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Colony

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

Small, 28mm; white


(opaque),
but older
colonies
maybe
yellowish,
round
Gamma
hemolytic

Lab
Characteristics

Source &
Transmission

Virulence Factors
(disease causing)

Associated
Diseases

Host
Defenses /
Immunity

Treatment /
Prevention

Non-motile
- Catalase (+)
- Coagulase (+)
- Dnase (+)
-Mannitol (+)

Can colonize nose &


skin; Not normal
Flora; GI & genital
tracts; Transmitted by
fomites, sneezes, food

- Beta lactamase pen resistant


- Mutatnt penicillin-binding
proteins (methicillin
resistance)

- 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

gamma, delta toxins

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)

Betalactamase (pen resistant)


Mutant penicillin-binding
proteins (methicillin
resistance) same as S.
Viridans

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

Urinary Tract Infect.


Upper UTI =
pyelonephritis

Mucous membranes
(lesser extent, GI)

Attachment to epithelial
cells

Lower UTI = cystitis

Inf. due to poor


hygiene & sexual
activity, especially in
young females

Urease: may mediate host


pathogenesis

Pyuria (puss in urine)

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 (+)

Small, graywhite, round

Non-motile

Human skin

* Hyaluronic acid

Mucous
membranes of
oropharynx (515%) & vaginal
tract

* Hemolysins (SLO & SLS)


- Streptolysins O
* beta hemolysis RBC, 02
* sens. => rhematic fever AGN
- Streptolysins S
* stable w/ O2, little to cause
disease

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

* Erythrogenic toxin (3) causes


red rash, Scarlet fever (use Dick
Test) chks toxin level, if red rash,
no AB) fever producing
(pyrogenic) are superantigens
(strep. Pyrogenic exotoxin)
* M Protein : antiphagocytic
- > 100 different serotypes
Essential for pathogenicity
- M proteins resemble x-reactive
antibodies lead to rheumatic
fever
- antiphagocytic
- adhesion factor
* Hyaluronidase degrades
hyaluronic acid
* Streptokinase: lyse clots
(spreading factor)
* Nuclease:degrade D/RNA
Spreading factor pus viscosity
DNase B = streptodornase (
antibody titer indicates recent S.
pyogenes infection

* Erysipelas : red rash on


face (slapped cheek)
* Necrotizing fasciitis: flesh
eating strep disease.
SPREADS!
Systemic Infections
Pharyngitis (strep throat,
tonsillitis)
Scarlet fever (scarlatina)
infection w/ erythrogenic
leads to red sandpaper
rash on trunk or strawberry
tongue
Puerperal fever (child birth
fever) uterine infection
Poststreptococcal infection
sequelae
- Acute Glomerulonephritis
(AGN): NO viable
organisms present, facial
edema & smoky urine
- Acute Rheumatic Fever
(ARF): NO viable
organisms present, include
migratory arthritis (aseptic),
M protein & heart tissue
leads to heart damage

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

CAMP test (+)


Beta Hemolytic

Mucous membranes
of vagina, male
urethra, throat, GI
tract

Neonatal meningitis (fever,


lethargy, & seizures)
invades through respiratory
tract
- Early onset: 0-5 days
infection (in utero)
- Late onset: 5-90 days

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

No growth > 6.5%


NaCl
Resistant
bacitracin
Hydralize sodium
hippurate

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

S. Bovis none (killed easily)

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: high resistant to


antibiotics (vancomycin
resistance) Adheres to
damaged heart valves &
urinary tract epithelial cells.

E. faecalis becomes bloodborne via urinary tract


infection (UTI) or GI
route.
UTI enterococal inf. Leads
to cystitis (lower) or
pyelonephritis (upper)
Sub-acute endocarditis:
from bacteremia.
Enterococcus ONLY infects
abnormal valves or
prostheses.
Bilary tract disease &
intraabdominal abscesses
Colon cancer prone to S.
bovis

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 (+)

Small, graywhite, round

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)

Capsule (Specific Soluble


substance) 80 serotypes
Identified w/ Capsule
swelling Quellung rxn

People
susceptible to
viral infection,
allergy
malnutrition,
alcoholism,
debilitation,
ciliary motion
==> aspirate into
lungs

Capsule protects phagocytosis


Non-encap. strains avirulent.

Sickle cell
anemia disease
Age related
Spread by
droplet nuclei

C reactive protein (CRP) and


used as indicator inflam
response as a marker
F antigen: part of C
carbohydrate, hide capsule
Ag are only exposed in nonencapsulated pneumococci
Pneumolysin similar to
Streptolysin O, Listeriolysin
O, & Tetanolysin (found in S.
Pyogenes, Listeria, C. Tetani)
fxn to inhibit ciliary movemt,
bactericidal actv PMN,
inhibit lymphocytic prolif.
Neuraminadase remove sugar
from host glycoprot
Peptide permeases:
adherence to host tissue
IgA protease: cleaves Iga
(blocks opsonization surface)
- Adhesins: fibronectin
- Autolysin: release toxin, infl
- Naturally competent

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)

alpha hemolytic: partial breakdown of RBC,

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 (+)

Small, graywhite, round

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

(No Group b/c


lack C cell
wall antigens
NO Lancefield
group)

alpha
hemolytic

Catalase (-) does


not produce
peroxide
alpha hemolytic
(-) for bile
solubility &
resistant to
optochin
(-) for inulin
fermentation
No group
carbohydrate
Media grown on
sugar produce
glycocalyx
composed of
dextran

Normal & Damaged


Acute Endocarditis
- S. Aureus

Abnormal & Damaged


Subacute Endocarditis
- S. Epidermis
- S. Bovis
- Enterococcus faecalis
- viridans

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)

Dental caries (tooth


decay) due to S. Mutans
which are localized by
large amounts of acid by
fermentation of sugars in
the mouth. Flourine in
water prevents adhesion.

Patients w/
heart
conditions are
at risk of
complications

Bacillus
Anthracis

Cell
Features

Colony
Features

Source &
Virulence Factors
Lab
Characteristics Transmission

Gram (+)

Large, graywhite, flat,


waxy, erose
colonies on
blood agar

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

Toxin is released &


blocks capillaries, if
untreated leads to
bacteremia (grows in
blood stream) & cause
blood to thicken. Can
be fatal if untreated in 4
days. Replicates in
blood!

ZOONOTIC
infection
associated w/
cattle

Anthrax toxin: plasmid


encoded, comprised of 3
different peptides
- Edema factor (EF), impairs
phagocytic ability (swelling)
- Lethal factor (LF),
pulmonary edema is
cytolytic for macrophages.
Stimulate production of
cytokines Skin turns black!
Zn metalloprotease,
cytokines
- Protective Antigen (PA)
Cellular uptake processed by
host protease to bind to EF or
LF ==> allows the factor EF
or LF to be internalized by
host cell by endocytosis. PA
is antigenic
LF and EF need PA to be
toxic
B. anthracis has PA + LF or
PA +EF is NOT as virulent as
EF + LF + PA. Leads to
vascular permeability &
neurotoxicity. No PA, then
virulent, no damage.
Endospore formation:
ensures survival of
bacteria in harsh
conditions. Spore
germination requires O2

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)

Emetic Food Poisoning:


upper GI disturbance w/
vomiting toxin forms in
rice ==> consume
reheated rice w/ toxin
==> food poisoning
symptoms arise in about
6 hrs after eating toxinladen food.
Diarrheal Food
Poisoning: lower GI
disturbance w/ diarrhea.
Toxin forms in meat /
vegetables ==> consume
reheated foods laden w/
bacteria (& toxin)
symptoms arise w/in
24hrs, food inf. May last
for 2 days
Post-traumatic
endophthalmitis (eye
infection) leads to
edema. Drug abusers are
risk, may cause
blindness
IV catheter & CNS shunt
inf & endocarditis w/
drug abusers, also
pneumonitis, bacteremia,
meningitis in
immunocompromised

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

Diphtheria toxin: strong,


slow acting binary toxin (has
A:B subunit motif) has
tissue specificity (heart,
nerves, kidney) acts
intracellularly following
internalization by pinocytosis
Detects for cardiotoxin.
Peptide B (shuttle protein)
binds to receptor on host
cells & aids Peptide A in its
transport into cell
Peptide A (ADPriboslyating enzyme)
ribosylates EF2 & stops
protein synthesis in host
cells
Toxin encoded for by
lysogenic phage (beta
phage). Synthesis
controlled by iron levels in
environment; toxin
expressed when iron levels
low and repressed when
iron levels high (repressor
contains iron, no repressor
when no iron) When iron
toxin expressed b/c lyse host
cell
Mycolic acid: (CHIEF
VIRULENCE FACTOR!)
similar to cord factor of M.
tuberculosis, toxic glycolipid
K antigen: adhesion in throat

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

Bacteria produce porphyrins, coral red pigment

Minutissimum

Organism grows on skin areas with high moisture (ex. skin folds)

Diagnosis of erythrasma is based on clinical


picture. Lesions when observed under UV
(365nm), Woods light appear pinkish to
coral red color

(Foot Associated
diphtheroid!)

Superificial infection w/ this organism ==> ex. Athletes Foot w/ scaly plaques especially
btw toes. Not pus forming and is called ERYTHRASMA

Non-invasive and treated with oral


erythromycin

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

Most labs can not


detect toxin
Spore stain useful

Spores normally
found in soil,
dust and in
decaying
organic matter.

Botulinum toxin: MOST


TOXIC COMPOUNDS
known. Eight
immunologically diff. toxins
produced

Vacuum-packed
canned goods,
the spores may
germinate &
produce toxin.
Food
intoxication

Types A, B, & E are most


commonly causing human
disease.

* Inadequate
canning, pH < 7,
smoked fish,
canned tuna
Infant botulism
associated w/
honey loaded
w/ spores &
wound infection
==> subsequent
toxin poisoning

Toxins are pre-formed in


food. Labile at 121 C at 15
min or boiling food for 20
min (heat sensitive)
Toxins are secreted, released
by cell autolysis.
Botulinum toxin acts as a
neurotoxin. It blocks the
release of acetylocholine
neurotransmitter from
poisoned neurons at
myoneural junctures. W/in
36hrs flaccid paralysis (Botox
for cosmetic purposes) Blocks
AcH w/ infants!
Endospores formation:
survivial in harsh conditions

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

Toxins A & B are


detected by lethal
effect on cell
cultures (within
24hrs)

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

Exotoxins A and B (==>


hemorrhagic necrosis)
Toxin A: enterotoxin causes
diarrhea & colitis
(hemorrhagic necrosis).
Cause infl. Damage to host
tissues
Toxin B: cytotxin lethal to
cultured cells.
Depolymerizes host actin
altering host cell cytoskeleton
==> cell loses shape ==>
necrosis
Endospore formation

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

5 different serotypes based on


exotoxins produced. All
serotypes ==> alpha toxin
(lecithinase)

Gas gangrene 80%


serotype A. Infection is
result of trauma or
surgery. Rapid spread,
tissue necrosis &
systemic intoxication
(via blood)

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

- Toxin blocks the


exocytosis of inhib.
Transmitters, Glycine, and
GABA. Results in spastic
(rigid) paralysis of voluntary
muscles due to un-opposed
excitation (tetani) of motor
neurons

Spastic paralysis due


to unremitting
muscle contraction.
Diagnosis: organism
may cultured
anaerobically
Difficult swallowing
due to LOCK JAW
Opisthotonos: arched
back & neck

LOCK JAW (TRISMUS)


for disease

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

Gram (+) rod


sometimes
branching

Cultured
anaerobically

Propionic acid
production

part of normal
flora of skin,
mouth & eyes

Lipases (Lipophilic)* split


off fatty acids from skin
lipids. Inhibit other bacteria
but can contribute to tissue
inflammation

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!

