Module 5.1 Flashcards

1
Q

Infectious agents/microbes

A

Organisms that cause infection/disease

Invade the human body to do so

Common types:
- Parasites
- Viruses
- Fungi
- Bacteria

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2
Q

Bacteria

A
  • Microscopic, unicellular, prokaryotic organisms
  • DNA is double-stranded, circular
  • Most have a cell wall outside plasma membrane
  • Cell structures differ from eukaryotes

Examples: Mycobacterium tuberculosis, Salmonella

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3
Q

Viruses

A

Obligate microbes: Must invade a host cell to replicate

Contain DNA or RNA with a protein coat

Central viral proteins infect specific host cell types

Can infect all forms of life (bacteria, plants, animals)

Examples: Influenza, Rhinovirus, Measles morbillivirus

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4
Q

Fungi

A

Unicellular or multicellular eukaryotes with thick cell walls made of complex carbohydrates

Cause superficial infections (skin, nails) or invade tissues and organs

Examples:
- Dermatophyte fungi (athlete’s foot)
- Aspergillus mould (respiratory tract infections)
- Candida species of yeast (thrush)

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5
Q

Parasites

A

Eukaryotes that cause disease in their host

Includes single-celled protozoa (replicate within cells), helminths (parasitic worms), and insects/arachnids

Ectoparasites (live outside host) can serve as vectors for diseases (e.g., malaria)

Examples:
- Plasmodium parasites (malaria)
- Sarcoptes scabiei (scabies)

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6
Q

are all microbes harmful?

A

no

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7
Q

Microbiome

A

Collection of microbes (viruses, bacteria, fungi, parasites) living symbiotically in/on humans

Found throughout the body, especially on skin and mucous membranes

Crucial to human health:
- Aid in digestion
- Prevent inflammation
- Protect against infection
- Produce vitamins not synthesized by humans

When in balance, support various bodily functions

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8
Q

Microbes as Pathogens

A

Imbalance in microbiome: When ‘good’ microbes are outnumbered by harmful ones, potential pathogens can become harmful

Example: Staphylococcus aureus
- Normally found on skin surface, but can enter deeper tissues/blood to cause infections (e.g., skin and soft tissue infections)

Always pathogenic: Some microbes are always harmful and not part of normal flora

Example: Rhinovirus
- Spread via droplets or direct contact, causing infections like the common cold

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9
Q

Innate immune response

A

First line of defense: Immediate, non-specific response to pathogens

Physical barriers: Skin and mucous membranes prevent entry

Chemical barriers: Enzymes in saliva, tears deter pathogens

Immune cells:
- Cause inflammation at infection site
- Engulf and destroy viruses/bacteria (phagocytosis)
- Prevents early-stage infections

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10
Q

Adaptive immune response

A

Takes several days: Activated after first contact with pathogen

Specific: Targets specific invader (antigen)

Recognition: System identifies non-self molecules

Response: Swelling, pus, redness, pain

Memory: Once cleared, system remembers antigen to fight future infections

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11
Q

what is the body’s first line of defense?

A

skin

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12
Q

Macrophage

A

Identify invaders: Recognize and attack pathogens

Cytokine release: Signal reinforcements (neutrophils, NK cells)

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13
Q

Innate immunity

A

Neutrophils, Natural Killer Cells, Macrophages

Non-specific response: Attack a wide range of pathogens

Sacrifice healthy tissue: To contain and limit infection

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14
Q

Adaptive immune system

A

dendritic cells, helper T cells, B cells

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15
Q

Dendritic cells

A

Dendritic cells: Collect pieces of the invader, travel to lymph nodes

Present antigen: To T cells, initiating communication

T cells activate B cells: Which then form antibodies

B cells: Release millions of antibodies to target the invader specifically

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16
Q

how pathogen causes infectious disease

A

1) Entry: Virus enters the body via oral/nasal passages, reaching the lungs.

2) Invasion and Colonization: Spike proteins bind to ACE2 receptors on lung cells to enter.

3) Evasion of Immune Response: Delays adaptive immune response to evade detection.

4) Infection: Virus hijacks cell machinery to replicate and spread to other cells.

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17
Q

Reservoir

A

Biological Reservoirs: Humans, animals (e.g., chickens, bats), etc.

Environmental Reservoirs: Soil, swamps, lakes, etc.
Pathogens can persist in these reservoirs for extended periods before potentially infecting new hosts.

