WEEK 2: BACTERIAL PATHOGENICITY Flashcards

1
Q

What is symbiosis?

A

All associations in which one species lives in or on the body of another.

-living together!!

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2
Q

Symbiosis is a fundamental concept in ecology and the study of interspecific relationships. There are several types of symbiotic relationships, including.

State The 3 types of symbiotic relationships.

A

Mutualism:

In mutualistic symbiosis, both species involved benefit from the relationship. This can involve mutual exchange of resources or services.

For example, pollination is a classic example of mutualism, where plants provide nectar to pollinators (like bees) in exchange for the transportation of pollen to other flowers, aiding in reproduction.

Commensalism:

In commensalism, one species benefits from the interaction, while the other species is neither helped nor harmed.

An example is the relationship between barnacles that attach to the shells of sea turtles. The barnacles benefit from being transported to new feeding areas while the turtles are not significantly affected.

Parasitism:

Parasitic symbiosis involves one species (the parasite) benefiting at the expense of the other species (the host), which is harmed by the interaction.

Common examples include parasitic worms or bacteria that live within a host organism and derive nutrients from the host’s tissues.

Amensalism:

Amensalism is a type of symbiosis where one species is negatively affected (harmed or inhibited) by the presence of another species, which is not significantly influenced in return.

For example, some plants release chemicals into the soil that inhibit the growth of nearby plants.

Predation:

While not always classified as a symbiotic relationship, predation is another ecological interaction where one species (the predator) hunts and consumes another species (the prey). This interaction is crucial for controlling population sizes and regulating ecosystem dynamics.

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3
Q

Define the following terms:
Commensal
Pathogen
Opportunistic pathogen

A

Commensal: One species of organism lives
harmlessly and in complete harmony in or on the
body of a larger species
❖ without causing any damage or disease
❖ part of the normal flora

Pathogen: A microorganism that lives on or in the
host and capable of causing disease.

Opportunistic pathogen: An agent capable of
causing disease only when the host’s resistance is
impaired

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4
Q

Define the following terms:
Infection
Disease
Pathogenesis

A
  1. Infection -

Any situation in which a microorganism is established and growing in a host, whether or not the host is harmed.

  1. Disease is a damage or injury to the host that impairs host function.
  2. Pathogenesis refers both to the mechanism of infection and to the mechanism by which disease develops.

o It refers to the sequence of events in the response of cells or tissues to the etiologic agent, from the initial stimulus to the ultimate expression of the disease.

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5
Q

What is infectivity?

What is infectious dose (ID50)?

A

Ability of a pathogen to establish an infection and its capacity for transmission.

 Infectivity -positively correlate with virulence.

 Infectious dose 50 (ID50): is the dose or
numbers of the agent required to infect 50% of
animals in a test group

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6
Q

What is virulence?

What is lethal dose 50 (LD50)?

A

The quantitative measure of pathogenicity or harmfulness of an infectious agent.

It measures the severity of the disease or damage caused by the agent once it has successfully infected a host.

 Relative ability of a pathogen to harm the
host.

 Lethal dose 50 (LD50)- the dose of an agent
that can kill 50% of the animals in a test group.

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7
Q

What is the difference between infectivity and virulence?

A

“infectivity” relates to the initial capability of an infectious agent to enter and infect a host, while

“virulence” pertains to the harmfulness or severity of the disease caused by the agent once it has successfully established an infection.

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8
Q

Describe the “iceberg” concept of infectious disease.

A

Tip of the Iceberg (Clinical Cases):

The “tip” of the iceberg represents the cases of an infectious disease that are clinically apparent and diagnosed.

These are individuals who exhibit symptoms, seek medical attention, and are officially recognized as having the disease.

These cases are typically documented, reported, and included in official disease statistics.

Below the Surface (Subclinical and Unrecognized Cases):

Beneath the water’s surface, the “iceberg” represents the subclinical or unrecognized cases of the disease.

