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MCD Year 1 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What colour does Gram-positive bacteria stain with the Gram stain?

A

Purple/blue

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2
Q

What colour does Gram-negative bacteria stain with the Gram stain?

A

Pink/red

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3
Q

What causes the differences in staining in bacteria between Gram positive and negative?

A

Gram-positive bacteria have cell membrane and surrounding cell wall
Gram negative have cytoplasmic membrane, surrounding peptidoglycan and then an outer membrane
Stains bind to the peptidoglycan, which cannot happen in gram negative, producing different colours

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4
Q

Give examples of pathogenic Gram-negative bacteria and the associated disease

A

Escherichia coli
Salmonella (tyhimurium- food poisoning, typhi- thypoid)
Shigella (dysentry)
Vibrio cholerae (cholera)
Neisseria (meningitidis- meningitis, gonorrhoeae- gonorrhea)

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5
Q

Give examples of pathogenic Gram-positive bacteria and the associated disease

A 
Staphylococcus aureus (skin disease, endocarditis, bacteraemia, joint diseases, pneumonia)
Streptococcus pneumoniae (pneumonia, meningitis, otitis media)
Streptococcus pyogenes (tonsilitis, necrotising fasciitis, bactereamia, scarlet fever)
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6
Q

Give examples of pathogenic mycobacterium and the associated disease

A 
Mycobacterium tuberculosis (TB)
Mycobacterium leprae (leprosy)
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7
Q

Give examples of extracellular pathogens

A

Staphylococcus
Streptococcus
Yersinia
Neisseria

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8
Q

Give examples of intracellular pathogens

A 
Listeria
Shigella
Salmonella
Mycobacterium
Coxiella
Chlamydia (obligate)
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9
Q

Do Gram-positive or Gram-negative bacteria have type III secretions?

A

Gram-negative

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10
Q

What two things are required for motility and invasion?

A

Flagella

Type III secretion system

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11
Q

What are type III secretions?

A

Similar to flagella machine but delivers virulence proteins (effectors) into host cell

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12
Q

How does Salmonella invade host cells?

A

Via type III secretions system

Bacertial virulene proteins (effectors) induce actin polymerisation, membrane ruffling and bacterial internalisation

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13
Q

How does Listeria invade cells, become mobile and spread between cells?

A

Free bacterium is phagocytosed by host cells by zipper mechanism
Bacteria escaped the endosome and initiates actin nucleation. This assembles an actin tail making the bacteria motile.
Protrusion formation allows cell-to-cell spread, and as it has come from a neighbouring cell it is not detected as foreign

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14
Q

What are the three mechanisms of horizontal gene transfer?

A

Transformation
Transduction
Conjugation

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15
Q

How do bacteria replicate?

A

Binary fission

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16
Q

What is the process of binary fission?

A

1) Duplication of chromosome
2) Continued growth of the cell
3) Division into two cells

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17
Q

What is the process of transformation in horizontal gene transfer?

A

Free DNA (a single-stranded segment) is taken into the bacterium using DNA uptake proteins

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18
Q

What is the process of transduction in horizontal gene transfer?

A 
A phage (virus) infects the bacterium, replicating it's DNA inside the bacterium and cutting bacterial DNA into small pieces.
Some bacterial DNA may then be packaged into phage heads. Bacterium lyses and new phage particles are released.
Phage particle injects bacterial DNa into new bacterial cell
Injected DNa may be incorporated into bacterial chromosome
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19
Q

What is the process of conjugation in horizontal gene transfer?

A

Donor bacterium has a transmissible plasmid
Two bacteria form a mating bridge
Plasmid enters mating bridge and is replicated
When bacteria separate they each have a plasmid copy

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20
Q

What is the pathogenicity island?

A

The driving force of evolution in bacteria. They are a distinct class of genomic island acquired through horizontal gene transfer

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21
Q

Give examples of routes of infection by bacteria

A 
Intrinsic and extrinsic
Upper respiratory tract
Urogenital tract
Broken skin
Gastrointestinal tract (faecal-oral)
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22
Q

How are upper respiratory tract infections usually acquired?

