Microbiology Unit 2

Front 1

IC
* Define dermatophyte, list 3 genera of dermatophytes, and name 3 dermatophytic infections.

Back 1

A group of molds that cause superficial mycoses of the hair, skin, and nails and utilize the protein keratin. Microsporum, Trichophyton, and Epidermophyton. Tinea capitis, tinea barbae, and tinea corporis.

Front 2

IC
* Describe what is meant by the term "dimorphic fungus", name 2 systemic infections caused by dimorphic fungi, and state how they are initially contracted.

Back 2

Fungi that exhibit two different growth forms. Outside the body they grow as a mold, producing hyphae and asexual reproductive spores, but in the body they grow in a non-mycelial form. Coccidioidomycosis and blastomycosis are both contracted by inhalation.

Front 3

IC
Name 2 opportunistic molds and the infections they cause

Back 3

Aspergillus and Rhizopus are the cause of opportunistic lung and wound infections in an immunosuppressed host.

Front 4

ID
Name at least 3 fungal virulence factors that promote fungal colonization.

Back 4

The ability to adhere to host cells, produce capsules allowing them to resist phagocytic engulfment, and be more resistant to phagocytic destruction (eg lyse macrophages).

Front 5

IA
Define mycosis.

Back 5

Fungal infections.

Front 6

IIA
Briefly describe protozoa.

Back 6

They are unicellular, eukaryotic, and lack cell walls; are in Kingdom Protista.

Front 7

IIA
Briefly describe 3 ways protozoans may reproduce asexually.

Back 7

1. fission: One cell splits into two.
2. schizogony: Multiple fission. The nucleus divides many times; the single cell then separates into numerous daughter cells.
3. budding: Buds form and pinch off of the parent cell.

Front 8

IIA
Define the following:
A. trophozoite
B. protozoan cyst.

Back 8

A. The vegetative form of a protozoan.
B. The dormant, protective form of some protozoa.

Front 9

IA
List 5 characteristics of fungi.

Back 9

1. are eukaryotic;
2. have a rigid cell wall;
3. are chemoheterotrophs (require organic compounds for both carbon and energy sources);
4. obtain their nutrients by absorption;
5. obtain nutrients as saprophytes (live off of decaying matter) or as parasites (live off of living matter).

Front 10

IB
Briefly describe yeasts and state how they reproduce asexually.

Back 10

They are unicellular, oval, fungi, are eukaryotes with thick polysaccaride cell wall (pathogen-associated molecular pattern). Yeast are facultative anaerobes that reproduce asexually through budding (some to produce blastospores as well).

Front 11

IA
Briefly describe pseudohyphae, blastospores, and chlamydospores and name a yeast producing these structures.

Back 11

Pseudohyphae are elongated buds that remain attached to each other. blastospores are asexual reproductive spores produced through budding. Chlamidospores are thick-walled survival spores. All are produced by the yeast Candida.

Front 12

IB
Name 3 potentially pathogenic yeasts and state the infections each causes.

Back 12

Candida albicans (candidiasis), Cryptococcus neoformans (cryptococcosis), and Pneumocystis carinii (Pneumocystis carinii pneumonia).

Front 13

IC
Define:
a. mold
b. hyphae
c. mycelium
d. vegetative mycelium
e. aerial mycelium.

Back 13

a. Multinucleated, filamentous fungi composed of hyphae.
b. A long filament of cells in fungi or actinomycetes.
c. The total mass of hyphae.
d. The portion of the mycelium of a mold that anchors the mold and absorbs nutrients.
e. The portion of the mycelium of a mold that produces asexual reproductive spores.

Front 14

IIIA
State 2 living and 3 nonliving characteristics of viruses.

Back 14

Living characteristics of viruses: a. They reproduce at a fantastic rate, but only in living host cells. b. They can mutate.
Nonliving characteristics of viruses:
a. They are acellular. b. They carry out no metabolism on their own and must replicate using the host cell's metabolic machinery. c. They possess DNA or RNA but never both.

Front 15

IIIA
List 3 criteria used to define a virus.

Back 15

a. They contain only one type of nucleic acid: DNA or RNA, but not both.
b. They are totally dependent on a host cell for replication. (They are strict intracellular parasites.)
c. Viral components must assemble into complete viruses (virions) to go from one host cell to another.

Front 16

IIIA
List 3 methods of cultivating viruses in the lab.

Back 16

Viruses are normally grown in animals, embryonated eggs, or in cell cultures.

Front 17

IIIA
*Discuss why bacteria can be cultivated on synthetic media such as nutrient broth whereas viruses cannot.

Back 17

Viruses have no metabolic machinery or means of replication out side of a host cell, therefore they cannot be grown on sythetic cultures.

Front 18

IIIA
Define bacteriophage.

Back 18

Viruses that infect only bacteria.

Front 19

IIIA
* Describe what an animal virus consists of structurally.

