Bacterial pathogens1

BacterialBacterial
PathogensPathogens
IMEC INC.
Quick Learning
Technique

WHAT STARTEDWHAT STARTED
MICRIOBIOLOGYMICRIOBIOLOGY
 Louis Pasteur and MILK
 They even named this Bacteria after
him—NAME IT?

Reproduction of
Bacteria
 Most of the time bacteria go through
Binary Fission
 Yet some can transfer genetic material
via transduction, transvection,
conjugation and viral phage

Glycolysis
 Most bacteria require energy just
like eukaryotic cells via
production of ATP
 Glycolysis is the make form of ths
production
 Simple glycolysis is call the
Emben-Meyerhof pathway

Other energy forms
 Alternative forms with with various
common bacteria- The Pentose Pathway,
also know as the hexo-monphosphate
shunt
 THE IS IMPORTANT WITH E-COLI &
ENTEROCOCCUS
 The next being very important as well,
because some are common related
NOSCOMIAL infections- The Entner-
Dourdoroff pathway
 PSEUDOMONAS

BACTERIAL
RESISTANCE
 Cell Membrane/Cell Wall
Structure
 Flagella/Pili
 Capsule Enzymes
 Endospore state

TOXINSTOXINS
 EXOTOXINS
 Both Gram +ve/ negative organism
 Plasmids, chomosomes, phage DNA
 ENDOTOXINSENDOTOXINS
 Gram Negative only
 Only by plasmids

Bacterial PathogensBacterial Pathogens
 Small (0.5-3.0 um) size
 Have no nuclear membrane
 No micro-organelle (except
ribosomes)
 Small ribosomes with (70s)sub-
unit: 50 S & 30S for protein
synthesis
 Have a single circular
dsDNA(haploid) and a smaller
circular plasmid

MetabolismMetabolism
 Bacteria tends to be either
aerobic or anaerobic in origin.
This helps diagnostically and can
sometimes be assimilated via a
good history and physical

Normal Flora
 Skin---S. Epidermitis
 Nose— S. aureus
 Oropharnx—Viridans Strep
 Colon— Fragilis.>E.coli
 Vagina--Lactobacillus

Common Causes of
Pneumonia
 Children
 Viral (RSV)
 Mycoplasma
 Chlamydia
 S. Pneumoniae
 Young Adults
 Mycoplasma
 S. Pneumoniae
 Adults over 40
 S.pneumoniae
 H.Influenza


Special Pneumoniae Groups
 AspirationAspiration
• AnaerobesAnaerobes
 NosocomialNosocomial
• Staphylococcus. / P. Auriginosa/ KlebsiellaStaphylococcus. / P. Auriginosa/ Klebsiella
 NeonatalNeonatal
• Group B Streptococci/ E.coliGroup B Streptococci/ E.coli
 AlcoholicAlcoholic
• S. PneumoniaeS. Pneumoniae
 ImmnocomprimisedImmnocomprimised
• Staphylococci, Gram (-ve), Pneumocystis in HIVStaphylococci, Gram (-ve), Pneumocystis in HIV

Causes of MeningitisCauses of Meningitis
 Newborn
• Group B Streptococci
• E.Coli
• Listeria
 Children
• S. pneumoniae
• N. Meningitidis
 Older than 6YO
• N. Menengitidis
• Enteroviruses

Causes of UTI’sCauses of UTI’s
 AmbulatoryAmbulatory
 E.coli (50-80%)E.coli (50-80%)
 Klebsiella (8-10%)Klebsiella (8-10%)
 Staphylococcus saprophyticusStaphylococcus saprophyticus (10-30% in young(10-30% in young
ambulatory womenambulatory women
 HospitalizedHospitalized
 E-coliE-coli
 ProteusProteus
 KlebseillaKlebseilla
 SerratiaSerratia
 PseudomonasPseudomonas

Bacterial PathogenBacterial Pathogen
Growth PhasesGrowth Phases
 LAG PHASELAG PHASE
 Turning on enzymesTurning on enzymes
 LOG PHASELOG PHASE
 Exponential Growth PhaseExponential Growth Phase
 STATIONARY PHASESTATIONARY PHASE
 Nutrients Used Up/Toxic products formNutrients Used Up/Toxic products form
 May also be due to pHMay also be due to pH
 DEATH AND DECLINEDEATH AND DECLINE

BACTERIAL CLASSIFIEDBACTERIAL CLASSIFIED
 GRAM STAINGRAM STAIN
 MORPHOLOGYMORPHOLOGY
 Organism, Colony in CultureOrganism, Colony in Culture
 METABOLIC CHARACTERMETABOLIC CHARACTER
 Hemolytic Property, NutritionalHemolytic Property, Nutritional
requirementsrequirements
 SEROLOGYSEROLOGY
 Genetic make-up, Phage typing,Genetic make-up, Phage typing,

BACTERIAL GENETICSBACTERIAL GENETICS
 DNADNA
 Purines (Adenine) & (Guanine)
 Pyrimidine (Thymine) & (Cytosine)
 The bacterial Chromosome is aThe bacterial Chromosome is a
dsDNAdsDNA loop without a membraneloop without a membrane
 Only One Copy (Only One Copy (HAPLOIDHAPLOID))
 Multiplication by Binary FisionMultiplication by Binary Fision

 PLASMIDSPLASMIDS
 Extra chromosomal geneticExtra chromosomal genetic
material not needed for bacterialmaterial not needed for bacterial
growth-growth-
 Can replicate by themselvesCan replicate by themselves
 Mostly Circular dsDNAMostly Circular dsDNA
 Some may be linearSome may be linear
 Transmitted via F-Pili byTransmitted via F-Pili by
ConjugationConjugation
 R-plasmid similar to FR-plasmid similar to F
• Can induce a resistance as in E-ColiCan induce a resistance as in E-Coli

 VIRULENCE PLASMIDSVIRULENCE PLASMIDS
 Transfer Virulence FactorsTransfer Virulence Factors
 ExampleExample
•E-COLI:E-COLI: LT & STLT & ST TOXINSTOXINS
•STAPH AUREUS:STAPH AUREUS: SSSSSS
•STEPTOCOCCI:STEPTOCOCCI: HEMOLYSINHEMOLYSIN