Lipophilic diphtheroid (appeared in the test bank)

grows in acne
lesions
metabolize skindervived lipids,
blocks sebaceous
glands cuase
acne & other
pustular rxn.
May enter via
wounds.

Able to enhance hosts


immune system to produce
a strong acute inflammatory
response

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

Grows on brainheart infusion


agar
anaerobically.

A. Israelii NOT very


virulent & actinomycoses
are polymicrobial infections
involves Strep. Sanguis,
Strep. Mitis, Prevotella,
Porphyromonas, Bacteroides,
Fusobacterium, Eikenella, &
Treponema denticola.

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)

Sulfar Granules are


yellow bacterial mats
(filaments) bound with
calcium phosphate

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

Aspirated into lungs:


leads to Lung
Actinomycosis (Farmers
Lung) chest pain,
pneumonitis, empyema,
hemoptysis, fever, may
spread & appear in X-rays

- Penicillin G

Swallowed ==>
abdominal disease.
Infection ==> appendix,
trauma, or performated
ulcer

----------------------------------Disease ===> section


----------------------------------A = Actino
A.mycosis
A.mycetoma
Obligate
Aerobic
Anaerobe
intracellular

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

Acid fast stain of


sputum or pus for
branching,
filamentous
bacteria.

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

Abundant in soil &


cause of
opportunistic
infections in
immunocompromised
patients w/ AIDS,
corticosteroids.
Most common:
- Infection initiates
via respiratory route
(inhale)
- Enters by skin
trauma w/ foot the
usual site of
infection

Virulence Factors

Associated Diseases

Host
Defenses &
Immunity

Treatment /
Prevention

Catalase & Superoxide


Dismutase enzymes: high
levels resist PMNs
intracellular oxidative burst.

Nocardiosis (not
contagious, but lethal, &
may relapse after
treatment)

Caught early:
Sulfonamide

Formation of long filaments


ability resist phagocytosis

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

Sepsis: spreads from lungs


via blood to other organs
often to CNS ==> brain
abscess, skin ==> kidney
lesion
Actinomycetoma (aerobic
actinomycosis): chronic
granulomatous infection of
subcutaneous tissues. Sinus
tracts are formed draining
pus to skin surface. Can
lead to damaged bone.
Foot is the usual site of
infection after injury:

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 (+)

Aerobically 510% CO2 &


grows
slowly!!!

Acid fast stain of


septum, but TB
is resistant.

Humans are the


reservoir

Cord factor composed of


trehalose dimycolate:
Leads to TNF induction
by immune cells, kill itself

TB is a pulmonary disease,
dissemination occurs by blood
STEPS in disease process:

Combination of
drugs, lasts up to
12 months.

1.Respiratory droplet reaches


alveloi: destruct of PMN by TB

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.

3.Caseating necrosis (cheesy)


==> hilar lymph n. (spreads
via - lymph w/ 2 output) to
a) lung (w/oxygenated)
- Adequate CMI (TDTH)
response ==> get granuloma
infect. stays contained

Granulomas
form w/
epithelioid
cells
surround
central
necrosis.

b) Spread via bloodstream, to


miliary TB kill . Shot-gun
pellet, lungs ,kidneys, GI. Inf.
Up to 20 yrs, inf reactivates &
develops Secondary TB

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

Catalase: is required for


isoniazid sensitivity (INH)
Protein antigens of outer
coat stimulate selfdestructive host
hypersensitivity (TDTH
mediated) & acquired
immunity
Sulfatides (multi-acylated
trehalose-2-sulfates):
inhibit phagosomelysosome fusion similar to
cord factor.
Wax D (mycoside): used
w/ oil & water (adjuvant,
enhance vaccine effective
in elicit ab response)
Lipoarabinomannin:
induce TNF alpha from
monocytes &
macrophages
INTRACELLULAR
pathogens, ex. chronic inf.
M. Tuberculosis survives
under acid, basic, & dry
conditions but readily
killed by heat
(pasteurization). Waxy is
a protective layer.

- Cavitating: inf. Blood to


kidney, bone marrow,brain, GI
- Consumption: waste away
- Extrapulmonary TB: Potts
disease, vertebral osteomyelit
(hunch back) SCROFULA =
cervical lymph nodes

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

1. Mott are low virulence


2. produce no catalase
3. protein antigens (killself)
4. survives in macrophages
5. survives in acid/basic, dry
6. MOTT are multi-drug
resistant

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

MOTT species are


ubiquitous in
nature
Cause disease by
opportunistic
infections
No person to person
transmission

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

Acid fast staining


Of sputum

Colonies
develop in 48 weeks

Cord factor: ( Trehalose


dimycolate) gathers M. Bovis
Into chains.

Causes pulmonary
infection, similar to TB

Chest X-ray

Mammals are only


reservoir b/c under
zoonotic.

T Cell Mediated
delayed
hypersensitivity
(TDTH)

Decontaminate
w/ concentrated
NaOH

Catalase (-) ==> INH (-),


resistant

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.

PPD skin test (+)

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

Proteins antigens of outer


surface stimulates selfdestructive host
hypersentivity
Other factors enable
organism to survive in
macrophages
(INTRACELLUULAR)
Waxy layer (mycolic acid w/
trehalose) contributes to
bacterias ability to survive
under acidic/basic, dry
conditions & to resist
exposure to many
disinfectants.
Multiple Drug Resistant
(MDR) b/c of the waxy layer
or porin size.

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

Acid fast stain of


sputum

MAC pulmonary inf.


common in AIDS patients

Grown on
MuellerHinton agar

Catalase (-)

1) MAC are organisms low


virulence
2) Do not produce catalase,
there INH becomes resistant
3)Protein antigens of outer
coat stimulate selfdestructive host hypersensit.
4) Bacterial factors enable
organism to survive in
macrophages. Therefore,
INTRACELLULAR
5) Bacteria survives in
acid/basic
6)MAC are naturally multdrug resistant

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

MAC species are


ubigquitous in
nature (soil, dust, &
throats) of normal
humans & animals
MAC can cause
disease by
OPPORTUNISTIC
infections of birds
& immunocompromised
humans, AIDS
patients w/ CD4
T cell.

PPD skin test


sometimes (+)
PPD(-) when
immunocompromised
patients w/ AIDS

Catalase (-)

Catalase (+)

M. Bovis
M. Leprae
M. Avium Intracellulare (MAC)
Acinetobacter

M. Tuberculosis
Norcadia

MAC pulmonary inf.


similar to TB
PPD(+) may appear (-) b/c
suppressed T cell, T_s
* Main route of inf. into
AIDS patients is the GI
tract.
MAC residing in macrophages INTRACELLULAR disseminate
from lymph nodes to
spleen & lungs forming
lesions. May spread to all
organ systems
Tubercle (granuloma)
formation in MAC inf. of
AIDS patients is NOT
observed. Tubercle seen
in M. Tuberculosis.

1st line drugs:


- ethambutol
- streptomycin
- rifampin

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

Acid-fast stain skin


test.

Humans &
armadillos are the
only reservoirs

1) Phenolic Glycolipid (PGL-1


antioxidant prevent phagocyte

Leprosy, lots of symptoms


Tuberculoid Leprosy:
Borderline (intermediary)
Leprosy subdivided to
Lepromatous Leprosy.
The patients progress of the
disease on hosts immune

Multi-drug
therapy dapson
w/ rifampin

2) LAM: along w/ PGL-1


inhibits T cell proliferation,
cause anergy (no
responsiveness)

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

3)Prefers lower temp. limits


infection to skin,
nasopharynx, & testicles.
Leprosy is primarily a skin
disease.
4) INTRACELLULAR
survival (no pain sensation)

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)

Male STD Gonorrhea: men


are systemic, at the urethral.
Leads to urethritis, painful
urination or dysurea w/
purulent discharge.

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.

1. Cell can add sialic acid to


LOS, more C resistant
2. Cell wall frag are released
3. Pili: attach to epithelial cells
especially urogenital cells +
mucosal surfaces undergoes
ANTIGENIC VARIATION
4. IgA protease: prevents IgAmediated opsonization on
mucous membranes
5. 3 outer membrane proteins
(omp) display antigenic
variation
- Protein I: Inhibit
phagolysomal fusion +
promote endocytosis
- Protein II:
Opacity protein, adhesion.
Undergoes antigenic + phase
variation. Therefore makes
macrophage difficult to kill
bacteria
- Protein III:
Porin protein, complex protein
I, binds IgG blocking AB =
Rmp, blocks C mediated
bactericidal ab f(x)
6. Beta lactamase: plasmid
encoded PPNG
7. Fe binding protiens
8. Invasiveness epithelia
engulf N. gonorrhea, via
INTRACELLULAR
9. Cell wall display toxicity
epithelial cells (tracheal
cytotoxin of B. pertussis)
10. Autolysis/natural comp.
11. Type IV pili: g(-) twitch,
cell specificity + phage abs

Female STD Gonorrhea:


inf. vaginal or anal.
Endocervical most common.
Inf. mostly asymptomatic
but vaginal discharge,
dysuria + bleeding may
occur. Untreated results in
salpingitis (Fallopian
tubes), cervicitis, and pelvic
inflammatory disease
(PID). Inf. of liver may
cause perihepatitis (FritzHugh-Curtis Syndrome) !!!
Neonates: purulent
conjunctivitis acquired by
newborn during passage via
birth canal (Ophthalmia
neonatorum)
Monoarticular arthritis
(single joint): #1 agent of
arthritis in young adults.
Found in female knees (due
to bacteremia)
Rash on leg!!!
Disseminate Gonococcal
Infection (DGI) ==>
septicemia ==> LOS ==>
toxicity ==> leads to chills
skin lesions (rash) ==>
spreads to joints ==>
endocarditis

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

Humans are the


only reservoirs.
Heathly
individuals may
be carriers of N.
meningitides.
2-8% of
population are
carriers but in
epidemic year
will increase to
40-90%,
colonizes the
nasopharynx.
Horizontal
transfer occurs
via respir.
droplets &
requires
intimate
contact (ass. w/
xchange of respir
secretions)
Activation of
infection in
carrier due to
depressed
immune
response.

