Microbial pathogenicity

Viral pathogenesis

process by which viral infection leads to disease

Primary replication of viral infection

virus replicates after initial host entry, determines if infection will be localized of systemic

Systemic spread of viral infection

virus spread via bloodstream + CNS

Secondary replication of viral infection

@ susceptible organs/tissue after systemic spread

cytolytic vs non-cytolytic productive infection (virus-cell interaction)

cytolytic - hot cell is permissive
non-cytolytic - leads to persistent infection

abortive/non-productive infection

virus doesn't complete replication cycle, cells non-permissive

Direct cell damage and death from viral infection may result from

cell energy diversion, shutoff of cell synthesis, competition of viral mRNA for ribosomes or for viral promoters + transcriptional enhancers

Indirect cell damage from viral infection can result from

viral genome integration, intro of mutations in host, inflammation, host immune response

What happens if virus enters cell but not produced/virus within cell as DNA

either cell remains normal or malignant transformation

Viral latency

virus is present in the form of its genome only and there is little (mRNA, not at protein level) or no expression of viral genes, common in DNA viruses

Viral persistence

virus replicates continuously in the body at a very low level (ex HIV)

Latent infection

patient recovers from initial infection but virus persists + infection may recur

Chronic infection

virus detectable for long time

Slow virus infection

prolonged period bw initial infection + appearance of disease (ex prions)

Stages of viral infection

incubation
prodromal
specific-illness
recovery

specific receptors, genetic constitution, age and physio states, and nutritional factors are all

Host factors related to virus infection

attenuated viruse

virus that lost virulence (ability to cause disease)

the signs and symptoms of a viral disease result from:

cell killing (from viral replication), loss of fnx
cell damage (from immune response)

cellular immunity plays the major role in _____________ whereas humoral immunity protects against ________

clearing virus infection
reinfection

horizontal transmittion

person to person, direct (secretions), indirect (contaminated food), blood

vertical transmission

perinatal, transplacental, @ delivery or during breastfeeding

Role of macrophages in systematic infections

they can either inactivate virus OR virus multiplies inside macrophage (HIV)

Tropism

range of host cells that can be infected by virus

Adherence/attachment

bacteria binds to surface of target cell

Dissemination/invasion

bacteria spreads from origin site to whole organism

Etiologic agent

the microorganism that causes the disease

Inapparent infection

infection in host w/o symptoms/signs, fxn not affected, mobilized immune system

Endogenous vs exogenous infection

endo - infectious agent already in body + was dormant
exo - bacteria outside body, found host

Bacterial infection pathogenesis

incubation
prodromal
acute (replication)
convalescence

Bacteria are pathogenic by

adherence to substrate, invasion, toxigenesis and ability to evade immune response

Infectious process of bacteria

1. Entry
2. Adherence
3. Bacterial multiplication
4. Dissemination
5. Elimination

Mechanisms of defense of respiratory tract

mucus and cilia (mechanically), IgA, macrophages and phagocytes in deep mucosal layer

Mechanisms of defense of GI tract

- gastric acid + intestinal pH
- proteolytic enzymes
- biliary salts
- mucus rich in IgA

Mechanisms of defense of genito-urinary tract

cervical mucus and vaginal pH

Mechanisms of defense of skin/mucosa

lipolysis of sebum (acidic)

Adherence step of infectious process of bacteria

adherence to epithelial cells, uses binding molecules, specific receptors and electric charge on cell surface

Bacteremia vs septicemia

*bacteremia*= bacteria present in the blood

*septicimia*= bacteria GROWING in the blood

the virulence factors that condition a bacterial strain virulence are

rate of multiplication and capacity of invasion

pili (somatic virulence factor)

adhesion fimbria

lectins (somatic virulence factor)

proteins that bind carbs

ligands (somatic virulence factor)

molecules that make specific binds w/ substrate

slime (somatic virulence factor)

substance around bacteria, mediates its non-specific attachment

capsule (somatic virulence factor)

role in antiphagocytosis and sometimes adherence

Vi surface antigen are for (somatic virulence factor)

gram - rods

coagulase (soluble virulence factor)

free or bound, in S.aureus

leucocidin (soluble virulence factor)

made by S.aureus after phagocytosed

catalse (soluble virulence factor)

inactivates free O2 radicals

Bacteria can produce 2 kinds of toxins:

proteic/exotoxins and lipopolysaccharidic/endotoxic

cytotoxic exotoxins act on

eukaryotic cell wall

AB toxins

type 3 - interfere w/ internal cell fxn
a - active
b - binding

what detach easily, have high molecular weight proteins, thermosensitive, antigens, decomposed by proteolytic enzymes?

exotoxins AB

_________ appear following disease or vaccine and can be transformed into _________

antitoxins, anatoxins

Endotoxins are produced by and reside in

gram - bacteria, ext cell wall

Endotoxins cannot be

transformed in anatoxins or decomposed by proteolytic enzymes

Which type of bacterial toxin is specific?

exotoxin

Endotoxins act by

stimulating cytokine release from macrophages