War against trees and banana lecture

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Last updated 8:25 PM on 10/6/26
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49 Terms

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What is Armillaria Root Rot?

Fungus that attacks the root and the base of trees, causing root rot. It’s a significant threat to many tree species and can lead to tree decline or death

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What is oak wilt?

Oak wilt primarily affects oak trees, causing wilting, browning, and defoliation. It’s particularly destructive to certain oak species

Red oaks: have sharp points on leaves; Oak Wilt is deadly for red oaks

White oaks: smoothly loaded; oak wilt slowly kills white oaks

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What is sudden oak death?

This water mold-like organism affects several tree species, including oak and other woody plants. It causes canker on the trunk and sudden death of infected trees.

Canker Circle trees and the xylem and phloem are killed; If cut, it will cause oozing showing that the mycelium is alive

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What is powdery mildew?

Powdery mildew fungi can infect a wide range of trees and shrubs. They cause a characteristic white powdery growth on leaves and may affect tree health if the Infections is severe

Thrive in moist and warm environment; happened when plants are planted too close to eachother

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What is Rhizosphaera Needle Cast?

This fungus affects conifers, such as spruce and pine trees, causing the browning and premature Shedding of needles

No more green color; looks dead

Pine needles are held together by vasicles at the bottom/connecting point to needle and tree→ fungus gets into vasicle and everything upstream dies

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What is Apple scab?

While primarily affecting apple trees, apple scab can also affect pair in other fruit trees. It causes lesions on leaves and fruits, reducing crop quality.

Apple trees: spread fast; long-term loss for orchards → farmers cut and burn them and takes about 8 to 7 years to grow

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What is cedar apple rust

This fungus affects apple and cedar trees. It produces distinctive rust colored galls on cedar trees and can damage apple fruit and leaves

Gall: Bulbous structure on tree/tree tumor; Has orange tentacles, falling off of gall which has a lot of spores


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What is phomopsis canker

This tree can infect various tree species, causing cankers on branches and trunks, as well as dieback

Seen in blueberries; can see random shrub dying

Zoom in on twig; little slit is the ascus busting out of the twig; starves the branch and takes the plants nutrients

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History of chestnut blight

In 1904, Hermann Merkel inspected Japanese chestnut trees, which were part of an effort to diversify American chestnut populations by introducing Asian chestnut varieties, which were believed to be resistant to the chestnut blight, a disease that was already causing concern in the United States. He noticed unusual symptoms, such as orange colored cankers. He sent samples to William Merrill. He Found that the fungus was responsible for the chestnut light disease that had already devastated American chestnut populations.


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Why was the discovery that the Japanese chestnut tree fungus was the chestnut blight important

It revealed that the import Japanese chestnut trees were carriers of the disease, even though they didn’t display severe symptoms. The discovery marked the beginning of efforts to control the spread of chestnut light in the United States. Despite efforts, the chestnut populations continued to decline.

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Chestnut blight overview

1) Japanese chestnuts resistant to blight /carrier

2) United States using Japanese chestnuts to diversify chestnut plants (Believe they were resistant to the chestnut disease)

3) United States chestnut plants were wiped out


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Why were chestnuts important?

It was an incredible source of nutrients, including fats, and calories; used to feed livestock and humans

The big wood was used to help with building

Was a keystone species that dictate to the surrounding environment and species

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What else impacted the chestnut tree population?

Lumberman were also killing them during the industrial Revolution because they need trees and open space to expand the United States

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What is the lifecycle of the chestnut bite?

1) Spore dispersal: release of asexual spores (conidia), produced on the surface of infected trees or in pycnidia→ can becarried by rain, wind, or insects to nearby, healthy, chestnut trees.

2) infection: when conidia lands on susceptible chestnut tree, they can germinate and penetrate into the bark through wounds or openings. Once inside the fungus begins to grow and reproduce.