 BACTERIOPHAGEBACTERIOPHAGE
 Contains HeadContains Head
 Sheath capsidSheath capsid
 Tail FibersTail Fibers
 PHAGE IS SPECIFIC TOPHAGE IS SPECIFIC TO
BACTERIA, AND BACTERIABACTERIA, AND BACTERIA
MUST BE IN PROPER RATIOMUST BE IN PROPER RATIO

BACTERIAL GENETICBACTERIAL GENETIC
MATERIAL EXCHANGEMATERIAL EXCHANGE
 TRANSFORMATION
 Only occurs in a few Genera-
 Usually between same species
 FREES DNA RELEASE
 TAKEN UP BY ANOTHER
 EXAMPLE:
•(Hemophilus, strep.Pneumonia)

 TRANSDUCTIONTRANSDUCTION
 Specialized via temperate phageSpecialized via temperate phage
• Integrated then spliced outIntegrated then spliced out
 Generalized via virulent phageGeneralized via virulent phage
 Transfer of DNA through Phage

CONJUGATION
 THIS IS TRANSFER VIA SEX PILI
 Donor (F+)/ Recipient (F-)

PolysaccarhidePolysaccarhide
InformationInformation
 Bacterial surface or secreted polysaccharides are
molecules that can function as barriers to protect bacterial
cells against environmental stresses, as well as act as
adhesins or recognition molecules. In some cases, these
molecules are immunodominant antigens eliciting a
vigorous immune response, while in other cases the
expression of polysaccharides camouflages the bacteria
from the immune system. Until recently, most studies on
the enzymatic steps and regulation of these molecules
were performed on the enteric gram negative bacteria
Escherichia coli and Salmonella typhimurium. With the
advent of modern bacterial genetics, techniques such as
construction and characterization of polysaccharide
mutants, cloning of genes and complementation of these
mutations, and expression of polysaccharides in
heterologous bacterial hosts has prompted investigations
into the roles and functions of these molecules for many
different bacteria.

BACTERIAL CLASSIFIEDBACTERIAL CLASSIFIED
 Other factors for Gram Positive+
 Cocci
 Catalase Positive-Catalase Positive-StaphStaph
 Catalase NegativeCatalase NegativeStrepStrep
 Bacillus
 Spore forming
• BacillusBacillus (aerobic)(aerobic)
• ClostridiumClostridium (anaerobic)(anaerobic)
 Non Spore forming
• CornyobacteriumCornyobacterium (non motile)(non motile)
• ListeriaListeria (motile)(motile)

GRAM-POSITIVEGRAM-POSITIVE
(+)(+)
ORGANISMSORGANISMS

GRAM POSITIVEGRAM POSITIVE
 Contain Cell Envelope with a Rigid
Cell Wall and a lipid bilayer
cytoplasmic membrane
 Cell Wall is made of Petidoglycan layer
(Thick) with Teichoic acid
 Peptidoglycan is made of polysaccarrides
(N-acetyl glucosamine & acetyl muramic acid)
 Which is covered interwoven with
Lipoteichoic Acid
 Thicker and Three dimensional compared Gram (-)

GRAM POSITIVE WALLGRAM POSITIVE WALL

AerobicAerobic
Gram Positive CocciGram Positive Cocci
 Staphylococci aureus
 Staphylococci epidermidis
 Staphylacoccus sp (coagulase
negative)
 Streptococcus pneumoniae
(viridans group)
 Streptococcus agalactiae
 Streptococcus pyogenese


STAPH AUREUS
Small ClustersSmall Clusters

Staphylococcus aureus
•Illness caused
oFood PoisoningFood Poisoning
o Pneumonia (often nosocomial)Pneumonia (often nosocomial)
oOther possibilities
oSkin and integumentary infections , Bacteremia, Toxic Shock SyndromeToxic Shock Syndrome , Meningitis ,Osteomyelitis
,Renal abscess
oEndocarditis ,Septic arthritis ,Impetigo
•Description
oGram positive
oCocci (grape-like clusters)
oFacultative anaerobes
oNon-spore-forming
oNon-motile
oNormal human flora
oWhen growth occurs in prepared food, enterotoxins are produced that cause food poisoning.
•Symptomology
oFood Poisoning symptoms (symptoms occur between 2 to 4 hours after ingestion)
oDiarrhea ,Nausea ,Vomiting ,Self limiting
oCAUSES
oUnsanitary food handling by colonized or infected food handlers
oImproper refrigeration following contamination
oAssociated foods
oCustards or custard-filled pastries
oDairy products
oMeats
oPotato salad
oSalads
oPneumonia symptoms
oChest pain ,Cough
oSevere shaking chill
oSustained fever
oArea and seasonality IV DRUG USERSIV DRUG USERS
oInhalation of droplets

STAPH AUREUSSTAPH AUREUS
Small ClustersSmall Clusters

STREP PYOGENESE
Classic Chains

STAPH EPIDERMATIS
(Common skin bacteria)

STREP PYOGENESE
 GROUP A (beta hemolytic)
 Viridan (y& a)
 ImpetigoImpetigo
 Rheumatic fever (M18 & M3 Serotypes)
 Mitral Stenosis (Ascoff bodies)
 Pancarditis
 Very complex enzyme structure
 SCARLET FEVER
 May cause Toxic Shock Syndrome
 Glomerulonephritis

Group A Beta-hemolytic Streptococci
•Illness caused
oPharyngitis (strep-throat)
oOther possibilities:
oScarlet fever
oPyoderma
oStreptococcal toxic shock syndrome
oRheumatic fever
•Description
oGram positive
oCoccus (spherical)
oFacultative anaerobes
o0.5 to 1.0um in diameter
oBeta hemolysis
oMucoid appearance
•Symptomology
oSymptoms develop 2 to 4 days after exposure to the pathogen
oFever , headache, malaise, sore throat
oDemographics
oAge and sex
oMost common in children between the ages of 5 to 10 years
oBoth sexes affected equally
oSeasonality
oWinter and spring
oTransmission
oPerson-to-person contact
oA person is most contagious when exibiting symptoms
oThroat and nose secretions
•Sample(s) to be collected
oThroat swabs
•Identification
oColony growth with a zone of inhibition around the disk indicates a presumptive identification of Group A beta Strep.
oGram staining produces Gram positive cocci in chains.

