• 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

1/110

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;

110 Cards in this Set

  • Front
  • Back

Mycology

Study of fungi

Filamentous/fleshy fungi

Molds and mushrooms

Nonfilamentous

Yeasts

Thallus

Major body of molds, composed of long, thin filaments

Hyphae

Filaments that compose the thallus

Septate hyphae

Cross linked walls in hyphae

Coenocytic hyphae

Molds that lack septate and appear to have one continuous cell with multiple nuclei

Vegetative hypha

Portion of hypha that is responsible for nutrient absorption

Aerial hypha

Portion of hypha that is responsible for reproduction

Mycelium

Hyphae that form a filamentous mass that is visible to the naked eye

How do you start a culture of fungi

Use the hyphae of a thallus

Pseudohypha

Short chains of bud cells on yeast

Fission of yeast

1. Cell elongates


2. organelles are replicated


3. Cell is pinched off at the node, two daughter cells are produced

Yeast's relationship to oxygen

Facultative anaerobic growth

Dimorphism

When they can grow as either yeast or molds

Conidospore

These are spores not enclosed by a sac

Sporangiospore

Spores which are enclosed by a sac

Asexual spores

Most common, produced from hyphae

Conidiophore

The stalk like structure in which conidiospores form off of

Sexual reproduction

1. Plasmogamy. Donor penetrate recipient


2. Karyogamy. Nuclei fuse together


3. Meiosis. Genetic recombination

How do fungi compete with bacteria

By living in highly acidic or sugary /salty environments

Molds relationship to oxygen

Aerobic

Mycosis

Fungal disease, usually chronic

Systematic mycosis

Located deep within the body that affect many areas

Subcutaneous mycosis

Fungal infections under the skin

Cutaneous mycosis

Fungal infection of epidermis, hair, nails

Keratinase

Breaks down keratin

Dermatophytes

Fungus that cause disease, Tolerate skin pH and produce keratinase

Innate immunity

Nonspecific, immediate response, TLRs, no memory

Adaptive immunity

specific recognition, delayed response

Mucociliary escalator

Synchronous movement of respiratory cilia to propel debris in mucus up the throat

Sebum

Prevents hair from drying out, forms protective film over the skin

Perspiration

Made by sweat glands to maintain temperature, eliminate waste and wash away microorganisms on skin

Lysozymes

Enzyme capable of breaking down peptidoglycan in bacterial cell wall

Gastric juice

In stomach, contains hydrochloric acid that destroys bacteria and toxins

Plasma

Fluid portion of blood that contains antibodies

Leukocytes

White blood cells that participate in immune responses

Platelets

Cell fragments that allow the body to form blood clots

Leukocytosis

During infections, white blood cell count increases

Leukopenia

During infections, white blood cell count decreases

Granulocytes

Neutrophils, basophils, eosinophils, dendritic cells

Agranulocytes

Monocytes, lymphocytes, T and B cells

Neutrophils

Polymorphic, active in initial stages of infection

Basophils

Call the shots, release histamine for inflammation

Eosinophils

Eat parasites and cause allergic reactions

Monocytes

Precursor of the macrophage, have to leave the blood first

NK cells

Use perforin and granzyme to kill even self cells

Phagocytosis

Ingestion of a microorganism by a cell

TLRs

Receptors on a cell that tell it what to attack

Inflammation

Defensive response to damage caused by a physical or chemical agent

Complement system

Defensive system consisting of 30+ proteins produced by the liver, inactive until infection

Three stages of the complement system

1. Cytolysis


2. Inflammation


3. Phagocytosis

Interferons

Interfere with viral multiplication

Transferrins

Make iron hard to get

Adaptive immunity has two parts

Humoral and cellular

Humoral immunity

Extracellular, B cells - > plasma cells, Mediated by antibodies

Cellular immunity

Intracellular, CD8 - > CTL, Mediated by T cells

Antigens

Molecules that cover foreign microbes not recognized as self

Epitope

Specific region on an antigen that an antibody can recognize

Cytokines

Chemical messengers

Interleukins

Communicate between leukocytes

Chemokines

Induce leukocytes to migrate toward an infected area

Clonal selection

Lymphocytes will first proliferate, then differentiate into a mature effector cell

