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79 Cards in this Set

  • Front
  • Back
Name 4 things an organism must do to cause an infectious disease.
a. Maintain a reservoir before and after infection
b. Leave the resevoir and gain access to the new host
c. Colonize the body
d. Harm the body
Define the following:
a. pathogenicity
b. virulence
a. refers to the difference in ability to harm between different species
b. Refers to difference in harmfulness between two strains of the same species.
Even though a microorgansim may be considered pathogenic, it still may not be able to cause disease upon entering the body. Why?
The amount of bacteria entering the host and the quality of the host's innate and acquired body defenses both affect whether the host will contract the disease.
* Briefly describe the mechanism by which invasins enable certain bacteria to enter host cells. Name 3 bacteria that are able to do this and name an infection that each bacterium causes.
Invasins activate the host cells cytoskeleton, permiting the bacteria to enter the cell by phagocytosis. Shigella casues bacillary dysentery. Escherichia coli causes dysentery-type infection. Salmonella causes gastroenteritis.
State what is meant by actin-based motility and state why this might be an advantage for a bacterium.
Comet-like actin tails that polymerize at the end of bacteria; they move the bacteria and allow it to invade other host cells. This is helpful for bacterial colonization.
Name two bacteria that use both invasins and motility to penetrate host cells and name an infection each causes.
Shigella, which causes dysentery, and Listeria monocytogenes, which causes food-borne infection.
State why it might be of an advantage for a bacterium trying to colonize the bladder or the intestines to be motile.
Mucosal membranes cover these surfaces and motile bacteria can swim through mucous and colonize the membrane.
* Name 2 pathogenic spirochetes and briefly descrbe why being extremely thin and having axial filaments may be an advantage to these bacteria.
Treponema pallidum and Leptospira. their thin bodies and internal flagella permit spirochetes to corkscrew through viscous liqids and their thin bodies permit the sprichetes to puncture the cytoplasmic membrane.
Describe the following as they relate to phagocytosis:

a. unenhanced attachment
b. enhanced attachment
c. ingestion
d. destruction
a. A recognition of and attahcment to pathogen-associated molecular patterns by endcytic pattern-recognition receptors on phagocytes.
b. The attachment of microbes to phagocytes by opsonins during the compliment pathway. Is more specific that unenhanced
c. the creation of pseudopods made of actin that engulf the microbe in a phagosome.
d. digrestion of the microbe by lysosmes containing microbicidal chemicals.
State what is meant by serum lysis of gram-negative bacteria and briefly describe one way a bacterium might resist this.
The cutting open of the cell wall with the gram-negative specific LPS serving as a bonding site for formation of Membrane Attach Complex (MAC). Some bacteria use sialic to prevent formation of complement enzyme C3 convertase.
State why the ability to compete for iron is important for bacteria to cause disease.
Since Fe is essential for both human and bacterial cell growth, not only will Fe cause the bacteria grow but the bacteria will kill human cells to gain Fe.
List 3 general categories of virulence factors that damage the host.
1. Ability to produce cell wall components that bond to host cells causing them to synthesize and secrete inflamatory cytokines and chemokines
2. Ability to produce harmful exotoxins
3. Ability to induce autoimmune responses
Briefly describe why inflammation during a minor or moderate infection is essentially beneficial while inflammation during a massive infection can cause considerable damage to the body.
When low numbers of bacteria are present, low levels of cell wall components are present, which triggers moderate inflammation. This inflammation kills the bacteria. But at high levels, bacterial infection causes excessive imflammation and can damage body cells as much as bacteria.
List 3 body defense pathways or processes promoted by cytokines such as tumor necrosis factor-alpha, interleulin-1, interleukin-6, and interleukin-8.
1. Inflammation
2. Complement pathways
3. Coagulation pathway
State the mechanism behind inflammation and state why it is primarily beneficial to the body.
Release of proimflammatory cytokines leads to vasodilation of blood vessels, which open and release plasma into surrounding tissues.

This is beneficial because most of the body defence elements are located in the blood.
