Podcast
Questions and Answers
Which of the following is NOT considered a general feature that enables bacterial pathogens to survive and infect the human body?
Which of the following is NOT considered a general feature that enables bacterial pathogens to survive and infect the human body?
- Ability to evade the host’s innate and adaptive immune defenses.
- Ability to attach to host cells for colonization.
- Ability to obtain essential nutrients for multiplication within the host.
- Ability to produce toxins that directly kill host cells. (correct)
In the context of bacterial infection, which phase of the in vitro growth curve corresponds to the expression of genes encoding proteins required to withstand the immune response?
In the context of bacterial infection, which phase of the in vitro growth curve corresponds to the expression of genes encoding proteins required to withstand the immune response?
- Death phase
- Stationary phase
- Exponential phase (correct)
- Lag phase
What is a key difference between the evolutionary development of intact skin/antibody responses versus many bacterial defense strategies?
What is a key difference between the evolutionary development of intact skin/antibody responses versus many bacterial defense strategies?
- Skin and antibody responses evolved specifically to target endospore-forming bacteria.
- Skin and antibody responses are relatively recent evolutionary developments without direct counterparts in protozoa. (correct)
- Bacterial defenses are solely focused on evading antibiotic treatments.
- Bacterial defenses are primarily effective against viral infections.
How does genome plasticity contribute to bacterial survival in external environments?
How does genome plasticity contribute to bacterial survival in external environments?
What is the primary function of the extracellular polysaccharide (EPS) slime found in biofilms?
What is the primary function of the extracellular polysaccharide (EPS) slime found in biofilms?
How might bacteria in a biofilm become more resistant to antibiotics compared to their free-living counterparts?
How might bacteria in a biofilm become more resistant to antibiotics compared to their free-living counterparts?
What is the role of the hook-shaped protein complex in a bacterial flagellum?
What is the role of the hook-shaped protein complex in a bacterial flagellum?
How does the flagellin protein contribute to the host's immune response?
How does the flagellin protein contribute to the host's immune response?
What is a key difference between swimming and swarming motility in bacteria?
What is a key difference between swimming and swarming motility in bacteria?
How does the mucin layer protect mucosal cells, and what challenge does it present to pathogenic bacteria?
How does the mucin layer protect mucosal cells, and what challenge does it present to pathogenic bacteria?
What is the role of M cells in the context of bacterial infection of the small intestine?
What is the role of M cells in the context of bacterial infection of the small intestine?
How does Helicobacter pylori overcome the challenges posed by the mucin layer in the stomach?
How does Helicobacter pylori overcome the challenges posed by the mucin layer in the stomach?
How do bacteria utilize secretory IgA (sIgA) proteases to enhance their colonization of mucosal surfaces?
How do bacteria utilize secretory IgA (sIgA) proteases to enhance their colonization of mucosal surfaces?
How do some bacteria evade opsonization by antibodies?
How do some bacteria evade opsonization by antibodies?
What is the primary mechanism by which antibacterial peptides like defensins kill bacteria?
What is the primary mechanism by which antibacterial peptides like defensins kill bacteria?
How do some bacteria resist the effects of antibacterial peptides?
How do some bacteria resist the effects of antibacterial peptides?
How does Brucella abortus demonstrate host specificity in its nutrient acquisition?
How does Brucella abortus demonstrate host specificity in its nutrient acquisition?
What is a siderophore, and how does it aid in bacterial survival within a host?
What is a siderophore, and how does it aid in bacterial survival within a host?
What is the primary function of bacterial hemolysins and cytolysins in the context of iron acquisition?
What is the primary function of bacterial hemolysins and cytolysins in the context of iron acquisition?
While adherence is often considered essential, how can Helicobacter pylori stay in a particular site without special structures for adherence?
While adherence is often considered essential, how can Helicobacter pylori stay in a particular site without special structures for adherence?
What is the bi-phasic model of bacterial attachment, and what role do pili play in this process?
What is the bi-phasic model of bacterial attachment, and what role do pili play in this process?
What is the role of lectins in bacterial adherence to host cells?
What is the role of lectins in bacterial adherence to host cells?
What is the function of the chaperone proteins (e.g., FimC or PapD) in the assembly of pili in Gram-negative bacteria?
What is the function of the chaperone proteins (e.g., FimC or PapD) in the assembly of pili in Gram-negative bacteria?
How does the assembly of pili in Gram-positive bacteria differ from that in Gram-negative bacteria?
How does the assembly of pili in Gram-positive bacteria differ from that in Gram-negative bacteria?
What is the role of sortase enzymes in the context of pili assembly in Gram-positive bacteria?
What is the role of sortase enzymes in the context of pili assembly in Gram-positive bacteria?
How do afimbrial adhesins differ from pili in mediating bacterial attachment to host cells?
How do afimbrial adhesins differ from pili in mediating bacterial attachment to host cells?
How does the M protein of Streptococcus pyogenes contribute to its virulence?
How does the M protein of Streptococcus pyogenes contribute to its virulence?
How does bacterial attachment to host cells trigger signal transduction?
How does bacterial attachment to host cells trigger signal transduction?
What is the significance of pili replacement (antigenic variation) in the context of host immunity?
What is the significance of pili replacement (antigenic variation) in the context of host immunity?
How do capsules protect bacteria from the host's inflammatory response?
How do capsules protect bacteria from the host's inflammatory response?
How does a capsule composed of hyaluronic acid or sialic acid subvert the host's immune response?
How does a capsule composed of hyaluronic acid or sialic acid subvert the host's immune response?
How do changes in the length of LPS O-antigen side chains contribute to bacterial resistance to complement-mediated killing?