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18
Q

Mode of Transmission of diseases

A

1) Direct Contact: Person-to-person (e.g., skin contact, sexual contact).

2) Droplets: Pathogens spread via respiratory droplets (e.g., sneezing, coughing).

3) Airborne: Pathogens that can remain suspended in air for extended periods (e.g., tuberculosis).

4) Vectors: Transmission via organisms like mosquitoes or fleas (e.g., malaria, plague).

5) Vehicles: Transmission through contaminated food, water, or surfaces (e.g., cholera, norovirus).

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19
Q

Opportunistic Conditions of diseases

A

Factors such as stress, surgery or old age could promote microbes of the normal flora ro become pathogenic, and others to evade the immune system.

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20
Q

how to prevent infectious diseases

A

Eliminated Reservoirs: Destroying the pathogen’s reservoir (e.g., mosquitoes for malaria) stops disease spread.

Enhanced Barriers: Prevent infections with barriers like masks, hand washing, and social distancing.

Distributed Vaccines: Vaccines train the immune system to fight infections before exposure.

Develop Targeted Medicines: Drugs (e.g., ivermectin for parasitic worms) help prevent or treat infections and reduce transmission.

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21
Q

Chickenpox Vaccination Programme in Canada

A

Chickenpox: Highly contagious viral disease, symptoms include a blister-like rash, fever, fatigue, and headache.

History: Once a hallmark of childhood in Canada, a vaccine was introduced in 1998 and subsidized in 2004.

Impact: Public health efforts have reduced prevalence by over 100-fold. It is now a routine childhood immunization.

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22
Q

First Nations and Infectious Disease Today: strep throat

A

Brody Meekis Tragedy: In 2014, 5-year-old Indigenous boy Brody Meekis from Sandy Lake First Nation died of strep throat.

Health Disparities: The community had limited healthcare resources, including an understaffed nursing station and unreliable medical transportation.

Missed Diagnosis: Brody’s condition likely went unnoticed by healthcare workers, who lacked proper training. Strep throat, a treatable infection, typically responds to antibiotics within a week.

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22
Q

Herd immunity

A

occurs when a significant proportion of the population is vaccinated and immune to the disease, can indirectly prevent those at risk from contracting the disease

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23
Q

Infectious Disease as a form of Colonization

A

Colonization & Disease: Europeans introduced infectious diseases like smallpox, tuberculosis, and measles to Indigenous populations with no prior immunity.

Impact: Devastating epidemics decimated communities, causing death and weakening survivors, which led to the loss of oral histories.

Consequences: While settlers used public health measures to protect themselves, Indigenous communities suffered. After population collapse, governments and churches exploited the situation to erase traditional cultures and impose oppressive systems.

