Chapter 15: Mechanisms of Pathogenicity Flashcards
Disease
Any condition in which the normal structure or function of the body is damaged or imparied
Infection
A successful colonization of the hoast by a microorganism
Infectious disease
Any disease directly caused by the effect of a pathogen
Pathogen
May be a bactureium, virus, fungi or yeast, viroid, prion
single celled organisms (not parasites) or a cellular
Fungal infections
not in temperate climates
require humid/ moist conditions
if aquaired can be very serious
systemic infeciton with antifungals can still be upwards of 40% mortality
superfical infection
skin and mucus layers
systemic infeciton
all throughout the body
Viroid
tiny virus without a capsid
mainly attack plants and single celled organisms
dont really attack humans
Communicalble disease
capable of being spread from person to person
non-communicable disease
not capable of being spread from person to person
usually from the environment ot a host
(a bacterium like vibrio vulnificans entering a cut from the soil)
Contagious disease
a disease easily spread from person to person
an infectious disease
Zoonotic disease
A disease pread between a non-human host to a human host
animal to human
(not usually insects, those are usually refered to as vectors), but his can be the case?
Perioids of disease
incubation
prodromal
illness
decline
convalescence
incubation
after colonization but not enough pathogens to cause signs and symptoms
prodromal
start of signs and symptoms, not definitive or diagnostic
illness
signs and symptoms are most severe and obvious or diagnostic
Decline
decrease in the number of pathogens in the body, decrease in severity of signs and symptoms
Convalescence
return to normal function (health), may be long term or permanent damage
Acute disease
fast progression through the periods, hours to days
Chronic disease
slow progression through the periods, weeks to months
Latent disease
pathogen becomes dormant, ro replication, usually no cultavatable pathogens in blood or other samples
may be life long
Molecular kochs postulates
revision of kochs postualtes to demonstrate that a single gene is responsible for pathogenicity
virulence factors???
the pathogenic phenotype should be associated only with pathogenic strains
Inactive (mutate, delete) the gene suspected of encoding the virulence factor, this should reduce pathogenicity
replace the inactivated gene with a functional copy, this should restore pathogenicity
Why are some strains for a species pathogenic while others are not
Molecular kochs postulates
In Gram-negative bacteria, this is often due to the presence of a gene in pathogenic staisn abstent in non-pathogenic strains
virulence factors???
Pathogenicity
the ability of a microorganism to cause disease
should be a yes/ no definition
Virulence
The degree to which a microorganism can cause disease
variable from avirulent (not pathogenic) to hihghly virulent
Infectious does (median) ID50
the number of pathogens required to cause infection in 50% of test subjects
Lethal dose (median) LD50
the number of pathogens required to kill 50% of test subjects
fig 15.5 x-axis (dose) is in a logarithmic scale
Primary pathogen
a pathogen which can cause disease regardless of the state of the immune system of the host
Opportunistic pathogen
can only infect a damaged or immuno-compromised host
5 stages of pathogenesis
exposure
adhesion
invasion
infeciton
transmission
Exposure
some type of physical contact with the pathogen, not necessarily the start on an infection
not every exposure results in infection, but every infection comes from exposure
Adhesion
some mechanism by which the pathogen sticks to cells of the body or to mucosal membranes
portals of entry
skin (damaged)
mucosal membranes
parenteral - through the skin or mucosus membbranes
adhesins on pathogen stick to receptors on host cells
Invasion
pathogen spreads throughout tissue locally or throughout the whole body, usually through the bloodstream
can produce factors whcih aid in invasion (proteaases, lipases, toxins)
=> morphology = membrane ruffling to induce its self to be phagocytosed
salmonella and lysteria
some bacteral and all viral pathogens enter inside cells by endocytosis, some bacteria are ingested by host phagocytes and reproduce inside these cells
Infection
pathogens reproduces in or on the host
local infection is in a small part of the host
pretty much the same thing for a fungal infection
systemic infection is when the pathogen spreads throughout the body (blood stream)
secondary infection is when a second different pathogen infects a host after disease caused by the first pathogen
= example = influenza increases the risk of streptococcus pneumonia secondary infections which cause death
Transmission
for a disease to reamin in a host population it must spread from the infected host to a new one
may leave by the original portal on entry or a new route
= fecal oral route or really the oral fecal route
= most airborne diseases enter and leave through the respiratory tract
Virulence factors of bacteria and viruses
virulence factors are individual properties or mechanisms which allow pathogenicity and increase virulence
a product of a single or a couple of genes
sometimes, cumulative effect of bacteria leads to virulence.
best example is a toxin is produced that causes the symptoms of a disease
adhesion
pathogens need a mechanism to stick to hosts
A virulence factor
often is specific to a host species or type of cell = trophism = species specificity, is also tissue specificity
mediated by specific molecules both on the host and the pathogen
Exozymes
Type of virulence factor
are soluable, not toxins, are protiens
are SECREATED enzymes which damage the host, increase the spread of the pathogen or increase it’s survival
proteses hydrolyse the protein which connect cells into tissue, destroy antibodies, kill cells
killing cells allows an entry point, also releases nutrients (like the iron from haemolysis)
(phospho)lipases damage membranes and kill cells
nucleases breakdown DNA which can trap cells (puss) (NETosis)
Toxins
type of virulence factors
protiens or not
often enzymes, sometimes not
compounds which damage the host and usually kill host cells
the production of toxins is called toxigenicity
Portal of entry
how the pathogen gets into you
nose, mouth, cuts or abbression
skin is only a portal of entry unless it is damaged (except fungi)
mucosal membranes are the major point on entry
disease symtpoms and outcomes depend on the portal of entry
Parenteral
going through the skin
(or sometimes a mucus membrane)
usually from injetions, Or insect bites
skin damage
Adhesions
used by the pathogen to stick to receptors on host cells
sometimes just refered to as a receptor? but more specific?
endotoxins
not enzymes
ex= LPS, lipid A which is very toxin
= induction of fever, and septic shock
ex= fragmented peptidoglycan induces fever and inflammation (not as toxic as lipid a)
Exotoxins
are protein toxins with enzymatic activity
may cause all the symptoms of the disease such as tetanus toxin in tetanus
(see table 15.10)
AB toxins have two different proteins, A for binding to a host receptor and B which is the actual toxin
(See enzymology notes)
superantigen
are proteins which cause an excessive stimulaiton of immune system cells which can damage the host
causes toxic shock syndrome = low blood pressure, shock, organ failure death
lots of cytokines
Virulence factors for immune evasion
in mammals the immune system detects and kills or removes pathogens
many bacterial and viral pathogens have evolved mostly protiens (exozymes) whihc interfere or suppress the immune system
capsules inhibit phagocytosis by mactophages (polysaccharides) = streptococcus pneumonia
=> these interfere or suppress the immune system
produce catalase to break down hydrogen peroxide
protein A and G bind antibodies (non-catalytic inactivaiton of antibodies)
M protiens prevents complement activaiton (and thus the complement cascade, MAC attack)
many viruses down regulate interferon production
antigenic variation many many O antigens in salmonella and e. coli. Or phase variatiohn in lyseria
