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87 Cards in this Set

  • Front
  • Back
Organisms live together, both benefit (Ecoli in GI tract)
Mutualism
one organism benefits, the other is not particularly benefited or harmed; to eat at the same table. (Most GI tract microbes; we provide a warm wet place to live with food, we don’t get all that much in return.)
Commensalism
one organism benefits at the other’s expense (Disease-causing bacteria; to them, we’re dinner.)
Parasitism
presence of microbes (where they don’t belong).
Contamination
multiplication of parasitic organisms in/on host.
Infection
used to describe infection of larger organisms, e.g. lice.
Infestation
malfunction in or damage to the host.
Disease
Disease is a condition of the ____?
Host
a parasite capable of causing disease
Pathogen
ability of pathogen to cause disease
Pathogenicity
relative ability to cause disease.
Virulence
attenuation means?
Weakened
microbes normally found on the body.
Normal microbiota
always found on human tissues.
Resident microbiota
come and go, can include potential pathogens.
Transient microbiota
Where do microbes live?
GI tract (crowded), respiratory tract, skin, genito-urinary tract, fluids
causes disease
pathogen
can cause disease under the right circumstance
opportunistic pathogen
decomposes dead stuff
Saprotroph
What determines whether we get sick? (Not always clear cut)
Inf Dis = N x V / HF
Types of diseases:
Inherited diseases: caused by a faulty gene.
Congenital: due to damage during development.
Degenerative diseases, due to age or lifestyle
Nutritional, endocrine, mental, immunological, neoplastic (cancer), idiopathic; same caveat.
Iatrogenic: caused by doctor.
Nosocomial infections: occur in hospital.
Infectious disease: caused by infectious agents like:
Bacteria, viruses, fungi, etc.
can be spread from one person to another
communicable
highly communicable, can easily be spread from one person to another.
Contagious
are not spread from one host to another.
Non-communicable
How bacteria can cause disease:
Invasive (usualy through tissues)
Toxigenic (produce and release toxins which dissolve in blood stream)
Host processes (inflamation over responding, causing damage.
How viruses can cause disease:
Viruses multiply inside host cells, using cell resources, often killing cells.
Viruses stimulate the immune system to fight back; infected cells are killed.
Viruses alter cell cycle regulation to promote their own replication; may lead to cancer.
Fungi, Protists, and worms
Produce enzymes that damage host cells
Multiply in host cells and kill them
Cause allergic reactions or inflammation
Steps in an infectious disease:
Entry and attachment
Deal with host defense
Damage
Escape
Things that bacteria have that improve their abilities to cause disease:
Virulence Factors-Fimbriae, capsules, enzymes, toxins
A protective mechanism, but can cause local damage.
Inflamation
What are Endotoxins and Toxic Shock Syndrome toxins?
Super antigents (Cause massive over response of WBS
Followed by decreased responsiveness)
The study of disease is called?
Epidemiology
the study of the causes of disease
Etiology
What is signs and symptoms?
Signs are observable/measurable
Symptoms are experienced by patient
collection of signs and symptoms
Syndrome
# of new cases during a time period
Incidence
ongoing cases at any one time
Prevalence
Death and sickness per total population over a given period of time.
Mortality and morbidity rate:
The first epidemiological study. Cholera was found to be spreading by water. London in 1854
John Snow was credited
Refers to how long the disease lasts..(Acute, subacute, chronic)?
Acute is short lived, subacute longer,chronic longest
Refers to how long the disease lasts....(Local, focal, systemic)?
A local infection is in one specific place, systemic means throughout the body. Focal: started somewhere
Refers to how long the disease lasts....(Primary, secondary, superinfection)?
Primary: the first or main infection
Secondary: a second infection once weakened by a first one.
Super infection usually blamed on antibiotic Rx
bacteria in the blood
Bacteremia
a disease condition, microbes actively growing in, infecting blood.
Septicemia
viruses in the blood, common in systemic infections
Viremia
infection comes from outside the host. Examples: common cold, STD.
Exogenous
host is original source of infection. Examples: boils on skin spread by fingers from Staph sinus infection; E. coli urinary tract infection.
Endogenous
Weakened immune system, poor lung clearance from bed rest, surgical wounds, bedsores, etc.
Compromised host
Where do germs live?
Humans, animals, non living (soil and water)
Entry portals for infections:
Glands, follicles that open to outside
Larger openings: respiratory system, digestive system, genito-urinary tract
Cuts, bites, burns, surgical incisions
Crossing the placenta, infecting the fetus
Exit portals for infections:
Coughing sneezing speaking: from mouth
Excretory systems: GI tract, in feces; in urine
From sex: vaginal fluid, semen
From blood: insect bites, shared needles
Types of transmission for microbes:
Contact-
Direct contact: touching, kissing, sex, endogenous spread (one part of you to another)
Vehicles- water, food, airborne
Vectors-Typically arthropods (insects, ticks)
Koch’s Postulates:
1.Microbe must be found in every instance of the disease.