Back 19

a. Genome: one type of single or double circular or linear nucleic acid.
b. Capsid: protein shell surrounding genome.
c. Enevelope: most have an enevelope surrounding the capsid; is derived from host cell membranes.

Front 20

IIIC
Describe how most animal viruses obtain their envelope.

Back 20

It is derived from host cell membranes by a process called budding.

Front 21

IIIC
State why some bacteriophages are more complex than typical polyhedral or helical viruses.

Back 21

Some bacteriophages possess complex tail structures consisting of a contractile sheath, a base plate, pins, and tail fibers.

Front 22

IIIF
** List and describe the steps involved in the productive life cycle of animal viruses, comparing naked and enveloped viruses.

Back 22

a. Adsorption: binding of attachment sites on the viral surface with receptor sites on the host cell cytoplasmic membrane.
b. Penetration:
1. Eneveloped: the envelope may fuse with the cell cytoplasmic membrane and the nucleocapsid enters cytoplasm or usually enter by endocytosis.
2. Naked: rearrangement of capsid proteins allowing the viral nucleic acid to pass through the membrane or enter by endocytosis.
c. Uncoating: release of the viral genome.
1. viral envelope is first removed and viral capsid is then enzymatically removed.
2. naked viruses entering by endocytosis, the endocytic vesicle and the viral capsid are enzymatically removed.
d. Replication: viral genome directs the host cell's metabolic machinery to synthesize viral enzymes and viral parts.
e. Maturation: the capsid is assembled around the genome.
f. Release:
1: The host cell may or may not be lysed. The viruses obtain their envelopes from host cell membranes by budding. Those obtaining their envelopes from the nucleus or the Golgi are then released via transport vesicles.
2: With naked viruses, the infected cell usually disintegrates and the virions are released.
g. Reinfection: As many as 10,000 to 50,000 animal viruses may be produced by a single infected host cell.

Front 23

IIIE
Define eclipse period.

Back 23

The period during a virus life cycle between uncoating and maturation during which no intact virions are seen within the infected host cell.

Front 24

IIIF
State the primary reason why some viruses become latent.

Back 24

Viral latency is thought to result primarily from the lack of production of specific host cell proteins that are required for the activation of the viral genes responsible for turning on viral replication.

Front 25

IIIF
Define provirus.

Back 25

An animal virus that has inserted its DNA into the chromosomes of its host cell. During its life cycle, HIV becomes a provirus.

Front 26

IIIF
Name 4 herpes viruses that may have a latent cycle, state in what cell types they become latent, and name the diseases each cause.

Back 26

1. (HSV-1) which usually causes fever blisters and become latent in the body of neurons.
2. (HSV-2) which usually causes genital herpes and becomes latent in the body of neurons.
3. (VZV) which causes chickenpox and is latent in nuerons.
4. (EBV) causes mononucleosis and is latent in B-lymphocytes.

Front 27

IIIF3
Name 4 types of cells HIV primarily infects and briefly explain why.

Back 27

T4-helper lymphocytes, monocytes, macrophages, and dendritic cells because they all have the necessary CD4 receptors.

Front 28

IIIF3
* Describe the role of chemokine receptors in determining what types of cells HIV preferentially infects.

Back 28

M-trophic HIV usually spreads the infection to macrophages because they have the chemkine receptor CCR5. Later in infection mutation allows dual tropic HIV to bind to CXCR4 chemokine receptor on T4-cells as well. Finally, T-tropic HIV in late stage infection only bind to receptor CXCR4.

Front 29

IIID
List the 6 types of nucleic acid that may be found among the viruses.

Back 29

a. (+/-) double-stranded DNA:The (-) DNA strand is directly transcribed into viral mRNA.
b. (+) DNA or (-) DNA: converted into dsDNA and the (-) DNA strand is transcribed into viral mRNA.
c. (+) RNA: (+) RNA is copied into (-) RNA that is transcribed into viral mRNA.
d. (-) RNA: (-) RNA is copied into a (+) RNA which functions as viral mRNA.
e. (+/-) double-stranded RNA: The (+) of the (+/-) RNA functions as viral mRNA.
f. (+) RNA: (+) RNA is reverse transcribed into (-) DNA that makes a complementary copy to become (+/-) DNA. The (-) DNA is transcribed into viral mRNA.

Front 30

IIIG1
Define the following:
a. lytic bacteriophage
b. eclipse period

Back 30

a. Bacteriophages that replicate through the lytic life cycle.
b. The time during which no intact viruses are in the cell.

Front 31

IIIG
Name the 2 types of bacteriophage life cycles and state what the bacteriophage capable of each is called.

Back 31

Bacteria capable of the lytic life cycle are called lytic bacteriophages. Bacteria capable of the lysogenic life cycle are termed temperate phages.

Front 32

IIIH
Briefly describe 3 different ways viruses can evade host immune defenses and give an example of a virus that uses each mechanism.

