytes
INTRACELLULAR
survival
Production by L.
pneumophila of
proteolytic enzymes:
Cytotoxin: blocks
PMN oxidative burst
Capsule = F1 fraction
Phosphatase: blocks
superoxide anion
production by
stimulated PMN
Hemolysin
(legolysin)
MIP gene product
(macrophage
infectivity
potentiator) promotes
phagocytosis by
binding to a
complement factor
Beta lactamase
Infections may be
nosocomial or community
acquired (hotels or cruise
ship)
2. Pontiac Fever: fever,
chills, nausea, &
headaches develop w/in
48 hrs after infection (flulike symptoms). Occurs
more often in younger
patients.
Cell
mediated
immunity
most
important &
activation of
macrophage
Acquired
immunity
obtained
(protect
against
subsequent
infection)
Cephalosporins
& aminoglycosides
Prevention:
Very hot water
flashing! 80C for
30 min or use
UV light.
Chlorination is
not very
effective since L.
pneumophila
survives by
colonizing
water-dwelling
amebae
G (-) bacilli
EQ!
Cell
Features
Colony
Features
Lab Charact.
Source &
Transmission
Virulence
Factors
Associated
Diseases
Host
Defenses
Immun.
Treatment /
Prevention
Pseudomonas
aeruginosa
G(-)
Oxidase (+)
Widely
distributed in
nature (soil &
water) often
associated w/
moist areas in
hospitals
Exotoxin A (diphtheria toxinlike toxin) A subunit has ADPribosyl transferase activity & B
subunit binds to cell. Leads to
inhibit protein synthesis.
Target cell: heart & liver.
1. Necrotizing
bronchopneumonia:
fever, cough,
purulent sputum, &
lung abscesses.
Immunocompetent
patients
have
Multi-drug
treatment
(Kirby-Bauer
test, antibiotic
resist. Profile)
1. Gentamycin
+ azlocillin
2. Augmentin
Strong beta
hemolysis
Many will
fluoresce
under UV
light due to
pyoverdin
(fluorescein)
production
Catalase (+)
No sugar
fermentation but
glucose is
oxidized
May be found in
swimming pool
& whirlpools
which are
inadequately
chlorinated, &
raw vegetables
Nosocomial
infections
Pyocyanin
production
(blue-green
pigment)
Found to exist in
disinfectant &
eyewash
solutions.
Beta-hemolysis
Intact skin
important
to resist this
organism.
No
immunity
to reinfection
Sensitive Pen:
Aztreonam
For meningitis:
Ceftazidime
UTI & Respir.
Disease
Quinolone
Prevent burn
wound infect :
Daily wound
debridgement
use topical Ag
sulfadiazine
Disinfect
whirlpools w/
iodine
disinfectants,
not recomm.
b/c organism
survives inside
biofilm.
Chlorination
effective to kill
pseudomonas
P. Aeruginos
sensitive to
pH. Acetic acid
(vinegar)!!!
Mycolplasma
pneumoniae
(EATONs
agent &
PPLO)
Cell
Features
Colony Features
Lab
Characteristic
Source &
Transmission
Virulence
Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Smallest,
free-living
organisms
Growth leads to
mulberry colonies
w/ older colonies
fried egg colony,
slow growth
1. Antimicrobial
resistance: b/c of lack
of cell wall, innately
penicillin resistant.
Does not make cell
wall
1. Atypical pneuomia
(walking pneuomonia)
most common cause,
infection is mild or
aymptomatic but can be
fatal. Chest x-ray show
unilateral lower lobar
involvement
Symptoms: interstitial
pneumonia w/ nonproductive (persistant)
cough & inspiratory
crackles, fever, chills,
headache & chest pain
Complictions: lead to CNS
& heart complications
Ab & T cells
important
Doxycycline
(leads to yellow
teeth in children)
Pliable
Cell
membrane,
contain
sterol
No cell wall
G(null)
Aerobic
Motile
Special
nutrient req.
cholesterol
cell
membrane
Glucose
fermentation(+)
Tetrazolium dye
reduction: turn
blue to yellow
Detected:
Stain w/
fluorescent labeled
ab, ELISA; latex
agglutination
Horizontal
transmission via
respiratory
droplets mostly
among teens &
young adults.
2. Adhesion Protein
P1: mediates
adhesion to epithelial
cells, ciliated cells &
RBC
3. Production of H202
possibly contributes
to mucosal damage &
damage to RBC
4. Mycoplasma,
survive intracellulary,
cause most damage
extracellularly
2. Raynauds
phenomenon occur to
cold-agglutination
antibodies, leads to
necrosis of fingers & toes
if in sickle cell anemia
patients
3. Endocarditis (inflame.
Of heart muscles)
4. Guillain-Barre Syndr.
(asc paralysis more
commonly associated w/
Campylobacter infection)
Associated
w/ auto-ab
production
(IgM cold
agglutinin)
Cytokines
activated
EXCEPT
IL-2
Erythromycin
for children &
preg. women
G (-) bacilli
Cell
Features
Colony Features
Lab
Characteristic
Source &
Transmission
Virulence
Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Helicobacter
pylori
G(-)
Organism grows on
selective agar
Oxidase (+)
Catalase (+)
TSI (-)
Urease (+)
Nalidixic acid
resist.
Nitrate reduct. (-)
Hippurate
hydrolysis (-)
Cephalothin sensit.
Human GI tract is
reservoir. Oral
fecal route is
involved in
horiztonal
transmission
(human to human)
1. LPS
2. Motility burrow through
mucin layer stomach lining
1. Chronic
Gastritis:
Causative agent!!!
Acute infection of
stomach
epithelium.
Organism causes
superficial mucosal
inflammation & is
non-invasive.
Symptoms: nausea,
abdominal
discomfort.
Immunocompetent
patients have
chronic
inflammator
y response
w/
moncytes,
macrophages
&
lymphocytes
in stomach
mucosa.
Combination of
drugs:
2. Duodenal peptic
ulcer: (#1 causative
agent) follows
chronic gastritis.
Symptoms:
burning abdominal
pain 1-3hr after
meals that may be
relieved by eating
& antacids.
Complications
include: bleeding,
& perforation of GI
tract
Antibody
formation
not
protective
therefore
patients after
treatment
may relapse
Pleomorphic
(s-shaped,
bacilli,
curved rods,
spirochete)
Produce:
corkscrew
motility
Microaerophilic
(grow in 6%
O2, 10%
CO2)
somewhat
tolerant to
stomach
acidity
Chocolate agar or
modified ThayerMartin incubate for
a > 1 week under
microaerophilic
conditions
(chocolatization
detoxifies agar)
Endoscopy: detect
by biopsy.
14C-urea in food &
look for 14CO2 in
patients breath &
serology
3. Resistance to stomach
acidity enhanced by
movement of Helicobacter
into & within the protective
mucous layer of the stomach
(not epithelia).
Microaerophilic nature
organism helps survival
4. Enzymes:
a) Mucinase causes
breakthrough of mucous
layer in stomach (resist acid)
b) Urease: stomach lining
produce small amounts of
urea .. leads to ulceration
5. Adhesion factors: attach
to stomach (resist peristalsis)
6. Hemolysin (128kD) found
w/ cytotoxin protein
7. Vacuolating toxin: 50%
isolates virulence of strain
(pathogenicity island*
virulence,
8.Cag protein: stimulates
host prod. of IL-8 & other
signal transduction events
9. Catalase / superoxide
dismutase: protects from
intracellular killing phago.
10. Produce acid inhibitory
protein (induce
hypochlorhydrin)
3. Gastric
carcinoma: chronic
gastritis
Pepto-bismol
(Bismuth salts),
amoxicillin, &
metronidazole.
Pen. Sensitive:
Sub. Amox w/
Tetracycline
Also include
proton pump
inhibitor ex.
omeprazole
G (-) bacilli
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence
Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Vibrio
cholerae
g(-)
Grows blood
agar
Oxidase (+)
Lactose (+)
Sucrose (+)
Indole (+)
Methyl Red (+)
Urease (-)
Human GI tract is
reservoir for this
organism
Explosive Diarrhea!
Cholera, remains in
SI (duodenum) &
non-invasive.
Large
inoculum
needed to
infect
Immediate &
continuous IV
or fluid
replacement
along w/
electroylates
comma
shaped
bacilli
(curved
rods)
motile
(flagella)
Enrich in
highly
alkaline
medium
(loves higher
pH)
ThiosulfateCitrate-BileSucrose
(TCBS) agar
Can grow
w/o salt
HALOPHIC
Chk rice-water
stool for motile
bacteria, culture on
TCBS media & see
if yellow b/c V.
cholerae ferment
sucrose
Replenish w/
NaCl / KCl
add glucose to
improve
uptake of salts
by intestinal
cells. (try
Gatorade!)
Tetracycline is
used for severe
cases
Enterotoxigenic
Escherichia
Coli (E.Coli)
AKA (ETEC)
Dr.
Trachmans
favorite pet
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
g(-) rod in
pairs &
chains
Grows on
almost any
medium,
forms large
gray colonies,
on blood
agar, some
strains are
hemolytic
Oxidase (-)
Lactose (+)
Sucrose (+)
------------------------Indole (+)
Methyl red (+)
VogesProskauer (-)
Citrate (-)
{IMViC assays}
==> unique E.Coli
------------------------TSI butt & slant
yellow w/ gas
prod.
Enteritis or
Travellers diarrhea
(Turista). Noninvasive & remains in
the lumen of SI.
sIgA against
CFA & other
bacterial
components
combats
infection.
Fluid &
electrolyte
replacement :
NaCl, KCL,
glucose, &
water.
anaerobic
strains are
motile
H2S (-)
Serology:
Kaufman White
Scheme
REMEMBER: KOH
K = capsule, fibriae
O = LPS somatic
H = H ag, flagella
Culture on
MacConkeylactose medium &
blood agar
Symptoms: mild,
watery diarrhea
similar to V. Cholera
EXCEPT the mucus.
Antibiotics not
given
prophylaxively
but use
norfloxacin .
