Bacteria and Host interactions Flashcards
1
Q
Mutualism or Symbiosis
A
Both microbes and thier host benefit from the interaction
2
Q
Commensalism
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Microbes benefit and the host is not affected.
The microb involved in commensalism is called a commensal
3
Q
Normal Flora
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Microbes that establish a more or less permanent residence but do not produce disease under normal conditions,
- Protective Functions:
- Prevent the entry and establishment (overgrowth) of other bacteria, including pathogenic bacteria
4
Q
Parasitism
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Microbes benefit from the host while harming the host.
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Parasite
- an organism that benefits at the expence of another organism.
- Harm ranges from no recognizable damage to overt damage even death.
5
Q
Pathogen
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any disease-causing microorganism
specifically used to refer to bacterial, fungus, and viral agents of disease.
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Q
Saprophyte
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A bacterium that is in the environment and does not cause any disease
7
Q
Molecular Postulates
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Koch’s postulates are now supplemented and often supplanted by certain molecular criteria, which use percise genetic techniques to determine the pathogenicity of microorganisms
- THe virulence factor gene of its product should be found in pathogenic strains but not in the nonpathogenic strains of the suspected organism
- The genes for virulence must be expressed during the disease process
- Introduction of a virulence gene should change nonpathogenic stains to a pathogenic strain, whereas disrupting the function of the virulence gene should reduce the virulence of the organism
- Antibodies or immune cells for the virulence gene products should be protective.
8
Q
Etilogy
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Cause of disease
9
Q
Koch’s Postulates
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Robert Koch:
- was the first one to demonstrate taht bacteria cause disease, by studying anthrax
Koch’s Postulates:
- The pathogen must be present in every case of the disease
- The pathogen must be isolated from the diseased and grown in pure culture.
- The pathogen from the pure culture must cause disease when it is inoculated into a healthy, susceptible animal
- The pathogen must then be recovered from the inoculated animal
Exceptions:
- Some bacteria cannot be cultured in laboratory media
- Some infectious diseases are saused by different pathogens, which makes it difficult to identify which particular organism is involved
- Some infectious diseases are acaused by mixed Infections (polymicrobial infections)
- Some pathogens cause several disease conditions
10
Q
Pathogenesis
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The process by which the etiologic agent causes the disease
11
Q
Pathogenicicty
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Potential of an organism to cause disease.
Is shaped by the genetic makeup of the pathogen
12
Q
Viulence
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Relative pathogenicicty or a measure of the degree or severity of disease.
Describes attributes of the pathogen that promote pathogenicity.
Can be:
- Highly virulent
- Moderately virulent
- Avirulent
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Q
Virulence Factors
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Substances contained in or secreted by the pathogen that confer virulence to the microorganism.
Include cell surface proteinds, cell surgace carbohydrates, toxins, hydrolytic enzymes
14
Q
Invasiveness
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Ability to enter, survive, multiply, and spread within host tissues
15
Q
Primary Pathogen
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A microbe that can initiate disease on its own
16
Q
Secondary pathogen
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A microbe that invades or extablishes itself in host tissues due to the presence of a primary invader.
17
Q
Opportunistic Pathogen
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A microbe, often part of the normal flora, that is normally not pathogenic, but can cause disease upon lowered host resistance or when intorduced into a different location.
18
Q
Extracellular Pathogen
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Grows and multiplies in the space and fluids surroinding the cells.
In the laboratory, they are grown in conventional culture bacteriological media.
Majority of pathogens
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Q
Intracellular Pathogen
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Grows and multiplies inside cells.
Internalized by both phagocytic and nonphagocytic cells
20
Q
Facultatively Intracellular Pathogens
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Have the ability to grow and multiply both inside and outside the cell.
In the laboratory, they can be cultivated in culture media in the absence of living cells
21
Q
Obligately Intracellular Pathogen
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Grows and multiplies only inside the cells.
In the laboratory, they cannot be cultivated in conventional bacteriological media.
Lack the ability to grow independently, and can be grown in cell culture.
22
Q
Mechanism of Intracellular Survival
A
Nonphagocytic Cell uptake:
- Ability of the bacteria to enter nonphagocytic cell requires specific uptake mechanisms.
- Essentially three options to avoid being killed once taken into the cell:
- Escape the phagosome:
- produces hemolysin to break out of the phagolysosome. Escape the effects of the lysosomal enzymes and grow in the cytoplasm
- Prevent Fusion of Phagosome and lysosome:
- Prevent fusion by secreting proteins that interfere with the cell-signaling pathways taht cause phagosome-lysosome fusion
- Survive the harsh environment:
- Some pathogens are able to survive the harsh environments of the phagolysosome.