3) Canker formation: as fungus spreads, canker form on the bark→ Typically sunken areas with orange or red margins; disrupt flow of nutrients and water within tree, weakening it and causing damage

4) Sap production: in response to infection, trees produce gum like sap, or resin in an attempt to seal off the infection and prevent further spread; often ineffective in stopping the disease

5) reproduction: within canker, fungus produce perithecia which releases sexual spores called ascospores→ Can be dispersed to other chestnut trees

6) Secondary infections: Ascospores from perithecia can initiate new infections on nearby trees, continuing the cycle of trees; significant effect in the rapid spread of chestnut

7) Tree declined and death: Overtime, Repeated canker formation and disruption of the trees, vascular system, can cause the chestnut tree to decline in health and may eventually die if they are unable to transport nutrients and water effectively

<p>1) Spore dispersal: release of asexual spores (conidia), produced on the surface of infected trees or in pycnidia→ can becarried by rain, wind, or insects to nearby, healthy, chestnut trees.</p><p>2) infection: when conidia lands on susceptible chestnut tree, they can germinate and penetrate into the bark through wounds or openings. Once inside the fungus begins to grow and reproduce.</p><p>3) Canker formation: as fungus spreads, canker form on the bark→ Typically sunken areas with orange or red margins; disrupt flow of nutrients and water within tree, weakening it and causing damage</p><p>4) Sap production: in response to infection, trees produce gum like sap, or resin in an attempt to seal off the infection and prevent further spread; often ineffective in stopping the disease</p><p>5) reproduction: within canker, fungus produce perithecia which releases sexual spores called ascospores→ Can be dispersed to other chestnut trees</p><p>6) Secondary infections: Ascospores from perithecia can initiate new infections on nearby trees, continuing the cycle of trees; significant effect in the rapid spread of chestnut</p><p>7) Tree declined and death: Overtime, Repeated canker formation and disruption of the trees, vascular system, can cause the chestnut tree to decline in health and may eventually die if they are unable to transport nutrients and water effectively</p>
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overview of Dutch Elm disease

Spread by a Beatles; gets into the trunk and makes tunnels/galleries in bark → dies quickly

Can test for disease by cutting a rectangular band in the bar to look for the galleries

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History of Dutch Elm disease

Was accidentally introduced to North America in early 20th century; first identified in a shipment of Elmwood bound for Ohio in 1930s and quickly spread across the continent. This rapid spread quickly impacted, urban and rural areas

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Importance of Elm trees in the effect of their loss on ecosystems

They are an important component of ecosystems, providing habitat and food for various wildlife species. The loss of Elms had ecological repercussions, affect affecting the wildlife that dependent on these trees.

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Importance of Elm trees in the effect of their loss on urban areas

Were widely planted in cities in towns for their aesthetic, beauty and shape providing qualities. Dutch Elm disease had a catastrophic effect on urban landscapes, leading to loss of countless mature Elm trees that were defining feature of mini streets and parks. Their loss transformed the visual character of cities across America.

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Elm tree’s cultural historical significance

Often associated with local history and community identity; loss had cultural and sentimental, implications

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Cooperative efforts in Dutch Elm disease and developments

Dutch elm disease sparked considerable research in cooperative efforts among scientists and government agencies to understand and combat the disease. This collaborated response contribute to advancements in plant pathology and disease management techniques.

Played a role in the development of urban forestry and the establishment of programs to protect and maintain urban tree populations

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Symptoms of Dutch Elm disease

Wilting: Leaves on one or more branches, turn, yellow, brown, and then eventually wilt during growing season

Flagging: affected branches, often die quickly leading to the flagging or browning of entire sections of the trees canopy

Brown streaking: the bark is peel Back on infected branches, showing visible brown streaking beneath the bark

Fungal mat: In some cases fungal mats may be visible on the bark, especially during summer months; have a slimy or Dutch cheese appearance