Associated Diseases

Host
Defenses &
Immunity

Treatment /
Prevention

1. Capsule made of polysac: 13


serogroups A,B,C,W-135, Y
provides antigenic variety,
encapsulated strains resist
phagocyt + facilitate invade

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.

Diagnosis: from spinal


tap. CSF, chk pressure,
cloudiness, culture (+), #
of PMN & low glucose
(confirm septic meningitis)

Pili available
may get
activation to
complement,
results
inflammation
and pus
formation.

Pili: attach to epithelial (nonciliated) cells. Antigenic


variation
IgA protease: (similar to
gonorrheae) prevent IgA
opsonization on mucosal
surfaces
Beta lactamase: plasmid
encoded
Iron-binding protein:
scavenging Fe from transferin,
lactoferrin of host
Protein II ONLY!!! = Opacity
Protein, involved in adhesion.
Undergoes antigenic + phase
variation
Facultative intracellular
pathogen: enter phagocytic
vesicles & avoids death. Similar
to N. Gonorrhea in non-ciliated
mucosal cells
Type IV pili: adhesion, twitch
motility
Intracellular: into m.phage

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

Does not ferment


sugars but
glucose oxidized

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

Virulence Factors Associated Diseases


1. LPS (endotoxin)
2. drug resistance(s)

Acinetobacter species are


hospital acquired in warm
seasons
Post-surgical infections of
soft tissue with abscesses is
often seen.
Organism may be also
involved w/ respiratory tract
infections and urinary tract
infections.

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

1. Capsule: A good marker for


vaccine effectiveness but ab is
Coccobacilli
not protective.
Horizontal
2. Exotoxin
(WHOOPING
transmission is
Singly or
3. PERTUSSIS TOXIN (PT) is
Oxidase (+)
COUGH!)
by respiratory
pairs, chairs
heat-labile binary toxin.
droplets among
Deactivates inhibitory GTP
Direct
children
Obligate
binding* proteins (Gi) by ADPfluorescent Ab
aerobe
ribosylating them
test (DFA)
HIGHLY
Active B (adhesion factor)
Produce small
CONTAGIOUS
NO carbocomposed 5 unique polypeptides
pearl-like or
ELISA
(90% gets
hydrate
& mediates w/ A subunit,
metallic colonies
infected)
fermentation
results in cAMP. Toxin blocks
& oxides
PMN & inhibits movement by
Produce small zone
amino acids
chemotaxis & activates
of hemolysis
pancreatic insulin production by
Non-motile
Islet cells.
CO2 help growth
Cyclolysin: dual f(x) toxin,
Requires:
hemolsyin + adenylate cyclase
Cell sensitive to
nicotinic acid heat, dry, & chem..
4. Adenylate Cyclase: inhibit cell
f(x), especially WBC, edema
Blood, helps
factor of B. anthracis.
neutralize inhibitory
Hemolysin: inhibit leukocyte
effects of fatty acid,
chemotaxis, phago & killing
sulfides & H202
5. tracheal cytotoxin:
peptidoglycan frag, damages
Phase II & II less
ciliated cells. Stim IL-1 release
virulent. No blood
6. Adhesion factors: pili
on phase IV.
(fimbriae) display phase
variation on/off
VIR gene
7. Filamentous Hemagglutinin
(FHA) attach to ciliate epithelial
Phase variation
cells
(exp. on/off gene)
8. Pertactin: adhesion factor
9. LPS = endotoxin Lipid A & X,
X more potent!!!
** B. bronchispetica: motile, causes cough in dogs, kennel cough, unique-nitrate reduction (+), mild symptoms
Phase
Description
Phase I
Pili & O-antigen expressed
Phase II & III
Bacteria express different antigens, less virulent
Phase IV
Pili & O-antigen NOT expressed. Avirulent
Bordetella
pertussis

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

1. Capsule: Type b is most


commonly associated w/
disease including meningitis
(90% caused by strains) Type b
capsule is composed of
polyribitol phosphate (PRP)
Capsules can elicit Quellung
rxn (serotyping)

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

2. IgA protease: prevents


opsonization by IgA
3. Beta lactamase: encoded on
plasmid, confers resistance to
penicillin
4. Pili: adhesion factor, not
well characterized
5. LOS

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 (+)

Humans are the


only reservoir
in genital tracts

1. LPS
(endotoxin)

na

Erythromycin

Requires only heme


(Factor X) no need
NAD b/c can
synthesize

Requires Factor X
(heme)

H. ducreyi causes SOFT chancre


(chancroid), painful, gential
lesions & lymphadenopathy
(enlarged lymph nodes). Enters
via break in skin. Can carry to
inguinal lymph nodes &
multiply. May result in massive
swelling. Highly contagious.

Coccobacilli
bipolar stain
facultative
anaerobic
Non-motile

Glucose is
fermented

Hortizontal
transmission
occurs via sexual
contact

Vancomycin
resistant

Alternative:
Sulfa drugs
(sulfonamide) or
streptomycin

Exam Question: What is the causative agent of cahncroid? H. ducreyi

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

1. Lobar pneumonia &


bronchopneumonia: associated
w/ hospital acquisition by
alcoholics, diabetics, & patients
w/ chronic pulmonary disease.
Symptoms include: fever,
productive cough, empyema,
hemoptysis (spit blood) & thick
currant jelly sputum.

Ab made
against
capsule

Cefotaxime &
gentamycin

(Friedlanders
bacillus)

Large & long


bacilli
facultative
anaerobic
Non-motile

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

2. Urinary Tract Infection:


common in hospital settings, b/c
compromised by surgery,
catheters, bladder retention etc
3. Bacteremia caused by
Klebsiella & E. Coli in hospital
settings.
4. Tropical sprue

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(-)

Grows very slowly


on BCYE (buffered
charcoal yeast
extract) agar
produce small
iridescent colonies

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(-)

Has Bluegreen color &


grape-like
odor

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

Long & thin


bacilli in
chains or
singles
Cant carry out
fermendation,
can use any
carbon source
oxidatively
Opportunist
Resistant to
many
chemical
disinfectants
Associated w/
resistance to
many
antibiotics.
Produce a
biofilm which
contributes to
antibiotic
resistant &
ability to grow
in presence of
disinfectants

Strong beta
hemolysis
Many will
fluoresce
under UV
light due to
pyoverdin
(fluorescein)
production

Catalase (+)
No sugar
fermentation but
glucose is
oxidized

Nitrate red. (+)

May be found in
swimming pool
& whirlpools
which are
inadequately
chlorinated, &
raw vegetables

Fruity (grapelike) odor

Nosocomial
infections

Pyocyanin
production
(blue-green
pigment)

Found to exist in
disinfectant &
eyewash
solutions.

Triple sugar iron


(TSI) (-)
Citrate (+)

Beta-hemolysis

#1 (most common) non-fermenting g(-), bacillus nosocomial infectious disease agent

Exoenzyme S: mediates burn


wound inf & lung inf of cystic
fibrosis (CF)
Hemolysins: disrupt
membrane lipids & acts
synergistically w/
phospholipase
Phospholipase C: disrupts
membranes & rhamnolipid
(inhibits ciliary action in
respiratory
Lipases & lecithinases destroys tissue & blood cell,
inflam
Mucoid ExPoly. (MEP) =
alginate, form biofilms:adhere,
immbolize organism. Biofilm,
resist. to drugs & disinfectants
(iodine). Glycocalx resist
phagocytosis. Collagenase:
degrade collagen Elastase;
cleaves IgA, IgG, &
complement. Alkaline
protease.
PYOYANIN: blue-green
pigment w/ bacteriocidal
activity. Pyoverdine =
fluorescein (green-yellow UV)
Multiple Antibiotic Resistance:
beta-lactamase, acetylating
enzymes.

2. Burn wound infs:


black blue wound,
fruity smell spreads
into adjacent healthy
tissues. #1 problem
in burn patients. Use
Woods UV to see P.
aeruginosa. Seen in
post-surgical wound
infections.
3. UTI:
catheterization
4. Sepsis/bacteremia:
septic shock & death.
5. Corneal keratitis:
contact lens lead to
blindness
6. Otitis externa
(swimmers ear):
cause otitis media
7. Pseudomonas
folliculitis: skin
abrasions, unchlorinated hot tubes
8. Osteochondritis:
puncture wound of
foot. Tennis shoes
9. Podiatrically
important infect
nail. Eats nail & turn
into green goo

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

Use gram staining


to rule out any
other causative
agents

Humans are only


reservoir

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

Cholera toxin (CT) A subunit


(ADP-ribosylates) cytoplasmic G
protein (G_s) regulates host
adenylate cyclase. cAMP
levels, induce intestinal cells to
release Cl- ions into lumen.
Toxin inhibits Na+ absorp,
ions, water release (diarrhea!)

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

Transmitted by oralfecal route (by


drinking water &
intaking raw &
undercooked seafood,
unpeeled fruits)
Hortizontal
transmission amongst
humans
Large inoculum
(10^7 10^11 cells)
b/c are killed by
stomach acidity
Exist in salt water for
long periods of time /
found associated w/
plankton, shellfish,

LPS: endotoxin, 6 serotypes


01: NON-INVASIVE cause
epidemics, no age preference but
usually in children, preg.
Women, long-term immunity.
Non-01: sporadic infections
0139: INVASIVE infection in
indiv. > 40 yrs, no immunity
gained, possible reinfection.
Flagelluem (H antigen): an
adherence factor. Motility
bacteria to enter into mucous
layer, non-motile is avirulent.
Adhesion factors: mediate
bacterial adherence to SI
epithelium. AF + CT to cause
full-blown disease

rice water diarrhea


(large vol. 1
liter/hr) rice: is
mucus from
intestinal wall.
No fever involved
Untreated patients
may die in hrs due to
hypotension,
dehydration, &
shock.
Complications:
- electrolyte
imbalance
- metabolic acidosis
- hypoglycemia: kid
- abortions
Dehydrationleads to:
- sunken eyes
- loss of skin turgor
- patient, comatose
- death

TCP-ACF: Toxin Co-regulate


Pilis pathogenicity island.
Acidic polysacc. Capsule found
ONLY in 0139 strain. It is
INVASIVE. Can go out of
intestine & cause infection
Test question: Given tainted water w/ cholera w/ a dosage of 100 organisms, would a normal person be sick? No b/c it requires a lot more, but Shigella could kill you

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.