- Escape the phagosome:
23
Q
Infection
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the invasion or colonization of the body by a pathogenic organism.
Presence of a particular organism in a part of the body where it is not normally found
24
Q
disease
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occurs when an infection results in any change from a state of health.
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Infectious Disease
disease caused by a microorganism
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Contagious disease
infectious disease that is readily spread from an infected animal to another animal
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Primary Infection
Infection in a previously healthy host
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Secondary infection
occurs along with or immediately following another infection
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Exogenous infection
infection caused by bacteria that originate from outside the animal
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Endogenous infection
infection that originates from within the animal
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Latent infection
infection in which the causative agent remains inactive for a period of time but then becomes active to cause an infection
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Zoonotic infection (zoonosis)
infection or a disease, primarily of animals, that can be transmitted to humans.
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Nosocomial infection
infection that is acquired in a hospital.
Major problem in human medicine
Caused by a variety of organisms, including bacteria, fungi, viruses, parasites, and other agents.
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Sporadic Disease
disease that only occurs occasionally
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Endemic disease
disease that is constantly present in a population
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Epidemic disease
disease that occurs in a relatively short period of time in a large number of animals in a population or herd
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Pandemic Disease
Endemic disease that occurs worldwide
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Acute infection
the symptoms have a rapid onset and are usually severe and last only for a short time
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Peracute disease
A higher degree of acute disease
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Chronic Disease
infections develop more slowly, are less severe and last longer (months to years)
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Subclinical, or subacute infections
mild, in which case the symptoms do not occur and the disease will not be noticed.
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Localized
Abcesses
the invading bacteria is confined to a relatively small area of the body.
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Systemic (generalized) infections
bacteria or their toxins are spread throughout the animals body.
spread is generally becuase of entry of the organism into the circulation, blood or lymph, then blood.
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Focal infections
bacteria from a local infection enter blood or lymph and spread to other parts of the body, where they are confined to specific areas of the body
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Bacteremia
Bacteria circulating in the blood
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Septicemia
Bacteria multiplying in the blood
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Toxemia
Toxin circulating in the blood
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Infections and infectious diseases
an infectious disease begins with the entry of the organism into an animal
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Incubation period
interval between the entry and the first symptoms or signs of illness
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Illness
follows incubation period.
symptoms and signs of hte disease occur
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Symptoms (subjective changes)
are effects of the disease experienced by the patient
* pain
* nausea
* lack of appetite
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Signs (objective changes)
are efects of the disease observed by examining the patient
* skin rashes
* swelling
* abscess formation
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Convalescence
period during which the animal recuperates and recovers from the disease.
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Predisposing Factors
factor that makes the animal more susceptible toa disease and may alter the course of the disease.
* inadequate nutrition
* stress
* age
* environent
* preexisting illness
* immune suppression
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Requirements for infection
there are four fundemantal requirements fora pathogen to be able to cause infection
1. enter the host (mode on infection)
2. Evade or compromise the host defenses
3. multiply and get established locally or spread to other parts of the body (invasion)
4. Damage the host.
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Virulence factors
Virulence factors are contained in the bacterial cells or secreted, which allow the pathogen to enter, evade, establish, and damage the host.
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1. Entry into the animal body
Bacteria must first gain entry into the body in order to set up infection.
Natural defense mechanisms and barriers, such as skin, mucus, celiated epithelium, and secretions containg antibacterial susbstances make it difficult for bacterial to gain entry into the body.
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Skin
based on the surface area skin is the largest organ.
it is an important defense barrier against disease.
Intact skin is impermeable to most microorganinsms.
Some microbes can enter through hair follicles or openings of sweat glands.
Certain fungi can grow in the skin to cuase disease
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Mucous Membranes
Many bacteria gain access by penetrating the mucous membrane lining the respiratory, gastrointestinal, and genitourinary tracts and the conjunctiva of the eye.
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Parenteral Route
bacteria in some instances can gain access by being directly deposited below the skin or mucous membrane when theses physical barreirs are broken or injured.
* Punctures
* bites
* cuts
* splitting caused by dryness
* wounds
* surgery
* insect bites
* larval migration
*
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Ingestion
the pathogen is ingested through contaminatied feed and water.
The entry of the pathogen is via the mucous membrane of the gastrointestinal tract
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Inhalation
pathogen is inhaled as aerosols or infectious droplets
entry of the pathogen is via the mucous membrane of the respiratory tract
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Venereal
Pathogen is transmitted by sexual contact
Entery of the pathogen is via the mucous membranes of the urogenital tract
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Vector-borne (parenteral)
pathogen is deposited in the subcutaneous tissues or directly into the blood by insect bites.
