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An overview of various Gram positive and negative bacteria, including their physiology, structure, virulence, epidemiology, and diseases. Topics covered include Staphylococcus aureus, Streptococcus species, Bacillus cereus, Actinomyces israelii, and Neisseria meningitidis, among others. The document also discusses various toxins, vaccines, and treatments associated with these bacteria.
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Organism
Physiology/Structure
Virulence
Epidemiology
Diseases
Tx
Staph Aureus
Gram (+) cocci formedin clustersFacultative AnaerobesCatalase (+)Coagulase (+)Β‐Hemolytic
A^ protein
evades phagocytosis Coagulase
forms fibrin clot around organism, protecting it fromphagocytosis Toxic
Shock
Syndrome
Toxin
produces the
superantigen
that leads to toxic shock. Exfoliatin
causes the skin to slough off, disrupts desmosomes. Enterotoxin
causes gastroenteritis
Is normal flora found in mucousmembranes and skin. Transmissioncan either be endogenous orexogenous.Common contamination is found infood workers that
sneeze
on their
hands, then
don’t
wash
. Found on
food that has been left out, like potatoesalid.
Gastroenteritis
usually self limiting. Can
be caused by ingestion of bacteria (thensubsequent production of toxin) or byingestion of
heat^
stabile
toxin
produced
before organism was killed by cooking. Scalded
Skin^
Syndrome
local infection
produces a toxin distally. Causes mildepidermal tears, with a “sunburn likerash” Toxic
Shock
associated with
tampons
left in too long, toxin is a
superantigen
that causes fever, hypotension, and death Infective
Endocarditis
acute onset
endocarditis with fever, malaise, and aheart murmur. Caused by
cytolytic
toxins
Gastroenteritis is self limiting,and the organism is passedwith stoolIt is gram (+) withpenicillinase activity, so Beta‐Lactams don’t work.Methacillin and Nafcillin weredrugs of choice because oftheir resistance topenicillinase.
(methicillin resistant staphaureus) has made treatmentmore difficulty. Vancomycin
is now the drug of choice, though resistantstrains are being identified.
Enterrococcus(Fecalis andFecium)
Gram
(+)^ Coccus
, it is
one of the StrepSpecies Lancefield
Group
Can grown in
Bile^ or in^ High
Salt^ (6.5%) γ^ Hemolytic PYR^ (+)
Survives
Bile^ and
Salt^ so can
colonize in the gall bladder.
They are part of the normal flora of theGI and GU tract. During a procedure,they can be dislodged or displaced andpresented to where they should no be. Normal
Flora Most^
prevalent
bacteria
of^ GI
tract
Endogenous
Transmission
Cholecystitis
Penicillin
Strep^
Pyogenes
Gram
(+)^ Coccus Lancelfield Group A β^ Hemolytic Bacitracin
Sensitive to separate it fromStrep Agalactiae
Theme is “escape or spread” M^ protein
O^ –^ Oxygen
Labile,
antigenic
cytolysin that causes lysis of cells. Streptolysin
S^ –^ Oxygen
Stabile,
non^ antigenic
cytolysin that causes lysis of cells.“ASE”s Streptokinase, DNAase,Hyalurindase, all makes it easier tospread in tissue.Exotoxin A‐C that are
superantigens
and cause symptoms of scarlet fever
Human throat, transmitted by aerosoldroplets or endogenous infection.Sequellae of Disease (to fit better) Rheumatic
Fever
of untreated pharyngitis ONLY. This isa type II hypersensitivity reaction,where antibodies to the strep
cross
react
with
heart
tissue
. Causes
endocartitis, a chorea, fever, andarthralgia. Poststreptococcal
Glomerular
Nephritis
Pharyngitis
fever
palms
and^ soles
are^ spared.
There is also a
strawberry
tongue
that presents bright
red with many bumps.Impetigo ‐ just like staph aureus Necrotizing
Fasciitis
‐ infection that
causes “flesh‐eating bacteria.” Rapidspread through fascial layer can involvelarge amounts of tissue requiringdebreidment or amputation.
Culture all negatives on a rapidtest. β^ Lactams
work well. In those with allergies, usemacrolides.
