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Block 1 > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

Describe what is meant by the term communicable disease

A

Communicable disease is defined by diseases which can be transmitted from one host to another unaffected individual. Grows in host before being shed.

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2
Q

Describe the different types of microbes and infectious agents

A
  • Prokaryotic organisms - single cell organisms with no nucleus or defined organelles. (e.g. bacteria)
  • Eukaryotic organisms - single or multi-celled organisms with defined nucleus and organelles. (e.g. fungi, protozoa, helminths, malaria, pinworms, tapeworms/
  • Viruses - DNA or RNA surrounded by protein capsule; obligate parasite
  • Prions - Infectious proteins
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3
Q

Define opportunistic infection

A

In immunocompromised host, the indigenous flora gain access to normally sterile tissue/sites of the body, colonizes the site, and causes

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4
Q

Describe the obligatory steps in microbial infection and transmission between hosts

A

Pathogens must colonize a host and invade a target tissue or organ for disease to be caused.

Transmission between hosts:

  • respiratory or salivary spread
  • faecal-oral spread
  • venereal (sexual) spread
  • Vectors (insects)
  • Vertebrae (animals) reservoir
  • Vector-vertebrate (animals and insects) reservoir
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5
Q

Describe the chronology of vaccine development (e.g. contributions of Jenner, Pasteur)

A

Edward Jenner - gave people cowpox and noticed they didn’t get small pox afterwards

Louis Pasteur - Debunk the theory of spontaneous generation of microbes. Boiled bacteria broth, sealed flask, and showed that no new cells grew.

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6
Q

Describe the sanitary movement; Van Leeuwenhoek, microscopes and the discovery of “animalcules” and Lister’s contribution

A
  • Sanitary movement - Need for clean water and air in highly populated areas
  • Dr. John Snow - traced the source of cholera outbreak to a waterhole in London
  • Van Leeuwenhoek - Invented microscope and observed ubiquity of microscopic life
  • Dr Joseph Lister - Surgical fever and abscess are due to bacteria in wounds.
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7
Q

Describe the contagion theory

A

Contagion theory: communicable diseases were the work of an external and transmissible

Miasma theory: Disease was due to “bad air” that caused the imbalance of “blood, phlegm, black and yellow bile”

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8
Q

Discuss Koch’s postulates and the germ theory of communicable disease

A

Germ theory of communicable disease: Diseases are caused by microorganisms which will invade hosts and grow and reproduce within their host to cause disease

Koch’s postulates

  • microbe must be present in every case of the disease
  • Microbe must be isolated from the diseased host and grown in pure culture
  • disease must be reproduced when a pure culture is introduced into a non-diseased susceptible host
  • Microbe must be recoverable from an experimentally infected host.

Modifications on Koch’s postulates - not all microbes can be cultured in vitro and so many communicable diseases do not have experimental animal models

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9
Q

Outline advances in bacterial culture and staining

A

Advances in bacterial culture

  • Koch used solid media for pure cultures
  • Gelatin -> Agar

gram staining - used to determine if peptidoglycan wall is present on a bacteria species

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10
Q

Describe the discovery of toxin-mediated diseases

A
  • In 1888 Yersin and Emile Roux isolated a toxin secreted by the diptheria bacteria
  • showed that the toxin alone caused symptoms of the disease
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11
Q

Describe the discovery of the role of insects in disease transmission

A

In 1898 Ross and Grassi demonstrated that malaria was transmitted by anopheles mosquitoes.

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12
Q

Describe the discovery of viruses

A
  • Reed showed yellow fever was caused by agent that could pass through porcelain filter
  • In 1898 Loeffler and Frosch demonstrate that filtrates of lesion fluid collected from animals infected with foot–and-mouth diseases could transmit the disease into susceptible animals
  • Visualization of viruses was only achieved in the mid 20th century via electron microscopes.
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13
Q

Describe how poliomyelitis drove vaccine research

A
  • Epidemic of poliomyelitis led to governments to conduct research of vaccination against polio
  • Jonas Salk developed an inactivated polio vaccine in 1955
  • Albert Sabin generated a second Polio vaccine which could be given orally and was able to transmit from person to person. It was used to eradicate Poliomyelitis
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14
Q

Describe the discovery of penicillin, antibiotics and antivirals

A
  • Alexander Fleming discovered antibacterial properties of fungal toxin Penicillin
  • while working on staphylococci, penicillium mould was surrounded by a bacteria-free zone
  • Penicillin mould culture prevented growth of staphylococci even diluted 800 times
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15
Q

Outline the classification of bacteria

A

Gram staining:

