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Questions and Answers
What does H.pylori produce to neutralize stomach acid in its vicinity?
What does H.pylori produce to neutralize stomach acid in its vicinity?
How does Bordetella pertussis compromise the host’s respiratory function?
How does Bordetella pertussis compromise the host’s respiratory function?
What type of secretion system does Enteropathogenic E.coli (EPEC) use?
What type of secretion system does Enteropathogenic E.coli (EPEC) use?
What effect does pertussis toxin have on the host's G protein?
What effect does pertussis toxin have on the host's G protein?
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What is a key characteristic of H.pylori in relation to disease?
What is a key characteristic of H.pylori in relation to disease?
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What role do flagella play for H.pylori in the stomach?
What role do flagella play for H.pylori in the stomach?
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What is the primary outcome of the adhesion of Bordetella pertussis to ciliated epithelial cells?
What is the primary outcome of the adhesion of Bordetella pertussis to ciliated epithelial cells?
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What is the function of the receptor protein Tri in Enteropathogenic E.coli (EPEC)?
What is the function of the receptor protein Tri in Enteropathogenic E.coli (EPEC)?
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Which of the following is NOT one of the six general categories that viruses rely on to be successful?
Which of the following is NOT one of the six general categories that viruses rely on to be successful?
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How does a virus acquire an envelope?
How does a virus acquire an envelope?
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What is the role of the capsid in a virus?
What is the role of the capsid in a virus?
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What is one method by which pathogens, such as Yersinia pestis, enter their host?
What is one method by which pathogens, such as Yersinia pestis, enter their host?
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Which of the following best describes the function of viral genome replication?
Which of the following best describes the function of viral genome replication?
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Why is it significant that vaccination and immunization lead to decreased disease incidence?
Why is it significant that vaccination and immunization lead to decreased disease incidence?
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How does H. pylori persist in the stomachs of its host?
How does H. pylori persist in the stomachs of its host?
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What is indicated by the statement 'a single virion can produce thousands of progeny'?
What is indicated by the statement 'a single virion can produce thousands of progeny'?
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What unique structure is formed on the cell surface due to the action of certain pathogenic bacteria?
What unique structure is formed on the cell surface due to the action of certain pathogenic bacteria?
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Which receptor is primarily used by HIV in its early stages of infection?
Which receptor is primarily used by HIV in its early stages of infection?
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Who might have immunity to HIV infection?
Who might have immunity to HIV infection?
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Which of the following correctly describes the 'fusion with plasma membrane' entry strategy of HIV?
Which of the following correctly describes the 'fusion with plasma membrane' entry strategy of HIV?
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What is the primary action of the zipper mechanism used by bacteria?
What is the primary action of the zipper mechanism used by bacteria?
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Which strategy employs endosomal membrane disruption to release viral content into the cytosol?
Which strategy employs endosomal membrane disruption to release viral content into the cytosol?
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Which cells are most efficiently infected by HIV variants that utilize CXCR4?
Which cells are most efficiently infected by HIV variants that utilize CXCR4?
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What role do Rho family small GTPases and Arp2/3 complex play in the action of bacterial mechanisms?
What role do Rho family small GTPases and Arp2/3 complex play in the action of bacterial mechanisms?
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What is the role of actin filaments in the movement of bacterial pathogens within host cells?
What is the role of actin filaments in the movement of bacterial pathogens within host cells?
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What is the primary mechanism by which L.monocytogenes escapes the phagosomal membrane?
What is the primary mechanism by which L.monocytogenes escapes the phagosomal membrane?
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How do pathogens facilitate their entry into neighboring cells without exposure to the extracellular environment?
How do pathogens facilitate their entry into neighboring cells without exposure to the extracellular environment?
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How does M.tuberculosis evade the phagosome?
How does M.tuberculosis evade the phagosome?
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What is the function of effector proteins secreted by bacteria in relation to host cell actin?
What is the function of effector proteins secreted by bacteria in relation to host cell actin?
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In how do viruses utilize the axonal transport system for their movement within host neurons?
In how do viruses utilize the axonal transport system for their movement within host neurons?
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What strategy does S.enterica employ to slow phagosomal maturation?
What strategy does S.enterica employ to slow phagosomal maturation?
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What do the effector proteins injected by L.pneumophila do?
What do the effector proteins injected by L.pneumophila do?
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What is the consequence of bacterial pathogens colliding with the host cell membrane?
What is the consequence of bacterial pathogens colliding with the host cell membrane?
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What unique movement strategy do some viruses use once they infect sensory neurons?
What unique movement strategy do some viruses use once they infect sensory neurons?
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At what pH level does listeriolysin O become less active in L.monocytogenes?
At what pH level does listeriolysin O become less active in L.monocytogenes?
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Which system does L.pneumophila use to inject its effector proteins into the phagocyte?
Which system does L.pneumophila use to inject its effector proteins into the phagocyte?
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What happens to the actin filaments as the bacterial pathogens advance through the cytosol?
What happens to the actin filaments as the bacterial pathogens advance through the cytosol?
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What is a significant outcome of S.enterica's alteration of phagosome maturation?
What is a significant outcome of S.enterica's alteration of phagosome maturation?
