Midterm Flashcards
(125 cards)
1
Q
Who was Robert Hooke?
A
First to describe microbes in the late 1600s. He illustrated the fruiting structure of molds.
2
Q
Who was Antoni Wan Leeuwenhoek?
A
First to report protozoa and bacteria, calling them animalcules in 1600s (were not called microorganisms until the end of the 19th century).
3
Q
Who was Louis Pasteur?
A
He developed the germ theory of disease in 1857. This led to effective sterilization procedures in medicine, pasteurization of milk, and heating of food to improve survival rate and decrease disease. He also developed vaccines against anthrax, fowl cholera, and rabis using weakened pathogens. He established the Pasteur Institute in Paris.
4
Q
What is the germ theory of disease?
A
Microorganisms are responsible for disease, specifically pathogens.
5
Q
Who was Robert Koch?
A
Examined the blood of infected animals and identified the pathogens responsible for anthrax and TB. He was the first to photograph bacteria in diseased tissues, use steam to sterilize petri dishes, use petri dishes, bacteria transfer lab techniques, estimate the bacterial number in solution, and recognized bacteria as distinct species. Won nobel in 1905.
6
Q
What were Koch postulates?
A
Suspected causative agent must be found in every case of disease and absent from healthy hosts
Agent must be isolated and grown outside the host
When agent is introduced to a healthy susceptible host, the host must get the disease
Same agent must be found in the diseased experimental host.
7
Q
Name some deadly historical pandemics.
A
Small pox: 300+ million Measles: 200 million Spanish flu: 50-100 million Black death: 75 million HIV/AIDS: 25+ million
8
Q
What are some different types of microbes?
A
Bacteria Archaea Fungi Protozoa Algae Small, multi-cellular animals
9
Q
Describe eukaryotes.
A
Have nucleus and internal membrane bound organelles and complex
Are larger (10-100um)
Composed of algae, protozoa, fungi, animals, and plants
Cell wall present only in plants and fungi
Have large 80S ribosomes
10
Q
Describe prokaryotes.
A
Lack nucleus and internal membrane bound structures
Typically smaller (1.0-10um)
Composed of bacteria and archaea
General have a cell wall made of peptidoglycan
Contains small 70s ribosomes.
11
Q
What is the function of bacterial cell walls?
A
Provide structure and shape to protect the cell, giving the bacteria their characteristic shape. It also assists some cells in attaching to other cells or resisting antimicrobial drugs. Generally it is composed of peptidoglycan.
12
Q
What are the different bacteria shapes?
A
Coccus (spheres) Rod Spirillium Spirochete Budding Filamentous
13
Q
What are the two different types of bacterial cell walls?
A
Gram positive: contain a thick peptidoglycan layer over a cytoplasmic membrane. Also contained teichoic acids. Purple.
Gram negative: has an outermsmbrane surrounding thin peptidoglycan layer and cytoplasmic membrane. Outer membrane contains phospholipid, proteins, and LPS. Pink.
14
Q
What does LPS cause?
A
Lipid A portion can cause fever, inflammation, shock and blood clotting due to being an endotoxin and making it very medically important.
15
Q
What are some functions of the cytoplasmic membrane?
A
Selectively permeable membrane Structure and support Protection Protein anchor Energy conservation
16
Q
What is the function of cytosol?
A
Contains nutrients, ions, carbohydrates, proteins, lipids, and wastes. May contain deposits that can be important for diagnosing certain pathogens.
17
Q
What are endospores?
A
Produced by some bacteria. Are a dormant structure that is important for durability and potential pathogenicity.
18
Q
What is the function of ribosome 70s?
A
Protein synthesis and translation
19
Q
What is the glycocalyx?
A
Capsules (attached) and smile layers (loose, water-soluble) composed of polysaccharides, polypeptides, or both. It can be thick or thin, rigid or flexible. It assists in attaching to surfaces of host tissues and biofilms, protects against phagocytosis, and protects from drying.
20
Q
What are fimbriae?
A
Short, filamentous protein structures that enable organisms to stick to surfaces such as tissues or form pellicles as well as enable motility on solid surfaces.
21
Q
What are pili?
A
A special time of fimbriae that is longer and allows for twitching motility or DNA transfer between cells. Generally on 1 to a few per cell.
22
Q
What are flagellum?
