Can plants get sick

Plants Get Sick Too!

  1. Abnormal tissue coloration—Tissue color may change (leaves, stems, roots). Examples include: chlorosis (yellowing), necrosis (browning), purpling, bronzing and reddening. Mosaic or mottled patterns may also appear on some tissues.
  2. Wilting—Water stress (too much or too little) can cause a plant to wilt. If a pathogen interferes with the uptake of water by the host plant, a part of the plant or the whole plant may die. Fungi belonging to the genera Verticillium and Fusarium and bacteria in the genus Xanthomonas are often associated with wilt diseases as they colonize the xylem of plants leading to a lack of water transport.
  3. Tissue death—Necrotic (dead) tissue can appear in leaves, stems, or root, either as spots or as entire organs. Decay of soft succulent tissue, as in damping off in young seedlings, is common and can result in other symptoms, such as bad odor from rotting tissues.
  4. Defoliation—As the infectious disease progresses, the plant may lose all its leaves and sometimes drop its fruit.
  5. Abnormal increase in tissue size—Some diseases increase cell numbers or cell size in the plant tissues, twisting and curling the leaves or forming galls on stems or roots.
  6. Dwarfing—In some cases the pathogenic organism will reduce cell number or size, stunting parts of the host plant or the whole host plant.
  7. Replacement of host plant tissue by tissue of the infectious organism—This occurs commonly where floral parts or fruits are involved. Examples include ergot on rye and other cereal crops caused by the fungus Claviceps purpurea and corn smut caused by the fungus Ustilago maydis.

Glossary of Important Plant Pathology Terms

Injury—damage caused by transitory interaction with an agent such as an insect, chemical or unfavorable environmental condition. Disease—abnormal functioning of an organism. Biotic—relating to life, as disease caused by living organisms. Abiotic—pertaining to the absence of life, as diseases not caused by living organisms. Pathogen—a disease-producing organism or agent, such as bacteria, viruses or fungi. Sign—indication of disease from direct observation of a pathogen or its parts. Symptom—indication of disease by reaction of the host, e.g., canker, leaf spot, wilt. Susceptible host—prone to develop disease when infected by a pathogen. Resistant host—possessing properties that prevent or impede disease development. Toxicity—capacity of a substance to interfere with the vital processes of an organism. Parasite—organism that lives in intimate association with another organism on which it depends for its nutrition; not necessarily a pathogen. Inoculum—pathogen or its parts, capable of causing infection when transferred to a favorable location.

For a complete list of definitions look on APSnet Illustrated Glossary of Plant Pathology: apsnet.org/edcenter/illglossary/Pages/default.aspx.

Introduction to Plant Disease Series

  • Plants Get Sick Too! An Introduction to Plant Diseases
  • Diagnosing Sick Plants
  • 20 Questions on Plant Diagnosis
  • Keeping Plants Healthy: An Overview of Integrated Plant Health Management
  • Viral Diseases of Plants
  • Bacterial Diseases of Plants
  • Fungal and Fungal-like Diseases of Plants
  • Nematode Diseases of Plants
  • Parasitic Higher Plants
  • Sanitation and Phytosanitation (SPS): The Importance of SPS in Global Movement of Plant Materials

These fact sheets can be found at OSU Extension’s Ohioline website: ohioline.osu.edu.

Plants do not have these sorts of immune cells, but that does not mean that their immune responses are any less impressive. On the contrary, plants exhibit a wide range of antimicrobial defences.

Plants and their pathogens have been evolving together for millions of years, so their relationships and their respective adaptations are complex. Pathogens come with baggage – biochemical baggage, known as pathogen-associated molecular patterns or PAMPs – and it this that plants need to be able to recognise. Examples of PAMPs include the proteins that make up the flagella of bacteria, lipopolysaccharides and peptidoglycans (which are found on the cell membrane of some bacteria) and chitin. Chitin is the main component of crustacean and insect body parts, as well as the cell walls of fungi.

If an organism made in part of chitin attacks a plant, the plant can produce chitinases, enzymes that can break down the chitin. That’s a very useful adaptation, but the story doesn’t end there. Many plant pathogens have evolved a response to this response. In such a situation, Cladosporium fulvum (a fungus) will, for example, secrete a lectin (a protein) that binds to the chitin in its cell walls, protecting it against the chitinases produced by the plant.

One of the most clever responses of plants to attack is the co-opt assistance from other organisms. When a tobacco hornworm caterpillar takes a bite from a tasty tobacco leaf, it triggers an emergency response from the tobacco plant. The tobacco plant releases green leaf volatiles (GLVs). These are the compounds that give freshly mowed grass its distinctive aroma. When the saliva of the hornworm caterpillar mixes with the GLVs released by the plant, they are changed, making them very effective at attracting predators, which then eat the herbivores that are consuming the plant. There are many other examples of this strategy throughout the plant kingdom.