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24
First Nations and Infectious Disease Today: TB
TB Introduction and Spread: Tuberculosis (TB), brought by European settlers, spread rapidly among Indigenous peoples due to overcrowded reserves, residential schools, and Indian hospitals. High Mortality Rates: TB caused some of the highest mortality rates in human populations. Ongoing Issue: Despite antibiotics reducing cases overall, TB continues to persist in Indigenous communities.
25
Gram positive
have a thick peptidoglycan wall
25
Introduction to Bacteria
Bacteria Evolution: Bacteria were among the first lifeforms on Earth and evolved into multicellular eukaryotes. Human Bacteria: Humans host trillions of bacteria, most of which are essential for health. Bacteria Classification: Bacteria are categorized into two groups based on their cell wall structure: Gram-positive and Gram-negative.
26
Gram negative
have a thin peptidoglycan wall surrounded by an outer membrane
27
Bacterial cell envelope
made up of two things important to outer structure Bacterial Cell Wall: The cell wall helps maintain internal pressure and prevents the bacterial cell from bursting. It consists of the plasma membrane and the cell wall. Therapeutic Target: Since eukaryotic cells don’t have cell walls, bacterial cell walls are a good target for therapeutic treatments.
28
Antimicrobials
any agent, natural or synthetic that stops growth of or kills microorganisms. Many antimicrobials happen to be antibiotics, but others like bleach, are not.
29
Antibiotics
small molecules used as medications produced by microorganisms that can stop the growth of or kill microorganisms. Hundreds of antibiotics on the market. Those given as medication can be characterized based on how they target and what they target *All antibiotics are antimicrobials, but not all antimicrobials are antibiotics*
30
Bacteriostatic drugs
inhibit bacterial growth, with the help of the host's immune system. Therefore, bacteriostatic drugs would never be used for life threatening infections.
31
Bactericidal drugs
kill susceptible bacteria, without any help from the host's immune system.
32
narrow-spectrum antibiotic
active against a small group of organisms - what they want to move to, to put less selective pressure on bacteria that are formed in the normal flora
33
broad-spectrum antibiotic
kills a wide range of bacteria
34
Serious infection for strep
start broad spectrum, once results are back, then a more narrow spectrum antibiotic is used
35
Cell wall synthesis inhibitors
Cell Wall Synthesis Inhibitors: Antibiotics like penicillin prevent proper bacterial cell wall formation by binding to enzymes that crosslink peptidoglycans. Effect: Without crosslinking, the cell wall can't form properly, causing the bacterium to die from osmotic rupture. Specificity: These antibiotics may be specific to Gram-positive or Gram-negative bacteria due to differences in cell wall structure and enzymes.
36
Metabolic Pathway Disruptors
Targeting Metabolic Pathways: Antibiotics can target metabolic pathways not present in human cells, like folate synthesis. Folate Synthesis: Humans acquire folate through diet, while bacteria synthesize it. Blocking this pathway disrupts bacterial growth. Combination Therapy: Cotrimoxazole is a combination of two antibiotics that block different stages of the folate synthesis pathway.
37
Protein Synthesis Inhibitors
Protein Synthesis Inhibitors: Antibiotics like doxycycline inhibit mRNA translation into proteins by targeting bacterial ribosomes. Selective Targeting: These antibiotics don’t affect eukaryotic (human) ribosomes, as bacterial ribosomes are structurally different. Lyme Disease Prevention: A single dose of doxycycline can prevent Lyme disease after a tick bite.
38
Cell Membrane Disruptors
Plasma Membrane Disruptors: Antibiotics like daptomycin create leaks in bacterial plasma membranes, disrupting key processes (protein synthesis, chemical gradients), leading to cell death. Side Effects: These drugs can also affect mammalian cells, especially disrupting mitochondrial function, resulting in more severe side effects compared to other antibiotics.
39
Nucleic Acid Synthesis Inhibitor
DNA Packaging & Inhibition: Bacterial DNA is tightly supercoiled by DNA gyrase, an enzyme absent in eukaryotic cells. Fluoroquinolones: These antibiotics inhibit DNA gyrase, preventing proper DNA supercoiling, causing DNA degradation and cell death.
40
Antibiotic Resistance Pathways
Alter Targets: Mutations change the drug target's structure, rendering the drug ineffective. Restrict Target Access: Drugs can't enter the cell, or are pumped out immediately. Develop Drug-Specific Enzymes: Bacteria create enzymes that destroy or modify antibiotics, making them ineffective.
41
Transfer of Antibiotic Resistance
Progeny Transmission: Antibiotic resistance genes are passed on to a bacterium’s progeny. Horizontal Gene Transfer: Resistance genes can spread to other drug-susceptible bacteria, leading to faster and more widespread resistance accumulation.
41
Development of Antibiotic Resistance
Infection: Host is infected with pathogenic bacteria, some drug-resistant. Treatment: Antibiotics kill most bacteria, but not the drug-resistant ones. Proliferation: Drug-resistant bacteria multiply, unaffected by the treatment. Gene Transfer: Drug-resistant bacteria can transfer resistance to drug-susceptible bacteria.
42
3 types of horizontal gene transfer