  • gram-positive bacteria have a much thicker peptidoglycan layer than Gram-negative bacteria
  • steps to gram stain:
    1) crystal violet applied to bind with peptidoglycans in wall (more retained in gram-positive)
    2) gram’s Iodine applied to seal in crystal violet dye
    3) Decolorizer (acetone/alcohol) washes away crystal violet from gram-negative bacteria
    4) Carbol fushsin/safranin counter-stain stains gram-negative bacteria pink

shape:

  • bacilli - elongated/rod-shaped bacteria
  • cocci - spherical shaped bacteria

Respiration:

  • anaerobes - can grow in environments without oxygen
  • Aerobes - require oxygen
  • Facultative anaerobes - use aerobic respiration when oxygen is present, but can switch to anaerobic

Reproduction:

  • clusters - staphylo- (multidirectional growth)
  • Chains - strepto- (one-dimensional growth)
  • Pairs - diplo- (unidirectional growth)

genomic similarity - Bacteria are classified together when strains share similar DNA sequences

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16
Q

Outline the rationale and importance of Gram staining

A
  • Very quick diagnostic tool for bacterial infection
  • Determining gram-stain of bacteria allows narrowing down of antibiotics in half. Certain antibiotics work on gram-positive and other on gram-negative
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17
Q

Outline the main features of Gram-positive staphylococcus aureus

A
  • gram-positive aerobic clustered cocci
  • Golden colour
  • Virulence: Structural components, toxins, and enzymes
  • Pathology: 1) Endocarditis: Fibrinogen on heart, 2) Toxic shock syndrome, 3) necrotic pneumonia (holes in lungs), 4) infection and necrosis of skin
  • Epidemiology: colonizes nasal mucosa and skin, spread through direct contact or contaminated materials
  • MRSA = Methicillin-resistant Staphylococcus aureus
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18
Q

Outline the main features of Gram-positive streptococcus pyogenes

A
  • Gram-positive aerobic cocci in long chains
  • Part of the normal flora in respiratory in respiratory, gastrointestinal and genital tracts
  • Virulence: Toxins and enzymes
  • Pathology: suppurative infection (i.e. to epidermis, dermis, and subcutaneous tissue), systemic infection, scarlet fever, post-streptococcal sequelae (acute glomerulonephritis, rheumatic fever)
  • Epidemiology: colonizes in skin and upper respiratory tract, spread through direct contact, respiratory droplets, and contaminated material
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19
Q

Outline the main features of gram-positive streptococcus pneumoniae

A
  • Gram-positive aerobic cocci in pairs
  • Virulence: Capsule (prevents phagocytosis) and pneumolysin
  • Pathology: pneumonia, meningitis, sinusitis
  • Epidemiology: colonizes nasal mucosa and skin, spread through endogenous spread from colonized nasopharynx (person-person spread is rare)
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20
Q

Outline the main features of gram-positive bacillus anthracis

A
  • Gram-positive aerobic bacilli in long chains
  • Causes anthrax infection: “Anthrax” = black necrotic wound
  • Spore forming bacteria
  • Virulence: Edema toxin and capsule
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21
Q

Outline the main features of gram-positive mycobacterium tuberculosis

A
  • Weakly gram-positive aerobic bacilli: complex lipid-rich wall with mycolic acid
  • Acid-fast bacteria (AFB) stained by Ziehl-Neelsen (ZN) stain
  • Difficult to culture (slow growing)
  • Pathology: 1) intracellular growth in alveolar macrophages, 2) granulomas prevent further spread (latent infected), 3) symptomatic disease state may occur during life
  • Epidemiology: 1/3 of world has TB, spread person-to-person by aerosol, Immunocompromised patients have higher risk of asymptomatic disease
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22
Q

Outline the main features of gram-positive listeria monocytogenes

A
  • Gram-positive aerobic short rods
  • Grown in high concentration of salt
  • Virulence: Haemolysins and intracellular pathogen
  • Pathology: Neonatal sepsis, meningitis, gastroenteritis
  • Epidemiology: in soil and mammal GIT, Transmission via foodborne or vertical, eating contaminated milk, cheese, or raw vegetables.
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23
Q

Outline the main features of gram-positive clostridium botulinum

A
  • Gram-positive anaerobic rods
  • spore-forming
  • In normal flora of GIT
  • Virulence: Produces exotoxins and haemolytic enzymes
  • Pathology: Blocks neurotransmitters in peripheral nerve endings (muscle weakness)
  • Epidemiology: Food-borne
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24
Q

Explain how bacteria are named

A

Genus name is capitalized, and the species name is written in lower case, all in italics

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25
Q

Outline the main characteristic of gram-negative cocci: Neisseria (general)

A
  • Gram-negative cocci pairs (i.e. diplococci)
  • Flattened adjacent sides
  • Capsule protects from phagocytosis
  • Epidemiology: Neisseria species are commensal in nasopharynx of 10% of humans, Respiratory spread person-to-person
  • Prevention: Vaccines, antibiotics
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26
Q