Back 32

1. Antigenic drift and antigenic shift refer to mutating and gaining new genome info respectively that alters binding site for antibodies (influenza)
2. Some block formation of MHC-I molecules which allows CLTs to recognize the cell as infected and destroy them (cytomegalovirus CMV).
3. Others block cell apoptosis (Epstein-Barr EBV).

Front 33

IIIC
Define the following:
a. capsid
b. capsomere
c. nucleocapsid.

Back 33

a. capsid - a hollow protein shell surrounding a viral genome and usually composed of protein subunits called capsomeres.
b. capsomere - the protein subunits forming a viral capsid.
c. nucleocapsid - a naked or nucleocapsid virus lacks an envelope and consists of only a genome and a capsid.

Front 34

IIIF5
Name 4 viruses that have been implicated in human cancers.

Back 34

Hepatitis B virus (HBV), hepatitis C virus (HCV), human papilloma viruses (HPV), and Epstein-Barr virus (EBV)

Front 35

IIIH
Briefly describe at least 6 ways viruses can damage infected host cells.

Back 35

1. inhibiting normal host cell DNA, RNA, or protein synthesis.
2. causing nicks or breaks in the host cell's chromosomes.
3. placing viral components on cytoplasmic membrane causing the cell to be recognized and destroyed by body's immune defenses.
4. depleting the host cell of essencial cellular materials.
5. stimulating body cells to release inflammatory cytokines and chemokines.
6. causing vasodilation and mucous secretion.

Front 36

IE
Briefly describe 4 ways antifungal chemotherapeutic agents may affect fungi and give an example of an antibiotic for each way.

Back 36

a. Interfere with nuclear division by preventing the aggregation of microtubules needed for mitosis (griseofulvin).
b. Interfere with normal nucleic acid synthesis (trimetrexate).
c. bind to ergosterol in cytoplasmic membrane, altering its structure and function and causing leakage of cellular needs (nystatin).
d. interfere with ergosterol biosynthesis thus alter the structure of the cytoplasmic membrane and function of several membrane-bound enzymes (miconazole).

Front 37

IIIJ
* State why antibiotics are of no use against viruses and what we must rely on to control viruses.

Back 37

Since viruses are acellular, they are not effected by antibiotlics that metabolic processes. Instead, chemotherpteutic agents are used.

Front 38

IIIJ
State the viruses the following antiviral agents are used against:
e. AZT (ZDV), didanosine, zalcitabine, stavudine, lamivudine, and abacavir
f. nevirapine, delavirdine, and efavirenz
g. saquinavir, ritonavir, idinavir, and nelfinavir

Back 38

e. HIV (nucleoside-analog reverse transcriptase inhibitors)
f. HIV non-nucleoside reverse transcriptase inhibitors
g. HIV protease inhibitors

Front 39

IIIJ
Compare how the following drugs exhibit their antiviral action against HIV and give two examples of each.
a. nucleoside-analog reverse transcriptase inhibitors
b. non-nucleoside reverse transcriptase inhibitors
c. protease inhibitors

Back 39

a. chemically resemble normal DNA nucleotides, and so are inserted in their place, but are non-functional. Prevents provirus formation.
Zalcitabine and zidovudine.
b. bind to an allosteric site that regulates reverse transcriptase activity instead of active site. Prevents provirus formation. Nevirapine and efavirenz.
c. bind to the active site of HIV protease and prevents it from splitting a polypeptide or polyprotein into smaller active proteins. prevents maturation. Saquinavir and idinavir.

Front 40

IIIK
Describe and give an example of an acute viral infection, a late complication following an acute infection, a latent viral infection, a chronic viral infection, and a slow viral infection.

Back 40

Acute infection means having a short course (e.g., cold viruses, influenza viruses). In acute complications, the virus is persistent or continually present (progressive encephalitis that can follow rubella). Latent infections are in equilibrium with body defenses and cannot be detected until symptomatic (VZV; chickenpox-shingles). Chronic infections: virus is present and can be detected and may (or not) be symptomatic (HCV: hepatitis C). In slow infections the virus slowly increases in number during asymptomatic period (HIV: AIDS).

Front 41

IVA
Compare adaptive (acquired) immunity with innate immunity.

Back 41

Adaptive immunity is antigen-specific defense, is activated over several days; developes during life-time. Innate immunity is antigen-nonspecific, is activated immediatly; is present at birth and is initial response to prevent infection.

Front 42

IVA
Define antigen, immunogen, and epitope.

Back 42

Antigen: a substance that reacts with antibody molecules and antigen receptors on lymphocytes.
Immunogen: an antigen that is recognized by the body as nonself and stimulates an adaptive immune response.
Epitope: fragments of an antigen that react with antibodies and lymphocyte receptors.

Front 43

IVB
Describe what is meant by anatomical barriers to infection.

Back 43

Tough, intact barriers that prevent the entry and colonization of many microbes.

Front 44

IVB
List 4 ways in which the body can physically remove microorganisms or their products.