In the case of a viral infection, the virus releases proteins known as effector proteins. These can be recognised by the plant’s resistance genes, or R genes. The response of R genes can trigger warning signals to be sent other part of the plant; they can even lead to changes in the local cell walls to prevent the virus spreading further. Plants can even be immunised against some diseases, by manipulating these R genes so their response lasts longer for more enduring protection.

Most plant pathogens feed on living plant tissue, so one way of limiting the spread of a pathogen is to isolate the area of attack and kill the surrounding cells. This is known as a hypersensitive response, and is basically selected cell suicide. One visible indication of this can be a patchy or mottled appearance of plant leaves.

Image by Andrew PurdamDeep down I think I knew that once I started looking into plant immunity, I was going to be impressed, and I have been. I have barely scratched the surface (epidermis?), so if you want to know more, here are a few useful places to start.

http://www.abc.net.au/science/articles/2012/06/12/3522493.htm

You’ll never see a tree barf or a flower sneeze. Still, plants get sick, much as we do. Their symptoms just look different. Their leaves may curl or drop. Their stems can break out in spots. Their fruit might shrivel.

One such plant sickness is called swollen shoot disease. Over the past two decades, it’s swept through cacao trees in Ivory Coast, a country in West Africa. Cacao is the main ingredient in chocolate. Hundreds of thousands of these trees have sickened or died. “We saw this rapid, rapid death. Trees were dying in one year,” Judy Brown says of the epidemic.

Brown works at the University of Arizona in Tucson. As a plant pathologist, she studies plant disease. Her specialty is viruses, the tiniest type of microbe. In people, viruses cause many illnesses, including the common cold. Viruses also are to blame for swollen shoot disease.

“Many people don’t realize that plants become sick from viruses,” says Brown. Other microbes, including bacteria and fungi, also make plants sick. Insects often spread viruses and other germs from plant to plant.

To stop that spread, farmers usually spray chemicals meant to kill germs or pests. They also may rip out and destroy sick plants. This keeps them from passing the disease on to healthy neighbors. In 2018, the Coffee and Cocoa Council in Ivory Coast announced a plan to uproot 3,000 square kilometers (about 1,200 square miles) of infected cacao trees. That’s an area around the size of Rhode Island.

Even such drastic measures may not go far enough to stop a dangerous disease.

Fortunately, scientists have other tricks up their sleeves. Researchers are working to understand crop diseases, identify sick plants, fight the attackers and breed plants that can fight illness on their own. They hope such efforts will keep foods like chocolate, bread and oranges on all of our plates for centuries to come.

Courtesy of Judy Brown Romain Aka (left) looks for signs of disease on a cacao tree. This plant pathologist works at the National Center for Agricultural Research in Ivory Coast. Together with Judy Brown, he studies swollen shoot disease.

Getting to know the enemy

Fighting any epidemic begins with understanding the disease. “You have to know who your enemy is,” Brown says. The foe she’s working to understand is swollen shoot disease.

It gets its name from one of its symptoms. Young branches of an infected tree will develop thick bulges. “We think those areas might be little virus factories,” she says. Inside the bulge, viruses may be multiplying rapidly. Leaves of infected trees grow smaller than normal, and often turn yellow or brown.

Different viruses can cause swollen shoot disease. Brown wanted to identify them. Scientists do this by reading a virus’s genome (GEE-nohm). That’s the complete pattern of nucleotides that tells a living thing how to grow. Nearly all living things have genomes made of DNA. Some viruses instead use a similar molecule, called RNA.

Each viral species has its own unique genome. Before Brown and her colleagues began working on the swollen shoot problem, they had identified seven viruses that cause the disease. Her team has turned up dozens of new ones. Today, the grand total stands at 84. Her team also has found that in some cases, more than one of these viruses has infected the same tree.

Identifying microbes by their DNA is a long, involved process. First, Brown collects an infected leaf. She separates the viral genetic material from all of the other molecules in the sample. Then she uses techniques similar to the ones police use to identify criminals. She makes many copies of the viral DNA (or RNA) so that it is easier to study. Computer programs then read through these copies, matching patterns to build up a complete readout of the genes.

For now, all of this happens in a lab. And it can take several weeks or longer. Brown wishes you could put a leaf into a handheld device to find out whether a tree was sick, even before any symptoms showed.