This category includes individuals who are infected with the pathogen but do not show symptoms or have mild, non-specific symptoms that may not lead them to seek medical care.

Some of these individuals may eventually develop symptoms, while others may remain asymptomatic throughout the course of their infection.

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9
Q

Whatare virulence factors?
Expression of virulence determinants are carefully regulated involves a form of chemical communication between bacteria known as _____________.

A

Factors that allow microorganisms to:
 invade the host cell.
 damage the host cells.
 resist the defenses of the host.

  • Expression of virulence determinants are carefully regulated involves a form of chemical communication between bacteria known as quorum sensing.
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10
Q

Outline mechanisms of acquiring bacterial virulence genes

A
  1. Horizontal Gene Transfer (HGT):

HGT is a major mechanism for acquiring virulence genes.
It involves the transfer of genetic material from one bacterium to another that is not its offspring. The primary methods of HGT include:

*Conjugation:
*Transformation:
*Transduction:

  1. Genomic Islands: Genomic islands are large segments of bacterial DNA that have been acquired through HGT and often contain virulence genes. These islands can integrate into the bacterial chromosome and become a permanent part of the genome.
  2. Plasmids and Mobile Genetic Elements:

Plasmids are small, circular pieces of DNA that can carry virulence genes and transfer them between bacteria.

They are considered mobile genetic elements and can move between different bacterial species.

  1. Integration of Prophages:

Some bacteria have temperate phages, which can integrate their DNA into the bacterial genome. This integration can sometimes bring with it virulence genes or alter the host’s gene expression to enhance virulence.

  1. Transposons: Transposons are genetic elements that can move within the bacterial genome. They may contain virulence genes or promote their transfer by facilitating recombination events.
  2. Gene Duplication and Divergence:

In some cases, virulence genes may arise through gene duplication events followed by divergence. A duplicated gene may acquire mutations that enable it to perform a new function associated with virulence.

  1. Mutations and Adaptations: Bacteria can acquire virulence by accumulating mutations over time. These mutations can lead to the expression of new virulence factors or the loss of factors that restrict pathogenicity.
  2. Genetic Rearrangements: Genetic rearrangements, such as inversions, deletions, or insertions, can result in the acquisition of virulence genes or the activation of silent virulence genes already present in the genome.

It’s important to note that not all bacteria with virulence genes are pathogenic, as the expression and regulation of these genes are influenced by various factors, including environmental conditions, host interactions, and the bacterium’s genetic background. Additionally, the presence of virulence genes does not guarantee the immediate development of disease; it is often a multifactorial process that depends on the interplay of multiple factors.

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11
Q

What are pathogenicity islands?

A

Pathogenicity islands are large genetic regions in the chromosome or on plasmids that contain sets of genes encoding numerous virulence factors that may require coordinated expression.

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12
Q

List the potential sources and possible routes of infection by bacteria.

A
  1. Human: Tuberculosis, Typhoid, Syphilis
  2. Animals: Anthrax, Tuberculosis, Brucellosis
  3. Insects: Plague, Typhus, Relapsing fever
  4. Soil, water: Tetanus, Cholera, Typhoid, Dysentery
  5. Food: Staphylococcus, food poisoning, Salmonellosis
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13
Q

Outline methods of transmission.

A

Contact
*Kissing
*Shaking hands
*Vertical
*Vector
*Animal

Indirect
*Fomites
*Vehicles
*Air
*Fecal-oral

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14
Q

Outline 3 ways in which Infectious agents establish infection and damage tissues.

A
  1. They can come into contact or enter host cells and directly cause cell death.
  2. They may release
    I. Toxins that kill cells at a distance
    ii. Enzymes that degrade tissue components, damage blood vessels and cause ischemic necrosis.
  3. Induce host immune responses (a double-edged sword!)
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15
Q

What is microbial pathogenesis?

A

Microbial Pathogenesis: Process by which organisms cause disease.

