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Block 6 week 3 > Bacterial Pathogenesis - Sumby > Flashcards

Bacterial Pathogenesis - Sumby Flashcards

1
Q

What is the microbiome?

A

The microbiome/microbiota/microbial flora is the aggregate of microorganisms that normally colonize the human body. The bacteria in our bodies outnumbers human cells 3 to 1.

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2
Q

Name the types of relationships between microbes and their hosts.

A
  1. mutualistic - the relationship provides benefits to both host and microbe.
  2. commensal - the relationship provides benefit to either the host or the microbe.
  3. Parasitic - the relationship provides a benefit to the microbe only.
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3
Q

What are the benefits of the human microbiome?

A
  1. facilitates nutrient acquisition
  2. ‘educates’ the innate defenses and stimulates both innate and adaptive immune systems
  3. helps to maintain epithelial boundary functions and integrity
  4. provides colonization resistance against pathogens
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4
Q

Is the microbiome the same for everyone?

A

No, and this difference can be associated with multiples conditions such as psoriasis, obesity, inflammatory bowel diseases and colorectal carcinoma.

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5
Q

Is the microbiome made up of the same microbes throughout the body?

A

No, it varies according to the different parts of the body.

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6
Q

What is fecal microbiota transplantation?

A

It is a therapy for treating Clostridium difficile infections. Infections with this bacteria are normally treated with oral antibiotics such as Vancomycin but it is spore forming so relapse infections are common.

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7
Q

Does the diversity and abundance of different bacterial species vary from person to person?

A

Yes.

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8
Q

Does the diversity and abundance of different bacterial species vary over time in a single person?

A

Yes.

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9
Q

Would 2 people who live together have the same microbiome?

A

No, they would be similar but not identical.

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10
Q

Does H. pylori alter the diversity of the stomach microbiome?

A

Yes, this pathogen tends to take over when it is present - replacing the natural species and leading to pathology.

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11
Q

What is incubation period?

A

The time between the moment the person is exposed to the microbe or toxin and the appearance of symptoms. The incubation period varies for microbes so this can be a good diagnostic clue.

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12
Q

What is the prodrome period?

A

The time during infection in which nonspecific symptoms occur.

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13
Q

What is the disease period?

A

The time during infection in which specific clinical signs and symptoms occur.

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14
Q

What is the recovery period?

A

The time during infection in which symptoms resolve and health is restored.

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15
Q

What can happen after the recovery period?

A

Some people can become chronic carriers of the organism they were infected with and some may develop latent (microbe dormant) infection.

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16
Q

What are the stages of infection?

A
  1. Incubation period - no signs or symptoms.
  2. prodrome period - general, vague symptoms.
  3. Disease period or illness - most severe and specific signs and symptoms.
  4. Recovery period - includes decline (declining symptoms) and convalescence (no signs or symptoms ).
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17
Q

Give an example of a latent infection.

A

TB is the most common latent infection - bacteria are dormant until reactivated by some trigger such as immunocompromise.

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18
Q

How can infection spread?

A

Modes of transmission include human- to human either by direct contact or via a vector and nonhuman to human. Nonhuman sources could be animals, soil, water, food etc.

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19
Q

Describe zoonoses.

A

This term is used to describe human diseases for which animals are the reservoir. The pathogens involved are called zoonotic pathogens.

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20
Q

What are the main portals of entry into the body for infection?

A
  1. respiratory tract
  2. GI tract
  3. GU tract
  4. skin
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21
Q

What is a fomite?

A

Any object capable of carrying infectious organisms - ie a damp towel.

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22
Q

Define infectious dose.

A

The dose of microbe required to cause infection. This amount can change if something occurs in the stomach that increases its pH - such as taking bicarbonate. Different organisms have different infectious doses.

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23
Q

What must a bacteria do in order to be a successful pathogen?