Pepto-bismol
(bismuth salts
are inhibitory)
Enterohemorrhagic
E. Coli
AKA (EHEC)
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
g(-)
Grows on
almost any
agar forming
large gray
colonies
Oxidase (-)
Lactose (+)
Indole (+)
Methyl (+)
Urease (-)
TSI (-) for H2S
Citrate (-)
VogesProskauer (-)
SORBITAL util (-)
Serology 0157H7
Human GI tract is
reservoir. Oral-fecal
route by drinking
contaminated water
& undercooked
Hemorrhagic colitis:
stays in lumen of LI &
non-invasive. Blood
diarrhea. Blood due
to cytokine activity
combined w/ SLT.
Secretory
IgA against
bacterial
components
combats
infection.
Noninflammator
y response
to infection.
Noninvasive
Fluid &
electrolyte
replacement.
bacilli pairs
or chains
motile
anaerobic
Consume
unpasteurized fruit
juices, playing in
contaminated water
Hemolytic-Uremic
Syndrome: result in
acute renal failure,
hemolytic anemia &
thrombocytopenia,
5% of cases. w/
platelet numbers.
Complication
(sequelae) seen in
children & in
immunocompromised or
elderly.
Antibiotics not
used for
prophylaxis.
Prevention:
- well cooked
meals, burgers
& pasteurized
fruit juices
Better treat:
- fluids + salts
- chlorinate
water
Non-invasive
Invasive
- ETEC
- Vibrio cholerae
- EPEC
- EHEC
- Shigella
- Salmonella
I
E.Coli
Enterobacter
aerogenes
Organisms
E.Coli, Klebsiella, Enterobacter
Shigella, Salmonella, Proteus, Pseudomonas (Acinetobacter)
Serratia, Vibrio
Salmonella
Typhimurium
AKA
(S. enteritidis
or S. enterica)
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
g(-)
Grows on
almost any
agar medium
large
Oxidase (-)
Lactose (-)
Indole (-)
Methyl red (+)
VogesProskauer (-)
Indole (-)
Citrate (+)
TSI (+) H2S
Urease (-)
Non-typical
Salmonellosis
(Enterco-colitis):
Initial invasion of
mucosal cells of
ileum & large
intestines may be
followed by systemic
invasion.
Most often is
self-limiting
Serology:
Kaufman White
Scheme
REMEMBER: KOH
K = capsule, fibriae
O = LPS somatic
H = H ag, flagella
Use antacids
predispose for
infection.
Strong
inflammatio
n response
w/ PMN &
T-Cells.
CMI is
important
b/c of
intracellular
location.
rod in pairs
or chains
anaerobic
motile
Culture stools on
selective medium
Which organisms are associated w/ Reiters syndrome? Salmonella typhimurium & typhi
Symptoms: FEVER,
nausea, water
diarrhea, headache,
enteric inflammation,
& pus in stools.
Entercocolitis may
mimic appendicitis
Bacteremia: intestines
to blood stream.
Leads to endocarditis,
bile duct infection,
septic arthritis,
pneumonia. AIDS
patient may have
recurrent bacteremia
Osteomyelitis:
salmonella bone
infections arising
from bacteremia seen
in sickle cell anemia
patients
Post-inf. Reiters
Syndrom: arthritis,
HLA-B27
Treatment
enterocolitis:
- fluid &
electrolyte
replacement
Antibiotics
dont eliminate
Salmonella
from GI but
duration.
Ciproflaxin,
TMP-SMZ
(bactrim) used
for systemic
infections
Avoid raw
eggs & use of
antacids
Wash hands
before eating
Salmonella
Typhi
AKA
S. paratyhpi
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Def.Im.
Treatment
/ Prevent
g(-)
Grows on
almost any
agar medium
forms large
gray colonies
Oxidase (-)
Lactose (-)
Indole (-)
Methyl red (+)
VogesProskauer (-)
Citrate (+)
TSI (-) H2S
Urease (-)
Human GI tract is
main reservoir for
these organisms
Stomach
acid kills
Salmonella.
Large
amounts of
inoculum
causes the
infection
Antibiotics
ciproflaxin
Oral-fecal route by
consuming
contaminated water
& food.
Typhoid Salmonellosis
(Enteric fever) &
paratyphoid fever. 2
stages:
Serology:
Kaufman White
Scheme
REMEMBER: KOH
K = capsule, fibriae
O = LPS somatic
H = H ag, flagella
Hortizontal
transmission
rod in pairs
or chains
anaerobic
motile
Issue
1-3
2-3
Incubation
Hepatoslenomegaly
Bradycardia
ROSE SPOT
on trunk
Secondary
infections
GI tract
2-3
2-3
4
Symptoms:
- FEVER
- abdominal pain
- headache
- water diarrhea
- enteric inflammation
- pus in stool
Bacteremia: intest. to
blood stream, subacute
endocarditis, bile duct
inf.
Reiters Syndrome:
arthritis (see S. enterica)
Abortion: enteric fever
Systemic Inf:
- TMP-SMZ
(Bactrim)
- Amoxicillin
- chlororamphenicol
Misc notes:
Ciproflaxin
eliminates
carrier state
Shigella
species
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment
Prevent
g(-)
Grows on
almost any
agar forming
large gray
colonies. On
EMB,
organism is
colorless or
white
Oxidase (-)
Lactose (-)
Indole (-)
Methyl red (+)
Urease (-)
TSI (-) for H2S
Citrate (-)
VogesProskauer (-)
1. Bacillary
Dysentery
(shigellosis): invades
mucosa of LI but not
underlying muscle
Strong acute
inflammatory
response to
infection by
PMN.
Infection is
self-limited.
Symptoms include:
Watery diarrhea
progresses to bloody
diarrhea, fever, &
inflammation w/ pus
in stools. Toxin kill
mucosal cells of
intestine. Often
found in children &
elderly.
Secretory IgA
against
bacterial
infection
rods in
pairs or
chains
non-motile
Lactose (-)
NONMOTILE
NON-MOTILE!!!
SERENY TEST:
(inoculate guinea
pig or rabbit eyes)
anaerobe
Five Fs:
- food
- fingers
- feces
- flies
- fomites
Common among
homosexual men
Commandeering of Actin
filaments in host cell for
mobility in host cell ==> helps
spread to nearby cells
-------------------Innately
non-motile but
once inside the
host becomes
motile b/c of
actin filaments
Shigella Type
S. boydii
S. flexneri
S. sonnei
S. dyenteriae
CMI important
b/c of
intracellular
location
2. Hemolytic-Uremic
Syndrome: Shigella
infection may result
in actue renal failure,
hemolytic anemia, &
thrombocytopenia.
3. Post-Shigellosis
Reiters Syndrome:
arthritis associated
w/ HLA B27
Serogroup
C
B
D
A
# serotypes
18
14
1
12
Comments
Most common in developing countries
Most common serogroup in US, acquired when traveling to endemic area (NON-MOTILE!!!)
Most common in remainder of world, most pathogenic, most invasive, produces Shiga toxin (LACTOSE (+)!!!)
Test question: Which pair organisms are associated wit h hemolytic-uremic disease? Shigella dysenteriae & EHEC
Fluid &
electrolyte
replacement.
Antibiotics
shortens
duration but
not lessen
intensity
Bactrim
(TMP-SMZ)
used for
serious
cases, stop
transmission
.
Nalidixic
acid or
newer
quinolones
Prevent
from
consuming
uncontaimin
ted food &
water
Bacteroides
fragilis
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
g(-)
Grows
anaerobically
on complex
agar
medium,
brain heart
infusion
forms gray
glistening
colonies due
to capsular
polysacch.
Anaerobic growth,
penicillin resistant
Human GI tract is
resvoir for
Bacteroides
1. Polysaccharide capsule
(K antigen): major VF w/
anti-phagocytic activities.
Attach to peritoneal
mesothelium
1. Intraabdominal
Disease (abscesses):
opportunistic, associated
w/ post-op. peritonitis,
inf. abdomen w/
intestinal contents
gunshots, stab wounds,
surgery, cancer, (80% by
b. fragilis) UTI in women
lead to pelvic abscesss
(PID), & brain & lung
infection
Both
humoral &
CMI
involved in
combating
Bacteroides
infections
Debridgement
& surgical
drainage
before
antibiotic
treatment
- clindamycin
slender
rods, pleomorphic
obligate
anaerobe
non-motile
capsule
NO
endotoxin
activity b/c
it lacks
Lipid A !!!
Superoxide
dismutase (+)
Catalase (+)
Indole (+/-)
Growth in 20% bile
Antibiotic Resistant
- colistin
- kanamycin
- vancoymcin
MOST numerous
bacterial species in
human body
Outnumbers E. coli
in colon.
Alcoholics, immunocompromised
patients, patient w/
anesthesia can lead to
pulmonary infections
(opportuntistic)
Mixed w/
an/aerobes
May have synergistic
interaction
-------------------Obligate
anaerobe ::
facultaitive &
anaeroebe
(10,000: 1 ratio)
5. Crepitant cellulites
(especially in foot),
usually post-op inf.
6. DIABETIC FOOT
INFECTIONS
(FECAL FALL OUT)!!!
Seriously ill:
- chloramphenicol
Alternatives:
- erythromycin
or moxalactam
Proteus
mirabilis
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
g(-)
Grows on
blood agar
forms large
swarming
colonies w/
blood agar
only w/
putrid odor
Oxidase (-)
Lactose (-)
Indole (-)
Methyl red (+)
Urease (+)
TSI & SIM (+) for
H2S
Citrate (+)
VogesProskauer (-)
1. Urinary tract
infections: a)
pyelonephritis
b)cystitis. Infections
may be acute or
chronic.
IgA, IgG,
made
against
various
bacterial
components.
Ampicillin for
cystitis
Symptoms:
pain
fever
pyuria
hematuria
urination
(synchuria)
PMN
involved in
acute
infections
(pus is
formed)
pairs or
chains rods
facultative
anaerobe
highlymotile b/c
peritrichou
s flagella
Phenylalanine
deaminase (+)
distinguish from
P. vulgaris!!!
Nosocomial or
iatrogenic infection
UTI can happen in
healthy & immunocompromised w/
large inoculum ==>
opportunistic
3. LPS (endotoxin)
Hortizontal
transmission
Macrophage
s & T cells
respond to
chronic
infections
Proteus
vulgaris
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
g(-)
rod, pairs,
chains
Grows on
blood agar
forms large
swarming
colonies w/
blood agar
only w/
putrid odor
Oxidase (-)
Lactose (-)
Indole (+)
Methyl red (+)
Urease (+)
TSI & SIM (+) for
H2S
Citrate (-)
VogesProskauer (-)
Normal flora of
human LI (colon)
1. Urinary tract
infections: a)
pyelonephritis
b)cystitis. Infections
may be acute or
chronic.