How do changes in the length of LPS O-antigen side chains contribute to bacterial resistance to complement-mediated killing?
Which of the following bacterial strategies primarily facilitates the spread of bacterial species to new hosts, ensuring their survival?
Which of the following bacterial strategies primarily facilitates the spread of bacterial species to new hosts, ensuring their survival?
In the context of bacterial infection, the expression of genes encoding toxins and degradative enzymes is most likely to be upregulated during which phase, according to the in vitro growth curve model?
In the context of bacterial infection, the expression of genes encoding toxins and degradative enzymes is most likely to be upregulated during which phase, according to the in vitro growth curve model?
Considering the evolutionary context, why might intact skin and antibody responses be considered particularly effective host defenses against bacterial pathogens?
Considering the evolutionary context, why might intact skin and antibody responses be considered particularly effective host defenses against bacterial pathogens?
Which of the following environmental factors is NOT mentioned as a major challenge to bacterial survival outside of a host?
Which of the following environmental factors is NOT mentioned as a major challenge to bacterial survival outside of a host?
How do bacterial endospores contribute to the survival of certain Gram-positive bacteria in harsh external environments?
How do bacterial endospores contribute to the survival of certain Gram-positive bacteria in harsh external environments?
What is the primary role of the extracellular polysaccharide (EPS) slime in bacterial biofilms?
What is the primary role of the extracellular polysaccharide (EPS) slime in bacterial biofilms?
Why are bacteria within biofilms often more resistant to antibiotics and disinfectants compared to planktonic (free-living) bacteria?
Why are bacteria within biofilms often more resistant to antibiotics and disinfectants compared to planktonic (free-living) bacteria?
In the context of dental plaque formation, what metabolic shift occurs in bacteria closest to the tooth surface, and what is its consequence?
In the context of dental plaque formation, what metabolic shift occurs in bacteria closest to the tooth surface, and what is its consequence?
Subacute bacterial endocarditis, caused by α-hemolytic streptococci, is highlighted as an example of:
Subacute bacterial endocarditis, caused by α-hemolytic streptococci, is highlighted as an example of:
What is a possible explanation for the limited effectiveness of antibiotic prophylaxis in preventing subacute bacterial endocarditis, despite the causative bacteria being susceptible to penicillin?
What is a possible explanation for the limited effectiveness of antibiotic prophylaxis in preventing subacute bacterial endocarditis, despite the causative bacteria being susceptible to penicillin?
Which bacterial structure is primarily responsible for motility in liquid environments, such as water or urine?
Which bacterial structure is primarily responsible for motility in liquid environments, such as water or urine?
How does the rotation of a bacterial flagellum facilitate movement?
How does the rotation of a bacterial flagellum facilitate movement?
What is the key difference between 'swimming' and 'swarming' motility in bacteria, as described in the text?
What is the key difference between 'swimming' and 'swarming' motility in bacteria, as described in the text?
How does the mucin layer protect mucosal cells from bacterial infection?
How does the mucin layer protect mucosal cells from bacterial infection?
How does Helicobacter pylori overcome the challenge posed by the mucin layer in the stomach to colonize the gastric mucosa?
How does Helicobacter pylori overcome the challenge posed by the mucin layer in the stomach to colonize the gastric mucosa?
What is the proposed mechanism by which secretory IgA (sIgA) proteases enhance bacterial colonization of mucosal surfaces?
What is the proposed mechanism by which secretory IgA (sIgA) proteases enhance bacterial colonization of mucosal surfaces?
How do some bacteria evade opsonization by antibodies, specifically mentioning Protein A of Staphylococcus aureus and Protein G of Streptococcus pyogenes?
How do some bacteria evade opsonization by antibodies, specifically mentioning Protein A of Staphylococcus aureus and Protein G of Streptococcus pyogenes?
What is the primary mechanism of action of antibacterial peptides like defensins in killing bacteria?
What is the primary mechanism of action of antibacterial peptides like defensins in killing bacteria?
How do some bacteria develop resistance to antibacterial peptides like defensins? Mentioning LPS modification as a specific mechanism.
How do some bacteria develop resistance to antibacterial peptides like defensins? Mentioning LPS modification as a specific mechanism.
Brucella abortus exhibits host specificity by preferentially proliferating in the placenta of pregnant cows due to the presence of high concentrations of:
Brucella abortus exhibits host specificity by preferentially proliferating in the placenta of pregnant cows due to the presence of high concentrations of:
What are siderophores, and how do they contribute to bacterial survival within a host environment?
What are siderophores, and how do they contribute to bacterial survival within a host environment?
What is the primary function of bacterial hemolysins and cytolysins in the context of iron acquisition, as suggested in the text?
What is the primary function of bacterial hemolysins and cytolysins in the context of iron acquisition, as suggested in the text?
While adherence is often considered crucial for bacterial colonization, how can Helicobacter pylori effectively colonize the stomach without relying on specialized adherence structures in the initial stage?
While adherence is often considered crucial for bacterial colonization, how can Helicobacter pylori effectively colonize the stomach without relying on specialized adherence structures in the initial stage?
Describe the bi-phasic model of bacterial attachment using pili, and what role do pili play in the initial phase?
Describe the bi-phasic model of bacterial attachment using pili, and what role do pili play in the initial phase?
How does the assembly of pili in Gram-positive bacteria differ significantly from that in Gram-negative bacteria, particularly regarding covalent linkages?
How does the assembly of pili in Gram-positive bacteria differ significantly from that in Gram-negative bacteria, particularly regarding covalent linkages?
