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Revision for Exams > Pathogens and Pathogenesis > Flashcards

Pathogens and Pathogenesis Flashcards

1
Q

How has technology spread disease?

A

Via airplane travel, use of blood banks and suburban sprawl.

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2
Q

What are examples of diseases that have spread due to technological advances?

A

Lyme disease = suburban development
E.coli O157:H7 = meat processing plants
COVID-19 and travel

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3
Q

What are bioweapons?

A

Highly virulent infectious agents or toxins

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4
Q

What are the implications of biowarfare?

A

Inflict massive casualties, rapid onset symptoms, death or temporary incapacitation.

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5
Q

What are the implications of Bioterrorism?

A

Widespread panic, disruption of society

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6
Q

What is the modern drug discovery process?

A
  1. Use genomics to identify new targets.
  2. Design compounds to inhibit the targets
  3. Alter the compounds to optimize MIC.
  4. Determine the spectrum of the compound
  5. Determine the pharmaceutical properties.
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7
Q

What are Antibiotics?

A

Secondary metabolites, not essential for microorganism survival, enhances ability to survive

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8
Q

How do Protein synthesis inhibitors work?

A

They either interact with the 30S or 50S subunit of the ribosome

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9
Q

What are examples of drugs that interact with the 30S subunit of the ribosome?

A

Aminoglycosides and Tetracyclines

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10
Q

What do Aminoglycosides do?

A

Cause translational misreading of mRNA.

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11
Q

What do Tetracyclines do?

A

Block binding of charged tRNAs to a site on the ribosome

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12
Q

What type of agent are Aminoglycosides?

A

Bactericidal - include streptomycin

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13
Q

What type of agent are Tetracyclines?

A

Bacteriostatic, include doxycycline

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14
Q

What are some drugs that interact with the 50S subunit?

A

Macrolides, Lincosamides, Chloramphenicol, Oxazolidinones, Strepogramins

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15
Q

What do Macrolides and Lincosamides do?

A

Inhibit translocation

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16
Q

What do Chloramphenicols do?

A

Inhibit peptidyl transferase activity

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17
Q

What do Oxazolidinones do?

A

Prevent formation of the 70S ribosome initiation complex

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18
Q

What do Streptogramins do?

A

Streptogramin A - Block tRNA binding
Streptogramin B - Blocks translocation

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19
Q

What are some examples of RNA synthesis inhibitors?

A

Rifampin and Actinomycin D

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20
Q

How does Rifampin work?

A

Binds to beta subunit of RNA polymerase to prevent the elongation step of transcription

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21
Q

How does Actinomycin D work?

A

Binds to DNA, prevents the initiation step of transcription

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22
Q

Downside of Actinomycin D?

A

It is not selectively toxic

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23
Q

Examples of DNA synthesis inhibitors?

A

Quinolones, Metronizadole, Sulfa Drugs

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24
Q

Examples of Quinolone drugs?

A

Nalidixic acid, ciprofloxacin

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25
Q

How do Quinolone drugs work?

A

Block bacterial DNA gyrase, preventing DNA replication

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26
Q

How does Metronizadole work?

A

It is non-toxic unless it is metabolised by anaerobes.

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27
Q

How do Sulfa Drugs work?

A

They are PABA analogues (folic acid precursor)

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28
Q

What are some drugs that disrupt cell membranes?

A

Gramicidin and Polymyxin

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29
Q

How does Gramicidin work?

A

Forms cation channels, which ions can leak through

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30
Q

How does Polymyxin work?

A

Destroys cell membranes - detergent like

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31
Q

What are bacterial drug targets?

A
  • Cell Wall
  • Cell Membrane
  • DNA synthesis
  • RNA synthesis
  • Protein Synthesis
  • Metabolism
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32
Q

What are the stages of Peptidoglycan synthesis?

A
  1. Precursors are synthesized in the cytoplasm (UDP-NAG and UDP-NAM)
  2. They are then carried across the cell membrane by bactoprenol
  3. The precursors are polymerised via transglycosylase.
  4. The peptide side chains are crosslinked by transpeptides.
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33
Q

What are some Beta-Lactam antibiotics?