IgA, IgG,
made
against
various
bacterial
components.
Ampicillin for
cystitis
Phenylalanine
deaminase (-)
distinguish from
P. mirabilis!!!
Hortizontal
transmission
Symptoms:
pain
fever
pyuria
hematuria
urination
(synchuria)
PMN
involved in
acute
infections
(pus is
formed)
facultative
anaerobe
motile b/c
peritrichous
flagella
Nosocomial or
iatrogenic infection
UTI occur in
immunocompromised
3. LPS (endotoxin)
4. Multiple drug resistance
Proteus mirabilis
Indole (-)
Citrate (+)
Phenylalanine
deaminase (+)
distinguish from
P. vulgaris!!!
Proteus Vulgaris
Indole (+)
Citrate (-)
Phenylalanine
deaminase (-)
Macrophage
s & T cells
respond to
chronic
infections
Europathogenic
E. Coli (UPEC)
Extraintestinal E.
coli infection
Cell
Features
Colony
Features
Lab
Characteristic
Source &
Transmission
Virulence Factors
Associated
Diseases
Host
Defenses
Immunity
Treatment /
Prevention
g(-)
rod, pairs,
chains
Grows on
almost any
agar surface
forming
large gray
colonies. On
EMB, have
metallic
sheen (b/c
eosin)
Oxidase (-)
Lactose (+)
Sucrose (+)
Indole (+)
Methyl red (+)
Urease (-)
TSI (-) for H2S
Citrate (-)
Normal flora of
human LI (colon)
1. Urinary tract
infections: (#1 cause
of UTI, 80-90%)
a)pyelonephritis
infection of kidneys.
Infections may be
acute or chronic.
Most nosocomially
acquired infections
are complicated &
present as
pelonephritist. They
are opporunitic &
infect
IgA, IgG,
made
against
various
bacterial
components.
Ampicillin for
cystitis
PMN
involved in
acute
infections
(pus is
formed)
Ampicillin &
gentamycin -
facultative
anaerobe
motile
Enterobacter
yields larger
colonies
VogesProskauer
(+) This unique!!!
Nosocomial or
iatrogenic infection
UTI occur in
immunocompromised
primarily
Hortizontal &
Vertical transmission
Macrophage
s & T cells
respond to
chronic
infections
L
theZoonotic
(GI infect)
Cell
Features
Colony
Features
Source &
Lab
Characteristics Transmission
Campylobacter
g(-)
CAMPY
agar
supplement
w/ blood &
other
nutrients
Oxidase (+)
Catalase (+)
Hippurate
Hydrolysis (+)
jejuni
PLEOMORPHIC
Curved
rods, spiral
forms w/
coccobacilli
Microaerophilic
(6% O2 &
10% CO2)
Motile (can
penetrate SI
& multiply)
Darting
motility
Grows from
4 - 42C to
inhibit other
bacteria
Urease (-),
[differentiate from
helicobacter]
Fecal specimen:
CAMPY AGAR
+vancomycin
+cefoperazone
Grows @ 42C,
O2 & CO2
Animal GI tract
(zoonotic infection)
Contact w/ infected:
animals, dogs, cats,
fowl (chicken), but
NOT eggs!
Even animal scratches
(did you see her nails?)
Improper handling:
- utensils & cooking
Raw unpasterurized
milk or water
contaminated (feces)
b/c bacteria survives in
milk for up to 5 weeks
when stored at 4C
Sensitive to chemical
disinfectants, acidity, &
chlorination
Relate to spontaneous
abortion(effect) infant
b/c infected
genitourinary tract xover placenta
Oral-fecal route (man
to man transmission) *
in children
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
1. CT like enterotoxin
2. cytotoxin (not Shigalike) results in bloody
diarrhea
3. LPS (endotoxin)
4. Flagellum: bacterial
motility; darting
movement
5. adherence factor
6. grows well w/ bile
7. can be invasive
1. ENTERCOLITIS: acute
infection of epithelium of SI
(jejunum & ileum) & LI.
Common in children
Acute
inflammatory
response by
PMN. Both Tcell mediated
immunity &
secretory IgA &
IgG.
Erythromycin
Zoonotic
(GI infect)
Cell
Features
Colony
Features
Lab
Source &
Characteristics Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Yersinia
Enterocolitica
g(-)
Grows on
blood agar
Oxidase (-)
Catalase (+)
Lactose (-)
Urease (+)
Methyl red (+)
VogeProskauer (-)
1. V and W antigens:
unknown f(x) but
essential (found in Y.
pestis)
1. (Hemorrhagic)
Enterocolitis: Acute infection
of the epithelium of the SI
(ileum) & LI. Symptoms of GI
tract include: fever, nausea,
abdominal discomfort,
headache, water diarrhea
which may be bloody + pus
(enteric inflammation).
Acute
inflammatory
response by
PMN. Both Tcell mediated
immunity &
secretory IgA &
IgG.
short rod
motile
No
siderophore,
so needs
iron for
growth
non-motile
at 37C or in
host
Tolerates at
cold storage
4C
facultative
anaerobe
Animal GI tract is
reservoir therefore
zoonotic infection
Water contaminated
w/ animal feces may
also be involved.
Oral-fecal route
involved man-man
transmission
Raw milk (also from
cold-stored blood)
Y. enterocolitica is
NOT need insect
vector for transmission
2. Enterotoxin: YST is
heat-stable enterotoxin
similar to ETEC (E.coli)
3. LPS (endotoxin)
4. Flagellum: mediates
motility outside of host,
but non-motile at 37C
Y. enterocolitica is destroyed
by stomach acidity, large
inocula 10^9 cells to be
infected.
5. Serum resistance:
(plasmid encoded)
7. Genes, invasiveness:
- Inv gene (invasion),
surface protein
- Ail gene (adherence
invasion locus),
facilitate entry into
specific cells
8. FACULTATIVE
INTRACELLULAR
9. Pathogenicity island
10. Type III secrete
proteins
VF regulated by
calcium & by
temperature
4. Reiter syndrome:
- post-infection, arthritis,
associated w/ HLA-B27
Bacteremia w/ this organism ;
therefore, can be blood-borne
by transfusions
W/ Y.
enterocolitica
sepsis,
gentamycin of
Bactrim used
Use good
hygiene
Fever
related
infection
Cell
Features
Colony
Features
Lab
Source &
Characteristics Transmission
Brucella
Species
g(-)
Grows
slowly on
blood agar
Oxidase (-/+)
Cabalase (+)
Urease (+/-)
TSI (+/-)
No fermentation
N03 reduction
coccobacilli
aerobic
non-motile
Requires
blood media
LPS: associated
antigens, A =
abortus antigen &
M = (melitensis)
antigen, are
present
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
1. Superoxide dismutase:
Allows survival w/in
PMN & phagocytes
1. Brucellosis: Enteric
Fever simlar to Typhoid
Fever. Systemic infection
involves multiple organs,
include GI tract, liver, (RES
= reticular epithelial organs.
Organs , macrophages
(spleen, liver, bone marrow,
lymph nodes, kidneys)
May result in enlargement,
endocarditis & p.neumonia.
Ab (IgM, IgG)
Treated w/
(a)
oral doxycycline
+ intramuscular
gentamycin
Symptoms:
- malaise, chills, sweats, &
fatigue, weight loss, nonproductive cough & fever
(intermittent).
IgG indicates
relapse
2. Survives in reticular
endothelial cells. B.
Abortus block
acidification.
Intracelluarly releases 5
& inhibits
myeloperoxidase halide
system to generate toxic
oxygen.
3. LPS (endotoxin)
4. Serum resistance
2. UNDULANT FEVER/
BANGS DISEASE /
MALTA FEVER
- fever is intermittent or
diurnal. Untreated, results
in chronic flue conditions.
May also see bone & joint
infections, severe
depression, &
osteomyelitis.
or
(b)
doxycycline +
rifampin
difficult to treat
takes 4-6 weeks
& it is
intracellular
Pregnant
women should
use: Bactrimn +
gentamycin
Best to
pasteurization
of milk &
vaccination of
farm animals
Granuloma formation in
liver, spleen, bone marrow
& changes in the organs.
Brucella infections leads to
CHRONIC disease (test
bank: 10 day periodicity)
Infect a variety of animals & can cause disease in humans as opportunistic infections. Under goes UNDULANT FEVER (waves peaks & valleys)
Human
Disease
B. melitensis
- more infectious but primarily in goat & sheep
B. suis
- infections in swine
B. canis
- dogs, foxes, coyotes
- suppurative, destructive
disease w/ granuloma formation
Rickettsiallike agent
Cell
Features
Colony
Features
Lab
Characterist
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
Coxiella
Burnettii
g(-)
Grows in
cell culture
or in animals
or in
embryonated
eggs / tissue
culture
(needs to
grow w/
cells no
artificial
media
acceptable,
not even w/
blood)
Weil-Felix
Reaction
(Rickettsia have
antigen on
surface that
cross react w/
antigen on
certain Proteus
species)
Animals are
reseservoir for
Coxiella. Zoonotic
infection. Infected
farm animals cows,
goats, pigs, rabbits,
birds.
1. Superoxide dismutase
- survival within the
acidic phagolysosome
Tetracycline for
pneumonia
CMI and
cytokines lead
to intracellular
killing of
Coxiella.
Doxycycline +
TMP-SMZ
(Bactrim) w/
min. 2 years
coccobacilli
aerobic
related to
Rickettsia
2 phases growth
1. spore/cyst
- Dry phase
- animal urine
2. veget. phase
Not effective
spore compare
w/ other
endospores
b/c this is g(-)
** Obligate
Intracellular!
