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Gram Positive and Negative Bacteria: Structure, Virulence, and Diseases, Study notes of Physiology

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.

What you will learn

  • What are the key differences between Gram positive and negative bacteria?
  • What is the role of Actinomyces israelii in actinomycosis and how is it diagnosed?
  • How does Staphylococcus aureus cause toxic shock syndrome?
  • What are the common diseases caused by Streptococcus species?
  • How does Bacillus cereus produce toxins and what are the symptoms?

Typology: Study notes

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GramPositiveCocci:StrepandStaph
OrganismPhysiology/Structure Virulence Epidemiology Diseases Tx
StaphAureus Gram(+)cocciformed
inclusters
FacultativeAnaerobes
Catalase(+)
Coagulase(+)
Β‐Hemolytic
Aproteinevadesphagocytosis
Coagulaseformsfibrinclotaround
organism,protectingitfrom
phagocytosis
ToxicShockSyndromeToxin
producesthesuperantigenTSST‐1
thatleadstotoxicshock.
Exfoliatincausestheskintoslough
off,disruptsdesmosomes.
Enterotoxincausesgastroenteritis
Isnormalflorafoundinmucous
membranesandskin.Transmission
caneitherbeendogenousor
exogenous.
Commoncontaminationisfoundin
foodworkersthatsneezeontheir
hands,thendon’twash.Foundon
foodthathasbeenleftout,likepotatoe
salid.
Gastroenteritisusuallyselflimiting.Can
becausedbyingestionofbacteria(then
subsequentproductionoftoxin)orby
ingestionofheatstabiletoxinproduced
beforeorganismwaskilledbycooking.
ScaldedSkinSyndromelocalinfection
producesatoxindistally.Causesmild
epidermaltears,witha“sunburnlike
rash”
ToxicShockassociatedwithtampons
leftintoolong,toxinisasuperantigen
thatcausesfever,hypotension,anddeath
InfectiveEndocarditisacuteonset
endocarditiswithfever,malaise,anda
heartmurmur.Causedbycytolytic
toxins
Gastroenteritisisselflimiting,
andtheorganismispassed
withstool
Itisgram(+)with
penicillinaseactivity,soBeta‐
Lactamsdon’twork.
MethacillinandNafcillinwere
drugsofchoicebecauseof
theirresistanceto
penicillinase.MRSA
(methicillinresistantstaph
aureus)hasmadetreatment
moredifficulty.
Vancomycinisnowthedrug
ofchoice,thoughresistant
strainsarebeingidentified.
Enterrococcus
(Fecalisand
Fecium)
Gram(+)Coccus,itis
oneoftheStrep
Species
LancefieldGroupD’
CangrowninBileor
inHighSalt(6.5%)
γHemolytic
PYR(+)
SurvivesBileandSaltsocan
colonizeinthegallbladder.
Theyarepartofthenormalfloraofthe
GIandGUtract.Duringaprocedure,
theycanbedislodgedordisplacedand
presentedtowheretheyshouldnobe.
NormalFlora
MostprevalentbacteriaofGItract
EndogenousTransmission
UTIGIÆGU
Cholecystitis–infectionofthe
gallbladder.
Penicillin
StrepPyogenesGram(+)Coccus
LancelfieldGroupA
βHemolytic
BacitracinSensitive
toseparateitfrom
StrepAgalactiae
Themeis“escapeorspread”
Mprotein–antiphagocyticprotein.
M12isassociatedwithglomerular
nephritis
StreptolysinO–OxygenLabile,
antigeniccytolysinthatcauseslysis
ofcells.
StreptolysinSOxygenStabile,
nonantigeniccytolysinthatcauses
lysisofcells.
“ASE”sStreptokinase,DNAase,
Hyalurindase,allmakesiteasierto
spreadintissue.
ExotoxinA‐Cthataresuperantigens
andcausesymptomsofscarletfever
Humanthroat,transmittedbyaerosol
dropletsorendogenousinfection.
SequellaeofDisease(tofitbetter)
RheumaticFever–possiblesequella
ofuntreatedpharyngitisONLY.Thisis
atypeIIhypersensitivityreaction,
whereantibodiestothestrepcross
reactwithhearttissue.Causes
endocartitis,achorea,fever,and
arthralgia.
PoststreptococcalGlomerular
Nephritis–possiblesequellaof
untreatedstreppharyngitisorskin
infection.TypeIIIhypersensitivity
reaction.Immunecomplexesare
depositedinthekidney,causing
damage.AssociatedwithM12serotype
Pharyngitis–white,purulentlesionson
theoropharynx.
Scarletfever–ifstrepthroatis
untreateditcanthenbeaccompaniedby
scarletfever.Itisdescribedasasand‐
paperrash,alsocalledasunburn‐like
rash,inthattheskinisred.Thepalms
andsolesarespared.Thereisalsoa
strawberrytonguethatpresentsbright
redwithmanybumps.
Impetigo‐justlikestaphaureus
NecrotizingFasciitis‐infectionthat
causes“flesh‐eatingbacteria.”Rapid
spreadthroughfasciallayercaninvolve
largeamountsoftissuerequiring
debreidmentoramputation.
Cultureallnegativesonarapid
test.
βLactamsworkwell.
Inthosewithallergies,use
macrolides.
pf3
pf4
pf5
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Gram

Positive

Cocci:

Strep

and

Staph

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

TSST‐

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.

MRSA

(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

D’

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

UTI^ GI

Æ^ GU

Cholecystitis

  • infection of the gallbladder.