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16
Q

Describe the process of microbial pathogenesis.

A
  1. Exposure to pathogens
  2. Adherence to skin or mucosa
  3. Invasion into epithelium
  4. Colonization and growth: Production of virulent factors
  5. Toxicity
  6. Invasiveness and metastasis
  7. Tissue damage and disease
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17
Q

Give examples of bacterial pathogens transmitted by different routes and outline the ways in which they cause disease.

A
  1. Ingestion: Salmonella spp., Shigella spp., Yersinia enterocolitica, enterotoxigenic Escherichia coli, Vibrio spp., Campylobacter spp., Clostridium botulinum, Bacillus cereus, Listeria spp., Brucella spp.
  2. Inhalation
    Mycobacterium spp., Nocardia spp., Mycoplasma
    pneumoniae, Legionella spp., Bordetella, Chlamydophila psittacine, Chlamydophila pneumoniae, Streptococcus spp.
  3. Trauma /Skin
    Clostridium tetani, Clostridium perfringens,
    Staphylococcus aureus, Streptococcus spp, Bacillus
    anthracis, Pseudomonas spp.
  4. Arthropod bite: Rickettsia, Ehrlichia , Coxiella, Francisella , Borrelia spp., Yersinia pestis
  5. Sexual transmission: Neisseria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum
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18
Q

What are the following adherence factors?

A surface structure or macromolecule that binds a bacterium to a specific surface.

A complementary macromolecular binding site on a (eucaryotic) surface that binds specific adhesins or ligands.

A surface molecule that exhibits specific binding to a receptor molecule on another surface

Any protein that binds to a carbohydrate

The mucopolysaccharide layer of glycosaminoglycans covering animal cell mucosal surfaces.

Filamentous proteins on the surface of bacterial cells that may behave as adhesins for specific adherence.

Same as fimbriae

A specialized pilus that binds mating procaryotes together for the purpose of DNA transfer.

Fimbriae in Enterobacteriaceae which bind specifically to mannose terminated glycoproteins on eucaryotic cell surfaces.

A

Adhesin: A surface structure or macromolecule that binds a bacterium to a specific surface.

Receptor: A complementary macromolecular binding site on a (eucaryotic) surface that binds specific adhesins or ligands.

Ligand: A surface molecule that exhibits specific binding to a receptor molecule on another surface

Lectin: Any protein that binds to a carbohydrate

Mucous: The mucopolysaccharide layer of glycosaminoglycans covering animal cell mucosal surfaces.

Fimbriae: Filamentous proteins on the surface of bacterial cells that may behave as adhesins for specific adherence.

Common pili: Same as fimbriae

Sex pilus: A specialized pilus that binds mating procaryotes together for the purpose of DNA transfer.

Type 1 fimbriae: Fimbriae in Enterobacteriaceae which bind specifically to mannose terminated glycoproteins on eucaryotic cell surfaces.

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19
Q

Define the following adherence factors:

Type 4 pili:
Slime-layer:
Glycocalyx:
Capsule:
Lipopolysaccharide (LPS):
Teichoic acids and lipoteichoic acids (LTA):

A

Type 4 pili: Pili in certain Gram-positive and Gram-negative bacteria. In Pseudomonas, thought to play a role in adherence and biofilm formation.

Slime-layer: Proteins that form the outermost cell envelope component of a broad spectrum of bacteria, enabling them to adhere to host cell membranes and environmental surfaces in order to colonize.

Glycocalyx: A layer of exopolysaccharide fibers on the surface of bacterial cells which may be involved in adherence to a surface. Sometimes a general term for a capsule.

Capsule: A detectable layer of polysaccharide (rarely polypeptide) on the surface of a bacterial cell which may mediate specific or nonspecific attachment.

Lipopolysaccharide (LPS): A distinct cell wall component of the outer membrane of Gram-negative bacteria with the potential structural diversity to mediate specific adherence. Probably functions as an adhesin.