A
These enable the cells to be motile by swimming and can be anchored in the cell in various locations. They can be very long. They are anchored into a hook attached to a basal body implanted in the cell wall. Gram - contains 4 rings and gram + contains 2 rings.
23
Q
What are the different methods of oxygen use in microbes?
A
Aerobes: require oxygen
Anaerobes: do not require oxygen and may even be killed by exposure
Facultative anaerobes: can live with or without oxygen
Microaerophiles: can use oxygen only when present at levels reduced from that in the air
Aerotolerant anaerobes: can tolerate oxygen and grow in its presence even though they cannot use it.
24
Q
Why is oxygen toxic?
A
Certain toxic forms of oxygen can be formed in the cell as byproducts of reactions, damaging the cells. Generally enzymes are present to neutralize most of these toxic species.
25
What are some different requirements for microbial growth?
```
Temperature
Oxygen
Water
Nutrients
pH
Nitrogen
```
26
What are the different types of microbes based on pH?
Acidophile: low pH
Neutrophile: neutral pH
Akaliphile: high pH
27
How do bacteria grow?
Binary fission: cell elongation, septum formation (new membrane and cell wall), completion of septum formation of walls, cell separation. Exhibit logarithmic growth.
28
Describe the typical microbial growth curve.
Lag phase: bacteria adjust to environment
Log phase: rapid growth with maximum metabolic rate
Stationary phase: nutrients depleted with metabolites and by-products accumulating
Death: cells die faster than growing.
29
What are biofilms?
Responsible for 70% of all infections, particularly chronic, biofilms are polymicrobial communities and the primary residence of microbes in nature. Primary sites often include subgenus catheter, mouth, and artificial hip implants.
30
How do biofilms grow?
The bacteria attach, colonize, grow, display community behaviour, and then disperse and attach in new places, establishing a new biofilm. They have a complex adaptation process.
31
What are some advantages of forming a biofilm?
High tolerance against biocides and antibiotics
Protection against the human host immune defence
Increased metabolic diversity
Resistance to dehydration
Genetic exchange through horizontal gene transfer
Phenotypic versatility
32
What are some characteristics of biofilms?
Extracellular polymeric substance: slimy matrix full og DNA, polysaccharides, and proteins. This allows adherence to surfaces, interfaces, and cells to one another as well as quorum sensing (cell-to-cell communication).
33
What is Quorum sensing?
Cell-to-cell communication. Regulated the expression of up to 10% of genes. Also influences biofilm formation, virulence, motility, antibiotic resistance, and expression of eco-enzymes.
34
What are some difference methods of controlling microbial growth?
Physical: filtration, osmotic pressure, radiation, freezing, lyophilization
Chemical: halogens, oxidizing agents, enzymes, heavy metals, alcohols, phenols and phenolics, gaseous agents, surfactants
Microbial control
35
What are the different types of antimicrobial drugs?
Semisynthetic: chemically altered antibiotics that are more effective, longer lasting, or easier to administer than naturally occurring ones
Synthetics: antimicrobials that are completely synthesized in a lab
36
What are some common modes of action for antibiotics?
Inhibitors of cell wall synthesis: beta lactams (penicillin), glycopeptides (vancomycin), and peptide antibiotics (polymyxin B)
Inhibitors of nucleic acid synthesis: quinolones (ciprofloxacin)
Inhibitors of protein synthesis: macrolides (azithromycin), tetracycline and amino glycosides (gentamicin).
37
What are enteric pathogenic bacteria?
Bacteria in the enteric system that can cause diarrhea, bloody diarrhea, dysentery, etc.
38
How are nutrients absorbed in the gut?
Most of the absorption occurs in the small intestine through enterocytes on the villi and microvilli. This generally includes smile sugars, vitamins, and salts. It is regulated by hormones in the stomach and small intestine and nerves in the enteric nervous system, speeding up or delaying the movement of food.
39
What natural protection do we have in the gut against pathogens?
Enzymes in our saliva kill some of the bacteria and HCL in the stomach can sterilize others. The microbiota in the intestines can protect against harmful pathogens with the liver filtering out harmful toxins from the GI and blood. The body's immune system in the lymph nodes along with the ENS also help.
40
Compare the microbiota in the upper and lower digestive tracts.
Upper: microbes colonize surfaces of teeth, gingiva, lining of cheeks, and pharynx and are found in saliva in large numbers, with dozens of unidentified species.