A

Penicillins and cephalosporins

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34
Q

How do Beta-lactam antibiotics work?

A

By competitively inhibiting transpeptidases

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35
Q

How does Vancomycin work?

A

Binds ends of peptides and prevents the action of transglycosylases and peptidases.

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36
Q

How does Cycloserine work?

A

By inhibiting the formation of D-ala-D-ala dipeptide precursor.

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37
Q

How does Bacitracin work?

A

By blocking the lipid carrier bactoprenol. Meaning disaccharide subunits do not reach the periplasm

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38
Q

What are the classifications of antibiotics?

A
  • Bactericidal and Bacteriostatic
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39
Q

What do Bactericidal compounds do?

A

Kill target organisms, but are only effective if the organism is building a new cell wall.

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40
Q

What do bacteriostatic antibiotics do?

A

Prevent the growth of the organisms.

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41
Q

Broad Spectrum

A

Effective against many species

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42
Q

Narrow Spectrum

A

Effective against few or single species

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43
Q

Source of Antibiotics

A

Most are discovered as natural products that are then often modified by artificial means.

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44
Q

How does selective toxicity come into Antibiotic development?

A

Drug must affect target without being detrimental to host.
Can cause side effects and allergic responses.

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45
Q

How are issues with hosts avoided when developing Antibiotics?

A

They should target physiologies not present in the host. E.g Peptidoglycans, differences in ribosome structure and biochemical pathways missing in humans.

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46
Q

When was the importance of antibiotics in treating disease recognised?

A

1940s

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47
Q

What do mechanisms of antibiotic resistance include?

A

Modifying, destroying and pumping out the antibiotic

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48
Q

What tests strain sensitivity to antibiotics?

A

Kirby-Bauer susceptibility test - disks of antibiotics

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49
Q

What test determines MIC?

A

E-test, gradient of antibiotic on strep, drug must be above MIC in tissue to be effective.

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50
Q

What is MIC?

A

Minimal inhibitory concentration

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51
Q

How is MIC determined?

A

By diluting the antibiotic

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52
Q

What does No living colonies on a agar plate in a MIC test indicate?

A

Mininal lethal concentration, always higher than MIC

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53
Q

How does drug resistance develop?

A

Gene duplications/mutatins and HGT

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54
Q

How do bacteria resist antibiotics through target modification?

A

They can mutate their ribosomal proteins to confer resistance, happens with Streptomycin

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55
Q

How do bacteria resist antibiotics through destroying the antibiotic?

A

Beta-lactamase enzymes destroy penicillin

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56
Q

How do bacteria resist streptomycin through enzymes?

A

Adding modifying enzymes inactivates aminoglycoside antibiotics.

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57
Q

How do antibiotics specifically and non-specifically resist antibiotics?

A

Through pumping the antibiotic out of the cell.

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58
Q

How does drug resistance occur?

A

Antibiotic overuse, overprescription in agricultural settings

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59
Q

Who discovered streptomycin?

A

Selman Waksman

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60
Q

Who purified Penicillin?

A

Florey and Chain

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61
Q

What is a virulence factor?

A

Allows pathogens to cause disease

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62
Q

Where can virulence factors be found?

A

Pathogenicity islands in the chromosome, plasmids or even phage genomes

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63
Q

Which pathogen can make proteins to bind antibodies, evading the immune system?

A

Staphylococcus Aureus Cell Wall protein a

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64
Q

How does Staphylococcus Aureus Cell Wall Protein A work?

A

By binding Fc fragments of antibodies, which cause them to attach upside down, preventing opsonisation.

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65
Q

How can pathogens evade the immune system?

A

Alteration of surface antigens.
Causing apoptosis of phagocytes.
Binding of antibodies.

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66
Q

Which pathogens are able to overcome engulfment by phagosomes?

A

Shigella dysenteriae and Listeria Monocytogenes

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67
Q

How do pathogens overcome phagosome engulfment?

A

By using hemolysin

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68
Q

Which pathogens secrete proteins to prevent fusion with lysosomes?

A

Salmonella, Chlamydia, Mycobacterium and Legionella/

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69
Q

Which pathogens use non-pilus adhesins to mediate binding to host tissues?