Outline the main characteristic of gram-negative cocci: Neisseria gonorrhoeae (gonococcus)

A
  • Causes gonorrhoea (i.e. urethritis, epididymitis and pelvic inflammation)
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27
Q

Outline the main characteristic of gram-negative cocci: Neisseria meningitides (meningococcus)

A
  • Causes pharyngitis, sepsis and meningitis
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28
Q

Outline the main characteristics of gram-negative rods (general)

A
  • Many are part of normal flora of GIT

- Virulence: Surface antigens (O = outer membrane, H = flagella, K = capsule), adhesins, endotoxins

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29
Q

Outline the main characteristic of gram-negative rods: Escherichia coli

A
  • Facultative anaerobic
  • Pathology: Urinary infection, neonatal sepsis and meningitis, Intestinal infection -> Enterohaemorrhagic E. coli (EHEC) is most common: complicated by haemolytic uraemic syndrome (HUS)
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30
Q

Outline the main characteristics of gram-negative rods: Klebsiella

A
  • Klebsiella pneumoniae is most common
  • Facultative anaerobic
  • Virulence: large polysaccharide capsule (mucoid colonies)
  • Pathology: UTI, lobar pneumonia, liver abscesses, sepsis
  • Epidemiology: antibiotic resistant
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31
Q

Outline the main characteristics of gram-negative rods: salmonella

A
  • Intracellular pathogen
  • Facultative anaerobic
  • Pathology: non-typhoid salmonella - gastroenteritis in GIT mucosa, extra-intestinal infections; typhoid fever - caused by salmonella typhi, life-threatening systemic infection
  • Epidemiology: foodborne/waterborne, human-to-human transmission via fecal-oral route, animal contact
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32
Q

Outline the main characteristics of gram-negative rods: shigella

A
  • Facultative anaerobic
  • Non-motile, non-lactose fermenting
  • Virulence: shiga toxin damages intestinal and glomerular endothelium
  • Pathology: necrosis in colonic epithelium, dysentery: frequent low-volume stools with blood, mucous, and pus and abdominal cramping
  • Epidemiology: humans are the only reservoir, faecal-oral transmission, water and foodborne, infectious dose is low
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33
Q

Outline the main characteristics of gram-negative rods: bordetella

A
  • Bordetella pertussis causes ‘whooping cough’
  • Aerobic gram-negative rods
  • Vaccine contains pertussis toxin and filamentous haemagluttin
  • Epidemiology: humans are only reservoir, spread via respiratory droplets
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34
Q

Outline the main characteristics of gram-negative rods: legionella

A
  • Aerobic gram-negative rods
  • Grows between 20-45 degrees celsius in warm water sources
  • Legionella pneumophila is the cause of Legionnaire’s disease
  • Virulence: invades alveolar macrophages
  • Pathology: pneumonia
  • Epidemiology: contaminated water source; NO human-to-human transmission
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35
Q

Outline basic mechanisms of bacterial pathogenesis

A
  1. Acquire virulence genes
    - pathogenic bacterial contain genes that are not present in related non-pathogenic bacteria
    - Transformation: lysis of one cell releases DNA for other bacteria to integrate into own DNA
    - Transduction: bacteriaophage (virus) develop capsule of bacteria DNA and inject into another bacterium for recombination
    - Conjugation: A DNA plasmid moves between bacterial via a pilus (tube)
    - Virulence can also arise due to gene loss
  2. Switch virulence genes on:
    - genes switch on in response to environment
    - Quorum sensing - bacteria to know when there are enough bacteria to proliferate and survive within an infected host or also know if there are enough nutrients and space to grow. Switches ON virulence genes
  3. Avoid immune system
    - Hide in capsules, biofilms, or in phagocytes
    - Mimic host cells
    - immune evasion by changing antigens
    - Escape phagocytosis via phagocyte recruitment suppression, reduction of vascular permeability, or phagocyte enzyme inhibition
  4. Damage host tissues and spread through cells and organs
    - Colonization, proliferation and invasion of tissues
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36
Q

List bacterial mobile genetic elements

A

Plasmids - Extra-chromosomal DNA that can be incorporated via recombination with the chromosomal DNA into the genome. Passed via pilus

Prophage - Non-lytic bacteriophages (virus) which incorporate host bacteria DNA into capsid, then inject DNA into another bacterium for recombination

Pathogenecity Island - segment of the chromosome which harbours clusters of virulence genes

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37
Q

Outline bacterial protection and attack strategies

A

Enzyme production:

  • proteases help survival on mucosal surface
  • Coagulases/collagenase damage tissue
  • Hyaluronidase help spread