Organism
Physiology/Structure
Virulence
Epidemiology
Diseases
Tx
Strep^
Pneumoniae
Gram
(+)^ Coccus Lancet
Shaped Diplococci No Lancelfield Group α^ Hemolytic Optochin
Sensitive
to
separate it fromViridans group
Capsule
O^ – what is responsible for the
rust^
colored
sputum
associated with the disease. Destroys ciliated cells by inducingclassic complement.
Normal flora of the upper respiratorytract. They can be colonized, but not beinfected. Any immunocompromise(chronic pulmonary disease, viralinfection, spleen‐ectomy) can lead topathogenesis
Acute
Pneumonia
rapid onset of fever
and chills, pain on inspiration, and an X‐ray with infilitrates Otitis
Media
Meningitis
H. Influenzae b (later), now is leadingcause of meningitis in neonates.
Macrolides
for adult bacterial pneumonia Third
Generation Cephalosporin
for meningitis Vaccines
are available. The pediatric vaccine covers 7common serotypes protectingagainst meningitis.The adult vaccine covers 23common serotypes to protectagainst pneumonia
Viridans
group
Gram
(+)^ Coccus No Lancelfield Group α^ Hemolytic Optochin
Resistant
to
separate it from S.Penuemo
Dextran
Bioslime
that both protect
the organism from the immunesystem and
increases
adherence
to
teeth
or^ heart
valves
This is a variety of organisms such asS. Mutans. S.^ Mutans
is part of the normal flora of dental caries. These buggers causeplaque. Plaque then allows otherViridans group to colonize and causecavities
Subacute
Endocarditis
gives S. Mutans access to the bloodstream where it
colonizes
the^ mitral
valve
This is why people with prostethic valvesor previous valve problems getprophylactic antibiotics before dentalprocedures.
Penicillin
often prophylactic for endocarditis.In pharm, you learn you treatwith^ Clindamycin
or a
combination of
Vancomycin
Gentamycin
Organism
Physiology/Structure
Virulence
Epidemiology
Diseases
Diagnosis
Clostridium Tetani
Same as otherclostridium species, nodouble zone ofhemolysis
Tetanus
Toxin
(tetanospasmin)– causes spastic paralysis known asTetanus. Classic
AB^ toxin
that targets the
central nervous system, inhibitinginhibitory neurons by preventingvesicle transport and fusion.No fusion = no release. No release =disinhibition of skeletal muscles =contraction.Targets
and^ glycine
Found in
dirt,^
soil, or
dust.
Common presentation is a penetrating
wound
(such as a rusty
nail).
Tetanus^ Bacteria colonize a local infection,housed in necrotic tissue (anaerobicspace).Secrete exotoxin that travelseverywhere, targets the CNS inhibitoryneurons.Symptoms begin with
trismus
(lockjaw)
and^ risus
sardonic
us^ (a
smile that cannot be stopped)Progresses to a
spastic
paralysis
with
death resulting from spasm of diaphragm
Antitoxin
binds and neutralizes free toxin incirculation Toxoid
(aka the vaccine) conveys long termneutralization of toxin and active
immunity
. Survival
DOES NOT convey immunity.Give injections at separatesites Muscle
Relaxants
(benzos)
to alleviate contractions
Clostridium Botulinum
Same as otherclostridium species, nodouble zone ofhemolysis
BotulismToxin
AB^ toxin
that targets the
peripheral nerves, inhibiting NMJneurons by preventing vesicletransport and fusion.No fusion = no release. No release =inhibition of skeletal muscles =flaccid.Targets
ACh
It is also found in dirt, soil, or dust,that can cause the low‐yield woundbotulism.Found in
home
canned
foods
that are
not cooked well enough.Found in
honey
given to newborns.
Adult
Botulism
dipolia
and
dysphagia
, progressing to
flaccid
paralysis
and^ death
from
flaccid
diaphragm Infant
Botulism
with botulism in an infant less than oneyear old. Begins with
constipation
and
feeding
problems
progressing to
floppy
baby^
syndrome
Palliative care to provideventilator support Antitoxin
to alleviate circulating toxin (any toxin incells has already taken effect). Penicillin
to kill bacteria
Clostridium Difficle
Same as otherclostridium species, nodouble zone ofhemolysis
Toxin
A^ =^ Enterotoxin Causes inflammation and secretory diarrheaToxin B = CytotoxinDisrupts protein synthesis andcauses disorganization of thecytoskeleton.