A

Usually extrinsically-acquired from respiratory tract droplets or airbourne
Hand transmission can act as intermediate

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23
Q

What are the consequences of a bacterial infection acquired via the upper respiratory tract?

A

Upper respiratory tract infection (Pharyngitis, tonsilitis, sinusitis)
Lower respiratory tract infection (Bronchitis, pneumonia, pneumonitis)
Spread to adjacent tissue (Brain abscess, meningitis, empyema (pleural space), pericarditis)
Spread to bloodstream (Bacteraemia e.g.pneumococcal bacteraemia, meningococcal bacteraemia)

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24
Q

Where do intrinsic infections of the urogenital tract occur? Give examples

A

Large intestine
e.g. E. coli, Bacteroides ap. Proteis spp, Enterobacter spp, Klebsiella, Enterococci, Streptococcus group B, Candida/yeast

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25
Q

What types of extrinsic infections occur in the urogenital tract? Give examples

A 
Nosocomial infections (Urinary catheters)
Sexually transmitted infections (Neiserria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum (syphilis), HIV, HSV- viruses)
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26
Q

What are the consequences of urogenital infections?

A

UTI (cystitis-bladder, pyelonephritis-kidney)

Pelvic infection/STD (Gonococcal urethritis, pelvic inflammatory disease, tubo-ovarian abscess)

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27
Q

Give examples of pregnancy-related urogenital infections

A

Neonatal group B strep infection
Neonatal gonococcal conjunctivitis
Maternal endometritis (group A strep)

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28
Q

Give examples of infections that target broken skin, and where they usually occur

A

Skin and mouth bacteria (Staphylococcus aureus, Strepptococcus pyogenes)
Recent antibiotics/hospital (MRSA, pseudomonas)
Surgery/ bowel flora exposure (all of the above + Gram-negatives)
Unusual pathogens (Dog bites- pasteurella multocida, Medicinal leeches- aeromonas hydrophilia, Soil- clostridium tetani)

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29
Q

What are the consequences of infections via broken skin?

A 
Superficial infection
Cellulitis
Abscess
Fasciitis
Myositis
Gangrene/necrotic infection
Bacteraemia
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30
Q

What are the consequences of an infection acquired via the gastrointestinal tract?

A

Diarrhoeal illnesses (Vomiting only (e.g. toxins), diarrhoea and vomiting, diarrhoea only, dysentery- bloody diarrhoea)
Bacteremic/ systemic infections (Typhoid (S.typhi), Listeriosis (L. monocytogenes), Salmonellosis and septic arthritis, aortitis)
Toxin-mediated disease- Diarrhoea and vomitting (e.g. S. aureus enterotoxin), neurological (e.g.botulism)

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31
Q

What are the five factors that influence a pathogen’s infectivity?

A

Transmission to host
Ability to colonise host
Tropism- find unique niche (in or outside host)
Replicate
Immune evasion at site of colonisation or niche

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32
Q

What is infectivity?

A

The ability of a pathogen to establish an infection

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33
Q

What four factors influence a pathogen’s virulence?

A

Toxin production
Enzymes that degrade host molecules
Interruption of normal host processes
Complete immune evasion

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34
Q

What is virulence?

A

Virulence is how able a pathogen is, to cause disease

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35
Q

What is infectious dose? What is it affected by? (5) Give examples

A

Infectious dose is the number of bacteria required to initiate an infection. It can be affected by:

  • Route of transmission (Stomach acid means high dose required)
  • Ability to conolise (Enteropathogenic E. coli “EPEC” type 3 secretions for adherence)
  • Tropism and motility (Vibrio cholerae- high infective dose but flagella motility may help it reach gut epithelium)
  • Replication speed (Mycobacterium tuberculosis- low infective dose, very low replication rate, able to survive inside macrophages and resist killing)
  • Immune evasion site
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36
Q

What is the pathogenicity of Vibro cholerae?