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Dutch Elm disease lifecycle

Beetle has spores on bodies; beetle chews two bark; spores are there and start to grow inside the bark (fungus and conidia in xylem and phloem); fungus spreads through natural root graph between trees; beetles dig galleries under bark and lay eggs; fungus grows in galleries and beetles emerge carrying spores

<p>Beetle has spores on bodies; beetle chews two bark; spores are there and start to grow inside the bark (fungus and conidia in xylem and phloem); fungus spreads through natural root graph between trees; beetles dig galleries under bark and lay eggs; fungus grows in galleries and beetles emerge carrying spores</p>
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What is white pine blister Rust

A fungal disease caused by the pathogen Cronartium ribicola. This disease primarily affects white pine species, particularly eastern white pine, sugar pine, and western white Pine

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Characteristic of white pine blister rust

A heteroecious parasite infecting white pines and certain species of currents and gooseberries

Have devastating effects on valuable tree species, especially in North America

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History of white pine blister rust

Believe to have originated in Europe, where it has been known for centuries. First described in Austria mid 18th century. The pathogen was likely introduced in America 19th or early 20th century through importation of infected pine seedlings from Europe.


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Impact of white pine blister rust

Had a relatively limited impact when first introduced to North America due to presence of resistance in some white pine population. However, as the disease adapted to North American, White Pines and their native Ribes hosts, It became more destructive. Began causing world spread epidemic across the North America in early 20th century.

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Lifecycle of white pine blister rust

1) initial infection on Ribes hosts: The fungal spores of Cronartium ribicola are produced on infected white pine trees, and are dispersed by wind. When the spores land on leaves or stems of Ribes (Wild currents and gooseberries) They can infect Ribes host

2) Aeciospore production on Ribes hosts: The fungus produces aeciospores on Ribes host, which are then released

3) Infection of white pine hosts: these aeciospores Are carried by the wind to white pine trees. When they land on the needles of a susceptible, white pine, they can cause infection.

4) Growth of the fungus on white pines. The fungus grows on the inner bark/cambian of white Pines, causing canker or swelling on the branches and main stem

5) damage to white pine trees: as the infection spreads, it can damage branches, or the main stem, leading to dieback of branches or the entire tree. Canker disrupt flow of nutrients and water within trees, weakening it.


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Symptoms of white pine blister rust

Canker: raised, swollen areas on the branches or main stem, often Covered with white resinous Blisters; can disrupt the flow of nutrients and water leading to branch die back

Needle discoloration: infected white pines may show yellowing or browning of needles on Affected branch

Conifer rust, fruiting bodies: in late summer, the fungus produces distinctive orange sport producing structures/Telia on the surface of the cankers

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What is CODIT

→ Overall Plants do not have good adapted immunity system; every time they get an infection it is like brand new

Trees compartmentalize disease through a process known as compartmentation of decay in trees (CODIT)

CODIT is a series of defense mechanisms of the trees used to limit the spread of fungal and bacterial pathogens as well as other forms of decay within their woody tissue

Main goal is to protect the healthy parts of the trees from infection and decay

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How does CODIT work?

There’s a wound response→ When a tree is wounded, whether due to mechanical, insect feeding, or fungal damage, it initiates a wound response (Chemical and physical barriers, callus formation, Compartmentalization)

Chemical and physical barriers: Chemical barriers include production of compounds like phenolics, resins, and gums, which can inhibit spread a pathogens. Physical barriers are created by the formation of specialized cells which block the passage of pathogens through the trees of vascular system

Callus formation: trees produce callous tissue, which are essentially new wood tissue that grows over the wound; helps to seal off, exposed areas and prevent pathogens from moving deeper into the tree

Compartmentalization: The tree compartmentalize‘s the affect areas by isolating it from the healthy wood. It does this by creating distinct walls within the trees woody tissues.

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What are the CODIT walls?

Barriers that the tree forms within its wood to contain the infection or decay

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What are the four primary CODIT walls?

