bsci 223 - third exam

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131 Terms

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mutualism

both partners benefit

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commensalism

one partner benefits, one partner is not affected

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amensalism

one partner is harmed, one is not affected

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parasitism

one partner is harmed, one partner benefits

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normal microbiota

normally present in our bodies

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resident microbes

part of the normal microbiota, inhabit body for extended time periods

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transient microbes

temporary residents of body sites

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how do we know GI microbiota is beneficial?

gnotobiotic animals & fecal flora reconstitution

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fecal microbiota transplantation (FMT)

used to treat recurrent Clostridium difficile (C. diff) infections

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VOWST 

capsule that contains bacterial spores from healthy stool donors

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opportunistic pathogens

member of normal microbiota that causes diseases due to change in circumstances

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what factors contribute to pathogenic disease?

colonizing an unusual space

host immune suppression (ex. HIV)

changes in the normal microbiota (taking antibiotics)

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colonization

persistence of a microbe in a specfic site within the host’s body (setting up shop)

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infection

when a pathogen overcomes body’s external defenses, multiplies and becomes established in the body

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pathogen

a microorganism or agent that is able to cause disease

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disease

a defect in body function caused by infection

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pathogenicity

the ability to cause diseasev

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virulence 

the degree of pathogenicity

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virulence factors

bacterial products that contribute to pathogenicity

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what are the three bacterial portals of entry?

skin

mucous membranes

placenta

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receptors

usually specific carbohydrate or peptide residues on eukaryotic cell surfaces or matrix

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bacterial ligand (a.k.a adhesin)

typically a macromolecular component of bacterial cell surfaces

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adhesin

a molecule, often a protein, on the surface of microorganisms like bacteria and fungi that allows them to stick to surfaces, including host cells

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bacterial bioflms

bacteria bound within sticky web of polysaccharide that binds cells to each other and to a surface

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what are the adhesins of e.coli

pili or fimbriae

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quorum sensing

specific small molecules can turn on genes (like those that encode virulence factors)

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an antibiotic that disrupts the function of the 70S ribosome is likely to be an example of which type of antibiotic?

broad spectrum

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almost all bacteria have what?

70S ribosome

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Beta-lactamase is an enzyme secreted by bacterial cells that helps protect the cells from the effects of penicillin and other similar antibiotics. which part of penicillin’s structure is targeted by beta-lactamase?

beta-lactam ring

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<p>which conclusion is suggested by the data in these graphs?</p>

which conclusion is suggested by the data in these graphs?

antibiotic A is bacteriostatic, and antibiotic B is bactericidal

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ampilicillin-sensitive e.coli is plated on media containing ampicillin. the next day, a few colonies have grown. which of the following statements best explains the presence of these colonies?

some e.coli cells in your culture mutated or picked up an ampicillin-resistance gene before you plated the cells

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streptococcus pyogenes (group A strep)

variety of acute infections

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streptococcus agalactiae (group B strep)

neonatal sepsis and meningeal infection

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streptococcus pneeumoniae (pneumococcus)

cause of bacterial pneumonia and purulent meningitis

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<p>which of the plates in the figure below shows the conversion of hemoglobin to methemoglobin?</p>

which of the plates in the figure below shows the conversion of hemoglobin to methemoglobin?

C - alpha hemolysis

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which of the following statements about gnotobiotic (raised in a germ-free environment) animals are true?

gnotobiotic animals show increased susceptibility to pathogens

fecal flora reconstitution restores production of some vitamins in gnotobiotic mice

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which organisms are capable of causing diseases

members of resident normal flora

members of your transient normal flora

commensal organisms

pathogenic organisms

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virulence factor

a component, such as a toxin or enzyme, that a microorganism uses to cause disease by helping it colonize a host, invade tissues, evade the immune system, or damage host cells

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what is the most common portal of entry and infection site for a pathogen of humans?

through the mucus membranes of the respiratory tract

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organisms that live inside a cow’s rumen help the cow by breaking down hay and grass into useable nutrients for the cow. in return, the bacteria get a place to live and a continuous source of food, this is an example of which type of symbiosis?

mutualism

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you pick up a Campylobacter infection from contaminated food. you end up with diarrhea and the Campylobacter get food and housing. this is an example of which type of symbiosis?

parasitism

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a beneficial member of your normal gut microbiota picks up a toxin gene from a lysogenic phage. the toxin allows the bacteria to gain nutrients by lysing red blood cells. this is an example of which type of symbiosis?

parasitism

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which of the following can potentially change the composition of your resident microbiotia?

antibiotic use

stress

infection

diet

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susceptibility to infection by a pathogen is determined by which of the following?

where the pathogen comes into contact with the body

the adhesins present on the bacterial cell

the receptors present on the host cell

other microbial species that are present

immune response of the host

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which of the following statements is true about bacterial biofilms?

provide protection for bacterial members

they are prevalent in nature

they can consist of many bacterial species

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describe the hemolysis phenotype of S. pneumoniae

Alpha hemolysis

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what best describes S. pneumoniae?

bacteria

part of the normal microbiota

resides normally in the throat and nasopharynx

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what is true about S. pneumoniae?

it is an opportunistic pathogen

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what is the cell morphology of Streptococcus pneumoniae

diplococci

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which disease can be caused by infection with S. pneumoniae?

pneumonia

ear infections

bacteremia

meningitis

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what can contribute to disease symptoms?