The M protein of Streptococcus pyogenes, initially thought to be an adhesin, is now primarily recognized for its role in:
The M protein of Streptococcus pyogenes, initially thought to be an adhesin, is now primarily recognized for its role in:
How can bacterial attachment to host cells trigger signal transduction pathways in host cells?
How can bacterial attachment to host cells trigger signal transduction pathways in host cells?
How do bacterial capsules protect bacteria from the host's inflammatory response, particularly concerning complement and phagocytosis?
How do bacterial capsules protect bacteria from the host's inflammatory response, particularly concerning complement and phagocytosis?
How do changes in the length of LPS O-antigen side chains contribute to bacterial resistance to complement-mediated killing, specifically concerning the Membrane Attack Complex (MAC)?
How do changes in the length of LPS O-antigen side chains contribute to bacterial resistance to complement-mediated killing, specifically concerning the Membrane Attack Complex (MAC)?
Which of the following is LEAST directly related to a bacterium's ability to establish an infection within a host?
Which of the following is LEAST directly related to a bacterium's ability to establish an infection within a host?
In the context of bacterial infections, at what stage of the infection process are genes encoding toxins and degradative enzymes most likely to be upregulated?
In the context of bacterial infections, at what stage of the infection process are genes encoding toxins and degradative enzymes most likely to be upregulated?
Why might skin and antibody responses be effective defenses against bacterial pathogens?
Why might skin and antibody responses be effective defenses against bacterial pathogens?
What presents a significant challenge to bacterial survival in external environments?
What presents a significant challenge to bacterial survival in external environments?
What is the main function of endospores in certain Gram-positive bacteria?
What is the main function of endospores in certain Gram-positive bacteria?
How does the formation of biofilms enhance bacterial survival in various environments?
How does the formation of biofilms enhance bacterial survival in various environments?
What metabolic shift occurs in bacteria closest to the tooth surface within dental plaque biofilms, and how does this change contribute to dental caries?
What metabolic shift occurs in bacteria closest to the tooth surface within dental plaque biofilms, and how does this change contribute to dental caries?
How might the limited vascularization of the heart surface contribute to the challenge of treating subacute bacterial endocarditis with antibiotics?
How might the limited vascularization of the heart surface contribute to the challenge of treating subacute bacterial endocarditis with antibiotics?
How does the helical structure of a bacterial flagellum contribute to bacterial movement?
How does the helical structure of a bacterial flagellum contribute to bacterial movement?
What role do environmental signal sensors play in bacterial motility control?
What role do environmental signal sensors play in bacterial motility control?
How do spirochetes utilize their endoflagella to move through viscous media?
How do spirochetes utilize their endoflagella to move through viscous media?
How do bacteria, such as Borrelia burgdorferi and Yersinia pestis, breach the skin barrier to infect a host?
How do bacteria, such as Borrelia burgdorferi and Yersinia pestis, breach the skin barrier to infect a host?
What is a key reason why the mucin layer is difficult to study in the context of bacterial infection?
What is a key reason why the mucin layer is difficult to study in the context of bacterial infection?
How might the structure of the mucin layer facilitate bacterial transit to the mucosal cell surface?
How might the structure of the mucin layer facilitate bacterial transit to the mucosal cell surface?
Why are secretory IgA (sIgA) proteases thought to enhance bacterial colonization of mucosal surfaces?
Why are secretory IgA (sIgA) proteases thought to enhance bacterial colonization of mucosal surfaces?
What is an example of how bacteria avoid the host's antibody response by mimicking host molecules?
What is an example of how bacteria avoid the host's antibody response by mimicking host molecules?
How does the lipopolysaccharide (LPS) layer in gram-negative bacteria influence the bacteria's resistance to cationic defensins?
How does the lipopolysaccharide (LPS) layer in gram-negative bacteria influence the bacteria's resistance to cationic defensins?
What is the primary mechanism by which degradative enzymes enhance bacterial virulence?
What is the primary mechanism by which degradative enzymes enhance bacterial virulence?
Which of the following mechanisms is used by Gram-negative bacteria to acquire iron from host transferrin?
Which of the following mechanisms is used by Gram-negative bacteria to acquire iron from host transferrin?
What advantage do pili provide to bacteria during the initial stages of adherence by enabling them to make initial contact with a host cell?
What advantage do pili provide to bacteria during the initial stages of adherence by enabling them to make initial contact with a host cell?
Why is bacterial meningitis considered a particularly dangerous disease?
Why is bacterial meningitis considered a particularly dangerous disease?
What is a main characteristic shared by Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae type b that contributes to their ability to cause meningitis?
What is a main characteristic shared by Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae type b that contributes to their ability to cause meningitis?
How does the capsule of E. coli K1 contribute to its virulence in causing meningitis in newborns?
How does the capsule of E. coli K1 contribute to its virulence in causing meningitis in newborns?
What is the primary mechanism by which antibodies to capsular polysaccharides protect against bacterial meningitis?
What is the primary mechanism by which antibodies to capsular polysaccharides protect against bacterial meningitis?
Why was developing a vaccine against N. meningitidis type B more challenging compared to other types of N. meningitidis?
Why was developing a vaccine against N. meningitidis type B more challenging compared to other types of N. meningitidis?
Why are outbreaks of N. meningitidis meningitis in Africa frequently associated with the dry season?
Why are outbreaks of N. meningitidis meningitis in Africa frequently associated with the dry season?
Why can administering antibiotics that lyse bacteria sometimes worsen the condition of a patient with meningitis?
Why can administering antibiotics that lyse bacteria sometimes worsen the condition of a patient with meningitis?