Lower: the bacteria are mostly strict anaerobes though some facultative also reside there.
41
What are the different protective mechanisms that cause nausea and vomiting?
Peripheral pathways
Vestibular system
Chemoreceptor trigger zone
Cortex
42
What causes nausea and vomiting?
Stimulation of the Vomiting Centre (VC) in the medulla
43
What causes diarrhea?
Three different pathways:
1) absorption and secretion of water and electrolytes in the GI tract is thrown off balance
2) osmotic: fluid passively moves into a bowel lumen down the osmotic gradient
3) Secretory: bowel mucosa secretes fluid into the gut lumen due to the activation of a pathway by a toxin or due to inherent abnormalities in the enterocytes
44
Describe diarrhea.
Leading cause of infant/childhood mortality in developing countries and is shown as the second leading cause of death of children under age 5. Generally, watery diarrhea is caused by a loss of electrolytes and fluids
45
What makes a bacterium pathogenic?
Invasiveness and toxicity
46
Define invasiveness.
The ability of a pathogen to invade tissues, encompassing (1) mechanisms for colonization, (2) production of extracellular substances that promote the immediate invasion of tissues, and (3) ability to bypass or overcome host defence mechanisms which facilitate the actual invasive process.
47
What are some virulence factors and what do they help do?
Virulence factors help bacteria invade the host, cause disease and evade host defences. Some examples include adherence structures such as capsules, fimbriae, pili, and flagella, toxins, such as ends/exotoxins, and extracellular enzymes, such as hyaluronidase and streptokinase.
48
How do pathogens attach to host tissues?
Adhesions on the pathogen surface bind to a host receptor embedded the cytoplasmic membrane of the host cell.
49
Describe the bacterial interactions with the mucous membranes and epithelial cells.
The microbial cells perform a loose association with the mucous on the epithelial cells, adhere, and then colonize, entering the tissue between the epithelial cells.
50
Define pathogenicity.
The ability of a microorganism to cause disease
51
Define virulence
The degree/measure of pathogenicity, the relative ability to infect a host and cause disease. A more virulent pathogen will hit the LD50 mark with smaller colonies.
52
What type of enzyme does streptococci use and how does it work?
It produces hyaluronidase, an enzyme that promotes spreading of microbes in the tissues by breaking down the polysaccharide hyaluronic acid. This causes the host cells of separate, allowing the pathogen to spread between the host cells and invade into the deeper tissues.
53
What type of enzyme does clostridia use?
Collagenase, an enzyme that destroys collagen in order to access deeper tissues, as this is the major protein of connective tissues.
54
Compare endotoxins and exotoxins.
exotoxins: toxic proteins
Endotoxins: LPS/LipidA
55
How are exotoxins classified by structure and function? Location?
S&F: AB-exotoxin, cytolytic (membrane disruption), super-antigen
Loc: neurotoxin, enterotoxin, cytotoxin
56
Describe the actions of AB-Exotoxins.
In an AB-exotoxin, the AB complex binds to a receptor on the surface of the cell and it brought into a vesicle. Once in the vesicle, the A subunit disassociates and is released into the cytoplasm, releasing a H+.
57
Give an example of an AB-exotoxin.
Diphtheria Toxin
This inhibits protein synthesis. The AB complex binds to the receptor, and the A subunit crosses the membrane into the cell, where is catalyzes ADP-ribosylation (The addition of ADP to) of elongation factor 2. This causes EF-2 not to bind to the ribosome, ultimately blocking translation and leading to host cell head.
58
What is a cytotoxin exotoxin?
These are soluble, secreted proteins that can cause damage to host cytoplasm membranes and the lyrics of host cells. Cause pores in the membrane that allows free movement of components in and out of the cell.
59
Describe LPS.
The lipidA portion of LPS is responsible for its toxicity where as the polysaccharide portion is non-toxic, just makes the LPS complex soluble and immogenic. When both the lipidA and polysaccharide functions are delivered, it can cause fever, diarrhea, blood coagulation, etc.
60
What are some antiphagocytic factors exhibited by capsules?
This can result in either phagocytosis being blocked by the capsule or incomplete phagocytosis, in which the lysosome fails to bind and the bacteria reproduce in the vesicle.
61
Define epidemic.
The occurrence of more cases of a disease than expected in a given area or among a specific group of people over a particular period of time
62
Define pandemic.