(can also exist
outside of cell,
doesnt need
to be spread
by any vector)
Ox-19 (-)
Ox-2 (-)
Ox-K (-)
Indirect
fluorescent
antibody kit on
smear,
detection
important
(grown in yolk
sacs, look for
complement
fixing ab, inject
sputum, blood
into hamster)
Transmission occurs
by aeorsoles (contain
spores) from dried
urine, feces or milk.
Ingestion of raw milk
from infected animal
Spores / cysts survives
at 60C for 1 hr
therefore
pasteurization at 62.9C
Test Q Characteristic:
- Not vector borne,
difference btw
Rickettsial disease,
ticks can be involved in
transmitting Coxiella.
Ticks are NOT direct
source. Tick feces on
cattle hides get
transmitted when
human inhales these
spores.
2. * ACIDOPHILIC
- spore taken up by
phagocyte, metabolically
activated by acid of
phagolysosome
(multiplies)
3. LPS (endotoxin): phase
variation
a) phase I: highly inf.,
surface antigen blocked
b) phase II: less inf.
4. Cysts or spores allow
for Coxiella to survive for
long periods of time
under adverse conditions
2. Q Fever Pneumonia:
Atypical pneumonia w/
non-productive cough,
inspiratory crackles & flulike symptoms. No fluid in
lungs
3. Q Fever hepatitis/
Hepatosplenomegaly:
Fever & observe liver
granulomas (upon biopsy),
very rare as result of
chronic latent infection
4. Q Fever endocarditis
(subacute): culture (-),
associated w/ chronic
(latent) infection, valvular
heart disease w/ preexisting damage of valves.
Incubation months to years.
5. Chronic (latent)
infection: osteomyelitis,
neurological symptoms,
heptatis
Granulomas
formed by DTH
Rxn
Delayed Type
Hypersensitivity
Francisella
Tularensis
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
g(-)
Grows on
medium
containing
blood,
glucose, &
cysteine
(recommend
chocolate
agar +
cysteine)
It is
hazardous!
Transmitted by direct
method or by vector. Wild
animals are reservoir.
1. TULAREMIA (RABBIT
FEVER):
Difficult b/c
intracellular
2. LPS (endotoxin)
coccobacilli
(pleomorphic,
very small)
facultative
anaerobic,
but prefers
O2
non-motile
3. Survive in
monocytes and PMN
(protect from ab &
complement). Resistant
to lysosomal oxidans,
include HCl by PMN
and inhibits
phagosome-lysome
fusion
2. Ulceroglandular
tularemia: contact w/
infected animal, arthropod
bite, open ulcer at entry site
(ex. Lower extremity or
trunk), possible bacteremia
3. Oculoglandular tularemia
(eye): conjuctival ulcer,
regional lymph nodes, opens
& drains bloodstream, liver,
spleen, lungs. Invasiness &
goes to the blood stream.
4. Pneumonic tularemia: if
reach lungs by blood or by
respiratory route (aerosol)
then spread by person by
person. High mortality rate.
Especially inhaled version!
5. Typhoidal tularemia:
ingest food or water (larger
inoculum size) GI & fever
symptoms can cause sepsis
w/ multi-organ involvement,
even pneumonia
6. Glandar: painful
adenopathy w/ overlapping
ulcers
Antibotics:
tetracycline
gentamycin
streptomycin
chloramphenicol
penicillin (some)
Prevention:
Handling
animals, avoid
infected animals
Vaccine:
Live-attenuated
vaccine used
only on people
at risk animal
handlers
Bartonella
henselae
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence Factors
Associated Diseases
Treatment /
Prevention
g(-)
White, rough,
mixed w/ tan
circular
Oxidase (-)
Catalase (-)
1. LPS (endotoxin)
Self-limiting
1. Bartonellosis (CAT
SCRATCH FEVER): symptoms
begin 2 weeks exposed. Local
lymphadenopathy (lymph
nodes), fever, & pustules at
scratch site. It is self-limiting
last months to years. Forms
granuloma.
curved rods
aerobic
motile
twichting
motility
Grow slowly
on selected
blood agar
Easy to see w/
Ag
impregnation
techniques
15% CO2
Facultative
intracellular
pathogen
3. Facultative intracellular
pathogen
2. Bacillary angiomatosis: in
immunocompromised patients
(AIDS) observe chronic
spreading cutaneous & visceral
lesions, Kaposis sarcoma-like
lesions may appear, differ
histologically.
Bacteremia & sepsis may also
occur in these patients
3. Sub-acute bacterial
endocarditis
4. Bacillary peliosis hepatits
(Peliosis): cyst of blood-filled
granulomas
5. Conjunctiva infection
(Oculoglandular syndrome):
swelling of eye, jaw, cervical
lymph nodes
Can scratch
disease treat w/
needle aspiration
but NO
antibiotics
Bacillary
angiomatosis &
sepsis treated w/
erythromycin
Pasteurella
multocida
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
g(-)
Grows on
blood agar
produce
yellow
colonies w/
musty
odor
Oxidase (+)
Catalase (+)
Indole (+)
Methyl red (-)
Nonhemolytic
Sucrose
utilization (+)
1. LPS (endotoxin)
Penicillin or
ampicillin &
tetracycline.
3. Pili mediates
attachment
T-cell mediated
immunity is
important.
Strong acute
inflammatory
response w/
PMN is very
important
coccobacilli
w/ bipolar
staining
facultative
anaerobe
non-motile
intracellular
pathogen
Grows best
w/ 02 at
37C
2. Large polysaccharide,
capsule: antiphagocytic
4. beta lactamase: in
some strains
Allergic patients
- doxcycline
Avoid contact
w/ wild &
domestic
animals & birds
Flea
borne
Cell
Features
Colony
Features
Lab Charact.
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Yersinia
pestis
g(-)
Grows on
blood agar.
Oxidase (-)
Catalase (+)
Lactose (-)
Urease (-)
Methyl red (+)
VP (-)
BUBONIC PLAGUE:
w/in 2-3 days of flea-bite.
Symptoms include: fever,
chills, painful
lymphadenitis (buboes).
Inguinal, axillary, femoral
& cervical lymph nodes
involved, & may swell.
Bacteremia, sepsis
follows. Vasculitis may
lead to gangrene (Black
death, necrosis of
capillaries, blacken body).
Infection is fatal. If
swallowed, stools maybe
bloody + pus (enteric
inflammation). May last
for weeks w/ treatment.
Granulomas
are result of
DTH.
ASAP! w/
Streptomycin
short
coccobacilli
w/ bipolar
staining
facultative
anaerobe
non-motile
facultative
intracellular
pathogen
Epicellulargrows both
on tissue &
on plates
Grows best
at 28C w/
oxygen
4. Fibronolysin: produced,
breaks the clot & spreads
5. Iron acquisition:
- takes up iron (hemin) by
siderophore-independent
Produce siderophore (only one)
6. Protein capsule-complex:
Fraction1: not produced in rat
flea plasmid encoded allows
for survival inside of
phagocytes
7. Promote invasion &
proliferation within host cells
and resistant to killing by host
LCR plasmid products are
expressed at 37C and at Ca++
which directs V and W antigen
synthesis.
8. Pesticin: bacteriocin, makes
the organism more virulent
9. pur protein: allows uptake of
adenine & guanine nucleotides
10. pigment production
11. Pathogencity island
12. YopE, disrupt actin filament
13. YopJ/P: initiate apoptosis
14. Plasminogen activator
15. Type III: secretion system
Septic plague: NO
occurrence of buboes,
found in children bites
from flea. Leads to
intravascular coagulation
w/ vascular & renal
collapse.
Pneumonic plague:
already in lungs, inhales.
Results in
bronchopneumonia.
Symptoms include: fever,
cough w/ blood & loaded
w/ bacteria. Deadly &
rarest form. HIGHLY
INFECTIOUS! 90-100%
death rate.
Sylvatic plague: fleas on
rabbits, wild rats to fleas
on urban rats to human
fleas to human.
Acute
inflammatory
response by
PMNS. Both
CMI and
sIgA and IgG
are important
against
infection.
Chloramphenicol
Tetracylcine
Hypotension use
dopamine.
Disease is
prevented by
rodent control
but also need to
control rat flea &
human flea. Use
pesticides.
Rickettsia
Typhi
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
g(-)
Grown in
cell culture
Weil-Felix
Rxn
(agglutinate
w/ Proteus
vulgaris) ex:
1. LPS (endotoxin)
Ab may be
important
initial barriers
against
infection.
Previous
infection
confers longlasting
immunity.
Oral
doxycycline
(makes teeth
yellow in
children)
Aka
small
coccobacilli
R. Mooseri
non-motile
Vec./spec
Flea-ty
end
ENDEMIC
Radiates
outward
aerobic
OBLIGATE
INTRACELLULAR
PATHOGEN
Ox-19 (+)
Ox-2 (-)
Ox-K (-)
Maybe transmitted by
transovarian method
(moma fly to baby fly)
Also flea bites (w/ feces)
transmitted into bite
wound.
2. Factors inducing
phagocytosis. Inside
phagocytes the
organism survives &
enters into the host
endothelial cells. Evade
host cell lysis (escape
from cell).
3. Produe
phospholipase A
(lecithinase) which
lyses phagosomes
enabling rickettsia to
enter into host cell
cytoplasm.
4. Organism able to
survive in rat blood &
flea feces
5. Loosely adherent
slime layer.
1. Endemic flea-borne
TYPHUS aka Murine typhus
Systemic inf. following a flea
bite. Rickettsemia causes
vasculitis of the capillary
beds of many organs
particularly of the liver &
skin.
Typhus produces fever,
chills, headache, & macular
rash mosly on trunk
(hallmark) and may
eventually spread outward
to extremities.
This differs from Spotted Fever,
rash start on palms & soles &
radiate inward to trunk.
Observed crossimmunity w/
R. prowaseckii.
Preg. Women
are treated w/
chloramphenicol
Killing rat is
not enough, b/c
flea could jump
to humans.
Louse-Borne
Bartonella
Quintana
(Rochalimaea
Quintana)
Trench
warfare
Epidemic
responsible
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
g(-)
Grows very
slowly on
selective
agar
medium
Oxidase (-)
Catalase (-)
1. LPS (endotoxin)
2. Facultative
intracellular pathogen
1. Bartonellosis Trench
Fever (5 day fever).