** Describe endotoxin (LPS) and list 10 pathophysiological changes that endotoxin in the blood may cause
LPS - lipid A of the lipopolysaccharide found in the outer membrane of a gram-negative cell wall.
a. fever production
b. inflammation
c. tissue destruction
d. respiratory distress
e. capillary damage (leading to petechial rash, capillary leakage, and hypovolemia
f. intravascular coagulation
g. hypotension
h. decreased cardiac output
i. irreversible shock
j. wasting of the body
k. diarrhea (from endotoxin in intestines)
** Describe the mechanism behind how we now know LPS causes harm to the body, briefly indicating the role of macrophages, cytokines, and neutrophils in the process, and relate this to the amount of LPS released.
LPS binds to pattern recongition receptors on macrophages causing cytokines production, and on neutrophils stimulating toxin syntheis. Citokines promote inflammation and activate the complement and coagulatin pathway. These elements harm the body when huge amounts of LPS enter the body during infection, over stimulating the body defense so it damages itself.
Define nosocomial infection and name 3 common gram-negative bacteria that cause nosocomial infections.
Infections accquired during a hospital stay. Escherichia coli, Pseudomonas aeruginosa, and Enterobacter.
Name the parts of the gram-positive cell wall that function similarly to the LPS in the gram-negative cell wall in stimulating cytokine production and an inflammatory response.
Peptidoglycan monomers and teichoic acids.
Name 2 gram-positive bacteria that commonly cause nosocomial infections
Staphylococcus aureus and Enterococcus.
Name the parts of the acid-fast cell wall that function similarly to the LPS in the gram-negative cell wall in stimulating cytokine production and an inflammatory response.
Mycolic acid and muramyl dipeptide.
Name pathogenic 2 acid-fast bacteria and state the infection each causes.
Mycobacterium tuberculosis (tuberculosis) and Mycobacterium leprae (leprosy).
State the major way the body defends itself against exotoxins.
The production of antitoxins antibodies.
Define superantigen.
Bacterial toxins that interact with exceedingly large numbers of T4-lymphocytes.
1. Toxic shock syndrom toxin-1 (TSST-1) is produced by some strains of Staphylococcus aureus
2. Straptococcal pyrogenic exotoxin (Spe) is produced by some rare invasive strains and scarlet fever strains of Streptococcus pyrogenes
3. Staphylococal entertoxins (SE) are produced by many strains of S. aureus
4. Hormone analog (Sta; heat-stable toxin) is produced by Escherichia coli
* Briefly describe the roles of alpha toxin, kappa toxin, and mu toxin, and fermentation by Clostridium perfringens in the pathogenesis of gas gangrene.
Alpha toxin increases the permeability of capillaries and muscle cells by breaking down lecithin in cytoplasmic membranes. This results in the edema.
Kappa toxin breaks down supportive connective tissue (collagen) resulting in the mushy lesions.
Mu toxin breaks down the tissue cement.
Gas production is the result anaerobic fermentation of glucose by the organisms (forms H2 and CO2).
All of these occur at the same time and increase presure in the infection while dcreasing the resistance of the tissue, allowing the infection to spread quickly.
State how the following exotoxins cause harm and name a bacterium producing each:
a. leukocydin
b. Streptococcus Exotoxin B
c. elastase
d. pneumolysin
a. Causes lysis of white blood cells (Staphylococcus aureus).
b. Protease that destroys muscles or the sheath that covers the muscle (Streptococcus pyogenes).
c. destroys elastin, a protein of lung tissue (Pseudomonas aeruginosa).
d. Damages ciliated epithelial cells, lung tissue, and vascular endothelial cells by puting pores in host cell (Streptococcus pneumoniae).
State how the hemolysins, proteases, DNases, and streptokinase produced by Streptococcus pyogenes cause harm.
These hydrolytic enzymes destroy red blood cell membranes, cellular proteins, DNA, and fibrin respectively. The tissue damage due to These enzymes causes inflammation.
* Briefly describe how cell-to-cell signaling between individuals of a population of bacteria may play a role in pathogenicity.
It allows the bacteria to act as a community rather than an individual. Ex. Bacteria may wait to secrete toxins until they are numerous enough to overpower the bodily defenses.
State what is meant by autoimmunity.
When the body's immune defenses mistakenly attack the body.