Heading into the field, literally

No such handheld tool yet exists. But another researcher, working on a different disease, has made a portable DNA sequencing lab that fits inside a suitcase. Sequencing means finding the pattern of genes and other genetic material in a sample.

Diane Saunders works at the John Innes Centre in Norwich, in England. This plant pathologist specializes in a group of diseases that attack wheat. They’re known as rusts. Their common names are leaf rust, stripe rust and stem rust. All make their host plants break out in reddish-brown or yellow spots or stripes. They get their names from the fact that these lesions look a bit like rust on metal.

Petr Kosina/CIMMYT/Flickr (CC BY-NC-SA 2.0) The reddish-brown splotches on this wheat leaf reveal that the plant is infected with stem rust. Microbes called fungi cause the sickness.

Thousands of years ago, the Romans believed that the god Robigus was responsible for wheat rust. They threw a festival in his honor each year on April 25th. The festivities involved sacrificing an animal with reddish fur. Supposedly, this would please the god and protect the wheat.

Now scientists know that single-celled fungi cause plant rusts. Farmers can spray chemicals called fungicides on a field to kill the microbes. But that’s expensive. And sometimes the crop dies anyway, notes Ruth Wanyera in East Africa. She’s a plant pathologist at the Kenya Agricultural and Livestock Research Organization (KALRO) in Njoro.

She thinks a better approach is to plant crops that naturally withstand the fungal infection. Certain genes toughen plants up so they can fight off various types of fungus. But no wheat variety resists every type of disease. To choose which variety to plant, farmers must know which rust-causing microbes live in their region.

Until recently, the only way to figure out the identity of a fungus was to mail a sample to a lab. Getting a result would take “many, many months,” says Saunders. In fact, analysis would take longer than it took for the wheat to ripen. Farmers would have to plant their next crop before finding out which diseases had attacked the previous crop.

Diane Saunders/MARPLE Diagnostics Diane Saunders and a technician from the Ethiopian Institute of Agricultural Research try out the MARPLE tool in the back of a car. Here, they are cleaning a sample to remove everything except DNA.

So Saunders’ team put together a tool they call the Mobile And Real-time PLant disEase diagnostic kit, or MARPLE for short. (The name is a nod to Miss Marple, the British detective in a famous series of mystery novels by Agatha Christie). It’s like a miniature laboratory. To use the kit, someone first mashes up plant material and puts it through a series of steps very similar to what Brown does in her lab. After just a few days, a laptop computer spits out genetic information. It’s not the entire genome. But it’s enough information to identify a fungus.

The kit doesn’t need constant electricity or internet access. So researchers can bring it into wheat fields anywhere in the world. That’s exactly what Saunders did during a test of the technology in Holeta, Ethiopia last year. Her team worked with the Ethiopian Institute of Agricultural Research to test rust from real farmers’ fields. At the end of the 10-day trip, the group shared a list of the fungi they had found. “It was the earliest warning they’ve ever had about what strains they have in their country,” says Saunders. The team has submitted its research for publication.

So far, the tool can identify only strains of stripe rust. But Saunders hopes to one day add the ability to identify stem rust.

Breeding plants for battle

In the late 1990s, a new and very aggressive strain of stem rust appeared in Uganda. Named Ug99, it devastated farm fields in Africa and the Middle East. “It can turn a wheat field in a matter of days into nothing,” says Maricelis Acevedo. She is a plant pathologist at Cornell University in Ithaca, N.Y.

Realizing the crisis it posed, the scientific community began hunting for wheat genes that could resist the new disease. Acevedo studied one resistant plant, called Montenegrin spring wheat. She started with a genetic map of the plant. The map didn’t cover the plant’s complete genome, just a general outline of it. She also had the genetic map for a different wheat variety that easily died from the disease.

She bred the two types of wheat together. Some of the offspring inherited resistance to Ug99. Others didn’t. Acevedo repeated this process again and again over several generations. At the same time, she compared all the plants’ genetic information, hoping to puzzle out which genetic material made a plant resistant.

It was slow work. Each time she had to wait for a new generation of wheat plants to grow up before she could assess their resistance. After four years, however, her team showed that multiple genes work together to protect Montenegrin spring wheat from Ug99.

“Now we’re in the process of identifying if all these genes are fully necessary or if one or two genes provide most of the resistance,” says Acevedo. When her results are final, she’ll share them with breeders. From there, it may take up to 10 more years to produce a variety that’s ready for farmers’ fields.

Peter Lowe/CIMMYT/Flickr (CC BY-NC-SA 2.0) Ruth Wanyera (at center) teaches students and colleagues at KALRO Njoro about rust diseases. Here, she’s demonstrating how to judge the severity of an infection.