A 
Enormous infective dose: >1000000
Flagella used to penetrate mucus
Then makes 2 component toxin A + B
Binds to GM gangliosides on gut
Triggers cAMP
Chloride efflux
Na and water follow
Profuse diarrhoea ("rice water stools")
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37
Q

What is the effect of group B strep on neonates?

A

Genital tract colonisation with group B strep (from GI tract)- harmless to 30-40% of women leads to invasive group B strep infection in neonates: meningitis, septicaemia, death

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38
Q

What is an antibiotic?

A

An antimicrobial agent produced by a microorganism that kills of inhibits other microorganisms

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39
Q

What does a bactericidal antibiotic do?

A

Kills bacteria

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40
Q

What does a bacteriostatic antibiotic do?

A

Stops bacteria growing

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41
Q

Antibiotic resistance usually occurs soon after the emergence of a new antibiotic with the exception of which antibiotics? (2)

A

Vancomycin

Erythromycin

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42
Q

What effect does antibiotic resistance have on patients?

A

Increased morbidity
Increased mortality
Increased time to effective therapy
Requirement for additional approaches (e.g. surgery)
Use of expensive therapy (newer drugs)
Use of more toxic drugs (e.g. vancomycin)
Use of less effective ‘second choice’ antibiotics

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43
Q

What are the major Gram-negative antibiotic resistant bacterial pathogens?

A
  • Pseudomonas aeruginosa (CF, burn wound infections. Survives on abiotic surfaces)
  • E. coli (ESBL, Klebsiella spp NDM-1→ GI infection, neonatal meningitis, septicaemia, UTI)
  • Salmonella spp. (MDR- GI infection, typhoid fever)
  • Acinetobacter baumannii (MDRAB→ opportunistic, wounds, UTI, pneumonia (VAP). Survives on abiotic surfaces)
  • Neisseria gonorrhoeae
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44
Q

What are the major Gram-positive antibiotic resistant bacterial pathogens?

A
  • Staphylococcus aureus (MRSA, VISA→ Wound and skin infection, pneumonia, septicaemia, infective endocarditis)
  • Streptococcus pneumoniae (pneumonia, septicaemia)
  • Clostridium difficile (pseudomembranous colitis, antibiotic-associated diarrhoea)
  • Enterococcus spp (VRE→ UTI, bacteraemia, infective endocarditis)
  • Mycobacterium tuberculosis (MDRTB, XDRTB→tuberculosis)
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45
Q

What is the reason for the high rate of hospital acquired infections?

A

High density of susceptible people
Presence of pathogen
Staff vectors
Open wounds
Inserted medical devices (e.g. IV catheters)
Disruption of normal flora due to antibiotic prophylaxis/therapy

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46
Q

What is the mechanism of action of beta-lactams? Give antibiotic examples

A

Interferes with synthesis of peptidoglycan component of bacterial cell wall by binding to penicillin-binding proteins. PBPs catalyse a number of steps in the synthesis of peptidoglycans.
Beta-lactams bind PBPs with high affinity and inhibit their function
(except PBP2a of MRSA)
e.g. Penicillin, methicillin, cephalothin

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47
Q

What is the mechanism of action of tetracycline?

A

Bacteriostatic, broad spectrum antibiotic. Inhibits protein synthesis. Binds to 16S component of the 30S ribosomal subunit, preventing interaction of charged aminoacyl-tRNAs with the mRNA/ribosome complex. This prevents the elongation of the peptide

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48
Q

What is the mechanism of action of chloramphenicol?

A

Bacteriostatic, broad spectrum antibiotic. Inhibits protein synthesis. Binds to 50S ribosomal subunit and blocks peptide transfer step. Often used topically due to toxicity, however AB resistance is renewing interest in chloramphenicol as a systematic therapeutic.

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49
Q

What are the four mechanisms of antibiotic resistance? What antibiotic uses all four of these?

