Microbiology Chapter 16
Terms in this set (64)
It is an association in which both partners benefit. In the large intestine, some bacteria synthesize vitamin K and certain B vitamins. These nutrients are then available for the host to absorb. The bacteria residing in the intestine benefit as well, supplied with warmth and a variety of different energy sources
It is an association in which one partner benefits but the other remains unharmed. Many microbes living on the skin are neither harmful nor helpful to the human host, but they obtain food and other necessities from the host
It is an association in which one organism, the parasite, benefits at the expense of the other. All pathogens are parasites, but medical microbiologists often reserve the word parasite for eukaryotic pathogens such as protozoa and helminths
Microbes that typically inhabit body sites for extended periods are resident microbiota, whereas temporary occupants are transient microbiota
Streptococcus, Fusobacterium, Actinomyces, Leptotrichia, Veillonella
Streptococcus, Moraxella, Corynebacterium, Haemophilus, Neisseria, Mycoplasma
Bacteriodes, Escherichia, Proteus, Klebsiella, Lactobacillus, Streptococcus, Candida, Clostridium, Pseudomonas, Enterococcus
Streptococcus, Mycobacterium, Escherichia, Bacteroides
What is the normal microbiota's most significant contribution?
Protection against pathogens. The normal microbiota excludes pathogens by (1) covering binding sites that might otherwise be used for attachment, (2) consuming available nutrients, and (3) producing compounds toxic to other bacteria. When members of the normal microbiota are killed or their growth suppressed, as can happen during antibiotic treatment, pathogens may colonize and cause disease. Examples: Suppressed Lactobacillus in vagina can lead to yeast Candida albicans to multiply, resulting in vulvovaginal candidiasis. Oral antibiotics inhibit normal intestinal microbiota, allowing overgrowth of Clostridium difficil
How does the normal microbiota stimulate adaptive immunity?
They help develop mucosa-associated lymphoid tissue. In addition, antibodies produced against members of the microbiota bind to pathogen surfaces well. Our defenses learn to lessen the immune response to the many microbes that routinely inhabit the gut, as well as foods that pass through
Recent studies into actions of regulatory T cells indicate that early and consistent exposure to certain microbes in the gut stimulates these T cells, thereby preventing the immune system from overacting to harmless microbes and substances. This proposes that insufficient exposure to microbes can lead to allergies
This refers to a microbe establishing itself and multiplying on a body surface
When can you call a relationship an infection?
If the microbe has a parasitic relationship with the host, then the term infection can be used
This is an infection where symptoms either do not appear or are mild enough to go unnoticed
An infection that results in disease (a noticeable impairment of body function) is called this
The subjective effects of the disease experienced by the patient, such as pain and nausea
The objective evidence of the disease, such as a rash, pus formation, and swelling
What is the difference between primary and secondary infection?
For example, a respiratory illness that damages the mucociliary escalator makes a person more likely to develop pneumonia. The initial infection is a primary infection, an additional infection that occurs as a result of the primary infection is a secondary infection.
More simply, is a pathogen. It is a microbe or virus that causes disease in otherwise healthy individuals. Diseases such as plague, malaria, measles, influenza, diphtheria, tetanus, and tuberculosis are caused by primary pathogen
It is an opportunist, and causes disease only when the body's innate or adaptive defenses are compromised, or when introduced into an unusual location. Opportunists can be members of the normal microbiota or they can be common in the environment. For instance, Pseudomonas species are environmental bacteria that routinely come into contact with healthy individuals without harmful effect, yet they can cause fatal infections in individuals who have the genetic disease cystic fibrosis and also in burn patients. Many organisms not previously known to cause disease have now been shown to do so in severely immunocompromised patients
This refers to the degree of pathogenicity of an organism. An organism described as highly virulent is more likely to cause disease, particularly severe disease, than might otherwise be expected. Streptococcus pyogenes causes strep throat, for example, but certain strains are particularly virulent, causing diseases such as necrotizing fasciitis ("flesh-eating disease")
These are the traits of a microorganism that specifically allow it to cause disease. The genes encoding these traits can sometimes be transferred horizontally
What makes a disease communicable?