A
  1. colonize - enter a human host and become established.
  2. immune evasion - must avoid innate and adaptive immune defenses.
  3. reproduce - must acquire nutrients and replicate.
  4. disseminate - must exit host and be transmitted to a new host.
  5. death of the host is unusual.
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24
Q

What is adherence?

A

The process by which microbes attach to host cells or tissues.

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25
Q

What is colonization?

A

The asymptomatic harboring of microbes on or in the body.

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26
Q

Define infection.

A

A breach of host epithelial barrier with some host damage. Infections may be subclinical.

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27
Q

Define nosocomial infection.

A

A hospital-acquired infection.

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28
Q

Define disease.

A

Tissue destruction with specific signs and symptoms.

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29
Q

Define pathogen.

A

A microbe with the inherent capability of causing infection and disease in a host with an intact immune system. Opportunistic pathogens only cause disease in an immune compromise individual.

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30
Q

Define pathogenicity.

A

The ability of a microorganism to produce infection and disease in a host.

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31
Q

Define virulence.

A

A term that provides a quantitative measure of pathogenicity or the likelihood of causing disease.

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32
Q

What are virulence factors?

A

Gene products that enable a microbe to establish itself on or in a host.

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33
Q

Can pathogens show different virulence levels?

A

Yes, some may have low virulence and rarely cause illness even when normally present in the host, some are highly virulent.

34
Q

Name some virulence factors.

A
  1. Adhesin - promotes attachment of bacteria to host cells or tissues.
  2. Surface capsule or slime layer/glycocalyx - prevents phagocytosis.
  3. Secretion systems - inject regulatory molecules and toxins into host cells.
  4. Exotoxins - cytotoxic proteins, degradative enzymes and superantigens.
  5. Endotoxins - Produces by gram-neg bacteria to induce harmful inflammation.
35
Q

What structure do bacteria use for adhesion?

A

Fimbriae or Pili - fibers that extend from the surface of bacteria that mediate attachment to specific host cell or tissue components.

36
Q

What promotes pathogen adherence?

A

The virulence factor Adhesins and also bacterial capsules or slime layers. For example S. pyrogenes binds to epithelial cells via recognition of hyaluronic acid in its capsule by host cell hyaluronic acid binding protein (CD44).

37
Q

Name some adhesins.

A
  1. collagen-binding protein
  2. fibrinogen-binding protein
  3. fibronectin-binding protein
  4. laminin-binding protein
38
Q

In addition to functioning as an Adhesin, what else can bacteria capsules do?

A

They inhibit phagocytosis by inhibiting C3b deposition and access to deposited C3b and/or by inhibiting the access of host pattern recognition receptors to bacterial PAMP’s

39
Q

What is biofilm?

A

Biofilm consists of bacterial cells embedded in extracellular polymeric substance or EPS. EPS is a mixture of extracellular DNA, proteins and polysaccharides. Biofilm formation is part of the infectious cycle for many bacterial pathogens.

40
Q

What is the purpose of biofilm?

A

It facilitates the ability of the pathogenic bacteria to resist antibiotic treatments, trap nutrients for growth, adhere to environmental surfaces and resist flushing, live in close association with other bacteria and it also enhances immune evasion.

41
Q

Describe bacterial secretion systems.

A

These are a mechanism that many bacteria use to co-opt the cell for their own benefit. These are used to inject various effector molecules like toxins or enzymes into the host cell cytoplasm to alter cellular machinery or communication.

42
Q

Describe the Type 3 Secretion system.

A

This is the most common type of bacterial secretion system. It starts with the secretion apparatus/injectosome being assembled in the bacterial cell wall. It polymerizes to form a hollow needle that penetrates the host cell membrane and allows bacterial proteins to be injected.

43
Q

What is the difference between Types 1-3 bacterial secretion systems?

A

Type one allows secretions out of bacteria, Type two allows secretion into intracellular space and Type 3 allows secretion into the cell cytoplasm.

44
Q

What are some ways for bacteria get inside of cells and tissues?