STREP PNEUMONIAESTREP PNEUMONIAE
Small chains in tissueSmall chains in tissue

Streptococcus pneumoniae
•Illness caused
oPneumonia
•Description
oGram positive
oEncapsulated diplococcus (oval or lancet shaped)
oFacultative aerobes or microaerophilic
o0.5 to 1.2 um in diameter
•Symptomology
oBlood stained sputum
oChest pain
oCough
oSevere shaking chill
oSustained fever
•Demographics
oAge and sex
oChildren
oArea and seasonality
oUbiquitous
oCommon in cold months
oTransmission
oPerson-to-person through infectious droplets
oSpreading from colonized nasopharynx sites to:
oBlood, ears, lungs, meninges, and sinuses.
oComplications
o5 % mortality rate
oSputum
•Identification
oAn initial plating battery of BAP with P disk, MAC and CHOC agars should be run, along with a Gram stain, as with
all sputum samples.

Gram Positive BacilliGram Positive Bacilli
 Bacillus anthracis
 Bacillus cereus
 Lactobacillis sp.
 Listeria monocytogenes
 Nocardia sp.
 Coccobacillus –Rhodococcus
 Cornyebacterium diptheriae
 Proiombacterium Acnes

ANTHRAX
 SPORE FORMING RODSPORE FORMING ROD
 NON-MOTILENON-MOTILE
 HERBIVORE ANIMALSHERBIVORE ANIMALSHUMANSHUMANS
 TOXIN:TOXIN:
 LELE-Lethal FactorPulmonary Edema
 EFEF-Extra-cellular form of Adenyl
Cyclaseincreases intracellular cAMP
 PAPA- Promote EF and LE into cell
 (95% of Cases CUTANEOUS)
 TREATMENT--PENICILLIN

Bacillus Cereus
 FOOD POISONINGFOOD POISONING
 (RICE & VEGETABLES)(RICE & VEGETABLES)
 SPORE SURVIVES COOKINGSPORE SURVIVES COOKING
 BothBoth ENTEROTOXINSENTEROTOXINS
 HEAT LABILEHEAT LABILE—similar to CHOLERA—similar to CHOLERA
 HEAT STABILEHEAT STABILE—similar to Staph—similar to Staph
 TOXINS USUALLY < 24HRS DIARRHEATOXINS USUALLY < 24HRS DIARRHEA

AerobicAerobic
Gram Positive RodsGram Positive Rods

CORYNEBACTERIUMCORYNEBACTERIUM
DIPTHERIADIPTHERIA

CORYNEBACTERIUMCORYNEBACTERIUM
DIPTHERIADIPTHERIA
 Club Shaped, arranged in letter V, Y
 Infection (DROPLET NUCLEI) direct contact
 STRICT RESPIRATORY ISOLATIONSTRICT RESPIRATORY ISOLATION
 AEROBIC---USUALLY ON TONSILS
(coagulated) vascular congestion
 DO NOT SCRAPE
 ELK TEST----LOEFFLERS MEDIUM
 Toxin-EXOTOXIN that inhibits EF2
 Pseudomembranous Respiratory
 Heart Myocarditis—Fibrosis
 Neural Damage—Polyneuritis
 ANTI-TOXIN IS EQUINE –Severe Reaction


Listeria-MonocytogensListeria-Monocytogens
 ProducesProduces EndotoxinEndotoxin
 MOVES IN A TUMBLING MOTIONMOVES IN A TUMBLING MOTION
 Can Multiply in cold (CHEESE,Can Multiply in cold (CHEESE,
CABBAGE)CABBAGE)
 Listeriolysin-O (Beta-Hemolysis)Listeriolysin-O (Beta-Hemolysis)
 Immunocomprimized-may developImmunocomprimized-may develop
MeningitisMeningitis (3(3rdrd
most common)most common)
septicemiasepticemia
 New Born-Granulomatous septicumNew Born-Granulomatous septicum
 TX-Ampicillin, or SMX/TMPTX-Ampicillin, or SMX/TMP

NOCARDIA
 AEROBIC AFB
 Source-Decaying Organic Material
 N. asteroids (pulmonary)
 N. brasiliensis (sub-Q)
• Abscess
• May effect eyes
 DX-Sputum
 TX- Sulfa Drugs/ Amikacin

Nocardia
Acid fast stain, high power to show the long, filamentous acid fast
organisms

AneorobicAneorobic
Gram Positive Rods
 Actinomyces sp.
 Closteridium botulism
 Closteridium deficile
 Closteridium perfringens
 Closteridium tetani

ACTINOMYCETESACTINOMYCETES
 GRAM (+) Filamentous
 ANAEROBICCrevices around Teeth
 Many Strains
 Produces Abscesses (sub-Q tissue)
 Upper angle of Jaw
 Thoracic Empyema
 Abdominal-any organ
 Pelvis-Associated with IUD’s & PID
 DX-SULFER GRANULESDX-SULFER GRANULES
 Treat: Penicillin/AmpicillinTreat: Penicillin/Ampicillin

ACTINOMYCETESACTINOMYCETES
Note FilamentsNote Filaments

Botulism effects thisBotulism effects this
pathwaypathway

C. Botulism-
THE MOST POTENT TOXIN
 Extremely Lethal Preformed Toxin
 Neurotoxin—Blocks Ach release at
Presynaptic terminal
 Flaccid – Descending Paralysis
 Double vision, ptosis, general muscle
weakeness Resp failure
 Spores- if left in anaerobic condition
 JARS/ DENTED CANS
 TX- IgG to neutralize unbound
toxin/respiratory support
 ANTIBIOTICS not effective