Toxin production

  • Endotoxins - lipopolysaccharides from gram-negative bacteria
  • Exotoxins - proteins from gram-positive and gram-negative bacteria
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38
Q

Outline some host factors that alter susceptibility to infection

A

Host factors include:

  • immune status
  • Age
  • Genetics
  • Nutrition
  • Overall health
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39
Q

Define the term ‘virus’

A

Virus definition:

  • Ultramicroscopic infectious agent that ONLY replicated within cells of living hosts
  • obligate intracellular parasites = totally dependent upon host cells for replication (has no machinery)
  • RNA or DNA wrapped in thin protein coat
  • Virion - name for virus particle composed of nucleic acid, capsid and envelope (in some cases)
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40
Q

Outline the structure of a virus structure and the composition of the virus genome

A

Nucleic acid - genetic content is either DNA or RNA but not both:

  • DNA viruses can have ssDNA or dsDNA
  • RNA viruses can have dsRNA, positive sense ssRNA or negative sense ssRNA

Capsid - protein shell around nucleic acid

  • capsomeres = viral protein subunits that make up capsid
  • helical capsid - rod shaped shell
  • icosahedral capsid - roughly spherical shell
  • Complex capsid - neither helical or icosahedral

Envelope

  • lipid bilayer membrane surrounding the capsid of some viruses
  • derived from host cell membranes
  • contain encoded proteins
  • consequence: must remain in moist environment; very sensitive to environment (die in GIT)
  • Non-enveloped virus can spread easier, infective after drying, and are much more resilient
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41
Q

List the steps in the virus multiplication cycle

A
  • attachment - virus particle binds to the potential host cell via capsid/envelop to cell surface proteins
  • penetration - movement of the virus across plasma membrane
  • uncoating - loss of capsid proteins and release of nucleic acid (DNA/RNA)
  • byosynthesis - synthesis of viral proteins and viral nucleic acid using host cell
  • Assembly - association of viral structural proteins and nucleic acid form virions
  • Release - accumulation within the host cell leads to exit of virus from the infected cell

For DNA viruses, DNA is synthesized in nucleus
For RNA viruses, RNA is synthesized in cytoplasm

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42
Q

List the effects of viruses on cells

A
  • Cell-death - known as cytopathic effect (CPE); may induce apoptosis or necrosis
  • Transformation - cell phenotype properties become cancer-like
  • Latent infection - virus remains within cells with no obvious effects; may infect later with full effect
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43
Q

List important modes of virus transmission

A
  • Respiratory and salivary transmission: aerosis, salivary spread
  • Faecal-oral spread: person-to-person, fecal contaminated water/food
  • vector-mediated transmission (through other animals and insects)
  • sexual transmission
  • blood-borne transmission
  • vertical transmission (mother to baby)
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44
Q

Key requirements for successful viral infection

A
  • viral entry
  • immune response evasion
  • dissemination/spread within host
  • transmission to another host
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45
Q

Portals of entry into the host

A
  • Skin - break in surface
  • respiratory tract - inhalation of viruses as aerosols or droplets
  • Gastrointestinal tract - consuming contaminated substance
  • genitourinary tract - infection via sexual activity
  • conjunctiva - entry via the eye due to abrasion
46
Q

Outline the mechanisms of spread of viruses through the host via localized infection

A
  • Replication at the primary site of infection
  • only spread locally to adjacent cells (usually epithelial layer)
  • surface infection: only spread to epithelial tissue near infection site
  • e.g. influenza, rotaviruses
47
Q

Outline the mechanisms of spread of viruses through the host via disseminated infection

A
  • Must breech physical and immunological barriers
  • Infection extends beyond primary site of infection to preferred site of replication
  • via circulatory system (in blood): e.g. HIV, measles
  • via nervous system (in neurons): e.g. rabies, polio
  • infection spreading from one part of the body to another via blood vessels or lymph vessels
48
Q

Outline the mechanisms of spread of viruses through the systemic infection

A
  • Disseminated infection but many organs are involved
49
Q

List major genetic determinants of viral virulence

A

Genetic determinants of viral virulence:

  • multigenic (characteristic is specified by a combination of multiple genes)
  • ability to make recombinant DNA (virus can integrate DNA from other cells)
  • use of reassorted strains of viral components
50
Q

Outline the meaning of the term ‘tissue tropism’

A

Tissue tropism - cells and tissues of a host cell that can support the growth of a particular virus or bacteria

51
Q

Summarize mechanisms of viral disease production (with reference to clinical examples):

A

Viral destruction of tissues and organs - damage to cell or cell function due to virus replication:

  1. ruptured of infected cells during virus release
  2. apoptosis of infected cells in response to infection
  3. lose function of infected cells
  4. transform of infected cells by virus

Virus-induced immunopathology - damage due to host response to infection

  1. antibodies and immune cells destroy infected cells and tissue
  2. inflammation occurs resulting in swelling and rash
52
Q