They are infectious diseases that spread from one host to another. Some contagious diseases, such as colds and measles, are easily transmitted
It is the number of microbes necessary to establish an infection. Generally, it is expressed as ID50, an experimentally derived figure that indicates the number of microbial cells administered that resulted in disease in 50% of the test population
What is the course of an infectious disease?
it includes several stages: incubation period, illness, prodromal phase, and covalescence
The time between introduction of a microbe to a susceptible host and the onset of illness. This varies considerably, from only a few days for the common cold, to several weeks for hepatitis A, to many months for rabies, and even years for Hansen's disease
This follows the incubation period. During this period, a person will experience the signs and symptoms of the disease
In some cases, onset of illness is heralded by this phase--the early, vague symptoms such as malaise and headache
After the illness subsides, there is this period, the stage of recuperation and recovery from the disease. Even though there is no indication of infection during the incubation and convalescent periods, many infectious agents can still be spread during these stages
Characterized by symptoms that develop quickly but last only a short time; an example is strep throat
Develop slowly and last for months or years; an example is tuberculosis
Never completely eliminated; the microbe continues to exist in host tissues, often within host cells, without causing any symptoms. If there is a decrease in immunity, the latent infection may become reactivated and symptomatic
The microbe is limited to a small area; an example is a boil caused by Staphylococcus aureus
The infectious agent is disseminated (spread) throughout the body; and example is measles
This means that bacteria are circulating in the bloodstream. This does not necessarily imply a disease state
Indicates that toxins are circulating in the bloodstream. The organism that causes tetanus, for instance, produces a localized infection yet its toxins circulate in the bloodstream
Indicates that viral particles are circulating in the bloodstream
(1) the microorganism must be presented in every case of the disease (2) the organism must be grown in pure culture from diseased hosts (3) the same disease must be produced when a pure culture of the organism is introduced into susceptible hosts (4) the organism must be recovered from the experimentally infected hosts
What did Koch study to come up with his postulate?
Koch studied anthrax, he grew B anthracis from all cases examined; he introduced pure cultures of the organism into healthy susceptible mice, again causing the disease anthrax. Finally, he recovered the organism from the experimentally infected mice
When does Koch's postulates not work?
The second postulate cannot be fulfilled for organisms that cannot be grown in laboratory medium, such as Treponema pallidum (causes syphilis). In other cases, the third postulate does not always hold true. There are many cases, including cholera and polio, in which some infected people do not have symptoms of disease. In addition, some diseases are polymicrobial, meaning that multiple species act together to cause the illness. Also, suitable experimental animal hosts are not available for some diseases and it would not be ethical to test the postulates on humans because of safety concerns
Molecular Koch's postulates
Similar in principle to Koch's postulates, but they rely on molecular techniques to study a microbe's virulence factors. Particularly relevant in the study of pathogens such as E. coli and Streptococcus pyogenes, which can cause several different diseases depending on the virulence factors of a given strain. (1) the virulence factor gene or its product should be found in pathogenic strains of the organism (2) mutating the virulence gene to disrupt its function should reduce the virulence of the pathogen (3) reversion of the mutated virulence gene or replacement with a wild-type version should restore virulence to the strain
What are the four patterns that pathogenic mechanisms follow?