Clostridium botulinum
oBotulism
o25 % foodborne
o72 % infant botulism
o3 % wound botulism
•Description
oGram positive
oBacillus (rod shaped) , ANAEROBIC, SPORE FORMING
oSpore former
oNeuro-toxin is produced
•Symptomology
oSymptoms begin between 18 to 36 hours on average after eating contaminated foods
oEarly symptoms (as soon as 6 hours)
oBlurred or double vision
oDry mouth
oDifficulty in swallowing or speaking
oGeneral weakness , Short of Breath
oLate symptoms (as late as 10 days)
oComplete paralysis
oAge & sex
oInfants with infant botulism
oAll ages susceptible for food borne and wound botulism
oTransmission ---SOIL, WATER, FOODS
oIngestion of contaminated food (especially home canned foods)
oInoculation through skin with subsequent localized production of neurotoxin
oBLOOD SPECIMIN REQURED
oSTOOL SPECIMEN REQURED
•Identification
oEMG
oGram staining
oInjection of serum or stool into mice for observation of botulism signs.
NERVE CONDUCTION HAMPERED AT SYNAPSE—ACTYLCHOLINE

Clostridium TetaniClostridium Tetani
 Terminal spore (drum-stick)Terminal spore (drum-stick)
 Found in Soil, excrement of animalsFound in Soil, excrement of animals
 EXOTOXINEXOTOXIN
 TetanospasminTetanospasminnerve terminalsnerve terminals
 Lack of inhibitionLack of inhibition sustained contractionsustained contraction
 Localized tetanusLocalized tetanus
 Jaw Trismus/ Laryngeal SpasmJaw Trismus/ Laryngeal Spasm
 Neonatal-unhygenic umbilical sectionNeonatal-unhygenic umbilical section
 TX- Immediate DPT BoosterTX- Immediate DPT Booster
 Never Immunized-Give IgG plus BoosterNever Immunized-Give IgG plus Booster
 Clean Wound, Ventilate, DiazapamClean Wound, Ventilate, Diazapam
 Antibiotics: Metronidozole/PenicillinAntibiotics: Metronidozole/Penicillin

C. Perfringes
 Non-motile , encapsulated
 Grows in necrotic tissue
 Gas Gangrene (myonecrosis)
 CHO fermentationcrepitus at site
 Reservoir-Colon/Soil
 PIGBEL –food type NEW GUINEA
 TX-Hyperbaric O2, Debridement

Clostridium perfringes
•Illnesses caused
oGas gangrene , necrosis of muscle
Description
oGram positive
oBacillus (rod shaped)
oAnaerobic-Spores only produced in adverse conditions
oNon-motile (rapid growth resembles motile organisms)
oEntero-toxins are produced
•Symptomology
oGas formation, necrosis of muscle
oFood poisoning
oAverage of 8 to 22 hours after eating contaminated food
oDiarrhea
oIntestinal cramps
•Demographics
oAge and sex
oAll ages affected equally
oWorldwide
oNon-seasonal
oTransmission
oSoil , GI, water, associated foods (meat, Fish), Poultry

C. DifficileC. Difficile
 Caused by broad spectrum antibiotics
(CLINDAMYCIN, CEPHALOSPORINS)
 Release exotoxins
 Pseudomembranous Ulcerative Colitis
 TEST STOOL FOR EXOTOXIN
 Treat with Oral Vancomycin
 REMEMBER VAN/TRAIN

AneorobicAneorobic
Gram-positive cocci
 Peptostreptococcus sp

Gram (-) Cell Membrane
much thinner-no wall
(but more virulent)

AerobicAerobic
Gram Negative Cocci
 Neisseria Gonorrhea
 Neisseria Meningitidis
 Moraxella catarrhalis

GRAM NEGATIVE(-)
NEISSERIA GONOCCOCCUS
 Sexually Transmitted (STD)
 2nd
most common-Chlamydia is 1st
 Can present intracellular (inside Neutrophils)
 Urethritis and attaches with pili
• Prostatitis in Male
• PID in Women
• LPS Endotoxin with IgA1 Protease on Pili
 PURULENT DISCHARGE
 Can Cause Fitz-Hugh-Curtis Syndrome
 CULTURE-THAYER/MARTIN
 TX: 3rd
Generation Cephalosporins

GRAM NEGATIVE(-)
NEISSERIA MENINGITIDIS
 Pili-Capsule-(Bacteremia)
 Enters via Respiratory Droplets
• 5% Normal Flora
 Virulence in Capsule
• 9 capsular PS serotypes (A, B, C, D, X, Y, Z, W135,
29E) Meningitis is by ABC
• IgA Protease splits IgAHelps Adhesion
• ARMY RECRUITS
 Fulminate casesAdrenal Hemorrhage
 Waterhouse-Freidrichsen sydromeWaterhouse-Freidrichsen sydrome
 TX-Ceftriaxone,or Pen G(When Sensitive)
 REMEMBER AX TO THE HEAD

AerobicAerobic
Gram Negative Rods
BIG CLASS-MUST BE BROKEN DOWN
 Fastidious, Gram-negative Rods
 Enterbacteriaceae-(Glucose
Fermenting)
 Oxidase Positive
 Glucose-Nonfermenting

AGNR-EnterobactericaeEnterobactericae
(CHO ferm) Glucose
 Citrobacter
 Enterobacter
 Escherichia Coli
 Klebsiella pneumonia
 Proteus
 Salmonella Typhi, Salmonella Enteritis
 Serratia Marcescens
 Shigella
 Yersina Pestis, Yersinia entercolitica

ESCHERICHIA COLI
 Gram (-) Rods
• Catalase (+)
• Oxidase (-)
 (90% of UTI’s)-pneumonia & sepsis
 EXOTOXIN
 LT (heat labile)watery cholera like (adenyl
cyclase)
 ST (heat stabile)---(guanyl cyclase)
 Shiga like toxin –due to Plasmid Sharing
 ENDOTOXIN
 Lipid A of LPS
 EH-EC Most Common inhibit 60S
ribosome

Escherichia coli 0157:H7
•Illnesses caused
oHemorrhagic colitis
oOther Possibilities
oUrinary tract infections and neonatal meningitis
•Description
oGram negative
oFacultative anaerobe
oNon-spore-forming
oShiga-toxin (verotoxin) is produced
•Symptomology
oSevere cramping
oWatery diarrhea that ends up grossly bloody
oLow fever (occasionally)
oVomiting (occasionally)
•Demographics
oAge and sex
oAll ages affected equally
oCommonality in institutional settings
oWorldwide
oNon-seasonal
oTransmission
oFoodborne
oPerson-to-person contact in daycares, schools, and nursing home situations
oRequires about 50 - 100 organisms to cause an infection
oAssociated foods
oHemolytic Sitiations
oRenal failure thrombocytopenia and anemia
oCan be fatal
oOccurs in 15 % of infected persons
oOften occur in very young victims