An epidemic occurring over a very wide area and usually affecting a large proportion of the population.
63
Define endemic infection.
An infection that is consistently found in the population such as dental carries and gonorrhoea.
64
What are some important factors in infections?
```
Reservoirs of infection
Modes of transmission
Treatment
Human-pathogen interactions
Prevention
Epidemiology of infectious diseases
```
65
What is Vibrio spp. ?
A gram-negative, rod-shaped, facultative anaerobe. It is often found in warm, brackish water. It cause both cholera and non-cholera infections based on the different strains. The DNA consists of 2 chromosomes, II slightly smaller than I, which mostly encodes the essential proteins. Recombination and HGT events are common. Generally it is transmitted through oral or wound exposure and person to person transmission.
66
Describe the prevalence of cholera.
There are 100000 deaths per years with 50% of those occurring in children under 5. It is endemic in Asia, Africa, and Latin America. This is a climate driven disease, showing seasonal peak patterns during the warmer months and temperature contributing to outbreaks.
67
What are some routes of entry for invading pathogens?
The three major pathways include skin, mucous membranes, and the placenta as well as parenteral routes, such as cuts, bites, and surgery stabs.
68
How many cholera pandemics were there?
Seven
69
Describe the pathogenesis of Cholera toxin.
V. cholera O1 and O139 are the causative agents of cholera epidemics, with most of the other serotypes being harmless. O1 is typically the agents responsible, presenting as either classical (pandemics 1-6) or El Tor (pandemic 7)
70
How does the cholera toxin work?
The bacteria travels to the small intestine, where it releases a CtxAB complex. This complex binds to GM1 in the membrane and is taken into a vesicle. The CtxA is released once in the ER and travels into the cytoplasm. It binds to ARF6 and interacts with G protein coupled receptors, causing an increase in cAMP. This causes an increase in PKA which binds to CFTR and causes the release of Cl, HCO3, K, Na, and H2O, from the cell, resulting in Diarrhoea.
71
What is a periodontist?
A dentist that specializes in the prevention, diagnosis, and treatment of periodontal diseases and in the placement of dental implants.
72
What is periodontal disease?
Inflammation of the gingiva that extends into the adjacent attachment apparatus. This causes destruction of the periodontal ligament and the loss of the adjacent supporting bones.
73
When is the oral biofilm found?
Found on the tooth and surrounding epithelium (gums)
74
How prevalent is periodontal disease?
Loss of at least 2mm: 80% of adults and 90% of those 55-64
| Loss of at least 4mm: 50% of those 55-64
75
What are the different bacteria that often make up oral biofilms? Provide examples.
Early colonizers: actinomyces species
| Late: R. gingivalis, B. forsythus, T. denticola
76
How do biofilms bind to the tooth?
On top of the tooth, there is a layer called acquired pellicle made of glycoproteins that sit on the enamel. Salivary receptor sit on top of pellicle and attach to the early colonizers. Other colonizers then attach to this and amongst each other, gradually forming the biofilm. The longer this goes undisrupted, the larger it becomes and the more late colonizer bind, causing severe gum disease.
77
How do you remove dental biofilms?
Have to be removed manually as they are 500X more resistant to certain antibiotics as the same species in planktonic state.
78
What aspects can alter the oral microflora?
Susceptible host: genetics, smoking, stress
Pathogenic species: late colonizers
Absence of beneficial bacteria: streptococcus sanguinis
79
What is aggressive periodontitis?
Rapid rate of clinical attachment loss and bone loss. IT often has a genetic component, is more common among african american people, and is exacerbated by smoking
80
What are the clinical features of chronic periodontitis?
Gingival edema, erythema, bleeding on probing, pocketing, loss of clinical attachment to the bone. May also see suppurating on probing, pathological tooth migration, tooth mobility, and furcation involvement.
81
What are the risk factors of chronic periodontitis?
Primary: microbial biofilm
Contributing: smoking, medical problems (diabetes), genetics, stress, SES, age, etc.
82
What are the goals of periodontal therapy?
Disrupt or eliminate the biofilm, recreate an environment to prevent microbial recolonization through oral self0care methods, stop the progression of disease, and preserve the teeth.
83
What are the general steps to periodontal therapy?
Initial therapy
Re-evaluation
Surgical therapy
Supportive periodontal therapy
84
What are the two main branches to treatment for periodontal diseases?