A

Streptococcus Pyogenes and Bordetella Pertussis

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70
Q

What is Streptococcus Pyogenes’ non-pilus adhesin?

A

M protein, binds to fibronectin

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71
Q

What is Bordetella Pertussis’ non-pilus adhesin?

A

Pertactin, binds t integrin

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72
Q

What are adhesins?

A

Any microbial factor that promotes attachment

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73
Q

What do most bacterial utilise for attachment to host cells?

A

Pili

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74
Q

What are the main types of pili ?

A

Type 1 and Type 4

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75
Q

What do Type 1 pili do?

A

Adhere to mannose residues, producing static attachment to host cells. Grow from outer membrane

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76
Q

What do Type 4 pili do?

A

Involved in twitching motility, continually assemble and disassemble, grow from inner membrane

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77
Q

What is quorum sensing used for?

A

Detection of exotoxins made by other cells. Delays toxin synthesis until many bacteria are present.

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78
Q

How do bacteria recognise host environments?

A

Two-component signal transduction, recognising magnesium concentration and pH

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79
Q

Biofilms

A

Specialised, surface-attached communities

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80
Q

What sort of protein secretion pathway is Type 1?

A

Pilus-like

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81
Q

What sort of protein secretion pathway is Type 2?

A

Syringe like

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82
Q

What sort of protein secretion pathway is Type 4?

A

Conjugation system like

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83
Q

What are the 5 categories of protein exotoxins?

A
  1. Membrane disrupters
  2. Protein Synthesis disrupters
  3. Secondary messenger pathway disrupters
  4. Superantigens
  5. Proteases
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84
Q

What type of toxin is only made by Gram negative bacteria?

A

Endotoxin

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85
Q

What are two types of disease protection and prevention?

A

Vaccines and Herd Immunity

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86
Q

What is herd immunity?

A

When a large % of the community is vaccinated

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87
Q

What can vaccines be made from?

A

Killed/attenuated organisms or purified components of infectious agents

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88
Q

How does Type 4 secretion work??

A

Similar to conjugation pilus, secretes proteins only or proteins+DNA.
Secretes from cytoplasm or periplasm

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89
Q

Example of a pathogen that uses Type 4 secretion?

A

Bordetella pertussis

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90
Q

How does Type 3 secretion work?

A

Molecular syringe, inject proteins from cytoplasm into the host cell.
Genes for proteins are on pathogenicity islands.
Base of the needle complex spans the Inner membrane and outer membrane.

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91
Q

Which pathogens possess Type 3 secretion systems?

A

Salmonella, Yersinia and Shigella.

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92
Q

How does Type 2 secretion work?

A

Pilus can extend and retract. Proteins to be secreted from the periplasm are folded then secreted

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93
Q

How do endotoxins get out of bacterial cells?

A

Protein secretion systems, tend to use mechanisms already present in the bacteria.

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94
Q

How do Endotoxins work?

A

Present in LPS of outer membrane, Lipid A released as bacteria die, causing massive cytokine release. Triggers fever, shock and death.

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95
Q

What is alpha toxin prodced by?

A

Staphylococcus aureus

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96
Q

What does hemolytic alpha toxin do?

A

Breakdown iron components, uses them for survival and metabolism. Forms a transmembrane seven member pore in target cell membrane.

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97
Q

How does S.Aureus damage cellular membranes?

A

Through its alpha toxin. Causes release of haemoglobin from RBCs.

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98
Q

How does Shigella inhibit protein synthesis?

A

Shiga toxin attaches to ganglioside Gb3, entering the cell and cleaves 28s rRNA

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99
Q

How does E.coli activate secondary messenger pathways?

A

E.coli Heat stable toxin activates guanylate cyclase of intestinal epithelial cells; which causes osmotic imbalance.

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100
Q

What is Cholera toxin’s mode of action?