2.Obtain microbe in pure culture
3.Produce disease in susceptible host
4.Re-isolate original microbe
Stages of Disease:
Incubation
Prodromal
Illness (acute/invasive)
Decline
Convalescent
Frequency of disease terms:
Endemic, Epidemic, Pandemic, Sporadic
Endemic: continually present in low numbers
Epidemic: higher than normal occurrence
Pandemic: epidemic spreads worldwide
Sporadic: cases show up only occasionally
The more immune individuals, the harder it is for the disease to be spread among many people; the cycle of transmission is broken.
Herd Immunity
potentially harmful diseases which must be reported to the CDC or other Health Unit by physicians
Notifiable disease
Non-specific Host Defenses
-Physical barriers
-Cellular defense
-Processes:
phagocytosis
inflammation
-Chemical defenses
Non-specific Host Defenses -Physical barrier-skin
Skin-Layered tissue, puncture resistant.
High in keratin, water repellant.
Secretions maintain low pH.
Outer layers slough off, reducing microbial load.
Self-repairing.
Non-specific Host Defenses -Physical barrier- mucus
Mucus traps microbes
-Action of cilia:
propel mucus & microbes toward GI tract or to where they can be coughed out.
Non-specific Host Defenses: Cellular Barrier: Blood
60% Plasma
Water and salts (electrolytes)
Proteins: albumin, immunoglobulins, fibrinogen, complement, etc.

40% “Formed Elements” (cells mostly)
RBCs (erythrocytes, red cells) carry oxygen
WBCs (leukocytes, white cells) fight infection
Platelets involved in clotting, release prostaglandins.
White Blood Cells: Lymphocytes, Monocytes, Granulocytes
Lymphocytes: 20-50% of total,
T and B cells, deal with specific immunity
Monocytes: 2-8% of total,
“grow up” to become macrophages, “big eaters”
Granulocytes
Neutrophils: 50-70%, numerous short-lived phagocytes
Eosinophils: 1-5%, stain red, attack parasites
Basophils: 0.1%, stain blue, release histamine
Granulocytes named according to microscopic appearance, presence of granules, type of stain, etc.
Features inactive proteins becoming activated.
Platelets respond to physical roughness
Blood clotting
plasma without the clotting factors
Serum
Large and mean, clean up debris as well as microbes.
Important link between non-specific immunity and specific immunity
Macrophages
patrol bloodstream, stepping into tissues when “called”
Wandering macrophages
reside in specific organs, get fancy names like Kupffer cells, histiocytes, microglia, “dust cells”, depending on home.
Fixed macrophage
a process by which cells engulf and destroy microbial invaders, debris, foreign material.
Phagocytosis (Cell-eating)
the major phagocytic cells in the body:
Neutrophils (PMNs) and macrophages
phagocytes respond to (move toward) various chemicals (cytokines) released by host cells and by microbes.
Chemotaxis
cell binds to material/microbe.
Attachment
Phagocytosis steps in the process:
Chemotaxis, attachment, engulfment, digestion
Phagocytosis 2- target brought into cell by endocytosis. Now in cytoplasm in a vesicle.
Engulfment
Phagocytosis 2- vesicle (phagosome) containing microbe fuses with lysosome.
Digestion
Some microbes have found a way to interfere and save itself by:
Anti-phagocytic coatings
Capsules, M-protein; aren’t grabbed and engulfed
Prevent phagosome-lysosome fusion
Prevention of destruction in phago-lysosome
Hide from phagocytes by entering “non-professional” phagocytes.
Kill phagocytic cells
Attach to parasites (protozoa, worms) larger than they are, release enzymes that attack pest.
Eosinophils
Non-specific lymphocytes (different from T and B cells) which attack virus-infected cells and kill them.
Natural killer cells
Series of vessels and nodes
Drains off excess body fluids from
tissues, returns fluids to cardiovascular system
Lymph nodes filter out microbes
Nodes filled with macrophages and lymphocytes
Fluid flows thru slowly, maximizes contact
Parallel circulatory system
Largely all explained by increased blood flow and vessel permeability in area of injury; host response to tissue injury.
Inflammation
: a substance that causes fever
Pyrogen
Fatty acids in sebum on skin, low pH and are toxic
Lysozyme in tears, saliva, other fluids
Chemical defenses: Secretions
not being susceptible to disease
Immunity
Types of immunity:
Innate: you have it from birth
Acquired: after exposure, your body remembers specific invader.
An atigen is:
Large, foreign, molecularly complex
A molecule that is too small to be an antigen without piggy-backing onto another is a ____
hapten
The specific part of an antigen recognized by an antibody or receptor is called an _____
epitope
refers to body fluids
Humoral
refers to the direct involvement of cells to attack an infection
cell mediated