pathogen virulence factors

pathogen growth within the host

host immune response to the pathogen

treatment taken to kill pathogen

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what is true about the S. pneumoniae capsule?

it is a virulence factor

it helps S. pneumoniae infect host cells

it protects the bacterial cells against phagocytosis

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phagocytosis

a process where a cell "eats" a solid particle by engulfing it - ingestion of a solid (microbe or debris) by a eukaryotic cell 

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which S. pneumoniae virulence factors allow the bacterial cells to bind to receptors in host cells and become intracellular (living within the host cells)

phosphorylcholine

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which S. pneumoniae virulence factor creates pores in and destroys host epithelial cells?

pneumolysin

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<p>which organism is MORE infectious?</p>

which organism is MORE infectious?

organism #1

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during which stage of disease is it possible to transmit organisms and infect others?

incubation period

prodromal period

illness period

decline period

convalescence period

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the following description applies to which type of virulence factor?

a cell-associated molecule found only in Gram-negative bacterial cells. It is part of the LPS molecule found on the outer membrane, and can be released upon cell death, causing fever, chills, aches, and shock in the host

endotoxin

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S. pneumoniae virulence factor - capsule

primary factor, protects against phagocytosis

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S. pneumoniae virulence factor - adhesion pllus

helps S. pneumoniae adhere to respiratory cells

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RrgB

pilus backbone

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RrgA

adhesion

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S. pneumoniae virulence factor → PspA (pneumococcal surface protein)

found on every S. pneumoniae strain, protects cell from host complement system and is attached to cell walll by binding to telchoic acids

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S. pneumoniae virulence factor → phosphorylcholine

present in bacterial cell wall - binds to receptors in host cells, allowing bacteria to become intracellular

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S. pneumoniae virulence factor → pneumolysin

cytotoxin binds cholesterol in host cell membrane and creates pores → destroys ciliated epithelial cells and phagocytic cells

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S. pneumoniae virulence factor → SlgA protease

traps bacteria in mucin (main component in mucus) by attaching itself to bacteria at Ag-binding sites and to mucin at the Fc region

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pneumonia

organisms get into lower airways (lungs): usually when defense mechanisms are down

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sinusitis and otisis media

infections of the sinuses and ear, usually preceded by viral infection of respiratory tract

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bacteremia

occurs in 25-30% of patients with pneumococcal pneumonia and >80% of patients with meningitis, can lead to endocarditis

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meningitis

bacteria spreads into central nervous system

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polyvalent

affective against multiple serotypes

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pneumovax vaccine

uses 3 most common capsular polysacchararides covering 88% of invasive diseases

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protein conjugate vaccine (prevnar)

contains capsular polysaccharide from 7 common strains important for disease along w/ a protein antigen (used in young people)

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which of the following statements is true about bacterial virulence factors

they can be acquired & and they are not required for normal bacterial survival

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what is an example of a time when a virulence factor would not be encoded on a bacterial chromosome?

if it’s encoded on a plasmid and inserted through horizontal gene transfer

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group B strep uses pili to adhere to host cells. are pili proteins potential virulence factors?

yes

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<p>which gene(s) would you want to study as a potential virulence factor? </p>

which gene(s) would you want to study as a potential virulence factor?

all of them (pilABC)

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damage caused by microbe + consequences of immune response

disease

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to cause a disease… a pahogen must:

  1. enter a host

  2. adhere to host cells

  3. escape detection or removal

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what is koch’s 1st molecular postulate?

gene should be found in strains that cause disease and absent in strains that do not

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what is koch’s 2nd molecular postulate?

mutation of the gene should result in a reduction in virulence

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what is koch’s 3rd molecular postulate?

introduction of the gene should increase virulence

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what is koch’s 4th molecular postulate?

immune response to gene product should protect against infection

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infectivity

microbes’ ability ot infect host

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infective dose (ID50)

number of bacteria necessary to result in infection of 50% of hosts

ex. low ID50 = high infectivity

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lethal dose (LD50)

number of bacteria that results in death of 50% of hosts 

ex. low LD50 = high lethality

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hyluronidase + collagenase

can dissolve structural materials in the body

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coagulase

allows bacteria to form clot

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kinase

dissolves clot

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toxemia

presence of toxins in the bloodstream - carried beyond site of infections

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exotoxins

toxins secreted out of the cell

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endotoxins

coats surface of bacterial cell, can be released into environment. cell-associated

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to avoid immune clearance, bacteria cells can

hide within host cells

avoid killing by host proteins

avoid phagocytosis

avoid host immune killing mechanisms

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bacterial capsule

composed of chemicals not recognized as foreign - slippery and difficult for phagocytes to engulf

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antiphagocytic chemicals

prevent fusion of lysosome and phagocytic vesicles or destroy phagocytic cells

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which of the following is the body’s first line of defense against invading pathogens?

skin and mucous membranes

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non-specific barriers to infection include which of the following?

skin 

mucous membranes

tears

lysozyme (antibacterial component)

commensal S. pneumoniae in the nasopharynx

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phagocytic cells locate bacterial cells through which process?

chemotaxis

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which of the following is part of the innate immune response?

killing of bacterial invaders by phagocytosis

local inflammation at area of infection

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cytokines are…

cell communication molecules - regulatory proteins that act as intercellular messages when released by cells