Remember it is facultative
intracellular & has
periodicity cycle in 5 day
periods. Symptoms include
fever, headache, exhaustion.
temp. during this
periodicity (Quintana),
chills severe bone pain &
transient rash on trunk &
may see splenomegaly &
myalgia. Self limiting but
may relapse.
Doxycycline or
chloramphenicol
curved rods
motile
(twitching)
aerobic
OBLIGATE
INTRACELLULAR
PATHOGEN
2. Reemerged in AIDS
patient & homeless
(immuno-compromised)
Inhalation of louse feces is
another method of
transmission.
Epidemics is common.
Associated w/ filth &
poor santition.
Pregnant women
- erythromycin
Louse-Borne
Rickettsia
prowaseckii
Mnemonic
Vect/Spec/dis
Lousy pr-epi
Epidemic
responsible
Spreads
outward
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
g(-)
Grown in
cell culture
Weil-Felix
Rxn
(agglutinate
w/ Proteus
vulgaris) ex:
1. LPS (endotoxin)
1. Epidemic louse-borne
typhus:Systemic f(x)
following a louse bite.
Rickettsia cause vasculitis of
capillary beds of many
organs particularly of the
liver & the skin.
Ab may be
important
initial barriers
against
infection
Oral doxycycline
very small
coccobacilli
non-motile
aerobic
Ox-19 (+)
Ox-2 (-)
Ox-K (-)
OBLIGATE
INTRACELLULAR
PATHOGEN
2. Produce factors
inducing
phagocytosis. Inside
phagocytes the
organism survives and
enters into the host
endothelial cells.
Evade host cell lysis.
3. Produces
phospholipase A
(lecithinase) which
lyses phagosomes
enabling rickettsia to
enter into host cell
cytoplasm.
4. Organism is able to
survive in rat blood &
flea feces
Clotting abnormalities
Symptoms include:
- high fever, chills, heaches,
& pain
Rash mostly on trunk (key
feature!) & spreads
outward toward extremities
EXCEPT face, soles &
palms. (differs from
Spotted Fever which starts
from palms & soles &
radiate inwards to trunk)
5. Slime layer
Previous
infection
confers longlasting
immunity
Pregnant
women are
treated w/
chloramphenicol
Tick-Borne
Rickettsia
rickettsii
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses &
Immunity
Treatment /
Prevention
g(-)
Grown in
cell culture
Weil-Felix
Rxn
(agglutinate
w/ Proteus
vulgaris) ex:
1. LPS (endotoxin)
Ab may be
important
initial barriers
against inf.
Previous inf.
confers longlasting
immunity.
Oral do Oral
doxycycline
very small
coccobacilli
Mnemonic
vect/spec/dis
Ricky-ticky
spot
Caus. Agent:
Rocky Mount.
Spotted Fever
(RMSF)
#1 rickettsia
disease & nonvector borne
disease in US
pop.
Also note:
Ticks may
deliver
Rickettsia or
lyme disese
non-motile
aerobic
OBLIGATE
INTRACELLULAR
PATHOGEN
Ox-19 (+)
Ox-2 (+)
Ox-K (-)
Zoonotic infection of
man occurs by bite of
infected tick (vector).
Infected tick, organism
may be transmitted to
tick offspring by
transovarian method.
2. Produce factors
inducing
phagocytosis. Inside
phagocytes the
organism survives &
enters into the host
endothelial cells.
Evade host cell lysis.
3. Produces
phospholipase A
(lecithinase) which
lyses phagosomes
enabling rickettsia to
enter into host cell
cytoplasm (also
deacidify vacuole)
4. Organism is able to
survive in rat blood &
flea feces
5. Slime layer
Test Question: #1 non-vector borne disease in US Rocky Mountain Spotted Fever primarily found on East coast
Test Question: #1 vector borne disease in US Lyme disease (carried by tick)
Symptoms:
- rapid onset, high fever,
nausea, vomiting, myalgia,
headache see macular rash
Rash spreads from
extremities to trunk. (rash
works inward)
Disease may lead to
pulmonary failure, renal
failure, encephalitis, coma,
& death.
Pregnant
women are
treated w/
chloramphenicol
Prompt removal
of ticks also
important as
preventive
measure.
Test Question: Endoflagella (axial filaments) inside of outer membrane NOT exposed to
outside but can be shed in infected individual. Lives in intestines & in mouth
Serology
Chlamydia
-
Treponema
pallidum
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence
Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Thin (0.5 u)
tightly coiled
spirals (5-15u)
Can not be
cultured in
vitro!!!
Grows in
rabbit
testicles or
in rabbit
epithelial
cell culture
Darkfield &
immunofluorescent
methods &
SEROLOGY
Vertical transmission
(mother to child) through
the placenta in utero.
1. Glycolipid
instead of LPS
(Glycolipid is rich
in cardiolipin &
other
phospholipids to
test for syphillus)
g(-) difficult to
see b/c too thin
Look for
spirochetes
using direct
miscroscopy
Syphilis is
treated w/
penicillin (at all
stages) &
penicillin can
also be given
prophylactically.
Visualized w/
darkfield
microscopy! or
immunofluorescent
microscopy &
silver
impregnation
Moves using
axial filaments,
ENDOflagellae
Microaerophilic
Sensitive to
environmental
influences
Horizontal transmission
by sexual contact.
2. Motility
3. complex outer
membrane
structure w/ few
membrane bound
outer proteins
4. Outer membrane
promotes
adherence to host
cells by tips
bacteria
5. Hyaluronidase:
enables spirochete
to invade host
tissue
6. Survive
intracellularly
(phagocyctic cells)
& extracellularly in
host
7. fibronectin (antiphagocytic) blocks
phagocytosis
Little
protection
immunity
during 1
and 2 stages.
T cells are
involved in
gumma f(x)
If sensitive Pen.
Use ==>
erythromycin or
tetracycline
Leptospira
Interrogans
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence
Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
g(-) spirochete
Parasites of non-human
animals (ie livestock &
dogs). Best friend (dog
prone to infect man)
tighly coiled
spirals w/
unusual
hooked ends
Grows
rapidly in
complex
media
Serological
tests such as
agglutinating
complement
fixation or
lysis in
presence of
complement.
1. LPS (endotoxin)
thin
Can be
cultured in
vitro.
Oral
doxycycline,
erythromycin,
or penicillin
3. Outer surface
Use darkfield
microscopy,
immunofluorescent
miscroscopy or
stained by
Silver
impregnation
technique.
Uses fatty
acids &
alcohols as
carbon
source.
Obligate aerobe
Motility (via 2
endoflagellae
but least motile
of all
spirochetes)
__________
* Twitch
motility
differs from
spirochetes
Interrogans:
shape, question
marks ???
complex outer
membrane
structure
contains LPS
Likes
alkaline
conditions.
Culture from
blood, CSF, &
urine.
Zoonotic infection
Survives for months in
soil & water but sensitive
to Chlorine
2. Hyaluronidase
- invasiveness
4. Maybe hemolysin
5. Motility &
thinness (penetrate
intact mucous
membranes; skin
via small cuts or
abrasions)
Lyme
disease
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence
Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Borrelia
burgdorferi
Thin
Cultured in
vitro
Darkfield
microscopy
Stage 1:
Use ELISA
1. Glycolipid
(similar to
Treponema) NO
LPS
Grown on
BarbourStoennerKelly
medium
contains
bovine
serum
albumin
(BSA) &
rabbit
serum at
30C
#1 vector
borne
disease US
Loosely coiled
long spirals
(spirochete)
g (-)
Use darkfield
microscopy,
fluorescent
miscroscopy +
acridine
organe dye or
stained by
Silver
impregnation
technique.
Microaerophilic
Rotational
motility
(endoflagellae,
axial filaments)
DNA is
fragmented w/
some being
linear
Western blot
also PCR
2. Surface protein:
produces many
different surface
antigens during
infection.
ANTIGENIC
VARIATION
3. penetrate
epithelial cells
4. Survives in blood
& in tick ability to
resist phagocytosis
5. Hemolysin
Stage 1:
appears
- Erythema Migrans (EM) or
Erythema Chronicum Migrans:
Lesion or rash (Bulls eye lesion)
- Symptoms:
headache, fever, stiffneck, malaise,
& lymphadenopathy.
Stage 2:
- Lyme arthritis (uniarticular ie
involving 1 joint) Reversible w/
treatment.
- Symptoms: neuroborreliosis
(meningitis, peripheral
neuropathy, encephalitis, Bells
Palsy) may last for months years
Stage 3:
Follow a latent & asymptomatic
period. Late or Chronic Lyme
disease.
Symptoms: similar to stage 2 but
worse. Mostly arthritis.
Oral doxycycline
Stage 2 & 3:
IV ceftriaxone
Prevention Tips
Dress properly
w/o skin
exposed, use
insect repellent
Borrelia
recurrentis
relapse
fever
Epidemic
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence
Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Thin
Cultured in
vitro
Darkfield
microscopy
1. Glycolipid
2. Surface protein
(VARIABLE
MAJOR
PROTEIN) which
produces many
different surface
antigens, resulting
in several relapses
(ANTIGENIC
VARIATION).
Stage 1:
1st fever symptoms (maybe fatal
due to shock-hypotension).
Spirochetes from lice (or tick)
penetrate the skin & skin & spread
through the blood. Treat w/
antibodies will clear most
circulating organisms, so host
experience a non-febrile latency
period 7-10 days.
Oral doxycycline
Penicillin
Tetracycline
Chloramphenicol
3. ability to
penetrate epithelial
cells
Stage 2:
Spirochetes go through antigenic
variation & a new variant will be
produced. Results in bacteremia &
a second fever stage (relapse).
Loosely coiled
long spirals
(spirochete)
g (-)
Use darkfield
microscopy,
fluorescent
miscroscopy +
acridine
organe dye or
stained by
Silver
impregnation
technique.
Microaerophilic
Rotational
motility
(endoflagellae,
axial filaments)
DNA is
fragmented w/
some being
linear
Grows
slowly on
complex at
30C
4. Survives in blood
& in lice has the
ability to resist
phagocytosis
Cytokines
may be
involved in
disease
resolution
Erythromycin
(children &
pregnant women)
NOT
spirochetes!
Cell
Features
Colony
Features
Lab
Charact.