Ten years is a long time to wait for better wheat plants. In the meantime, climate change is causing more extreme weather around the world. When the weather is warmer, wetter or drier than normal, plants have trouble coping. That makes it harder for them to fight an infection.

In addition, new diseases or new strains of known diseases will continue to emerge. A plant that resists Ug99 may not fare as well against a slightly different strain of wheat rust. “The disease is windborne and keeps on mutating,” notes Wanyera. “Scientists have to be awake all the time.” The faster scientists can identify resistant genes and develop stronger wheat plants, the better.

The quickest way to create a stronger plant is by directly “editing” a plant’s genes in the lab. This is called genetic modification, or GM. Once scientists have identified all the genes they want in a plant, they can cut and paste them together. They don’t have to wait for many generations of thousands of baby plants to grow. “We know we can do it,” says Acevedo. “We have proof that it works.”

But the idea of changing a living thing’s genes makes many people nervous. Any technique that involves adding, deleting or altering genes in a lab is a form of genetic modification. A food that has gone through this type of process might be called a genetically modified organism, or GMO.

In the United States and Europe, many food products boast the label “non-GMO.” It means that none of the ingredients in the food contain genes that were modified in a lab. Scientific studies have shown that GM foods are safe to eat, concluded a massive 2016 review by the National Academy of Sciences. Still, many people refuse to buy products that contain such ingredients. So Acevedo and many others tend to breed crops using traditional, slower methods.

Animals for oranges

Genetic testing and modification aren’t the only way to find and fight crop diseases. Some researchers have recruited animals to join the battle.

The company F1K9 in Yalaha, Fla., trains dogs to sniff out bombs, drugs — and diseases. They’ll work with “any that’s got a nice, long nose and the desire to please,” says William Schneider. He is a molecular biologist with the company. Dogs he has helped train have been sniffing out citrus greening disease. (This plant ailment also goes by the name of huanglongbing, or HLB.)

Citrus greening disease affects all citrus fruit. That includes oranges, grapefruit, tangerines, lemons and limes. A sick tree produces skinny branches with tiny leaves. The small, hard fruit it produces also fall off before ripening. Eventually, an infected tree will die.

The disease arrived in Florida in 2005, then spread rapidly. Today, around four out of every five citrus trees in Florida have the disease. Citrus growers in the state now produce less than half of the fruit that they used to. In 2012, citrus greening disease made it to California, though the sickness has not yet spread to large orchards there.

A genetic test for citrus greening disease exists. But scientists sample just a few leaves at a time. So their testing might not catch the disease very soon after a tree is infected, a time when most of leaves show no symptoms. Yet even though it doesn’t appear sick, this tree can still infect its neighbors.

However, Schneider says, his dogs smell the entire tree at once. They often can detect the disease before genetic testing or human eyes identify a problem. Schneider’s company has brought their trained dogs to farmers’ groves in Florida and California. When the dogs find disease, farmers cut the infected trees down. This may help save the grove.

The disease the dogs are sniffing out is a bacterial infection. But the bacteria that cause citrus greening disease can’t hop between trees on their own. They move by hitching a ride on a tiny flying insect called the citrus psyllid (SILL-id). It sucks sap from trees. When this insects feeds on a sick tree, it picks up the bacteria. The next tree it visits may now become infected. In the United States, citrus psyllid is an invasive species. And it has no native predators.

Farmers can treat their trees with chemical insecticides. But in cities and backyards, these chemicals may not be safe to use. Another bug might be a better weapon.

Mike Lewis/Center of Invasive Species Research/UC Riverside The wasp Tamarixia radiata lays an egg on a young citrus psyllid. When the egg hatches, her young will devour its host.

In Asia, the original home of citrus trees, a tiny wasp called Tamarixia radiata hunts and eats psyllids. This wasp is as small as a grain of sand and harmless to people. It lays its eggs on young psyllids, called nymphs. Later, a baby wasp will hatch out of each egg and “eat the nymph alive,” notes David Morgan. He works for the California Department of Food and Agriculture in Riverside. As an entomologist, he studies insects.

Morgan and his colleagues, Mark and Christina Hoddle, wondered if wasps could help hunt psyllids in the United States. The Hoddles are a husband-and-wife team of entomologists who work at the University of California, Riverside. They’ve been raising baby T. radiata wasps for several years.

The researchers made sure that the wasps wouldn’t harm any native insects. Then in 2011, the Hoddles released several hundred wasps into the wild in California for the first time. Since then, they sent some 13 million of the tiny warriors in search of psyllids. In some places, this has brought down the population of citrus psyllids by almost 70 percent, says Morgan. Fewer psyllids means the chance that citrus greening disease will spread also is lower.

