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Microbiology –bacteria summary Gram +‘ve
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Microbiology – bacteria summary (updated)

Apr 06, 2018

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Page 1: Microbiology – bacteria summary (updated)

8/3/2019 Microbiology – bacteria summary (updated)

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Microbiology –bacteria summary

Gram +‘ve

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Cocci – aerobicGenus Species Description Virulence factors &

PathogenesisEpidemiology Diseases Treatment

Staphylococcus Aureus

(coagulase+’ve)

AnerobicNon-sporingNon-motileNon-capsulate /limited capsuleformationCatalse +’ve

Appear as“bunches of grapes”

Enterotoxins- food poisoning- heat stable-Toxic shock syndrome toxin (TSST-1)

Epidermolytic toxins- type A&B- cause blistering disease

cytotoxin →alpha toxin- pore formation- proinflammatory

protein A- disrupts opsonization- binds IgG in Fc region(bind Ig with irregular orientation todisrupt opsonization)Causes infection of sites of loweredresistance →damaged skin / mucousmembrane

Enterotoxin & TSST-1 = superantigens- activate T lymphocytes- release cytokines (TNF)

coagulase & bound coagulase (clumpingfactor)

Nuclease

Haemolysans

leukocidins

Nose of 30% of healthypeople

Skin, glands and mucousmembranes

Colonization:- nares, axilla, vagina,

pharynx

Skin infection

Osteomyelitis

Food poisoning

Inherentlysensitive tomanyantimicrobialagents

90% resistantto:

penicillin G(benzylpenicillin)

resitance via:β -lactamase(penicillinase)

antibiotics:- must use β -lactamaseresistantpenicillins- cloxacillin

- flucloxacillin

MRSA(Methicillin-resistant Staph.aureus)∴ usevancomycin

epidermidis

Coagulase–‘ve

Normal flora of 

cutaneousorgan system

Adhesion to biomaterials

- adhesion to silastic catheter bycapsular polysaccharide adhesion- forms biofilms →via extracellular slimesubstance

Major cause of 

foreign bodyinfection

resitance via:

β -lactamase

- vancomycin

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Streptococcus Pyogenes(pus forming)

aka →groupAstreptococcus→GAS(Lancefieldgrouping)

β -

haemolysin

Facultativeanaerobe:- makes ATP bynormal aerobicrespiration- ferments inabsence of O2

Non-sporingNon-motilecapsulatedCatalase –‘ve

M proteins- prevent opsonization by C3b- B cells can produce anti-M protein Ab →Ab also damages cardiac muscles∴ rheumatic fever

 Toxins- superantigens →do not requireprocessing by APC- bind directly to T cell MHC II(nonspecificly)∴ huge cytokine release

- rapid onset- pyrogenic- toxic onset syndrome∴”super bug” / “flesh eating bacteria”

capsule-hyaluronic acid- antiphagocytic

haemolysins→streptolysins O & S- lyse: eryhtrocytes, leucocytes, platelets

- β -haemolysis

hyalournidase

- degrades hyaluronic acid of groundsubstance

streptokinase- fibrinolysis ∴↑ spreading

DNAaseslocalized infections

suppurative infections(pus forming)

Pharyngitis

Skin infections

Rheumaticfever- type 2hypersensitivity

acuteglomerulonepgritis- immunecomplexdeposition inglmoeruli

Penicillin stilleffective forGoup Astreptococcal

antibiotics:- penicillin G &V

Specific M-proteinvaccines beingtested

typing:- β -haemolysis+’ve =pathogenic→clear zonearound colonyin blood agar- α -haemolysis= mostlycommensals →green for

oxidation byhydrogenperoxide (notactualhaemolysis)

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Pneumoniae(pneumococcus)

α -haemolysin

optochinsensitive

Pneumonia

Meningitis inchildren andadults

 Typing:- α -haemolysis

Viridians(green)

α -haemolysin

optochinresistant

Commensals

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Cocci – anaerobicGenus Species Description Virulence factors &

PathogenesisEpidemiology Diseases Treatment

Peptostreptococcus

 