Wall one: the outermost barrier formed; surrounds the immediate wooded area and contains the initial response to injury

Wall two: forms inward from wall one and represents the limit of the wound compartment (boundary or edge of the damaged area); as a secondary barrier to contain the spread of pathogens

Wall three: another inner barrier formed; further isolate the infected area from healthy wood

Wall four: at our most barrier and represents final defense; separates the infected wood from living healthy wood at the core of the trees

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Wall 1 (Reaction zone)

Outmost CODIT wall and is formed nearest the site of injury; often first wall of defense against invading pathogens

1) Chemical barriers: Tree produces chemical compounds such as phenolics and resins, Which help inhibit the spread of pathogens

2) Physical barriers: Cells May become suberizes (Develop a protective layer) And produce gums or callus tissue to block the passage of Pathogens

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Walk 2 (Compartmentalization zone)

Forms inward from wall one and represents the boundary of the wound compartment

1) Suberized cells: cells can become suberized Creating a durable physical layer

2) Chemical inhibitors: Chemical compounds produced by The tree may continue to inhibit the growth of pathogens in wall two


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Wall 3 (protection zone)

Another inner barrier that further isolate affected area

1) Chemical inhibitors: treatment continues to produce chemical compounds

2) formation of occlusions: specialized cells may form occlusions which are substances that block the vascular tissue and limit movement of pathogens

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Wall 4 ( Compartmentalization zone)

Innermost wall closest to center of tree; final defense against spread of pathogens

1) Formation of Heartwood: In some cases tree may form heartwood Which is denser and less susceptible to decay, then surrounding sapwood; protects the central core of tree from infection

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Healing of the tree overtime

Overtime the trees, natural defense mechanisms continue to work and the wounds heal, and the CODIT walls may become more effective at containing the disease. CODIT is not always completely successful in stopping the progression of disease, especially if the pathogen is highly aggressive

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Information on bananas

All bananas we’ve eaten are bananas that have mutation so that they don’t have viable seeds (they bread the seeds out and clone them)

You’ve probably eaten the same banana your entire life because the bananas are clones of each other; however, the bananas your grandparents would have been different

The artificial banana taste is from the original banana (Gros Michel)

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History of the original Gros Michel banana

An early 20th century the Gros Michel Banana was the primary banana exported and consumed globally→ Was known for its taste texture and resistance to the prevalent strain of Panama disease (TR1)

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The search for a new variety of bananas

As the Gros Michel Began to parish, banana producers scrambled for a variety that they could grow instead (That could be shipped easily grew quickly and could survive transport) → turned to conventional cavendish

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Cavedish and resistance

Resistance to race one but suspectible to TR4

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History of Cavendish

Descended from a plant grown in a hot house belonging to the Duke of Devonshire 180 yrs ago

Was not as hardy as the gros michel and required A change of transportation methods; Was not as delicious as the gros michel (Dole worried consumers wouldnt buy them; was resistant to TR1 fungus and became the banana we used today

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How the infection begins

Begins below:

Fungus in soil contact susceptible roots, hyphae enter and colonize root tissue, the fungus reaches the xylem and spreads into the rhizosome

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What occurs inside the xylem?

Fungal hyphae and microsporidia inside; colonize and host responses disrupt water transport

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Signs of the infected banana

Older leaves yellow, wilt, and collapse; internal vascular tissue becomes discolored

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What happens if the plant dies?

The fungi will remain; the thick wall survival spores (chlamydospores) help the fungus persist

→ Removing a diseased plant does not eliminate inoculum in the soil

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How does the fungus reach another farm?

Transport of spores from people, animals, insects, and railroads

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When TR4 reached the Americas

Columbia- 2019

Peru - 2021

Venezuela -2023

Ecuador- dec 2025 (Laboratory confirmation E Oro Province prompted an official pest alert

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What would confirm TR4?

Symptoms→ show where to begin to investigate

Culture and microscopy→ A fusarium-like fubgus is present

Validated molecular assay→ whether the target lineage is detected

→ A genetic ITS match cannot establish the race