A

1) Altered target site
2) Drug inactivation
3) Efflux
4) Altered metabolism
Pseudomonas aeruginosa uses all four mechanisms

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50
Q

What approaches are used to prevent emergence of drug resistant bacteria and nosocomial infections?

A

Better prescribing practices
Infection control
Combination therapy
Narrow vs broad spectrum antibiotic therapy

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51
Q

What are the main causes of human fungal infections? (4)

A

Candida albicans
Coccidioides immitis
Histoplasma capsulatum
Aspergillus fumigatus

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52
Q

How do fungi digest their food?

A

Extracellularly- they secrete hydrolytic enzymes which break down biopolymers to be absorbed for nutrition. Fungi are saphrophytes (live suspended in their own food source)

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53
Q

What types of illness are caused by fungi? (3)

A

1) Allergies
2) Mycotoxicoses
3) Mycoses

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54
Q

Give examples of allergies caused by fungi

A

Rhinitis
Dermatitis
Asthma
Allergic broncho-pulmonary aspergillosis (ABPA→ occurs in 2.5% of asthmatics)

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55
Q

What are mycotoxicoses? Give examples

A

A toxic reaction caused by ingestion or inhalation of a mycotoxin. Mycotoxins are secondary metabolites of moulds that exert a toxic effect on animals and humans
e.g. Amanita species, Psilocybin

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56
Q

What symptoms occur in Amanita species? What therapy?

A

Breathing problems, dizziness, severe vomiting, diarrhoea, dehydration, hepatic and renal failure 6 days later
Therapy- Gastric lavage and charcoal, liver transplant

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57
Q

What is the most carcinogenic natural compound known?

A

Aflatoxin produced by Aspergillus flavus

58
Q

What are the classifications of mycoses?

A

Superficial
Cutaneous
Sub-cutaneous
Systemic

59
Q

What is a superficial mycoses infection? Give examples

A

A superficial cosmetic fungal infection of the skin of hair shaft. No living tissue if invaded and there is no cellular response from the host
e.g. Black piedra (Piedraia hortae)
White piedra (Trichosporon beigelii)
Dandruff (Malassezia globosa)
Tinea nigra (Phaeoannellomyces werneckii)

60
Q

What is the mechanism of a cutaneous mycoses? Give examples

A

Dermatophytes or keratinophilic fungi
Produce extracellular enzymes (keratinases) which are capable of hydrolysing keratin. Inflammation if caused by the host response to metabolic by-products
e.g. Tinea capitis/ pedis/ corporis/ cruris/ unguium

61
Q

What is Tinea capitis?

A

Scalp ringworm
Superficial fungal infection of the skin of the scalp, eyebrows and eyelashes with a propensity for attacking hair shafts and follicles

62
Q

What is Tinea pedis?

A

Athletes foot

63
Q

What is Tinea corporis?

A

Ringworm

64
Q

What is a subcutaneous mycoses? Give examples

A

Chronic, localised infections of the skin and subcutaneous tissue following traumatic implantation of the aetilogic agent
e.g. Sporotrichosis (Sporothrix)
Chromoblastomycosis (several spp.)
Mycetoma (several spp.)
Sporotrichosis (Sporothrix schenckii- increasingly seen in combat blast wounds)

65
Q

What are systemic mycoses?

A

Affects internal organs. Primary infections can become established in a normal healthy host. Opportunistic require a compromised host in order to establish an infection

66
Q

Give examples of primary systemic mycoses infections

A

Coccidioides immitis
Histoplasma capsulatum
Blastomyces dermatiditis
Paracocidioides brasiliensis

67
Q

Give examples of opportunistic mycoses infections

A 
Cryptococcus neoformans
Candida
Aspergillus
Penicillium marneffei
The zygomycetes
Trichosporon beigelii
Fusarium
68
Q

How are fungal infections diagnosed?

