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Ways microbes can get into the body
skin, GI tract, upper respiratory tract, urogenital tract, placenta
portal specificity
most microbes have a preferred portal of entry
why are microbes attracted to humans as hosts?
nutrient rich, moist, stable pH, stable temp, lots of places to hang out
methods for microbes to get in through skin
breaks in skin, helminth digestive enzymes, insect vectors, needle injections
infectious dose
minimum number of microbes to cause disease
median infectious dose
number of microbes required to cause disease in 50% of inoculated animals
adhesion factors
used to bind receptor molecules on host cells to pathogens
types of adhesion factors
fimbriae, glycocalyx (biofilm), viral protein spikes, adhesive disks
how do cells avoid phagocytosis
capsules or coagulase
how do pathogens avoid host defenses?
avoid phagocytosis, camouflage, avoid immune cells by invading a cell
how do microbes damage host cells?
out-compete for nutrients, direct damage at entry site, toxins, disrupt immune response
siderophores
proteins that bind to iron and allow pathogens to out-compete host cells for iron
exotoxin
secreted proteins that target specific receptors on cells to cause damage
superantigens
trigger cytokine storm > toxic shock syndrome (S. aureus is an example)
endotoxin
consists of one lipopolysaccharide, only associated with Gram-negatives, general systemic effects
portals of exits
respiratory tract, GI tract, skin, urogenital tract, blood,
progress of an infection
getting in > adhesion > avoiding host defenses > disease caused by damage to host cell > disease transmission
exoenzymes
secreted enzymes that cause damage to host cells by breaking down tissues to allow deeper spread of bacteria
streptokinase
an exoenzyme that can cause flesh-eating disease. dissolves clots, so can also be used as a clot buster
pathology
study of disease
infection
successful invasion or colonization of a microbe within a host
microbial pathogenesis
the traits the microbe has that leads to the disease
normal microbiome
upper respiratory tract, GI tract, urogenical tract, skin
sterile body areas
nervous system, lower respiratory tract, cardiovascular ssytem
blood-brain barrier
endothelial cells, astrocytes, neurons
things that keep lower respiratory tract sterile
nasal hairs, mucous membranes, ciliary escalator, alveolar macrophages
holy trinity for nosocomial infections
microorganisms, compromised host, chain of transmission
incubation period
pathogens are multiplying but no signs or symptoms
prodromal period
pathogens still multiply, host begins to experience signs and symptoms and activation of immune system
period of illness
signs and symptoms of disease are most obvious and severe
period of convalescence
patient returns to normal functions
what does transmission of infection depend on?
the disease, pathogen, and mechanisms by which it develops and progresses
etiology
study of the causes of disease
etiologic agent
the pathogen or substance responsible for causing a particular disease
what is the purpose of Koch’s postulates
identify a microorganism as the cause of a specific infectious disease
reasons Koch’s postulates could not apply
opportunistic pathogens, varying immune system strengths, ethics for human exclusive diseases
epidemiology
science that studies when and where diseases occur and how they are transmitted
morbidity rate
number of people with the diesease/ number of all people
prevalence
number of people who are sick at a given time
incidence
number of new cases at a given time
mortality rate
number of deaths from a disease in a given population at a point in time
sporadic disease
occasionally without geographic concentration
endemic disease
constantly present in a population within a geographic region
common source spread
a single source for all infected
point source spread
common source for a short period of time
propagated spread
person to person, indirect or direct spread
3 types of reservoirs of infections
humans, animals, nonliving
passive carrier
not sick but can pick up and transmit disease
incubation carrier
active infection and spread to others during the incubation period
convalescent carrier
active infection and spread it to others during the convalescent periodc
chronic carriers
life-long infection and can spread disease throughout their life
asymptomatic
have an active infections but never show any signs or symptoms of disease
zoonosis
disease that occurs primarily in animals but can be transmitted to humans
two most common nonliving reservoirs
soil and water
fomite
a nonliving object that can transmit disease
mucociliary escalator
moves mucus away from lungs to stomach, coughed up, or sneezed out
intestinal tract lining
epithelial and mucus-secreting goblet cells
peristalsis
muscular contractions that help move mucus and other material through the GI tract
endothelia
epithelial cells that line the blood vessels, lymphatic vessels, and other tissues.
microbiome prevents pathogen attachment how
occupying binding sites and competing for nutrients
lysozyme
breaks down peptidoglycan
antimicrobial peptides
nonspecific antimicrobials secreted by skin, epithelial cells, immune cells
ion binding proteins
chemically bind and sequester iron, starves microbes
complement system
complement immune cells in destroying bacteria, connects innate and adaptive immunity
opsonization
sugar coating for phagocytic cell to come destroy it more easily
3 complement system mechanisms
opsonization, initiate inflammation, promot cytolysis
cytokines
proteins that are communication signals between cells
3 types of phagocyte white blood cells
neutrophils, dendritic cells, monocytes/macrophages
inflammatory response
vasodilation, redness, heat, increased BV permeability, swelling, pain, loss of function
diapedesis
when phagocytes squeeze between endothelial cells that line BV walls and into tissue during inflammation response
phases of phagocytosis
chemotaxis, adherence, ingestion, formation of a phagosome, formation of a phagolysosome, digestion, discharge
pyrogens
chemical that cause the hypothalamus to turn up the body temp by releasing prostaglandins.
humoral immunity
B cells release antibodies to fight pathogens in the blood
cell-mediated immunity
T-cells destroy cells that have been infected with pathogens inside them
epitope
portion of antigens that antibodies and T-cells can recognize and attach to
IgG
most abundant, can cross placenta
IgM
must stay in blood, not tissue. first in primary response
IgA
mucous membranes, dimer
IgD
b-cell receptor
IgE
allergic reactions
agglutination
cross-linking pathogens by antibodies, creating large aggregates, IgM
antibody titer
amount of a specific antibody to a specific epitope in the blood
inactivated vaccine
dead or inactive organism with heat or chemicals or radiation
attenuated vaccine
microbe is alive but reduced virulence
sub-unit vaccine
uses only a part of the microbe like its DNA or viral capsid
toxoid
toxin that has been inactivated by chemical treatment or mutations
anti-toxin
antibodies from another host/animal, purified, and administered to a patient who already has the disease
allergic reaction
secondary immune response to an allergen
hypersensitivity
unnecessary response/overreaction of the immune system
autoimmune disorder/disease
immune system recognizes its own tissues as foreign and attacks them.
type I
IgE, regular allergies
Type II
IgG and IgM, antibodiy-mediated cytotoxic, blood transfusions
Type III
IgG, immune complex formation, rheumatoid arthritis
Type IV
T-cell mediated cytotoxic, delayed. contact dermatitis, graft rejection
isohemagglutinins
naturally occuring IgM antibodies in plasma that can cross react with blood group antigens not present on one’s own RBCs.
allograft
person to person graft
isograft
identical twin graft
autograft
self tissue graft
xenograft
animal to human graft
Graft vs Host disease
transplanted tissue is capable of producing immune cells, recognizes the host as foreign and starts rejecting host cells, T-cells attack host cells