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How do some pathogens manipulate autophagy mechanisms in host cells?
How do some pathogens manipulate autophagy mechanisms in host cells?
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Which cellular structures do viruses acquire their envelope from during budding?
Which cellular structures do viruses acquire their envelope from during budding?
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What is one method that viruses use to manipulate the autophagy process in host cells?
What is one method that viruses use to manipulate the autophagy process in host cells?
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What is a consequence of viruses encoding proteins that modify the host's transcription/translation apparatus?
What is a consequence of viruses encoding proteins that modify the host's transcription/translation apparatus?
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What are the two main advantages that allow pathogens to evolve rapidly?
What are the two main advantages that allow pathogens to evolve rapidly?
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How does antigenic variation benefit trypanosomes?
How does antigenic variation benefit trypanosomes?
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What is a common reason that RNA and DNA replication is error-prone among viruses?
What is a common reason that RNA and DNA replication is error-prone among viruses?
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Which of the following describes the function of endonucleases encoded by some viruses?
Which of the following describes the function of endonucleases encoded by some viruses?
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In what way do selective pressures influence the evolution of pathogens?
In what way do selective pressures influence the evolution of pathogens?
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What is the primary role of a trypanosome's variable surface glycoprotein (VSG)?
What is the primary role of a trypanosome's variable surface glycoprotein (VSG)?
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Study Notes
Pathogens and Microbiota
- Pathogen: An organism, cell, virus, or prion that causes disease, exploiting host cell attributes for infection.
- Microbiota: Collective of microorganisms residing on or in an organism.
Primary and Opportunistic Pathogens
- Primary Pathogen: Causes overt disease in most healthy individuals, often spreading rapidly between hosts. Some can persistently infect a single host for years without overt symptoms.
- Opportunistic Pathogen: Normal flora microbes causing disease only when host immune systems are weakened or they gain access to normally sterile areas. Four characteristics of successful pathogens: Entering the host (breaking barrier), Finding a suitable niche, Avoiding the host's immune system, and Replicating to spread.
Gram-Positive and Gram-Negative Bacteria
- Gram-Positive Bacteria: Stain positive with Gram stain due to a thick peptidoglycan cell wall layer outside their plasma membrane.
- Gram-Negative Bacteria: Do not stain with Gram stain, due to a thin peptidoglycan cell wall outside their inner membrane, covered by an outer membrane.
- Lipopolysaccharide (LPS): Component of Gram-negative bacterial outer membranes.
- Pathogen-Associated Molecular Patterns (PAMPs): Shared molecular structures/molecules by many pathogenic bacteria and some viruses. PAMPs are recognized by the host immune system.
Horizontal Gene Transfer
- Horizontal gene transfer: Genes are transferred between bacteria and archaea via three mechanisms: natural transformation (release of naked DNA), transduction (infection by bacteriophages), or conjugation (sexual exchange).
- Genomics variation: Within a bacterial species, a certain degree of genomic variation is seen, with some bacterial species having core genomes common to all isolates and larger pangenomes containing additional genes present in subsets of isolates.
Bacterial Shapes and Structures
- Bacterial shapes: Various shapes like cocci (spherical), bacilli (rod-shaped), spirilla (spiral).
- Cell surface features: Gram-positive or gram-negative, and various appendages that may contribute to virulence.
Bacterial Pathogenicity
- Virulence genes: Encode proteins that contribute to an organism's ability to cause disease.
- Virulence factors: Proteins encoded by virulence genes that contribute to disease.
Pathogen Entry Strategies and Virulence
- Pathogen entry to host: Common entry points are wounds or by being transferred (e.g. to a non-immune host) via a vector.
- Yersinia pestis: Multiplies in the flea's foregut; block the digestive tract; transmitted to a new host.
- Helicobacter pylori: Persists in the stomach by neutralizing stomach acid using urease; was identified as a microbial cause of stomach ulcers.
- Bordetella pertussis: Colonizes respiratory epithelium; produces toxins that disable and kill ciliated cells (impeding host's clearing mechanism).
- Enteropathogenic E. coli (EPEC): Uses a type III secretion system to inject proteins, enabling the bacteria to attach to intestinal cells, triggering actin polymerization, and forming cellular protrusion (pedestal).
Viral Strategies and Mechanisms
- Viral Structures: Viruses can be either DNA or RNA viruses and have various morphologies.
- Viral Entry: Viruses use various strategies to enter cells which can include: (1) fusion with the host membrane, (2) endocytosis, (3) pore formation, (4) endosomal membrane disruption.
- HIV infection: HIV infection uses CD4, CCR5 co-receptor (early stages) and CXCR4 co-receptor to enter host cells.
Intracellular Pathogens
- Intracellular pathogens: Some pathogens use various strategies to survive within host cells and avoid the host's immune response mechanisms.
- L. monocytogenes: Avoids being killed by lysosomes, it secretes listeriolysin O, which disrupts the endosome/phagosome membrane; allowing replication in the cytoplasm.
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Description
Test your knowledge on various pathogens such as H.pylori, Bordetella pertussis, and Yersinia pestis. This quiz covers their mechanisms of action, effects on the host, and characteristics that contribute to disease. Challenge yourself with questions about virus structure and functioning as well.