Klebsiella Pneumoniae
 Flora:Colon and URT
 Major Cause of Nosocomial Infections
 Polysaccharide capsule
 K-&-O antigen
 Lactose FermenterLactose Fermenter
 Non-motile- (NO FLAGELLUM)Non-motile- (NO FLAGELLUM)
 Pulmonary-
 ALCOHOLIC, COPD, ICP, DM
 SPUTUM-”RED CURRENT JELLY”
 Urinary-indwelling (Foley)
 HIGH MOTALITY- SPITE OF A/B THERAPYHIGH MOTALITY- SPITE OF A/B THERAPY

Klebsiella Pneumoniae
Lung TissueLung Tissue

Klebsiella pneumoniae
•Illness caused
oPneumonia
oOpportunistic
•Description
oGram negaitive
oNon-motile
oAirborne
oNormal intestinal and skin flora
oNosocomial
oInfectous in the upper respiratory tract
•Symptomology
oChest pain
oDifficulty breathing
oFever
oThick bloody sputum (current jelly sputum)
oSputum
oBlood
•Identification
oAn initial plating battery of BAP with P disk, MAC and CHOC agars should be run, along with a
Gram stain, as with all sputum samples.Gram stain, as with all sputum samples.
oK. pneumoniae will produce mucoid non-hemolytic colonies on BAP, will be resistant to optocin, and will form pink
mucoid colonies surrounded by dark pink agar on MAC. These results on MAC are very indicative of K. pneumoniae.
oGram staining produces Gram negative rods.
oTo confirm K. pneumoniae MIO, TSI and LIA tests should be run.
oMIO results are non-motile, indole negative and ornithine negative. A.

Proteus Vulgaris &
Miribalis
 Very MotileVery Motile
 SWARMIMG
 UREASE POSITIVE-OXIDASE NEG
 UreaAmmoniaAlkaline UrineStones
 Proteus cross react with Rickettsia
 WEIL-FELIX REACTIONWEIL-FELIX REACTION
 OX-19OX-19
 Culture-Blood AgarCulture-Blood Agar
 TX-KANAMYCIN

Salmonella
 Unlike ShigellaUnlike Shigella Very MotileVery Motile
• Produces H2SProduces H2S
 Uncooked eggs/ PET TURTLEUncooked eggs/ PET TURTLE
 TYPHOID FEVERTYPHOID FEVER
 Vi Antigen. Diagnose with O-H-Vi antigenVi Antigen. Diagnose with O-H-Vi antigen
 S-Typhi can cause Osteomyolitis and and isS-Typhi can cause Osteomyolitis and and is
notorious in Asplenic patientsnotorious in Asplenic patients
 May show effects at PeyersMay show effects at Peyers
PatchPatchBleedingBleedingweek 3-4week 3-4
 Liver effects may present @ weeks 2-3Liver effects may present @ weeks 2-3
 TX-TX- Ciprofloxine, CeftriaxoneCiprofloxine, Ceftriaxone

Salmonella
•Description
oGram negative
oNon-spore-forming
oMotile with flagellum
oEnterotoxins produced
oHosts are animal and human
•Symptomology
oMain symptoms
oAbdominal cramps ,Diarrhea (2 to 7 days) Flu-like symptoms
oNausea
oVomiting
oPossible symptoms
oChills
oFever
oTransmission
oEating foods contaminated with animal feces
oFactory and kitchen surfaces
oHand contact
oRaw meat, poultry, and seafood
oSoil
oWater
oAssociated foods
oBeef
oEggs
oMilk
oStool

SERRETIA MARSCESENSSERRETIA MARSCESENS
 Gram (-)Gram (-)
 Common Nosocomial infection inCommon Nosocomial infection in
Urinary Track infectionsUrinary Track infections
 If becomes pathogenic can beIf becomes pathogenic can be
aggressive respiratory andaggressive respiratory and
systemicsystemic

Shigella
 Non H2S ProducingNon H2S Producing
 Non MOTILE
 Evades Gastric Acid, by somehow
having ability to live in HCl
 Fecal Contamination
 Gay Bowel Syndrome
 ANTI-O agglutination
 TX-CIPRO, SMX/TMP
 Fluid Replacement

ShigellaShigella
•Illness caused
oShigellae
•Description
oGram negative
oNon-spore-forming
oNon-motile
oProduces shiga toxin
oHosts are humans, rare in animals
•Symptomology
oMain symptoms
oAbdominal pain
oBlood, pus or mucus in stool
oDiarrhea
oAdditional symptoms
oCramps
oFever
oFound in polluted water with human
oNon-seasonal
oTransmission
oFecal oral route
oAssociated foods (transmitted from feces to food only)
oDairy products
oRaw vegetable
oSalads (potato, tuna, shrimp, macaroni, and chicken)
oStool
oRectal swabs

Yersinia Pestis
Note-Safety Pin Appearance

Yersinia Pestis
Bubonic PlagueBubonic Plague

Yersinia pestis
•Illnesses caused
oBubonic plague
oPneumonic plague
•Description
oGram negative
oNon-motile
oNon spore forming
oBacillus (rod-shaped)
oHumans and animals are hosts
oFleas are vectors
•Symptomology
oMalaise
oFever
oPain in lymph nodes (possibly due to swelling)
oBloody vomit
oBloody diarrhea
oSkin mottling
oPetechiae
oTransmission
oBite from an infected flea
oInhalation of infected droplets in the air
oSputum
•Identification
oAn initial plating battery of BAP, MAC, CHOC should be done as for all sputum specimens.
oA Gram stain produces Gram negative (red) rods.
oTSI, LIA, MIO, Citrate, and Oxidase tests will be negative.