Back 44

1. Mucus and cilia
2. The cough and sneeze reflex
3. Vomiting and diarrhea
4. The physical flushing action of body fluids

Front 45

IVB
* Describe how bacterial antagonism by normal flora bacteria acts as a nonspecific body defense mechanism and name 2 opportunistic microbes that may cause superinfection upon destruction of these normal flora.

Back 45

Normal flora act as a defense by:
a. producing metabolic products ant inhibit growth of some pathogens.
b. preventing colonization by covering host cells
c. depleting pathogens of nutrients
d. keeping immune system primed by stimulaing defenses.
Candida and Clostridium difficile.

Front 46

IVB
Briefly describe the process involved in the development of antibiotic-associated colitis.

Back 46

C. difficile survives antibiotic treatment by sporulation and germiates when colin is free from antibiotic. It over grows the colon because of absence of normal flora and secrets toxin A.

Front 47

IVC
* State the function of the following as they relate to innate immunity.
A. pathogen-associated molecular patterns
B. pattern-recognition receptors
C. endocytic pattern-recognition receptors
D. signaling pattern-recognition receptors
E. toll-like receptors

Back 47

A. allow the body to detect microbes by recognizing these unique molecules.
B. receptors used to recognize pathogen-associated molular patterns
C. promote attachment of microbes to phagocytes in order to engulf them.
D. secrete cytokines when they bind to microbial molecules.
E. specific singaling receptors that promote adaptive and inate responses.

Front 48

IVC
State the benefits of the following antimicrobial body molecules:
a. lysozyme
b. human beta-defensins
c. hydrochloric acid in gastric secretions
d. fatty acids and lactic acid in sebaceous secretions
e. lactoferrin and transferin

Back 48

a. breaks down peptidoglycan
b. forms pores in the cytoplasmic membrane of a variety of bacteria causing leakage of cellular needs.
c. destroy swallowed microbes.
d. inhibit microbes on the skin.
e. isolate Fe for human use only.

Front 49

IVC
Describe the following:
a. cytokines
b. chemokines
c. interferons

Back 49

a. low molecular weight, soluble proteins that are released in order to regulate intracellular activities pertaining to immunity.
b. cytokines that promote inflamation by allowing white blood cells to adhere to and than escape from blood vessels to infected site.
c. cytokines that prevent viral replication, activet various defenses, and fight tumors.

Front 50

IVD1
Briefly describe the beneficial effects of the following complement pathway products:
a. C5a
b. C3a
c. C3b
d. C4b
e. C5b6789n (MAC)

Back 50

a. triggers inflamation, chemoattractant for phagocytes
b. inflamation
c. remove harmful immune complexes, function as opsonins
d. function as opsonins, remove harmful immune complexes
e. lysis of gram-negative bacteria and human cells displaying foreign epitopes.

Front 51

IVD
Briefly describe how the classical complement pathway is activated and how C3 convertase is formed.

Back 51

To activate the classical complement pathway, IgG or IgM is made in response to an antigen. C3 is formed when antibodies Fab react with epitopes and then C1q binds to the Fc, follwed by C1r and C1s, all of which form C1, the first enzyme. C1 then cleaves C4 and C2 making C4b2a, which is C3 convertase.

Front 52

IVD
Name 3 complement pathways and briefly state how each is activated.

Back 52

1. the classical complement pathway is activated by antigen-antibody complexes
2. the lectin pathway is activated by interaction of microbial carbos with mannose-binding proteins
3. the alternative complement pathway is activated by C3b binding the microbes and antibodies

Front 53

IVD3
Briefly describe how the alternative complement pathway is activated and how C3 convertase is formed.

Back 53

C3b or C3i activate the pathway by binding to microbial surface components. Factor B binds to the cell bound C3b, making C3bB and is then split by Factor D, forming C3bBb. Properdin binds to this compound forming C3bBbP that functions as C3 convertase

Front 54

IVD4
Briefly describe 4 different ways microorganisms can circumvent the complement pathways.

Back 54

1. Capsules can prevent formation of C3 convertase, preventing formation of C3b and C4b and other proteins
2. Capsules rich in sialic acid collect protein H, a host regulatory protein that degrades C3b, hence C3 convertase as well.
3. Some capsules simply cover the C3b that binds, thereby preventing phagocytes from binding to them.
4. Capsules can resist unenhanced attachment.

Front 55

IVE
State the significance of the following:
a. an elevated white blood cell count
b. a shift to the left (elevated bands)

Back 55

a. indicates infection, inflammation, leukemia, or parasitic infestations
b. indicates active infection because of unusually high immature (band) neutrophils

Front 56

IVE1
State what type of cell monocytes differentiate into when they enter tissue.

Back 56

Macrophages

Front 57

IVE1
State 2 functions of platelets.

Back 57

Promote cloting and form platelet plugs, also produce vasodilators for inflammation.

Front 58

IVE2
*State 3 different functions of macrophages in body defense.

