Bacterial Virulence Mechanisms

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Questions and Answers

What are A-B toxins primarily composed of?

One polypeptide part

Four polypeptide parts

Three polypeptide parts

Two polypeptide parts (correct)

What is a characteristic effect of endotoxins on the human body?

Lead to increased capillary permeability (correct)

Stimulate an immediate immune response

Cause only localized symptoms

Induce effective antitoxin formation

What role do plasmids play in bacterial pathogenicity?

They are involved in cellular respiration

They eliminate immune responses from hosts

They can carry genes for virulence factors (correct)

They require a host to replicate

How do superantigens affect the immune system?

They stimulate excessive immune responses Signup and view all the answers

Which type of toxin is produced by bacteria to lyse host cells by disrupting their plasma membranes?

Membrane-disrupting toxins Signup and view all the answers

What is one mechanism by which viruses evade the host's immune defenses?

By having specific attachment sites Signup and view all the answers

What common symptom is associated with exposure to endotoxins?

Fever and chills Signup and view all the answers

What characterizes the intracellular growth of viruses?

They replicate inside host cells Signup and view all the answers

What do infected cells produce to protect neighboring uninfected cells from viruses?

Alpha and beta interferons Signup and view all the answers

Which mechanism is commonly employed by fungi to evade host defenses?

Producing proteases to modify host cell membranes Signup and view all the answers

What effect do trichothecenes produced by certain fungi have on the host?

Inhibit protein synthesis Signup and view all the answers

What is a characteristic pathogenic mechanism of protozoa?

Infecting red blood cells to cause rupture Signup and view all the answers

What is a consequence of the resistance to antifungal drugs in pathogenic fungi?

Decreased receptor synthesis Signup and view all the answers

Which protozoan is known to prevent normal digestion within macrophages?

Toxoplasma Signup and view all the answers

What is one of the mechanisms viruses employ to evade interferon responses?

Developing mechanisms that hinder interferon effectiveness Signup and view all the answers

What disease is caused by ergotism produced from Claviceps purpurea?

Hallucinations and gangrene Signup and view all the answers

Which bacterial pathogen requires low pH for replication within phagocytes?

Coxiella burnetii Signup and view all the answers

How do biofilms enhance resistance to phagocytosis?

By forming an extracellular polymeric substance Signup and view all the answers

What is the primary function of siderophores in pathogenic bacteria?

To sequester iron from host proteins Signup and view all the answers

Which of the following is NOT a mechanism by which microorganisms can damage host cells?

Causing systemic infection Signup and view all the answers

Which pathogen can escape or inhibit phagosome-lysosome fusion?

Mycobacterium tuberculosis Signup and view all the answers

What role does the extracellular polymeric substance (EPS) play in biofilms?

It provides structural support Signup and view all the answers

How do some pathogens directly acquire iron without using siderophores?

By binding to host iron-transport proteins Signup and view all the answers

What happens to phagocytes when they interact with the EPS of Pseudomonas aeruginosa?

They can be killed Signup and view all the answers

Which molecule is found in Streptococcus pyogenes and aids in attachment while resisting phagocytosis?

M Protein Signup and view all the answers

What role does Opa Protein play in Neisseria gonorrhoeae?

Facilitates attachment and entry into host cells Signup and view all the answers

Which enzyme produced by bacteria helps to form clots that protect them from phagocytosis?

Coagulase Signup and view all the answers

Which extracellular enzyme helps to spread infections like gas gangrene by breaking down collagen?

Collagenase Signup and view all the answers

What does the presence of mycolic acid in Mycobacterium tuberculosis help the bacterium achieve?

Resisting digestion by phagocytes Signup and view all the answers

Which bacterial function is triggered by adhesins leading to membrane ruffling in host cells?

Invasion Signup and view all the answers

Which bacteria use invasins to rearrange actin filaments in host cells?

Salmonella and E. coli Signup and view all the answers

What is the primary function of kinases produced by bacteria?

Breaking down fibrin clots Signup and view all the answers

How does HIV evade the immune system?

By hiding attachment sites from immune detection Signup and view all the answers

What is a direct outcome of cytopathic effects caused by viral infections?

Accumulation of viruses leading to cell death Signup and view all the answers

Which type of cytopathic effect directly results in cell death?

Cytocidal effects Signup and view all the answers

What occurs during the inclusion bodies formation cytopathic effect?

Viral components aggregate in infected cells Signup and view all the answers

Which cytopathic effect is characterized by the formation of large multinucleate cells?

Syncytium formation Signup and view all the answers

Which effect could lead to cancer due to viral infection?

Chromosomal damage Signup and view all the answers

What is a potential effect of the measles virus on the immune response?

Reduced IL-12 production Signup and view all the answers

Which of the following describes how viral proteins can affect host cells?