Most E.coli are


harmless
commensals of GI
tract

1. Heat-labile enterotoxin (LT):


cholera-like binary toxin
encoded in ENT plamids. It is
cytotonic! Active A subunit
ADP-ribosylates cytoplasmic G
protein (G_s) regulates host
adenylate cyclase. cAMP.
(diarrhea!)

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

Some E.coli contain


extrachromosomal
DNA such as large
ENT plasmids which
enable E.coli to be
pathogenic.
Enterotoxigenic E.coli
can colonize small
intestines.
Oral-fecal route by
consuming
contaminated water
Hortizontal
transmission from
human to human
TRAVELLERS
DIARRHEA or AKA
TURISTA

2. Heat-stable toxin (ST):


encoded by ENT plasmids,
activates guanylate cyclase &
cGMP levels. Blocks ion uptake
from lumen.
Heat Looks like Rxn
LT
Cholera
cAMP
ST
Yersinia E. cGMP
-------------------------------------------LPS:endotoxin, Oag, serum resist
Flagellum: H,ag bacteria enter
mucus layer. w/ phase variation
Pili: attachment to host cells.
2 Types
Mannose
Common pili Sensitive
P pili
Resistant
Sex pili: conjugative plasmids
transfer F+ plasmid or Hfr
(donor, male) to F- (female)
Fimbriae: attachment to host
cells SI (tissue specific) CFA
(colonization factor antigen)
Antibiotic & heavy metal resist:
Encode on conjugative plasmids
Capsule: protect from acidicity
E. coli produce hemolysins
E. coli produce siderophores (Fe
acquisition)

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

Enterotoxins: lysogenic phage


- Shiga-like toxin I (SLT-1):
toxin f(x) in LI. Results: cleavage
of euk 28s ribosomal RNA (60S).
Mucosal cells poisoned, inhibits
protein synthesis. Bloody stools.
Enterotoxins enter bloodstream
may be associated w/ kidney
damage.

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

- SLT-II (STX) : both of these are


called VEROTOXIN b/c of their
toxic effects on vero monkey
kidney cells.
- Enterohemolysin
- LPS (endotoxin)
- Pili: Adhesion, mediate
bacterial (attachment to large
intestinal epithelium. Plasmid
encoded
- capsule (possibly)

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

- ACID RESISTANT, ~50


bacteria to cause disease (like
Shigella). EHEC more acid resist
- EAE genes (similar to EPEC) >
attaching & effacing lesions

Non-invasive

Invasive

- ETEC
- Vibrio cholerae
- EPEC

- EHEC
- Shigella
- Salmonella
I

Lactose Ferm. sugar


Occurs
Not occur
Occurs slowly
M

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 (-)

Animal & human GI


tracts are reservoirs
(poultry, reptiles such
as turtles & iguana).
Oral-fecal route by
consume
contaminated water
or food involved in
hort. Transmission.

LPS = exotoxin: mediates


endotoxic shock, involves
inflammatory response of
intestinal mucosa. S. Resistant

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

Chronic carrier status


Cutting
boards/knives (need
to clean w/ bleach)
Raw eggs
Survives freezing
water, food or water
for several weeks

Invasion factor(s): bacteria


invades hosts mucosal cells of
the ileum & LI. Organism is able
to survive in macrophages, not
PMN.
Flagellum (H ag): strong
motility enable bacteria to enter
into mucus layer.
Inhibition of phagosomelysosome fusion: salmonella
multiply in macrophage, then
lyse macrophage & spread to
nearby cells.
Capsule (K ag): help bacteria
survive stomach acidity
Multi-drug resistant factors
Enterotoxin: epidermal growth
factor (EGFR) on host cell to
bind to, leads to Ca in cell.
leukotriene synthesis opens up
Ca channels lead to rearrange
actin. Results: leukotrienes
inflammation.
VIR genes turned on inside host
cell ==> antigenic variation
Pathogenicity island (SP-1, SP-2)
Expression of genes can adapt to
acidic environment

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

Vi antigen (capsule, hides


surface markers, removed by
boiling water). Bacteria resists
LPS = endotoxin: major VF in
mediating endotoxic shock,
involves in inflammatory
response of intestinal mucosa.
May mediate serum resistance.

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

DNA probe for Vi


antigen (capsule)
WIDAL test: look
for agglutinating ab
acute &
convalescent stages
(refer to B. Pertusis)
see 4x in ab
titers, If (-) rxn then
inconclusive.

Chronic carrier status


in humans is
possible survive in
GI tract w/
predilection (bias)
for gall bladder.

Invasion factor(s): bacteria


invades mucosal & epithelial
cells of ileum & LI using this
factor. Able to survive in
macrophages but not PMN.
Inhibition of phagosomelysosome fusion: Salmonella
multiply in macrophage, then
lyse macrophage & spread to
nearby cells
Flagellum (H ag): bacteria enters
mucus layer. Has phase var.
similar to E.Coli
Multi-drug resistant factors:
plasmid encoded beta lactamase
& chloramphenicol transferase.
Ability to adapt to acidic
environment expressed by genes

Invades Peyers patch of


ileum & LI infects
various organs &
tissues: liver, kidneys,
spleen, bone marrows,
gall bladder, skin
(ROSE SPOT TRUNK)
& heart
Wk

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

* Most invasive! Enterics are resistant to bile

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 (-)

Human GI tract & GI


tracts of higher
primates

Enterotoxin: Shiga toxin has


same activity. RNase activity
cleaves euks 28S ribosomal RNA.
Stops protein synthesis, results in
bloody diarrhea. Verotoxin:
ONLY S. dysenteriae (see chart
below)

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

Get specimen from


rectal swab,
sigmoidoscopy

Five Fs:
- food
- fingers
- feces
- flies
- fomites

LPS (endotoxin): epithelial


necrosis end of ileum & colon.

Common among
homosexual men

Invasion factors: similar to EIEC.


Plasmid encoded & mediates
invasion & destruction of
epithelium of colon.

Polysach. somatic O antigen to


avoid phagocytosis, serum
resistant

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

Can survive for


months, but it is
delicate.

Shigella are able to survive


acidity of stomach: infection
requires very small inoculum
50-300 cells

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

Multi-drug resistance plasmids

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

2. catalase & superoxide


dismutase: allows organism
to remain viable for days w/
O2 (aerotolerant)
3. Enzymes contribe to
Bacteroides (act as
spreading factor):
- heparinase for
intravascular clotting
- collagenase
- hyaluronidase
- lipases
- nucleases (DNases,
RNases)
- Pili / fimbriae

2. Soft tissue & cellulites:


mixed infections w/
peptostreptococcus,
bacteroides,
fusobacterium, &
actinomyces (all
anaerobes) Post-opt.,
cutaneous & or
mucotaneous infections.
UTI
3. Bacteremia: may cause
endocarditis & brain
abscesses
4. Upper/Lower infection

-------------------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 (-)

Normal flora human


LI (colon), crap found
in soil & water.

1. Urease: splits urea to NH4


ions ==> alkaline urine promotes
urolithiasis (kidney stones).
Destroys the urinary epithelium
& cause infection & impair
kidney fxn

1. Urinary tract
infections: a)
pyelonephritis
b)cystitis. Infections
may be acute or
chronic.

IgA, IgG,
made
against
various
bacterial
components.

Ampicillin for
cystitis

2. Strong motility: movies up


urinary tract

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

2. Urolithiasis: MgNH4 phosphate salts


form kidney stone
due to NH4
3. associated w/
bacteremia,
pneumonia,
endocarditis
UTI: contamination with fecal matter
a) lower UTI = cystitis, infection of urinary cyst, bladder
b) upper UTI = pyelonephritis, serior infection see blood, pus in urine
c) renal or kidney stones = urolithiasis (struvite) & apatite, formation due to production of urease (ie Proteus)

Macrophage
s & T cells
respond to
chronic
infections

Bactrim (TMPSMZ) for


pyelonephritis

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. Urease: splits urea to NH4


ions ==> alkaline urine promotes
urolithiasis (kidney stones).
Destroys the urinary epithelium
& cause infection & impair
kidney fxn

1. Urinary tract
infections: a)
pyelonephritis
b)cystitis. Infections
may be acute or
chronic.

IgA, IgG,
made
against
various
bacterial
components.

Ampicillin for
cystitis

2. Strong motility: movies up


urinary tract

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

2. Urolithiasis: MgNH4 phosphate salts


form kidney stone
due to NH4

Proteus mirabilis
Indole (-)
Citrate (+)
Phenylalanine
deaminase (+)
distinguish from
P. vulgaris!!!

Proteus Vulgaris
Indole (+)
Citrate (-)
Phenylalanine
deaminase (-)

Macrophage
s & T cells
respond to
chronic
infections

Bactrim (TMPSMZ) for


pyelonephritis

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. Polysaccharide capsule (more


infectious): strains w/ K1
capsule contains K1 sialic acid
associated w/ bacterial
meningitis. E. coli w/ K1 are
NOT immunogenic, protects
against phagocytosis & against
complement-mediated lysis.

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

2. Hemolysins: release cytokins,


leads to inflammation
Alpha hemo: disrupts
lymphocytes
Beta hemo: membrane-bound &
h& inhibits PMNs
3. Motility: flagella (H antigen)
b/c of phase variation
4. LPS (endotoxi) most inf.
isolates 04.05.075
5. Pili
a) P (PAP) pili involved in UTI,
attaches to uroepithelia. These
strains can cause pyelonephritis
P Pili are mannose resistant
Type 1 pili used for adhension
(see bolow)
6. S. Fimbria: not well reconigzed
7. Siderophores: chelate host Fe
released by RBC (hemolysins), &
take from transferrin & allow Fe
uptake by E. Coli
8. Serum resitant: resist
oposonization / destruction by
host complement factors or due
to k1 capsules

2. Urolithiasis: MgNH4 phosphate salts


form kidney stone
due to NH4 immunocompromised
b) Bacteremia &
sepsis: (#1 causative
nosocomial agent)
UPEC bacteremia is
complicated.
c) Neonatal
meningitis (#2
causative nosocomial
agent) cause sepsis &
death. Need lumbar
puncture: CSF
PMN, glucose
d) Opportunistic
pheumonia similar
ot Klebsiella
pneumoniae

Macrophage
s & T cells
respond to
chronic
infections

Bactrim (TMPSMZ) for


pyelonephritis

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.

Infection is selflimiting but


requires fluid &
electrolyte
replacement.