Back 58

1. killing microbes and infected and tumor cells with phagocytosis.
2. processing antigens so they can be recognized by T-lymphocytes during the adaptive immunity.
3.secreting cytokines that play a variety of roles in nonspecific body defense.

Front 59

IVE1
State 2 functions of platelets.

Back 59

Promote cloting and form platelet plugs, also produce vasodilators for inflammation.

Front 60

IVE1
State 2 functions of platelets.

Back 60

Promote cloting and form platelet plugs, also produce vasodilators for inflammation.

Front 61

IVE2
State the primary function of dendritic cells in body defense.

Back 61

Their primary function is to capture and present protein antigens to naive T-lymphocytes.

Front 62

IVE2
State the primary function of mast cells in body defense.

Back 62

They release histamine, leukotriens, and prostaglandins, chemicals that promotes inflammation (like basophils).

Front 63

IVFII
**Describe the following steps in phagocytosis:
a. activation
b. chemotaxis
c. attachment (unenhanced and enhanced)
d. ingestion
e. destruction

Back 63

a. Resting phagocytes are activated by inflammatory mediators such as bacterial products, complement proteins, proinflammatory cytokines, and prostaglandins. As a result, the phagocytes produce surface glycoprotein receptors (endocytic patern-recognition receptors) that increase their ability to adhere to surfaces and recognize microbes.
b. Chemotaxis is the movement of phagocytes toward an increasing concentration of some attractant such as bacterial factors, complement components, chemookines, fibrin split products, kinins, and phospholipids released by injured host cells.
c. Unenhanced attachment is a general recognition of what are called pathogen-associated molecular patterns by means of glycoprotein known as endocytic pattern-recognition receptors on the surface of the phagocytes. Enhanced attachment is the attachment of microbes to phagocytes by way of an antibody molecule called IgG or the complement proteins C3b and C4b produced during the complement pathways.
d. Following attachment, polymerization and then depolymerization of actin filaments send pseudopods out to engulf the microbe and place it in an endocytic vesicle called a phagosome.
e. Phagocytes contain membranous sacs called lysosomes (produced by the Golgi apparatus) that contain various digestive enzymes, microbicidal chemicals, and toxic oxygen radicals. The lysosomes fuse with the phagosomes containing the ingested microbes and the microbes are destroyed.

Front 64

IVFII
State what happens when either phagocytes are overwhelmed with microbes or they adhere to cells to large to be phagocytosed.

Back 64

The phagocyte will empty the contents of its lysosomes for extracellular killing. This also kills surrounding host cells and tissue.

Front 65

IVFII
*Describe what causes most of the tissue destruction seen during microbial infections

Back 65

If the phagocyte is overwhelmed with microorganisms, the phagocyte will empty the contents of its lysosomes by a process called degranulation in order to kill the microorganisms or cell extracellularly. These released lysosomal contents, however, also kill surrounding host cells and tissue. Most tissue destruction associated with infections is a result of this process.

Front 66

IVFII
Compare the oxygen-dependent and oxygen-independent killing systems of neutrophils and macrophages.

Back 66

In the oxygen-dependent system, phagocytes with the oxidase convert molecular oxygen into O2-, which combines with water to form hydrogen peroxide and hydroxyl radicals. The radicals can combines with chloride to create powerful oxidizing agents which oxidize most chemical groups foudn in proteins, enzymes, carbohydrates, DNA, and lipids. When sugars are initially broken down by these oxidizing agents, they produce lactic acid, which lowers the pH and allows acid hydrolases to effectively break down cellular proteins.
In the oxygen-independent system, some lysosomes contain cationic (def) proteins that alter cytoplasmic membranes, lysozyme which breaks down peptidoglycan, lactoferrin which deprives bacteria of needed iron, and various digestive enzymes which exhibit antimicrobial activity by breaking down proteins, RNA, phosphate compounds, lipids, and carbohydrates.

Front 67

IVFII
*Describe 4 specific different ways a microbe might resist phagocytosis. (Think of the steps in phagocytosis.)

Back 67

i. block chemotaxis
ii. capsules can resist unenhanced attachment by preventing the endocytic pattern-recognition receptors on phagocytes from recognizing bacterial cell wall components.
iii. depolymerize the actin microfilaments needed for phagocytic engulfment into the phagocytes
iv. Some bacteria are more resistant to phagocytic destruction once engulfed, such as Salmonela, which is resistant to toxic forms of oxygen and defensins.

Front 68

IC
Briefly describe the following fungal asexual reproductive spores:
a. conidiospores
b. macroconidia,
c. microconidia
d. sporangiospores
e. arthrospores.

Back 68

a. Mold spores borne externally on an aerial hypha called a conidiophore.
b. + c. characteristic asexual reproductive spores produced by Microsporum, Trichophyton, and Epidermophyton.
d. Mold spores borne internally within a sac or sporangium on an aerial hypha called a sporangiophore.
e. Mold spores produced by the fragmentation of vegetative hyphae.