A
  1. Toxin complex binds ganglioside GM1 on host membrane lipid rafts.
  2. Toxin is endocytosed.
  3. Phagosome migrates to endoplasmic reticulum.
  4. A1 subunit is removed from the B subunits and exported to the cytoplasm.
  5. The A1 peptide attaches an ADP ribose to an amino acid which regulates adenylate cyclase.
    6.Cyclic AMP rises and activate ion transport, causing electrolyte imbalance.
  6. Water from the cells follows the ions, causing diarrhea.
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101
Q

What are examples of ADP-ribosylating toxins?

A

Diptheria and Cholera

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102
Q

What produces Diptheria toxin?

A

Corynebacterium Diptheriae

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103
Q

What produces Cholera toxin?

A

Vibrio Cholerae

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104
Q

How does Cholera toxin work?

A

Ribosylates to overactivate adenylate cyclase
cAMP activates ion transport; water follows
Uncontrollable diarrhea

105
Q

How does Diptheria toxin work?

A

Ribosylates elongation factor 2
Blocks ribosome function; cell dies.
Forms psuedomembrane over trachea.

106
Q

How does the A unit of AB toxins work?

A

Has toxic activity through ADP ribosyltransferase

107
Q

How does the B unit of AB toxins work?

A

Binds to host cell, delivers A subunit.
Often 5 B subunits to form a pore for A entry.

108
Q

Which pathogens use AB toxins?

A

Shiga, Diptheria, Cholera

109
Q

How does tetanus toxin work?

A

Through retrograde movement. Toxin enters nervous system at the neuromuscular junction, travels against signal flow to inhibitory neurons.Cleaves VAMP protein involved in exocytosis, blocking GABA release.

110
Q

What do exotoxins do?

A

Subvert host function

111
Q

Why type of toxin is tetanus toxin?

112
Q

What type of toxin is Staphylococcus Aureus’ TSS toxin?

A

Superantigen

113
Q

What type of toxin is E.coli’s Heat stable toxin?

A

Secondary messenger pathway disrupters

114
Q

What is epidemiology?

A

Examines the distribution and determinants of disease frequency in human populations

115
Q

What is an epidemic

A

High disease frequency over a short period

116
Q

What is a pandemic?

A

Epidemic that occurs over a wide geographic area

117
Q

How are safety levels monitored in labs?

A

Biological Safety Levels

118
Q

What is the most severe BSL ?

A

BSL IV, complete isolation

119
Q

How is PCR used to detect pathogens?

A

Through amplification of small DNA fragments, can identify tiny numbers of bacteria.

120
Q

How are bacteria further categorised after PCR?

A

Restriction analysis to indicate strain

121
Q

How are gram-negative bacteria detected?

A

Analytical profile index strips

122
Q

What are issues with growing organisms on plates?

A

Inability to obtain pure cultures
Passage in the lab can lead to attenuation
SOme diseases are caused by combinations of microbes
Different strains of the same species can have different pathogenic properties

123
Q

What are the steps to Koch’s postulates?

A
  • Plate blood, streak it, forming singular colonies.
  • look for causative agent
  • Culture, reinject mouse and plate again
124
Q

How do we identify pathogens?

A
  1. Symptoms
  2. Isolation and growth of microorganism
  3. Reinfection
  4. Pattern of infection
  5. Biochemical/Metabolic properties
  6. Site of infection
  7. Drug sensitivity
125
Q

What is a physiochemical host defence mechanism?

126
Q

Examples of pathogens that can infect via Fomites?

A
  • MRSA and Streptococcus Pyogenes
127
Q

Examples of pathogens that can infect through accidental and direct pathways?

A

Staphylococcus epidermis (skin) and neisseria meningitides (saliva)

128
Q

Example of a pathogen that can infect through vertical transmission?

A

Treponema Pallidum (Syphillis)

129
Q

What does verticla transmission mean?

A

From parent to child

130
Q

What does accidental transmission mean?

A

Host who is not usually a part of the infectious cycle

131
Q

What does horizontal transmission mean?

A

From one member of the species to another.

132
Q

What are primary pathogens?

A

Cause disease in healthy hosts

133
Q

What are opportunistic pathogens?

A

Cause disease only in immunocompromised patients

134
Q

What is virulence?

A

A measure of the severity of a disease

135
Q

Examples of skin and soft tissue infections?