A

1) Sample acquisition
2) Microscopy
3) Culture
4) Identification

69
Q

What are the targets for antifungal therapy?

A

1) Cell membrane
2) DNA Synthesis
3) Cell wall

70
Q

What is the mechanism of action of cell membrane active antifungals? Give examples

A

Inhibit synthesis of ergosterol (the main sterol in the fungal membrane). Act upon fungal cytochrome P450 enzymes
e.g. Polyene antibiotics (Amphotericin B, lipid formulations, Nystatin)
Azole antifungals (Ketoconazole, itraconazole, fluconazole, voriconazole, miconazole, clotrimazole)

71
Q

Give an example of a fungal DNA/RNA synthesis inhibitor

A

Pyrimidine analogues- Flucytosine
Often combined with azoles in combination therapy: Fluconazole and Flucytosine is often used to treat cryptococcal meningitis

72
Q

What is the mechanism of action of cell wall active antifungals?

A

Major components are glucans and chitin. non-specific inhibition of β 1, 3 glucan synthase

73
Q

Give an example of a cell wall active antifungal

A

Echinocandins- Caspofungin (Cancidas)

74
Q

What is the mycelium made up of?

A

Hyphae

75
Q

What are Koch’s postulates?

A

Criteria for identifying a microorganism causing disease

1) Microorganism found in large numbers in diseased animals but not in healthy ones
2) Microorganism isolated from a diseased animal and grown in pure culture
3) Microorganism when injected into healthy host much produce the same disease
4) Microorganism recovered from experimental host, isolated and compared to first microorganism = identical

76
Q

What is a virus?

A

Infectious obligate intracellular parasite. DNA or RNA genome

77
Q

What is the morphology of a virus?

A
  • Filamentous
  • Isometric
  • Enveloped
  • Head and tail (infects bacteria)
78
Q

What are the different classes of virus?

A
  • DNA virus
  • RNA virus
  • Capsid
  • Enveloped
  • Non-enveloped
79
Q

What is a DNA virus? Give examples

A

Virus that has DNA as it’s genetic material and replicates using DNA dependent DNA polymerase
The DNA is usually double stranded but can be single stranded
ssDNA→ Parvovirus B19; fifth disease/ slap face
dsDNA→ HSV1; cold sores, smallpox, Papillomavirus; warts
dsDNA (retrovirus)→Hepatitis B; hepatocellular carcinoma

80
Q

What is an RNA virus? Give examples

A

Has RNA as it’s genetic material.
RNA (positive sense)→SARS, norovirus, poliovirus;poliomyelitis, dengue virus;DHF
dsRNA→ Rotavirus; diarrhoea
RNA (negative sense)→ Ebola, rabies, Lassa fever, influenza, Measles, Mumps
RNA (positive sense)- retrovirus (Include DNA intermediates in their replication cycle)→ HIV; AIDs

81
Q

What is a retrovirus? Give an example

A

An RNA virus that includes DNA intermediates in it’s replication cycle
e.g. HIV/ AIDs

82
Q

What is the difference between a positive and negative sense virus action once it gets inside a cell?

A

A positive sense virus can make protein as soon as it gets into a cell
A negative sense virus must translate it

83
Q

What type of virus has accessory genes? What is the effect of these and consequence of not having them?

A

DNA viruses have accessory genes that can modify the host immune response. RNA viruses do not have them and therefore do not have proof-reading mechanisms

84
Q

What is the process of virus replication?

A

1) Attachment to cell membrane
2) Entry into cell
3) Translation
4) Replication
5) Assembly
6) Exit

85
Q

What is the cytopathic effect of viruses usually a result of?

A

Lysing the cell- due to shut down of host protein synthesis or accumulation of viral proteins

86
Q

What are the methods of viral diagnosis?

A

Detecting

1) Viral genome (PCR)
2) Viral antigen (IFA, ELISA)
3) Virus particles (EM, HA)
4) Virus cytopathic effect in cultured cells (Virus isolation)
5) Antibodies to virus (serology)

87
Q

What routes can viruses enter the body through?