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Direct entry
they pathogen enters the site of infection
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2. evasion of host defenses
After the entry, inorder to establish an infection, the pathogen must overcome the host defenses.
Once the surface barriers are breached and pathogen reaches the underlying tissues, pathogen encounters two levels of host defenses: **innate resistance mechanisms and adaptive immune response**.
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3. Adherence
1. Adherence:
1. after entering the body, bacteria attache to the cells to facilitate colonization and infection.
2. **adhesion**:
1. process by which bacteria attach to cells
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Colonization and invasion
a pathogen must grow and multiply in order to establish itself on or within the host.
colonization is a prerequisite to set up the infection.
Pathogens have several mechanism to achieve internal spread.
* Some produce enzymes that can disrupt cell membranes. destroy the intracellylar matrix or disrupt the basement membrane that underlies epithelial cells
* Pathogens must go through or go between the cells. Some organisms after entry into the cells from the outside can emerge on the other side of the cells, extracellular but within the tissues.
* Another mechanism is by way of **M cells**, which are specialized cells taht are part of the mucosa-associated lymphoid tissue
* **endocytosis:**
* ****the pathogen attached to the normally nonphagocytic cell and is able to induce the cell to rearrange its actin molecules and ingest tha attached pathogen.
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4. Damage the Host
Infection could be local or spread to become systemic
Damage to the host may be caused by the direct action of the pathogen or by the host response to the infection.
The damage could be change in the physiology ofhte cell to the most dramatic effect , death,
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Virulence Factors.
are cell structures or substances elaborated by bacteria taht help establish the organism in the host and alter host functions to cause disease.
Encoded by virulence genes, include attachment structures, enzymes, toxins
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Extracellular Enzymes
Many virulence factors are extracellular enzymes that are secreted, for the most part, to obtain nutrients to the organism. the enzymes include hyaluronidases, proteases, DNAses, Collagenase.
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Hyaluronidase
An enzyme that promotes spreading of the organisms in tissues by breaking down hyluronic acid, a polysaccharide, that function as intracellular cement.
Also called the "spreading factor"
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Coagulase
enzyme causes fibrin formation form fibrinogen in blood.
Produced by pathogenic S. aureus.
The fibrin deposites on S. aureus act as a defense mechanism from host defenses.
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Streptokinase
fibrinolytic enzyme produces by S. pyogenes dissolves the fibrin clots, which are often formed at the site of infection to isolate the pathogen and limiting the spreadk.
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Toxins
Chemicals contianed in or produced by pathogens that damage tissues or trigger host immune responses that cause damage.
Often the primary factro contributing to **toxigenicity**
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Exotoxins
Produced inside the cell as part of the growth adn metabolism and are released extracellularly into the surrounding medium.
Are proteins and many have enzymatic activity, meaning even small amounts are damaging to the host.
Produced by Gram + and Gram - bacteria.
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Exotoxins are named on 4 characteristics
1. Based on the type of host cell attacked
1. Hemolysin - erythrocytes
2. leukotoxin - leukocytes
3. enterotoxin - enteryocytes
4. Neurotoxin - nerve cells
5. Cytotoxin - any cell
2. Based on the tissue, organ or system targeted
1. Neurotoxin
2. Enterotoxin
3. Dermonecrotic Toxin
3. Named for the disease
1. Cholera toxin
2. Tetanus toxin
3. Diphtheris toxin
4. Named for the bacteria
1. Bolulinum,
2. Cholera Toxin
3. Shiga Toxin
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Modes of action:
1. Cell memebrane damage
2. Protein Synthesis inhibition
3. Second messenger pathway disruption
4. Superantigens
5. Proteases
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Cell membrane Damage
Damage to the cell membrane causes leakage of cell contents resulting lysis and death of cells.
One type of membrane damaging tixins **Pore Forming** toxin.
Which inserts directly into the cytoplasmic membrane to form channels.
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Hemolysins
Membrane disrupting toxins that lyse red blood cells.
**alpha toxin** of S. aureus
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Leukotoxin
Membrane disrupting toxins taht lyse and kill phagocytes or white blood cells.
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Protein Sysnthesis Inhibition
These target ribosomes and inhibit protein synthesis.
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Second Messenger Pathway Disruption
Mess with cGMP and cAMP
These toxins subvert host cell secondary messenger pathways.