What is the purpose of administering corticosteroids along with antibiotics in children with bacterial meningitis?
What is the purpose of administering corticosteroids along with antibiotics in children with bacterial meningitis?
How does the bacterial enzyme that degrades C5a enhance bacterial survival?
How does the bacterial enzyme that degrades C5a enhance bacterial survival?
How do some bacteria evade complement activation by mimicking host molecules, as seen with H. pylori?
How do some bacteria evade complement activation by mimicking host molecules, as seen with H. pylori?
What is the primary advantage for intracellular pathogens to invade and live inside host cells?
What is the primary advantage for intracellular pathogens to invade and live inside host cells?
How do bacteria like Yersinia pseudotuberculosis induce non-phagocytic cells to engulf them?
How do bacteria like Yersinia pseudotuberculosis induce non-phagocytic cells to engulf them?
What role do integrin receptors play in the invasion of host cells by Yersinia pseudotuberculosis?
What role do integrin receptors play in the invasion of host cells by Yersinia pseudotuberculosis?
How does disruption of normal actin polymerization processes in mucosal cells contribute to the inflammatory response during bacterial invasion?
How does disruption of normal actin polymerization processes in mucosal cells contribute to the inflammatory response during bacterial invasion?
What is the immediate result of a bacterium being ingested by a host cell?
What is the immediate result of a bacterium being ingested by a host cell?
What is a major advantage for a bacterium to escape from the phagosome into the cytoplasm of a host cell?
What is a major advantage for a bacterium to escape from the phagosome into the cytoplasm of a host cell?
What is the role of listeriolysin O (LLO) in the intracellular life cycle of Listeria monocytogenes?
What is the role of listeriolysin O (LLO) in the intracellular life cycle of Listeria monocytogenes?
Why is the pH optimum of LLO's membrane lytic activity at 5.5 considered advantageous for Listeria?
Why is the pH optimum of LLO's membrane lytic activity at 5.5 considered advantageous for Listeria?
What is a common strategy employed by intracellular pathogens like Chlamydia and Coxiella to survive within host cells?
What is a common strategy employed by intracellular pathogens like Chlamydia and Coxiella to survive within host cells?
How do obligate intracellular pathogens, such as Chlamydia and Coxiella, typically survive outside of their host cells?
How do obligate intracellular pathogens, such as Chlamydia and Coxiella, typically survive outside of their host cells?
What is a key characteristic of facultative intracellular pathogens that distinguishes them from obligate intracellular pathogens?
What is a key characteristic of facultative intracellular pathogens that distinguishes them from obligate intracellular pathogens?
How does Legionella manipulate mammalian phagocytic cells to create a replicative environment?
How does Legionella manipulate mammalian phagocytic cells to create a replicative environment?
How does Salmonella Typhimurium avoid the full effects of phagolysosomal destruction within macrophages?
How does Salmonella Typhimurium avoid the full effects of phagolysosomal destruction within macrophages?
What role does cholesterol play in the entry of Mycobacterium tuberculosis into macrophages?
What role does cholesterol play in the entry of Mycobacterium tuberculosis into macrophages?
How does Mycobacterium tuberculosis impede phagocytic destruction after being internalized by a macrophage?
How does Mycobacterium tuberculosis impede phagocytic destruction after being internalized by a macrophage?
What is the role of the smooth to rough conversion in Brucella bacteria regarding host cell interaction?
What is the role of the smooth to rough conversion in Brucella bacteria regarding host cell interaction?
How does Coxiella burnetii ensure its survival within the phagolysosome?
How does Coxiella burnetii ensure its survival within the phagolysosome?
What is the purpose of bacterial enzymes like catalase and superoxide dismutase (Sod) that neutralize reactive forms of oxygen?
What is the purpose of bacterial enzymes like catalase and superoxide dismutase (Sod) that neutralize reactive forms of oxygen?
What is the function of periplasmic superoxide dismutases (Sods) like SodC1 in Salmonella enterica serovar Typhimurium?
What is the function of periplasmic superoxide dismutases (Sods) like SodC1 in Salmonella enterica serovar Typhimurium?
What are peroxiredoxins (Prx) and what role do they play in bacterial survival?
What are peroxiredoxins (Prx) and what role do they play in bacterial survival?
How does the flavohemoglobin (NOD) enzyme contribute to E. coli's resistance to nitric oxide (NO)?
How does the flavohemoglobin (NOD) enzyme contribute to E. coli's resistance to nitric oxide (NO)?
What is the role of ActA protein in the actin-based motility of Listeria monocytogenes?
What is the role of ActA protein in the actin-based motility of Listeria monocytogenes?
Why do bacteria secrete deoxyribonucleases (DNases) during infection?
Why do bacteria secrete deoxyribonucleases (DNases) during infection?
How does staphylokinase contribute to the dissemination of S. aureus during infections?
How does staphylokinase contribute to the dissemination of S. aureus during infections?
What characteristic defines opportunistic pathogens?
What characteristic defines opportunistic pathogens?
Why are opportunistic pathogens, such as S. epidermidis and E. faecalis, becoming increasingly problematic in hospital settings?
Why are opportunistic pathogens, such as S. epidermidis and E. faecalis, becoming increasingly problematic in hospital settings?
What advantage do many opportunistic pathogens have due to their location within the host?
What advantage do many opportunistic pathogens have due to their location within the host?
What is the primary reason why bacterial meningitis can develop so rapidly?
What is the primary reason why bacterial meningitis can develop so rapidly?
How does the capsule of E. coli K1 contribute to its ability to cause meningitis?
How does the capsule of E. coli K1 contribute to its ability to cause meningitis?