Dogs and wasps are joining scientists in the war against many diseases that threaten important crops. Cacao, wheat and citrus aren’t the only foods at risk. Epidemics of fungus affect banana, coffee and rice plants. When it comes to keeping food on our plates, every bit of help counts.

Patient With ‘Tree Man’ Syndrome Says He ‘Can Finally Live A Normal Life’

The growths on Mahmoud Taluli’s hands were the result of a severe case of a rare condition called epidermodysplasia verruciformis — sometimes referred to as “tree man” syndrome because the tumors can resemble wood or bark. At right: Taluli after his operation. Hadassah Medical Center hide caption

toggle caption Hadassah Medical Center

More than two years after doctors in Jerusalem removed thousands of barklike lesions that had prevented Mahmoud Taluli from using his hands for more than a decade, he continues his battle with a rare, incurable skin condition. But even with another surgery planned for later this summer — his fifth in the pioneering treatment at Hadassah Medical Center — Taluli considers himself a winner.

“After years of suffering and solitude, I can finally live a normal life,” said Taluli, 44, who lives in Gaza and suffers from epidermodysplasia verruciformis, an extremely rare condition caused by his immune system’s inability to fight off the ubiquitous human papillomavirus, resulting in painful gray and white growths on his hands and other parts of his body. His severe form of this condition has been documented only a handful of times around the world and has been nicknamed “tree man” syndrome because the large growths can resemble tree bark.

Last month, a man in Bangladesh with a similar condition made international headlines with his pleas for doctors to amputate his hands after a series of unsuccessful surgeries to remove his lesions. As in Taluli’s case, the lesions on the Bangladeshi patient keep growing back, leaving him in severe pain and unable to use his hands, according to media reports.

Although he has not spoken with that patient or his doctors, Michael Chernofsky, the senior hand and microvascular surgeon at Hadassah who is overseeing Taluli’s treatment, says that amputation is not a good solution. In fact, when Taluli first arrived for treatment at Hadassah in 2017, he said that doctors in Egypt and Jordan had recommended amputation of his hands — an option Taluli refused.

“Amputation is a nonstarter that would create more problems,” Chernofsky said, explaining that if the patient’s hands were cut off, the patient would likely continue to have severe pain from nerves severed in the amputation process. And the skin condition would continue to affect the rest of a patient’s body, he said.

“But I really feel bad for this patient in Bangladesh, and it seems like his desire for amputation is an index of his frustration levels,” he said.

Rare Skin Disease Ruined Gaza Man’s Life — Until Israeli Doctors Stepped In Sept. 1, 2017

Treating Taluli, and ultimately saving his hands, has been a long process — and it isn’t over yet. In four operations since 2017, doctors have removed thousands of lesions from his hands and other parts of his body. Using scalpels and other instruments, they make incisions that are often deep enough to require skin grafts to aid in healing. The operations have been largely successful in clearing away enough growths to allow Taluli to use his hands, but new growths continue to appear. The team will operate for a fifth time later this summer to remove new lesions on various areas of his body as well as some scar tissue from previous operations.

“We realized he was just reinfecting himself by touching lesions, then touching other parts of his body,” Chernofsky said. Not only are existing lesions at risk of spreading to other areas of his body, but if the deep roots of each lesion are not completely removed, the growth returns, Chernofsky said.

“You can’t just shave these off at the surface,” Chernofsky said. “You have to remove every last shred.” Removing the roots of the lesions also relieves the pain they cause as they compress nerves.

“In the beginning, I wasn’t sure our approach would work,” Chernofsky said, explaining there is no medical protocol for treating the condition. “We didn’t know if there would be anything viable left of his hands, but thank God it’s working.”

Doctors are now working to map Taluli’s genome to pinpoint the genetic abnormality that keeps his immune system from fighting off HPV, which comes in more than a hundred strains and can cause warts and even some types of cancer but is usually harmless. Taluli does not have the same genetic mutation that most other patients with the condition have, doctors said.

Ideally, the Hadassah doctors will develop some type of tailored immunological-based treatment for Taluli to allow his body to better fight HPV. They also hope to learn more about the still mysterious human papillomavirus virus and why it affects different people in different ways.

Another challenge is that Taluli lives in Gaza, where the ailing medical system does not offer physical therapy that would ensure better future function for his hands. Patients from the increasingly isolated and impoverished enclave also must obtain permission from Palestinian and Israeli officials to enter Israel for care. Taluli’s case has been approved so far, and he is thankful for the treatment.

“The surgery has completely changed my life,” he said in response to questions submitted by email. “I can play with my children. I can go to family events. I no longer need to cover my hands when I go out in public.”

