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170 Cards in this Set

  • Front
  • Back
pathology
study of disease
etiology
cause of disease
pathogenesis
manner in which disease develops
infection
invasion or colonization of the body by pathogenic mircobes
disease
any change from a state of health
abnormal state in which all or part of body isn't adjusted or is incapable of performing its normal functions
= occur without detectable disease
normal flora
organisms in or on the body that do not cause disease under normal conditions

certain locations in and on the body normally have microbial populations; other sites wont ( sterile)
transient flora
not permanent residents but may be present for several days, weeks, or months and then disappear
skin
restrict the growth of microorganisms

ex = Staphylococcus sp. S. aurues and S epidermidis
Corynebacterium sp
Proprionibacterium sp
Micrococcus sp
Candida sp
Eye ( conjunctiva)
continuation of skin and mucous membranes, therefore, will have similar organism

ex = S. epidermidis and S aureus
Corynebacterium sp
Proprionibacterium sp
Streptococcus sp
Micrococcus
nose and throat

nose
S. aureus
S. epidermidis
diptheroids
nose and throat

throat
S. aureus
S. epidermidis
Dipotheroids
Streptococcus pneumoniae
Haemophilus sp
Neisseria sp.
mouth

normal flora
Streptococcus sp
Lactobacillus
Neisseria sp
Haemophilus sp
Staphylococcus sp
Anareobes : Fusobacterium sp.
Veillonella sp
large intestine
coliforms : Escherichia coli
Citrobacter sp
Lactobacillus sp
Proteus sp
Klebsiella sp
Enterobacter sp
Enterococcus sp
Anaerobes : Fusobacterium sp
Genito-urinary systems

all mucous membranes having contact with outside
(continuation of the skin) will have normal flora

lower urethra of male and female
vagina
normal flora include: Skin organisms
Lactobacillus sp
Candida Sp
sterile sites
heart
liver
spleen
blood system
lymphatic system
all internal organs
microbial antagonism
microbial antagonism/competitive exclusion
competition among microbes
normal flora protect host against pathogens by:
competing for nutrients
producing harmful substances
affecting conditions such as pH and oxygen
symbiosis
relationship of 2 different organisms that live together
commensalism
one organism is benefitted, the other is unaffected
mutualism
both organisms are benefitted
parasitism
one organisms is benefitted and the other is harmed
opportunistic organisms
DO NOT cause disease in the healthy host
DOES cause disease in the immunocompromised
classification of disease
1. occurrence of a disease
2. severity or duration of disease
3. extent of host involvement
4. symptoms : subjective changes in the body function, as evidenced by patient
5. signs : objective, measurable changes, as evidenced by observer
communicable disease
disease that spreads from on host to another (either directly or indirectly)

contagious : spreads easily
non-communicable : infectious diseases that don't spread from person to person

contracted from environment or ourselves
occurrence of disease

1. incidence
2. prevalence
1. number of people in a population who develop a disease during a particular period of time (new cases)

2. the number of people who have a particular disease at a specified period of time ( new and old cases)
sporadic
occasional occurrence
endemic
occurs constantly in a population
epidemic
an increase in the incidence of a particular disease above the numbers normally seen
pandemic
am epidemic that occurs worldwide or across continents
acute disease
develops rapidly but lasts only a short time
chronic
develops more slowly, may be less severe, but is continuous or recurrent for a long time
subacute
intermediate to acute and chronic
latent
causative agent remains inactive for a long period of time and then reactivates and produces s/s
herd immunity
percent of population who are immune to a particular disease... if immune can't spread, can't get disease, can't spread disease to others...
local infection
limited to a small area of the body
systemic infection
organisms are spread throughout the body by the blood or lymphs
focal infection
a local infection is spread to a specific area and are combined there
septicemia
systemic infection due to organisms reproducing in the blood
bacteremia
presence of bacteria in the blood
toxemia
presence of toxins in the blood
viremia
presence of viruses in the blood
primary infection
an acute infection that causes the initial illness
secondary infection
a second organism causes an illness due to the host's weakened condition because of the primary infection
subclinical infection
infection in which no noticeable illness is seen
predisposing factors
gender
race
geographic location
nutritional status
age
occupation
immune status
development of disease
incubation period
prodromal period
period of illness
period of decline
period of convalescence
incubation period
time from initial exposure until first appearance of s/s