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Superantigens
These toxins activate the immune system and provoke a very intense immune response.
Nonspecifically stimulate the proliferation of T cells, which then release Cytokines.
Cytokines enter the blood stream and induce a number of symptoms including fever, vomiting, diarrhea, and sometines shock and death.
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Proteases
These toxins exert their biological activity because of their proteolytic activity.
Enzymes that break down protiens.
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Toxin Structure
Based on the structure of the molecule.
A-B toxin of RTX toxin
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A-B toxins
Have two subunits, designated A and B, both of which are polypetides.
The A part is the active component whit biological activity, and B part binds to the cell to allow transfer of A into the cell to exert its biological activity.
A subunit possesses enzymatic activity that is specific for each toxin.
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A-B toxin:
Shiga Toxin
Toxins are produced by *Shigella dysenteria* and enterohemorrhagic *E. coli* (EHEC)
The most common EHEC is a foodborne pathogen taht causes bloody diarrhea in humans. Cattle are major reservoirs of this organism.
Another serotype of EHEC causes a disease in pigs called **edema disease**
AB toxins with 5 B subunits and 1 A subunit, that bind to a glycolipid receptor, globotriaaosylceramide (GB3), at the surface of the epithelial or endothelial cells, permitting the toxin to be internalized by receptor-mediated endocytosis.
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A-B Toxins
Enterotoxins
Affect enterocytes lining the small intestine, generally causing massive secretion of fluid into the lumen of the intestine, leading to diarrhea.
AB toxins and exert their biological activity by stimulating cGMP and cAMP.
Affect ion balance in enterocytes causing secretion of electrolytes and water into the lumen.
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A-B Toxins:
Neurotoxins
Two major neutotoxins are tetanus and botulinum toxin
Both are AB toxins that block release of neurotransmitters involved in muscle activity.
Botulinum Toxin:
* is internalized at the neuromuscular junction, blocking the release of acetyl choline, and inhibits muscle contration.
Tetanus Toxin:
* From the site of infection is transported through the motor neurons to the spinal cord, where it binds specifically to ganglioside lipids at the inhibitory interneurons.
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RTX Toxin
Proteins are produced by a variety of _Gram negative bacteria_
Characterized by the presence of repetitions of glycine- or aspartic acid- rich sequences.
Typically 9 amino acid peptides.
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Virulence Genes
Pathogens carry genes that encode for the exotoxins.
Toxins are essential for the survival colonization and spread of the bacteria inside the host.
Targets for Diagnosis by PCR
Not essential for growth.
Horizon gene transfer
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Pathogenicity Islands
Chromosomes contain clusters of genes, generally longer than 30kb that encode virulence factors
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Endotoxins
Also called Lipopolysaccharides.
Part of the outer membrane of Gram - bacteria composed of lipopolysaccharides, phospholipids, and proteins.
Released when bacterial cells die naturally or digested by the phagocytes
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Alarm Reaction
At low concentrations of endotoxins
Fever, activation of complement. activationof macrophages, and stimulation of B-lymphocytes.
At high concentrations endotoxins cause shock and even death
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Fever
Is almost a universal symptom of endotoxin activity.
Fever is believed to occur as follows:
1. Gram negative bacteria are ingested by phagocytes and degraded in phagosomes releasing LPS
2. The endotoxins cause macrophages to produce a cytokine called Interleukin-1
3. IL-1 is carried via the blood to the hypothalamus, a center that regulates body temp.
4. The effects of IL-1 on the hypothalamus is mediated by the release of prostaglandins, which results in fever.
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Disseminated Intravasculat Coagulation (DIC)
Praticularly at high concentrations, is the activation of blood-clotting protiens, causing formation of blood clots.
These clots will block capillary blood flow resulting in decreased blood supply and tissue necrosis.
The deposition fo thrombi in small blood vessels resulting in damage because of oxygen deprivation.
Effect is most severe in the brain, kidneys, lungs, and adrenals
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Shock
In large doses, endotoxins can cause a condition of loss in blood pressure.
Phagocytosis of Gram - bacteria causes phagocytes to secrete a polypeptide called Tumer Necrosis Factor (TNF). TNF binds to many tissues and alters their metabolism.
TNF can cause damage to capillaries, causing their permeability to increase and loose large amounts of fluids, resulting in loss of blood pressure.
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Comparison of Bacterial Exotoxins and Endotoxins
Know the following table very well
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Portals of Exit
Bacteria leave the body via specific routes in secretions, excretions. discharges, or tissue that has been shed.
Exit allows spread of the pathogen to other susceptible hosts.
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