Microbiology (Unit 7)

Symbiotic Relationships

partnership/association b/w 2 species

3 types:

1. mutalism

2. commensalism

3. parasitism

Mutualism

= 2 species benefit from eo

• microbiome: all mo associated w certain species (resident/transient)

resident flora benefits:

• produce vitamins (ex. e.coli uses nutrients in intestine + makes vitamin K for us)

• competitive inhibition (uses all avaliable sites, competes for nutrients, prevents pathogen attachment)

• disruption of resident: susceptible to sec infections/colinization by pathogens

Resident vs. Transient Flora

part of human microbiome

• resident: mo constantly in/on our bodies (ex. intestines/skin)

• transient: mo temporarily found in/on our bodies

Commensalism

= 1 partner benefits while others unaffected

• resident flora

• ex. S. epidermidis → uses dead skin cells as nutrients (no benefit/cost for us)

Parasitism

= 1 partner benefits at expense of other partner

• ex. pathogens

Infection vs. Disease

• I: mo enters body w no change to health

• D: result of infection → change in health

Infection/Disease: Primary vs. Secondary

• P: occurs in host regardless of hosts resident flora/immune system (ex. cold/flu)

• S/oppurtunistic: occurs in situations that have alr compromised hosts defenses (ex. yeast infection, pneumonia)

Infection/Disease: Local vs. Systemic

• L: pathogen contained to sm location (1 system)

• S: pathogen spread throughout body (multiple systems)

sepsis = systemic (mo/toxins trigger inflam so severe that it damages more than infection)

Behaviour in Population

• communicable: infectious disease spread from person to person

• zoonotic: disease transmitted from non human host to humans

• non-communicable: infectious disease not spread from person to person (ex. acne)

Changes in State of Health

• sign: objective/measurable deviation from norm structure/func of host (ex. bp, # of mo cells, temp, rashes)

• symptom: subjective deviation from norm func of host + felt/ experienced by patient (ex. dizzy, pain, fatigue)

• syndrome: group of s/s characteristic of spec disease

• asymptomatic/subclinical: disease w no noticeable s/s

Severity of Disease

• acute: pathogenic changes occur over short period w full recovery after rapid onset (ex. flu)

• chronic: pathogenic changes occur over longer period w continued rep of causative pathogen (ex. liver inflam w hep B)

• latent: causative pathogen goes dormant for extended period wo active rep (ex. herpes simplex virus)

Analysis of Disease

morbidity: %/# of people w disease, includes

• prevelance: # of people w particular illness pop at a point in time

• incidence: # of new cases in period of time

mortality: %/# of people that died from disease

Frequency of Occurence

• sporadic: disease seen occasionally, wo geographical concentration (ex. tetanus)

• endemic: constantly present within spec geographical region (ex. cold)

• epidemic: lrger than expected # of cases in short time within a geographic region (ex. flu)

• pandemic: epidemic occurs on worldwide scale (ex. HIV)

Stages of a Disease (DIAGRAM!!)

1. incubation: after inital entry of pathogen into host

2. prodromal: patient feels gen s/s of illness (skip over quick)

3. illness: s/s most severe

4. decline: s/s begin to decrease (susceptible to secondary infections)

5. convalescence: recovery, pateint returns to norm

contagious at all stages

Etiology

• cause of disease, typically the causative organism (ex. S. aureus/measles virus)

• koch postulates help determine

4 Postulates

1. suspected pathogen must be found in every case of disease + not in healthy people

2. suspected pathogen can be isolated/grown in pure culture from diseased person

3. healthy test subject (susceptible) exposed to suspected pathogen + must devlop same s/s as diseased

4. pathogen isolated from 2nd person → identical to pathogen from 1st test subject

Exceptions to Kochs Postulates

1. resident flora → can be colonized w pathogens but not have s/s of disease

2. not all mo can be cultured (ex. viruses/some bacteria)

3. / 4

• ethical issues (esp human hosts) → deliberately infect humans

• everyone isnt equally susceptible (ex. immune system strength)

• some pathogens cause multiple diseases

Virulence & Infectious Dose

• pathogenicity: ability of microbial agent to cause disease

• virulence: degree to which organism can cause disease

• infectious dose: (aka ID50) # of pathogenic cells/virions needed to cause active infection in 50% of test pop

lower ID50 = smaller # of cells/virions needed

Infection Reservoir

= living org/nonliving site allows pathogen to rep/survive over long period of time

• humans: dont display symp = carriers

• animals = zoonoses

• nonliving sites: water, air, food

Contact Transmisson

= other humans

Direct:

• through kiss/touch/intercourse/droplet sprays (<1 meter)

• can include contact b/w mucus membranes + site specific

Indirect:

• use of inanimate objs called fomites that become contaminated

• ex. syringes, doorknob

Vehicle Transmission

= non living sites

• transmit pathogens through vehicles (ex. food/water) → poor sanitation

• transmit through air → aerosols= dust/fine particles travel >1 meter

Vectors Transmisson

= from animals (arthropod vectors + non)

