Infection, macroorganism defence and first epizootiological factor Flashcards
what is infection
active or passive invasion, colonisation and replication of a pathogen in human, animal or plant
what is an infectious disease
disease resulting from infection
infection in which infected macro organism organ function or health in general is impaired
infectivity
ability of pathogen to invade, recognise cell receptors multiply and spread inside of a host
communicable disease
an infectious disease transmitted from one individual to another, either by direct contact or indirectly by vectors or fomites
contagious disease
communicable disease transmitted by direct contact
infectious disease when it is easily transmitted by contact with an ill animal or their secretions (eg influenza)
conditions in which infections take place
natural or experimental
extent of infection
general or focal
mono infection
infection with a single kind of organism
mixed/polyinfection
infection of an organ or tissue by more than 1 micro-organism
primary infection
primary pathogens cause disease as a result of their presence or activity within the normal, healthy host.
secondary infection
infection by a micro-organism following an infection by another microorganism (primary infection)
opportunistic infection
opportunistic pathogens can cause an infectious disease in a host with depressed resistance or if they have unusual access to inside of the body
recurrent infection
too great in number, too severe or too long lasting
reinfection
an additional infection, with the same micro-organism, occurring after the first infection has resolved
relapse
a second episode of a disease due to reemergence of original infection
superinfection
an additional infection, with the same microorganism, occurring during the course of an existing infection
exogenous microbes
organisms fom outside the body
endogenous microbes
organisms from inside the body
auto infection
infection with bacteria or virus that persist on or in the body (saprophytes)
nosocomial
infection acquired in a health care facility, during a hospital stay
iatrogenic infection
infection after medical or surgical management, whether or not the patient was hospitalised
subclinical infection
infection that is nearly or completely asymptomatic
latent infection
an infection that is inactive or dormant
parasitic infection
one benefits at the extent of another
commensalism
one benefits but causes no harm
symbiotic infection
both benefit - eg gut microflora
balanced pathogenicity
microorganism causes smallest amount of damage compatible with the need to enter, multiply and be discharged from the body
why are some infections still lethal?
virulent variants emerged
not enough time to adapt
introduction to new population
host is irrelevant to survival
stages of infection
exposure (contact)
adhesion (colonisation)
invasion
multiplication
exit
portal of entry
anatomic site through which pathogens can pass in to host tissue
most vulnerable portals of entry
GI and respiratory tracts
adhesion
capability of pathogenic microbes to attach to cells of the body using adhesion factors. different pathogens use various mechanisms to adhere to cells
what do microbes attach to cells with
protein or carbs called adhesions are found on fimbriae and flagella of bacteria and capsid or membranes of viruses. they bind to specific glycoprotein receptors
invasion
dissemination of a pathogen throughout local tissues or body
what helps invasion
exoenzymes or toxins = virulence factors that allow them to colonise and damage host tissues as they spread deeper in to the body
how do intracellular pathogens invade
enter host cells and reproduce
portal of exit
a way for pathogen to transmit to new host in order to persist
Kochs postulates
1 - suspected causative agent must be absent from all healthy organisms but present in all diseased organisms
2 - the causative agent must be isolated from the diseased organism and grown in pure culture
3 - the cultured agent must cause the same disease when inoculated in to a heathy susceptible organism
4 - the same causative agent must then be reisolated from the inoculated diseased organism
kochs postulates are wrong because
- assume that pathogen are only found in diseased, not healthy individuals (doesn’t consider asymptomatic)
- 1 pathogen can cause several disease conditions and 1 disease condition can be caused by several different microorganisms
- not all healthy test subjects are equally susceptible to disease
- all pathogens can be grown in pure culture and that animals are reliable models for human disease
molecular kochs postulates
- phenotype of disease should be associated only with pathogenic strains of a species
- inactivation of suspected genes associated with pathogenicity should result in a measurable loss of pathogenicity
- reversion of the inactive genes should restore the disease phenotype
vogralink chain
virulence and infective dose
source of infection
mode of transmission
portal of entry
host susceptibility
pathogenicity
the ability of an organism to cause disease
virulence
the degree of pathogenicity caused by the organism
virulence influence by
dose, route of infection, species, age, gender, susceptibility of host and environmental factors
pathogenicity v virulence
pathogenicity for a given host and pathogen is absolute
virulence is variable
pathogenicity is all or none - it is either pathogenic or not
pathogenicity is applied to groups or species whereas virulence is intended for within group or species comparisons
virulence can be measured by
mean time to death
mean time to appearance of symptoms
measurement of fever, weight loss etc
measurement of pathological lesions etc
important indicators of virulence
measured using controlled experiments with lab animals
median infective dose
median lethal dose
virulence factors are
properties (gene products) that enable a microorganism to establish itself on or within a host of a particular species and enhance its potential to cause disease
virulence factors help to
invade the hots
evade the host defences
multiply
exit
cause disease
bacterial virulence factors
- adherence components - colonise mucosal sites by using pili to adhere to cells
- capsules - protect from opsonization and phagocytosis
- invasion enzymes - exoenzymes all them to invade cells and deeper tissues
- toxins - exo or endotoxins
toxigenicity
ability of pathogen to produce toxins
examples of exoenzymes
hyaluronidase breaks down polysaccharide that glues host cells together
collagenase
fibrinolytic enzymes (streptokinase) destroys fibrin of blood clots so they escape
coagulase promotes blood clotting - protection
nucleases, lipases etc
exotoxins
small toxins that are released in to cell surroundings (extracellular toxins)
produced by bacteria during infection or directly ingested eg contaminated food
3 types of exotoxins
cytolytic
superantigens
A-B toxins
cytolytic toxins
lead to cell lysis
affect cell membrane by forming pores or disrupting the phospholipid bilayer
hemolysins
lecithinase and phospholipase - degrade phospholipids
leukocidins - kill WBC
superantigens
exotoxins that trigger an excessive, non specific stimulation of immune cells to secrete cytokines.
for example the toxic shock syndrome toxin from S.aureus
A-B toxins
2 components (initially linked together). one binds to the host receptor, the other enters and damages the cell
Diphtheria toxin
Tetanus toxin
Botulinum toxin
cholera toxin
cholera B fragment activates adenylate cyclase, increasing the concentration of cAMP and stimulating the secretion of Na and HCO3 - leads to massive water loss through diarrhoea which can be fatal
tetanus toxin
binds to motor neurons, blocks glycine-stimulated relaxation and leads to spastic paralysis
botulinum toxin
most toxic substance known - found in improperly canned food
binds to presynaptic motor neurons, prevents release of acetylcholine and leads to flaccid paralysis
endotoxins
lipopolysaccharide found on the outer membrane of gram negative bacteria
released when cell dies or when bacteria undergo binary fission
lipid component (lipid A) is responsible for toxic properties
lipid A triggers the immune systems inflammatory response
they are not destroyed by heat
viral virulence factors
1 - viral replication
2 - invasivenes ( adhesion)
3 - tropism
4 - modify the host defuse mechanism
how do viruses modify host defence mechanism
virokines - not required for viral replication but influence viral pathogenesis by inhibiting the body’s immune response
enable virus to spread in host
intrinsic cell killing effects
types of virokines
inhibitors of T cel cytotoxicity
inhibitors of cytokine s
inhibitors of complement system
inhibitors of antibody mediated cytolysis
cytokine mimics