Sara Toth Stub is a Jerusalem-based journalist. You can follow her work on Twitter: @saratothstub.

‘Tree man’ returns to hospital with fresh ‘bark’ growth as his condition gets worse

A Bangladeshi man who gained international attention after his rare condition caused massive growths resembling tree bark on his hands is reportedly back in the hospital with symptoms worse than before his initial surgeries. Abul Bajandar, who was diagnosed with epidermodysplasia verruciformis (EV), has reportedly already undergone 25 operations to remove 11 pounds worth of growths.

EV is an inherited genodermatosis that stems from chronic HPV, which causes patients to develop polymorphous cutaneous lesions and leaves them at high risk of developing non-melanoma skin cancer. According to the Genetic and Rare Diseases Information Center (GARD), while the exact number of patients who have EV is unknown, it’s been reported at least 200 times so far.

The condition is incurable, but surgical treatment is an option for some patients.

Bajandar’s condition worsened after he skipped a number of doctors appointments.Getty Images

Bajandar had undergone several surgeries in 2016 after the growths left him unable to eat, drink, work or hold his own daughter. But 28-year-old allegedly skipped appointments with his doctors last year, and the growths have not only returned but allegedly have thickened and spread to his feet and body.

“I made a mistake by leaving the hospital,” Bajandar told AFP “I sought alternative treatment but could not find any. I now understand I should have stayed and continued the treatment.”

Samanta Lal Sen, a plastic surgeon reportedly caring for Bajandar, told The Sun that doctors would ideally resume treatment “soon,” but that they have to start “from the very beginning.”

“We’ll have to conduct more surgeries,” she told the news outlet.

PMC

Numerous viruses infect plant, however, none of them so far is known as pathogen to animal and human beings. Only three families, Bunyaviridae, Rhabdoviridae and Reoviridae contain viruses known to infect plant, animal and human. Philippe Colson and coworkers from France reported in the recent issue of PLoS ONE that Pepper mild mottle virus (PMMoV), a plant virus might infecting human being . The findings trigger to reevaluate the dogmatic concept that plant viruses are safe to human health even though numerous viruses are consumed through various types of fresh foods and food-products.

Colson et al. tested stool samples of 304 adults and 137 children and 21 various food products containing chilli-pepper (Sauce, spicy powder ect) for the presence of PMMoV using real-time PCR, sequencing, and electron microscopy. PMMoV was detected in 57% of food products, 7.2% of stool samples of adults and 0.7% of children. Viral RNA sequence was recovered, virus particles were visualized and the virus present in food product was viable as it infected the host plants. In the case-control study, fever, abdominal pains and pruritus were found significantly common in the patients detected with PMMoV. Anti-PMMoV IgM antibodies were detected in all PMMoV positive patients indicating specific immune response to PMMoV. Based on these findings, Colson et al. concluded that PMMoV might infect humans and cause clinical symptoms.

PMMoV, a rod-shaped non-envelop positive sense ssRNA virus belongs to the genus Tobamovirus and commonly infects chilli-pepper. The members under the genus Tobamovirus are highly stable, contagious and require no specific insect-vector for transmission from one host to another host. Tobacco mosaic virus, the type species of the genus Tobamovirus, is well known for its stability in dead tissues of tobacco (cigarette) and also in sputum and thoracentesis fluids of cigarette smokers . PMMoV has been shown widespread in wastewater in USA . Cucumber green mottle mosaic virus, another tobamovirus was detected in the water of Yamuna river in India and the recovered virus from water was infectious on several host plants . Several of such examples show that tobamoviruses are highly stable outside living host-cell. Therefore, presence of biologically active PMMoV in food products and human stools are not surprising. Prior to the work of Colson et al. , PMMoV was shown as the major RNA virus in human stool by Zhang et al. . The interesting observation of Colson et al. is that PMMoV is not a mere gut-inhabitant flora in human being, it interacts with the immune system and generates anti-PMMoV IgM antibody. Furthermore, PMMoV positive patients were correlated with specific clinical symptoms. Although, as they also have pointed out, the symptoms like abdominal pain and fever may be due to spicy food.