Outline factors related to persistent and latent infections

A

Persistent infections

  • not cleared effectively by the immune response
  • virus products continue to be produced for long periods
  • two types: slow/chronic and latent

Chronic persistent infection:

  • virus is never fully cleared (associated with immunopathology)
  • viral products produced in low quantities for a long period of time
  • periods where person is contagious with NO symptoms
  • Amplified reinfection after virions accumulate
  • E.g. HIV, measles

Latent persistent infection

  • Infectious virus is completely cleared, but genome persists in cells (undetectable)
  • Periodic virus re-awakening with new infectious virus
  • may or may not be response
  • e.g. Herpes
53
Q

Outline mechanisms of viral oncogenesis

A
  • oncovirus contains RNA/DNA in capsule that can insert viral oncogenes into the host genome
  • via retrovirus, can insert segments into host genome that will cause cancer
  • viruses can insert in regions that are already cancerous
54
Q

Describe the appropriate choice of test for pathogen detection and antibody response including the influence of time-frame on choice of diagnostic test

A

Pathogen detection: during early and height of disease

  • Culture independent: microscopy, antigen detection, nucleic acid amplification
  • Culture dependent: microbial diagnosis, antimicrobial susceptibility

Antibody response: during convalescent period
- serology

55
Q

Explain the culture-independent detection technique of microscopy and the purpose of this technique

A

Microscopy-based diagnosis:

  • direct examination of specimens
  • can use special stains to identify specific microorganisms: e.g. gram-staining for bacteria, e.g. fluorescent antibodies for viruses
  • purpose: detection of potential pathogens, assesment of quality of specimen (e.g. epithelial cell in urine -> contamination)
  • Pros: fast and cheap, sometimes sufficient for diagnosis
  • Cons: limited specificity, frequent false-negatives (low microbial load)
56
Q

Explain the culture-independent detection technique of antigen detection with antibodies, including the role of direct immunofluorescence and point-of-care tests (POCT)

A

Antigen-antibody detection:

  • steps: 1) fix antigen to surface slide, 2) add fluorescently-labelled antibody, 3) wash and apply UV light
  • Pros and cons same as microscopy
  • POCT - Point of Care test: sample taken and tested immediately, need confirmation by standard lab test, very fast
57
Q

Explain the culture-independent detection technique of nucleic acid amplification techniques - e.g: PCR Nucleic ACid Amplification (NAA)

A
  • Detection of microbial DNA
  • PCR -> Add specific primers for microbial DNA and amplify with thermal cycles: PCR involves 3 cycles.
    1) Denaturation - heating to ~95 degrees celsius to break H-bonds between the two DNA strands
    2) Annealing - cooling to ~70 degrees Celsius to anneal primers to the strands
    3) Synthesis - heat to optimal temperature of DNA polymerase to synthesize
  • Pros: high sensitivity, fast
  • cons: false positives (cros contamination), hard to interpret positive results
58
Q

Explain the culture-dependent detection technique of culture-based diagnostics and describe the rationale behind the use of various solid media, substrates, biochemical and cell wall structure properties

A

Pathogen isolation

  • culture microbe on solid media:
    1) sheep-blood Agar - haemolytic bacteria grow
    2) Mannitol salt agar: selects for gram-positive bacteria, microbes that metabolize mannitol turn agar YELLOW, e.g. Staphylococci
    3) MacConkey Agar: selects gram-negative bacteria, microbe that metabolize lactose turn agar RED
    4) CHROMagar - selective agars
59
Q

Describe the use of cell cultures including their pros and cons

A

Pros:

  • very specific and sensitive (“gold standard)
  • examine multiple microbes
  • Assess antimicrobial infections

Cons:

  • very expensive
  • can be slow
60
Q

Explain the process of microbial DNA sequencing and its clinical usage

A
  • Use PCR to amplify “conserved” essential microbial genes
  • Match DNA vs ‘reference’ sequences in databases (need +99% for species identification)
  • Can be performed directly from clinical samples (not just cultures)
61
Q

Explain the process of antibiotic susceptibility testing, the disk diffusion test, rationale behind the dilution test and the meaning of minimal inhibitory concentration (MIC)

A

Antibiotic susceptibility testing

1) Disk diffusion tests:
- Seed agar with standardized amount of bacteria
- Filter paper discs are saturated with antibiotics are placed on agar
- Incubate and see if bacteria grow around disk

2) Dilution tests:
- Quantitative estimates of susceptibility to antibiotics
- Minimal inhibitory concentration (MIC) = lowest (antibiotic) that inhibits growth in vitro
- Place standard bacteria broth and add antibiotics, diluting by double each step

