Task 3 pt2 Flashcards by Miraya W

Sanger chain termination method

Target DNA is isolated and amplified with PCR
Double strands of DNA seperated with heated (95C)
Reaction is cooled to (50C) so that primer can attatch to a DNA strand
Reaction is heated again to (60C) so that DNA polymerase binds to primer and begins making new strand usin free nucleotides and ddNTP terminator nucleotides of specific base with fluresecent tag added
When ddNTP randomly binds to completeary DNA bases, terminates the chain
Cycle continues until all positions on tenplate strand identified

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Conditions for sanger method

Each ddNATP for each base is done in seperate sample tubes and after placed into different walls of gel electrophrises to see the length of terminated chains

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Case study for epidemic
Name

Equine infleueza Virus
strain of Influenza Type A Virus

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Case study for epidemic
Transmission

● Breeding stallions from Japan showed signs of EIV infection following importation
● Direct contact: Spread between horse via nasal discharges, can be inhaled by non affected horses
● Direct: Contaminated farm equipment (i.e. feed buckets and tack)
● Indirect: Humans can also carry the virus on skin, hair, clothing or shoes

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Case study for epidemic
management

● Govt put a halt on all movement of horse between locations
● Performed quarantine operations to isolate affected & unaffected horses
● Horses were given anti-inflammatory drugs to fight the virus

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Case study for epidemic
Preventative measures

● Ensure horses are up to date with vaccinations
● Continuous monitoring of strain
● Avoid sharing equipment between horses

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Case study for epidemic
Control measures

● Affected horses should be isolated from unaffected horses to minimise the transmission of disease.
● New horses should be quarantined for 14 days before grouping the new horses with existing unaffected horses.

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Animal disease
name

Foot and mouth disease

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Animal disease
Cause

Virus, apthovirus of the family Picornaviridae with 7 strains

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Animal disease
how does the pathogen enter the host

Through breath, secretions (spit, snot) and excretions (urine), animal products

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Animal disease
Effect on animal

Affecting: cattle, sheep, pig, cloven-hoofed wildlife
Symptoms: blisters, ulcers in mouth, shivering, loss of appetite/weight loss, depression, drooling/hyperventilation, fever, ruptured blisters,

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Animal disease
distrbution

Circulate 77% of global live stock population
Aus, NZ, Indonesia, Central, North America is free from FMD

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Animal disease
Prevention/control

Burning the carcasses, burying in mass graves, slaughters, euthanasian,
Quarantining new animals, foot washes, regular cleaning of pens, building, vehicles, equipment

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Animal disease
Effects on agriculture/economy

Case Study: UK 2001
* Total animals slaughtered: 6.5million animals euthanized/slaughtered
* Total cost to the economy: $13 billion

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Plant disease
Name

Panama disease (bananas) Fungus: Fusarim oxysporum

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Plant disease
Cause

TR4 strain –> affecting all banana species, Cavandish banana mostly

Plant disease
Effect on plant

Symptoms
- Yellowing and browning of leaf margins
- Stem splitting at base of plant
- Does not affect the fruit

Plant disease
Distribution

Race 1, 2, 4 present QLD
First detected in Aus near Darwin in1997,North Queensland in 2015
Present in many South East Asian countries

Plant disease
Prevention/control

Prevention
- Managing movement of soil, water, plant material entering and exiting farms
- Panama TR4 Grower kit –> latest info on disease and security practices
- Strict quarantine to slow down movement of fungus

Control
- Surveillance and compliance programs (self-reporting)
* Inspect bananas for disease
* Photos and documentation

Plant disease
Effects on agriculture/economy

Far North QLD grows 95% of Aus bananas
Banana industry supporting income, jobs, produce
Does not infect fruit
Whole plantations wiped out
Global loss of 18.2 billion USD

Adaptions to faciliate entry
Prion

Adherance: Host B lymphocytes: secreting factors that enable prions to invade follicular dendritic cells in
lymphoid tissue.
Invasion: From lymphoid tissue, they invade nervous tissue through the autonomic nerves and travel to the brain.
● PrPSC is able to bind to surface of neuron → neuron synapse degradation

