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what does disease study?
Pathology
how is pathology informed
Pathogenesis
what does pathogenesis develop?
Diseases
sisease
abnormal state in which the body is not performing normal functions.
symptoms
Subjective characteristics of disease felt by the patient as a result of the disease(ie. pain)
signs
objective changes that can be observed and measured as a result of the disease (ie. fever, edema)
syndrome
characterization of a disease: determined by specific signs&symptoms of a disease (confirmed with lab tests; like a diagnoses)
communical Disease
classification of disease within a pop: spread from host to host (flu, chicken pox)
noncommunicable disease
classification of disease within a pop: not spread from host to host (includes microbes that live outside the body and when introduced they cause disease. tetnus)
reservoir
habitat of an infectious agent (not necessarily where its located, just where it can survive)
carriers
living organism w/ the pathogen reproducing in them & shedding into environment
carrier symptoms?
can range from NO symptoms at all to very prominent/obvious symptoms
what is direct transmission
contact person-person:
physical contact, no intermediate (rhinovirus & flu, ghonorrhea (sexually transmitted))
what is droplet transmission?
contact person-person:
microbes spread from respiratory droplets over SHORT distances <1m (sneezing/coughing, rhinovirus, flu)
what is indirect transmission
contact person-person:
transmission via non-living organism (fomite)
what is a fomite? what type of transmission is it involved in?
inanimate objects that become contaminated (bedding, toys, surgical instr. money...). involved in indirect contact transmission
what is airborne transmission?
vehicle transmission:
respiratory agents are dispersed into the air via dust particles (>1m long distances)
what is water/food borne transmission?
vehicle transmission:
waterborne: untreated water allows pathogens to replicate
food borne: undercooked, poorly refrigerated, unsanitary preparation
what are vectors
living organisms that transfer a pathogen from one person to another (anthropods: fleas, ticks, mosquitos, vertebraes: dogs, rodents) classified as vector transmission
what is mechanical transmission
type of vector transmission: (passive transport) antrhopod carried pathogen on is feet and makes contact w/ food. transmission occurs when human consumes food
what is biological transmission?
type of vehicle transmission: (active transport) anthropod bites an infected person and picks of pathogen in blood. injects into next host when feeding.
what is the end result of all routes of transmission?
infection! a susceptible host become infected
what is epidemiology?
study of the occurrence, distribution, and determinants of health and disease in a population
descriptive epidemiology
COLLECTION and analysis of data (general)
analytical epidemiology
analyzes a SPECIFIC disease, determines probable cause
experimental epidemiology
includes and hypothesis and controlled experiments (clinical trials with a test & control group
what is an outbreak?
numerous cases over a SHORT period of time (where cases are minimal)
non-outbreak cases vs. outbreak cases
non outbreak cases are considered the baselines of cases
endemic
a disease constantly present at LOW INCIDENCE in a population (common cold; viral)
epidemic
a disease the infects an unusually HIGH number of individuals in a population (influenza; viral)
pandemic
widespread, WORLDWIDE. a type of epidemic
human host-host epidemic
begins with one infected person: slow and steady progression followed by gradual decline (due to variable incubation times) cases are reported over LONGER time period (chicken pox, influenza)
common source epidemic
originates from a contaminated "common source" rapic increase in infected individuals due to many getting sick over a SHORT time period (common result is cholera/intestinal diseases)
incidence
number of NEW cases of a disease during paticular time (indicates SPREAD)
prevalence
number of NEW and EXISTING cases at a particular time (regardless of first appearance) (indicated HOW LONG a disease can persist in a pop)
mortality
deaths in a population , calculated as mortality rate (death/population)*100
disease progression: stage (1)
infection: organism invades, colonizes, and grows in host (host becomes infected!)
primary vs. secondary infection
primary: causes initial illness
secondary: opportunistic infection after primary
local infection
pathogens limited to small area of body
systemic infection (generalized)
infection throughout the body
disease progression: stage (2)
incubation: duration b/w infection & appearance of symptoms
disease progression: stage (3)
prodromal period: SHORT period after incubation; early, mild symptoms
disease progression: stage (4)
acute period: disease is most active, most severe symptoms
disease progression: stage (5)
decline period: symptoms subside
disease progression: stage (6)
convalescent period: patient regains strength and returns to normal
hospital environments
- diseased patients are pathogen reservoirs & carriers
- often patients share rooms
- healthcare workers move from patient to patient
- surgical procedures expose organs to contaminants
healthcare-associated infection (HAI)
an infection acquired while receiving treatment in a healthcare facility
predisposing factors
factors that make the body more susceptible to disease (gender, age, inheritance, climate/weather, vaccination, lifestyle, chemotherapy, fatigue...)
acute disease
symptoms develop rapidly but the disease lasts only a short time (influenza)
latent disease
causative agent is inactive for a time but then activates and produces symptoms
chronic disease
a disease that develops gradually and continues over a long period of time (tuberculosis, mononucleosis)
escherichia coli
part of normal intestinal microbiota, mostly harmless, main cause of diarrheal diseases and UTI's
enterohemorrhagic e. coli
causes food borne illness
- transmission: contaminated food/water (undercooked beef)
- incubation: 2-5 days
- symptoms last: >8 days
- shiga toxins
what are shiga toxins?