A
  • Boils; scalded skin syndrome (staphylococcus aureus)
  • Necrotising Fascitis (Streptococcus pyogenes)
136
Q

Examples of respiratory tract infections?

A
  • Pneumonia
  • Tuberculosis
137
Q

Examples of GI tract infections

A
  • EHEC - enterohemorrhagic E.coli
  • Salmonella
    -Shigella
  • Helicobacter pylori
138
Q

Example of a pathogen that causes UTIs.

A

Uropathogenic E.coli

139
Q

Examples of systemic diseases?

A
  • Yersinia Pestis and Borrelia Burgdorferi (Lyme disease)
140
Q

What are the Clostridium toxins?

A
  • Botulin and Tetanus
141
Q

How does C.Botulinum work?

A

It is an anaerobe that grows in canned foods.
Spores survive unless it is autoclaved.
Toxins block the release of acetylcholine = flaccid paralysis

142
Q

How does C.Tetani work?

A
  • Anaerobe, grows in puncture wounds.
    Blood flow becomes interrupted, tissue becomes anaerobic.
    Blocks release of GABA, inhibitory transmitter.

Causes spastic paralysis

143
Q

What is Meningitis?

A

Infection of meninges of the brain.
Bacteria crosses blood-brain barrier

144
Q

How does Neisseria Meningitidis cause Meningitis?

A
  • Thick capsule
  • crosses from the capillaries into the cerebrospinal fluid
    Once in the meninges, it is difficult to treat
145
Q

What species caries Borrelia Burgdorferi?

A

Ixodes Sacapularis tick

146
Q

What are the 3 stages of Lyme disease?

A

Rash, Joint muscle nerve pain, arthiritis.

147
Q

What does yersinia in the lymph nodes cause?

A

Bubonic Plague

148
Q

What does yersinia in the blood cause?

A

Septicemic plague

149
Q

What does inhaled yersinia cause?

A

Pneumonic Plague

150
Q

What is Endocarditis?

A

Inflammation of the hearts inner lining

151
Q

What is Septicemia?

A

Presence of microbes in the blood.

152
Q

What is Streptococcus Mutans caused by?

A

Dental procedures.
Grows on damaged heart valves, forming biofilms.
DIfficult to treat

153
Q

How does Neisseria Gonnorrhoeae cause disease?

A

Binds to CD4 T cells, inhibiting. T cell activation.

Women are asymptomatic reservoirs

154
Q

How does Chlamydia cause disease?

A

Intracellular lifecycle, reticulate bodies.
Live within immune cells

155
Q

What are the types of Syphillis?

A

Primary - Chancre at the site of the infection
Secondary - Generalised rash
Tertiary - effects on heart and CNS

156
Q

Uropathogenic E.coli

A
  • Invades bladder up from the urethra
  • Causee 75% of UTIs
157
Q

How do active infections of the urinary tract occur?

A

Descending or ascending infection from the kidneys or infection from urethra migrates.

158
Q

What is the most frequent cause of diarrhea?

A

Campylobacter Jejuni

159
Q

What is most food poisoning caused by?

A

Staphyloccocus Aureus

160
Q

What causes Gastric ulcers?

A

Helicobacter Pylori

161
Q

How does Helicobacter Pylori cause stomach ulcers?

A

Secretes urease, causes urea to convert to ammonimum ions that neutralise stomach acid.
This allows the bacteria to burrow into protective mucus layers.

162
Q

EHEC

A

Enterohemorrhagic

163
Q

ETEC

164
Q

EAEC

A

Aggregative

165
Q

What does EIEC produce?

A

Shiga toxin

166
Q

How is knowledge of a patients history vital?

A

Can give answers to where disease came from.
Hobbies/Travel/Occupation etc

167
Q

Which pathogen is linked to farmers?

A

Q fever caused by Coxiella Burnetti

168
Q

Which pathogen is linked to hunters?

A

Francisella Tularensis

169
Q

Gram positive bacteria have:

A

Thick Peptidoglycan layer

170
Q

Gram negative bacteria have:

A

Two lipid bilayers with a think peptidoglycan layer between them

171
Q

What does the Mucin layer do?