Name 3 bacterial diseases that may result from autoimmunity.
Rheumatic fever, chronic Lyme disease, and tertiary syphilis.
Define the following:
A. selective toxicity
B. broad spectrum antibiotic
C. narrow spectrum antibiotic
D. cidal
E. static
F. antibiotic
G. synthetic drug
a. chemical being used inhibits or kills the intended pathogen w/o seriously harming the host.
b. generally effective against a variety of gram+ and gram- bacteria.
c. works against a few specific microbes.
d. agent kills the organism.
e. inhibits the organism's growth.
f. metabolic products of one microorganism that inhibit or kill others.
g. antimicrobial drugs synthesized by chemical procedures in a lab.
State the functions of the A component and the B component in A-B toxins
B (binding) component is specific to certain host cells: it binds the exotoxin to a receptor molecule on the host cell memebane. The exotoxin then translocates across the cell membrane. Then the A (active) component separates and enters the host cell's cytoplam, catalyzing a reactino that removes the ADP-ribosyl group from NAD and attaching it to a host cell protein (ADP-ribosylation). This interferes with the functin of the host cell protein.
State which of the following antibiotics 1) inhibit peptidoglycan synthesis; 2) inhibit nucleic acid synthesis; 3) alter bacterial 30S ribosomal subunits blocking translation; or 4) alter bacterial 50S ribosomal subunits blocking translation.
1. penicillins, monobactams, carbapenems, cephalosporins, and vancomycin
2. fluoroquinolones (norfloxacin, lomefloxacin, fleroxacin, ciprofloxacin, enoxacin, trovafloxacin, etc.), sulfonamides and trimethoprim, and metronidazole
3. aminoglycosides (streptomycin, neomycin, netilmicin, tobramycin, gentamicin, amikacin, etc.) and tetracyclines (tetracycline, doxycycline, demeclocycline, minocycline, etc.)
4. macrolides (erythromycin, azithromycin, clarithromycin, dirithromycin, troleandomycin, etc.), oxazolidinones (linezolid), and streptogramins
Name 2 bacteria that have low-permeability membrane barriers and are thereby intrinsically resistant to many antibiotics.
Pseudomonas aeruginosa, Mycobacterium tuberculosis.
** Describe 3 mechanisms (changes in the bacterium) that may enable a bacterium to resist an antibiotic.
1. Producing an enzyme capable of destroying or inactivating the antibiotic;
2. Altering the target site receptor for the antibiotic to reduce or block its binding; and
3. Preventing the entry of the antibiotic into the bacterium and/or actively transporting the antibiotic out of the bacterium.
* Describe R (Resistance) plasmids and state their significance to medical microbiology.
Small molecules of circular, extrachromosomal DNA found in some bacteria and containing genes coding for multiple antiobiotic resistance and often a conjugation (sex) pilus. The pilus means that not only is the microbe resistant by it can pass its resistance on, creating a resistant infection.
State what the following stand for: MRSA, MDRSA, VRE, and MDRTB.
MRSA (methicillin-resistant Staphylococcus aureus), MDRSA (multiple drug resistant Staphylococcus aureus), VRE (vancomycin-resistant Enterococcus), MDRTB (multiple drug resistant Mycobacterium tuberculosis)
Define conjugative transposons.
Transposons normally found within the bacterial nucleoid that can excise and transfer themselves from the donor bacterium's nucleoid to the nucleoid of a recipient bacterium.
Describe mycoplasmas and name the most common mycoplasma infection of humans.
The only prokaryotic organisms that naturally lack a cell wall and have sterols in their cytoplasmic membrane. Mycoplasmas are the smallest microorganisms that can independently grow on a cell-free medium. Mycoplasma pneumoniae is common cause of both upper and lower respiratory infections
Define tolerance
Tolerant bacterium is not killed but simply stops growing when the antibiotic is present.
Describe rickettsias and name 4 rickettsial infections of humans and the vector involved
Rickettsias are small, mostly obligate intracellular parasites unable to make their own ATP. Rickettsia rickettsii causes Rocky Mountain Spotted Fever (ticks). Rickettsia prowazekii causes epidemic typhus (lice). Rickettsia typhi causes endemic typhus fever (fleas). Erlichia causes human granulocytic erlichiosis (deer tick).