AnaerobicNon-sporing

Normal flora of skin, oral cavity,colon,genitourinarytract

1. Abscesses:- brain- lung

2. Aspirationpneumonia

3. Gingivitis +other periodontaldiseases

Bacilli – aerobicGenus Species Description Virulence factors &

Pathogenesis

Epidemiology Diseases Treatment

Listeria Monocytogenes

Intracellularpathogen

Found in environment and animals

Contaminates food

Humans = local carriers

Adults:- asymptomaticGIT carrier- influenza like

antibiotics:- penicillin →Prolongedampicillin

β -lactamaseinhibitor:- clavulanic acid

Resistant:- cephalosporins(intrinsically)

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Bacilli – anaerobicGenus Species Description Virulence factors &

PathogenesisEpidemiology Diseases Treatment

Clostridium Tetani Anaerobicsporing

 Toxins:tetanospasmin- neurotoxin →very leathal- blocks neurotransmitter release for 3-4 days

enzymes:- oxygen-labile haemolysin (tetanolysin)Spread:

1. ascending tetanus wound to trunk →viapheripheral nerves

2. Descending →Haematogenous→via lymp =lock jay

Found in soil &animal feces

spores enter deeptissue with lowoxygen tension

1. Tetanus- vascillatingspasms- respiratory arrest- death if dose ishigh

Diagnosis:- smear fromlesion

Immunization:- active → tetanustoxoid (neutralizeunbound toxin)

- passive →immunoglobulins

Supportive:- mechanicalventilation- muscle relaxants

- sedation- nutrition

antibiotics:- metronidazole(kills vegetative

bacteria)- penicillin G & VBotulium anaerobic

Sporing Toxins:1. neurotoxins- 7 forms (A-G)- invasion of peripheral nerves →blocks releaseof Ach ∴ flaccid paralysis →ocular andrespiratory muscles- blurred vision- trouble swallowing

Highly resistantspores

Found in feces,blood, food

Vaccine:- toxoid vaccinehelps clearunbound toxin → if given immediatelyBUT questionableefficacy

Antibiotics:- penicillin

supportive care

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Perfringens Anaerobicsporing

 Toxins:exotoxins- deep tissue necrosis- gas production causing crepitus

1. Clostridialmyonecrosis→gas gangrene- complications →shock,haemolysis, renalfailure, metabolicacidosis, coma

2. Enteric infection

-food poisoning- enteritis necrosis

- neutropenicenterocolitis

3. Soft tissueinfections- polymicrobialinfection- crepitantcellulitis- suppurativemyositis

- Extensivedebridement- possibleamputation

antibiotics:- penicillin G & V

sometimeshyperbaric O2

Difficile Anaerobicsporing

 Toxins:- Enterotoxin- cytotoxin

Antibiotics kills many GIT flora other thandifficile∴ multiplies and produces toxins

complications:- hypoproteinaemia-toxic colonic perforation- peritonitis

Part of normal GITflora in manyindividuals

1. Antibiotic-associateddiarrhoea +pseudomembranous colitis

watery →blooddiarrhoea 4-9 dayspost antibiotics

Discontinueantibiotic

supportive:- rehydrate

avoid anti-motilitydrugs

antibiotics:- metronidazole- vancomycin (if severe)

Propionibacterium

Normal flora of theskin

Opportunisticinfections:- prosthetic devices- CNS shunts

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Bifidobacterium

Questionable pathogenic potential - Predisposingcondition- dental extraction

Eubacterium Female genital tract- ICUD(contraceptive)

Predisposingcondition

Chronicperiodontaldisease

Actinomycetes Israelii Actinomycosis- chronic,granulomatousinfective disease- multipleabscesses, sinustracts, fistulae →erupt to thesurface →drainpus containingsulphur granules

Antibiotics:long coursepenicillin

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Gram –‘ve

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Cocci - aerobicGenus Species Description Virulence factors &

PathogenesisEpidemiology Diseases Treatment

Neisseria

(describedby Neisser)

meningitidis Obligate humanpathogens

Diplococci(axis of pairparallel →sideby side)

Oval cocci to“bean shaped”

Found insideneutrophils(polymorphonuclear pus cells)

Capsule(determinesserogroup)