Plant viruses, such as tospovirus, rhabdovirus, reovirus, begomovirus and nanovirus are expected to have some linkage beyond their plant-hosts to insect and animal hosts. Tospoviruses, enveloped negative stranded ssRNA plant viruses, are worldwide distributed infecting numerous plants including a wide variety of freshly consumed vegetables, such as tomato, chilli-pepper, lettuce, onion, watermelon, muskmelon etc. Tomato spotted wilt virus, the type species of the genus Tospovirus is known to replicate in insect-vector, thrips and in two human cell lines . Groundnut bud necrosis virus, one of the commonly occurring tospovirus in India, could be transmitted to tobacco plant from tissues of a ripen tomato fruit (unpublished results) (Fig. 1). This means live tospoviruses are consumed while eating fresh salad. To our opinion, tospoviruses are one group of plant viruses that may have potential for host-switching to human or higher animal. Tomato yellow leaf curl virus, a begomovirus (ssDNA virus) affects tomato cultivation in several countries in the world is known to reduce the lifespan and fecundity of its insect-vector, Bemisia tabaci, and the virus is transmitted to the next generation through eggs of B. tabaci. Viruses undergo alteration to inhabit in a new niche. Vertebrate-infecting ssDNA viruses, circoviruses are of such example, which have evolved from plant-infecting nanoviruses though host-switching event and then recombination with vertebrate-infecting virus . Recently, Dangre et al. predicted major histocompatibility complex (MHC) binding affinity of coat proteins from five species under the genus Nanovirus. The MHC molecules are cell surface glycoproteins, which play an important role in the host immune system, autoimmunity and reproductive success. The presence of MHC binding peptide in nanovirus prompted Dangre et al. to forecast that man might be the future host of nanovirus.

Tomato fruit showing symptoms (rings and uneven ripening indicated by arrows) (a) of Groundnut bud necrosis virus (b)

Plant based food and water are obvious route through plant viruses can get access to human body. The other possible route of access of plant virus directly to human cells is through insects that feed on both plant and human. The insect may be vector, host or both for a virus. Mosquito is one possible insect that feed on both plant and human and is a carrier of viruses under the plant and human viruses containing families, Bunyaviridae, Rhabdoviridae and Reoviridae.

To establish plant virus as human pathogen, evidence of its entry into cell, replication therein and finally fulfillment of Koch’s postulation is necessary. However, there is no rigid rule that plant virus can not break the barrier of their host kingdom and invade human or animal. It is possible that some plant virus may have direct or indirect role as human pathogen, but at this moment, no such study is available to consider plant virus as human pathogen.

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Viral Diseases of Plants

This is the fifth fact sheet in a series of ten designed to provide an overview of key concepts in plant pathology. Plant pathology is the study of plant disease including the reasons why plants get sick and how to control or manage healthy plants.

Viruses are intracellular (inside cells) pathogenic particles that infect other living organisms. Human diseases caused by viruses include chickenpox, herpes, influenza, rabies, small pox and AIDS (acquired immunodeficiency syndrome). Although these are the viruses most of us are familiar with, the first virus ever described and from which the term was eventually derived was tobacco mosaic virus or TMV (the term virus was derived from the original description of the causal agent of TMV—“contagium vivum fluidum” or contagious living fluid). TMV was discovered by Martinus W. Beijerinck, a Dutch microbiologist, in 1898.

Figure 1. Symptoms of impatiens necrotic spot virus on pepper leaves. Image courtesy Rayapati A. Naidu, © The American Phytopathological Society.

Morphology

Virus particles are extremely small and can be seen only with an electron microscope. Most plant viruses are either rod-shaped or isometric (polyhedral). TMV, potato virus Y (PVY), and cucumber mosaic virus (CMV) are examples of a short rigid rod-shaped, a long flexuous rod-shaped, and an isometric virus, respectively. Viruses consist of an inner core of nucleic acid (either ribonucleic acid or deoxyribonucleic acid ) surrounded by an outer sheath or coat of protein (referred to as the capsid). The capsid is further enclosed by a membrane in most human and animal viruses that helps the virus pass through the cell membrane in these types of cells. Since the cell membrane in plants is surrounded by a rigid cell wall, plant viruses require a wound for their initial entrance into a plant cell. Wounds in plants can occur naturally, such as in the branching of lateral roots. They may also be the result of agronomic or horticultural practices, or other mechanical means; fungal, nematode, or parasitic plant infections; or by insects. In some cases, the organism creating the wound can also carry and transmit the virus. Organisms that transmit pathogens are called vectors. Mechanical and insect vector transmission are the two most important means by which plant viruses spread. The activity of humans in propagating plants by budding and grafting or by cuttings is one of the chief ways viral diseases spread. In fact, plant virologists use grafting and budding procedures to transmit and detect viruses in their studies. The seedling offspring of a virus-infected plant is usually, but not always, free of the virus, depending on the plant species and the kind of virus. Insect transmission is perhaps the most important means of virus transmission in the field. Insects in the order Homoptera, such as aphids, planthoppers, leafhoppers, whiteflies and mealy bugs—that have piercing sucking mouthparts—are the most common and economically important vectors of plant viruses. Some plant viruses can also be transmitted in pollen grains or by seed.