Part of the
normal
GI^ Flora
When on
broad
spectrum
antibiotics
the normal flora is eliminated. This ishighly resistant, so then grows in thespace left by the previous flora.
Psuedomembranous
Colitis
secretory diarrhea that results from theenterotoxin. Ulcerations can bevisualized on endoscopy resulting fromCytotoxin. Cultures will be positive(normal flora), but a
tox^ screen
of stool
will confirm diagnosis.
Discontinue antibiotic therapy.Give^ oral
vancomycin
(one of
the few drugs it is NOTresistant to). You must give itorally because vancomycincannot penetrate GI barrier,and the infection is in the GItract.
Lactobacillus
Low^ yield
organism
Know that it maintains the vaginal pHto prevent exogenous infection. Whengiving broad‐spectrum antibiotics, youcan kill lactobacillus, and allowovergrowth of other organisms (likecandida)
Actinomyces Israelii
Facultatively anaerobic/strictly anaerobic NOT^ acidfast
(contrast to^ Nocardia) Grow^
slowly Filamentous
hyphae Resemble
“grains
of
sand”
‐>^ sulfur
granules NOT^ found
on^ skin
Colonize
GI,^ female
genital
tracts
Actinomycosis
-^ chronic granulomatous
lesions
‐>^ suppurative
and^ form
abscesses
No^ person
to^ person
spread
Disease
from^ soil
or^ water Cervicofacial
infections
‐>^ poor
oral^ hygiene;
invasive
dental
procedure Thoracic
infections
‐>^ Hx^ of
aspiration
‐>
spreads
to^ lung
‐adjoining
tissues
Abdominal
infections
‐>^ GI^ surgery;
trauma
to
bowel Pelvic^
infections
‐>^ secondary
manifestation
of^ abdominal
actinomycosis;
primary
infection
of^ woman
with^ IUD CNS^ ‐>
hematogenous
spread
from^ other
tissues
Most^
cases:
Cervico
facial
‐>^ draining
sinus
tracts
along
angle
of^ jaw/neck
Difficult Culturing
is^ slow Sulfur
granules
‐>^ tin,
gram
positive,
branching
rods^ around
periphery
Nocardia Asteroides
Gram
(+)^ branching rods. Partially
Acid^
Fast Aerobic
Ill defined pathogenesis
Reservoir is Soil and Dust, thus there isan exogenous inoculation via traumaor inhalation.
(Inhalation)
Cavitary Broncholpulmonary
Nocardosis
often associated with immunecompromised patients. Symptoms arefever, cough, diffuse pneumonia withcavitation of the lungs.Spread via the blood to the brain.(Traumatic Implantation)
Subcutaneous
nocardosis
Sulfonamides
Listeria monocytogenes
G+ve^
coccobacili ‐> arranged in pairsresemblingenterococciFaculative anaerobesMotile at room temp,weakly β‐hemolytic,capable of growth at 4 °C^ and
high^
salt concentration
Facultative
intracellular
pathogen
that can avoid Ab‐mediated clearanceVirulent Strains produce cellattachment factors (
internallins
hemolysins (
listeriolysin
O,^ two
phospholipase
Cs), and a protein that mediates actin‐directed motility(ActA
“Actin rockets” – cell to cellmovement
Isolated in soil, water, and vegetationDisease assoc. with consumption ofcontaminated food products(unpasteurized milk)Transplacental spread from mother toneonate(vaginal transmission) HIGH
Young, elderly, Pregnant, pts with defective cellular immunity
Neonatal
Disease
Amnionitis:
1.^ Early
onset
disease
“ granulomatosis
infantiseptica
disseminated ascesses andgranulomas in multiple organs2. Late^ onset
disease
: acquired at or
shortly after birth. Presents asmeningitis or meningoencephalitisw/ septicemia Healthy^ Adults: Influenza like (with or withoutgastroenteritis) Pregnant^ women/cell
mediated
immune
defects: Primary bacteremia or disseminateddisease (hypotension and meningitis)
Microscopy ‐> insensitiveCulture 2‐3 days or coldenrichment
Organism
Physiology/Structure
Virulence
Epidemiology
Diseases
Diagnosis
Neisseria Meningitidis
Gram
(^ )^ Cocci Diplococci
with flattened
sides Oxidase
Glu^ +,
Maltose+ Facultative Intrallecular Found in respiratorytract and causesmeningitis
Capsule
Pili^ for attachment
Found in the human nasopharynx.About 5‐10% are carriers of theorganism.Usually transmitted through respiratory
droplets
that colonizes
the pharynx and spreads to themenignese. College
Dorms
,^ Military
Recruits
other close quarters
Adult
Meningitis Begins with a
Stiff^ Neck,
Photophobia
Petechial Rash. Once the rash starts, thepatient declines rapidly.Fulminant cases develop bruising, DIC,and death. This can happen in hours.