Production of toxins that are then ingested, Colonization of mucous membranes of the host, followed by toxin production, Invasion of host tissues, Invasion of host tissues, followed by toxin production
Production of toxins that are then ingested
The microbe does not grow on or in the host, so this is not an infection but rather a foodborne intoxication, a form of food poisoning. The only virulence determinant is toxin production. Relatively few bacteria cause foodborne intoxication; these include Clostridium botulinum, and toxin-producing strains of Staphylococcus aureus
Colonization of mucous membranes of the host, followed by toxin production
The microbe adheres to a mucous membrane such as the lining of the intestinal or upper respiratory tracts and multiplies to high numbers. There, it produces a toxin that interferes with cell function
Invasion of host tissues
The microbe penetrates the first-line defenses and then multiplies within the tissues. Organisms that do this generally have mechanisms to avoid destruction by macrophages; some also have mechanisms to avoid antibodies
Invasion of host tissues, followed by toxin production
these microbes are similar to those in the previous category, but in addition to invading, they also make toxins
The pathogen becomes less virulent while the host becomes less susceptible
Where are adhesins located and how are they used?
They are often located at the tips of pili (pili used for attachment are often called fimbriae). They can also be a component of other surface structures such as capsules or various cell wall proteins
Where do adhesins attach?
The molecule to which an adhesion attaches is called the receptor. They have distinct roles for host cells; the microbes merely exploit the molecules for their own use. Receptors are typically glycoproteins or glycolipids, and the adhesion binds to the sugar portion
How specific is adhesion-receptor binding?
It is highly specific, dictating the type of cells to which the bacterium can attach. For instance, the adhesion of common E. coli strains allow them to adhere to cells that line the large intestine, where the strains multiply as part of the normal microbiota. Pathogenic E. coli strains have additional adhesins, broadening the range of tissues to which they can attach
How do microorganisms colonize a mucosal surface?
The pathogen must deal with the host's defenses that protect those surfaces. For example, the body uses lactoferrin and transferrin to bind iron, thereby limiting the growth of microbes
What are siderophores used for?
Some pathogens respond by producing their own iron-binding molecules, siderophores
How do these microorganisms avoid secretory IgA?
Pathogens have evolved mechanisms to avoid these antibodies. Mechanisms include rapid turnover of pili (to shed any bound antibody), antigenic variation, and IgA proteases (enzymes that cleave IgA antibodies)
How does the type III secretion system work and what does it do?
It is a syringelike structure that injects proteins into eukaryotic cells. The infected protein, referred to as effector proteins, induce changes such as altering the cell's cytoskeleton structure. Some effector proteins direct the host cell to engulf the bacterial cell
Which bacteria rely on skin damaging injuries to penetrate?
Staphylococcus aureus enters tissues via a cut or wound
How do pathogens enter the mucous membrane?
Direct uptake or exploiting antigen-sampling process.
Direct uptake by cells
Some pathogens induce non-phagocytic cells to engulf them. The pathogen first attaches to a cell, then triggers the process for endocytosis. Gram-negative bacteria often infect effector proteins that induce engulfment by host cells
Exploiting antigen-sampling process
Mucosa-associated lymphoid tissue samples material from the mucosal surface, and some pathogens use this process to cross the membranes. Several pathogens use M cells to cross the intestinal barrier. M cells transport material from the lumen of the intestine to the Peyer's patches. Most microbes delivered this way are destroyed by the macrophages in the Peyer's patches, but pathogens have mechanisms to avoid this fate. The freed bacterial cells then bind to the base of the mucosal epithelial cells and cause these non-phagocytic cells to engulf the, using a mechanism similar to that of Salmonella. Some pathogens invade by means of alveolar macrophages, which engulf material that enters the lungs. Mycobacterium tuberculosis produces surface proteins that direct their uptake by macrophages
Injected effector proteins cause actin molecules in the host cell cytoplasm to rearrange, resulting in the characteristic membrane ruffling on the cell's surface. The ruffles enclose the bacterial cells, bringing them into the intestinal cell
How can a pathogen exploit the antigen-sampling process?
(1) macrophages in the Peyer's patches engulf material that passes through M cells. Shigella cells survive and replicate, causing the phagocytes to undergo apoptosis. (2) Shigella cells attach to the base of the epithelial cells and induce these cells to engulf them (3) within an epithelial cell, Shigella cells cause the host actin to polymerize. This propels the bacterial cell, sometimes with enough force to push it into the next cell
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