dependent on: organism
virulence/pathogenicity
resistance of host
prodromal period
doesn't occur in all diseases
occurs relatively short time

mild symptoms of general aches and malaise ( tiredness)
period of illness
period of time when the disease is most severe

pt exhibits s/s
one of 2 things happen:
treatment is successful and pt recovers
or isn't and pt dies
period of decline
s/s subside

pt begins to recover
this is the time in which pts are vulnerable to 2nd infections
period of convalescence
pt regains strength and body returns to the pre-diseased state

not necessarily healthy
reservoirs
are sources that provide the organism with adequate conditions for survival, multiplication, and an opportunity for transmission

can be: human, animal, non-living
human reservoirs
transmitted from person to person:
current active disease : s/s present
incubation or recovery : s/s not present
during a carrier state
transmitted directly or indirectly
animal reservoirs
disease occur primarily in animals (wild or domestic) and can be transmitted to people are called zoonoses

occur by many routes:
direct contact with infected animals
contact with waste products of animals
contamination of food and/or water
insect vectors
non-living reservoirs
soil harbors- fungi/bacterial spores
water can be contaminated with feces of humans or
other animals
contact transmission
direct
indirect
droplet
vehicle transmission
water
food
air
vectors
mechanical transmission
biological transmission
emerging infectious disease
new or changing
showing an increase in incidence in the recent past
shows the potential to increase in the future

ex: Anthrax-bioterrorism
Toxigenic E. coli non 0157:H7
Acinetobacter
Pandemic influenza
epidemiology
studies diseases occurring in populations, not individuals

investigates the underlying reason
what intervene or control will prevent the spread of disease
descriptive epidemiology
retrospective studies- looking back at what happened

prospective studies- choosing a group of disease and follow them forward to see if and when disease develops
analytical epidemiology
case control studies- look for factors that may have preceded the disease and see if cases differ from controls
experimental epidemiology
clinical trails
pathogenicity
the ability of a microorganisms to cause disease by overcoming the defenses of a host
virulence
the degree or extent of pathogenicity
portals of entry
3 primary routes of entry (or portals of entry)
mucous membranes
skin
parenteral

portal of entry and exit are often the same
mucous membranes
enter thru mucous membranes of resp tract or GI tract
esp if mucous membranes are damaged

EX : resp = influenza, TB, common cold
GI = polio, Hep. A, Shigella
GU = STDs- chlamydia, gonorrhea, syphilis
skin
unbroken skin is impenetrable to most microorganisms

some microbes have adapted to penetrate = syphillis
hookworm larvae
broken skin or routes thru hair follicles and sweat
gland ducts are common routes
some fungi actually infect the hair, skin or nails
parenteral routes
directly deposited into tissues beneath skin or mucous membranes

punctures (incl needlesticks), inj., bites, cuts, wounds, surgery, etc.

ex= tetanus, gangrene, Hep B&C and HIV via sticks
infectious dose
number of organisms needed to cause disease

chance of disease occurring is dependent on the number of microbe the host is exposed to

dependent on microbe and virulence of pathogen
attachment
adherence or adhesion is required in pathogenicity
adhesins or ligands
on the pathogen bind to complementary receptors on the host's cell surface
pathogens penetrate host defenses
aka virulence factors
capsules
cell wall components
enzymes
antigenic variation
penetration into the cytoskeleton
capsules
impair phagocytosis- ability of certain host cells to engulf and destroy microbes

ex : Streptococcus pneumoniae
Klebsiella pneumoniae
Haemophilus influenzae
Bacillus anthracis
cell wall components
chemical substances in the cell wall which contribute to virulence

ex = Streptococcus pyogenes- M protein that mediates attachment to host epithelial cells and helps resist phagocytosis
Mycobacterium tuberculosis - waxy substance in the cell wall that resists digestion by phagocytes
enzymes

coagulases
clot production, walls off the bacteria and prevents phagocytosis and isolates the microbe from other host defenses
enzymes

kinases
break down clots , and allow invasion into the tissues
enzymes

collagenase
breaks down collagen, allowing spread of the organisms
antigenic variation
ability of an organism to alter surface antigens so that antibodies against that organism are no longer effective

ex = influenza virus
Neisseria gonorrhoeae
penetration of the cytoskeleton
penetration into the host cell or the ability to move through and between host cells
exotoxins
produced within bacteria and secreted to the outside
( most often Gram + organisms)