A

1) The epithelial layers; respiratory tract, GI tract, genital tract
2) Directly into the blood through a bite or needle
3) Through the skin, often following an abrasion

88
Q

What is tropism?

A

The predilection of viruses to infect certain types of tissues and not others.
Can be defined by:
- receptor interactions (susceptibility)
- ability to use the host cell to complete replication (permissivity)
- whether the virus can reach tissue (accessibility)

89
Q

Give examples of modes of transmission of viruses

A
  • Measles virus→ Receptors: CD155 (SLAM) and Nectin 4. Entry to new host uses SLAM on immune cells. Exit from infected host uses Nectin4 on airway epithelia
  • Influenza→ Receptors: NA and HA. Entry through endosomes. Low endosomal pH triggers fusion- HA cleavage is required for exposure of fusion peptide
90
Q

What does iatrogenic mean?

A

Illness caused by medical examination or treatment

91
Q

What does nosocomial mean?

A

Infection acquired in hospital

92
Q

What is vertical transmission?

A

From parent to offspring

93
Q

What is horizontal transmission?

A

All other forms

94
Q

What is viraemia?

A

Virus in the blood

95
Q

How does a varicella zoster virus infection occur?

A

1) Virus enters body through peripheral route
2) Can infect many cell types including PBMCs (peripheral blood mononuclear cells) and skin cells
3) This leads to mild self-limiting illness in most childhood cases
4) From the skin site, it can infect sensory neurones where is remains latent
5) In herpes zoster, or shingles, occurring in adulthood when cellular immunity is impaired, virus is reactivated in the sensory neurone and causes a painful rash at the nerve endings

96
Q

What are the different outcomes of infection by viruses?

A 
Acute infection
Persistent infection
Latent infection
Slow infection
Oncogenesis
97
Q

Describe the process of a typical acute infection

A

Infection and viral replication until it reaches the threshold to activate adaptive immune response.
Induction of adaptive immune response
Adaptive response
Virus cleared, then memory

98
Q

Give examples of acute infection, including those which are fatal and accidental pathogenesis

A

Colds and influenza
Death→ smallpox- variola virus (Viral growth factors induce proliferation of the skin resulting in pox)
Dengue haemorrhagic fever (leakage of blood plasma from the capillaries)
Accidental pathogenesis→ poliovirus (faecal-oral transmission. Neurovirulent virus infects motor neurons causing paralysis)
Rubella (Mild rash except in early stage foetus where virus has strong tropism for dividing neural tissue= deafness, eye abnormality, congenital heart disease)

99
Q

What is a persistent viral infection? How do viruses do this?

A

Chronic infection with low-level replication of viruses in tissues which regenerate
e.g. Papillomavirus in warts, hepatitis B and C
Evading immune system surveillance: MHC downregulation, compensation for lost MHC class I, HCMV cytomegalovirus. Infecting tissues with reduced immune surveillance

100
Q

Explain the process of latency in herpes simplex virus

A

1) Primary site of infection: productive infection of epithelial cells. Infection by retrograde transport
2) Secondary site of infection and site of latent infection: sensory neuron
3) Site of recurrent infection: productive infection of epithelial cells

101
Q

How do viruses lead to oncogenesis?

A

May encode oncogenes
Interfere with the cell cycle in order to enhance their own repliation
Papilloma viruses encode inhibitors of tumour suppressor p53, E6 and E7 genes forcing the cell into S phase

102
Q

Give examples of oncoviruses and the cancer they cause

A

HTLV-1 causes adult leukaemia
Hepatitis B and C cause hepatocellular carcinoma (Hepadnavirus utilises a reverse transcription step in it’s replication cycle)
Epstein-Barr virus causes Burkitt’s lymphoma, Hodgkin’s lymphoma and nasopharyngeal carcinoma (In most, causes a lytic infection in childhood or infectious mononucleosis in young adulthood and then remains latent in B cells. Passed on in saliva)

103
Q

What affects the outcome of a virus?