Teichoic acids and lipoteichoic acids (LTA):
Cell wall components of Gram-positive bacteria that may be involved in nonspecific or specific adherence.

20
Q

State the functions of a capsule.

A
  • Attachment
    -Prevent phagocytosis
    -Protects from complement- mediated lysis in serum or blood
21
Q

Give examples of encapsulated microorganisms.

A

Examples of Encapsulated
 Staphylococcus aureus
 Streptococcus pneumoniae
 Streptococcus pyogenes
(group A)
 Streptococcus agalactiae
(group B)
 Bacillus anthracis
Neisseria meningitidis
 Haemophilus influenzae
 Escherichia coli
 Klebsiella pneumoniae
 Salmonella spp.
 Yersinia pestis
 Campylobacter fetus
 Pseudomonas aeruginosa
 Bacteroides fragilis
 Cryptococcus neoformans
(yeast)

22
Q

Biofilms has a 3-step lifecycle. Describe it.

What is the function of biofilms.

Give an example of a natural biofilm.

A

The biofilm life cycle in three steps: attachment, growth of colonies (development), and periodic detachment of planktonic cells.

Less susceptible to phagocytosis, drugs,
or neutralizing antibodies.

Dental plaque is an example of a natural biofilm.

23
Q

State examples of diseases caused by biofilms.

A

. Periodontal disease
* Urinary tract infections
* Prosthetic joints and heart valve
* Kidney stones
* Osteomyelitis
* Endocarditis
* Cystic fibrosis
* Atherosclerosis
* Sinusitis
* Otitis media.

24
Q

Name microorganisms that form biofilms.

A

Staphylococcus epidermidis
Pseudomonas aeruginosa
Escherichia coli
Legionella
Vibrio
Leptospira interorgan
Streptococcus

25
Q

Outline mechanism of entry into host cells.

A

➢Coating of bacteria with antibodies /
Compliments/ protein (Opsonization)
➢Phagocytosis
➢Endocytosis
➢Pore formation
➢Type 3 and 4 Secretion System
➢Rearrangement of host cell cytoskeleton

26
Q

Pathogen multiplies and colonize in the tissues.
Presence of appropriate nutrients and environmental conditions make it suitable for them to grow.

State them.

A
  • Temperature
  • pH
  • Presence or absence of oxygen
  • Special proteins produced to colonize the host tissues.
    ✓Production of urease by Helicobacter pylori
    ✓Siderophores help obtain iron from environment.-
    Iron is a growth limiting micronutrient, e.g.: E coli, Neisseria, Salmonella
27
Q

What is invasiveness?

Virulence of pathogens depends on ______and ____________ resulting in host damage.

A

Ability of pathogens to enter host cells or tissues, spread, and cause diseases.

Virulence of pathogens depends on toxicity and invasiveness resulting in host damage.

Many pathogens produce enzymes and toxins that indirectly or directly enhance invasiveness.

28
Q

SOME EXTRACELLULAR BACTERIAL PROTEINS THAT ARE CONSIDERED INVASINS

  1. Hyaluronidase:
  2. Collagenase
  3. Neuraminidase
  4. Coagulase
  5. Kinases
  6. Leucocidin
A
  1. Hyaluronidase:
    Streptococci, Staphylococci, Clostridia
    Degrades hyaluronic of connective tissue.
  2. Collagenase
    Clostridium species
    Dissolves collagen framework of muscles.
  3. Neuraminidase
    Vibrio cholerae, Shigella
    Degrades neuraminic acid of intestinal mucosa.
  4. Coagulase
    Staphylococcus aureus
    Converts fibrinogen to fibrin which causes clotting.
  5. Kinases
    Staphylococci and streptococci
    Converts plasminogen to plasmin which digests fibrin.
  6. Leucocidin
    Staphylococcus aureus
    Disrupts neutrophil membranes and causes discharge of lysosomal granules.
29
Q

SOME EXTRACELLULAR BACTERIAL PROTEINS THAT ARE CONSIDERED INVASINS

Streptococcus pyogenes
Repels phagocytes and disrupts phagocyte membrane and causes discharge of lysosomal granules.