A

Lysozymes digest bacterial peptidoglycans.
sIgA prevents bacterial attachment to mucosal cells.
Lactoferrin binds iron to prevent bacterial growth

172
Q

What is the major cause of many nosocomial infections?

173
Q

What is the primary defense against respiratory issues?

A

Mucociliary escalator

174
Q

First lines of defence against disease:

A
  1. Skin
  2. Saliva
  3. Tears
  4. Mucus lining
  5. Stomach aciid
  6. Good gut bacteria
175
Q

What causes colitis?

A

Clostridium dificile

176
Q

What type of parasite is Blastocystis?

A

Gastrointestinal

177
Q

What are the four cellular forms of blastocystis?

A
  • Vacuolar
  • Granular
  • Cyst
  • Amoeboid
178
Q

What are Blastocystis cells?

A

Strictly anaerobic, cells die within minutes when exposed to oxygen
Deflate like balloons.

179
Q

What phenotype do some blastocystis cells show when exposed to oxygen?

A

“Medusa head”, membrane extrusions can be seen around the cell.

180
Q

What is the definition of Stramenopiles?

A

Having flagellar hairs

181
Q

Why is blastocystis categorized as a stramenopile if it doesn’t have flagellum?

A

Must have arisen from a related member

182
Q

How many different Blastocystis subtypes are there?

A

At least 30
12 in humans
Vary in prevalence in different hosts

183
Q

How is Blastocystis transmitted?

A

Mainly fecal-oral. Zoonotic, but also located in water and soil.

184
Q

What vary in the different subtypes of Blastocystis?

A

DNA base composition, size of the genome, number of genes and number of introns

185
Q

What is Blastocystis?

A

Common gut commensal with reduced abundance in IBD cases.

186
Q

What is the hygeine hypothesis?

A

When the body’s immune system is no longer challenged by infectious organisms, making it more likely to be inappropriately stimulated. This leads to increased susceptibility to allergies and autoimmune diseases.

187
Q

What is Diabetes mellitus incidence related to?

A

Corresponding declines in helminth infections

188
Q

Parasites that are used to treat medical conditions?

A
  • Helminths
  • Larvae
  • Leech
  • Malaria
189
Q

What type of mitochondria does Blastocystis have?

A

Similar to Anaerobic mitochondria/Hydrogenosome

190
Q

What do Blastocystis carriers have?

A
  • Lower BMI
  • Absence of GIT issues
  • Higher bacterial richness and diversity
191
Q

What is cryptosporidium related to?

A

Plasmodium

192
Q

What does cryptosporidium lack that plasmodium retains?

A

Apicoplast

193
Q

Why is Cryptosporidium so concerning?

A

No drug currently for treatment

194
Q

What is cryptosporidium associated with in children?

A

Stunted growth

195
Q

Why is cryptosporidium such a difficult organism to study?

A

There is no culturing system for it

196
Q

What makes cryptosporidium so infectious?

A

Oocysts resistant disinfectants
Low infectious dose
Many sources and transmission routes

197
Q

Who is at risk of Cryptosporidium infection?

A
  • Contaminated water/food intake
  • Travel to less industrialised countries
  • Recreational water users
  • Contact with farmed animals
  • Childcare settings
  • Contact with other ill people
198
Q

Who bears the greatest burden from cryptosporidiosis?

A
  • Immunocompromised
  • Young Children
  • Malnourished children
199
Q

What are the clinical concerns of cryptosporidiosis?

A
  1. Lack of treatment regimen
  2. Long term health effects
  3. Potential for large scale outbreaks
200
Q

Symptoms of cryptosporidiosis?

A

Gastrointestinal symptoms, diarrhoea, abdominal pain, vomiting, fever, anorexia

201
Q

How have Cryptosporidium host-pathogen interactions been studied?

A

Metabolomics, Proteomics and microscopy. Identification of metabolites.

202
Q

Which metabolic pathways influence host metabolism upon infection with Cryptosporidium?

A
  • Amino Acid biosynthesis
  • Sugar metabolism
  • CoA biosynthesis
  • Taurine biosynthesis
203
Q

Which group do Trypanosomes and Leishmania fall under?