Why are antibodies to capsular polysaccharides protective against bacterial meningitis?
Why are antibodies to capsular polysaccharides protective against bacterial meningitis?
Why did developing a vaccine against N. meningitidis type B prove more challenging compared to other types?
Why did developing a vaccine against N. meningitidis type B prove more challenging compared to other types?
How might dry conditions contribute to outbreaks of N. meningitidis meningitis?
How might dry conditions contribute to outbreaks of N. meningitidis meningitis?
What is the rationale for administering corticosteroids alongside antibiotics in children with bacterial meningitis?
What is the rationale for administering corticosteroids alongside antibiotics in children with bacterial meningitis?
How does immune mimicry, as seen with H. pylori, help bacteria evade the host immune response?
How does immune mimicry, as seen with H. pylori, help bacteria evade the host immune response?
How does ActA protein contribute to the actin-based motility of Listeria monocytogenes?
How does ActA protein contribute to the actin-based motility of Listeria monocytogenes?
Why does the presence of a capsule in bacteria like Neisseria meningitidis and Streptococcus pneumoniae contribute to the rapid progression of meningitis?
Why does the presence of a capsule in bacteria like Neisseria meningitidis and Streptococcus pneumoniae contribute to the rapid progression of meningitis?
Serum resistance is a critical factor in the pathogenesis of bacterial meningitis. How does Streptococcus pneumoniae, a Gram-positive bacterium, achieve serum resistance?
Serum resistance is a critical factor in the pathogenesis of bacterial meningitis. How does Streptococcus pneumoniae, a Gram-positive bacterium, achieve serum resistance?
Why are antibodies against capsular polysaccharides considered a crucial protective defense against bacterial meningitis?
Why are antibodies against capsular polysaccharides considered a crucial protective defense against bacterial meningitis?
Developing a vaccine against Neisseria meningitidis serogroup B was particularly challenging because its capsule is composed of sialic acid residues. What is the primary reason sialic acid capsules pose a challenge for vaccine development?
Developing a vaccine against Neisseria meningitidis serogroup B was particularly challenging because its capsule is composed of sialic acid residues. What is the primary reason sialic acid capsules pose a challenge for vaccine development?
Outbreaks of Neisseria meningitidis meningitis in Africa are often associated with the dry season. What is the most likely explanation for this correlation?
Outbreaks of Neisseria meningitidis meningitis in Africa are often associated with the dry season. What is the most likely explanation for this correlation?
Why can the administration of antibiotics that lyse bacteria sometimes initially worsen the condition of a patient with bacterial meningitis?
Why can the administration of antibiotics that lyse bacteria sometimes initially worsen the condition of a patient with bacterial meningitis?
Corticosteroids are often administered alongside antibiotics in children with bacterial meningitis. What is the rationale for this adjunctive therapy?
Corticosteroids are often administered alongside antibiotics in children with bacterial meningitis. What is the rationale for this adjunctive therapy?
Some Gram-positive bacteria produce an enzyme that degrades C5a. How does this enzyme contribute to bacterial virulence?
Some Gram-positive bacteria produce an enzyme that degrades C5a. How does this enzyme contribute to bacterial virulence?
Helicobacter pylori produces LPS with O-antigen carbohydrate moieties that mimic human Lewis antigens. What is the proposed benefit of this immune mimicry for H. pylori?
Helicobacter pylori produces LPS with O-antigen carbohydrate moieties that mimic human Lewis antigens. What is the proposed benefit of this immune mimicry for H. pylori?
Intracellular pathogens like Chlamydia and Coxiella have evolved to live inside host cells. What is the primary advantage of this intracellular lifestyle for these bacteria?
Intracellular pathogens like Chlamydia and Coxiella have evolved to live inside host cells. What is the primary advantage of this intracellular lifestyle for these bacteria?
Invasins are bacterial surface proteins that facilitate entry into host cells. How do invasins like the one used by Yersinia pseudotuberculosis function to promote bacterial uptake by non-phagocytic cells?
Invasins are bacterial surface proteins that facilitate entry into host cells. How do invasins like the one used by Yersinia pseudotuberculosis function to promote bacterial uptake by non-phagocytic cells?
Listeria monocytogenes escapes from the phagosome into the cytoplasm using listeriolysin O (LLO). What is the significance of LLO's optimal activity at pH 5.5 for Listeria's intracellular survival strategy?
Listeria monocytogenes escapes from the phagosome into the cytoplasm using listeriolysin O (LLO). What is the significance of LLO's optimal activity at pH 5.5 for Listeria's intracellular survival strategy?
Obligate intracellular pathogens like Chlamydia and Coxiella prevent phagolysosomal fusion. What is the primary consequence of preventing this fusion for their survival?
Obligate intracellular pathogens like Chlamydia and Coxiella prevent phagolysosomal fusion. What is the primary consequence of preventing this fusion for their survival?
Facultative intracellular pathogens like Legionella and Salmonella can survive both inside and outside of host cells. What distinguishes them from obligate intracellular pathogens in terms of their survival capabilities?
Facultative intracellular pathogens like Legionella and Salmonella can survive both inside and outside of host cells. What distinguishes them from obligate intracellular pathogens in terms of their survival capabilities?
Bacteria produce enzymes like catalase and superoxide dismutase (Sod) to neutralize reactive oxygen species. What is the primary function of these enzymes in bacterial survival during phagocytosis?
Bacteria produce enzymes like catalase and superoxide dismutase (Sod) to neutralize reactive oxygen species. What is the primary function of these enzymes in bacterial survival during phagocytosis?