A 
Virus sequence
Virus load
Host immune response/status
Host co-morbidity
Co-infections
Other medications
Host genetics
Host age/gender
104
Q

What predisposing co-morbidities lead to severe influenza?

A 
Asthmatics and respiratory viruses
Obesity
Immunosuppression
Immundeficiency
Eldery
Diabetes mellitus
Pregnancy
105
Q

What is the function of HIV integrase?

A

An enzyme found in retroviruses that permits the viral DNA to be integrated into the DNA of the infected cell

106
Q

What is the replication cycle of HIV?

A

1) Fusion of the HIV cell to the host cell surface (HIV GP120 binds to CD4 receptor)
2) HIV RNA, reverse transcriptase, integrase and other viral proteins enter the host cell
3) Viral DNA is formed by reverse transcription
4) Viral DNA is transported across the nucleus and integrates into the host DNA
5) New viral RNA is used as genomic RNA, and to make viral proteins
6) New viral RNA and proteins move to cell surface and a new, immature HIV virus forms
7) The virus matures by protease releasing individual HIV proteins

107
Q

What is the function of HIV protease?

A

An enzyme that hydrolyses or cuts proteins and is important in the final steps of HIV maturation

108
Q

What are the properties of a good vaccine? (6)

A

Stimulates an effective immune response
Safe- no adverse reactions
Inexpensive to manufacture and distribute
Stable
Easy to administer
Simple for manufacturer and regulatory authroities to control

109
Q

How does herd immunity affect a disease?

A

if it is high enough the disease will die out

110
Q

What are the phases of a clinical trial?

A

Phase 1→ Assesses safety- small number of adults
Phase 2→ Assesses immune response and expands safety- includes all groups likely to have the vaccine
Phase 3→ Protection studies- placebo, double blind trials

111
Q

What phase of clinical trials is vaccine efficacy determined in?

A

Phase 3 trials

112
Q

What is the formula to calculate vaccine efficacy?

A

Attack rate in vaccinated group/Attack rate in unvaccinated group

113
Q

When do you calculate the herd effect of a vaccine?

A

After trials following introduction of the vaccine

114
Q

What is the formula for herd effect?

A

1-(attack rate unvaccinated post-introduction/attack rate unvaccinated pre-introduction)

115
Q

What does a vaccine formulation contain? (3)

A

1) Antigen (to stimulate the immune response to the target disease)
2) Adjuvant (to enhance and modulate the immune response)
3) Excipients (buffer, salts, saccharides and proteins to maintain the pH, osmolarity and stability of the vaccine plus preservative)

116
Q

What types of antigen can be used in a vaccine? (5)

A

1) Live attenuated organisms
2) Killed whole organisms
3) Purified component vaccines
4) Conjugates
5) DNA vaccines

117
Q

What are conjugate vaccines?

A

Carbohydrate chemically linked to immunogenic protein

118
Q

In what situations are conjugate vaccines useful?

A

Where humoral immunity is required

119
Q

What conjugate vaccines are licensed?

A

Hib vaccine (Haemophilus influenzae)
Pneumococcal conjugates
MenC conjugates
Meningococcal A, C, W, Y conjugates

120
Q

What are the advantages of live attenuated vaccines?

A

1) Provides rapid, broad, long-lived immunity
2) Cellular immunity
3) Immune system challenged at the right site

121
Q

What are the disadvantages of live attenuated vaccines?

A

1) Complex
2) Hard to define and ensure safety
3) Difficult to license and control
4) May revert

122
Q

Give an example of a killed whole cell vaccine and the versions of this vaccine available

A

Cholera vaccine

  • Killed whole cell parenteral vaccine
  • Killed whole cell oral vaccine
  • Dukoral (drink formulation)
123
Q

What adjuvents are used in vaccines?