Formerly Penicillin (whichmay still work).Currently use
doxycyline
or
cirpofloxain. Vaccine is available that is athe^ polysaccharide
capsular
vaccine
covering all types not B.
NeiserriaGonorrheaHigh‐Yield imageis a gram stain ofexudate fromsomeone withgonnorhea withthe gram negativediplococci INSIDEthe PMNs
Gram
(^ )^ Cocci Diplococci
with flattened
sides Oxidase
Glu+^
Maltose FacultativeIntracellularFound in theurogenital tract andcauses gonorrhea
No Capsule Antigenic
Variation
antigen to avoid detection Outer
Membrane
Proteins
1 =^ Por Protein that decreases phagolysosome fusion in PMNs andincreases transcytosisOMP 2 = Opa = adhesion molecule IgA^ Protease
‐ evades mucosal epithelium defenses. Pili^ ‐ increase adhesion
Human genital tract and is transmittedas an STD or to a child in birth.
Gonorrhea‐^
Males = urethritis and proctitis. Purulent
yellow
discharge
with
painful urination.‐ Females = variable symptomsincluding
Pelvic
Inflammatory
Disease
,^ Salpingitis
, and
Intramenstrual
Bleeding
. It may
go unnoticed, and females are oftenthe carriers‐ Infants ‐ opthalmia and blindnessif untreated
Beta‐Lactamases areabundant, so we now use cephalosporins
There is a special agar called Thayer
Martin
Agar
that is a
chocolate agar + antibioticsthat grows only gonorrhea
MoraxellaCatarrhalisPrevious low‐yield organism,that has beencoming up on theboards
Gram
(^ )^ Cocci Diplococcus
Normal flora of the upper respiratorytractTransmited through the respiratorydroplets
Otitis
Media
-^ strep pneumo is the most common cause, but Moraxella can causeear aches Sinusitis -^ same thing as Otitis Media Bronchitis - especially in the older population
Augementin or thirdgeneration cephalosporing
Organism
Physiology/Structure
Virulence
Epidemiology
Diseases
Diagnosis
Tx
Yersinia
Pestis
Gram
(^ )^ Rod Bipolar
Staining
, they look
like a safety pin or adumbbell. There is stainingat either end, but clear inthe middle. Facultative
Intracellular
produces granulomas
Coagulase
F1^ Antigen
can inhibit phagocytosis Type
III^ Secretion
System
Cause of the plague, theblack death.Common in the
desert southwest. Transmitted by the
bite
of^ a^ flea
or by human‐ human contact viarespiratory droplets
Pneumonic
Plague
=septic pulmonary
embolus from the bubonic plague, orinhalation. This is highly contagious, highlyfatal, and is a target of
bioterrorism
Cutaneous =
Bubonic
Plaque
= Black Death.
This is from the flea bites that generate the axillary
bubos
and conjunctivitis. Its called the Black death because you get DIC and theextremities, without an adequate bloodsupply, necrose, turn black, and fall off.
Aminoglycosides Control the animals, the vector (therats). Killing rodents is a bad idea, thefleas will all go to humans!