Peroxiredoxins (Prx) are thiol-dependent antioxidant defense systems in bacteria. What is their role in bacterial survival against host defenses?
Peroxiredoxins (Prx) are thiol-dependent antioxidant defense systems in bacteria. What is their role in bacterial survival against host defenses?
ActA protein in Listeria monocytogenes is essential for actin-based motility. How does ActA facilitate the intracellular spread of Listeria?
ActA protein in Listeria monocytogenes is essential for actin-based motility. How does ActA facilitate the intracellular spread of Listeria?
Bacteria secrete deoxyribonucleases (DNases) as 'spreading factors'. What is the primary function of bacterial DNases during infection?
Bacteria secrete deoxyribonucleases (DNases) as 'spreading factors'. What is the primary function of bacterial DNases during infection?
Opportunistic pathogens like Staphylococcus epidermidis and Enterococcus faecalis are increasingly problematic in hospital settings. What is a key factor contributing to their success as opportunists in these environments?
Opportunistic pathogens like Staphylococcus epidermidis and Enterococcus faecalis are increasingly problematic in hospital settings. What is a key factor contributing to their success as opportunists in these environments?
Why are opportunistic pathogens often found to be located in areas of the body that are somewhat 'protected' from the immune system?
Why are opportunistic pathogens often found to be located in areas of the body that are somewhat 'protected' from the immune system?
Flashcards
Virulence Factors
Virulence Factors
Molecules or strategies used by pathogenic bacteria to cause disease.
Lag Phase
Lag Phase
Initial phase of bacterial growth, where genes for host cell attachment are activated.
Exponential Phase
Exponential Phase
Phase where genes for withstanding the immune response are activated
Stationary phase
Stationary phase
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Endospores
Endospores
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Biofilms
Biofilms
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EPS Slime
EPS Slime
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Subacute Bacterial Endocarditis
Subacute Bacterial Endocarditis
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Flagella
Flagella
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Chemotaxis
Chemotaxis
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Mucus
Mucus
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Mucinase
Mucinase
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M cells
M cells
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sIgA Proteases
sIgA Proteases
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Antigenic Variation
Antigenic Variation
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Defensins
Defensins
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Degradative Enzymes
Degradative Enzymes
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Siderophores
Siderophores
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Pili (Fimbriae)
Pili (Fimbriae)
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Afimbrial Adhesins
Afimbrial Adhesins
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Capsule
Capsule
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Bacterial Meningitis
Bacterial Meningitis
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Antiphagocytic Capsules
Antiphagocytic Capsules
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Serum Resistance
Serum Resistance
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Membrane Attack Complex (MAC)
Membrane Attack Complex (MAC)
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Opsonization
Opsonization
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Conjugate Vaccine
Conjugate Vaccine
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Bacterial Toxicity
Bacterial Toxicity
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Invasins
Invasins
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Phagosome
Phagosome
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Listeriolysin O (LLO)
Listeriolysin O (LLO)
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Sequestration Vacuoles
Sequestration Vacuoles
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Elementary Body (EB)
Elementary Body (EB)
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Reticulate Body (RB)
Reticulate Body (RB)
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Spreading Factors
Spreading Factors
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Opportunistic Pathogens
Opportunistic Pathogens
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Catalase and Superoxide Dismutase (SOD)
Catalase and Superoxide Dismutase (SOD)
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Peroxiredoxins (Prx)
Peroxiredoxins (Prx)
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ActA
ActA
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Study Notes
Bacterial Meningitis
- Bacterial meningitis is a life-threatening disease that can cause death or irreversible neurological damage
- It develops rapidly due to bacterial replication in the blood caused by antiphagocytic capsules and the ability to avoid complement-mediated killing
- Common causes include Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae type b
- These bacteria all produce polysaccharide capsules and dangerous strains are serum resistant
- Bacterial capsules protect bacteria from phagocytes once they enter the bloodstream
- N. meningitidis can become serum resistant by attaching sialic acid residues to their LPS molecules
- H. influenzae type b strains can become serum resistant by modification of LPS O-antigen side chains
- S. pneumoniae is naturally serum resistant due to the lack of an LPS-type molecule that can bind to the MAC
- E. coli K1 produces a capsule composed of sialic acid residues that does not bind C3b, preventing MAC component assembly
- The innate defense mechanisms of serum and blood are rendered ineffective by capsules and complement avoidance, except for transferrin-mediated iron sequestration
- N. meningitidis and H. influenzae can acquire iron from transferrin
- Antibodies to capsular polysaccharides opsonize the bacteria, facilitating phagocytosis and killing by neutrophils and macrophages
- People who develop antibodies against capsular antigens are protected from the disease
- H. influenzae type b primarily affects children aged 5 months to 5 years because older individuals develop antibodies due to nasopharyngeal colonization
- A conjugate vaccine is available that consists of capsular polysaccharide attached to a protein
- Older capsular polysaccharide vaccines against S. pneumoniae exist, but newer conjugate vaccines are more effective in children
- Vaccines against N. meningitidis are challenging to develop because type B capsules consist of sialic residues and do not evoke an antibody response
- Meningococcal vaccines exist for serogroups B, C, and Y (commonly seen in the United States), as well as serogroups A and W (found in other parts of the world)
- MPSV4 is a polysaccharide-based vaccine targeting serogroups A, C, W, and Y for high-risk children aged 2–10