Describe chlamydias and state the human infections each species may cause
Chlamydias are coccoid bacteria that are small and lack peptidoglycan in their cell walls. They are also obligate intracellular parasites. The infectious for is the elementary body, while the reticulate body is the form that divides by binary fission into more elementary bodies. Chlamydia trachomatis causes trachoma, LGV, nongenococcal urethritis, PID, neonatal respiratory and eye infections. C. trachomatis is leading cause of female reproductive problems in U.S. C. pheumoniae can cause pheumonia, pharyngitis, bronchitis, and sinusitis.
Briefly describe the life cycle of chlamydias
The infectious form of Chlamydias is the elementary body, about .3 micrometers. The host cell phagocatizes the elementary body and places it in a vacuole where it develops into a larger reticular body, which divides by binary fission into two more elementary bodies.
Briefly describe what is meant by the endosymbiotic theory
Endosymbiotic theory is that little bacteria got enveloped by an amoeba-like cell and turned into the first mitochondria and chloroplast.
State 4 different body defense functions of the body's complement pathways.
1. inflamation
2. phagocyte chemotaxis
3. opsonization (enhanced attachment)
4. lysis of biological membranes
Define exotoxin and list three types of exotoxins.
Toxins released both from live and dead bacteria and somes time injected directly into human cells.
1. Superantigens (Type I toxins)
2. A-B toxins; toxins that interfere with host cells (Type III)
3. Exotoxins that damage host cell membranes (Type II)
**Briefly describe 3 different mechanisms by which bacteria can adhere to host cells and colonize. Name 2 bacteria that utilize each mechanism and name an infection each bacterium causes.
2. Adhesins are proteins in bacterial cell wall that allow the bacteria to bind closely with the host by means of specific host cell receptors. Streptococcus pyogenes causes streptococcal pharyngitis (strep throat). Bordetella pertussis causes pertussis (whooping cough).
State an advantage for bacteria in being able to switch the adhesive tips of their pili.
Allows them to adhere to different types of cells and evade immune defenses
*Briefly describe 3 ways capsules may enable bacteria to resist phagocytic engulfment, name 3 pathogenic bacteria that produce capsules, and state an infection each causes.
Capsules can prevent C3 convertase syntethesis, which in turn blocks opsonins and other protein production. Some capsules simply cover the C3b that binds to the bacterial surface and prevent the C3b receptor on phagocytes from making contact with the C3b. They also resist unenhanced attachment by preventing the glycoprotein receptors on phagocytes from recognizing the bacterial cell wall components. Streptococcus pneumoniae (lobar pneumonia), Bacillus anthracis (anthrax), and Bordetella pertussis(whooping cough)
State 4 beneficial functions of our antibody molecules.
1. stick bacteria to phagocytes
2. block their attachment to host cells
3. activate the classical complement pathway
4. clump bacteria together
3. Capsules (biofilms) are colonies sticking to hosts collectively with a capsular mass. Streptococcus mutans causes cavities in teeth. Escherichia coli causes hemorrhagic diarrhea and hemolytic uremic syndrome.
** Briefly describe 3 different mechanisms by which bacteria adhere to host cells and colonize and name 2 bacteria that untilze each and the infection they cause.
1. Pili are long shafts of protein at the end of which are adhesive tips that are shaped to fit into specific receptors on a host. Neisseria gonorrhoeae causes gonorrhea. Neisseria meningitidis casues meningococcal meningitis.
* List 6 virulence factors that promote bacterial colonization of the host.
1. Adhere to host cells; resist physical removal.
2. Invade host cells.
3. Contact host cells.
4. Resist innate immune defenses (phagocytosis and complement)
5. Evade adaptive immune defenses
6. Compete for iron, other nutrients
State 2 mechanisms other than capsules that certain bacteria might use to resist phagocytic engulfment.
a. Coagulase (Staphylococcus aureus) causes fibrin clots to form around the organism that help enable it to resist phagocytosis.
b. Yersinia use a Type III secretion systems to deliver proteins that depolymerize the actin microfilaments needed for phagocytic engulfment into the phagocytes
State 6 different ways bacteria might be able to resist phagocytic destruction once engulfed.