62
Q

Describe the use of serology based lab diagnostics to measure antibody response, including the use of specific and non-specific tests, and enzyme immunoassay (EIA)

A

serology-based lab diagnosis - a measurement of antibody response:

  • Steps:
    1) fix known antigen on plate
    2) add patient serum; wash
    3) add labelled anti-human antibodies; wash
    4) Add UV or substrate
  • Relative concentrations of immunoglobulins will indicate the exposure or infection of the individual:
    1) IgM -> Recent or current infection
    2) IgG -> Current or past infection

EIA - Enzyme ImmunoAssay (EIA):

  • Anti-human antibodies are enzyme-labelled
  • Add colourless substrate
  • Enzymes make colourless substrate into coloured products

ELISA - plate-based assay designed to quantify substances such as peptides etc. EIA is another name for ELISA

63
Q

Explain the time-frame when IgM and IgG will appear in the serum and how their presence or absence can be used to identify the presence of current or past infection and/or immunization

A

IgM -> Recent or current infection
IgG -> current or past infection

4-fold increase in antibody quantity between maximum IgM and IgG

serological evidence of infection:

  • presence/absence of specific antibody
  • four-fold increase in antibody titre
  • seroconversion
64
Q

Describe the clinical significance of acute and convalescent sera and explain the meaning of seroconversion and a four-fold increase in antibody titre

A

Acute sera - serum taken from patient and stored
Convalescent sera - serum taken from a patient two to three weeks later

If there is a large change in the level of antibodies between the sera, then an infection has occurred, and the body is mounting an immune response:
- 4 fold increase is sufficient to infer that there is an infection

65
Q

Describe the pros and cons of serology

A

Pros:

  • convenient sample (2-5 days)
  • Main method for lab diagnosis of viral infections

Cons:

  • Invasive infectious diseases only
  • Retrospective (weeks before detectable antibodies are produced due to infection)
  • Cross-reacting antibodies affect specificity of results
  • Previous vaccination make interpretation difficult
66
Q

Define antimicrobial agent

A

chemical that kills or inhibits the growth of microorganisms

67
Q

Describe antibiotic

A

chemical produced by a micro-organism that kills or inhibits the growth of another microorganism:
- semi-synthetic antibodies: natural base, but modified chemically to new “antibiotic”

68
Q

Outline the classification of microbials by spectrum of activity and mechanism of action

A

Spectrum of activity:

  • classified based on which groups of microbes the antibiotic kills
  • broad = kill multiple groups of microbes; Narrow = kills one group of microbes
  • No antibiotic kills ALL types of microbes

Mechanism of action:
- antimicrobials are classified by their mechanism of action

69
Q

Describe action of beta-lactams and vancomycin

A

Disruption of cell wall:

  • binds PBPS and enzymes responsible for peptidoglycan synthesis
  • inhibits cross-linkage of peptidoglycan layers
70
Q

Describe action of aminoglycosides, tetracyclines and macrolides

A

Inhibition of Protein synthesis:

  • Premature release of aberrant chains from 30S ribosomal subunit
  • Prevent polypeptide elongation at 30S ribosomal subunit
  • Prevent polypeptide elongation at 50S ribosomal subunit
71
Q

Describe action of quinolones

A

Inhibition of nucleic acid synthesis:

- prevent DNA replication

72
Q

Describe action of sulfonamides and trimethoprim

A

Inhibition of synthesis of essential metabolites

- Disrupt folic acid synthesis

73
Q

Outline classification of antibiotics by chemical structure

A
  • Beta-lactams: penicillins -> -cillin, cephalomsporins -> Ceph- or Cef -, carbapenems -> Meropenem
  • glycopeptides -> vancomycin
  • tetracyclines -> -cycline
  • amynoglycosides -> gentamicin
  • macrolides -> -mycin
  • quinolones -> -floxacin
  • antimetabolites
74
Q

Briefly describe the mechanism of action, spectrum of activity and example of penicillins

A
  • Inhibits cell wall synthesis in bacteria
  • Gram-positive bacteria and gram-negative bacteria that have a cell wall
  • Examples: anything ending in -cillin
75
Q

Briefly describe cephalosporins

A
  • Same as penicillin
  • Bacteria; broader with higher generations
  • Anything beginning with Cef- or Ceph-
76
Q

Briefly describe carbapenems

A
  • Same as penicillin
  • Gram-negative rods
  • Meropenem
77
Q

Briefly describe Glycopeptides

A
  • Inhibit peptidoglycan cell wall synthesis (inhibits cross-linkage of layers)
  • Gram-positive bacterial
  • Vancomycin
78
Q

Briefly describe tetracyclines

A
  • Protein synthesis inhibitor (prevent 30S ribosomal subunit elongation)
  • Gram-positive and gram-negative bacteria
  • cycline
79
Q