1.easily diffused into blood and rapidly transported
2.harmful in small amounts
3.function by destroying host's cells or inhibiting metabolic functions
4. diseases caused by exotoxins are caused by toxins not the bacteria
5. disease-specific s/s
6. body produces antibodies to toxins = anitoxins
exotoxins

botulism
neurotoxin- prevents transmission of nerve impulses resulting in flaccid paralysis
exotoxin

tetanus
neurotoxin- blocks nerve impulses to muscle relaxation resulting in uncontrollable muscle contractions
exotoxin

staph food poisoning
enterotoxin- secretion of fluids and electrolytes resulting in diarrhea
exotoxin

diphtheria
cytotoxin- inhibits protein synthesis
endotoxins
part of the outer cell walls of gram - bacteria

released when gram - bacteria die, lysing cell walls, releasing endotoxin

work by stimulating macrophages to release cytokines which are toxic at high levels

endotoxins do not promote effective antitoxin formation

produce the same s/s regardless of the microbe
endotoxins
s/s : chills, fever, weakness, generalized aches, sometimes shock and death

can also activate blood clotting proteins resulting in DIC ( disseminated intravascular coagulation)
endotoxins

shock
shock = any life-threatening decrease in blood pressure
endotoxins

septic shock
caused by bacteria
endotoxins

endotoxins shock
caused by gram - bacteria
portals of exit
microbes leave the body via SPECIFIC ROUTES

ex: secretions, excretions, discharges or tissues that have been shed

are related to infected part of body

most common are resp and GI, but also GU, skin, and wound infections, and blood
Immunity
ability to ward off disease caused by microbes or their products and to protect against environmental agents
immunity defenses designed to :
keep microorganisms out
remove microbes if they do get in
combat them if they remain inside
susceptibility
lack of immunity
nonspecific or innate immunity
defenses present at birth
always present
respond rapidly to protect against disease
acts against all microbes in same way
does not involve specific recognition or memory
lines of defense
1. skin and mucous membrane
2. phagocytosis, inflammation, fever, and other antimicrobial substances or cells
3. specialized cells and antibody production
defense

skin and mucous membrane
physical factors : barriers to entry or processes that remove microbes

chemical factors : substances made by the body that inhibit microbial growth or that destroy microbes
chemical

sebum
an oily substance produced in the sebaceous gland

prevents hair from drying
protective film on the skin
one of its components are fatty acids which keep pH of skin low (3-5)
chemical factors

perspiration
produced by sweat glands

helps maintain body temp
eliminates certain wastes
flushes microbes from surface the skin
contains lysozyme- an enzyme that can break down bacterial cell walls
chemical factors

gastric juices
produced by glands in stomach
consists of HCL, enzymes and mucus
very high acidity (pH 1.2-3) destroys bacteria and most bacterial toxins
phagocytosis
blood
formed elements : erythrocytes, leukocytes, thrombocytes

liquid components: serum w/o clotting factors
plasma with clotting factors
leukocytosis
increase in WBC
leukopenia
decrease in WBC
granulocytes
presence of granules in the cytoplasma

neutrophils are phagocytes
monocytes
become macrophages after leaving circulating blood (into tissues). are phagocytes
lymphocytes
active in specific immunity
phagocytes
cells that can ingest microbes

are activated by components in or on the bacteria
mechanism of phagocytosis
1. chemotaxis
2. adherence
3. ingestion
a. formation of phagosome
4. digestion
a. fusion with lysosome to form phagolysosome
b. residual body of indigestible materials
5. discharge of waste materials
inflammation
tissue damage that triggers this defensive response

