Microbiology Host Microbe Interaction
Terms in this set (71)
Define microbiota or normal flora:
the group of microorganisms that colonizes the body surfaces but does not usually cause disease
When do they establish in our body?
soon after birth
List the specific sites where these microorganisms can be found:
nose, mouth, throat, skin, large intestine, vagina, urethra
Why does P.acnes causing Acne occur during puberty and why acne disappear with time?
Give one example of bacteria that are not found in vegetarians but do exist in non vegetarians.
List all the advantages that are provided by the normal flora to their host:
protection against potentially harmful microorganisms and development of the immune system. Excludes pathogens by covering binding sites that might otherwise be used for attachment, consuming available nutrients, and producing compounds that are toxic to other bacteria.
Give specific examples for the above:
Lactobacillus species in the vagina normally suppress growth of the yeast Candida albicans. In hair follicles of the skin, Propionibacterium species degrade the lipids found in skin glands, releasing fatty acids that inhibit the growth of many pathogens. In the gastrointestinal tract, some strains of E. coli synthesize colicins, proteins toxic to other strains of bacteria.
What are probiotics and why are they important for our health?
Probiotics are live beneficial microbes. They're important to our health because they replace good bacteria that has been lost from taking antibiotics, treat diarrhea and other diseases, and are beneficial for brain function and cholesterol.
organism or virus causing a disease
the ability of an organism or virus to cause disease
organism that causes disease only in hosts with impaired defense mechanisms or when introduced into an unusual location
growth and multiplication of a parasitic organism or virus in or on the body of the host with or without the production of disease; ex. Urinary tract infections - Escherichia coli, other Enterobacteriaceae, Staphylococcus saprophyticus, Pseudomonas aeruginosa
process resulting in tissue damage or alteration of function, producing body changes noticeable by physical examination or laboratory tests; ex. measles
initial infection; ex. various respiratory illnesses that damage the mucociliary escalator making a person more likely to develop pneumonia
an additional infection that occurs as a result of the primary infection; ex. pneumonia is the secondary infection to various respiratory illnesses
time between first exposure and the illness (infected but not yet experiencing the illness--still contageous) pathogen specific for how long this lasts
Period of illness:
experiencing signs & symptoms. begins prodromal: nonspecific symptoms like headache/body aches, then begin to experience more specific signs / symptoms
the time when a person is recovering, still can be infectious
usually sudden onset of symptoms, last for a short period of time then is resolved
onset is usually gradual, lasts for months years or even lifetime
the pathogen only infects one specific part of the body
the pathogen spreads throughout the body causing more serious symptoms
pathogen remains in the body unactive until something triggers it to reactivate (ie mono or chicken pox-->shingles)
virus circulating through the blood
bacteria is circulating through the blood
toxins are circulating in the blood
adhesins-allow the pathogen to attach to host cells, usually located at tips of pilli...attaches to RECEPTOR of host cell
Non specific adherence:
-glycocalyx → capsule/slime layer eg: dental plaque result of accumulation of capsules (glucan) in strep mutans
-surface proteins: intimin binds Enterohemmorgatic E.Coli to epithelial cells of large intestine
-adhesins on fimbrae: allow enterotoxogenic E.coli to bind to specific glycoprotein receptors in epithelial cells of small intestine
Colonization and hiding from the immune system give an example of a bacteria like Streptococcus group A may use during colonization:
-pathogen must compete with normal microbiota
-fight host immune system by:
-rapid turnover of pili → shed any IgA that may have bound
-antigenic variation by altering the types of pili
-IgA protease: enzymes cleave the IgA antibodies
-use siderophores: help them get the iron/nutrients from the host cells
"sense" the density of cells within their population
List three ways by which bacteria may avoid phagocytosis:
1.prevent an encounter with phagocytes
-C5A peptidase: enzyme that degrades complement proteins → no signal for phagocyte to come
-membrane damaging toxins: kills the cell around the pathogen, try to lyce it
2.avoid recognition & attachment
-affect opsonins that signal phagocytes
-capsule: surround the bacteria, inactivate all opsonins that attach to it
-M proteins: part of cell wall that acts like a capsule does -- bind complement protein & inactivates
-FC receptors: bind to the FC region of antibody and interferes with their function
3.survive within the phagocytes
-escape from the phagosome (capsule within the phagocyte), live in intracellular membrane
-prevent phagosome-lysosome fusion: wont be broken apart
-survive within the phagolysosome
lipopolysaccharides (LPS) IN GRAM -
-make up outer layer of gram - cell wall, NOT inside of the cell
-cannot be converted into a toxoid for vaccinations
-attached to the cell membrane, part of the structure of the cell wall
-ex: septic shock -- systematic bacterial infection
-heat stable, cant destroy with heat
-why IV fluids have to be sterile & free of endotoxins, cant kill with heat
-produced by gram + and gram - bacteria
-proteins with very specific damaging effects
-secreted by bacteria OR leak into fluids when bacteria lyses
-can act locally or be carried throughout the blood stream
-immune system tries to neutralize with antibodies, but it takes antibodies a while to get working
-toxoids from: tetanus, diptheria, pertussis
-can be used to make vaccines
-if NOT vaccinated and exposed to an exotoxin, can inject a person with antitoxin (ex: neutralize tetanus toxoid)
List the three outcome of toxicity that result from the endotoxin:
fever, pain, malase chock blood coagulation
UTI, typhoid, menigococcal meningitis
What is an A-B toxin ?
