• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/114

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

114 Cards in this Set

  • Front
  • Back
Constitutive genes
their products are constantly produced at a fixed rate.
Promoter
region of DNA where RNA polymerase initiates transcription.
Operator
region of DNA; “stop” or “go” signal for transcription of structural genes.
Operon
Operator and promoter sites and the structural genes they control.
Repression
inhibits gene expression; decreases synthesis of enzymes.
Vertical gene transfer
genes are passed from an organism to its offspring.
Horizontal gene transfer
genes passed to other microbes of the same generation.
What are Three types of Horizontal Gene Transfer:
1. Transformation.
2. Conjugation.
3. Transduction
Transformation
transfer of genes between bacteria as “naked” “DNA.
Competence
recipient cell is in a state that allows it to take up DNA.
Plasmid
circular piece of DNA; replicates independently from chromosome.
● Carry genes that are not essential for normal growth of cells.
Resistance factors (R factors)
plasmids that carry toxin, antibiotic resistance, etc. genes.
Pathology
study of disease.
Etiology
the cause of disease.
Pathogenesis
the way a disease develops.
Infection
invasion or colonization of body by a pathogen.
Disease
occurs when infection results in change of health.
Normal microbiota
colonize the body but don’t normally produce disease.
Transient microbiota
present for days-weeks and then disappear.
Microbial antagonism
normal flora prevents overgrowth of harmful microbes.

► Protect host against colonization by:
• Competing for nutrients.
• Producing substances harmful to other microbes.
• Affect pH and available oxygen.
Symbiosis
relationship between normal microbiota and host.
Commensalism
one organism benefits, other is unaffected.
Mutualism
benefits both organisms.
Parasitism
one organism benefits at the expense of the other.
Opportunistic Pathogens
don’t cause disease in their normal habitat.

Cause disease if they:
► Gain access to other body sites.
► Host is weakened.
Koch’s Postulates
used to study the etiology of any infectious disease.
Symptoms
subjective changes not apparent to observer (pain, malaise).
Signs
objective changes doctor can observe and measure (lesions, fever).
Syndrome
specific group of symptoms or signs; always accompany particular disease.
Communicable disease
spreads from one host to another.
• Chickenpox, tuberculosis, genital herpes.
Contagious disease
easily spread from one person to another.
• Chickenpox, measles.
Non-communicable disease
not spread from one host to another.
• Tetanus.
Sporadic disease
occurs occasionally (typhoid fever).
Endemic disease
constantly present in the population (common cold).
Epidemic disease
many people in a given area get the disease in a short period of time (influenza, AIDS).
Pandemic disease
worldwide epidemic (influenza).
Acute disease
develops rapidly, lasts a short time (influenza).
Chronic disease
develops slowly, often less severe, likely to be continual or recurrent (mononucleosis).
Subacute disease
between acute and chronic (subacute sclerosing panencephalitis).
Latent disease
agent inactive for a time, becomes active, produces symptoms (shingles).
Immunity of a population determines:
► The rate at which a disease spreads
► Number of individuals infected.
Vaccination
enough people in a population are protected to prevent rapid spread.
Herd immunity
many immune individuals present in a population.
Local infection
microbes limited to a small area (boils, abscesses).
Systemic infection
microbes and their products spread through body by lymph/blood (measles).
Focal infection
local infection spreads to another area where its confined (arise from teeth, tonsils).
Sepsis
toxic inflammatory condition from spread of microbes or their toxins from an infected area.
Septicemia
blood poisoning; systemic infection from multiplying pathogens in the blood.
Bacteremia
bacteria in the blood.
Toxemia
toxins in the blood (tetanus).
Viremia
viruses in the blood.
Reservoir
source of pathogens for infectious disease.
Transmission
to susceptible host; direct contact, vehicle, or vector.
Invasion
microbe enters host and multiplies.
Pathogenesis
microbe injures host.
Incubation period
interval between infection and appearance of signs or symptoms.
Prodromal period
short period in some diseases; early, mild symptoms.
Period of illness
clear signs and symptoms, disease is most severe; immune system or treatment end this period or patient dies.
Period of decline
signs and symptoms subside; vulnerable to secondary infection.
Period of convalescence
body returns to prediseased state.
Reservoirs of Infection
source of disease causing organisms.
Zoonoses
disease that occurs in animals, can be transmitted to humans.
Direct contact transmission
physical contact, no intermediate object involved.

• Kissing, touching, sexual intercourse.
Indirect contact transmission
transmitted via a nonliving object (fomite).