Enterobacteriaciae family
Gram (‐) Rods Catalase
Fermenters – at least Glu+
Endotoxin
Wall K^ =^ Kapsular H^ =^ Flagella
Escherlichia
Coli (E.Coli)
Same As Enterobacteriaciaefamily.
Pili^ – attach and establishinfection in the mucosa ofthe GI tract or the urinarytract. Capsule
Normal flora of thehuman Gut.There can be anengodenous displacementfrom the GI (such as inUTI) or can be exogenous(such as fecal oral)
Most^
common
cause
of^ UTI
Neonatal
meningitis
. This is the second most
common cause of neonatal meningitides afterStrep Agalactiae.
K1^ serotype
implicated
Fluroquinolone Third generation cephalosporin
ETEC Enterotoxigenic E.^ Coli
Same As Enterobacteriaciaefamily.
Enterotoxins
they are cyclic‐something inducers.One is cAMP, the other iscGMP. Regardless of themechanism, they both causewatery diarrhea.^ Heat
Labile
Toxin
causes ADP‐Ribosylation ofGαs^ that stimulates AC
cAMP^ Heat
Stabile
Toxin
causes ADP‐Ribosylation of Guanine
Cyclase
increasing
cGMP.
Same as E. Coli
Montezuma’s Revenge. ETEC causes Travler’sDiarrhea. This is a
watery
diarrhea
because
it is noninvasive.
Usually Self Limiting. Replace fluidseither IV or Oral.
EHEC EnteroHemorrhagic E.^ Coli
Same As Enterobacteriaciaefamily.Know the
serotype is the mostimplicated. Non^ Sorbitol
fermenter (most E.Coli are sorbitol
Shigga
Like
Toxin
classic AB toxin that causes ADP^
Robsylation
of^ the
60s^ ribosome
reducing affinity
for^ EF
1.^ Called verotoxin.
Same as E.Coli, but canalso be from bovine fecesor unpasteurized milk.EHEC can be rememberedas Hamburger (the Jack‐in‐the‐Box E. Colioutbreak).
Dysentery
. EHEC causes Hemorrhagic diarrhea. This is an exception to the rule.Normally bloody diarrhea means invasiveorganisms. This is
non^ invasive
. Therefore,
there will be
(+)^ Blood
(^ )^ Pus
Hemolytic
Uremic
Syndrome
sequella of EHEC is renal failure.
. Death of
EHEC will release its toxin and LPS thatincreases the risk of HUS.
In culture will have a
halo
around cells, because oftheir capsule. Lac+
Endotoxin
–LPS from it being Gram (‐)
Usually an endogenoustransmission
Community
acquired
pneumonia
. Common
cause of community acquired. Strep Pneumois the most common cause, but Klebsiella isstill right there. Use the gram stain toseparate.Causes a
thick
like^ jelly,
red^ sputum
without
a pungent odor (such as in the case of aaspiration pneumonia).
Third generation
Cephalosporin
Pasturella Multocida think^
and^ CAT BITES
Small
Gram
(^ )^ Rods Facultative
Intracellular facultative
Anaerobe
Reservoir is the mouths ofcats, transmitted frombites or licks. Don’tconfuse this with Cat‐Scratch fever, which iscaused by a scratch, not alick or a bite likePasturella
Rapidly
Spreading
Cellulitis
from the site of
the lick or bite, there will be a cellulitis thatwill spread within hours.
Amoxyclin
and^ Augmentin Because it is so rapid spreading, theygive an IM injection of antibiotics.