Streptococci, Staphylococci Clostridia
Destroy red blood cells (and other cells) by lysis.

Clostridium perfringens
Destroy lecithin in cell membranes.

Clostridium perfringens
Destroy phospholipids in cell membrane.

Bacillus anthracis
One component (EF) is an adenylate cyclase which causes increased levels of intracellular cyclic AMP.

Bordetella pertussis
One toxin component is an adenylate cyclase that acts locally producing an increase in intracellular cyclic AMP.

A
  1. Streptolysin
    Streptococcus pyogenes
    Repels phagocytes and disrupts phagocyte membrane and causes discharge of lysosomal granules.
  2. Hemolysins
    Streptococci, Staphylococci Clostridia
    Destroy red blood cells (and other cells) by lysis.
  3. Lecithinases
    Clostridium perfringens
    Destroy lecithin in cell membranes.
  4. Phospholipases
    Clostridium perfringens
    Destroy phospholipids in cell membrane.
  5. Anthrax EF
    Bacillus anthracis
    One component (EF) is an adenylate cyclase which causes increased levels of intracellular cyclic AMP.
  6. Pertussis AC
    Bordetella pertussis
    One toxin component is an adenylate cyclase that acts locally producing an increase in intracellular cyclic AMP.
30
Q

What is toxicity?

There are 2 types of toxins. Describe the 2.

A

The ability of an organism to cause disease by means of a preformed toxin that inhibits host cell function or kills host cells.

Endotoxins: Are toxic substances that are an integral part of the cell wall of Gram-negative bacteria.
They are not actively secreted by the bacteria but are released when the bacterial cells are lysed or destroyed.

Exotoxins are toxic proteins or enzymes actively secreted by living bacterial cells into their surrounding environment.

These proteins have specific targets in the host organism.

31
Q

State the 3 categories of exotoxins.

A

➢AB toxins
➢Cytolytic toxins
➢Super antigen toxins

32
Q

Describe structure of AB Toxin.

Describe the mechanism they use to result in toxicity in hosts.

A

AB Toxins:

Structure:

AB toxins are typically composed of two subunits: A (active) and B (binding) subunits.

The A subunit is responsible for the toxic activity, while the B subunit binds to host cells.

Mechanism:

The B subunit binds to specific receptors on the host cell’s surface, facilitating the entry of the A subunit into the cell. Once inside the cell, the A subunit exerts its toxic effects.

Examples: Diphtheria toxin and cholera toxin are examples of AB toxins. Diphtheria toxin inhibits protein synthesis in host cells, leading to cell death, while cholera toxin induces the secretion of excess fluid and electrolytes from intestinal cells, causing severe diarrhea.

33
Q

State the 3 types of AB toxins.

A

Neurotoxins
Cytotoxins
Enterotoxins

34
Q

Neurotoxins are types of AB toxins.

What is their function?

Describe their mechanism of action.

A

Function:

Neurotoxins are toxins that specifically target and affect the nervous system. They interfere with the normal functioning of neurons (nerve cells) and can lead to a variety of neurological symptoms and conditions.

Mechanism:

Neurotoxins may block neurotransmission, disrupt ion channels, or damage nerve cells directly. The effects can range from muscle weakness and paralysis to seizures and altered mental states.

Examples:

Botulinum toxin (produced by Clostridium botulinum) is a well-known neurotoxin that causes muscle paralysis and is used for medical and cosmetic purposes.

Tetanus toxin (produced by Clostridium tetani) leads to muscle stiffness and spasms, while certain snake venoms contain neurotoxins that can cause paralysis.

35
Q

What is the function of cytolytic Toxins?