found in e.coli; targets blood vessels in intestinal lining
- the body responds by sending platelets to stop bleeding (forms clotts)
- decreased blood flow to organs can cause organ failure
*key symptom is bloody diarrhea (5-10% lead to kidney failure
infection vs. disease
infection: growth of microbes in host
disease: when those pathogens affect normal functioning of host
pathogenicity
potential ability of a pathogen to causes disease in host
virulence
ACTUAL ability of a pathogen to infect or damage a host
ID 50
expression of virulence: number of microbes required to produce an infection in 50% of healthy humans (lower the number the easier is is for infection to occur)
O-antigen
in contact w/ environment:
advantage: varies among bacterial strains (unique)
disadvantage: target for human immune response (antigen) location for viral attachment
portal of entry: mucous membrane
penetrates mucous linings of respiratory tract(inhalation), GI tract, urinary tract
portal of entry: skin
entry via hair follicles (unbroken skin is impermeable to microbes)
portal of entry: parenteral routes
if barriers are penetrated (cuts, bites, injections) microbes can be deposited directly into tissues
Mechanism of bacterial entry
"lock & key" mechanism
- bacteria = ADHESIN
- host = RECEPTOR
adherance
process of pathogens adhering to a host cell
adhesins
located on glycocalyx of pathogen (polysaccharide layer on the outside of the cell wall)
can also be on pathogenic pili (adhere to host) or flagella (mobility)
phagocytosis
once inside the cell, hosts tries to detroy microbe via this process.
lysozyme
digestive enzyme that break down peptidoglycan
lysosome
cell vesicle that contains numerous digestive enzymes
capsule formation
evade host: glycocalyx released by a bacterium can form a capsule around cell wall (reduces phagocytosis effectiveness increasing survival)
two microbes that use capsules
Streptococcus pneumonieae (causes pneumonia disease)
Bacillus anthracis (causes antrax disease)
enzyme release
evade host: coagulases, enzyme that forms clots when contacts fibrinogen (used by some staphylococcus).
kinases excreted when microbe is ready for release (used by some streptococcus)
antigenic variation
evade host: some microbes can change surface antigens resulting in the inability for host antibodies to bind and destroy the microbe
siderophores
direct damage: microbial proteins secreted iinto the environment and binds to IRON (affects host by using host nutrients and increases microbial growth) (
exotoxins
produced internally then secreted OUT (gram pos AND gram neg bacteria)
endotoxins
part of lipopolysaccharide layer (LPS) which can be released (gram neg ONLY)
exotoxin details
production is coupled to growth/metabolism during exponential phase, easily diffusible into blood, enzymes that destroy host cells
treatment: anti-toxin injections (specific antibodies for a specific exotoxin)
A-B exotoxins
A - enzymatic component - Attacks cell
B - binding component - Binds toxin to host cell receptor (glycoprotein or glycolipid).
After binding (B); A is transported into cell
botulinum toxin
clostridium botulinum
tetanus toxin
clostridium tetani
anthrax toxin
bacillus anthracis
endotoxin detail
part of LPS:
lipid A = portion of LPS secretes toxins when cell wall lyses during binary fission (ONLY gram neg like salmonella of e. coli
reaction = chills, fever, aches, weakness, death
portals of exit
The same as portals of entry (allows for movement from one host to another)
resp - coughing/sneezing, GI - feces, blood - anthropods, needles/syringes
immune system
bodys defense system against disease causing organisms, malfuntioning cells, and foreign particles
innate immunity
defenses gained from birth
adaptive imunity
response to a specific causative agent; defenses target a specific pathogen inside and outside host
first line of defense: physical
innate: physical factors
- skin: epidermis is constantly shed, extreme dryness inhibits growth
- mucous membranes: secretes mucus/glycoproteins that prevent desiccation of cilia, also traps microbes preventing further entry into body
first line of defense: chemical
innate chemical factors - perspiration, lysozyme (breaks down peptidoglycan=lysis), earwax (pH 3-5), saliva, gastric juice (pH 1-3), vaginal secretions (pH 3-5)
low pH inhibits microbial growth
second line of defense
phagocyte production (white blood cells), fever.
infection attracts WBC's
white blood cell count
high count in blod may indicate bacterial infection (normally found throughout blood, but will enter tissues if invaders are detected)
neutrophils
phagocytic 70%: early stages of an infection
eosinophils
phagocytic 0.5-1%: produce toxic proteins that target parasites
monocytes
phagocytic 2-4%: mature into macrophages in tissues
dendritic cells
phagocytic 3-8%: located in skin and mucous membranes
free macrophages
wandering, roam tissues and gather at sites of infection
fixed macrophages
residents in tissues and organs (liver, lings...)
mechanism of phagocytosis
1) chemotaxis: chem signals from damages cells attract phagocytes
2) adherance: TLR's bind to PAMP's releasing cytokines and initiating phagocytosis
3) ingestion: phagosome
4) digestion: lysosome fuse with phagosome (release lysoZYME to breakdown)
5) exocytosis: fragments released
Host defensive cells
macrophages and dendritic cells
host cell receptors
toll-like receptors (TLRs)
what do TLRs bind to?
pathogen-associated molecular patterns (PAMPs)
PAMPs
in bacteria - lipopolysaccharide (gram neg), flagella (all), peptidoglycan (gram pos), DNA (all)
in viruses - genetic info