Bordetella
Pertussis
Small
gram
(^ )^ rod Nonmitile Strictly
Aerobic Grow Singly or in pairs Encapsulated Requires a long growthperiod on a special agar,called the Bordet
Gengou Bordet = Bordetella
Pertussis
Toxin
AB toxin that targets theciliary cells. It is a cAMPtoxin, causing edema andfluid. This causes increase inhistamine sensitivity,leukocytosis and an increasein insulin, leading tohypoglycemia.Dermonecrotic Toxin Adenylate
Cyclase
Toxin
secreted AC that is taken upTracheal CytotoxinFilamentous HemagglutinEndotoxin
Colonizes the respiratoryepithelium and cab bespread via respiratorydroplets (the coughing,sneezing, and hand‐to‐hand contact)
Whooping
Cough
week of incubation.‐^
Catarrhal
Stage
highly
infectious
stage
with nonspecific
symptoms such as low grade fever,malaise, rhinitis. Weeks 2‐3 ‐ Paroxysmal
Stage
noninfectious, but
stereotypical
phase
. This stage has frequent bouts that come and go (paroxysmal) ofsevere fits of coughing followed by astrong inspiration against a narrowedglottis causing the “whoop.” They canbecome cyanotic or vomit. Weeks 3‐6 ‐ Convalescence
Stage
dies out, with lessening paroxysmalstage symptoms. Weeks 6‐on
Erythromycin
is drug of choice to give to household contacts and those in thecatarrhal phase. Isolate
the catarrhal and early paroxysmal phases Vaccinate
with the DPT vaccine.
Vibrio
Cholera
Curved,
Gram
(^ )^ Rod
with
polar
flagella Oxidase
Grow on Alkaline but notAcidicMotile
Pilus
cAMP
increases that leads to tremendous fluidextrusion
The reservoir for cholerais the human colon. It istransmitted fecal‐oral, butoften by
contaminated water
. It^ requires
a^ very
high^ infectious
dose. El^ Tor
strain causes epidemicsThe classic strain has notbeen so bad
Cholera
rice^ water
stools
, looking white/clear
like water while cooking rice.
Treat with
fluid
and^ electrolyte replacement, both oral and IV.Prevent cholera by boiling water andvegetables, cooking your food
Helicobacter
Pylori
Gram
(^ )^ curved
rod^ with
a^ Single
polar
flagella (sounds like Cholera)Only organism that cangrow and replicate in thestomach
Urease
converts urea and acid into bicarbonate andammonia, which neutralizesthe acid, allowing it to live inthe stomach Adhesins
allow colonization and prevent dislodgementfrom gastric mucosa Mucinase
degrades the mucin protective barrier Vacuolating
Cytotoxin induces vacuoles in humancells. Cytoxin
Associated
Gene
encodes another cytotoxin.These HP are more virulent
Humans are the onlyknown reservoir and it isthought that it istransmitable fecal to oralor oral to oral.The mode of transmissionhas not yet beenestablished, despite itsprominence in GI disease.
Gastric/Duodenal
Ulcer
mucinase degrades the protective lining of thestomach, allowing acid to reach the mucosalsurface.In addition, the cytotoxins cause
autolysis
of
macrophages
and^ neutrophils
inducing a
strong inflammatory reaction, alsocontributing to the disease.Can lead to
cancer
. Either the
reactive
oxygen
species
damaging DNA post lysis and inflammation or through
viral
infection
of
the epithelium from the compromised barrier,gastric tumors may result.This is a
Type
1 Carcinogenic
Agent
, a highly
board relevant point.
Serology can detect antibodies, but willonly tell you if there ever was aninfection. Golden
standard
is the
biopsy
with
culture
Use the
Urea
Breath
Test^
to determine
if someone has HP. You feed the patientradioactive urea, and, if there is HP, theywill expire radioactive CO
2 (converted
from the bicarb the HP made) Endoscopy
can be made to identify gastric ulcers.Treat the
ulcers
with^
Proton
Pump
Inhibitors
treating the symptoms. Treat the bug with
Amoxicillin
Clarithromycin
Proteus
Mirabillis and^ Vulgaris Mirabillis
of infection
Small Gram (‐) Rods thatare part of theenterobacteriacae family Swarming
Motility
from
its peritrichous flagella Urease
Nonlactose
Fermenting
Extreme MotilityUreaseEndotoxin LPS from gram (‐)
Pretty much ubiquitous inthe environment andwithin the
normal
flora
of the GI tract.Most cases in humans areendogenous.
UTI^ if there is a UTI via proteus (E Coli mostcommon), there is an increased risk of
kidney
stones
by reducing the pH of the urine.
Fluroquinilone Treat kidney stones with pain meds (forpassing) or sonic disruption to removestones.