Adaptions to faciliate entry
Viruses

Adhesion:
makes contact electrostatically to the cell’s host surface
Viral surface proteins coat adhere to host cell surface receptors
Enters the cell through endocytosis (most likely)
RNA viruses: must reach cytoplasm
DNA viruses: much reach nucleus

Adaptions to facilitate entry
Bacteria

● Pili binding with the host cells’ surface receptor proteins
● Adhesins on the surface of the bacterial cell resist washing action of secretions such as urine, mucus, cilia.
● Translocation of bacterial proteins causes host cell membrane engulfment of bacteria.
enter a cell via phagocytosis

Adaptions to facilitate entry
Protozoa

Receptors on the protozoan’s surface can bind with the host cell’s surface or cell
membrane.
After successful binding, the protozoan secretes adhesive proteins to strengthen the attachment.
Next the protozoan begins to corkscrew itself through the
cell membrane.
Proteins are then released to form a vacuole membrane around the
protozoan to protect it from lysosome digestion.

Adaptions to facilitate entry Fungi

The hyphae are able to penetrate the host cell’s membrane by either: * applying great pressure at a small surface area thus penetrating the cell membrane * by secreting enzymes that can break down a portion of the cell membrane Evasion mechanisms include: * cell wall and capsules protect the fungus from host cell attack. * heat shock proteins that allow fungi to tolerate body temps of 37°C * reduced fungicidal power of macrophages * suppression of cytokine production of host cells

Adaptions to faciliate entry Macroparasities

Eg. Ticks - can inject their mouth through the cell membrane and secrete saliva and neurotoxins into the cytoplasm. The saliva contains chemicals that stop the initiation of the immune response. Eg. Hookworms – larvae are able to penetrate the skin. Once they enter, they are carried via blood to the heart and lungs. Upon coughing and swallowing, they are transferred to the intestines where they mature and develop eggs.

Adaptions to facilitate transmission Air borne

● Able to remain suspended in air for long periods. ● Resists drying out. ● Pathogen causes sneezing and coughing, which causes ejection and transmission to the new host. e.g. influenza virus

Adaptions to facilitate transmission Water-borne

● Able to colonise and proliferate in water, so environmental reservoirs are present (e.g. from faecal material). ● Modified outer surface structures (e.g. fimbria, flagella) allow motility. ● Many are not destroyed by simple boiling of water or other water-treatment processes. e.g * Legionella

adaptions to facilitate transmission Vector-borne

● Pathogen not affected when absorbed by or bound to a vector. Therefore, they have adapted to survive inside the vector's body. ● surface receptor proteins that can attach to vector → pili and adhesion proteins e.g. malaria, dengue fever, zika virus

Adaptions to facilitate transmission Sexual transmission

● Ability to enter the uterus. ● Able to survive in placenta and transmit disease when organisms consume placenta. e.g. HIV/AIDS, chlamidia

Passive defence Physical barriers

Thick cuticle, cell walls and small stomata → inhibit pathogen entry ○ Some pathogens secrete enzymes to break down the cuticle, and so plants with thicker cuticles are better able to withstand this. Bark: protects pathogens from invading food source, sap, in the phloem beneath the bark tree

Passive defence Chemical barriers

● Antimicrobial chemicals such as nicotine which naturally occurs in some plants. ● Naturally occurring enzyme inhibitors. ● Stomata may close in response to the presence of bacteria, through chemical signalling methods involving detection of PAMPs. (pathogen-associated molecular patterns)

Active defence Rapid active responses

● Plant recognitions → change in permeability of cell wall ○ Allows movement of ions & activates certain genes ● Release hydrogen peroxide in an oxidative burst → kill microbes directly ● Reinforcement of cell wall w/ aggregates of cytoplasm → cell wall apposition

Active defence Delayed active response

● Limit spread of pathogen ● Repair wounds in bark through cork cell production and gum secretion ● Lysozyme-like chemicals released ● Salicylic acid act as signals agent of subsequent infections and play a role in the plant’s ‘memory’ of a particular pathogen → system acquired resistance