Surgical and non-surgical
85
What is the non-surgical treatment for periodontal diseases?
A very deep cleaning under the gums. This aims to decrease the pocket depth, increase recession, and increase clinical attachment level. May also use in conjunction with antibiotic therapy in aggressive periodontitis to eradicate aa.
86
What are the two antibiotics sometimes used in aggressive periodontitis?
Amoxicillin: bacteriocidal that inhibits cell wall synthesis of gram positive and some gram negative species
Metronidazole: bacteriocidal that inhibits DNA synthesis of strict anaerobes, protozoa, and some gram negative bacilli.
87
What is a gingivectomy?
A procedure used to remove excess soft tissue.
88
What is open flap curettage?
A surgical technique used in very severe bone loss with a high degree of tartar. Involves opening up a bit of the gum, cleaning it, then closes it.
89
What is osseous surgery?
This involves modifying the bone to lower the gum line, changing the oxygen levels of the pockets. This prevents the survival of strict anaerobes and results in healthier gums.
90
What is guided tissue regeneration?
This process can help bone regrow in incidents of vertical bone loss. The gums are cut open and the bone graft is added to the area of missing bone then stitched up. The blood supply still present in the old bone allows a new blood supply to develop in the bone graft, allowing them to grow into one another.
91
What virulence factors does V. cholerae have?
Flagella and motility
| LPS
92
What regulates the Cholera toxin?
Bile
Reduced oxygen
Bicarbonate
Unsaturated fatty acid
93
What mediates the cholera toxin?
The complex regulatory network including CT regulator (tour), TCP regulator (txT) and quorum sensing.
94
What are some barriers to widespread cholera vaccines?
Political and cultural hesitancy in vaccine acceptance
Costs
Lack of supportive infrastructure for storage and delivery
Long-term prevention under debate
95
Describe campylobacter.
A gram negative, motile rod, microaerophilic, non-fermenting bacteria. Spiral shaped with a single flagella at each pole, it is commonly found in the intestinal tracts of many wile and agriculture-associated animals. It is the leading cause of bacterial diarrheal diseases in many areas worldwide.
96
What can campylobacter cause?
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Mild to severe diarrhea
Bloody diarrhea
Nausea
Stomach pain
Fever
Vomiting
```
97
What bacteria is responsible of the most food borne illnesses in the european union?
C. jejuni
98
Describe C. jejune.
This bacteria colonizes mucous layers in the epithelium in the lower intestinal tract where there are plenty of nutrients and carbon sources. A single flagella at each pole distinguishes virulent strains and an extracellular capsular polysaccharide aids in colonization of chicken and pathogenesis. Other virulence factors include adhesins, cytotoxins, and lipid A
99
How is C- jejuni spread?
Spread through the focal oral route through contaminated food or drink, contact with the faces of infected humans, and contact with the faces of domestic or wild animals.
100
How is C. jejuni treated?
Diagnosed by stool sample culturing, it is often just left to run its course although antibiotics, specifically azithromycin, are sometimes used. In rare cases, it can lead to arthritis and guillain barre syndrome.
101
Describe a virus
Tiny, acellular, infectious agent having either DNA or RNA. They neither grow nor respond to the environment and cannot reproduce independently, instead recruiting the cell's metabolic pathways to increase their numbers.
102
Compare the intercellular and extracellular states of viruses.
Extracellular: called a virion, it has a protein cost surrounding nucleic acid, together called a nucleocapsids, and some have a phospholipid envelope.
Intracellular: the capsid is removed and the virus exists as nucleic acid.
103
How does a virus chose a host?
Most viruses only infect a particular host due to their affinity for complementary proteins on the cell surface. Some are even more specific, only infecting a particular type of cell in their host.
104
Describe the capsid of a virus
Composed of capsomeres (proteinaceous subunits), they provide protection for viral nucleic acid and are a means of attaching to the host cells.
105
Describe the viral envelope.
Acquired from the host cell during replication or release, it is a portion of the host membrane that is composed of a phospholipid bilayer and proteins. These proteins often play a role in host recognition. Enveloped viruses are less fragile than naked viruses.
106
How are viruses classified?
Type of nucleic acid
Presence of an envelope
Shape
Size
107
What virus causes small pox?
Orthopoxvirus
108
Describe lytic replication.