causes: microbial infection, heat, electricity, sharp objects or chemicals

4 signs: redness, pain, heat, and swelling
loss of function depending on site and extent of damage
functions of inflammation
1.to destroy the agent and remove by-products from the body
2. if destruction is not possible : limit the effects by confining or walling it off
3. repair or replace tissue damaged
stages of inflammation
1. vasodilation and increased permeablility of blood vessels
2. phagocytic migration and phagocytosis
3. tissue repair
fever
elevated high body temp produced in response to a bacterial or viral infection
1. fever is considered a defense against disease
speeds up body's reactions
complications : dehydration, seizures, acidosis
complement system
causes cytolysis of microbes, promotes phagocytosis, contributes to inflammation
interferons
protects uninfected cells from viral infections
transferrins
inhibit growth of bacteria by reducing available iron
antimicrobial peptides
cause lysis of bacteria
natural killer cells
kill infected targets cells which are then phagocytized
adaptive or acquired immunity
develops during an individual's lifetime
3 important components :
1. specificity
2. memory
3. recognition
ANTIbody Generators
adaptive immunity

active
body produces antibody in response to an antigen
takes longer to develop, persists longer, involves memory
adaptive immunity

passive
body receives pre-formed antibody from another source
immediately available, short duration, no memory involved
adaptive immunity

natural
born with
adaptive immunity

artificial
man-made/produced
natural

active
immunity produced in response to exposure and subsequent recovery from a disease
natural

passive
immunity produced from antibody transfer from Mom to offspring across the placenta or thru breast milk
artificial

active
immunity produced in response to injection of man-made antigen (vaccine)
artificial

passive
immunity produced in response to injection of preformed antibodies (immunglobuline or Ig)
antigens (Ag)
proteins that provoke a response like mircoorganisms

( ANTIbody GENerators)
antibodies (Ab)
proteins made in response to the antigen

these proteins are made by the immune system
antigens
proteins or large polysaccharides

1. can be components of invading microbes- like capsules, cell walls, flagella, fimbriae, toxins
2. antibodies interact and recognize specific regions on the Ag called epitopes or antigenic determinants
antibodies
made in response to the SPECIFIC ANTIGEN

1. are globular proteins called IMMUNOGLOBULINS
2. have unique structure allowing them to bind to the antigenic determinants on the antigen
3.HELP TO NEUTRALIZE OR DESTROY THE AG
5 classes of immunoglobulins
IgG
IgM
IgA
IgE
IgD
IgG
80% of Ab in serum
has ability cross placenta
functions:
1. enhances phagocytosis
2. neutralizes viruses and toxins
3. protects fetus and newborn
IgM
5-10% of Ab in serum
pentamer- 5 monomers
to large to cross the placenta and generally stays in blood vessels
FIRST Ab produced in response to an Ag
relatively short-lived
IgA
1.relatively small amount in serum but most common Ig in mucous membranes and body secretions
2. dimer structure
3. functions as localized protection on mucosal surfaces
IgD
1.monomer structure
2.very small amt in serum
3.found on the surface of B lymphs
4.functions in initiation of the immune response
IgE
1.monomer structure
2.very,very small amount in serum
3.bind to mast cells and basophils involved in allergic reactions
Ag-Ab complexes and their results
1.binding of an antibody to an antigen protects the host by tagging "foreign" cells and molecule for destruction by phagocytes and complement
2.mechanisms include:
1.agglutination
2. opsonization
3. neutralization
4. Ab-dependent cell-mediated sytotoxicity
5. activation complement leading to inflammation and cell lysis
immunological memory
original exposure to an antigen has a lag time
process of immunity creates MEMORY CELLS
second exposure to an antigen, the memory cells are reactivated and respond very quickly- becoming protective quickly
primary response
Primary
IgM
slow onset
low magnitude
short-lived
secondary response
secondary
IgG ( or IgA or IgE)
rapid onset
high magnitude
long-lived
active disease
presence of IG
titer
measure the amount of antibody present
humoral immunity-antibody mediated
B lymphocytes produce antibody
present in serum and lymph
cellular immunity-cell mediated
T lymphocytes
present in tissues
humoral immunity