-two subparts: A subunit - toxic part (contains the enzyme that does the damage) B subunit - binds to the surface of the target cell (tells you which cell the toxin will effect)
-botulinum toxin: in chlostridium botulinium causes botulism → FLACID paralysis acts as motor neuron end plate to prevent release of acetylcholine, lack of stimulus to muscle fibers, irreversable relaxation of muscles
-Tetanospasmin: in clostridium tetani causes tetanus → SPASTIC paralysis
tetanus toxin binds to interneuron to prevent release of glycine, result in lack of inhibitory signals to motor neurons, constant release of acetycholine to muscle fibers → irreversable contraction of muscles
-cholera toxin: binds to intestinal cells (enterocytes--epithelial), triggers endocytosis of the toxin stimulates the overproduction of cAMP → watery diarrhea
-produced by Corynebacteria diptherea blocks the protein synthesis and affects the nerve, heart and kidneys
superantigens: induce excess stimulation of helper T cells, release large amount of cytokines which enter blood stream and cause fever, nausea, diarrhea, circulatory failure, shock (death)
staph aureus strain: food poisoning and toxic shock syndrome
strep. pyogenes: erythrogenic SPE scarlet fever and toxic shock syndrom
What is the difference between cytotoxic toxin and cytolytic toxin?
cytolytic toxin: disrupt the host cell membrane → leakage of cell content
cytotoxic toxin: leads to cell death
Give three examples of cytolytic toxins:
alpha toxin, phospholipase: clostridium perfringens
alpha toxin in staph aureus
List all the invasive enzymes that are associated with Staph.aureus (See skin diseases associate with Staph. Aureus )
List all the virulence factors which allow S.aureus to hide/destroy from the immune system(See skin diseases associate with Staph. Aureus )
1. The neurotoxins produced by Clostridium botulinum and Clostridium tetani are examples of virulence
2. The necrotizing enzymes produced by Clostridium perfringens and Streptococcus pyogenes are examples of virulence factors.
3. coagulases are exoenzymes that cause clot formation.
4. enterotoxins are exoenzymes that dissolve clots.
5. kinases are produced by Clostridium difficle, Salmonella spp., Shigella spp., Vibrio cholerae, and
certain serotypes of E. coli.
6. endotoxin is a virulence factor that is found in (and released from) the cell walls of Gram-negative
7. The molecules on the surfaces of host cells that pathogens are able to recognize and attach to are known as
receptors or integrins
8. Molecules on the surfaces of pathogens that are able to recognize and bind to molecules on the surfaces of
host cells are known as ligands or adhesins
9. hyaluronidase is also known as "spreading factor."
10. leukocidins are toxins that destroy white blood cell
Bacterial capsules protect bacteria from being phagocytized by leukocytes.
A headache is a classic example of a sign of a disease.
False. a headache is a symptom not a sign
In order to cause disease, all bacterial pathogens must first attach to some tissue in the body.
False. some bacterial pathogens can cause disease without attaching to tissue
Rickettsias and chlamydias are examples of obligate intracellular pathogens.
Babesia spp., Ehrlichia spp., and Plasmodium spp. are examples of intraerythrocytic pathogens.
False. Ehriichia spp. are intraleukocytic pathogens
The exoenzyme that causes toxic shock syndrome is called erthyrogenic toxin.
False. the erthyrogenic toxin causes scarlet fever
The neurotoxins produced by Clostridium botulinum and Clostridium tetani cause a spastic, rigid type of
False. Clostridium Botulinum causes a flacid type of paralysis
Although most people use the terms "infection" and "infectious disease" synonymously, microbiologists define
infection as colonization by a pathogen.
Avirulent strains do not cause disease.
It is thought that the waxes in the cell walls of Mycobacterium tuberculosis protect this pathogen from digestion
How are microbes able to resist immunologic clearance? Give at least one example of each mechanism
1. Encapsulation → Staphylococcus Aureus
2. Intracellular Growth →
4. IgG Binding Proteins
5. Inhibition of Phagolysosome Fusion
6.Resistance to Lysosomal Enzymes
What are the two general types of exotoxins ? list examples of each type
A-B Toxins: Neurotoxins, enterotoxins, cytotoxins
Superantigens: Staph. aureus, Strep group A
Cytolytic toxins: Leukocidins, alpha toxin, phospholipase
Name three routes by which exogenous pathogens can infect a person. List 5 examples that use each route.
3. Arthropod Bite/wound on skin
microbe lacks the ability to cause disease
establish microbial growth on a body surface
able to produce disease in a host with impaired defenses
The most successful parasites are the ones that live in harmony with their hosts.
Infection always leads to disease.
A disease is an infection that impairs the normal state of health
Obligate intracellular parasites may be grown in special synthetic media
During incubation and convalescence a person may still spread infectious organisms
The infectious dose of most pathogens is about equal.
A strong attachment of a microorganism to a host cell automatically leads to disease.
High concentrations of some bacteria are necessary for successful invasion because only at high density are their virulence genes expressed.
Only Gram-positive bacteria produce exotoxins.