Describe their MOA.

A

Cytolytic Toxins:

Function: Cytolytic toxins, also known as pore-forming toxins, disrupt the integrity of host cell membranes, leading to cell lysis or death.

Mechanism:

These toxins can form pores or channels in the host cell membrane, causing the influx of ions and osmotic imbalance, which leads to cell swelling and lysis.

Examples: Hemolysins produced by Staphylococcus aureus and Streptococcus pyogenes are examples of cytolytic toxins.

They can lyse red blood cells and other host cells.

36
Q

Describe the MOA of the Tetanus toxin

A

Clostridium tetani – spastic paralysis-Tetanus.

Tetanus toxin also an AB protein neurotoxin.
Binds to the inhibitory interneurons in the dorsal root and blocks release of inhibitory neurotransmitter glycine, which then unable
to inhibit release of acetyl choline leading to uncontrolled contractions of the muscles-Tetanus, lockjaw or trismus.

37
Q

Botulinum toxin is a neurotoxin.

What is it produced by?
How does it result in flaccid muscle paralysis?

A

Clostridium botulinum

  • Act at the NMJ blocking release of acetyl choline, preventing muscle contraction and flaccid paralysis and death by suffocation.
  • Botulinum toxin most potent biological toxin.
  • One milligram of the toxin is enough to kill more than 1 million guinea pigs.
38
Q

What is the function of cytotoxins?

Describe their mechanism of action.

A

Cytotoxins:

Function:

Cytotoxins are toxins that primarily target and damage various types of host cells. They can disrupt cellular structures and functions, leading to cell death.

Mechanism:

Cytotoxins may act by disrupting cell membranes, interfering with cellular processes, or triggering apoptosis (programmed cell death).

The effects can manifest as tissue damage and inflammation.

Examples: Cytotoxins can be produced by various pathogens, including bacteria and some venomous animals.

For instance, the cytolysins produced by certain bacteria like Streptococcus pyogenes can damage host cells and contribute to diseases such as streptococcal pharyngitis.

39
Q

What is the function of enterotoxins?

Describe their MOA.

A

Function:

Enterotoxins are toxins that specifically target the cells of the intestines (enterocytes).

They affect the gastrointestinal system and can lead to symptoms such as diarrhea, vomiting, and abdominal cramps.

Mechanism:

Enterotoxins typically disrupt the normal functions of enterocytes, causing increased secretion of fluids into the gut and alterations in ion transport.

These effects result in diarrhea and dehydration.

Examples:
Cholera toxin (produced by Vibrio cholerae) is a well-known enterotoxin that leads to the profuse, watery diarrhea characteristic of cholera.

Other pathogens, such as some strains of Escherichia coli, also produce enterotoxins that contribute to food poisoning and traveler’s diarrhea.

40
Q

A subset of exotoxins
 Affects the small intestine causing secretion of fluid into the intestinal lumen
 Results in vomiting and diarrhoea.
 Acquired by ingestion of contaminated food or water with
➢ Staphylococcus aureus, Clostridium perfringens, Bacillus cereus, Cholera,
Escherichia coli and Salmonella enterica serovar Typhimurium.

What toxins are those?
Are they endotoxins or exotoxins?

A

Enterotoxins

41
Q

What is the function of superantigen toxins?

Describe their MOA.

A

Superantigen Toxins:

Function:

Superantigens are a class of toxins that induce an excessive and non-specific activation of the host’s immune system, particularly T cells.

Mechanism:

Superantigens bind to major histocompatibility complex (MHC) class II molecules on antigen-presenting cells and simultaneously to specific T-cell receptors, leading to the activation of a large number of T cells.

This uncontrolled immune response can result in cytokine storms and inflammation.

Examples: Staphylococcal enterotoxins and toxic shock syndrome toxin (TSST-1) produced by Staphylococcus aureus are examples of superantigen toxins. They can cause conditions such as toxic shock syndrome and food poisoning.