Source &
Transmission
Virulence
Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Chlamydia
trachomatis
Grows in
cell culture
Difficult to
diagnose.
1. Intracellular
survival
a) stimulates nonphagocytic
epithelial cycle to
engulf them
Ab not
effective.
Oral doxycycline
Most
common
STD
compact
inclusion body
w/ glycogen,
make folic acid
therefore
sensitive to
sulfonamide
ONLY!!!
(differs from .
C. psittachi)
LGV test
dead bacteria
injected
under skin &
look for DTH.
Serology
15-20
different
serotypes
b)Inhibit
phagosomelysosome fusion
(all 3 chlamydia
have them!)
2. Unusual life
cycle: elementary
bodies can infect
host macrophages
& epithelial cells,
becomes reticulate
bodies & produce
new elementary
bodies ==>
released when host
cell lyses.
3. Endotoxin
4. toxic factor
5. Type III Secretion
system
PMN
effective in
killing.
Sulfonamide
(unique)
Erythromycin
Cefoxitin &
doxycycline if
concurrent w/
N. gonorrhea
infection
Antibiotics such
as erythromycin
or tetracycline
are used in form
of eyedrops for
new borns.
NOT
spirochetes!
Cell
Features
Colony
Features
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Chlamydia
psittaci
(psittaci)
Grows in
cell culture
1. Intracellular survival:
a) stimulates nonphagocytic epithelial cycle
to engulf them
Ab not
effective.
Doxycycline and
azithromycin
Psittacosis (ornithosis)
PARROT FEVER:
Can exist as asymptomatic,
likely to be severe,
frequently fatal
pneumonia. Can involve
other organs: jaundice,
acute thyroiditis,
meningitis w/ delirium. It
is a latent infection. Lung
inhaled form it is atypical
pneumonia. Spread by
human to human.
PMN very
effective in
killing.
Alternatives:
Ofloxacin,
erythromycin,
amoxicillin
(pregnant women)
Parrot
Fever
diffuse
inclusion body
no glycogen
cant synthesize
folic acid,
resistant to
sulfonamide!
Previous
infection
provides no
immunity &
subsequently
see relapse &
reinfection.
Quarantine
imported birds
NOT
spirochetes!
Cell
Features
Colony
Features
Source &
Transmission
Virulence Factors
Associated Diseases
Host
Defenses
Immunity
Treatment /
Prevention
Chlamydia
pneumoniae
Grows in
cell culture
1. Intracellular survival:
a) stimulates nonphagocytic epithelial
cycle to engulf them
1. Atypical pneumonia:
(sneezing or coughing): mild
or asymptomatic but in
elderly, it can be fatal.
Involves in the lower lobe.
Pneumonia and bronchitis in
adolescents & adults is often
seen w/ pharyngitis and
sinusitis.
Other Symptoms: nonproductive cough, fever,
chills, headache & malaise.
Complication of coronary
artery disease &
endocarditis.
Ab not
effective.
Doxycycline and
azithromycin
PMN very
effective in
killing.
Alternatives:
Ofloxacin,
erythromycin,
amoxicillin
(pregnant women)
diffuse
inclusion body
no glycogen
cant synthesize
folic acid,
resistant to
sulfonamide!
Previous
infection
provides no
immunity &
subsequently
see relapse &
reinfection.
Mycology (Fungi)
Characteristics:
Eukaryotic cells w/ cell walls (no peptigylcan)
o Chitin, cellulose, glucans, mannans (ex. polymers of sugars)
o Non-photosynthetic, Heterotrophs, saprophytes, or saprobes, parasites
Cell membrane
o Ergosterol
o No motility
Cryptocococucus neoformans (only one with capsule), anti-phagocytic!
2 forms:
a) unicellular yeast (chains)
b) multicellular mold (septate) (filaments structures aka hyphae)
-
c)Dimorphism triggers:
1) 25C ==> forms macrocondia (mold), Chlamydia spore
2) 37C ==> budding yeast form a non-mold form (C. immitis)
d)Reproduction:
Anamorphic
- Asexual
-
Telomorphic
- Sexual
Thallospores:
arthrospores: barrel shaped, thick-walled produced by hyphae fragmentation
chlamydospores: swelling of hyphal fragment, thick double wall
blastospores: simple budding from parent cells
Sexual Reproduction (cells are 2N), Perfect state
oopspores
zygospores
ascospores (sac)
basidiospores: club shaped (mushroom)
Zygomycetes: (phycomycetes):
ex. bread molds, most primitive, filaments, aseptate, sexual & asexual
(sporangium formation)
Ascomycetes (Ascomycotmia):
Asexual
- conidia
Sexual
- ascospores (incl. dermatophytes) and spherules
Basidiomycetes:
septate hyphae, sexual spores
Deuteromycetes (Fungi Imperfectii)
has sexual stages
Culture Fungi:
Sabouraud agar
o Slightly lower pH (more acidic)
o Contains dextrose & peptone
o Chloramphenicol to inhibit bacteria
o Cyclohexamide (Acti-Dione) inhibit saprophytes
Molds grows away from plate, looks fuzzy
o Vegetative hyphae = roots
Yeasts creamy opaque colonies
Dermatophyte Test Medium (DTM)
inhibits bacteria
cyclohexamide to inhibit saprophytic molds
dermatophytes turn medium yellow ==> red
Corn-meal Agar
test for spore formation
visualize chlyamydospore & blastocondia
production candida albicans
Monomorphic fungi
dermatophytes
o E (NS)
o M (SH)
o T (NSH)
Cryptoccous neoformans (encapsulated, endosporulating, spherules)
Aspergillus fumigatus (fungus ball)
Dimorphic fungi
Histoplasma (dusty environment, bird feces)
blastomyces (valley fever)
coccidiodies
sporothrix (rose garden cuts)
Lab diagnosis:
Potassium hydroxide: (KOH) used for diagnosis + heat for ID
Calcofluor: fluroscent stain, UV microscope
Gomori methenamine silver stain (GMS): tissue stains red & fungus blue
Lactophenol cotton blue dye: (stain hyphae): aniline stains fungal
India ink & test for capsule (-) stain ==> cryptoccocus neoformans
3 types of transmission:
Anthropophilic ==> human to human
Zoophilic ==> animal to human, ex. Microsporum canis
Geophilic ==> soil to human, ex. microsporum gypseum
Candida pseudohyphae, burrows into tissue
yeast disseminate easier body via blood
Antifungal agents: (ex. Nystatin, Amphotericin B)
Trichophyton (NSH)
Thermal morphic
moid
Cell features
Diagnosis
Disease
Dxn
Mentagrophytes
Yes
Rubrum
Yes
Tonsurans
Yes
Septate hyphae,
spiral,
microconidia,
grape-like cluster
Septate hyphae,
oval, tear-drop,
peg-shaped, cigar
shaped
Bright RED*
Tinea Capitis
Tinea Corporis
Tinea Cruris
Tinea Pedis
Tinea Ungium
Onychomycosis
Scraping of
infected skin, nail,
KOH
Black dot
Black spores lead
to tinea capitis
INDI Organisms # 4
Virus
Size & Structure
Enveloped: picked up from nucleus or p.membrane or created from cytoplasm ether sensitive
DNA Viruses
o
Are dsDNA except parvovirus
o
Are icosahedral, except poxvirus (brick, complex shaped)
o
Replicate their DNA in nucleus, except poxvirus
Virus Family
DNA type
Parvovirus
Papovirus
ssDNA
dsDNA
circular
dsDNA
linear
dsDNA
linear
Adenovirus
Herpes virus
Poxvirus
dsDNA
linear
Virion
(associated polymerase)
No
No
Envelope
Major viruses
Naked
Naked
Nucleus
Nucleus
No
Naked
Nucleus
B-19
Papilloma
Polyoma
Adenoviruses
No
Enveloped
(nuclear)
Nuclues; virus
assemble in nucleus
Yes
Enveloped
Cytoplasm
(DNA dept RNA
polyermase)
Enveloped
Nucleus, RNA
intermediate
Variola
Vaccinia
Molluscum
Contagiosum
Hep. B
Yes
Partially
dsDNA
circular
Mnemonic: Parvas Papa Adds Her Poxes to Hepas
Hepadnavirus
(+)RNA Viruses
Virus Family
RNA structure
Virion
(associated polymerase)
No polymerase
Envelope
Shape
Multiplies
Major viruses
Calicivirus
ss(+) RNA
Linear
Non-segmented
ss(+) RNA
Linear
Non-segmented
Naked
icosahedral
cytoplasm
Norwalk agent
hepatitis E
No polymerase
Naked
icosahedral
cytoplasm
No polymerase
Enveloped
icosahedral
cytoplasm
ss(+) RNA
No polymerase
Linear
Non-segmented
Coronavirus
ss(+) RNA
No polymerase
Linear
Non-segmented
RNA dep.
Retrovirus
Diploid
DNA
ss(+) RNA
Polymerase
Linear
Non-segmented
Mnemonic: Call Pico and Flo To Come Rightaway
Enveloped
icosahedral
cytoplasm
Enveloped
Helical
cytoplasm
Polio,
Enteroviruses
Rhino
Coxsackie
Hepatitis A
Yellow fever,
dengue, St.
Louis
encephalitis
Hepatitis C
Rubella, WEE,
EEE, Venez
encephalitis
Cornoavirus
Enveloped
Icosahedral
or
truncated
conical
Nucleus
Picornavirus
Flaviviros
Togavirus
ss(+) RNA
Linear
Non-segmented
HIV, HTLV,
Sarcoma
Papovaviruses:
virus types:
o
Papilloma: HPV types 1-58+. Causes human, cat, dog, & rabbit warts
o
Polyoma: found in mice which are asymoptomatic. If induced into newborn animals results in malignant tumors
virus structure:
o
icosohedral capsid virion, dsDNA, circular, replicated & assembled in nucleus
o
p53 and RB regulates cell growth but papovaviruses binds to them to promote cell growth
o
T angitens regulates transcription with the p53 and RB, T antigen is found w/ viral DNA for replication to continue in cell.