2. Enterotoxin invades the


epithelial cell, superificially
Symptoms:
- fever
- nausea
- abdominal discomfort
- watery diarrhea
Severe cases:
- cytotoxin production
(bloody diarrhea + pus) or
enteric inflammation & last
for about a week (self limit)
- Extraintestinal disease:
survives intracellularly 7days
2. Guillain-Barre Syndrome:
- ascending paralytic disease
- viral inf. (influenza, EpsteinBarr Virus EBV)
3. Abortion: organisms
invasiveness can invade fetus
or across placenta during a
septicemia or ascending inf.
4. Reiter syndrome:
- post-infection, arthritis,
associated w/ HLA-B27

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.

Infection is selflimiting but


requires fluid &
electrolyte
replacement.

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)

2. Terminal ileitis: lead to


peritonitis

6. YadA gene: outer


membrane protein,
adhesion to epithelial
cells

3. Septicemia: rare; lesions


internal organs

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

Animals are reservoir


for Brucella species.
Zoonotic infection of
man occurs by contact
w/ infected farm
animals such as cows,
goats, & pigs.
Hygiene (handwash!)
Ingestion of raw milk
Erythritol levels in
placenta (breast,
uterus, epididymis)

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.

CD4 & CD8


Tcells, cytokines
IFN gamma, &
IL-2.
Granulomas are
formed by
delayed
hypersensitivity
rxn.

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. abortus (Bang & Malta fever)


- Primarily cause disease in cattle
- abortion in animals, rich in euorthrodol
- mild disease w/ suppurative
complications uncommon, self-limited

B. melitensis
- more infectious but primarily in goat & sheep

B. suis
- infections in swine

B. canis
- dogs, foxes, coyotes

- severe acute disease w/ complications such as


granuloma formation, becomes chronic

- suppurative, destructive
disease w/ granuloma formation

- mild disease. Suppurative


complications

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

1. Q (Query) Fever: acute


febrile disease: symptoms
include: flu-like disease
w/ fever, headache, chest
pain, chills, malaise, severe
sweats. VERY
INFECTIOUS! 10 bacteria
may cause illness. Usually
self limiting, but may
become latent infection &
chronic, which may
reactived (use cortisone).

Igm & IgG


useful.

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. Lipid capsule: blocks


phagocytosis & blocks
opsonizaiton

1. TULAREMIA (RABBIT
FEVER):

Difficult b/c
intracellular

Zoonotic infection of man


occurs by contact w/
infected wild animals Duch
as beaver, rabbit, squirrel &
deer.

2. LPS (endotoxin)

IgM & IgG are


ineffective
against
infection.
Granulomas are
formed by DTH
rxn. T cell
mediated
immunity is
important to
activate
phagocytosis
for intracellular
killing,

coccobacilli
(pleomorphic,
very small)
facultative
anaerobic,
but prefers
O2
non-motile

RABBIT FEVER can be


fatal!
Transmissin occurs by
tick, mosquito, or fly
vectors. Contaminated
water (ex. Contaminated
H20) maybe envolved in
transmission also in
stagnant water.
Transmitted via aerosols
Inoculum size to be ill:
10 bugs tick bites
50 bugs if inhale
10^8 ingested

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 (-)

Cats (blood) are reservoir

1. LPS (endotoxin)

Self-limiting

Zoonotic infection of man


occurs by the bite or
scratching of an infected
cat

2. Type IV pili adhesion,


twitch motility

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

Man to man transmission


NOT observered

Facultative
intracellular
pathogen

Can survive in saliva,


inhale lice feces, crushed
lice
Causes conjuctiva infection

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 (+)

Animals & birds are


reservoir, upper
respiratory tract & saliva
are involved in
transmission.

1. LPS (endotoxin)

Acute cellulitis: symptoms


include erythrema, swelling,
& pain at bite / scratch site.
Usually the host injuries
occur on leg, arm, or face.

Penicillin or
ampicillin &
tetracycline.

Zoonotic infection of man


occurs by the bite or
scratching by infected dog
or cat.

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

Man to man transmission


not observed
Commensals in some
animals

2. Large polysaccharide,
capsule: antiphagocytic

4. beta lactamase: in
some strains

Associated w/ severe bites!


Complications include:
- tendonitis
- osteomyelitis
- abscess formation
Leads to systemic septicemia
or meningitis
AIDS patient: complication
includes sepsis

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 (-)

Animals are the


reservoir Zoonotic
(also Vector-borne
infection)

1. LPS: fatal, septic shock


2. V and W antigens: exact f(x)
unknown but involved in
extracellular survival as well as
intracellular survival &
multiplication in macrophage;
Resists phagocytic killing & are
facultative intracellular
pathogens.
3. Coagulase: blood to clot
during flea bloodmeal,
regurgitate into the next bite

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

Gram satn &


Waysons satn
to look for
bipolar cells
Direct immunofluorescence

Fleas from infected


animals RODENTS,
rats, & squirrels
involved in
transmission of disease
to humans. Fatal
transmission, &
survives for several
months in infected
carcasses, sputum, &
flea feces.
May cause enteric
disease from ingest
contaminatation.
Inhalation of
aerosolized Y. Petsis
from infected humans
or while handling
infected live animals
carcasses.
Pneumonic Plaque
(rare & deadly!)
Sylvatic plaque
(transmit by fleas on
rabbits, squirrels vs.
urban plaque spread by
rats) Flea jumps onto
human. Then spread
human to human.
Organism survives in
animal blood & flea gut

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:

Vertebrate animals are


reservori for R. typhi in
particular rats. Zoonotic
infection of man occurs by
bite of infected flea
(vector). In infected flea
(rat, cat).

1. LPS (endotoxin)

Highly infectious (but lowest


pathogenicity of the
Rickettsia). 10 organisms to
cause disease!

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 (-)

Humans were thought to


be only reservoir BUT
cats too. Indirect
transmission from man
to man occurs by BITE of
the VECTOR, the body
louse

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.

Both IgM and


IgG are
important

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:

Humans are primary


animal reservoir but
other animals can also be
reservoir. Flying
squirrels. Zoonotic
infection of man occurs
by bite of infected louse
(vector). Arthropod
likely to be squirrel flea.

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.

Infected louse may be


transmitted to man via
inhalation of dried lice
feces or by bite wound or
crushed into the skin.
NOT passed transovarian
Unlike other rickettsia
diseases: can also see
man to vector to man
transmission. Still needs
the vector as source!

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

See neurological changes


include delirium & stupor.

More life threatening:


Bartonella Quintana

During cold weather may


lead to gangrene of feet &
fingers.
2. Brill-Zinsser Disease:
Reactivated epidemic
typhus (BuZy Pissing) (less
severe than primary
infection) May occur years
after initial disease.
Chronic carrier w/ less
intense rashes b/c of partial
immunity.
3. Copmlications: CNS
dysf(x), myocarditis

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:

Animals (wild mammals


& birds) & hard ticks

1. LPS (endotoxin)

1. Rocky Mountain Spotted


Fever (RMSF): Systemic inf.
following a tick bite (tick
saliva). Rickettsemia
causing vasculitis of the
capillary beds of many
organs particularly of the
lungs & skin producing a
fulminant disease.

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)

Has to be attached 24-48


hr in order to become
encouraged w/ blood &
to transmit the organism
to man.

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.

Spirochetes (cork screw)


-

outer most layer is referred to as an outer sheath (glycosaminoglycan)


underneath is the outer membrane (peptidoglycan, lipids + covalently linked
proteins)
encase the periplasmic space where endoflagellae are located
directly underneath the periplasmic space is inner membrane (cytoplasm)
Cytoplasmic tubules (body fibrils)
NO LPS
Has a layer of peptidoglycan

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

a) Non-specific blood tests: (agglutination) indicate present infection, since


individual become (+) upon infection but levels decrease during chronic disease.
Tests for Syphilis
1. Complement Fixation (Wasserman) indirect test: used to detect presence of
reagin antibodies (reagan is antibodies directed against cardiolipin)
Cardiolipin is an antigen which is released by damage host cells & present on
the treponeme.
2. Rapid Plasma Reagin (RPR): also a reagent cardiolipin & is a carbon
agglutination test
3. Venereal Disease Research Lab (VDRL) test: Cardiolipin + serum, check for
clumping (means + results of antibodies against cardiolipin) AKA Flocculation
test
4. Treponemal Specific Blood tests
5. Fluorescent treponemal antibody Absorption test (FTA-abs)
6. T. pallidum Hemagglutinin Assay (TPHA)
Vocabulary Disease Symptoms:
1. Charcots disease: trophic degeneration of knee joint. Loss sensation due to
neurosyphilus
2. Condyloma: fusion of 2nd syphilitic lesions around the anal areas
3. Gummata: ulcerous skin lesion (chewy gum)
4. Hutchinsons teeth : teeth are translucent. Incisor-like
5. Saber shins: affects long bones
6. Saddlenose: perforated nasal septum
7. Tabes dorsalis: destruction of dorsal roots of spinal cord

Chlamydia
-

Gram (-), obligate intracellular organisms w/ unusual life cycle


NOT spirochetes!!!
Obligate intracellular parasites !!! Can not synthesize ATP!
o No cytochromes or flavoproteins. Cant metabolize glucose to pyruvic
acid using pentose phosphate pathway

Chlamydia Life Cycle:


1. Small dense cell: ELEMENTARY BODY (infectious form but NOT replicating)
it is outside of the host. Enters the host via phagocytosis DNA:RNA, 1:1 ratio =
infectious particle
2. Next 8 hr, elementary body reorganizes into large, less dense cell called
reticulate (or initial) body
3. Reticulate body: (this replicates) , grows in size & divides by binary fission
(DNA:RNA ratio is 1:4) this is NON-INFECTIOUS form
4. 24-48 hr, reticulate bodies reorganize into dense elementary bodies &
developmental cycle is complete when host cell liberates the small dense
infectious cells.

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!!!

Man is only reservoir.

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)

Syphilis (3rd most common STD)

g(-) difficult to
see b/c too thin

Look for
spirochetes
using direct
miscroscopy

IgG and IgM


develops by
end of 2nd
stage are
important.
Immunity
takes a long
time to
develop in
part b/c so
there are few
proteins on
surface of T.
palladium.

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.

Highly infectious! Less


than 10 spirochetes to
cause disease!