A

Kinetoplastids, which are derived from Euglenozoa

204
Q

What does Trypanosoma Brucei cause?

A

Sleeping Sickness

205
Q

What are the 3 important kinetoplastid diseases?

A

Trypanosoma Brucei/Cruzi and Leishmania

206
Q

What are the two types of Trypanosoma Brucei?

A

Gambiense and Rhodesiense, split based on vector transmission

207
Q

Why do Trypanosomas utilise Antigenic variation?

A

To maintain chronic infection and to constantly evade the immune system

208
Q

How do Trypanosomes vary their antigens?

A

They alter their surface proteins which cause waves of parasitemia.

209
Q

How many genes and pseudogenes encode the variable surface glycoproteins?

A

More than 1,000, change VSGs every couple of days

210
Q

Why do Trypanosomes possess both genes and pseudogenes?

A

To avoid selective pressures, allows them to adapt better as a single celled organism

211
Q

What does Trypanosoma Brucei Gambiense affecr?

A

CNS, slow onset but chronic trypanosomasis

212
Q

What does Trypanosoma Brucei Rhodesiense affect?

A

Widespread organ damage, fast onset acute trypanosomasis

213
Q

What is the vector for Trypanosoma Brucei?

A

Tsetse Fly

214
Q

What happens in the Human lifecycle of Trypanosomas?

A
  1. Tsetse fly takes a blood meal
  2. Infects bloodstream, and converts into bloodstream trypomastigotes, which carry to other sites.
  3. These multiply via binary fission in various bodily fluids.
215
Q

What happens in the Insect lifecycle of Trypanosomas?

A
  1. Tsetse fly takes an infected blood meal from human
  2. Bloodstream trypomastigotes transform into procyclic trypomastigotes in their midgut.
  3. These multiply via binary fission
  4. When procyclic trypomastigotes leave the midgut they become epimastigotes.
  5. These multiply in the salivary glands and transform into metacyclic trypomastigotes.
216
Q

What happens to the physiology of Trypomastigotes in human blood?

A

They become stumpy, due to the high glucose levels

217
Q

What is characteristic about Trypanosome cells?

A
  • Huge Flagella
  • Kinetoplastids and Glycosomes = both not present in humans
218
Q

What is the glycosome?

A

Unit for Glycolysis in Trypanosomes
Allows for high glycolytic activity

219
Q

What is the kinetoplast?

A

Single Mitochondrion
Has compact mitochondrial DNA = makes up about 25% of DNA content of the cells

220
Q

What is Kinetoplast DNA composed of?

A

Mini Circles - 5-10,000 copies
Maxi Circles - 20-50 copies

221
Q

What does Mini circle kDNA do?

A

Guide RNAs to decode maxi circle genes

222
Q

Why does Trypanosomas have such a complex Mitochondrial genome?

A

Protects against selective pressure
It is energetically costly

223
Q

What is the insect stage of Trypanosomas reliant on?

A

The mitochondria for ATP

224
Q

How is ATP generated in Trypanosoma?

A

Via ETC and proton pumping ATPase, partly encoded by mitochondrial DNA

225
Q

What is critical for proton translocation in Trypanosomas?

A

FoF1 ATP synthase

226
Q

What is key for ATP export in Trypanosoma?

A

ADP/ATP translocase, exports ATP in return for ADP.
Flagella requires large amont of ATP

227
Q

What is unique about the ETC in the bloodstream stages of Trypanosomas?

A

They lack complexes 1,2, and 3.
Means no proton gradient is formed = no energy
FoF1 is functioning in the opposite direction.
Takes ATP and exports it to maintain the H+ gradient

228
Q

What are two types of Trypanosomes that occur in other vectors?

A
  • Evansi - surra
  • Equiperdum - horses/camel
229
Q

What is different about T.Evansi and Equiperdum?

A

They are Dyskinetoplastic (no kinetoplast) and are transmitted without an insect lifecycle

230
Q

What does Evansi and Equiperdum being Dyskinetoplastic mean?

A

Lack of kDNA, no functional mitochondrial gene expression.
Cannot produce ATP via oxidative phosphorylation
Reliant on other methods of trnasmission

231
Q

What has a lack of kinetoplast shown in lab strains?