Front 69

IIB
State a disease caused by each of the following protozoans and indicate their means of motility and how they are transmitted to humans:
f. Balantidium coli
g. Plasmodium species
h. Toxoplasma gondii
i. Cryptosporidium

Back 69

f. causes a diarrhea-type infection; cilia (fecal-oral route).
g. cause malaria; transmitted female Anopheles mosquito; non-motile.
h. causes toxoplasmosis is contracted by inhaling or ingesting cysts from the feces of infected domestic cats; non-motile.
i. causes diarrhea; non-motile (fecal-oral route).

Front 70

IIB
State a disease caused by each of the following protozoans and indicate their means of motility and how they are transmitted to humans:
a. Entamoeba histolytica
b. Acanthamoeba
c. Giardia intestinalis
d. Trichomonas vaginalis
e. Trypanosoma brucei-gambiens

Back 70

a. Causes amoebic dysentery. Amoebas move by extending lobelike projections of their cytoplasm called pseudopodia (fecal-oral route).
b. Infects the eye, blood, spinal cord, and brain; amoeba is transmitted by waterborne cysts.
c. causes gastrointestinal infection called giardiasis; move with flagella (fecal-oral route).
d. infects the vagina and the male urinary tract; flagella (sexual contact).
e. causes African sleeping sickness and is transmitted by the bite of an infected Tsetse fly; flagella.

Front 71

IIIF3
** Describe the life cycle of the retrovirus HIV-1 (Human Immunodeficiency Virus Type-1).
(recomend studying from text)

Back 71

1. Adsorption: envelope gp120 adsorbs to a CD4 and chemokine receptor of human cells like T4-cells.
2. Penetration: binding of gp120 and CD4 causes shape change that lets envelope fuse with membrane; the core then enters the cell.
3. Uncoating + Production of Provirus: Uncoating occurs. HIV uses viral reverse transcriptase to make a DNA copy of the RNA genome (which is degraded) and then host enzymes to make it double-stranded. Viral DNA inserts into host DNA to become a provirus.
After integration, the HIV proviral DNA can exist in either a latent or productive state. If it is productive:
4. Replication of HIV: viral RNA and mRNA are transcribed from DNA. mRNA is used in ribsomes to make viral needs; viral gps are placed on host cell membrane.
5. Assembly: Gp 41 is synthesised and achors newly synthesized gp120 to host membranes. Maturation: occurs in forming bud or after release. Protein core assembles around the viral ssRNA genome.
6. Release: HIV is released and gets envelope from cyto. membrane, cells usually die.
7. Reinfection: Free viruses now infect new hosts; HIV can be transmited through cell-to-cell contact too.

Front 72

IIIF4
* State where in the body most replication of HIV occurs and explain why, during the chronic asymptomatic period of HIV infection, relatively few HIV and HIV-infected cells are found in the bloodstream.

Back 72

The main site for HIV replication in in the lymph nodes. HIV can either be carried directly to the lymph nodes by a healthy immune system, or it can infect monocytes, macrophages, or dendritic cells which will carry it to the lymph nodes. During the incubation period a steady-state infection persists where T4-lymphocyte death and T4-lymphocyte replacement by the body are in equilibrium.

Front 73

IIIG2
* Describe the lysogenic life cycle of temperate phages (including spontaneous induction).

Back 73

When a temperate phage infects a bacterium it becomes a prophage. To do this, it enters like in the lytic life cycle, but does not shut down the cell; instead, it inserts its DNA into the host's DNA. Rarely, spontainious induction takes place, when the phage genes are activated and the phage finishes the lytic cycle.

Front 74

IIIF
State the major difference between the productive life cycle of animal viruses and the latent life cycle.

Back 74

In the latent life cycle the virus may not replicate or produce symptoms right away.

Front 75

IIIE
Define viroid and name an infection caused by a viroid. * Define prion and name an infection caused by a prion.

Back 75

Viroids are small, circular, single-stranded molecules of infectious RNA lacking even a protein coat. Cadang-cadang (coconuts). Prions are infectious protein particles thought to be responsible for a group of transmissible and/or inherited neurodegenerative diseases. Kuru.

Front 76

IIIG2
Define the following:
a. temperate phage
b. lysogen
c. prophage

Back 76

a. A bacteriophage having a lysogenic life cycle and capable of inserting its DNA into that of the host bacterium.
b. A bacterium containing a prophage.
c. a pacteriophage that has incorporated its genome into the host's DNA.

Front 77

IIII
* Describe the process of lysogenic conversion and give 2 examples of exotoxins that result from lysogenic conversion.

Back 77

When the added DNA of a prophage gives a bacterium a new genetic trait such as the ability to produce an exotoxin. Diphtheria exotoxin, shiga toxins.

Front 78

IIIG1
* Describe the steps involved in the lytic life cycle of bacteriophages.