42
Q

-Hyper stimulate large number of T lymphocytes
-Induce an immune response that is 2000x stronger than normal resulting in extensive inflammation and tissue damage.
-Produces large quantities of cytokines - interleukin 1, tumor necrosis factor leading to systemic inflammatory responses
-Rapid vasodilation and decrease in blood pressure, resulting in shock.

What toxin is this?
Is it an endotoxin or exotoxin?

A

Superantigen toxin
Exotoxin

43
Q

Superantigens result in rapid vasodilation and decrease in blood pressure, resulting in shock.

State 2 microorganisms that result in Toxic shock syndrome.

A

Toxic Shock Syndrome
➢ Staphylococcus aureus
➢ Streptococcus pyogenes

44
Q

Toxic lipopolysaccharides produced by Gram negative bacteria
as part of the outer layer of their cell envelope.
▪ Endotoxins cell bound -released in large amounts when the cell
lyse.
▪ Lipid A portion responsible for toxicity
▪ Polysaccharide fraction makes the complex water soluble and
immunogenic
▪ Endotoxins less toxic than exotoxins
▪ LD 50 for endotoxin for mice is 200-300 ug per animal
▪ LD 50 for botulinum toxin is 25 pg about 10million times less.
➢ Neisseria meningitidis
➢ Escherichia coli
➢ Shigella
➢ Salmonella

What toxins are those?

A

Endotoxins

45
Q

State 3 characteristics of Intracellular bacteria.

A

 Avoid hosts defenses - antibodies
 Ready access to host nutrient supply
 Antibiotics have difficulty entering cells

46
Q

State examples of intracellular bacteria.

A

➢ Mycobacterium tuberculosis
➢ M.leprae
➢ Chlamydia trachomatis
➢ Rickettsia
➢ Coxiella
➢ Yersinia species
➢ Neisseria sp.
➢ Brucella spp.
➢ Francisella spp.
➢ Coxiella burnetii
➢ Listeria monocytogenes
➢ Legionella pneumophila

47
Q

Differentiate between endotoxins and exotoxins.

  1. Composition
  2. Fever producing?
  3. Toxicity
  4. Release
  5. Toxic mechanism
  6. Location
A
  1. COMPOSITION
    *Endotoxins are primarily composed of lipopolysaccharides (LPS), which are complex molecules found in the outer membrane of Gram-negative bacteria. LPS consists of lipid A, core polysaccharide, and O-antigen components.

*Exotoxins are typically proteins or enzymes. They are highly specific in their action, often affecting particular cellular processes or structures in the host.

  1. FEVER PRODUCING

*Endotoxins: YES
*Exotoxins: NO

  1. TOXICITY
    -Endotoxins: Low, but may be fatal in high doses
    -Exotoxins: High
  2. LOCATION:

*Endotoxins are components of the cell wall of Gram-negative bacteria.
They are typically not actively secreted but are released when the bacterial cells are lysed or disintegrate.

*Exotoxins are proteins or enzymes actively secreted by living bacterial cells into their surrounding environment.
They are produced by both Gram-negative and Gram-positive bacteria.

  1. TOXIC MECHANISM:

*Endotoxins induce an immune response in the host, primarily by binding to Toll-like receptors (TLRs) on immune cells.
This immune response can lead to the release of pro-inflammatory cytokines, resulting in fever, inflammation, and, in severe cases, septic shock.

*Exotoxins can disrupt various host cell functions and physiological processes, often leading to tissue damage and disease symptoms.
They have a wide range of specific targets, such as cell membranes, intracellular processes, and signal transduction pathways.

  1. RELEASE:

*Endotoxins are released when the bacterial cells are lysed or disintegrate, which can occur during bacterial infection or antibiotic treatment.

*Exotoxins are actively secreted by living bacterial cells and are typically soluble proteins. They can affect host cells at a distance from the site of bacterial growth.