A

Trypanosomes are easier to mutate, they become more susceptible to drugs.

232
Q

What have experiments that knockout the ADP/ATP carrier in Trypanosomes shown?

A

They are able to discard functions and stay a live, maybe not the best drug target as they survive.

233
Q

What could have been the reason for superior mutations in Evansi and Equiperdum?

A

The lack of tsetse as a host may have prompted them or the fact that these mutations occured may have avoided the use of tsetse

234
Q

What is a drug that targets Kinetoplasts in Trypanosomes?

A

Acriflavine

235
Q

What is a concern about Trypanosomes?

A

Single nucleotide changes can make trypanosomes completely independent of their kDNA and gene products –> may make kinetoplasts a less worthy drug target

236
Q

What is Plasmodium a type of?

A

Apicomplexa, obligate parasite

237
Q

What is the apical complex of Plasmodium formed of?

A

Preconocoidal Ring
Polar ring
Conoid
Microtubules

238
Q

What is the function of the Apical complex?

A

It is an invasion mechanism, works to penetrate blood cells/epithelial cells. Secretes proteins to manipulate cells

239
Q

What does Plasmodium use as a vector?

240
Q

What is the most deadly Plasmodium species?

A

Plasmodium Falciparum

241
Q

What does Plasmodium require to mate and mature into sporozoites?

A

10-18 days at a temperature of >21 degrees

242
Q

What is an unusual location for Plasmodium replication?

A

Car tyres, provides a humid environment due to collection of rain water

243
Q

What is efficacy of Malaria transmission dependent on?

A

The vector

244
Q

What are the majority of Malaria carriers?

A

Female Anopheles due to the presence of hormone 20-E

245
Q

What does the presence of 20-E mean in female mosquitos?

A

Increased longevity, increased blood feeding preferences, and increased lipid transporters which assist the development of Plasmodium by reducing the parasites immune system.

246
Q

What are typical symptoms of malaria?

A

Fever, Chills, Nausea, Sweat, Headaches, Vomiting and Diarrhoea

247
Q

What is the worst type of malaria and what typically causes it?

A

Complicated Malaria and Plasmodium Falciparum

248
Q

What are the symptoms of complicated Malaria?

A

Severe Anemia, Organ damage, Coma and Hypoglycaemia. Associated with higher levels of mortality

249
Q

What are the 3 lifecycles of malaria?

A

Insect, Liver and Human

250
Q

What is the process of Plasmodium infection in humans?

A
  1. Mosquito infects human with sporozoites
  2. These form merozoites in the liver which explode
  3. Triggers asexual cycle in which Plasmodium forms rings in RBCs
  4. Leads to sexual differentiation into gametocytes
  5. These then go on to infect other vectors through blood meals
251
Q

Why is it effective to know about a parasite’s lifecycle?

A

We can target drugs/vaccines to it

252
Q

What varies between different plasmodium species?

A

Mechanisms/Factors used to invade host cells

253
Q

What has recent research shown about Plasmodium transmission?

A

Mononemes are excreted in the bloodstream from merozoites - encoded by the parasite

254
Q

What do Mononemes do?

A

They are secretory organelles which manipulate cellular architecture of RBCs. They are able to hijack host cell mitochondria

255
Q

What is significant about Apicoplasts in Plasmodium?

A

If you deplete = Parasites die, essential for survival.
They are present in all life stages of the parasite, provide a good/easy drug target

256
Q

What is the function of Apicoplasts in Plasmodium?

A

They fuel metabolic pathways of the Organelle

257
Q

What is unique about mitochondria in Plasmodium?

A

They only have one and it is more active in the insect host

258
Q

What is a drug used in Malaria-stricken countries?

A

Atovaquone, resistance has been shown in insects but prevents transmission

259
Q

How does Atovaquone prevent transission of Malaria?

A

Parasites with atovaquone resistant CytB genes do not generate viable progeny by self fertilisation = lower transmission.
Lower prevalence of mosquitos that are not susceptible to the drug.

Revision for Exams (5 decks)

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