A
  1. They use proteins called Invasins. For example - S. pyrogenes produces hyaluronidase to degrade the extracellular matrix and gets in between epithelial cells. Invasins can be intracellular or extracellular
  2. Some bacteria bind to cell surface receptors and induce their own endocytosis. Some of these will escape the vacuole and some will multiply in the phagolysosome. Some will remain intracellular and some will escape into the submucosa via transcytosis.
45
Q

What are exotoxins?

A

Exotoxins are toxins or proteins synthesized and used by bacteria to affect host cells. These exotoxins are either secreted into the environment or are found associated with the microbial surface.

46
Q

Are exotoxins specific to the host cell?

A

Yes, most exhibit host cell specificity by binding to specific receptors. They are antigenic and induce antibodies called antitoxins.

47
Q

What are toxoids?

A

These are exotoxins that have been modified. They are antigenic but not toxic. An example is the tetanus toxoid vaccine.

48
Q

Describe the classification of exotoxins.

A

Type 1 - cell surface active. For example the superantigen toxic shock syndrome toxin.
Type 2 - membrane damaging. For example the Clostridal a-toxin which has phospholipase activity.
Type 3 - Intracellular. For example the AB toxins like cholera toxin.
Extracellular damaging exotoxins. For example the hydrolytic enzymes such as hyaluronidase and collagenase.

49
Q

Describe the mode of action of cholera toxin.

A

Cholera toxin is a Type 3 exotoxin of Vibrio cholerae. It has several domains - 2 A and 5 B. The B domain binds to receptors on cell surface and the entire complex is endocytosed. Inside, the A1 subunit becomes active by cleavage from A2. A1 then catalyses the ADP-ribosylation of a G-protein (Gs subunit). This increases adenylate cyclase activity which increases intracellular concentration of cAMP which in turn leads to increased efflux of chloride ions and thus secretion of water and other ions. This causes massive amounts of watery diarrhea.

50
Q

How do superantigens work?

A

They bind simultaneously to T cell receptors and MHC class II molecules outside of the normal binding site. It then hyper-stimulates T cells to secrete cytokines leading to a cytokine storm and inflammation mediated host damage. Because superantigens do not have to bind to the normal peptide binding site they don’t need T cell specificity and so can activate up to 20% or our body’s T cells.

51
Q

Give a couple examples of superantigens.

A
  1. Toxic shock syndrome toxin and staphylococcal enterotoxins secreted by S. aureus.
  2. Streptococcal pyrogenic exotoxins secreted by S. pyrogenes.
52
Q

What are endotoxins?

A

Endotoxins are lip polysaccharides located in the outer membrane of gram-neg bacteria. They are not secreted and are poorly antigenic.

53
Q

How do endotoxins work?

A

The lipid A component of LPS induces the overproduction of cytokines such as TNF-a and other inflammatory mediators from macrophages. This results in inflammation mediated damage via sepsis, septic shock, fever, hypotension, disseminated intravascular coagulation (DIC), and multi-organ system failure (MOSF).

54
Q

How does LPS activation lead to DIC?

A

LPS activates the coagulation cascade and the complement cascade resulting in increased vascular permeability.

55
Q

How are virulence factors regulated?

A
  1. environmental cues

2. Quorum sensing

56
Q

How does environment affect production of virulence factors?

A

Factors such as temperature, pH and osmolarity may control the expression of virulence genes. Examples are:

  1. In C. diphtheria the gene for diphtheria toxin is regulated by iron concentration. Free iron levels are normally low in humans and C. diphtheria sense this.
  2. In B. burgdorferi expression of surface proteins is regulated by temperature.
  3. In V. cholerae the gene for cholera toxin is regulated by pH and temperature.
57
Q

What is quorum sensing?

A

The production and release by individual bacteria of molecules called autoinducers that modulate gene expression in response to the density of a bacterial population. This facilitates coordinated responses by bacterial populations.

58
Q

What are some coordinated responses that can be mediated via quorum sensing?