A 
Delivery systems
- mineral salts
- surface active agents
- synthetic microparticles
- oil-water emulsions
- liposomes
Immune potentiators
- toxins and lipids
- nucleic acids
- peptidoglycan
- carbohydrates
- peptides
- cytokines and hormones
124
Q

What is a prophylactic approach to virus control?

A

Preventing disease before the aetiological agent it acquired, by vaccination or giving drug before infection

125
Q

What is a therapeutic approach to virus control?

A

Treating the disease after the host has been infected e.g. antiviral drugs

126
Q

How is a live attenuated virus produced for a vaccine?

A

1) Pathogenic virus is isolated from a patient and grown in human cultured cells
2) The cultured virus is used to infect monkey cells
3) The virus acquires many mutations that allow it to grow well in monkey cells
4) The virus no longer grows in human cells and may be a candidate for a vaccine

127
Q

For what viral infections is vaccination a successful strategy?

A 
Influenza
Poliovirus
Rotavirus
Shingles
HIV vaccine? ( Thai trial RV-144)
Ebola vaccine
128
Q

Name two vaccines available for the flu

A

FluMist- delivered intranasally

Tamiflu- neuraminidase receptors

129
Q

What disease has been eradicated using successful vaccination programme?

A

Smallpox

130
Q

What drug is a successful antiviral agent?

A

Interferons- induces the hosts natural antiviral response

131
Q

Why is acyclovir an effective antiviral agent?

A

It is only activated inside virus infected cells

It has a higher affinity for viral DNA polymerase than for host cell polymerase

132
Q

What is Acyclovir’s mechanism of action?

A

1) Acyclovir is converted by viral thymidine kinase to Acyclovir monophosphate
2) Acyclovir monophosphate is then converted by host cell kinase to acyclovir triphosphate
3) Acyclovir triphosphate competitively inhibits and inactivates viral DNA polymerases preventing viral DNA synthesis without affecting normal cellular processes
It has a higher affinity for viral DNA polymerase than for host cell polymerase

133
Q

Give examples of targets for antiviral agents and the associated drug

A

1) Fusion- Amantadine
2) Protein synthesis- Amantadine
3) RNA polymerase- Ribavirin
4) Release- Zanamivir, oseltamivir

134
Q

Why was neuraminidase a target for antiviral agent research? Give drug examples

A

Neuraminidase (enzyme) destroys cell surface receptors. Inhibiting it inhibits virus spread
e.g. Sialic acid, Relenza, Tamiflu

135
Q

How do HIV antiretrovirals work?

A

Allosteric inhibitors
Integrase inhibitors
Entry inhibitors
Protease inhibitors

136
Q

What is antigenic drift?

A

A mechanism for variation in viruses that involves the accumulation of mutations within the genes that code for antibody-binding sites.
vaccines need to be updated every year to accommodate this

137
Q

What is antigenic shift?

A

The process by which two or more different strains of a virus, or strains of two or more different viruses, combine to form a new subtype having a mixture of the surface antigens of the two or more original strains.

138
Q

What are arboviruses? Give examples

A

Viruses that are transmitted by arthropod vectors

e.g. Yellow fever, Dengue, West Nile, chikingunya

139
Q

What is the vector of West Nile virus?

A

Culex tarsalis

140
Q

What is the SARS virus? How has it spread?

A

Severe Acute Respiratory Syndrome
Coronavirus- zoonotic infection
Large (30kb) positive sense RNA genome. Envelope spike protein. Receptor is human ACE-2 protein
Virus isolated from masked palm civets and raccoon dogs is almost identical
S protein is highly plastic and can adapt to different receptors overcoming host range barriers

141
Q

What is MERS?

A

Middle Eastern Respiratory Syndrome

A zoonotic infection from camels- receptor DPP4 expressed in the lungs

142
Q

What was the mechanism behind the swine flu outbreak?

A 
H1N1 was already present in human population
Antigenic shift (co-infected cells within a host). Pigs mixing the strains of virus created a more virulent strain

MCD Year 1 (10 decks)

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