Penicillin

Strep^

Pyogenes

Gram

(+)^ Coccus Lancelfield Group A β^ Hemolytic Bacitracin

Sensitive to separate it fromStrep Agalactiae

Theme is “escape or spread” M^ protein

  • antiphagocytic protein. M12 is associated with glomerularnephritis Streptolysin

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

  • possible sequella

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

  • possible sequella of untreated strep pharyngitis or skininfection. Type III hypersensitivityreaction. Immune complexes aredeposited in the kidney, causingdamage. Associated with M12 serotype

Pharyngitis

  • white, purulent lesions on the oropharynx. Scarlet

fever

  • if strep throat is untreated it can then be accompanied byscarlet fever. It is described as a sand‐paper rash, also called a sun burn‐likerash, in that the skin is red. The

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

  • most important virulence factor IgA^ protease - cleaves IgA that allows colonization of mucosa. Pneumolysin

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

  • most common cause of otitis media in children, despite vaccine. Sinusitus - same as otitis media, commonly causes sinusitis in kids Adult

Meningitis

  • since the vaccine for

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

  • dental surgery

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

GABA

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

  • causes spastic paralysis known as Botulism. Classic

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

  • food contaminated with botulism is not cooked or preparedwell enough. Begins with

dipolia

and

dysphagia

, progressing to

flaccid

paralysis

and^ death

from

flaccid

diaphragm Infant

Botulism

  • honey contaminated

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

  • watery,

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

URT,^

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

  • training type of sinus tracts and granules. This is similar toactinomyces only with a traumaticimplantation.

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

RISK:

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

Gram

Negative

Cocci:

Neisseria

and

Moraxella

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

  • 5 different serotypes of capsule. B is the most common foundin the US. It is NOT covered in thevaccine, but all others are. IgA^ Protease - helps colonize the respiratory epithelium Endotoxin

=^ LPS

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

  • changes its

antigen to avoid detection Outer

Membrane

Proteins

(OMP)

OMP^

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

Gram

Negative

Rods

–^ all

gram

negative

bacteria

have

LPS,

the^

endotoxin,

which

poses

a^ risk

of^ sepsis,

shock,

and

death

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

  • molecular syringe thatallows for toxins to beinjected into host cell.

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

  • all gram negative bacteria possessLPS or LOS.Antigens:^ O^ =^ Cell

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

– (LT)

causes ADP‐Ribosylation ofGαs^ that stimulates AC

Æ

cAMP^ Heat

Stabile

Toxin

– (ST)

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

O157:H

serotype is the mostimplicated. Non^ Sorbitol

fermenter (most E.Coli are sorbitol

Shigga

Like

Toxin

  • a

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

(HUS). A

sequella of EHEC is renal failure.

DO^ NOT

GIVE

ANTIBIOTICS

. 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^

CATS^

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

  • classic

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

  • comes in 3 phases after a

week of incubation.‐^

Catarrhal

Stage

  • the

highly

infectious

stage

with nonspecific

symptoms such as low grade fever,malaise, rhinitis. Weeks 2‐3 ‐ Paroxysmal

Stage

  • this is the

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

  • the disease

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

  • the Tcp Pilus allows for adhesion to mucosalepithelium Flagella - makes it motile Toxin - cholera toxin is a classic AB toxin. It activatesGαvia ADP‐Ribosylation. Its^ causes

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

  • excessive diarrhea up to 20L/day. Causes

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

  • the urease and

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

=^ 90%

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

L.

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

X

(heme)

and/or

V^ (NAD)

factor

for^ growth H. influenzae subdividedserologically (a to f),biochemically (biotypes I to

H.^ influenze

type b is clinically most virulent (

PRP

-^ 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

H.

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

H.

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

H.

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

H.

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

  • LPS in gram (‐)

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.

Enterobacteriaciae

Nonlactose

Fermenters

“ShYPS”

Lactose

Fermenters

–^ “CEEK”

Shigella

Citrobacter

–^ Tulane

doesn’t

discuss

it

Yersinia

Escherichia

–^ E^ Coli

Proteus

Enterobacter

Salmonella

Klebsiella

Spore

Formers

“ Start

off^ the

Gram

Positive

Rods”

Bacillus Clostridium Capsules:

“Some

Killers

Have

Pretty

Nice

Capsules”

S^ –^ S.

Pyogenes

K^ –^ Klebsiella

Pneumoniae

H^ –^ Haemophilus

Influenza

P^ –^ Pseudomonas

Aeruginosa

N^ –^ Neisseria

(Meningiditis

only)

C^ –^ Cryptococcus

Motile,^ (fungus)

HS^2

producing

Non^

motile,

non^

H2S^ producing

Urease

Positive

Klebsiella

Pneumoniae

Helicobacter

Pylori

Proteus

Toxins

Intracellular

Growth

Facultative

Obligate

Listeria

Monocytogenes

Mycobacteria

Leprae

Salmonella

Genus

Rickettsia

Rickettsii

Shigella

Genus

Coxiella

Burnetti

Mycobacteria

TB^

Erlichia

Brucella

Genus

Chlamydia

Species

Bartonella The^ “ABCs”

of^ Anaerobic

bacteria

A^ –^ Actinomyces

(gram

B^ –^ Bacteroides C^ –^ Clostridium

(gram

Acid^

Fast^

Bacteria

Mycobacteria

(TB^ and

Leprosy)

Nocardia