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

1. Primary syphilis: systemic inf


following sexual contact.
Typically hard, painless chancre
forms site of entry (genitals, mouth
or anus) w/ spirochemia
(spirochetes in blood stream)
Sympt. 4-6 weeks. Most
contagious stage. May see > 1
chancre in AIDS patient.
2. Secondary syphilis: persistent
spirochemia, 3 weeks 3 months.
Papular rash develops entire
body. Spreads from trunk to soles,
genitalia, & mucous surfaces.
AKA Great Pox (Great Imitation)
w/ fever & soar throat. Spirochete
may invade any organ of body.
Rash may last up to many months.
Contagious. Organism may be
isolated from rash. May develop
LATENT disease. Condylomata
(bacteria continue to multiply &
deep-seated lesions)
3. Tertiary syphilis (LUES)
NOT CONTAGIOUS! Disease
affect any organ, may re-occur. T.
pallidum, only observed in the
CSF. Lesions on tongue, gummata
lesions, & other effects on skin,
bones, & blindness & Charcots
knee
4. Congenital syphilis:
transplacental inf. of fetus at 12
latent stages in mother. Death of
fetus (blindness or deafness). Also:
saddle nose, saber shins, skin rash,
Hutchinsons teeth, heart
malformation, & liver damage.

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.

Severe case: (effect liver & kidney)


LEPTOSPIROSIS which is usually
a biphasic disease. Moves quickly
& effects blood.

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.

Animal kidneys are


resvoir. Eating kidney,
or consuming water
contaminated w/ animal
urine.

IgM & IgG


are
important
Autoimmune
response
may be
involved in
disease
process

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)

a) Leptospiremic phase: presence


of leptospires in blood & CSF.
Abrupt onset of fever, shaking
chills, headache, & myalgia.
b) Immune phase: Accompanied
by IgM production. Aseptic
meningitis (no bacteria in blood
but effects brain) . Onset of
hepatic & renal failure &
widespread hemorrhages & shock.
Also known as Weils Disease due
to an autoimmune response
causing liver damage b/c of
molecular mimicry. AKA
INFECTIOUS JAUNDICE
(yellow/green liver) .
Has 2 phases:
1. Anicteric phase: w/o liver
2. Icteric phase: w/ liver involve

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

IgG and IgM


against outer
surface
antigens
(Osps)
important
but undergo
antigenic
variation.

Stage 1:

Use ELISA

1. Glycolipid
(similar to
Treponema) NO
LPS

LYME DISEASE: > 1 stage

Grown on
BarbourStoennerKelly
medium
contains
bovine
serum
albumin
(BSA) &
rabbit
serum at
30C

Primary reservoir is the


mouse including white
food mouse, dusty footed
wood rat, chipmunks,
and DEER.

#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

Vectors are the primarily


Ixodid ticks

Infection of man occurs


by tick bite & transfer of
organism during tickengorgement!
Transmitted in vector by
transovarian route. Also
tick saliva or deposition
of feces into wound.

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

Humans are believed to


be only reservoir
(epidemic form of
disease).

1. Glycolipid

Relapsing Fever: > 1 stage

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.

IgM & IgG


against outer
surface
antigens are
important
leads to
complementdependent
lysis.

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

Vectors for the epidemic


organism are lice
(therefore, louse-borne
disease)
Endemic form of disease
is found in animal &
human reservoirs &
appear to be spread by
ticks.

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

g (-) does not


have typical
cell wall of
peptidoglycan
but sensitive to
Penicillin

Grows in
cell culture

Difficult to
diagnose.

Humans are reservoir.

1. Intracellular
survival
a) stimulates nonphagocytic
epithelial cycle to
engulf them

Male STD: most common STD in


US. Urethritis involve urethral
discharge. (SYPMTOMATIC)

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

Infection of man occurs


by sexual contact & by
autoinoculation to other
parts of body.
Mother to child
transmission is possible
at birth.
Maybe transmitted by
direct contact with
fingers, contaminated
towels & clothing.
Can be transmitted
sexually to other adults
leading to genital
symptoms. Can be
spread by fingers,
towels, clothing can
even spread in
chlorinated water
(swimming pool
conjunctivitis)

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

Female STD: Cervicitis,


endometritis, PID involve
discharge. May cause sterility
women are ASYPMTOMATIC
Swimming Pool Conjunctivitis:
Spread by fingers, fomites & even
chlorinated water into eye.
ADULT INCLUSION
CONJUCTIVITIS: STD
TRACHOMA:
Chronic eye inflammation by
infecting eye.
Lymphogranuloma venerum:,
(LGV): develop into buboes and
lead to elephantiasis of genitalia &
rectal structures as result of
perirectal scarring.
Neonatal infection:
Due to vaginal passage can cause
disease by either being aspirated
into lung or by conjuctiva of
neonate.
a) Infant atypical pneumonia:
- long term complications & otitis
media
b)Inclusion conjunctivitis:
may have similar to trachoma
Reiters Syndrome:
Arthritis, periostitis on calcaneus
(heel) pain AKA Lovers Heel

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)

g (-) does not


have typical
cell wall of
peptidoglycan
but sensitive to
Penicillin

Grows in
cell culture

Contact w/ parrots &


other psittacine birds can
spread to other animals
(cattle, swine, cats, dogs)

1. Intracellular survival:
a) stimulates nonphagocytic epithelial cycle
to engulf them

Ab not
effective.

Doxycycline and
azithromycin

Can get into:


environment from feces
& survive a long time !

b) inhibit phagosomelysosome fusion


(all 3 chlamydia have
them!)

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!

2. Unusual life cycle:


Elementary bodies can
infect host macrophages &
epithelial cells
3. Endotoxin similar to LPS
4. Toxic factor
5. Type III secretion system

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

g (-) does not


have typical
cell wall of
peptidoglycan
but sensitive to
Penicillin

Grows in
cell culture

Humans are reservoir.


Occurs in respiratory
droplets.

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!

Epidemics are possible


TWAR strain caused
acute respiratory disease.

b) inhibit phagosomelysosome fusion (all 3


chlamydia have them!)
2. Unusual life cycle:
Elementary bodies can
infect host macrophages
& epithelial cells
3. Endotoxin similar to
LPS
4. Type III secretion
system

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)
-

Coenocytic: several nuclei present in cytoplasm of 1 cell (multinucleated)


Mat of hyphae = mycelium or thallus
Vegetative hyphae = penetrates substrates for nutrient acquestion
Reproductive hyphae: aerial structures for reproduction

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

Sexual form NOT identified: (Fungi Imperfectii or deuteromycetes)


99% of ASEXUAL spore
o Fragmentation
o Fission (equal size)
o Budding (new buds, vary in size)
o Spore formation: mostly budding
o Yeasts: fission, budding
Spores produced in sac sporangium w/ spores sporangiospores

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)

Polyenes: creates large pores in fungal cell membrane by binding to erogsterol

Azoles: ex. ketoconaxole, fluconaxole, itraconazole, inhibit ergosterol, block


cytochrome P450 enzyme

Allylamine: ex. naftine, binafine, terbinafine, lamisil


o tolinaftate : ex. tinacitin ==> ergosterol

Griseaans : inhibit microtubule so cells do not divide

Potassium iodide (KI) : antifungal therapy to treat sporothrix schenckii infection


Mycotic Infection:
cutaneous
superificial
subcutaneous
systemic
CUTANEOUS INFECTION (Dermatophyte infection):
Dermatophytes:
invade keratinized & cutaneous areas
produce keratinase, collagenase, elastase
affect stratum corneum (skin)
grown best at 25C
not invasive
Tineas (ringworm)
Tinea Capitis (scalp) itch on scalp w/ 3 patterns
Caused by microsporum species (M. canis, use Woods light)
o Endothrix: inside hair shaft
o Ecotothrix: outside hair shaft
o Favic: hyphae

arthoconidia & air bubbles form inside hair

Honey comb pattern

Tinea Corporis (non-hairy parts of body)


mistaken for lupus
scaly
popular eruptions
Tinea Pedis (Athletes foot)
public showers, swimming pools, watery lesions btw toes, show peeling &
cracking of skin
caused by: Trichophyton rubrum & T. mentagrophytes
Tinea Favosa (form of scalp)
yellow, cap-shaped crusts
looks like a honey comb
T. Schoenleinii (fluoresces yellow-green)
Tinea Unguinum (nails - infection)
superificial, only pits of nails
involvement of nail surface w/ invasion beneath nail plate
onychomycosis (nail infection) caused by non-Dermatophytic
o saprobe fungi ex. Aspergillas
Fungal finger nails ex. car wash workers, common cause Candida Albicans
Tinea Cruris (Jock Itch)
can be epidemic form w/ exchange of clothing, towels, scaling lesions, itchy &
often dry
Dermaphytids
not grown on Sabouraud
allergy response w/ dermatophyte infections
IDs (severe itching especially after antifungal agent)
Fungal organism NOT present
Epidermophyton (NS):
thermally monomorphic, no microconidia but macroconidia, cigar shape
Microsporum (SH)
thermally monomorphic
Trichophyton (NSH)
thermally monomorphic

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

Various size &


shape
microconidia w/
large spherical
conidia

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

Microscporum Gypseum Complex (M. Canis & M. Audouinii)


thermally monomorphic mold
Cell feature
- Septate hyphae
- microconidi, along the hyphae & club shaped
Dxn
- KOH, non-treated test w/ sabouraud agar for microsporum canis
use woods lamp (yellow-green) fluorescence
Disease
- Tinea capitis
- Tinea Cruris
- Tinea Pedis
Transmission
- dog ==> human (zoophilic) & geophilic transmisin
Treatment
- affected skin, kept cool & dry
- apply topicl antifungal agents (cream)
- tinea capitis ==> oral griseofulvin
- Lamisil
Hortaea Wereckii = Exophiala Werneckii :
Dematiaceous fungi or pigmented fungi
o Non-invasive
o Pigmented (b/c melanin production)
Disease:
o Produce superificial inf. of skin, Tinea Nigra (black growth on skin)
but non-invasive
o Skin infections, non-scaly, smooth, brown-black painless spots

Malassezia furfur & M. Ovalis (Pityrosporum ovale)


Dimorphic & long hyphae
Comes from furfaraceous or scaly
Cell feature
- yeast like cells
- hyphae are usually absent
- spaghetti & meatballs
Dxn
Disease
- Superficial inf. Of skin (Tinea Versicolor, Pityriassis Versicolor)
- skin-inf. non-itchy, scaly, pale spots on shoulders & back, chest, &
upper arms!
Treatment
Woods Light, orange-red fluorescent hyphae
Piedraia Hortae
dark/black hard nodule hair shaft (Black Piedra)
Disease
- Base of the hair to fall out
Trichosporon Beigelii (T. aschii, T. mucoides, T. inkin)
baige associated w/ white Piedra
Disease
- Superificial infection of hair roots

SUBCUTANEOUS INFECTION (Dimorphic)


stays localized
Sporothrix Schenckii (Gardeners w/ hay, rose bushes, ferns) puncture of skin
thermally dimorphic yeast-like fungus dematiaceous
daisy clusters
Cigar shaped budding yeast (37C)
Wrinkled round brown, black colonies
Infectious occurs (scratches, punctures) during gardening from wood, splinters,
Prevelant in South US
Zoonotic transmission: armadillo & infected cats
Disease
- painless nodules forming along lymphatic channels
Treatment
Potassium iodide
Madurella Spores
thermally monomorphic molds, dematiaceous
true fungal infection, brown-colored
Disease
fungal mycetoma (Eumycetoma)
madura foot, resembles nocardiasis (actinomycetoma)
Treatment
- difficult to cure