Legionella
Slender, pleomorphic,G‐ve rodsStains poorly w/commonreagents – Use
Silver
Stain
Nutritionally fastidious ‐> L^ cysteine
and^ enhanced growth
with^
iron^ salts Non fermentative
Capable of replication in ALVEOLAR MACROPHAGES
(and
amoebae in nature)Prevents phagolysosomefusion
Sporadic, epidemic,nosocomial infectionsAerosol Transmission(Air conditioning units,but^ no
person
to person
Commonly found innatural bodies of water(rivers and streams)Estimated btw 10k to 20kcases in US annually High^
risk:^ compromised pulmonary function, ptswith decreased cellularimmunity (transplant)
1.^ Legionnaires’
disease
(legionellosis)
incubation period of 2‐10 dayssystemic signs of acute illness appear abruptMultiorgan disease (GI, CNS, liver, Kidneys)Primary manifestation – pneumonia (severe)2.^ Pontiac
fever Self limiting, febrile illnessFevers, chills, myalgia, malaise, headacheSymptoms develop over 12 hrs, last 2‐5 days
Microscopy
: insensitive DFA – fluorescence Culture
Buffered charcoal yeast extract (BCYE)and Fe+Cys Antigen
tests:
sensitive for
pneumophila
serogroup 1 Seroconversion
: must be demonstrated
‐> 6 mo. To develop PCR: Sensitivity and specificity approachingculture
mental states).
Borrelia Burgdorferi
Gram
(^ )^ Spirochete
It is invasive, and will infectthe heart, joint, and CNS.
Nymphs (on mice) andTicks (on deer).We usually here aboutthis disease with deerticks from Lyme CT. Ixodes
is the genus of tick that spreads theorganism.
Lyme
Disease
This is the number 1 vector‐borne disease.You get a
bulls
eye^ rash
at the bite site. It
starts out with flu‐like symptoms with swollenlymph.Once the organism disseminates, then you seenerve effects (such as
bell’s
palsy
Migratory
Arthralgia
develops from Type III
hypersentivity reactions depositing into thejoints. Cardiac
Arrythmias
may result from the
disease as well.
Serologydiagnoses theproblem via ELISAor PCR.Treatment is doxycycline
Leptospira interrogans Low^ yield Spirochete
Gram
(^ )^ Spirochete
, with
little hooks at the end
Unknown
pathogenesis
Zoonotic disease withtransmission throughwater contaminated withanimal urine. You will seethis in patients who jet skior who work in sewers.
Swineherd’s
Disease
or^ Mud
Fever
gastrointestinal symptoms + flu‐likesymptoms that
may^ progress to hepatic or liver failure.
Rickettsia Rickettsia
Ricketsii
Energy parasite. They needyour ATP, and are an^ obligate
intracellular parasite
with leaky epitheliumVery tiny, so you wouldn’tsee them on a gram stain,even though they areconsidered
Gram
(^ )^ rods
Invade the
vascular endothelial
cells
causing
vasculitis and permittingthem to move through theblood strea,
Reservoir is ticks. Thevector is a tick bite.Requires a long feedingtime in order to transmitthe bacteria. The bacteriamay be passed toprogeny.
Rocky
Mountain
Spotted
Fever.
Rash is
critical for the diagnosis. When not present,the disease is usually missed until too late, asthis disease is rapidly fatal.Confusion, N/V/D + headache. It looks likemeningitis, but then the rash comes on. Therash is a
maculopapular
that^ turns
petechial
that^ starts
on^ the
hands
and^ feet
and^ moves
to^ the
trunk.
Includes
palms
and^ soles
Start treatmentwithoutconfirmation fromserologicalindirect antibodytest.Weil‐Felix is anold test, that mightcreep on theboards.
Doxyclcine
and protection againstthe vector.