Immune evasion via capsule

Bacteremia

Antibodies and complementare essential for host immuneresponse

Carriers in:nasopharynxoropharynx

Increased incidence inwinter

Spread by kissing

Spread via respiratorydroplets

Meningococcalmeningitis

Danger of majorout break-endemic &epidemicsituations

2/3 of casesunder age of 5

Vaccine preventable(based on capsuleserogroups)- last 3 years-immunityprophylaxis- herd immunity →vaccinate populationgroups to avoid

outbreakscatch early → treatearly- chemoprophylaxis- if danger of outbreak treatmentshould begin beforedefinite diagnosis- notifiable

Antibiotics:- penicillin G & V

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gonococcus Non-capsule Pili(phase variation)

Antibiotics:- penicillin G & V

Cocci – anaerobicGenus Species Description Virulence factors &

PathogenesisEpidemiology Diseases Treatment

Veillonella often contaminates skin

commensal of:- mouth, upper RT, GIT,vagina

1. Osteomyelitis

2. Periodontitis

1. antibiotics

2. Surgery- incision,drainage,debridement,removal of foreignbodies

3. Improvecirculation→oxygen

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Bacilli – aerobicGenus Species Description Virulence factors &

PathogenesisEpidemiology Diseases Treatment

Enterobacteria

Escherichia

Coli ?

strains

Aerobic(use / fermentcarbohydrates)

GITcommensals ?

Found in: soil,plants water

EPEC

enteropathogenic

Adherent bacteria

Adheres to gut wall(upper intestine)

- loss of microvilli ∴↓water &electrolyte absorption

Common in tropics- bad hygiene

Infantile diarrhoea- mild fever, malaise,vomiting- large amount of mucous

in stool →no blood

Supportive- replacement of water & electrolytes

avoid exposure toinfecting agent- “boil it, peel it, orleave it”

no antibiotictreatmentrecommended- diarrhoea normallyself-limiting

in VTEC- antibiotics

associated withdevelopment of HUS

antimicrobialprophylaxis→notadvised →development of resistance

ETEC

Enterotoxogenic

 Toxins 1. fimbriae →adherence toepithelial membrane of smallintestine

2. enterotoxins- heat stable and heat labile- hyper secretion of fluids andelectrolytes in to lumen

 Tropical and subtropicalclimates

Contaminated food andwater

Poor sanitation

Diarrhoea in adults andinfants

traveler’s diarrhoea

Major cause of death inchildren <5

rapid onsetno blood1-5 days

EIEC

enteroinvasive

Invasive bacteria

Direct penetration, invasionand destruction of intestinalmucosa

Food borne

Out breaks in schoolsand hospitals for thementally handicapped

Dysentery

- scanty stool with pus,mucous, blood

Fever, abdominal cramps,malaise

VTEC

Verocytotoxiogenic

(aka→enterohaemorragic)

 Toxins

Cytotoxins- VT1- VT2

Out breaks- nursing homes- day care centres

food- hamburger meat,cooked meat- unpasteurized milk

Severe in old and young

hemorrhagic:- diarrhoea- colitis- uremic syndrome(HUS)→ ↓platelets, hemolyticanaemia, renal failure

no leukocytes in stoolFever, abdominal cramps

EAggEC

entero-aggregative

Adherent bacteria

Adheres to mucosal surface of intestine

Rare in industrializedcountry

Chronic diarrhoea(malnourished children)

Colonized but notpathogenic

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Shigella Dysenteriae(serogroup A)

Closely relatedto Escherichia

Non-motilenon-capsulate

Invasive bacteria:Superficial invasion of the gut

 Toxin:Shiga Toxin- destroys epithelial cells- necrosis- neurotoxic- meningism(triad of nuchal rigidity [stiff neck], photophobia,headache)- coma

 Transmission:- human to human- low infective dose →10 viable bacteria

4 F’s:FingersFaecesFliesFood

No animal reservoir

Most common in children

Dysentery:- Bloody diarrhoea

Bacteraemia = rare

β -lactamaseinhibitor:- clavulanic acid

Vibrio Cholerae ToxinEnterotoxin

Non-invasive

Outbreaks / epidemics

Contaminated water

Watery diarrhoea(20-30 liters/day)

Rapid onsetHypovolemic shockMetabolic acidosis

Cyanoticsunken eyes and cheeksPoor skin tugor

Detection:- fresh fecal sample→1-2hours- rectal swab

vaccine:- given to groups inhigh risk areas

Dukoral:- 85-90% efficiency- all ages- for 4-6 months

Parahaemolyticus

Acquired from food- mainly raw seafood

Dysentery-like picture

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Salmonella Enterica

typhiNon-typhi

Aerobicnon-sporingrods(coccobacillus)motile

Enter macrophages??