1. trick cell into engulfing them in a protective vacuole.
2. resistant to the toxins and defensins
3. escape from phagosome into the cytoplasm.
4. block transport machinery that allows lysosome to fuse with phagosome
5. prevent the acidification of the phagosome.
6. kill phagocytes with exotoxin leukocidin or induce macrophage apoptosis.
Define the following:
A. vasodilation
B. septicemia
C. hypotension
D. hypovolemia
E. septic shock
a. increased blood vessel diameter and permeability
b. microorganisms enter bloodstream and cause harm
c. drop in blood pressure
d. decreased volume of circulating blood
e. circulatory collapse
f. (disseminated intravascular coagulation) blood clots form within blood vessels throughtout body
g. (acute respiratory distress syndrom) respiratory failure resulting from inflammation, injury to capillaries in lungs, and pulmonary edema
h. multiple system organ failure
*Briefly describe the mechanism behind the shock cascade that can occur during septicemia.
Blood vessels dilate and neutrophils adhere to capillary walls. Chemokines cause them to dump their proteases and oxygen radicals, damaging capillary walls. Plasma leaves the bloodstream and enters tissue, decreasing volume of blood. Increased capillary permeability leads to inflamation in lungs, injury to capillaries in aveoli of lungs, and pulmonary edema (ARDS). Blood-clotting pathway causes blood to clot within vessels (DIC). Combination of hypotension, hypovelomia, DIC, and ARDS leads to acidosis, decreased cardiac output, circulatory collapse, multiple system organ failure (MSOF), and death.
Define cytokine and chemokine and name 4 proinflammatory cytokines.
Cytokine - intercellular proteins produced by one cell that bind to other cells and influence their activity.
Chemokine - cytokines that promote inflammation by sticking white blood cells to vessels, causing them to leak out.
1. tumor necrosis factor-alpha (TNF-alpha)
2. interleukin-1 (Il-1)
3. interleukin-6 (Il-6)
4. interleukin-8 (Il-8)
Briefly describe the role of LPS in gram-negative septic shock and gram-negative meningitis.
In both cases LPS is the endotoxin that initiates the cytokine creation causing the shock cascade.
Superantigens (Type I toxins) bind directly to the outsided of HMC-II molecules and are recognized by many T4-lymphocytes. This results in the secretion of excessive amounts of cytokine Il-2, which can lead to production of other cytokines which can eventually cause the shock cascade.
** Describe 6 different ways antibiotics or disinfectants may affect bacterial structures and functions and ultimately harm the cell. Give 2 examples of antibiotics or disinfectants for each mode of action.
1.Inhibit normal synthesis of peptidoglycan (cephalosporins and penicillins).
2. Inhibit acid-fast cell wall synthesis and other cell wall synthesis(INH (isoniazid) and ethambutol)
3. Alter the cytoplasmic membrane (polymixins, alcohol)
4. Inhibit normal nucleic acid replication (sulfonamides, fluoroquinolones)
5. Inactivate Bacterial enzymes (Cl and Iodine)
6. alter bacterial ribosomes (macrolides, aminoglycosides)
* Describe the composition of a gram-positive cell wall indicating the possible functions of peptidoglycan, teichoic acids, and surface proteins
Gram-positive cell wall has 20-80nm thick peptidoglycan (60-90%), with teichoic acids, lipoteichoic acids, and proteins. The peptidoglycan gives shape and prevents osmotic lysis. peptidoglycan and teichoic acid also activate the body's defence pathways. The proteins can be enzymes, adhesins, and invasins.
* Briefly describe how components of the gram-positive cell wall can promote inflammation
Peptidoglycan and teichoic acids are pathogen associated molecular patters that bind to pattern-recognition receptors and trigger innate immune defences, such as inflammation, fever, and phagocytosis.
* Describe the composition of a gram-negative cell wall indicating the possible functions of peptidoglycan, lipopolysaccharides, porins, and surface proteins
The gram-negative cell wall has an inner layer of 2-3 nm thick 10-20% peptidoglycan. This layer gives shape and prevents osmotic lysis. The outer membrane is a lipid bilayer composed of phospholipids, LPS, porins, and surface proteins.