This viral replication usually results in the death and lysis of host cells. There are five stages: attachment, entry, synthesis, assembly, and release.
109
How does the replication of animal viruses differ from bacteriophages?
Same basic replication pathway with differences resulting from presence of envelope around some viruses, the eukaryotic nature of animal cells, and the lack of cell walls in animals.
110
How do animal viruses attach to host cell?
Animal viruses do not have tails or tail fibres, but there is a chemical attraction between the viral protein and the cell receptor, with glycoprotein spikes or other attachment molecules that mediate attachment.
111
How are DNA viruses of animals synthesized?
Each type of animal virus requires different strategies depending on its nucleic acid. DNA viruses often enter the nucleus and RNA often replicate in the cytoplasm. Involves considering how the mRNA is synthesized and what serves as the template for nucleic acid replication.
112
How do dsDNA viruses replicate?
Similar to the replication of cellular DNA, the viral genome replicates in the nucleus and the viral proteins are made in the cytoplasm. There are some exceptions, such as the Hep B virus, which replicates DNA from an RNA intermediate.
113
How do ssDNA viruses replicate?
Cells do not use ssDNA so the DNA strand folds back on itself to form dsDNA, which is replicated by cellular DNA polymerase, with the newly replicated strand being released as ssDNA.
114
How do (+) ssRNA viruses replicate?
ssRNA is transcribed by viral RNA polymers ace. Complementary (-)ssRNA then acts as a template for further transcription, resulting in copies of the +ssRNA. The original is also used for the translation of viral proteins.
115
How do (-) ssRNA viruses replicate?
-ssRNA is transcribed by RNA-dependent RNA transcriptase to create a complementary +ssRNA that acts as a template for further transcription of -ssRNA and translation of viral proteins
116
How do ds RNA viruses replicate?
The dsDNA is unwound in the cell. The-ssDNA and +ssRNA is transcribed by the viral RNA polymerase to make complementary RNA strands, resulting in dsRNA. The +ssRNA also acts as a template for protein translation.
117
Describe orthopoxvirus variola.
An enveloped, brick-shaped, complex capsid, dsDNA virus. It has a human host and causes small pox, a disease that caused between 300 and 500 million deaths. It infects the internal organs, causing fever, malaise, and delirium, moving via the blood to the skin and producing pox.
118
What are the two major forms of variola?
Major: causes severe disease with a 20-40% mortality rate by the 7th day.
Minor: Causes a milder form of the disease with 1% mortality.
119
What are some virulence factors of variola?
Adhesion molecules allow the attachment to human host cells, triggering endocytosis. They carry genes for transcription enzymes which allow replication in the cytoplasm. It remains stable in aerosol form, making it highly contagious between people.
120
Who was Edward Jenner?
Father of immunology. He carried out variation to protect his patients from smallpox, which involved infecting them with variola minor. He created the first small pox vaccine in 1796 using cowpox. Eradication program began in 1967 and was declared eradicated in 1980.
121
What factors enabled the eradication of smallpox?
The vaccine was inexpensive, stable, and effective, there are no animal reservoirs, symptoms were quickly obvious, there are no asymptomatic cases, and the virus is only spread via close contact.
122
Describe poliovirus.
An enterovirus, that is small, makes, (+)ssRNA. It is protected by a capsized and generally resistant to mild sewage treatment and heat, common methods of disinfecting water. It is transmitted through the fecal-oral route and heron-person via droplets. It infects the oropharynx and intestinal mucosa or the upper respiratory tract and infect the underlying lymphatic tissue.
123
Describe Polio.
Caused by one of three serotypes of poliovirus, with the last case of wild polio in America in the 1979.
124
What four conditions can be caused by poliovirus?
Asymptomatic infections (90%)
Minor polio - abortive poliomyelitis (5%)
Non paralytic polio - aseptic meningitis (1-2%)
Paralytic polio - minor illness (0.1-2%)
125
Compare the two polio vaccines.
Inactivated polio vaccine: effective and inexpensive, stable during transport and storage, and poses no risk of vaccine related illness BUT requires booster to achieve lifeline immunity, painful, requires higher community vaccination rate.
Oral polio vaccine: Induces secretory antibody response smilier to natural infection, easy to administer, heard immunity BUT requires booster, more expensive, less stable, mutate into disease-causing form, poses risk in immunocompromised patients.