1. primary bacteraemicphase:Invades ileal mucosa →multiplies in mesentericlymphoid tissue→enters blood via thoracicduct→ liver, gall bladder, spleen,kidneys and bone marrowbecome infected

2. Second (heavier)bacteraemic phase:7-10 day incubation period →conincides with fever

3. Further infection of GITfrom gall bladder →Preyer’spatches and lymphoid tissueinvolved → inflammatoryresponse → typhoid ulcers

 Transmission:- human to human

Fever:- enteric fever- typhoid fever(if causative agent istyphi)

long termasymptomatic carriers:- chronic excretion- biliary →necrotizingcholecystitis- urinary tact- dangerous for foodhandlers to be carriers

Diarrhoea

found in:- CSF- Stool, urine, blood

Detection:Blood cultures →ESBL-producing salmonella

Vaccine:- live attenuated Ty21a →approved for travelers

β -lactamaseinhibitor:- clavulanic acid

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Bacilli – anaerobicGenus Species Description Virulence factors &

PathogenesisEpidemiology Diseases Treatment

BacteroidesPorphyromonasPrevotella

Fusobacterium

Fragilis Normal flora:– oral cavity, GIT, vagina

1. abscessformation

2. Periodontal

disease- Vincent’sangina →acutenecrotizingulcerativegingervitis

3. postaspirationpleuro-pulmonarydisease

4. Genital tract

infections

1. antibiotics

2. Surgery- incision,

drainage,debridement,removal of foreignbodies

3. Improvecirculation→oxygen

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Rods (coccobacilli)Genus Species Description Virulence factors &

PathogenesisEpidemiology Diseases Treatment

Nosocomial infections

Pseudomonas Aeruginosa Rods(coccobacilli)

Nonenterobactericacea

Non-fastidious(simplenutritionalneeds)

Ubiquitous innature

opportunistic,nosocomialpathogens

Obligateaerobiccapsulate

(mucoidpolysaccharide)glucoseoxidizer

4-42˚C

 Toxins:- exotoxins A- lipopolysaccharide

Enzymes:- protease- phospholipase C

Invasins:- elastase- hemolysins- cytotoxin- pyocyanin

Adhesins:- pili- alginate capsule-biofilm

Genetic attributes:- transduction, conjugation,

antimicrobial resistanceOpportunistic pathogen

Can infect almost all tissue

Systemic infections incompromised patients can be50% fatality rate

Survives in:- hydrotherapy baths- hot tubs- swimming pools

Can infect alltissues

oppertunisitcpathogen- systemicinfection incompromised

host → 50%fatality rate

Resistance:- high [] of salts andanti-septics

antibiotics:- piperacillin(ureidopenicillins) +tazobactam

(β -lactamaseinhibitors)

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Acinetobacter

akinetos =“unable tomove”

Bactrim = “rod”

Baumannii AerobicNon-motile

20-30˚C

- Attachment- persistence on surfaces- secretion of enzymes andtoxins

Enters via:- open wounds- catheters- breathing tubes- Fomites- contaminated parentralsolutions

pathogen amongstwounded soldiers

moist and dry conditions

normal flora of oropharynxof some hosts

colonizes:- skin, wounds, GIT, resp.tact

Resistance:- resistant toall availabledrugs fortherapy

Stenotrophomonas

stenos =“narrow”trophos = “whofeeds”

monas = “ aunit”

Maltophilia

malt + philos=“friend of malt”

Low virulenceOpportunistic pathogen

rarely a true pathogen on itsown

Colonizes fluids in hospitalsettings

1. Nosocomialpneumonia

2. Present inmany cysticfibrosispatients

Resistance:

- β lactams-aminoglycosides- inherent tocarbapenems

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BacilliGenus Species Description Virulence factors &

PathogenesisEpidemiology Diseases Treatment

Fastidious

Pasturella Multocida Fastidious Colonizes mucousmembranes, upper resp.tract and GIT of mammalsand birds

 Transmission:- bites and scratches

1. Localized infectionfrom scratch

2. resp. tract infection

3. Systemic disease(life threatening)- meningitis- bacteremia

Antibiotics:- penicillin

Legionella pneumophilia Ubiquitous

 Transmission:- inhalation of aerosols

1. Legionnaire’s disease=febrile disease(associated with fever)+ pneumonia +extrapulmonaryinvolvement

2. Pontiac fever =without pulmonaryinvolvement

3. Asymptomaticinfection 

Antibiotics:- quinolones(ciprofloxacin,ofloxacin)- macrolides

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Haemophilus Influenzae Capsulate(serotype B)non-motileCatalase +’veoxidase +’ve

Fastidious

Can be bacilli to coccobacilli→pleomorphic

Obligate human parasite

Capsule:- 6 serotypes- serotype B most common

enzymes:- IgA proteases

10% of upper respiratorytract flora

Growth = 5-10% CO2 

 Transmission:- repertory drops

entrance:- mucous membranes

Systemic:(encapsulated strains)- acute epiglottis- laryngotrachealinfection- cellulitis / arthritis- pneumonia- septicemia- conjunctivitis

local:(unencasulated – non

typable)- otitis media-sinusitis- pneumonia- bronchitis

Lab cultures:Requires- X factor →haemin/haematin(blood)

- V factor →NAD(nicotinamide-adeninedinucleotide)→ from S.aureus

β -lactamase inhibitor:

- clavulanic acid

adjunctive medication:- steroids

Resistance:- ampicillin (penicillin)vaccine:- HiB →serotype B

HACEK group

HaemophilusActinobacillus

CardiobateriumEikenellaKingella

aphrophilusactionomycet

em-comitanshominiscorrodenskingae

Fastidious Found in human oralcavity

1. endocarditis- long duration of symptoms→ largevegetations with

potential to embolise

2. Skin and soft tissueinfections

3. Eye →keratitis,corneal ulcers

Antibiotics:- penicillin

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Diarrhoeal pathogens

1. Ingestion of preformed toxins

- Clostridium botulinum- Clostridium perfringens

- Staphylococcus aureus- Bacillus cereus

Clinical:- Usually watery diarrhoea (water + electrolytes)

2. Toxins produced in the gut

- Vibrio cholerae- ETEC- Clostridium difficile

- Aeromonas sp.

Clinical:- Usually watery diarrhoea- Bacteria &/ toxins found in stool

3. Invasive bacteria

- salmonella- shigella- VTEC (aka →EHEC)- EIEC- Yersinia enterocolitica- Vibrio parahaemolyticus- Clostridium difficile

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Clinical:- dysentery / inflammatory diarrhoea- leukocytes (pus) & erythrocytes (blood) usually found in stool

4. adherent bacteria

- EPEC- EAEC

Clinical:- mucous diarrhoea

nosocomial infectionInfection Predisposing factorsCatheter-associated bacteruria Indwelling urinary catheterIntravenous line infection Central intravenous catheterUrosepsis Urinary tract instrumentation

Primary bacteremia Arterial monitoring devicesPseudobacteremia Contamination of blood during collection / processing of blood culture

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Anaerobic infection- Ubiquitous in nature and commensals of GIT- Weak pathogens ??- Produce toxins- Cause polymicrobial infections

Clinical:

- foul smelling discharge / odour- abscesses, necrotic tissue, gangrene- large quantity of gas production in tissue→creptitus (crackling & popping sounds/sensation under skin/joints)- black discolouration of tissue- sulphur granules- blood in exudate

situation suggestive:- bite wound infected- previous antimicrobial therapy- gram stained tissue yields organisms but no growth on culture

treatment- antimicrobial therapy- surgery → incision, drainage, debridement, removal of foreign bodies- improve circulation →oxygen