MHC 1

Antigens are found on all body cells except RBCs. Mark host cells as self

MHC 2

Contain immune cells called antigen presenting cells, stimulate immune response

Antigen presentation

Antigens processed into fragments and presented to T cells

Helper T cells

CD4 cells that tell us which immune response to use

Antigen presenting cells

Dendritic cells, macrophages, B cells

B cells

Humoral, present antigens to T cells

Clonal expansion

CD4 cells first proliferate, then differentiate, a few become memory cells

TH1

IL2, produce cytokines that activate cellular immunity

TH2

Humeral, IL4, Produce cytokines associated with B cells and allergic reactions

Clonal deletion

Destroys any harmful B cells

Affinity

Strength of the bond between an antigen and antibody

Agglutination

When antibodies cause antigens to lump together

Opsonization

Coating of antigens with antibodies that enhance phagocytosis

Neutralization

IgG antibodies inactivate viruses by blocking their attachment to host cells and destroy toxins

ADCC

Ability of antibodies of humeral system and cells of cellular system to stimulate NKs to kill large invaders

Hypersensitivity

Antigenic response beyond which is normal, allergies

Anaphylaxis

Reaction caused when certain antigens combine with IgE antibodies

T independent antigens

Elicit the production of antibodies by B cells without T cell involvement

T dependent antigens

Requires presence of T Helper cells to stimulate antibody production by B cells

Chemotherapy

Use of synthetic or naturally derived compounds to combat infectious disease in a living host

Antibiotics

Naturally occurring substances that kill or inhibit organisms

Chemosynthetic agents

Synthetic compounds which are selectively toxic to organisms

Minimum inhibitory concentration

Minimum concentration needed to prevent the replication of a certain microbe

Chemotherapeutic index

Minimum dose of a drug that is toxic to the host divided by the effective therapeutic dose (want HIGH)

Broad spectrum antibiotics

Inhibit a large range of G+ and G- bacteria

Narrow spectrum antibiotics

Act only against a few groups of bacteria, penicillin

Inhibitors of cell wall synthesis

Penicillin, cephalosporins, bacitracin, carbapenems, vancomycin, isoniazid

Penicillin

Only gram +, inhibits crosslinking of peptidoglycan

Cephalosporins

Gram +&-, alternative to penicillin, damages kidneys

Bacitracin

Gram +, applied topically, Nephrotoxic

Carbapenems

Use primaxin and cilastatin, inhibit cell wall synthesis, little side effects

Vancomycin

Glycopeptide antibiotics, narrow and toxic, gram +, damage to ears and kidneys

Isoniazid

Inhibits mycolic acid, damages liver

Inhibits cell membrane function

Polymyxin B

Polymyxin B

Nephrotoxic, increases Permiability

Inhibitors of protein synthesis

Aminoglycosides, tetracycline, chloramphenicol, macrolides, lincosamides, streptogramins, oxazolidinones

Aminoglycosides

Bind to 30S ribosome, results in misread mRNA, hearing defects, kidney damage

Tetracycline

Prevent binding of trna to 30S ribosome, discolors teeth, kidney and liver damage

Chloramphenicol

Penetrate BBB, last resort, gram +/-, gray syndrome

Macrolides

Prevents syphilis in babies, used for people with penicillin allergies, liver damage, gastrointestinal distress

Lincosamides

Binds to 50S ribosome and prevents elongation, gram +&-, pseudomembranosus colitis

Streptogramins

Bind to 50S ribosome, causing premature chain termination, muscle aches, rash, headache

Oxazilidinones

Binds to 50S ribosome, inhibits initiation of protein chain formation, toxic to mitochondria

Inhibit nucleic acids

Sulfonamides, floroquinolones, rifampin

Sulfonamides

Inhibit folic acid synthesis, damage kidneys and liver

Floroquinolones

Inhibit DNA gyrase in DNA replication, affects cartilage development, gastrointestinal distress, allergies

Rifampin

Inhibits rna synthesis, always with isoniazid, liver damage, gastrointestinal distress