- MCV4 is a conjugate-based vaccine targeting either A, C, W, and Y or C, Y, and H. influenzae type b, recommended for children 11+ and high-risk adults
- MCV4 is longer lasting than MPSV4
- There is a recombinant meningococcal vaccine available against serogroup B
- During N. meningitidis outbreaks, many may be colonized, but only a small percentage develop the disease
- Host susceptibility is affected by the integrity of the mucosal membranes
- N. meningitidis outbreaks are associated with the dry season due to compromised mucosal barriers
- Acute viral respiratory infections may also be a predisposing factor
- People with deficiencies in late complement components are more prone to meningitis
- Release of toxic cell wall components triggers toxic shock and death
- Antibiotics can worsen a patient's condition due to the release of toxic compounds from lysing bacteria
- Corticosteroids are administered with antibiotics to counteract the inflammatory effect of toxic compounds released from lysing bacteria
Other Strategies to Avoid Complement and Phagocytosis
- Some bacteria produce an enzyme that degrades C5a
- Many bacteria produce toxic proteins that kill phagocytes, prevent their activation/migration, block cytoskeletal changes, or reduce the oxidative burst
- Some bacteria can directly deliver inhibitory toxins into host immune cells and block intracellular signaling pathways
- Some bacteria have an LPS-type molecule that does not elicit strong host responses
- H. pylori O antigen contains carbohydrate moieties identical to human Lewis antigens, which could help prevent an effective immune response
- H. pylori elicits an inflammatory response that can result in gastritis/gastric ulcers and patients with symptomatic disease often have antibodies that cross-react with antigens on gastric mucosal tissue
- Salt concentrations in the stomach increase CagA production
- Low iron levels increase T4SS-associated pili adherence to α5β1-integrin on epithelial cells and translocation of CagA into epithelial cells
Invasion and Uptake by Host Cells
- Intracellular pathogens hide from the host immune system by invading and living inside host cells
- They can avoid complement or neutralizing antibodies
- They also gain access to available nutrients
- Many intracellular bacteria can enter host cells that are not naturally phagocytic
- They attach to the host cell surface and cause changes in the host cell cytoskeleton that result in their engulfment
- Bacterial surface proteins that provoke phagocytic engulfment of the bacterium by host cells are called invasins
- Yersinia invasin (encoded by the invA gene) gains entry into M cells of Peyer’s patches and thereby transit into the underlying tissues
- Mammalian receptors that are partners for invasin are members of the β1 integrin family of cell adhesion molecules that are found on the apical surface of M cells in Peyer’s patches
- Invasin binding to the integrin receptors causes clustering and activation of the signaling, which in turn triggers actin rearrangements in the M cells and engulfment of the bacteria
- Bacterial invasion of mucosal cells triggers these cells to release chemokines and cytokines that are known to be important for mobilizing phagocytes and other immune defenses
- Disruption of normal actin polymerization processes and the presence of bacteria within mucosal cells, sets off the cytokine/chemokine alarm system that initiates the inflammatory response
- Bacterial products such as LPS can trigger these inflammatory responses through activation of Toll-like receptors even without uptake by phagocytes or bacterial invasion of host cells
Surviving Phagocytosis
- Bacteria that have been ingested by host cells are enclosed in a membrane vesicle called a phagosome, which then fuses with lysosomes
- A vast majority of bacteria are killed by this process
- Some bacteria manage to evade, survive, and even multiply inside phagocytes
- The only effective host responses left against bacteria that can survive inside normal phagocytes are the activated macrophage response or the cytotoxic T cell response
Escape from the Phagosome
- Invading bacterium escapes from the phagosome before it merges with the lysosome
- Cytoplasm is abundant in nutrients, protection from antibodies and complement, and partial protection from some antibiotics
- The only effective host defense against bacteria that do this appears to be the cytotoxic T cell (CD8+) response or the natural killer (NK) cell response
- Escape from the phagosome is mediated by a bacterial protein toxin that disrupts membranes by degrading membrane lipids or by forming pores in the membrane
- L. monocytogenes induces its own uptake and then quickly escapes the phagosome
- One of the proteins responsible for the escape from the phagosome is a pore-forming hemolysin, called listeriolysin O (LLO)
- The optimal pH for the membrane lytic activity of LLO is 5.5 (similar to that of the phagolysosome)
- The lytic activity of LLO is reduced once Listeria has escaped from the phagosome
Prevention of Phagolysosomal Fusion
- Many intracellular pathogens produce factors that allow them to prevent phagosome-lysosome fusion and promote sequestration of the bacteria in specialized vacuoles
- Some examples are Chlamydia, Coxiella, Legionella, Salmonella, Mycobacterium, and Brucella
- Obligate intracellular pathogens, such as Chlamydia and Coxiella, generally have two developmental life cycles that enable them to survive the external environment during transmission from host to host and the harsh environment of the phagocyte
- In Chlamydia the extracellular infectious form of the bacterium that permits transmission from one host to the next is the small metabolically inactive elementary body (EB)
- The metabolically active form of the bacterium that replicates inside the host cell is the larger, noninfectious reticulate body (RB)
- The EB is contained within a specialized vacuole, called the inclusion, where the EB converts into the replicative RB form
- The RBs convert back into EBs and are released from the cell through lysis or extrusion release of packaged EB-filled vesicles
- The metabolically inactive, small-cell variant (SCV) form of Coxiella burnetii is highly infectious
- After the SCVs invade and form a Coxiella-containing vacuole (CCV), they convert into the metabolically active, large-cell variant (LCV) form that can replicate, but only after recruitment of the V-ATPase (proton pump) and acidification of the CCV
- LCVs replicate in an expanding CCV for four to seven days before converting back into SCVs, which are then released from the cell
- Unlike obligate intracellular pathogens, facultative pathogens can survive and replicate both outside the host in the external environment and within the host phagocyte
- The macrophage invasin Mip appears to facilitate the uptake process of Legionella cells
- Not only do the vacuoles not acidify to the same extent as normal phagosomes, but they also leave the normal pathway that leads to phagolysosomal fusion
- Salmonella Typhimurium triggers actin rearrangements that lead to the formation of ruffle-like structures in the host cell membrane.