• mechanical: animal carries pathogen from 1 host to another wo being infected

• biological: pathogen reproduces within biological vector that transmits pathogen from 1 host to another

Pathogenesis

progression of a disease

steps:

1. exposure

2. adhesion

3. invasion

4. infection

Pathogenesis: Exposure/Portal of Entry

first

1. skin (enters/causes infection of intact skin)

2. mucus mems (ex. resp/gi/urogenital tracts → most common)

3. parenteral (wound (cut/bite)/ invasive procedures (IV/surgery)

pathogens exit same way they enter

Pathogenesis: Adhesion

second

= microbes attach to host tissues/cells

• bacteria: fimbriae, capsule, biofilm, adhesins

• viruses: spikes, fibers

• helminths: hooks (round), oral suckers (flukes)

Pathogenesis: Invasion → Entry of Pathogen into Host Tissues/Cells

third

• endocytosis (cells forced to uptake pathogen → through production of invasins)

• phagocytosis (wbcs consume pathogens → pathogens take over + rep inside phagocytes)

Pathogenesis: Invasion → Mechs to Evade Host Defenses

third

• capsule/M proteins/mycolic acid = evade phagocytosis

• Ig proteases = prevent ab-mediated killing

• coagulase = trigger clot formation (bacteria hide)

• kinases = dissolve clots (bacteria escape)

• antigenic variation = alteration of surface proteins (no longer recognizable)

Pathogenesis: Infection → Production of Exoenzymes

• glycohydrolases (degrade CT by seperating cells, allow pathogens deeper in body ex. hyaluronidase)

• nucleases (degrade DNA webs, by neutrophils, leave cell + spread to other tissues)

• phospholipases (degrade cell mems → lysis of target cell)

• proteases (digest proteins → AA, allows pathogen deeper in body)

Pathogenesis: Infection → Production of Toxins

• toxin: produced by mo that can harm cells/tissues or trigger damaging immune responses

• toxingenicity: ability to produce toxins

• toxemia: toxins in blood

Endotoxins

• production: produced inside bacteria as part of metabolism + secreted out of cell

• molecule: protein (often enzymes) → destroyed by heat

• bacteria: mainly gram pos (some neg)

• amount needed to be toxic: smaller

• effects: spec

Exotoxins

• production: part of outer mem of cell wall (lipid A- part of LPS), released during lysis/multiplication

• molecule: lipid → not destroyed by heat

• bacteria: gram neg

• amount needed to be toxic: larger

• effects: non-spec

Exotoxins Examples

• A-B: active + binding components (ex. tetanus/cholera toxin)

• cytolytic: leads to lysis of host cell (ex. C. difficile toxin + S. pyogenes → hemolysin)

• superantigens: intense immune respones → sudden release of toxins (ex. TSS toxin)

Endotoxins Examples

• all endotoxins lead to same gen symps → fever, muscle ache, nausea (varried severity)

• ex. EHEC, N. meninigitidis

(treating w antibiotics (kill/lyse bacteria)→ cause ↑ endotoxin release)

Epidemiology

= study of geographical location, timing, occurance, transmission of diseases

studies used: observational & experimental

Observational Studies

= info gathered, subjects not manipulated, 2 types

• descriptive: gather info about disease outbreak → form inital hypothesis (interview patients, examin samples/med records)

• analytical: select spec groups → form stronger hypothesis about cause of outbreak

Experimental Studies

• evaluate hypothesis → study connection b/w disease + possible causes/treatments

• subjs manipulated through clinical studies (efficacy of drugs, dietary items. phys exercise)

• use double blind to ↓ bias

Healthcare Associated Infections (HAI)

infection aquired at healthcare facility (not cause of visit)

Top 3 HAI (Most to Least Common)

1. surgical site infection (S. aureus, S. epidermidis) & pneumonia (ex. S. pneumoniae)

2. urinary tract infections (E.coli, S. epidermidis, S. aureus)

3. prim bloodstream infections (S. aureus, S.epidermidis)

Factors Leading to Infections in Healthcare Settings

1. ↑ prevelance of pathogens

• sick patients can carry, lrg variety of pathogens

2. weak immune system

• immunocompromised cuz of illness, meds, invasive procedures allow pathogen entry

3. chain of transmission

• people are direct link / fomites indirectly transmit pathogens

Universal Precautions

= aka infection control procedure → treat all blood/body fluids as potentially infectious to ↓ transmisson

relating to 3 factors leading to HAI:

• factor 1: isolate sick people

• factor 2: isolate immunocompromised patients, aseptic tech + cleaning during invasive procedures

• factor 3: handwashing (prevent transmission), appropriate levels of cleaning for fomites

(wear personal protective equipment to help all 3 factors)