A
  1. biofilm production
  2. virulence factor secretion
  3. sporulation
  4. competence for DNA uptake
59
Q

What can inhibit quorum sensing?

A

RNAIII-inhibiting protein (RIP).

60
Q

What makes a bacteria pathogenic?

A

The expression of virulence factors.

61
Q

Where are virulence factors encoded in bacteria?

A

They can be in the bacterial chromosome - in which case they will be present in all isolates of a given pathogenic species - or they can be carried on mobile genetic elements such as plasmids, bacteriophages or pathogenicity islands (PIA’s). This is how different isolates of the same bacterial species can have widely different virulence characteristics.

62
Q

Give examples of some virulence factors that can be plasmid encoded.

A
  1. Heat labile and heat stable enterotoxins that cause diarrhea in plasmids of E. coli.
  2. Adherence factors and gene products involved in mucosal invasion in plasmids of E. coli and Shigella.
  3. Capsule essential for virulence and edema factor, lethal factor and protective antigen essential to virulence in B. anthracis plasmids.
63
Q

Give some examples of virulence factors that are phage encoded.

A
  1. Shiga-like toxin which inhibits cell protein synthesis in E. coli bacteriophages.
  2. Cholera toxin in V. cholerae bacteriophages.
  3. Streptococcal pyrogenic exotoxins/superantigens (SpecA, SpecC, SpecH, SpeI, SpeK, and SpeL) in S. pyrogenes bactriophages.
64
Q

Give some examples of virulence factors that are PAI encoded.

A
  1. Type III secretion system and effector proteins on PIA in E. coli.
  2. Toxic shock syndrome toxin/superantigen on PIA in S. aureus.
  3. The R28 adhesion which promotes attachment to host epithelial cells on PIA of S. pyrogenes.
65
Q

Describe some characteristics of Plasmids.

A
  1. most replicate extra-chromosomally
  2. range in size from one to hundreds of kb
  3. may contain genes that encode for virulence factors and or antibiotic resistance genes
  4. some pathogen isolates have many plasmids, others have none
66
Q

What virulence factors are encoded on plasmids in B. anthracis?

A

Both pXO1 and pXO2 are virulence factors essential to pathogenesis that are encoded on plasmids. pXO1 codes for toxin components. pXO2 codes for capsule biosynthesis genes.

67
Q

How are bacteriophages important to pathogenicity?

A

Some lysogenic phages encode key virulence factors for some bacteria. For example Shiga-like toxin of E. coli. Some pathogens have no integrated phage while others have many. Ten percent of S. pyrogenes chromosome is integrated phage DNA.

68
Q

What is the difference between a lytic and a lysogenic phage?

A

Once a phage injects its DNA into a bacterium there are two fates. The lysogenic cycle is when the DNA is incorporated in host chromosome (called a prophage) and remains there inactive until a precipitating event. The lytic cycle is when the phage DNA uses bacterial machinery to replicate. The DNA is then packaged and the bacteria lyses releasing all the phages to infect other bacteria.

69
Q

What are pathogenicity islands?

A

Collections of genes that are clustered together which may encode virulence factors. PIA’s are usually acquired via conjugation. An example is the locus of enterocyte effacement PIA which is present in the genomes of two different E. coli pathotypes. This PIA encodes multiple virulence factors.

70
Q

Name some bacterial defenses against host immunologic clearance.

A
  1. encapsulation
  2. antigenic mimicry
  3. antigenic variation
  4. Anti-Ig proteases
  5. destruction of phagocytes
  6. intracellular replication
  7. inhibition of chemotaxis
  8. inhibition of phagocytosis
  9. inhibition of phagolysosomal fusion
  10. resistance to lysosomal enzymes
71
Q

How have bacteria evolved means to avoid opsonization by antibodies?

A

They modify their surface proteins. Two processes that allow this are:

  1. phase variation - the expression of surface proteins are swiched on or off
  2. antigenic variation - surface antigens are switched from one type to another
72
Q

What are the mechanisms of phase variation and antigenic variation?