- In these special Salmonella-containing vacuoles, the bacteria replicate
- M. tuberculosis uses multiple strategies for impeding phagocytic destruction.
- Bacterial recruitment of several host proteins to the phagosome surface prevents phagolysosomal fusion at the early endosome stage
- M. tuberculosis secretes a phosphatase, SapM, that hydrolyzes membrane phospholipid PI3P and prevents transition to late endosomes
- B. abortus traffics among three subcellular compartments during its intracellular life cycle
- Egress from the cell, which is still poorly understood, occurs after about three days and appears to involve formation of an autophagosome-like vacuole (aBCV) that promotes spread to adjoining host cells
Neutralization or Resistance to Phagolysosomal Components
- Some bacteria are acid-tolerant and can survive for periods of time within the acidic phagolysosomal compartments
- C. burnetii is an obligate intracellular pathogen that is remarkably resistant to the conditions found within the phagolysosome
- Coxiella employs the acidic environment of these degradative, phagolysosomal-like compartments with pH ∼5 to activate its metabolic activity and express an arsenal of proteins that protect the bacterium from phagocytic oxidative burst
Resistance to Reactive Oxygen and Nitrogen Species
- Some mechanisms include production of enzymes, such as catalase and superoxide dismutase (Sod), that neutralize reactive forms of oxygen
- M. tuberculosis has a thick cell envelope that is comprised of an abundance of oxygen and nitrogen radical scavengers, such as lipoarabinomannan and phenolic glycolipids
- S. enterica serovar Typhimurium produces four Sods: two cytoplasmic Sods (SodA and SodB) and two periplasmic Sods (SodC1 and SodC2)
- SodC1 enhances survival within the macrophage during infection because it remains tethered within the periplasm through noncovalent binding to the peptide portion of peptidoglycan and is inherently resistant to proteases
- Many bacteria possess thiol-dependent antioxidant defense systems, called peroxiredoxins (Prx), that catalyze the reduction of hydrogen peroxide, organic hydroperoxides, and peroxynitrite
- The strategies described previously that reduce O2- levels in bacterial cells also protect against highly reactive nitrogen species, such as peroxynitrite (ONOO-)
- Additional ways that some bacteria resist killing by NO include conversion of NO into NO3-
- In E. coli, resistance to NO is mediated by a flavohemoglobin, also called nitric oxide dioxygenase (NOD), which is normally part of the bacterial respiratory system
Cell-to-Cell Spread
- Condensation of actin on one end of the bacteria propels them through the host cell cytoplasm and into adjacent cells
- Only three bacterial species are able to use this actin-based motility to promote cell-to-cell spread with one being the Gram-positive, foodborne pathogen Listeria species
- Another is is the Gram-negative causative agent of dysentery, Shigella species
- The third is the causative agent of Rocky Mountain spotted fever, Rickettsia rickettsii
- The ability of these intracellular pathogens to spread within host cells and tissues very effectively enables them to evade the host’s humoral immune response
- The process of actin nucleation by the bacterium requires only one bacterial protein, a surface protein called ActA that assembles actin filaments by interacting with the host cytoskeletal proteins, profilin and Arp2/3
- L. monocytogenes also uses membrane-damaging toxins to escape from the double-membrane vacuole into the cytoplasm, where they once again continue to grow and spread from cell to cell
Tissue Penetration and Dissemination
- Material in the region is viscous pus consisting of DNA and proteins from dead phagocytes and other cells, which will trap some bacteria
- Many bacteria, however, secrete deoxyribonucleases (DNases) that degrade DNA, thereby thinning the pus and making it easier for the pathogen to disseminate
- Some bacteria produce hyaluronidases that degrade the charged polysaccharide hyaluronic acid in connective tissue, thereby also degrading the extracellular matrix and allowing spread along tissue planes
- The term “spreading factors” is sometimes used to refer to these enzymes collectively
- S. aureus can cause life-threatening infections, including “flesh-eating” skin infections (necrotizing fasciitis)
- S. aureus produces a wide variety of degradative and proteolytic enzymes that aid in dissemination
Beyond Virulence Factors
- Bacteria that appear to possess few or none of the virulence factors described thus far can nonetheless cause serious infections
- Such bacteria preferentially infect people whose defenses are compromised in some way (opportunists)
- Most common causes of serious infections in hospitalized patients or cancer patients are the opportunistic pathogens
- B. fragilis, a Gram-negative obligate anaerobe found in the colon, produces a capsule and has an altered LPS, and the Gram-positive S. epidermidis has cell-surface adhesins that bind extracellular matrix proteins and plastic surfaces
- One feature is that they are constantly present in high numbers in the body or in the environment.
- The capsule of B. fragilis function less as an antiphagocytic mechanism than as a factor that elicits an inflammatory response
- The surface adhesins of S. epidermidis allow it to bind tightly to medical implants rather than to mammalian cells
- Many of them are able to take advantage of locations in the body that are somewhat protected from the immune system
- Damaged tissue is quite anoxic (lacking in oxygen), so strict anaerobes, such as Bacteroides species, are quite happy to grow in these areas
- Still another feature that many opportunists have in common is their resistance to multiple antibiotics
- The combination of impaired host defenses and a multidrug-resistant bacterium is a dangerous one
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