Back 78

a. Adsorption: the phage adsorbs to receptor sites on the host.
b. Penetration: phage injects its genome into the bacterial cytoplasm.
c. Replication: the phage replicates its genome and uses the bacterium's metabolic machinery.
d. Maturation: viral components assemble around viral genome.
e. Release: lysozyme breaks down the bacterial peptidoglycan causing osmotic lysis.
f. Reinfection: 50-200 new phages.

Front 79

IIIF3
* Describe the role of chemokine receptors in determining what types of cells HIV preferentially infects.

Back 79

The correct chemokine receptor is necessary for gp120 to continue the process of adsorption begun by CD4 receptors

Front 80

IIIF5
State the normal function the following:
a. proto-oncogenes
b. tumor suppressor genes

Back 80

a. regulatory genes that promote cell proliferation.
b. regulatory genes that inhibit cell proliferation.

Front 81

IIIB
Compare the size of most viruses to that of bacteria. List 4 shapes of viruses.

Back 81

Viruses are usually much smaller (5 to 300 nm); are submicroscopic.
a. Helical viruses: virus consisting of nucleic acid surrounded by a hollow protein cylinder or capsid and possessing a helical structure.
b. Polyhedral viruses: viruses consisting of nucleic acid surrounded by hollow, multi-sided, protein capsid.
c. Enveloped virus: A virus consisting of nucleic acid within either a helical or polyhedral core and surrounded by an envelope.
d. Binal (complex) virus: virus that has neither helical nor polyhedral forms or has combinations of these forms. Formerly called complex.

Front 82

IIIJ
State the viruses the following antiviral agents are used against:
a. amantadine, rimantidine, zanamivar, and oseltamivir
b. acyclovir, famciclovir, and valacyclovir
c. vidarabine
d. foscarnet, gancyclovir, and cidofovir

Back 82

a. Influenza A and/or B
b. Herpes simplex viruses (HSV) and/or Varicella-zoster virus (VZV).
c. HSV encephalitis and for shingles.
d. Cytomegalovirus (CMV).

Front 83

IIIF5
Describe how certain viruses may contribute to the development of tumors by altering proto-oncogenes or tumor-suppressor genes.

Back 83

They may cause long term damage to tissues resulting in large scale cell regeneration which increases the chances of natural mutation in proto-oncogenes and tumor suppressor genes. Some viruses may alter the normal function of the genes.

Front 84

IVG
Briefly describe the healing stage of late inflammation.

Back 84

Cytokines from macrophages stimulate prolifereation of endothelial cells, which form new capilaries, and fibroblasts, which form scar tissue from collagen.

Front 85

IVG
Briefly describe the problems that arise from chronic inflammation.

Back 85

It can result in extensive damage and scaring as neutrophils constantly discharge lysosome and oxidizing agents.

Front 86

IVH
Name 2 bacteria that can obtain their iron from human iron-binding proteins.

Back 86

Neisseria gonorrhoeae, Neisseria meningitidis.

Front 87

IVI
* Describe the mechanism behind fever induction and indicate its possible benefits.

Back 87

Activated macrophages and leukocytes release cytokines that stimulate anterior hypothalamus of brain to increase body temp with prostaglandins. Fever raises temp above optimum for bacteria, stimulates proinflammatory cytokins, and increases enzymatic reactions and speeds up metabolism.

Front 88

IVJ
State the functions of the following acute phase proteins:
a. C-reactive protein
b. mannose-binding lectin

Back 88

a. binds to phospholipids in microbial membranes, functioning as an opsonin, and actives classical complement pathway.
b. binds to mannose sugar, functioning as opsonin, and activates lectin pathway.

Front 89

IVJ
"Activated macrophages and leukocytes" means...

Back 89

pathogen-associated molecular patterns have bound to their toll like receptors and stimulated release of proinflammatory cytokines like TNF-alpha, Il-1, Il-6.

Front 90

IVFI
Briefly describe the function of the following in phagocytosis:
a. inflammation
b. lymph nodules
c. lymph nodes
d. spleen

Back 90

a. Inflammation allows phagocytes to enter the tissue and go to the site of infection as a result of vasodilation and increased capillary permeability.
b. Lymph nodules contain phagocytes that remove microorganisms that enter the mucous membranes and the skin
c. Lymph nodes contain phagocytes that remove microorganisms from the lymph.
d. The spleen contains phagocytes that remove microorganisms from the blood.

Front 91

IVE
*Describe and state the major functions of the following leukocytes:
a. neutrophils
b. basophils
c. eosinophils
d. monocytes

Back 91

a. form majority of leukocytes, stain clear (hence neutrophil), have lobed neucleus. Function as phagocytes, contain microbicidal granules, promote inflammation by promoting bradykinins.(granulocyte)
b. 0-1% of leukocytes, stain methylene blue, lobed nucleus. Promote inflammation with histamine.(granulocyte)
c. 1-4% of luekocytes, granules stain red. Contain granules for killing infectious organisms, can phagocytose or kill large pathogens extracellularly, promote inflammation with leukotrienes.
(granulocyte)
d. 2-8% of leukocytes. Important phagocytes, differenciate into macrophages when leave blood for tissue, which are important phagocytes and APCs. (Are agranulocytes)

Front 92

IVE
State what each of the following determine:
a. CBC (complete blood count)
b. leukocyte differential count.