B cells or B lymphocytes
lymphs that have matured in the bone marrow

recognize free or extracellular antigens and make antibody
process of humoral immunity
1. B cells binds the antigen and becomes activated
2. activated B cells undergo clonal expansion or proliferation ( all of these cells are identical)
3. some of these cells differentiate into plasma cells which produce antibody
4. some of these cells become long-lived memory cells
cellular immunity
1.T cells or T lymphocytes mature under the influence of the thymus
2. they respond to antigens and secrete cytokines
cytokines are chemical messengers that tell other cells what to do
3. T cells respond to intracellular organisms-viruses, bacteria, parasites
process of cellular immunity
1. the helper T cells is activated when the antigen is present
2.activated helper T cells
1.proliferate and secrete cytokines that activate
macrophages, enhancing phagocytic activity
2.secrete cytokines that activate cytotoxic cells
into cytotoxic T lymphocytes (CTLs)
3. produce cytokines that activate B cells
4. memory cells are also produced
specificity of antibodies
using knowledge of immunology and to antigens, we apply it to 2 situations

vaccines
diagnostic tests
vaccines

natural active
immunity produced in response to exposure and subsequent recovery from a disease
vaccines

natural passive
immunity produced from antibody transfer from mom to offspring across the placenta or thru breast milk
vaccines

artificial active
immunity produced in response to injection of a man-made antigen (vaccine)
vaccines

artificial passive
immunity produced in response to injection of preformed antibodies (Immunoglobulin or Ig)
principle of vaccination
to provoke the primary immune response

when exposed to the organism again the response willl be:
1.rapid
2. effective and
3. prevent the development of disease
disease prevention
ways to prevent disease transmission:
1.sanitation
2.control of vector
3.isolation and quarantine
4.vaccines
an effective VACCINE is the best method of disease control
types of vaccines
attenuated whole-agent vaccines
inactivated whole-agent vaccines
toxoids
subunit vaccines
conjugated vaccines
nucleic acid vaccines
attenuated whole-great vaccines
use living-but attenuated (weakened) microbes
1. most closely mimic actual infection
2. lifelong immunity
3. effectiveness of 95%
4. ex= MMR, oral polio vaccine (Sabin)
inactivated whole-great vaccines
use microbes that have been killed- usually by formalin or phenol

ex = influenza vaccine
injectible polio vaccine (Salk)
pneumococcal polysaccharide
vaccine (Pneumovax)
toxoids
inactivated toxins

1. are directed at the toxins produced by a pathogen
2. ex = diptheria and tetanus toxoids
3. required series of vaccines and boosters
subunit vaccines
use only antigenic fragments that stimulate the immune system
1. fragments can NEVER reproduce in host
2. contain little extra material-fewer side effects
3. ex = Hepatitis B vaccine
conjugated vaccines
developed due to POOR IMMUNE RESPONSE in young children
1. polysaccharides are attached to proteins which the child's system can recognize and respond to

ex = pneumococcal conjugate vaccine, HiB (Haemophilus influenza type B)
diagnostic Immunology
2 critical components of a diagnostic test are :

1.sensitivity- test is positive when a person has the
disease
2. specificity- test is negative when a person doesn't
have the disease
monoclonal antibodies
used in diagnostic tests because they :

are uniform
are highly specific
can be produced in large quantities
precipitation reactions
1. involve the reaction of soluble antigens with either IgM or IgG antibodies to form large, interlocking lattices (visible)

2. occur only when the ratio of antigen to antibody is optimal
agglutination reactions
agglutination reactions involve either particulate antigens (such as cells) or antigens adhering to particles

these antigens can be linked together by antibodies to form visible CLUMPS
titers
the amt of Ab present in the serum

1.seroconversion= before illness no antibody present; during illness detectable antibody
2.rise in titer= during the acute phase of disease, antibody was present, during the convalescent period the amt of antibody was elevated
samples taken 2 weeks apart
significant rise= fourfold increase
complement fixation
during most Ag-Ab reactions, complement binds to the complex and is used up or fixed

complement fixation is used to detect very small amts of Ab
direct FA test
used for clinical specimens
ex= virus isolation
indirect FA test
detects specific antibody in serum following exposure
Indirect ELISA
detects antibody
Direct ELISA
detects antigen