AGNR-Fastidious
 Bordetella pertussis
 Brucella sp.
 Camplyobacter
 Francisella
 Haemophilis influenza, Haemophilis ducreyi
 Heliobacter pylori
 Legionella pneumophila

B. Pertussis
 Filimentous
 Agglutinin stimulates cilia
 G-Proteins stimulate adenyl cyclasecAMP
 Cough severe (Whooping cough)
 Highly Contagious
 B of BCG Vaccine
 Only 1000-4000 a year now
 DX-Agglutinin via ELISA

Haemophilus influenzaHaemophilus influenza
 Gram Negative
 Loves factor X(hematin) and V (NAD)
 PS Capsule (poly ribitol) a-f
 Risk ½ -3 years
 Meningitis
 Acute Epiglottitis (Major Cause)
 Septic Arthritis
 Sepsis
 DX-Latex Agglutination/Chocolate Agar
 TX-Ceftriaxone / Amoxicillin
 th

Haemophilus influenzae
•Illness caused
oPneumonia
oOther possibilities:
oEar and sinus infections
oMeningitis
oArthritis
oPulmonary disease in the elderly
•Description
oGram negative
oBacillus
oAerobic or faculatative anaerobic
oNon-spore-forming
oNon-motile
oEncapsulated
o0.2 um in length by 0.3 to 2.0 um in diameter
•Symptomology
oChest pain
oCough
oFever
oPleuritic pain
oSneezing
oWatery eyes
•Demographics
oAge and sex
oCommon in children under the age of 1
oCommon in the elderly
oTransmission
oDirect contact
oInhalation of infected respiratory droplets that contain the bacteria
oThe bacteria is spread to the ears, sinuses, and lower respiratory tract form the upper respiratory tract
oCommon in day care centers
oSputum
oBronchial washings
•Identification
oAn initial plating battery of BAP, CHOC and MAC agars should be done, along with a Gram stain, as with any sputum sample.
oGrowth only on the CHOC agar and a Gram stain producing Gram negative rods indicates the probability of Heamophilus.
oX and V factor testing will distinguish between Heamophilus strains. Growth around the X, V and XV strips indicates the presents of H.
influenzae.

Campylobactor jejuni
oGasteroenteritis
oOther possibilities
oMeningitis
•Description
oGram negative
oBacillus (curved) Motile
o.3 to .6 um in diameter
oMicroaerophilic
oEnterotoxins, cytopathic toxins, and endotoxins are produced
•Symptomologymamaast 1 week or longer
oAbdominal pain, diarrhea, fever, mailase, gross bloody stool possible
oBowel movements may be up to 10 per day during peak of disease
oSelf-limiting
oWorldwide
oUnderdeveloped areas have less severity
oMore common in warm months
oYear-round
oTransmission
oFecal-oral
oFood handlers
oPerson to person contact
oAssociated foods
oContaminated food
oContaminated poultry
oMilk
oWater
oAn oxidase test will be positive.
oGram stain produces curved Gram negative rods.
oA catalase test will also be positive.
oCan be hard to be detected by Gram stain, may be detected by darkfield or phase contrast microscopy (rarely done).

Camplyobacter JejuniCamplyobacter Jejuni
 CURVED ROD with POLAR FLAGELLUMCURVED ROD with POLAR FLAGELLUM
 Very common cause of IntestinalVery common cause of Intestinal
disordersdisorders (Bacterial Enteritis)(Bacterial Enteritis)
 Villus bluntingVillus blunting
 Mucosal inflammationMucosal inflammation
 Usually self limited to 3-5 daysUsually self limited to 3-5 days
 From Milk, Pork and animal contactFrom Milk, Pork and animal contact
 Has toxin, nothing PS, PurelentHas toxin, nothing PS, Purelent
exudativeexudative
 TX- Erythromycin

Heliobacter PyloriHeliobacter Pylori
 Has a capsule (S) “SLIMY LAYER”
 1st Duodenel Ulcer
 2nd
Gastric
 Can be systemic, endocardic
 Attacks Vascular tissue
 Urease Producing
 Has Flagella,Motile
 TX- Bismuth, Metrodiazonole
 Key neutralize and treat

F. Tuleremia
 Arthrop Vector Hunting Season
 Minnesota, Arizona, Oklahoma
 Ulcero-
glandular/Pneumonic/Ocular/
 Ulcero Glandular common- 80%
 Pneumonic-15%

Brucella
 UNDULENT FEVER-MALTA FEVERUNDULENT FEVER-MALTA FEVER
• Dr. David Bruce
 Highly virulent
 Contact with meat & placenta of
animal
 ALSO SEEN ON DAIRY FARMS
 Caseating Granulomatous lesions
 DX-Blood/lymph—(SA)
 Tx-Doxycyclin--Gentamycin

Pasteurella
P. Multicida
 CATS/DOG BITES
 CELLULITIS
 Seen with DF2 Canimorus (+)
 Rat bite fever
 TX-Long Term A/B
 Keep Clean---DO NOT SUTURE

Erysipeloid
 Human Bite & Fishing
 Painful with swelling
 Keep Clean---DO NOT SUTURE

AGNR- OXIDASE +
(CHO FERM)
Aeromonas sp.
Vibrio Cholerae
Vibrio parahaemolyticus
Vibrio vulnificus

Vibrio Cholera
 El TorEl Tor & classic (Ogawa, Inaba)
 Lives in coastal brackish water (Ganges River)
 Caused many (7) pandemic
 O139 ,O1 Serotypes
 Non invasive yet very powerful LT toxin
 Effects cAMPCrypt cells of intestinal lumen
 Changes Osmolarity (Na-Cl-K-HCO3 are lost)
 Rice water diarrhea
 Death in hours if untreated
 TX-Doxycycline

Non-Glucose Fermenting
 Actinobacter sp.
 Flavobacterium
menengosepticum
Pseudomonas
aeruginosa
 Burkholderia cepacia,
 B. psudomallei

PSEUDOMONADACAEPSEUDOMONADACAE
 P. Aeruginosa
 NosocomialNosocomial-Water in Hospital
 Common Respiratory Therapy Problem
 Grape like Scent- very prodominant
 Green /blue flourescenceGreen /blue flourescence
 Exotoxin Aactivating EF2
 Cystic Fibrosis
 COPD
 Diabetic Patients
 Burns Wounds

PSEUDOMONADACAEPSEUDOMONADACAE
Protegrin binding with p. AeruginosaProtegrin binding with p. Aeruginosa

ANAEROBIC
Gram-Neg Rods
 Bacteroides Fragilis
 Bacteroides Sp.
 Fusobacterium sp.
 Prevotella sp.