*Briefly describe 4 ways a bacterium might evade our immune defenses and name a bacterium that does each.
1. Change adhesive tips on pili or surface proteins (Nisseria gonorrhoeae)
2. Create capsules which resemble carbos in human tissue prevent recognition (Neiseria meningitidis)
3. Produce proteins that bind to the Fc portion of antibodies (Staph aureus)
4. Immunoglobin proteases that degrade the antibodies (Helicobacter pylori)
State how enterotoxins cause harm and name a bacterium producing it.
High levels of cAMP and cGMP cause loss of electrolytes and water that results in diarrhea. Clostridium perfringens. (An A-B toxin)
State how the following exotoxins cause harm and name a bacterium producing each: pertussis exotoxin.
Causes high levels of cAMP, which results in increased respiratory secretions and mucous production and contributes to coughing. Bordetella pertussis. (A-B)
State how the following exotoxins cause harm and name a bacterium producing each: Pseudomonas exotoxin A
Similar to the diphtheria exotoxin. It results in tissue damage and inhibits phagocytic activity. Pseudomonas aeruginosa.
State how the following exotoxins cause harm and name a bacterium producing each: botulism exotoxin
Is an A-B neurotoxin that acts on the nervous system by preventing muscle stimulation leading to flaccid paralysis (weakened mucsles). Clostridium botulinum.
State how the following exotoxins cause harm and name a bacterium producing each: tetanus exotoxin
It is an A-B neurotoxin that prevents relaxing of muscles and causes spastic paralysis (simultaneous contraction of opposing flexor and extensor muscles). Clostridium tetani.
State how the following exotoxins cause harm and name a bacterium producing each: invasive adenylate cyclase
An A-B toxin that stimulates the synthesis of cAMP contributing to cough and excess mucus production. Bordetella pertussis.
State how the following exotoxins cause harm and name a bacterium producing each: Helicobacter toxins
A-B toxins that interact with the epithelial cells of the stomach causing them to produce chemokines resulting in extracellular killing by the phagocytes. Helicobacter pylori.
State how diptheria exotoxin causes harm and name a bacterium that produces it.
It is an A-B toxin that interferes with host cell protein synthesis. Cells of the heart, nerve tissue, and kidneys have receptors for this exotoxin. Corynebacterium diphtheriae.
State how cholera exotoxin causes harm and name a bacterium producing it.
It is an A-B toxin that blocks intestinal epithelial cells from taking in sodium and stimulates them to secrete large quantities of chloride. Water and other electrolytes osmotically follow. This causes loss of fluids, diarrhea, and severe dehydration. Vibrio cholerae.
State how the following exotoxins cause harm and name a bacterium producing each: anthrax lethal toxin and edema toxin.
Both A-B toxins share protective antigen (PA) as B component; different A parts. Lethal Factor (LF) at low levels inhibits porinflamitory cytokine production, reducing immune responce. At high levels is cytolytic for macrophages, causing chemokine induced shock. Edema factor generates cyclic AMP in host cells, impairs phagocytosis and production of chemokines. Bacillus anthracis.
State how the following exotoxins cause harm and name a bacterium producing each: shiga toxin
A-B toxin that cleaves host cell rRNA stopping host cell protein synthesis and also causes blood vessel damage. Shigella and some E coli.
Name three major types of photosynthetic bacteria and briefly describe where its photosynthetic system is located.
cyanobacteria: extensive thylakoid membrane system
green bacteria: in chlorosomes that are independent of the cytoplasmic membrane
purple bacteria: spherical or lamellar membrane systems that are continuous with the cytoplasmic membrane.
State the function of the following inclusion bodies:
A. cyanophycin granules
B. carboxysomes
C. gas vacuoles
D. polyhydroxybutyrate and glycogen granules
E. magnetosomes
F. volutin granules and sulfur granules
a. store nitrogen
b. CO2 fixation
c. regulate buoyancy
d. energy reserve
e. tiny magnets
f. store phosphate and store sulfur respectively.