Back 92

a. detemines the total number of both leukocytes and erythrocytes
b. determines the number of each type of leukocyte

Front 93

IVD
State 5 beneficial innate defense functions associated with all complement pathways.

Back 93

1. trigger inflammation
2. chemotactically attract phagocytes to infection
3. enhanced attachment or opsonization
4. lysis of gram-negatives cells and human cells with foreign epitopes
5. involved in activation of B-lyphocytes
6. remove harmful immune complexes from body.

Front 94

IVG
* Briefly describe the process of diapedesis, indicating the role of selectins, integrins, and adhesion molecules such as ICAMs and VCAMs.

Back 94

Proinflammatory cytokines from macrophages and vascular endothelials cause v. endothelials to increase expression of adhesion molecules (selectins, ICAMs, VCAMs etc.), increase blood flow and dilate vessels. Selectins slow leukocytes, cause them to roll. The cytokines also cause v. endothelial cells to produce chemokines, which stimulate integrins on leukocytes. Activated integrins cause leukocytes to bind to adhesion molecules like ICAMs. Once they have adhered, the leukocytes squeeze between endothelial cells in to the tissue and are attracted to infection by chemokines.

Front 95

IVH
Describe how the body deprives microorganisms of iron.

Back 95

1. the body absorbs less Fe
2. more Fe is stored as ferritin
3. increased numbers of human Fe-binding proteins lactoferrin and transferrin.
4. prior stationing of lactoferrin at common invasion sites; transferrin enters tissue during inflamation.

Front 96

IVJ
Briefly describe the mechanism behind the acute phase response.

Back 96

Activated macrophages produce cytokines that stimulate hepatocyes in liver to sythesize acute phase proteins.

Front 97

IVD1
Briefly describe how the lectin pathway is activated and how C3 convertase is formed.

Back 97

Activation takes place when mannan-binding proteins (MBP) bind to mannose in microbial carbos. MASP1 and 2 also bind to MBP forming a protien, like C1 of classical, that is able to cleave C4 and C2 into C4bC2a, C3 convertase.

Front 98

IVG
** Describe the mechanism of inflammation, indicating the various beneficial effects associated with plasma leakage and diapedesis.

Back 98

Smooth muscles around larger blood vessels contract to slow the flow of blood through the smaller blood vessels at the infected or injured site. The endothelial cells that make up the wall of the smaller blood vessels contract, increasing capillary permeability. This allows plasma leakage, so clotting factors, antibodies, proteins of the complement pathway, nutrients, lysozomes and beta-defensins, and transferrins can enter the tissue. Diapedesis, the process of leukocytes adhering to endothelial cells of the capillaries and leaking out through gaps between the cells, has the following benefits: Leukocytes leave the blood and enter the tissue for 1) phagocytosis; 2) more vasodilation; 3) exposure of immunocompetent cells (B-lymphocytes and T-lymphocytes to microorganisms and other antigens; 4) killing of infected cells and cancer cells by (CTLs) and NK cells.

Front 99

IIIF4
* State the median incubation period for AIDS and, in terms of viral load, exhaustion of the lymphopoietic system, and immune responses, briefly describe what marks the progression to AIDS.

Back 99

The median incubation period is ca 10 yrs. AIDS is marked by increase in viral load and immunoresistance; the immune system weakens due to destruction of T4 lymmphocytes and leads to inability to replace CTLs.

Front 100

IA
Name 3 groups of fungi.

Back 100

Includes yeasts, molds, and fleshy fungi.

Front 101

IC
State how molds reproduce asexually.

Back 101

They reproduce primarily by means of asexual reproductive spores

Front 102

IIID
State what criteria are used in viral classification.

Back 102

Type of nucleic acid they have in their genome, the shape of their capsid (helical or polyhedral), and whether they are enveloped or naked.

Front 103

IVE1
*Describe and state the major functions of the following leukocytes:
e. B-lymphocytes
f. T4-lymphocytes
g. T8-lymphocytes
h. NK cells

Back 103

e,f,g. 25-40% of leukcytes (WBC), circulate between blood and lymph, mediate the adaptive immunity.(agranulocytes)
e. mediate humoral immunity (antibodies), differenciate into plasma cells, have B-cell receptors .
f. mediate adaptive immunity through cytokines, have CD4 molecules and T-cell receptors (TCRs).
g. mediate cellular immunity, differenciate into T8-suppressor cells and cytotoxic TLs (CTLs), have CD8 molecules and TCRs.
h. kill cells w/o MHC-I on surface or bound by antibody. (agranulocytes)