B. Fragilis
 Not seen as Primary
 But is seen in many intra-abdominal
and retro-peritoneal infection septic
infections
 It may also be present in Lung
Abscesses
 Lesion usually resemble common
pyogenic (pus forming) infections

Many difficult to stain
 Borrelia burgodorferi, BorreliaBorrelia burgodorferi, Borrelia
recurrentsrecurrents
 BartonellaBartonella
 ChlamydiaChlamydia
 CalymatobacteriumCalymatobacterium
 Coxiella burnettiCoxiella burnetti
 Legionella spLegionella sp
 Leptospira spLeptospira sp

CHLAMYDIA
 Is Gram negative, but no muramic acid in Peptidoglycan
 Obligate IntracellularObligate Intracellular
• Needs host ATP
• Has both DNA and RNA
 Infects Columnar cells
 Inclusion bodiesInclusion bodies
 3 types
 C. Trachoma
• Most common STD-URETHRITIS
• INCLUSION CONJUNCTIVITIS (Pannus)
• Infantile Pneumonia
 C. Pneumoniae
• Taiwan Group (TWAR)
 C. Psittaci
• Atypical Pneumonia
• PARROT FEVER
TX-ERYTHROMYCIN, DOXYCYCLIN

Legionella pneumophilia
 In 1976, Philadephia, Am. LegionIn 1976, Philadephia, Am. Legion
 Small pleomorphic coccobacillusSmall pleomorphic coccobacillus
 Source-Water-(coolers/Air units)Source-Water-(coolers/Air units)
 33rdrd
most Common cause of CABPmost Common cause of CABP
 Pt had recently been incarceratedPt had recently been incarcerated
 Increased incidence in Hairy CellIncreased incidence in Hairy Cell
LeukemiaLeukemia
 PONTIAC FEVERPONTIAC FEVER
 Resolves in a weekResolves in a week
 TX-Erythromycin / RifampinTX-Erythromycin / Rifampin
 Biggest mistake in American MedicineBiggest mistake in American Medicine

Many ACID FAST
or Difficult
 Mycobacterium TuberculosisMycobacterium Tuberculosis
 Mycobacterium LeprosyMycobacterium Leprosy
 Mycobacterium Avium,Mycobacterium Avium,
 Mycobacterium IntracellulareMycobacterium Intracellulare
 Rickettsia RickettsiiRickettsia Rickettsii
 Trepenema pallidumTrepenema pallidum

Mycobacteria can also beMycobacteria can also be
stained with Auraminestained with Auramine

MYCOBACTERIUMMYCOBACTERIUM
 ACID FAST STAINACID FAST STAIN
 Mycolic Acid in cell wall lipidsMycolic Acid in cell wall lipids
 Zeihl-Neilsen StainZeihl-Neilsen Stain (need heat)(need heat)
 KINYOUN STAINKINYOUN STAIN
 No HeatNo Heat
 FLOURESCENT STAINFLOURESCENT STAIN
 AuramineAuramine-apple green flouro-apple green flouro on a darkon a dark
backgroundbackground

M. TuberculosisM. Tuberculosis
 Slender, grooved granular Rod
 Slow Growth (3-6) weeksSlow Growth (3-6) weeks
 OBLIGATE AEROBEOBLIGATE AEROBE—Needs O2—Needs O2
 Resistant to DryingResistant to Drying
 Primary TB
 Caseating Granulomatous infection that isCaseating Granulomatous infection that is
produces by Macrophage release of TNFproduces by Macrophage release of TNF
 Cheesy necrotic cellCheesy necrotic cell. May calcify. May calcify increasedincreased
collegencollegen
 Hilar LymphHilar Lymph (GHON FOCUS)(GHON FOCUS)
 2ndary TB (10% Risk)
 ReactivatedReactivated Chronic low grade feverChronic low grade fever
 MILIARYMILIARY (ALL ORGANS)(ALL ORGANS)

 MAY BE SEEN ON CHEST X-RAYMAY BE SEEN ON CHEST X-RAY
 PPDPPD (TUBERCULIN TEST) +ve(TUBERCULIN TEST) +ve
• 5 units Intra-dermal5 units Intra-dermal
 BCGBCG required in many countriesrequired in many countries
• Bacillus Calmette-Guerine (attenuatedBacillus Calmette-Guerine (attenuated
Bovine)Bovine)

 POPULATIONS of INFECTIONSPOPULATIONS of INFECTIONS
 OLD AGEOLD AGE
 URBAN POOR (LOW SOCIO CLASS)URBAN POOR (LOW SOCIO CLASS)
 AIDSAIDS

TB DRUGS
 ISONIAZID
 RIFAMPIN
 PYRAZIAMIDE
 ETHAMBUTOL
 STREPTOMYCIN
 AMINOSALICYCLIC ACID
 ETHONAMIDE
 CYCLOSERINE

M. Leprae (Hansen’s Disease)
 World wide
 US-200 new cases ayear
 Cooler parts of body (face)
• Testis, and superficial nerves
 2 types
 Lepramatous (increased CD8, DQ1)
• Lepromin Skin Test (NEG)Lepromin Skin Test (NEG)
• Severe, Highly infectious, blocks T-4 helper
response Disfigured Skin
• Cartilage destroyed, testicular atrophy, nerve
damage, loss of digits
 Tuberculoid (increased CD4, DR2)
• Lepromin Skin Test (POS)Lepromin Skin Test (POS)
• Localized, may have hair loss

Mycobacterium avium-intracellulare infection is marked by
numerous acid fast organisms growing within macrophages.
Lots of bright red rods are seen, particularly in macrophages,
in this acid fast stain of lymph node.