Briefly describe Amynoglycosides

A
  • Protein synthesis inhibitor (premature release of 30S ribosomal subunit
  • Broad
  • e.g. Getamicin
80
Q

Briefly describe macrolides

A
  • Protein synthesis inhibitor (prevent 50S ribosomal subunit elongation)
  • Gram-positive and gram-negative bacteria
  • mycin (except Vancomycin)
81
Q

Briefly describe quinolones

A
  • DNA replication inhibitor
  • Broad
  • e.g. -floxacin
82
Q

Briefly describe antimetabolites

A
  • Disrupt folic acid synthesis
  • Gram-negative bacteria
  • e.g. Sulfonamides or Trimethoprim
83
Q

Outline resistance mechanisms of antibiotic resistance and factors promoting antibiotic resistance

A

mechanisms of resistance:

  • Enzymatic inactivation of antibiotic
  • Prevention of penetration of drug
  • Alteration of drug’s target site (microbe mutations)
  • Rapid ejection of the drug

Promotion of resistance:

  • Inappropriate antibiotic prescriptions (over prescription)
  • Spread of resistant microbes in health-care facilities
84
Q

Outline antiviral agents (molecular targets, examples of drugs for treatment of influenza, Hepatitis C virus, herpes simplex virus and HIV, antiviral resistance)

A

Anti-viral agents:

  • Narrow spectrum of activity
  • Inhibit replication of the virus and do not interfere with host metabolism

Antiviral drug resistance

  • Mutations within the viral genome selected by drug pressure
  • Very fast resistance due to: very fast replication, high mutation rate in RNA, degree of selective drug pressure
85
Q

Describe protozoa

A
  • Includes sporozoa, flagellates, amoebae, ciliate
  • single celled eukaryotes
  • undergo both sexual and asexual reproduction
  • Transmission via person-to-person and insect vectors
86
Q

Describe Helminths

A
  • includes nematodes (round worm), cestodes (flat worm), trematodes (tape worm)
  • helminths are multicellular eukaryotes (worms)
  • large multicellular organisms
  • transmission via person-to-person, skin penetration and insect vectors
87
Q

Describe arthropods: insects and arachnids

A
  • Attach to skin and take blood meals
88
Q

Describe mites and lice

A
  • live permanently on host and can cause skin irritation and allergic sensitization
89
Q

Define the term ‘protozoa’

A

Unicellular eukaryotic organisms that can be parasitic

90
Q

Define the term ‘helminth’

A

multicellular eukaryotic organisms known as parasitic worms

91
Q

Outline main features of entamoeba histolytica

A
  • Intestinal protozoa infection
  • prevalent in tropical regions
  • causes ulcers in bowel mucosa and abscesses in liver
  • Symptoms: blood in feces, abdominal pain
  • Transmission: Fecal-oral via water/food
92
Q

Outline main features of malaria

A
  • Blood-borne protozoa infection
  • Invades liver to reproduce
  • Endemic in Africa and South East Asia
  • Transmission: Vector from female anopheline mosquitos
  • Two species: 1) Plasmodium falciparum -> affects brain; continuous fever; high mortality
    2) plasmodium vivax -> causes chronic edema; spikes of fever; low mortality
  • Life cycle is split between humans and mosquitos; both species required
93
Q

Outline main features of hookworm

A
  • Intestinal nematode infection
  • Found in all tropical regions
  • Life cycle: eggs in feces -> larvae penetrate skin -> larvae migrate to lungs then intestine -> mature hookworms in intestines
  • Symptoms: anaemia (low iron) due to blood loss
  • transmission: Larvae ingested or penetrate skin
94
Q

Outline main features of lymphatic filariasis - Bruga malayi

A
  • Tissue nematode infection
  • In all tropical regions
  • Disease of poverty
  • Infect lymphatic tissue of host
  • Symptoms: blockage of lymphatic flow due to inflammation, elephantiasis
  • Transmission: mosquitos
  • Life cycle: 1) adult parasite in human produce sheathed larvae, 2) sheathed larvae mature into infective larvae in mosquito, 3) mosquito bite infect human with larvae which mature in lymphatic tissue
95
Q

Outline main features of pig tapeworm - Taenia solium

A
  • Intestinal cestode infection
  • Symptoms: larvae causes cysts to form in brain and other organs
  • Transmission: eating raw pork
  • Life cycle: 1) adult in human produces egg; excreted in faeces, 2) pig ingests eggs; hatch and move to muscles, 3) human eats pig and adult matures in small intestine
96
Q

Outline the main features of schistosomiasis

A
  • Trematode infection
  • Symptoms: chronic inflammation, urinary and intestinal bleeding, lesions in liver
  • Transmission: freshwater with snails
  • Life cycle:
    1) larvae release from snails
    2) penetrate skin of humans in fresh water
    3) mature in liver
    4) Male and female travel to bladder or small intestines to lay eggs
    5) eggs shed in feces or urine
97
Q