A

Phase variation:

  1. site specific inversion of DNA - a promoter is required for the transcription of the surface protein.The promoter is flanked by inversion factors on either side and these cause inversion of the promoter so that the protein is not transcribed.
  2. Slipped -strand mispairing

Antigenic variation -

  1. Homologous recombination from silent loci to transcribed loci
  2. Slipped-strand mispairing
73
Q

How can some microbes avoid humoral immunity?

A

By being intracellular bacteria.

74
Q

Give some examples of intracellular pathogenic bacteria.

A
  1. Mycobacterium spp.
  2. Brucella spp.
  3. Francisella spp.
  4. Rickettsia spp.
  5. Legionella pneumophila
  6. Listeria monocytogenes
  7. Salmonella Typhi
  8. Shigella dysenteriae
  9. Yersinia pestis
  10. Chlamydia spp.
75
Q

How do some microbes inhibit killing after they are phagocytosed?

A
  1. inhibition of phagosome-lysosome fusion. This mechanism used by Legionella, Mycobacterium and Chlamydia.
  2. Resistance to lysosomal enzymes. This mechanism is used by Salmonella, Coxiella and Mycobacteria.
  3. Escape from the phagolysosome. This mechanism used by Listeria, Franciscella, and Rickettsia.
76
Q

What are some important functions of mobile genetic elements?

A
  1. They code for virulence factors - the type of virulence factors will then determine the pathotype and the resultant disease.
  2. They can also affect the regulation of the virulence factors.
77
Q

Give some examples of pathotypes and the different mobile genetic elements present.

A

The following are all pathotypes of E. coli.

  1. ETEC - causes diarrhea - virulence factor enterotoxin is encoded on a plasmid called pENT.
  2. EPEC - causes diarrhea - needs the plasmid pEAF and also has the LEE pathogenicity island.
  3. EHEC - can cause diarrhea or hemorrhagic colitis - needs the integrated Stx phage (codes for Shiga-toxin) and the LEE pathogenicity island.
  4. EIEC - causes a syndrome with profuse diarrhea and high fever similar to Shigellosis. Needs the invasion plasmid and also has a Black hole (deleted genes).
  5. UPEC - causes uncomplicated UTI’s and needs a pathogenicity island.
78
Q

Give an example of how mobile genetic elements can regulate virulence factors.

A

In EHEC bacteria (form of E. coli) the use of antibiotics leads to HUS or hemolytic uremic syndrome. HUS is caused by Shiga-like toxin produced by EHEC. The way this happens is that an integrated phage codes for the Shiga-like toxin and when antibiotics are introduced the cell becomes stressed. The lytic phase is induced and there is increased transcription and production Shiga-like toxin. The phage causes production of Lyase and the cell lyses releasing the the toxin.

79
Q

Describe hemolytic uremic syndrome.

A

This syndrome is the result of the rapid and premature destruction of erythrocytes. This overwhelms the filtering system of the kidneys and causes kidney failure. It is caused by Shiga-like toxin.

80
Q

Name some ways that bacteria such as S. pyrogenes evade the host immune response.

A
  1. Degradation of NET’s - NET’s are formed by dead neutrophils, they can trap and kill bacteria. Bacteria can produce enzymes that degrade NET’s.
  2. Antimicrobial peptide resistance - some bacteria can inactivate or cleave these peptides or they may cause their surfaces to become positively charged so that they repel the positively charged peptides.
  3. Phagocyte uptake impairment - some bacteria produce a protein called MAC that binds to receptors on phagocytes and prevents uptake.
  4. complement deposition interference
  5. cloaking of opsonins - via binding of bacterial M protein to fibrinogen or fibronectin.
  6. Nonopsonic binding or antibody degradation - can produce enzymes that degrade antibodies.
  7. Chemokine degradation - can produce proteins to degrade chemokines so neutrophils are not attracted.
  8. phagocyte lysis - can produce proteins that lead to phagocyte lysis

Block 6 week 3 (5 decks)

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