SYSTEMIC INFECTIONS: (Inhales into lungs)


ALL thermally dimorphic
True, frank, primary pathogens
Via respiratory rate (inhaled spores)
Blastomyces dermatitidis:
yeast like fungus, looks like figure 8s
multi-nucleated, forms granules of skin
no cell wall, bird droppings
Mississippi river to East coast
Dxn
- multi-nucleated budding yeasts, single broad-based 888s
Disease
NAmerica blastomycosis (mild pulmonary inf), skin lesion
Formation of granulomas of skin & bone
Paracoccidiodes brasiliensis:
- thermally dimorphic yeast-like fungus
- UNINUCLEATE!, multiple budding mother cell w/ buds having narrow bones
- Cause systemic infection, more mucosal surface
- Found mostly in S. America blastomycosis (granulomatous spreads to lungs to other
mucous surfaces of nose, mouth, & GI tract)
-Looks like ships wheel, steering wheel, pilot wheel
- endemic
Coccidioides Immitis (C.Posadasii)
dimorphic fungus: changes form to spherule at at 37C
Cell feature
terminal arthrospores attached directly to hyphae
spherules in tissue specimens, barrel shapped!
Transmission
direct inhalation (mold spores, arthrospores) from soil &
dry climates Southwest US (Central or S. America)
likes Nitrogen associated w/ bird droppings (feces)
Disease
Coccidiomycosis, highly infectious disease flue-like
pulmonary infection, CNS (Meningitis)!!!
Leads to erythema nodosum (DTH response, red tender
nodule on skin)
Desert rheumatism San Joaquin Valley FeverCali
ID test looks for DTH response
Histoplamsa Capsulatum Var. Capsulatum:
dimorphic yeast-like fungus & small oval microconidia
spiny macroconidia attatched to hyphae, knobby (tuberculate macronidia)
Transmission
- direct inhalation of small molds (microconidia) from soil or bird
droppings. They are spiny & knobby looking!
- Mississippi + endemic, Ohio River, S. America, & Africa
Disease
- Most common respiratory mycotic inf pneumonia, granuloma
- reticuloendothelial system (RES) found intracellularly w/in
macrophages. Like at TB test can use DTH
- Chronic disease: reactivation enlarged granuloma, liver, spleen

OPPORTUNISTIC INFECTIONS: (Colorized, immunocompromised state of host)


Aspergillus fumigatus:
thermally monomorphic mold
inhale spores immunocompromised patients
Fungus ball (aspergilloma) spore germinate (Farmers Lung) HAY FEVER!!!
A. Flavus produces aflatoxin potent liver carcinogen. INVASIVE!!!
Candida Albicans:
Dimorphic but NOT thermally but grown on corn-meal produce pseudophyae
Use as diagnositic: Germ tubes test (true hyphae) this is a unique feature!
Part of normal flora (FurFur & tricosporum???)
Produces ==> chlamydospores are unique to this candida
cream-colored pasty colonies
Transmission
- normal commensals of human & animal GI, resp, tracts skin &
female genital tracts
Disease
ORAL THRUSH: (AIDS immunocompromised)
- produce white patches in mouth & tongue continue to GI tract
Cutaneous candidiasis: diper rash
INTERTRIGINAS CANDIASIS (Intertrigo):
- appendages immersed in H20 long periods, moist parts in diabetes
ONYCHOMYCOSIS: nail inection
VAGINITIS: (Moniliasis): vaginal infection of women
Chronic Mucocutaneous Infection:
- CMI failure (T-cell deficiencies) infection associated w/ skin, oral
mucosa, respiratory mucosa, GI & GU mucosal surfaces
- antibiotics
Treatment
Cryptococcus Neoformans:
capsule, visible w/ India ink
thermally monomorphic yeast
capsule is anti-phagocytic
Cell feature
- oval shapped
Dxn
- Mayers stain to see PINK capsules
- CSF sample prep. w/ 10% KOH & India ink
Disease
- result in cryptococcosis (pulmonary infection)
- to meninges & brain thrives on CSF (Meningitis)
- occurs often immunocompromised
- can be unrecognized or asymptomtic
Transmission
- Via inhalation of yeast found in soil & pigeon droppings
Treatment
- Ampotericin B & Latex agglutination!
Mucormycosis (Phycomycosis or Zygomcosis): mucor, absidia, rhizopus species
invades tissues, brain (nasally) it is a bright mold!
Cell feature
aseptate or coenocytic & invasive
member of Zygomycetes (phycomycetes)
sporangia form at 90 degree angle from hyphae

INDI Organisms # 4
Virus
Size & Structure

20-300 nm size (picornavirus ==> poxvirus) appears spheres or rods

Contain either DNA or RNA, NOT both!

All have a protein coat, capsid (repeating capsomers)


o
Capsid could is outer surface
o
Others could have lipoprotein envelope composed of phospholipids bilayer

Enveloped: picked up from nucleus or p.membrane or created from cytoplasm ether sensitive

Composed of nucleic acid & capsid protein is called nucleocapsid

Shape: spherical (icosahedral) or helical symmetry


o
Exception: poxvirus looks like a brick shaped (complex)

All human viruses have helical nucleocapsid are enveloped

No naked helical viruses infect humans.

Icosahedral nucleocapsid can be either enveloped or naked


Viral Nucleic Acids

Retroviruses: have two copies of genome (diploid)

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

DNA replicates in:

Major viruses

Naked
Naked

Nucleus
Nucleus

No

Naked

Nucleus

B-19
Papilloma
Polyoma
Adenoviruses

No

Enveloped
(nuclear)

Nuclues; virus
assemble in nucleus

HSV: VaricellaZoster, EBV

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:

group of DNA viruses that produce benign & malignant tumors

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)

Hyperkeratosis: inflammation w/ excess growth of prickle cells of skin

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

Important misc facts:


o
Associated with conjunctivitis, GI tract, and upper respiratory disease (common cold).
o
Produce tumors in baby hamsters but NOT in humans.
o
Most common infection of tonsils & adenoids in early child life is from adeno types 3 & 7 and is latent.
Parvoviruses

The ONLY ssDNA, naked, icosahedral, linear, e-nucleated w/ mature RBC


non-defective
defective
replicates only in multiplying host cells

requires helper virus (Dependo virus) ex. of


helper virus is (Adenovirusand Herpes Virus)

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

dsDNA, enveloped, icosahedral, linear shaped,

tegument: contains viral proteins & enzymes involved in initial replication

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

- Herpes Type 1 & 2 (HSV-1 & HSV-2)


- Varicella-Zoster:
a) chicken pox: (varicella portion) acute infection (children)
b) shingles: reactivation of virus of chicken pox
- Epstein Barr Virus (EBV)
a) Burkitts lymphoma (tumor in jaw), nasopharyngeal carcinoma
b) infectious mononucleosis

HSV-1 (usually infects above waist)


- Location of latent: Trigeminal dorsal root ganglia
- Acute herpetic gingivostomatitis: most common
infection for Type 1. Gums swollen! Similar to herpes
labialis. Oral herpes. Self-limiting.
- Eczema Herpeticum:(Kaposis similar to Herp 8) infect
fingers (herpes whitlow)
- Keratoconjunctivitis: infects eye
- Herpes labialis:(cold sores!!) NOT common cold, most
common recurrent disease.
- Encephalitis: residual neurologic defects

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)

HSV-2 (usually infects below waist)


- Location of latent: Lumbo-sacral dorsal root ganglia
- Genital Herpes: lesions develop in genital organs.
- Neonatal Herpes: transmitted to new borns
- Aseptic meningitis:mild, self-limiting

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

Cytomegalovirus (Herpes 5) Latent in Leukocytes


o
Disease:

Most infection of infants, caused by intrauterine or early postnatal infection (pass to child)

Teratogenic: virus causes severe congenital anomalies in infants (mental retardation)

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

Also found in Conventional slow virus disease: involves brain infection


o
Treatment:

Ganciclovir, foscarnet, cidofovir

Vaccine is not effective

Epstein Barr Virus (EBV) latent in B cells are leukocytes


o
Disease:

Burkitts Lymphoma & Nasopharyngeal Carcinoma

Chromosomal translocation breakages are associated

Associated with Kissing Disease (mono, results in large lymph nodes & spleen)

Use Paul Bunnel test to detect mono

WBC ex. Downey cells: B cells infected by EBV

Herpes Virus 6:

Lymphotrophic & ubiquitous associated w/ childrens disease

Childhood exanthema subitum (roseola)

Associated with multiple sclerosis

Herpes Virus 8:

Associated w/ Kaposis sarcoma, (found in Type I) problem w/ immunocompromised

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

Rhinoviruses (nose): common cold

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

D antigencity: is the native complete virus HAS VIRUS RNA


o
Host: man is the ONLY natural host
o
Virus replication: adsorption (complete particles) ==> penetration ==> uncoating ==> translation (replication) ==> synthesis of
vRNA ==> maturation ==> release
o
Disease: Starts oral route. Multiples in tonsil, lymph nodes, Peyers patches in SI. Asymptomatic shedding
Infection
Ingested virus
Alimentary phase
Oropharyngeal, virus in throat, intestinal mucosa
Lymphatic phase
Tonsils, deep cervical lymph nodes, virus in feces, peyers patch,
Viremic phase
Blood
Neurological phase
CNS, extraneural tissue, regional nerve ganglia
o

o
o
o

Infection: 90% in oropharnyx region

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.

Paralytic poliomyelitis: flaccid paralysis, uncoordinated, painful spasms on nonparalyzed muscles

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:

Nonspecific febrile illness: Can lead to polio-like paralytic disease

Herpangia:fever, soar throat, anorexia, vomiting, abdominal pain, vesicles in palate, uvula. Self limiting. Not herpes!

Pleurodynia: chest pain (Bornholm disease: Devils grip)

Hand-Foot-Mouth: oral & pharyngeal ulcers which may spread to arms & legs w/ mild fever

Mycoardiopathy: mycocardial disease in adults & children

Common cold: upper respiratory infection

Diabetes Melitis:abrupt onset of diabetes after infection w/ coxsackie


o
Control:

Spread by feces, pharyngeal secretions, sewage

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

Associated with common cold & SARS

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)

associated w/ the influenza

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,

Reyes syndrome: encephalopathy & fatty liver associated w/ Influenza B

Associated w/ Guillain-Barre Syndrome: ascending paralysis

Otitis media
Treatment:
Anti-viral
- Amantadine hydrocholoride & rimantadine
- Tamiflu
- Relenza (works against NA
- drug blocks uncoating (blocks replication)
Vaccine

Vaccine is prepared in eggs

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)

Acute highly infectious disease: w/ rash & respiratory symptoms


o
3C (cough, coryza, conjunctivitis)
o
Lacks neuraminidase
o
Kopliks spots: vesicles in the mouth. Appear tiny red patches w/ white specks on buccal mucosa
o
Measles can impair CMI (cell mediated immunity)

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.