• Tissues, towels, bedding, cups, money.
Droplet transmission
spread in mucus droplets that travel short distances.

• Sneezing, coughing, talking.
Vehicle Transmission
disease transmitted by a medium; food, water, blood, etc.

Waterborne, Airborne, Foodborne
Vectors
Animals/insects that carry pathogens from one host to another.
Nosocomial (Hospital-Acquired) Infections Result from an interaction of:
► Microbes in the hospital.
► Compromised hosts.
► Chain of transmission in the hospital.
Epidemiology
study of when and where diseases occur and how they’re transmitted in populations.
Morbidity
number of people that contract the disease during a particular period of time.
Mortality
number of deaths that occur from those diseases.
Adhesins (ligand)
surface molecule on pathogen that binds to receptors on host tissue cells.
Surface receptors
molecule on host cell that is specific to host cell tissue; complementary to the adhesin.
► Mostly carbohydrates.
Phagocytosis:
host cell engulfs and destroys microbes.
Coagulases

.
convert fibrinogen in blood plasma to fibrin; fibrin clots blood.
Kinases
breaks down fibrin; digest clots.
Hyaluronidase
breaks down hyaluronic acid.
Collagenase
breaks down collagen.
Antigen
foreign substance/molecule.
Siderophores
Iron-binding proteins secreted by pathogens.
IgA proteases
destroy IgA antibodies made against pathogens.
Exotoxins
produced inside and secreted. Gm(+) AND gm(-)

• Signs and symptoms depend on type of exotoxin; no fever results except from superantigens.
Endotoxins
part of gram (-) cell wall. ONLY gram (-) →→ LIPID A
>>Results in Fever<<
Three types of exotoxins:
(#1) A-B toxins:
• Two polypeptide parts (A and B); A is enzyme; B is binding portion.
• Bacteria releases A-B exotoxin.
• B part binds to receptor on host cell.
• A-B toxin transported into host cell by pinocytosis.
• A & B separate.
à A inhibits protein synthesis; cell death.
à B is released from cell.
Three types of exotoxins:
(#2) Membrane-disrupting toxins:
• Lyse host cells by disrupting plasma membrane.
• Form pores in membrane (S. aureus) or disrupt phospholipids (C. perfringens).
• Some are hemolysins: disrupt membrane of red and white blood cells = cell lysis.
• Streptococci sp. and staphylococci sp.
Three types of exotoxins:
(#3) Superantigens:
• Bacterial proteins that provoke intense immune response
• Result in: fever, nausea, vomiting, diarrhea, shock and death.
• Staphylococcus aureus toxin: toxic shock.
Shock
life-threatening decrease in blood pressure.
Immunity
ability to fight off disease caused by microbes and their products.
Leukocytosis
increase in total white blood cell count during infection.
Leukopenia
decrease in total white blood cell count during infection.
● Fixed macrophages
located in certain tissues and organs of the body (liver, lungs, etc.)
● Wandering macrophages
roam tissues and go to sites of infection.
Natural Killer (NK) cells
kill wide variety of infected body cells and some tumor cells.
Perforin
makes channels in membrane and causes fluids to flow into cell = cell lyse (cytolysis).
Granzymes
cause target cell suicide (apoptosis).1
Chemotaxis
chemical attraction of phagocytes to microbes.
Adherence
attachment of phagocyte to microbe.
Opsonization
coating of microbes with serum proteins; aids phagocytosis.
What Are Four signs and symptoms of inflammation?
► Redness, pain, heat, and swelling.
► Sometimes a fifth: loss of function.
Acute inflammation
cause is removed over short period of time; response is intense.
Chronic inflammation
cause is difficult to remove; response is longer, but less intense.
Edema
swelling caused by fluid build up.
Margination:
phagocytes stick to inner surface of blood vessels.
Emigration
collected phagocytes squeeze between cells of blood vessels to injured area.
Lectins
proteins that bind to carbohydrates.
Induction
turns on transcription of a gene or genes.

Inducer: molecule that turns on transcription.
Carriers
carry and transmit pathogen without showing signs of illness.
cytokines
chemical messengers produced by immune cells.
Ex: (IL-1 and TNF-a)
Phagosome
sac surrounding the microbe.
Phagolysosome
Fuses with lysosome containing digestive enzymes
Induction
turns on transcription of a gene or genes.
I gene
regulatory gene; encodes repressor protein.
Antigenic variation
alteration of surface antigens by some pathogens.

► Host immune response against pathogen.
► Pathogen alters surface antigens and is unaffected by antibodies.
Abscess forms
localized collection of pus (dead cells, body fluids).