FINAL Flashcards by Joseph Nesbitt

the lag phase

This period of little or no cell division, called the lag phase, can last for or several days. During this time, the cells are not dormant; they are undergoing a period of intense metabolic activity

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multiplication of DNA animal virus

❶–❷ Following attachment, entry, and uncoating, the viral DNA is released into the nucleus of the host cell.

❸ Transcription of a portion of the viral DNA—the “early” genes—occurs next. Translation follows. The products of these genes are enzymes that are required for the multiplication of viral DNA. In most DNA viruses, early transcription is carried out with the host’s transcriptase (RNA polymerase); poxviruses, however, contain their own transcriptase.

❹ Sometime after the initiation of DNA replication, transcription and translation of the remaining “late” viral genes occur. Late proteins include capsid and other structural proteins.

❺ This leads to the synthesis of capsid proteins, which occurs in the cytoplasm of the host cell.

❻ After the capsid proteins migrate into the nucleus of the host cell, maturation occurs; the viral DNA and capsid proteins assemble to form complete viruses.

❼ Complete viruses are then released from the host cell.

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Major difference bw maturation of RNA virus and DNA

The multiplication of RNA viruses is essentially the same as that of DNA viruses, except RNA viruses multiply in the host cell’s cytoplasm.

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steps of RNA virus replication

After uncoating, single-stranded RNA (ssRNA) viruses with a strand genome are able to synthesize proteins directly from their strand. Using the strand as a template, they transcribe strands to produce additional strands to serve as mRNA and be incorporated into capsid proteins as the viral genome. (b, blue arrow) The ssRNA viruses with a strand genome must transcribe a strand to serve as mRNA before they begin synthesizing proteins. The mRNA transcribes additional strands for incorporation into capsid protein. (c, yellow arrow) The dsRNA viruses transcribe a + strand in capsid proteins to protect dsRNA from cellular destruction.

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Replication of retrovirus

Is actually a ssRNA(+) containing reverse transcriptase or RNA dependent DNA polymerase

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Best description of parental route of entry

M/o deposited under the skin

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Examples of infections using parental route of entry

HIV, hepatitis, tetanus

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Salmonella typhi preferred portal of entry

GI tract (mucous membrane)

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Streptococcus pneumonia: portal of entry

Resp tract (mucous membrane)

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Yersinia pestis portal of entry

Black plague - parental route

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Virulence often expressed as

ID50

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Potency often expressed as

LD50

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Bacteria forms of adherence to cells

Glycocalyx of Streptococcus mutans: surface of teeth
Fimbriae of enteropathogenic Escherichia coli: specific cells in small intestine
Fimbriae ofNeisseria gonorrhoeae: cells in genitourinary tract
Tapered end as a hook: Treponema pallidum

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What does streptococcus use to adhere to host

Glycocalyx

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How does N. Gonnorhoeae ahere to GI tract

finmbraie

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How does treponema pallidum adhere to GI tract

Tapered end is hooked

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Adhesins or ligands

glycoproteins or lipoproteins) on microbes bind to receptors (carbohydrates) on host cells; altering one can block adherence

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Invasin

Invasins rearrange nearby host cell cytoskeleton and induce ruffling

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How does a capsule contribute to a bacteria virulence (ex of bacteria)

impair phagocytosis

Streptococcus pneumoniae

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How does having a waxy layer contribute to virulence plus example

Waxy layer: resist digestion by phagocytes
Mycobacterium tuberculosis

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How is Coagulase used to evade host defenses

Coagulate the fibrinogen in blood
Staphylococcus aureus

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How does kinase allow for evading host defenses

Digest fibrin clots
Streptococcus pyogenes, Staphylococcus aureus

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Hyaluronidase use in virulence

Hydrolyses hyaluronic acid that holds together some cells in body (i.e. connective tissue)
Streptococcus spp, Clostridium spp

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Collaginase purpose

Hydrolzyses collagen

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Which bacteria uses IgA proteases

N. Gonnohoreae

What does a bacteria alter on itself to avoid detection and become a different strain

Antigens

2 ways that pathogens damage host cells

Siderophores and direct damage

Characteristics of Exotoxin

mostly Gram +ve (but found in both) Yes neutralized by antigen Does not cause fever Small lethal dose

Characteristics of endotoxin

ONLY G- Present in LPS of outer membrane Causes fever Unaffected by antitoxin Large lethal dose (relatively)

During what phase of bacterial grwoth are exotoxins secreted?

Log phase

The primary function of the humoral,

AKA antibody-mediated, immune response is to control freely circulating pathogens.