MMR is a live attenuated virus vaccine


Reoviruses

ONLY dsRNA, naked, icosahedral, 10 segments, double capsid

Disease:
o
Rotavirus: affects children w/ diarrhea. Looks like wheel shaped. Can see genetic re-assortment (shift in orthomyxovirus
Toga Virus (cloak)

(+)ssRNA, enveloped, 3 proteins

Rubella (German Measles) Rubivirus


o
Rubella virus:

Transmitted by (starts in) respiratory tract. Highly infectious. Spread in blood.

Symptoms: rash begins on face, low fever, enlarged lymph nodes & spleen.

Congenital Rubella Syndrome:


o
Complications involve cardiovascular, hematologic, neurologic, opthalmlogic, osteologic, & auditory systems.
o
Mental retardation may occur
o
Teratogenic: CONGENITAL ANOMALIES

Leads to spontaneous abortion

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

Rabies multiplies in muscle & connective tissue at the infection.


o
3 stages in human rabies:

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

Depressive (paralytic) phase: convulsive seizures, coma, and death

Lab Diagnosis
o
Presence of Negir bodies in nerve cells.
o
Antibodies can be detected by immunofluorescence, complement fixation, or neutralization.

Immunity & Prevention


o
Passive and active immunization at the same time!
o
Give promptly to build antibodies to prevent virus attacking nervous system.
o
Vaccines include: human diploid cell vaccine, duck embryo vaccine, nerve tissue vaccine (brains of animals) inject into individuals.
Arboviruses (Flavi, alphaviruses)

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:

PrPc: wildform, native, found on surface

PrPsc: infectious form, tertiary structure


o
Replication: If PrPsc interacts with PrPc in the body will interact and change confirmation and infect near nerve cell & cause
spongiform appearance.
Conventional Slow Virus Disease
- Subacute sclerosing panencephalitis (SSPE) measles virus

Unconventional Slow Virus Diseases


- Kuru: Neuro. disease in & children. Cannibalism. A prion
- Creutzfeldt-Jakob: dementia, lesions resemble kuru
- Scrapie: agent in brain. Sheep affected. spongiform encephal.
- Transmissible mink encephalopathy: infects brain of mink
- Bovine Encephalopathy (MAD COWS disease): spongiform

Hepatitis Viruses

Definition: acute infections of the liver (jaundice) may lead to liver cancer (necrosis of hepatocytes)

Viruses: herpes simplex, herpes-zoster virus, Epstein-Barr virus, coxsackieviruses


o
Viruses replicate primarily in the liver (viral hepatits):

Hep A (HAV): infectious hepatitis w/ short incubation

Hep B (HBV): serum hepatitis w/ long incubation due to blood/fluid exchange

Hep C (HCV): non-A and non-B

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

RNA or DNA the cancer originates from a single cell

Function of oncogene: protein kinases codes for tyrosine kinase that phosphorlyates proteins at tyrosine & causes fibrin network

Human Leukemia-Sarcoma Virus:


o
Human Trophic cell leukemia virus HTLV-I and HTLV-II

They are diploid cells, w/ 2 copies of genome, NOT segmented

HTLV-1 via tax (transcriptional activation) activates IL-1, IL-2 receptor


o
HIV

Binds to CD4 and chemokine receptor

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

Anti-protease drugs: (ex. Saquinavir or Ritavir)

Inhibit protease from cleaving the polyprotein into the virus.

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)

gag = group specific antigen, capsid proteins

pol = polymeras, protease, integrase

env = enveloped glycoproteins

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?

(-)sense means infected


What type of vaccine do you need for rabies?

both live & dead vaccine


What are the 3 phases of Rhabdovirus?

Prodromal ==> excitement ==> depression


Which are associated with the common cold?

coxsackieviruses

rhinoviruses

adenoviruses

cornoviruses
Which deals with cold sore?
* Herpes labialis

Which viruses do you see coryza?

Coronavirus

paramyxovruses - Measles (Rubeola) which includes the 3Cs

What is the treatment for polio?

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:

ectoparasite: live outside of organism

endoparasite: live inside of organism

facultative: can have free form or w/in the organism

obligate: completely establish only inside, cant live outside

incidental: establish doesnt belong (its like an accident)

temporary: part of life cycle in organism, later goes outside

permanent: remains inside host

pathogenic: causes injury, by trauma, toxins or damage

pseudoparasite: like a parasite artifact

coprozoic: termites able to digest cellulose (in the gut)

Needs:

Moisture & reasonable temperature

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:

Parasites can exist in 3 forms


o
Sporozite: resistant, quiescent (nothing happening)
o
Trophozoite: active eating stage
o
Larval forms:worms, cysts

Lab diagnosis: Intestinal & biliary parasites


o
Feces (check 1st), intestinal material, Entero-Test method (get capsule w/ string parasite wrapped around when taken out)

Common Human Infections


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Protozaons
o
Nemathelminthes (round worms)
o
Platyhelminthes (flukes)
o
Arthropoda (fleas & ticks)

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

- keratitis (eye) may lead to


blindness
- Chronic granulomatous
amebic encephalitis

Giadrdiasis / Giardia
lamblia

protracted diarrhea and


malabsorption syndrome

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

- skin lesion at bite site,


fever, lymphadenopathy
- CNS involvement:
progressive mental, coma,
death due to pneumonia
- Starvation, sepsis

metratrypanosomes,
transmitted by bite
of TseTse fly

American
Trypanosomiasis /
Trypanosoma cruzi

- Chagas disease (in


children) acute: visceral
organs, heart, unilateral
opthalmia, palpebral
edema, eyes
- Chronic disease (adults) :
megaesophagus,
megacolon, enlarged heart
visceral leishmaniasis (kalaazar), destruction of
macrophages, enlarged liver
& spleen, protracted fever

trypomastigoes
(body form) &
transmitted by
reduviid bug
(kissing bug) feces

blood &
trypomastigotes

Promastigotes &
Phlebotomus
(sandfly)

bone marrow
aspirate &
macrophages

Balantidiasis

diarrhea & dysentery

- cysts, transmitted
food & water
contaminated by
pigs

stool, cyst

Plasmodiasis
Malaria, plasmodium
vivax, ovale,
malariea, falciparium
Toxoplasmosis
Toxoplasma gondii

periodic fever, chills,


hepatosplenomegaly,
anemia

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

- reservoir in dogs &


foxes
- thatched roofs,
breeding places for
sandflies
largest protozoal
parasite

- 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

definitive host cat


family

pyramethamine +
sulfadiazine

specific
antibodies that
bind to T. cruzi
antigens

- Iodoquinol

Babesiosis / Babesia
microti

Nantucket fever, resembles


malaria

bite of nymph of
hard tick, Ixodes
sacapularis

blood &
organism in
RBC

Cryptosporidiosis

profuse, watery diarrhea

oocysts, feces of
animals, human
feces & respiratory
secretions

stool, gut
tissue, oocyts
observed via
phase contrast
microscopy,
acid-fast
stained
material

Helminth Diseases (Round worms)


Disease name/agent
Clinical condition
Ascariasis/
Most common in
lumbricoides
children, abdominal pain,
obstruction or worm
migration
Hookworm / necator
- Epigastric pain
americanus or
- anemia
ancyclostoma
duodenale
Stronglyoidiasis /
Watery, mucous diarrhea
stercoralis
Enterobiasis / E.
vermicularis
Trichinelliasis /
larvae ingestion of
meat

Anal pruritus

Schistosomiasis /
mansoni,
haematobium

Fever, lymph node &


liver enlargement,
obstruction of vessels of
urinary bladder, intestine,
liver
Tapeworm infection,
adult worm infect
(asymptomatic) beef,
epigastric fullness, nausea
Fish tape worm,
asymptomatic, diarrhea,
anemia b/c lack of B12
Mild symptoms, loss of
worm

* Taeniasis / saginata
(beef) solium (pork)

* Diphyllobothriasis /
latum
* Tapeworm disease /
Rat tapeworm /
Hymenolepsis
diminuta
* Dwarf tapeworm /
Hymenolepsis nana

clindamycin + quinine

antibiotics not effective,


immunocompetent self
limiting, supportive care,
paromomycin (some
success)

Infective form
Eggs, feces contaminated
food or soil

Diagnostic
Stool/ eggs

Comments

Treatment
- Mebendazole
- pyrantel pamoate

- larvae, (soil, on vegetative


penetrate skin)

Stool /eggs

Controlled by sanitary
disposal of human feces

- Mebendazole
- pyrantel pamoate

Larvae / larvae in soil or


vegetation penetrate skin

Stool /eggs

- Thiobendazole

Eggs / ingestion of eggs

anal contact
spec/eggs
curled up
larvae in
muscle,
antibodies

ONLY nematode worm


reproduce in host. Free
living & parasitic phase
Pinworm, seatworm
infection
Muscle worm infection

T. solium may cause serious


CNS infection (cysticercosis)

- prazquantel
(unhooks)

Muscle biopsy, serum,

Abdominal pain, nausea


& vomiting in heavy inf

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 (cercariae), larvae in


snail infested water
penetrate skin

Larvae (cysticercus),
ingestion of
raw/undercooked pork or
beef
Larvae (plerocercoid),
ingestion of raw
fish/undercooked fish
Larvae, ingestion of
infected cereals (flour)

Larvae, hand to mouth


contact, ingestion of mouse
feces

Stool /
eggs, worm
segments

- prazquantel
(unhooks)

Stool /
eggs, worm
segments
Eggs in
feces

Eggs in
feces

- prazquantel
(unhooks)

Most common tape worm in


southeast US, children
affected

- 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

What is the difference between polio vs. poxvirus?


Polio (+sRNA)
Poxvirus (dsDNA)
- Subgroup of the piconovirus
- largest
- vaccinated w/ Salk & Sabin
- eradicated
What is the difference btw the measles (rubeola) vs. German measles (rubella)?
measles (rubeola)
German measles (rubella)
- acute infectious disease w/ rash & respiratory - subcategory of toga virus
- 3C
- (+)ssRNA, enveloped
- no neuraminidase
- rash on face
- Kopliks spot
- congenital anomalies
- impairs CMI
- SSPE
- RSV: blocks resp. tract in young children