By causing antigenic changes on cell surfaces Signup and view all the answers

Study Notes

Bacterial Encapsulation

Encapsulation enhances virulence by preventing phagocytosis and complement activation
Examples of encapsulated bacteria include: Klebsiella pneumoniae, Haemophilus influenzae, Bacillus anthracis, and Yersinia pestis

Bacterial Cell Wall Components

M Protein (found in Streptococcus pyogenes) aids in attachment and resists phagocytosis
Opa Protein (present in Neisseria gonorrhoeae) facilitates attachment and entry into host cells
Mycolic Acid (in Mycobacterium tuberculosis) helps resist digestion by phagocytes

Bacterial Exoenzymes

Coagulases convert fibrinogen to fibrin, forming protective clots
Kinases (like streptokinase) break down fibrin clots
Hyaluronidase hydrolyzes hyaluronic acid, aiding tissue spread
Collagenase breaks down collagen, facilitating spread of infections like gas gangrene
Some bacteria produce IgA proteases to destroy IgA antibodies, aiding adherence

Bacterial Penetration of Host

Pathogens attach using adhesins, triggering host cell signals for entry
Bacteria like Salmonella and E. coli use invasins to rearrange actin filaments in host cells, leading to membrane ruffling and engulfment
Once inside, some bacteria like Shigella and Listeria can use actin for movement

Bacterial Survival Inside Phagocytes

Coxiella burnetii requires low pH for replication within phagocytes
Some bacteria escape or inhibit phagosome-lysosome fusion (Mycobacterium tuberculosis, HIV)

Bacterial Biofilms

Biofilms enhance resistance to phagocytosis
Phagocytes struggle to penetrate the extracellular polymeric substance (EPS)
EPS shields bacterial antigens from immune recognition and can even kill phagocytes (Pseudomonas aeruginosa)

Bacterial Iron Requirements

Most pathogenic bacteria require iron for growth
Free iron levels in the human body are low
Siderophores are proteins secreted by bacteria to bind and sequester iron from host iron-transport proteins (e.g., transferrin, lactoferrin).
The iron-siderophore complex is taken up by bacterial receptors, allowing bacteria to acquire essential iron

Damage Mechanisms of Microorganisms

Using the host's nutrients
Causing direct damage at the site of invasion
Producing toxins that affect distant sites
Inducing hypersensitivity reactions

Exotoxin Types

A-B Toxins: Composed of two polypeptide parts (A for activity, B for binding). Example: diphtheria toxin
Membrane-Disrupting Toxins: Lyse host cells by disrupting plasma membranes; examples include leukocidins and hemolysins
Superantigens: Stimulate excessive immune responses by activating T cells nonspecifically, leading to severe symptoms like shock

Endotoxin Effects

Common symptoms include chills, fever, weakness, and potentially septic shock due to increased capillary permeability and fluid loss
Endotoxins do not promote effective antitoxin formation

Plasmids and Pathogenicity

Plasmids carry genes for virulence factors (e.g., toxins, adhesins)
Lysogeny: Some bacteriophages integrate their DNA into bacterial genomes, leading to new pathogenic traits in lysogenic bacteria

Pathogenic Properties of Viruses

Access to Host: Viruses must gain entry into a host organism.
Evasion of Immune Defenses: Successful viruses evade the host's immune system.
Cell Damage: Viruses cause damage or death to host cells while replicating

Viral Mechanisms for Evading Host Defenses

Intracellular Growth: Viruses can replicate inside host cells, inaccessible to immune components
Attachment Sites: Viruses possess specific sites that bind to receptors on target cells, facilitating entry (Example: Rabies virus mimics acetylcholine to enter cells)
HIV Evasion: Hides attachment sites from immune detection, targets CD4 proteins on T lymphocytes, making it difficult for antibodies to neutralize the virus

Cytopathic Effects (CPE) of Viruses

Cell Death: Viral infections typically lead to host cell death via: Accumulation of viruses, Disruption of cellular functions (e.g., DNA/RNA/protein synthesis)
Types of CPE: Cytocidal Effects (directly result in cell death), Noncytocidal Effects (cause damage without killing the cell)

Specific Cytopathic Effects of Viruses

Inhibition of Macromolecular Synthesis: Some viruses halt cellular processes (e.g., Simplexvirus stops mitosis)
Lysosomal Enzyme Release: Host cell lysosomes release enzymes, leading to cell destruction
Inclusion Bodies Formation: Viral components aggregate in infected cells, aiding in diagnosis (e.g., Negri bodies in rabies)
Syncytium Formation: Infected cells may fuse to form large multinucleate cells seen in measles and mumps
Functional Changes Without Visible Damage: Example includes measles virus reducing IL-12 production, impairing immune response
Antigenic Changes on Cell Surfaces: Viral proteins alter host cell antigens, prompting immune targeting
Chromosomal Damage: Some viruses induce chromosomal breakage or activate oncogenes, leading to cancer risks
Cell Transformation: Certain viruses can transform host cells into abnormal growth patterns, losing contact inhibition

Interferon Production

Infected cells produce alpha and beta interferons to protect neighboring uninfected cells: Inhibit viral and host protein synthesis, Induce apoptosis in infected cells
Many viruses have evolved mechanisms to evade interferon responses

Pathogenic Properties of Fungi, Protozoa, Helminths, and Algae

Toxins: Trichothecenes (inhibit protein synthesis, cause headaches, chills, nausea), Ergotism (caused by Claviceps purpurea, leading to hallucinations and gangrene)
Virulence Factors: Proteases for attachment, capsule production (Cryptococcus neoformans), resistance to antifungal drugs
General Characteristics: Protozoa can cause disease through their presence and metabolic waste products
Cell Invasion: Plasmodium invades red blood cells, Toxoplasma prevents normal digestion within macrophages, Giardia intestinalis attaches to host cells and digests tissue fluids
Evasion of Host Defenses: Some protozoa use antigenic variation to evade the immune system (Trypanosoma)

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Description

This quiz covers various strategies that bacteria employ to enhance their virulence, including encapsulation, cell wall components, and exoenzymes. You will explore specific examples of bacteria and their mechanisms of evading host defenses. Test your knowledge on how these features contribute to bacterial infections.