Helper T cell

Activated by two signals 1. Binding of T cell receptor to processed antigen 2. Costimulatory cytokine

Cell mostly responsible for enhanced secondary response to an antigen

Memory cells

This type of immunity is acquired via injection of antibodies from an individual or host that has immunological memory to the specific pathogen or antigen.

artificially acquired passive immunity

This type of immunity is acquired when a person is vaccinated for a specific type of infection via the introduction of antigens. These antigens normally have undergone some type of modification and may not confer the same type of long-lasting memory that would occur with unmodified antigens

artificially acquired active immunity

What type of defenses are the first line defenses?

External Secretions: Skin pH 3-5 (inhibit microbes) Lysozyme: Enzyme in skin, saliva and tear secretions Fungistatic fatty acid in sebum (oily skin) Lactic acid bacteria in vagina: Produce lactic acid (acidic pH) Stomach acid is lethal to most bacteria: Helicobacter pylori survives stomach pH Normal Microflora:

Complement systems

An antimircrobial substance produced by the body composed of Special proteins that attack and lyse microbes

Interferons

Antimicrobial substance of proteins secreted by virus infected cells that inhibit viral multiplication

Defensins

Antimicrobial proteins secreted by activated macrophages to destroy pathogens

Antigen

Antibody

Describe physical differences bw mature T cell and Mature B cell

B cell Y shaped with two IDENTICAL light chains and two IDENTICAL heavy chains Two differnt (straight) chains

CD antigens stands for

Clusters of differentiation

Most T cells are

Helper (65%)`

What MHC class do T cells

MHC 1 or MHC 2

Most osre throats can be treated by

Penecillum

Analytical epidimology

Comparing healthy individuals to sick (florence nightinggale)

Descriptive epidemiolgy

Gathering information of all sorts

Streptococcus Pyogenes

Low G+C Lactobacillus

First step In DNA virus multiplication

Synthesis of DNA

Differnce bw vehicle transmission and vector

Vehicle is air, water, food Vector is biological (animal) or passive (FLy on food)

How can botulism ingestion be easily avoided

Boiling food

Cornebacterium diptheria

High G+C G+ producing exotoxins

Salmonella produces toxins?

Endotoxins

Vibrio cholera produces toxins?q

Exotoxins

Do phagocytes use complements or lysozumes?

COmplements but no lysozymes

Neutrophils with a defextive lysozyme are unable to do what to a pathogen

Digest it

Normal microbiota of the skin

Micrococci M. luteus M. roseus Staphylococci S. epidermidis S. aureus Diphtheroids (pleomorphic rods) Corynebacterium xerosis (aerobic) Propionibacterium acnes (anaerobic)

Ampicillin

Semisynthetic (penecilin) Extended-spectrum beta lactam antibiotic

Cephalosporins does whar

Inhibits cell wall synthesis

Bacitracin, Colistin, and vancomyosin are

Polypeptide antibiotics that inhibit cell wall synthesis

isonicotinylhydrazine and ethambutol are

Antimycobacterial antibiotics inhibitors of cell wall synthessi mycolic acid synthesis

Pseudonomas are

G- Gamma proteobacteria

Tetracyclines Macrolides (e.g. Erythromycin) Chloramphenicol Aminoglycoside are all

Broad spectrum Inhibitors of Protein Synthesis

Rifamycin, Quinolones and fluoroquinolones Nalidixic acid, Ciprofloxacin (CIPRO)

3. Inhibitors of DNA/RNA Synthesis and treatment for antrhax

Polymyxin B

4. Injury to the Plasma Membrane effective against g- like psudonomonas

Sulfonamides, Trimethoprim, and SXT –

Competitive Inhibitors of Enzymes

2 major bacteria genera involved in diseases of the skin

Staphylococcus Streptococcus

Describe S.Epidermis

Very common on skin (90%) Opportunistic infection (broken skin or catheter) Produce biofilm `

What bacteria CAN be found on the skin, is not NORMAL skin flora, and causees a wide range of diseases?

Streptococci

P. aeruginosa. resists antibiotics

Pump out drug Efflux pumps

How does S.aureus resist antibiotics

Prevents entrance

How is MRSA durg resistant

Alteration of target enzyme or organellec (Binding proteins of penicillin)

M protein or Capsule prevents adherence to macrophage

Streptococcus pyogenes, S. pneumoniae

Leukocidins kill mcrophages:

Staphylococcus aureus

Lysis of phagolysosome

Listeria monocytogenes

Escape from the phagosome

Shigella

Prevent fusion of phagosome with lysosome

HIV and M. tuberculosis

Survive in phagolysosome (advantage?)

Coxiella bunetii