M. Avium Intercellulare
 AIDS PATIENTS
 OCCURS LATE IN DISEASE WHEN
CD4 COUNT IS LOW
 Watery Diarrhea, wieght loss

Rickettsia Rickettsi
IntracellularIntracellular

Rickettsia Rickettsi
 ROCKY MOUNTAIN SPOTTED FEVER
 Dock tickDock tick—Eastern states
 Wood tickWood tick-Western states
 Profilerates in the endothelium and
attacks smooth muscle cells
 Hemorrhage may be serious
 Ankle, soles, palms, wrist
 Severe cases, cardiac renal,encephalitis
 DX-If recent tick exposure, do latex
test, If a skin lesion PCR
 Treat-Doxycyclin

Rickettsia
(Typhus Group)(Typhus Group)
 Endemic and Epidemic
 Large Populations, During War-time, also
world wide distributiion
 Rash-leading to collapse and
delerium, Mortality is low
 Agents-
 R.Prowazacki
 R. Typhi ( RAT RELATED)
 Vectors
 Louse
 Reservior
 Flying squirrel (FLEA RELATED)

BartonellaBartonella
 Trench Fever
 R. Quinata
• (louse bornhuman)
 Cat Scratch Fever
 B. Hensele
• (papules, pustules, crusts)
 Oroyo Fever
 B. Bacilliformus (Sand Fly)
• Deforms RBC’s, marked Anemia, seen in high
altitudes like the ANDES MOUNTAINS

DONAVANOSIS
Granuloma Inguinale
 Calymmatobacterium granulomatisCalymmatobacterium granulomatis
 STDSTD
 Increased in TropicsIncreased in Tropics
 Sub Q swellingSub Q swelling
 TX-Tetracyclin, ErythromycinTX-Tetracyclin, Erythromycin

Mycoplasma
 Smallest Free living organism knownSmallest Free living organism known
 No cell wallNo cell wall
 Aerosolized respiratory dropletsAerosolized respiratory droplets
 WALKING PNEUMONIAWALKING PNEUMONIA
 AtypicalAtypical
 X-ray looks extremely badX-ray looks extremely bad
 TX-TX- Erythromycin, TetracyclinErythromycin, Tetracyclin

Mycoplasma pneumoniae
•Illness caused
oMild upper respiratory tract disease
oPrimary atypical pneumonia
•Description
oClassified as gram negative due to no cell wall
oFacultitive anaerobe
oVarried shapes
oPleomorphic
oSpherical
oPear-shaped
oFilamentous
oSmallest free-living cells
oRequires a complex media
•Symptomology
oMild upper respiratory tract disease
oHeadache
oLow fever
oPredominant cough
oWeakness
oPrimary atypical pneumonia
oChest pain ,Difficulty breathing ,Little sputum ,Fever ,Cough
oHeadache
oWeakness
Transmission
oNasal Secretions ,Close contact ,Airborn droplets (sometimes)
oSputum
oThroat washings
•Identification
oCold agglutinins
oComplement fixation
oCulture
oELISA

Treponema Pallidum
Spirochete-SyphilisSpirochete-Syphilis

SYPHILIS (T. Pallidium)
 STD-Can enter via mucosa or dermal abrasion
 3 stages
 Primary Syphilis (CHANCRE)
• Secondary-Mucosal Lesions (palms, sole, tongue)
• Condylomata-cluster of warts (perineum, anus,
vulva)
 Latent
• After 6 weeks
• STS remains Positive
 Tertiary
• 6-40 years
• (GUMMA) 15%---skin and bone
• Cardiovascular 10%
• Neuro-syphilis 8%
VDRL/Hemaglutin—Jarisch-Herxheimer reaction

Leptospira (Weil’s DX)
 Smaller than Treponema Pallidum
 Hooked end
 Organisms in Blood and CSF
 FEVER
 PHOTOPHOBIA

Borrelia BurgodorferiBorrelia Burgodorferi
 LYME DISEASELYME DISEASE
 NE,NW, and MidwestNE,NW, and Midwest
 Most common vector borne infection in theMost common vector borne infection in the
U.S.U.S.
 Vector-Ixodes TickVector-Ixodes Tick
 Three StagesThree Stages
 1. Acute—Erythema1. Acute—Erythema
 2. Dissemination, encephalopathy, (CN2. Dissemination, encephalopathy, (CN
VII-Bells Palsy)---MycocarditisVII-Bells Palsy)---Mycocarditis
 3. Late. Destructive Arthritis, neuropathy3. Late. Destructive Arthritis, neuropathy
 Culture-Modified Kelly’sCulture-Modified Kelly’s

Borrelia Burgodorferi
Difficult to StainDifficult to Stain

Ixodes Tick-FemaleIxodes Tick-Female

Causes of MeningitisCauses of Meningitis
 Newborn
• Group B Streptococci
• E.Coli
• Listeria
 Children
• S. pnemoniae
• N. Meningtidis
 Older than 6YO
• N. Menengitidis
• Enteroviruses

Causes of UTI’sCauses of UTI’s
 AmbulatoryAmbulatory
 E.coli (50-80%)E.coli (50-80%)
 Klebsiella (8-10%)Klebsiella (8-10%)
 Staphylococcus saprophyticus (10-30% inStaphylococcus saprophyticus (10-30% in
young ambulatory womenyoung ambulatory women
 HospitalizedHospitalized
 E-coliE-coli
 ProteusProteus
 KlebseillaKlebseilla
 SerratiaSerratia
 PseudomonasPseudomonas

Pyogenic Cocci Bacteria
 Staphylococcus aurues
 Streptococcus pyogenes
 Streptococcus Pneumoniae
 Neisseria Menegitidis
 Neisseria Gonorrhoeae

Common Gram Negative
Infections
 Escherichia Coli
 Klebsiella Pneumonae
 Enterobacter Aerogenes
 Proteus spp.
 Pseudomonas sp.
 Legionella spp.

Rare Gram Negative
Infections
 Calymmatatobacterium
donavons
 Heamophilis ducreyi
 Klebseilla rhinoschleromatis
 Bartonella bacilliforms

Contagious Childhood Bacteria
 Hemophilus influenze
 Hemophilus pertusis
 Cornyobacterium diptheria

Enteropathic Infections
 Enterpathogenic E-coli
 Shigella Sp
 Vibrio cholera
 Campylobacter jejuni
 Yersinia enterocolitica
 Salmonella spp (1000 strains)

Zoonotic Bacteria Infections
 Bacillus Anthracis
 Listeria monocytogenes
 Yersinia pestis
 Franciella tuleremia
 Brucella sp
 Lerptospira sp (many groups)
 Borrelia burgodorferi

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