Papovaviruses:
o
Papillomaviruses replicate in the squamous epithelium of skin & mucous membranes to produce warts
o
Skin warts, anogenital warts (cervical cancer, 16,18 where E1 & E2 become inactivated so that E6 binds to p53 & E7 w/ RB)
Koliocytosis: infectious human papillomavirus of epi layer of uterine cervix or external genitals (condylomata acuminata)
Treatment warts:
o
Remove surgically cryotherapy (liq. N2), electric, or chemical means (ex. podophyllin)
o
Laryngeal warts: remove surgically but NOT w/ irradiation b/c could induce malignant changes
o
Imiquimod + IFN can promote faster healing applied to topically (ex. external genital regions)
o
Cidofovir: antiviral nucleoside inhibits viral DNA polyermase
Adenovirus:
Virus structure:
o
dsDNA, naked, icosahedral, linear shaped, fiber (attachment protein + hemagglutinin activity)
o
47 different types, permissive, found in human adenoids & tonsils
Disease:
o
Erythema infectiosum (fifth disease) - comment: remember a 5 finger slap in the face you get this redness!
o
1 of 5 common childhood exanthems or rashes (looks like slapped cheek (facial rash)
o
Chronic hemolytic anemia (ex. sickle cell anemia) leads to aplastic crisis (lytic on RBC)
o
Immunodeficient can lead to chronic anemia
transmitted:
o
vertically (cross placenta) results in spontaneous abortion associated w/ HYDROPS FETALIS
Herpesviruses
Lab diagnosis:
o
Tsanck smear (scrapings of infection) see Cowdry Type A cells (acidophilic intranuclear inclusion bodies) see syncytia
Virus replication:
o
Virus induces synthesis of viral thymidine kinase & DNA polymerase
o
Phosphonoacetic acid inhibits herpesvirus replication by inhibiting viral DNA polyermase
o
Viral protein are made in cytoplasm & enters the nucleus where they assemble w/ the DNA into virus particles
o
Virus buds from nuclear membrane, pickup lipid bilayer & viral proteins that have been inserted into it.
o
Infection can be lytic or lead to latent infection
Latent in nerves
Latent in
leukocytes-WBC
Varicella-Zoster
Chicken pox (multiple crops)
- occurs in children via mucosa the upper respiratory tract
- swelling of epi cells, eosinophilic inclusions found in
nuclei of infected cells & end up attacking nerve cells
- virus replication occurs in the nucleus
- incubation time: 2-3 weeks
- symptoms: fever, fash, vesicles appear
- differs from small pox (1 crop)
Shingles
- occurs in the posterior nerve & ganglia (Dorsal RG)
- reactivation of the chicken pox
- triggered by stress, immunocompromise, trauma
Treatment:
o
Acyclovir, vidarabine, idoxiuridine, trifluoridine
Most infection of infants, caused by intrauterine or early postnatal infection (pass to child)
Cytomegalovirus cells found in the epi tissues of liver, lungs, kidneys, lungs, GI, parotid gland, pancreas, etc.
o
Virus recovery:
Virus can be recovered from the mouth, urine, liver, adenoids, kidneys & peripheral blood leukocytes
Diagnosis of virus infection by owl cellsor owl eyes in the urine. Basophilic intranuclear inclusion body
Associated with Kissing Disease (mono, results in large lymph nodes & spleen)
Herpes Virus 6:
Herpes Virus 8:
Poxvirus
Virus structure:
o
Largest DNA, enucleated, complexed shape
Virus replication:
o
ONLY DNA replicates in the cytoplasm
o
Replicate in enucleated cells
Virus DNA and proteins are packaged into virus particles occurring in cytoplasm in the Guarnieri bodies
Small pox:
o
2 variants, enters in the mucous membranes of upper respiratory tract with incubation of 12-16 days.
o
Virus multiplies in lymphoid tissues with infection throughout the body. May result in scaring.
o
Diagnosis: Incoluated in embyronated eggs
o
Treatment: cidofovir (inhibits DNA polyermase) also it is safer w/ less side effects
Molluscum contagiosum
o
An ex. of a pox virus leads to skin infection, benign tumor, it is a nodular-wart-like growth
o
Transmitted: direct contact or fomites & spread by STD
o
Treatment: curettage (scrape) or liquid N2
Picornaviruses
Enteroviruses (intestine)
o
Polio and coxsackie viruses
Cardiovirus: in rodents
Virus characteristics:
o
(+)ssRNA, naked, icosahedral, smallest RNA virus, nucleic acid is infectious
o
Poliovirus: stable in acidic environment pH 3-9. Found in GI tract & in feces
o
Rhinoviruses: unstable in acidic environment pH 5-6. Found in oropharynx area
o
Replicates at 33C.
Poliovirus
o
Smallest RNA, 3 serotypes (1-3): 1&2, 2&3 cross react, 1 & 3 doesnt cross react
o
Inactivated by UV, drying. 1M MgCl2 thermally stabilizes b/c of the capsid proteins.
o
Immunological properties:
C antigencity is the empty capsid which lacks the vRNA. NO VIRUS RNA
o
o
o
Abortive: most common form. Malaise, fever, drowsiness, headache, nausea, vomiting constipation, & sore throat.
Nonparalytic: asceptic meningitis similar to symptoms from abortive with stiffness & pain in back & neck.
Factors alters the disease: fatigue, tonsillectomy incidence, pregnancy, age, steroids
Lab diagnosis: CSF in leukocytes
Treatment: aridone (binds to receptors change confirmation)
Prevention & Control: Vaccine
Salk Formaline Inactivation Virus
Sabin Live Attenuated Virus
- grown in monkey kidney
- grown in human diploid cells in culture
- inactivated could induce polio
- given orally: IgA
- boosters needed 3-5 years
- long term immunity
- develops IgG & IgM
- reverts to virulence
- no herd immunity
- herd immunity (virus cant spread, buffer zone)
Coxsackieviruses (enterovirus)
o
Coxsackie A: Found mostly in respiratory region. flaccid paralysis
o
Coxsackie B: Found mostly in the body region.
spastic paralysis
o
Diseases:
Herpangia:fever, soar throat, anorexia, vomiting, abdominal pain, vesicles in palate, uvula. Self limiting. Not herpes!
Hand-Foot-Mouth: oral & pharyngeal ulcers which may spread to arms & legs w/ mild fever
Rhinoviruses
o
Virus characteristics:
o
o
Common cold, at pH < 6-7 (unstable in acidic environment), found in nasopharyngeal cavity, not found in GI tract
H&M strains
Host: man
Control: Vaccine is not possible b/c too many serotypes!
Coronarviruses
Virus structure:
o
(+)ssRNA virus, enveloped, naked, helical, lipid containing, 2 glycoproteins at its surface (E1 & E2 (activtes HA)
Multiplication:
o
Different in sized viral mRNAs transcribed from vRNA
o
Occurs in cytoplasm: assembly by budding into ER & Golgi apparatus. Released by fusion via exocytosis
o
Multiplication is max. at ~32C
Pathogenesis:
o
Aerosol and large droplets
o
Coryzas (swelling of mucosal membrane of oropharynx), sneezing, nasal congestion, etc
o
Some can cause gastroenteritis
Prevention:
o
No vaccine or regulation available
Orthomyxoviruses (Myxoviruses)
Virus structure:
o
(-)ssRNA, enveloped, helical, segmented, own polyermase, infectious respiratory disease, 3 forms (A,B,C)
o
A type: replicate in humans & animals, B & C type: not as virulent
Hemagglutinin (HA)
- glycoprotein binds to cell receptors
- main antigen against neutralizing antibody
Neuraminidase ( NA)
- removes sialic acid virus spread in
respiratory tract
Ribonucleoprotein (RNP)
- code for structural & non-structural proteins
- capsid, it goes into the nucleus
Virus replication:
o
Virus attach to receptor (HA) enters cell
o
pH change so fuses w/ membrane & release RNP
o
Viral polymerase cleaves host mRNA & uses capped primer to transcribe the vRNP.
o
mRNA & vRNA made in nucleus
o
HA & NA made in RER ==> SER until cell membrane & gets glycosylated
o
Virus made by budding from cell
Antigenic shift
Antigenic drift
-b/c of high error of RNA polymerase
- re-assortment
- can have co-infection
- can be pandemic
- change in nucleic acid of virus
Complications:
o
Associated w/ lung infection (pneumonia)
Pneumonia: primary influenza, combined viral & bacterial, secondary bacterial pneumonia,
Otitis media
Treatment:
Anti-viral
- Amantadine hydrocholoride & rimantadine
- Tamiflu
- Relenza (works against NA
- drug blocks uncoating (blocks replication)
Vaccine
Paramyxovruses
Virus structure:
o
(-)ssRNA, enveloped, helical, non-segmented, HN and F proteins (2 spikes), contain RNA polymerase
o
F protein (fusion) causes lyses of rbc when mixed w/ virus
Replication:
o
Synthesis of mRNA & proteins occur at the cytoplasm
o
HN & F proteins are assembled in the cell plasma membrane
Virus types:
o
parainfluenza types 1-5: Infects humans & non-humans
o
mumps: paramyxovirus
o
measles: morbillivirus
o
respiratory syncticial virus:
Parainfluenzas:
Upper respiratory disease: fever, rhinitis, pharyngitis, CROUP syndrome (laryngoracheobraonch) (barking cough difficult to
breath)
MUMPS
Pathogenesis:
o
Asymptomatic
o
Acute onset of parotitis w painful swelling in salivary glands & transmitted in saliva & respiratory secretions
o
Forms multinucleated cells (F protein) causes fusion of several cells (syncytia formation)
o
May lead to male sterility because cant expand due to tunica albuginea
o
Stensens duct: parotitis
Measles (Rubeola)
Complications:
o
Subacute sclerosing panenceophalitis (SSPE):
latent in individuals, brain cells have nuclear & cytoplasmic includsions of measles ribonucleoprotein, slow virus
o
Herpes 6 (multiple sclerosis)
Respiratory Syncytial Virus (RSV)
o
Blocks breathing respiratory tract of young children < year old causes bronchitis & pneumonia .produce syncytia.
Disease:
o
Rotavirus: affects children w/ diarrhea. Looks like wheel shaped. Can see genetic re-assortment (shift in orthomyxovirus
Toga Virus (cloak)
Symptoms: rash begins on face, low fever, enlarged lymph nodes & spleen.