transformation: Extracellular DNA taken up by a bacterium and incorporated into its genome Conjugation: Direct cell-to-cell contact through plasmid gene transfer to a recipient cell. Transduction: Transfer of gene through the infection with a bacteriophage (bacterial virus)
43
Maintenance of Antibiotic Resistance
Metabolic Cost: Maintaining antibiotic resistance requires extra energy for processes like protein production and structural alterations. Evolutionary Perspective: If the antibiotic is no longer present, non-resistant bacteria can grow faster as they don't waste energy on resistance. Selective Pressure: Antibiotic-resistant strains survive only when the antibiotic is present; without it, they die off.
44
Andres Story
Semi-conscious due to brain trauma Open fracture on right leg Surveillance cultures taken for MRSA and carbapenem-resistant organisms Central line placed for meds, fluids, nutrition, and blood draws had low blood pressure increased WBC count pos test for MRSA Most common treatment = vancomycin
45
MRSA
Common cause of skin and soft tissue infections. Can be treated with antibiotics, but options are limited due to resistance. Antibiotic-Resistant Bacteria in Canada MRSA has become a persistent and serious health concern, causing severe complications and deaths. In response to rising cases, Canada implemented public health programs in 2010. Despite efforts, MRSA rates remain nearly twice as high as in the early 2000s.
46
CPO
Carbapenem-Resistant Organisms Often resistant to multiple antibiotic classes. Some strains are resistant to all available antibiotics, making treatment very difficult.
47
Development of antibiotic resistance of MRSA
S. aureus developed resistance to penicillin via beta-lactamase, which destroys the drug. Methicillin was introduced in 1959 to bypass beta-lactamase. S. aureus evolved again—mutated penicillin-binding protein—making methicillin ineffective. By the mid-1980s, MRSA had become widespread, especially in hospitals.
48
Vancomycin-resistant Enterococci (VRE)
extremely common
49
overuse of antibiotics in hospitals
Non-prescription use and unregulated sales are widespread in low- and middle-income countries. China: Hospitals rely on antibiotic sales for revenue. Illegal pharmacy sales without prescriptions are common. India: Doctors often receive compensation from pharmaceutical companies, encouraging overprescription.
49
Vancomycin-resistant S. aureus (VRSA)
very rare for now leave few antibiotic choices remaining for treatment.
50
Evidence of Worldwide Antibiotic Resistance
Decades of extensive antibiotic use (~75 years) created selective pressure, leading to widespread resistance. Beta-lactamases are a key example: ~2,800 types identified—a 10x increase since pre-1990. Carbapenem resistance: First seen in 2008, now global. Carbapenems treat multidrug-resistant infections—resistant strains may have no treatment options left.
51
Overuse of Antibiotics
Excessive use of antibiotics worldwide is creating an ideal environment for bacteria to develop resistance.
52
overuse of antibiotics in Agriculture and Aquaculture
Widespread use to promote growth and prevent disease in densely housed animals. Major driver of global antibiotic overuse, especially in agriculture and aquaculture. In Canada, agriculture accounts for 82% of antibiotic use. The majority of global antibiotic production goes to agriculture, aquaculture, and veterinary use.
53
Burden of Antibiotic Resistance
In 2018, ~26% of infections were antibiotic-resistant; expected to rise to 40% by 2050 (PHAC) Annual deaths: ~5,400 (2018) → projected 13,700 by 2050 Economic impact: ~$1.4 billion/year Due to longer infection duration, costlier treatments, and more complications for survivors
54
Preventing Antibiotic Resistance
PHAC Strategy to Combat Antibiotic Resistance Surveillance – Monitor antibiotic use & resistance trends Stewardship – Promote appropriate antibiotic use in all sectors Research & Innovation – Support ongoing antibiotic discovery & development Infection Prevention & Control – Enforce hygiene & sanitation best practices
55
Regulation of Antibiotic Use in High-Income Countries
1) EU Ban on Antibiotics in Food Production (2006) 2) Medical Guidelines – Prescribing limited to clear, evidence-based guidelines 3) Conflicts of Interest – No gifts from pharmaceutical companies, and limited drug ads to patients 4) Prescription Statistics – Tracking prescriptions for various antibiotic classes 5) Hospital Screening – Resistant organisms screened and isolated in hospitals and long-term care settings
56
Antibiotic Use in Low- and Middle- Income Countries
1) Unregulated Antibiotic Sales – Antibiotics sold without prescriptions, often without oversight 2) Medical Ethics – Weaker enforcement of ethical guidelines compared to high-income countries 3) Lack of Resources – Limited access to accurate testing, funding, and leadership in healthcare 4) Quality Issues – Poor quality antibiotics may contribute to increased resistance
57
Antibiotic Drug Discovery is Languishing
1900-1919: Salvarsan (early antibiotic) 1920-1939: Sulfonamides 1940-1979: The "Golden Age" – over 20 new classes of antibiotics, MRSA detected 1980-1999: Only 3 new classes, VRE (Vancomycin-resistant Enterococci) detected 2000-Present: 5 new classes, VRSA (Vancomycin-resistant Staphylococcus aureus) detected, UN declares antibiotic resistance a global threat
58
challenges of antibiotic Drug Discovery is Languishing
Limited new antibiotics discovered since the 1970s. The pharmaceutical industry is not motivated to invest in new antibiotics due to limited profitability. Need: 20 new antibiotic classes in the next 20-50 years to combat resistance.