Rickettsia Prowazekii Considered
low yield^ for
Boards
Same as Ricketsii
Endemic
Typhus
Rickettsia
Typhi Considered
low yield^ for
Boards
Same as Ricketsii
Haemophilus
(and related
bacteria)
Small,
pleomorphic,
G^ ve
rods or coccobaciliFacultative anaerobes,fermentative Most^
species
require
(heme)
and/or
factor
for^ growth H. influenzae subdividedserologically (a to f),biochemically (biotypes I to
H.^ influenze
type b is clinically most virulent (
-^ polyribitol
phosphate
in capsule)PRP – ribose, ribitol,phosphate Haemophilus
adhere to host cells via pili and non‐pilusstructures IgA^ Protease
Noncapsular
Haemophilis commonly colonized inhumans; encapsulated Haemophilis
(H. influenze type b) UNCOMMONmembers of normal floraDisease caused by
influenze
type b was primary a pediatricproblem ‐> eliminated inimmunized populations
Haemophilis
influenzae Meningitis
: unimmunized children ‐> fever, severe headache, systemic signs Epiglottitis
: unimmunized children ‐> initial pharyngitis, fever, difficulty breathing,progresses to cellulitis and swelling ofsupraglottic tissues ‐> obstruction of airway Pneumonia
: inflammation and consolidation of lungs observed primarily in the ELDERLYwith underlying chronic pulmonary disease;typically caused by nontypeable strains Haemophilus
ducreyi
Microscopy
sensitive test inCSF, synovial fluid,lower respiratoryspecimens Culture
chocolate agar Antigen
tests
less useful for
influenzae
type b infections
VIII), and clinically(biogroup
aegypticus
Satellite Phenomena – youcan grow Haemophilusnext to staph because it isbeta‐hemolytic andreleases the heme and NADinto the medium on a bloodagar.
H.^ ducreyi
disease is uncommon in the USWith the exception of
ducreyi,
which is spread by sexual contact, most Haemophilus
infections are cased by pts bacterialflora (endogenousinfections)
Chancroid
: STD ‐> tender papule with an erythematous base ‐> progresses to painfululceration and lympathadenopathy. This is adistractor with Syphilis (treponema) becausethey are both spirochetes, and both cause achancer. Yoyu “do cry with ducreyi” meaningthat it is a painful chancer.
following vaccine
Bacteroides
Fragilis
Gram
(^ )^ Rod
Reduced
Endotoxin Capsule
Normal part of the GIflora. Traumaticdisplacement (surgery)can permit movementinto other compartments.
Sepsis: weak, because the endotoxin ismodified. Peritonitis:
This isn’t terribly high yield, but man you don’t want this kind of peritonitis. Itwill cause massive necrosis of the peritoneumand the intrabdominal contents
Francisella Tularensis (potentially
low yield^ accept
it^ is^ a Bioterror
agent)
Zoonotic Small
Gram
(^ )^ Rod Facultative
Intracellular pathogens
(cause granulomas)
Tick bite (the ulcero‐glandular form)Associated with huntingand skinning Wabbits.This can cause atraumatic implanation orinhalation while youshred its flesheverywhere.If you eat the rabbitwithout cooking it well,you could ingest it as well
Tuleremia: Ulcer at bite site and regional lymph swellingfrom tick. Traumatic Implantation fromwabbit skinning can cause it as well.If you inhale it or eat it, you will developtularemia in the GI tract.
Live^ Attenuated Vaccine
broad‐spectrumcephalosporins,azithromycin, orfluoroquinolonesMany strains areresistant toampicillinActiveimmunizationwith^ conjugated PRP^ vaccines prevents most
influenzae
type b infectionsRifampinprophylaxis ‐>children at highrisk for disease
Brucella (potentially
low yield^ accept
it^ is^ a Bioterror
agent)
Zoonotic Small
Gram
(^ )^ Rod Facultative
Intracellular pathogens
(cause granulomas)
Endotoxin
Passes readily betweenanimals and humans.Usually contained indomestic livestock (largeanimal veterinarians)Species depends on theanimal it infects.Abrotus = cattleSewis = pigsMalatensis = goats
Brucellosis –
undulant
fever
because it goes
up and down. They are flu‐like symptoms withprofuse sweating.
Serum Agglutination test^ is prettymuch all you cando. Rifampin &Doxycycline for 6weeks (facultativeintracellular aretough)We can
vaccinate cattle
or^ high
risk individuals
Pasturizationhelps spread.