List the major groups of medically important fungi (mycoses = fungal infection)

A
  • Superficial mycoses: malassezia
  • Cutaneous mycoses: e.g. trichophyton and microsporum
  • Sub-cutaneous mycoses: e.g. sporotix
  • Systemic mycoses: e.g. coccidiodies and cryptococcus
  • Opportunistic mycoses: e.g. candida
98
Q

Outline the main features of opportunistic mycoses and their clinical consequences

A
  • Opportunistic fungi are usually not infectious in healthy people
  • Cause infection in immunocompromised hosts
  • Fungi may be part of normal flora that overgrows
  • E.g. candidiasis
99
Q

Define the terms ‘yeast’, ‘mould’ and ‘dimorphic fungi’

A

Yeast - unicellular fungi, reproduce by budding or fusion
Moulds - multicellular fungi consisting of hyphae (branching filament)

Dimorphic fungi - fungi that can exist as moulds or yeasts with unicellular or multicellular arrangements.

  • yeast phase in host (37 degrees celsius)
  • mould phase in environment (20 degrees celsius)
100
Q

Outline the main features of clinically significant fungi: Tinea

A

Tinea is highl inflammatory dermaophyte infection

  • superficial mycoses
  • occurs in outer skin
  • occurs all over the body (e.g. Tineas pedis = foot, tinea capitis = hair/scalp)
101
Q

Outline the main features of clinically significant fungi: candida

A
  • Candidiasis - an infection caused by members of the Candida genus
  • Opportunistic mycosis
  • Localized to the mouth, skin, vagina, fingers, nails or the GI tract
  • Can become systemic in fungal sepsis
102
Q

Outline the main features of clinically significant fungi: Sporotrichosis

A
  • Caused by sporothrix schenkii
  • white in culture and ages to black
  • dimorphic fungi
  • subcutaneous mycosis
  • causes chronic infection and granulomas in subcutaneous tissue
  • Epidemiology: in decaying vegetation and hay; common of gardeners and farmers
103
Q

Outline the main features of clinically significant fungi: cryptococcus

A
  • Systemic mycoses
  • encapsulated yeast
  • culture as smooth, white mucoid colonies
  • Pathology:
    1) Act like opportunistic pathogens (affect immunocompromised people)
    2) invade lungs and CNS
    3) pulmonary infection
    4) meningitis
  • Lab diagnostic:
    1) microscopy (observe capsular “halos”)
    2) DNA detection via PCR
    3) Detection of antigens in blood
    4) Fungal culturing
  • Epidemiology:
    1) caused by inhalation of yeast cells
    2) isolated from pigeon dropping and Red River Gum Tree
104
Q

Summarize what infection control is and why it is important

A

Infection control: describes ways to prevent the transmission of infection within a health facility

1) Direct transmission: via contact with humans
2) indirect transmission: via environment, equipment and waste

105
Q

Define standard precautions and outline their application

A

Standard precautions: Treat all people as potentially infectious and apply precautions regardless of symptoms

  • Use when exposed to body fluids, mucous membranes, or breaks in skin
  • three methods of standard precautions:
    1) work practices (wash hands, no eating in risk areas)
    2) Engineering control (sharps containers, waste management)
    3) Personal protective equipment
106
Q

Summarize the importance of hand hygiene

A
  • Hand hygiene is the single most important intervention before and after patient contact
  • Hand washing station at convenient locations
  • Alcohol-based hand rubs at point of care
107
Q

List additional protective devices used in infection control

A

Personal protective equipment includes:

  • Gloves
  • Gowns
  • Masks
108
Q

Define additional precautions and outline their application

A

Use additional precautions when the communicable disease has a specific mode of transmission:

  • Contact: isolated patient in private room, use gloves and gown, disinfect environment
  • Droplet: Spread in liquid droplets, use same procedures are contact with masks
  • Airborne: spread in air currents, use negative pressure room and air-tight masks
109
Q

Outline the role of environmental decontamination

A
  • Environmental decontamination - decontaminate all surfaces where infectious agents could be spread on
110
Q

Outline the roles of disinfection and sterilization

A
  • Disinfection - decreases the number of transmissible diseases on a surface/area to non-infectious levels
  • Sterilization - eliminates completely the transmissible organisms

Methods of disinfection and sterilization:

  • heat
  • chemical
  • gas
  • radiation
111
Q

Outline the roles of monitoring and surveillance for drug-resistant organisms and health-care associated infection

A

Monitoring drug-resistant organisms helps select treatment that is most likely to succeed and help prevent more resistance from developing

Block 1 (9 decks)

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