MISC: T.O.R.C.H.
To
Toxoplasma
R
Rubella (German measle) TogaVirus
C
Cytomegalovirus & Coxsackievirus
H
Herpes Virus
Rhabdovirus
Virus structure:
o
bullet shaped, enveloped, made up of 5 proteins w/ 1-protein outside (glycoprotein G)
o
(-)ssRNA, helical, contains RNA polymerase
o
Cytoplasmic replication
Rabies Disease
o
Infection of CNS of all warm blooded animals (mammals)
o
Transmitted via bite wounds with saliva
Prodromal phase: malaise, anorexia, headache, nausea, vomiting, sore throat, & fever.
Excitement phase: salivation & perspiration. Hydrophobia (fear of water) b/c fear of swallowing due to pain
Lab Diagnosis
o
Presence of Negir bodies in nerve cells.
o
Antibodies can be detected by immunofluorescence, complement fixation, or neutralization.
Virus characteristics:
o
(+)ssRNA, lipid envelop (less stable), icosahedral
o
transferred by arthropods (West Nile virus)
Disease characteristics:
o
o
West Nile Virus (Flavivirus) spread by mosquitoes. Elder & immunocompromised more at risk for developing encephalitis.
Asymptomatic
Fevers, encephalitis (fatal, multiplies in non-neural tissue, found in blood,), hemorrhagic fever
Slow viruses
Incubation periods are long & may appear many years later and are categorized conventional & unconventional.
o
Causes: spongiform
o
Symptoms include: loss of muscle control, shivering, tremors, & dementia
o
There is no inflammation, no immune response, no antigencity
Prions: Infectious protein, no nucleic acid, cause degenerative neurological disease (scrapie)
o
2 types of prions:
Hepatitis Viruses
Definition: acute infections of the liver (jaundice) may lead to liver cancer (necrosis of hepatocytes)
Hep D: super infection, more severe than other Hep, found mostly in pregnant women
HAV: Picornovirus
o
(+)ssRNA, no envelop, enterovirus, spread by fecal-oral route (water, shellfish(raw clams)), infect liver, no cross react w/ Hep B
o
Disease: acute infection
HBV: Hepadnavirus
o
dsDNA, enveloped, icosahedral, circular, variable in length.
o
Made up of 2 major proteins and 1 minor protein.
o
Can be seen as: Dane particle (complete virus), Sphere, or Filament with surface (s antigen)
o
Risk in drug abusers, transfusions, high promiscuous populations, infected blood, breast milk, saliva, nasopharyngeal, semen,
menstrual fluid, blood.
o
Disease: acute & chronic infection
o
Replication: vRNA (pregenome RNA) copied into DNA by reverse transcriptase. Enzyme removes original vRNA and a double
stranded DNA is formed. Virus is formed by budding.
HCV: Flavivirus
o
(+)ssRNA, enveloped, icosahedral, lipid virus, related to plant virus, may cross a mammalian & plant virus
o
called non-A & non-B hepatitis
o
Disease: acute & chronic infection
HDV: delta agent (viroid like) Fulminant hepatitis
o
ssRNA contains HBV surface protein. HDV is defective virus needs a helper fxn ex w/ HBV
o
super infection, intensify and becomes severe mostly in pregnant women
Oncogenes Virus
Function of oncogene: protein kinases codes for tyrosine kinase that phosphorlyates proteins at tyrosine & causes fibrin network
Treatment :
AZT (azido-dideoxythymidine)
Used for viral reverse transcriptase to prevent DNA replication, competes thymidine & terminates DNA
growth. WBC
Chain termination which does not allow anything to attach to the genome
Protease cleaves the gag & pol to produce nucleocapsid proteins inhibits production of infection but does NOT
cure infection.
Replication:
o
o
o
o
o
Virus enters, cytoplasm is where the reverse transcriptase copies vRNA into complementary DNA
DNA is called PROVIRUS & is found in linear & dsDNA form.
DNA provirus gets into nucleus w/ pregenome chromosome, transcribes w/ infected virus
mRNA translated into polyprotein (pp) ==> pp cleaved by proteus & assembled in plasma membrane
virus buds from cell
Glycoprotein (glycosylated)
LTR = aka long term repeats, these are promoters to enhance transcription factor binding sites
Misc:
What replicates in the cytoplasm?
pox virus
cornovirus
paramyxovirus
rhabdovirus
Guillan Baire Syndrome found in?
EBV herpes
Influenza (ortho)
What is the difference between (+/-) sense?
coxsackieviruses
rhinoviruses
adenoviruses
cornoviruses
Which deals with cold sore?
* Herpes labialis
Coronavirus
aridone
Parasitology
definition: reciprocal association, species depend upon another for its existence. Maybe temp. or permanent
association:
o
symbiosis:
o
mutualism:
o
commensalisms:
o
parasite: weaker organism that obtains food & shelter from another & derives all benefits from association
Types:
Needs:
Sources of infection:
o
Contamination, food, insects, animals, another person/fomite
Hosts:
o
Definitive host: parasite reaches the sexual stage!
o
Intermediate host:
o
Paratenic host: it is a transfer host, of a parasite that is not essential to (neither hindering nor hastening) parasites life cycle
o
Incidental host: accidental
o
Dead-end host:
o
Reservoir host:
Protozoan Infections
Disease name/agent
Amebiasis
Entameoba histolytica
Clinical condition
intestinal diarrhea,
dysentery
Infective form
cyst, transmitted via
food, water, anal
intercourse
Acanthamebiasis
agent Acnthamoeba
sp
Giadrdiasis / Giardia
lamblia
Trichomoniassis
Vaginal
vaginitis, itching,
inflammation, discharge
- trophosoites, eye
(contact lenses, soil,
water sewage)
found in brain tissue
- maybe free living
ameba
cysts, persons to
person contact, food,
water (campers)
trophozoite
transmitted by
veneral
African
Trypanosomiasis
sleeping sickness,
trypanosome brucei
gambiense,
trypanosome brucei
rhodesiense
metratrypanosomes,
transmitted by bite
of TseTse fly
American
Trypanosomiasis /
Trypanosoma cruzi
trypomastigoes
(body form) &
transmitted by
reduviid bug
(kissing bug) feces
blood &
trypomastigotes
Promastigotes &
Phlebotomus
(sandfly)
bone marrow
aspirate &
macrophages
Balantidiasis
- cysts, transmitted
food & water
contaminated by
pigs
stool, cyst
Plasmodiasis
Malaria, plasmodium
vivax, ovale,
malariea, falciparium
Toxoplasmosis
Toxoplasma gondii
Leishmaniasis
- primary infection
asymptomatic or mild
- congenital infections
(anomalies of CNS, eyes)
- immunocompromised:
disseminated infection
involving CNS
ingestion oocyts,
meat containing
tissue cysts
Diagnostic
Comments
Can go into liver to
cause abscesses
Treatment
- metronidazole (M) +
iodoquinol (intestinal)
- (M) and dehydroemetine
+ chloroquine
(extraintestinal)
Topical miconazole for eye
infection
stool, duodenal
contents, cysts,
trophozoites
vaginal
discharge,
scrapings,
trophozoite
blood, CSF,
lymph node
aspirates,
trypanosomes
animal reservoir
(beavers, muskrats)
pap smears, males
(asymptomatic), no cyst
form
- quinacrine HCL,
- metronidazole
- furazolidine
- metranidazole
Winterbottoms sign
(posterior cervical
chain enlargement)
- Gambian,
- eflonithine,
- Rhodesian,
- Suramin,
- Rhodesian encephalitis,
- Melarsoprol B
- xenodiagnosis:
person suspected
having acute disease
- Host & resvoirs:
domestic and wild
animals
- Nifurtimox
- benznidazole
- antimony compounds
blood, cyclical
plasmodial
forms in RBC
drug resistant in
falciparum malaria
Chloroquine PO4,
primaquine PO4, quinine
for falciparum malaria
serum, tissues,
organism not
readily
observed or
cultured from
humans
pyramethamine +
sulfadiazine
specific
antibodies that
bind to T. cruzi
antigens
- Iodoquinol
Babesiosis / Babesia
microti
bite of nymph of
hard tick, Ixodes
sacapularis
blood &
organism in
RBC
Cryptosporidiosis
oocysts, feces of
animals, human
feces & respiratory
secretions
stool, gut
tissue, oocyts
observed via
phase contrast
microscopy,
acid-fast
stained
material
Anal pruritus
Schistosomiasis /
mansoni,
haematobium
* Taeniasis / saginata
(beef) solium (pork)
* Diphyllobothriasis /
latum
* Tapeworm disease /
Rat tapeworm /
Hymenolepsis
diminuta
* Dwarf tapeworm /
Hymenolepsis nana
clindamycin + quinine
Infective form
Eggs, feces contaminated
food or soil
Diagnostic
Stool/ eggs
Comments
Treatment
- Mebendazole
- pyrantel pamoate
Stool /eggs
Controlled by sanitary
disposal of human feces
- Mebendazole
- pyrantel pamoate
Stool /eggs
- Thiobendazole
anal contact
spec/eggs
curled up
larvae in
muscle,
antibodies
- prazquantel
(unhooks)
important infection of
domestic & wild
animals & deer mice,
field mice important
reservoir
Immunocompromised,
fatal diarrhea,
dehydration,
parenteral nutrition,
supportive
- Mebendazole
- pyrantel pamoate
- steroids (severe)
- Thiobendazole
(adult)
Larvae (cysticercus),
ingestion of
raw/undercooked pork or
beef
Larvae (plerocercoid),
ingestion of raw
fish/undercooked fish
Larvae, ingestion of
infected cereals (flour)
Stool /
eggs, worm
segments
- prazquantel
(unhooks)
Stool /
eggs, worm
segments
Eggs in
feces
Eggs in
feces
- prazquantel
(unhooks)
- prazquantel
(unhooks)
8/19/2006
Additional materials
- Levines last lecture on parasitology
- Enterococcus
- M. Marium (Group I)
- IMVIC (relevant lactose & gas), pg 33
- UPEC
- Bortonella Quintana
- Coxsacckie
- Coronavirus
- Orthomyxovirus
- West Nile Virus (arbo virus) ==> What family does it belong to? Flavivirus
- Oncogene