lesson 1 Flashcards
determinants that would influence the outcome of an interaction
host immune system and pathogens’ virulence factors
the disturbance in the state of health wherein the body cannot carry its normal function
disease
refers to the multiplication of the parasite within the host body
infection
means the organism is present on the surface of the skin and mucous membranes
contamination
one that harbors parasite
host
one that benefits from the symbiotic relationship and harms the host
parasite
the capacity of the pathogen to produce disease
pathogenicity
pathogenicity of an organism depends on ___
its ability to evade the defense mechanism of the host
intensity of the disease produced by the pathogens or the degree of pathogenicity
virulence
factors that are produced by a microorganism and evoke disease
virulence factors
virulence factors help bacteria to
- invade host
- cause disease
- evade host defenses
examples of virulence factors
bacterial toxins and enzymes
type of barriers of immune system
physical
innate
specific
progression of an infectious disease
incubation
prodromal
invasisve
decline
convalescent
period of time beginning with the initial infection through to the point where individual presents clinical signs.
incubation phase
The agent localized and begun to multiply; asymptomatic but capable of transmitting the disease agent to others
incubation phase
- short and present non- specific mild signs. e.g. redness and swelling, depression and anorexia.
prodromal phase
characteristic of a particular disease are apparent
invasive phase
signs are at greatest intensity; when pathogen has invaded and damaged host tissues
acme
what phasse is acme present
invasive
examples of invasive phase
cough, fever, swollen lymph nodes, vomiting, diarrhea
characterized by decline in signs associated with the disease
decline phase
secondary infection may occur this time as the immune system has been compromised during the interaction with the original pathogen
decline phase
host begins to repair the damage caused by the presence of pathogen, and the host recovers.
convalescent phase
This phase may be infectious if the disease is associated with scab or accessible lesions.
convalescent phase
major virulence factors are
adhesins, capsules and toxins
help the bacterium bind to intestinal epithelium,
adhesins
2 classification of toxins based on how they are released
exotoxins and endotoxins
differentiate endotoxins from exotoxins
exotoxins are soluble substances released in the host tissues while endotoxines are part of the bacterial wall and released when the bacterium dies or divide
organisms producing endotoxins and exotoxins
gram negative-endo
gram positive- exo
location of exotoxins in cells
extracellular, excreted into the medium
location of endotoxins in cells
bound within bacterial cell wall. released upon its death
chemical nature of exotoxins and endotoxins
exo- polypeptides
endo- lipopolysaccharide complex
exo and endo stability
exo- unstable(can be natured at 60 C by UV light)
endo- relatively stable(can withsatance several hours above 60 C)
toxicity of endo and exo
exo-among the most powerful toxins
endo- weak but can be fatal in large doses
100-1million times as strong as strychnine
exotoxins
capsules are prevents phagocytosis
capsules
elaboration result to various damaging effects to the host.
toxins
exotoxins effect on tissue
highly specific. some act as a neuurotoxins or cardiac muscle toxins
fever production exo and end
exo-little or no fever
endo- rapid rise in temp to high fever
endotoxins effect on tissue
nonspecific. ache all over systemic effects or local site reactions
antigenicity of endo and exo
exo- strong. stimulates antibody production and immunity
endo- weak. recovery from disease often does not produce immunity
toxoid conversion and use endo exo
exo- by treatment with heat or chemicals. toxoid to immunize against toxins
endo- cannot be converted to toxoid. cannot be used to immunize
examples of exotoxins
botulism, gas gangrene, tetanus, diphtheria
endotoxins examples
salmonellosis, tularemia, endotoxic shock
the disease triad
host
pathogen
environment
events in all infectious disease
encounter
entry and colonization
evading host defenses
multiplication
damage
where agents meet the host
encounter
after attachments to receptors of host cells by means of specific adhesion molecules present on its surface
entry and colonization
proteins that promote tighter binding of bacteria to host cells following initial binding bia pilii
adhesins
promotes attachment in small intestine
pili-K88/K99 of e coli
mechanisms that destroy host defenses
evading host defense
examples of evading host defense
production of extracellular matrices
imactivation of cell responses
interference with the humoral immune responses
ability of organism to invoke deleterious effects
damage
how does bacteria damage cells
through toxin production and direct cell and cellular function damage