Figure 2. Symptoms on pepper produced by tomato spotted wilt tospovirus. Image courtesy H. R. Pappu, © The American Phytopathological Society.

Pathogen Biology

Viruses are obligate parasites; that is, they require a living host in order to grow and multiply. Once in a wounded cell, the virus particle sheds its protein coat and the nucleic acid then directs the production of multiple copies of itself and related proteins leading to the development of new virus particles. Cell-to-cell movement of plant viruses occurs through the cytoplasmic “bridges” between cells called plasmodesmata and move systemical y throughout infected plants via the phloem. Although the details of plant virus replication are complex and beyond the scope of this fact sheet, the general idea is that plant viruses cause disease in part by causing a reallocation of photosynthates and a disruption of normal cel ular processes as they replicate. Interestingly, many kinds of plants are infected with viruses and show no symptoms. Such infections are referred to as being latent. Some viruses, such as cucumber mosaic virus (CMV) and cowpea mosaic virus (CPMV), occur as a complex of multiple component particles, each containing different nucleic acid cores. In multi-component viruses, all components have to be present in a plant for infection and replication to take place.

Figure 3. Rose mosaic virus. Image courtesy J. Lotz and P. Lehman, © The American Phytopathological Society.

Viruses are difficult to classify and, for lack of anything better, they were given descriptive (and sometimes colorful) names based on the disease they cause—for example, tobacco ring spot, watermelon mosaic, barley yellow dwarf, potato mop top, citrus tristeza, sugar beet curly top, lettuce mosaic, maize dwarf mosaic, potato leaf roll, peach yellow bud mosaic, African cassava mosaic, carnation streak, and tomato spotted wilt. Many of these viruses infect multiple plant species. For example, tobacco ring spot virus causes a bud blight in soybeans; maize dwarf mosaic infects sorghum, Sudan grass, sugarcane and Johnson grass in addition to corn.

Control

Once plants are infected, little can be done to free them from the virus.

1. Genetic Host Resistance
  • Since different cultivars and species show different degrees of resistance to some viruses, resistant types should be planted whenever they are available. Recent advances in plant cell molecular biology and virology have led to the development of genetically modified plants with superior resistance to some viruses.
2. Cultural Practices

There are numerous cultural practices that can be used to reduce plant losses due to virus infection.

  • Scouting and removal of symptomatic plants or known alternative weed or volunteer plants that may serve as a reservoir for a given virus.
  • For cutting, grafting or propagating seedlings vegetatively, use cleaner or sanitized tools and equipment, and disposable overcoat; wash hands frequently.
  • Rotations to non-host crops.
  • Geographic isolation of production facilities may also help avoid losses caused by plant viruses.
  • The isolation of newly received plant material prior to its introduction into the rest of a production system can also minimize the unintentional introduction of pathogens.

Some viruses are permanently inactivated by prolonged exposure of infected tissue to relatively high temperatures—for example, 20 to 30 days at 38 degrees C (100 degrees F). This procedure, called heat therapy, frees individual plants or cuttings of the virus. The clean tissue is then used as a propagative source, allowing large-scale production of virus-free plants. This has been done with many cultivars of fruit and ornamental species. If insect vectors and infected plant material are kept out of the new virus-clean plantings, subsequent reinfection is unlikely, particularly if the planting is at a distance from virus-infected plantings. For orchard, ornamental nursery, and floricultural crops, the best management approach is the planting of stock that has been propagated from known virus-clean or certified sources. The citrus industries in both Florida and California, for example, have set up certification and registration programs to assure that citrus nursery stock is propagated from the most pathogenfree propagative materials available. A similar certification program exists for seed potatoes. Another successful way to eliminate viruses, particularly from herbaceous plants, is to use meristematic tip culturing techniques and tissue culturing to develop virus-free callus tissue that can then be used to generate new virus-free clones of the original plant.

This procedure is based on the fact that virus is usually not present in the actively growing shoot tip of an infected plant. This procedure has been used to clear many herbaceous cultivars of viruses.

3. Chemical Applications and 4. Biological Control
  • There are no chemical sprays or biological control approaches to eradicate viruses, although insecticides and biocontrol products can be used to control insect vectors.
4. Government Regulatory Measures
  • Management of insect vector populations in the field can be difficult to impossible unless coordinated on a regional basis but may be highly effective in closed production systems such as greenhouses or interiorscapes.
  • Plants Get Sick Too! An Introduction to Plant Diseases
  • Diagnosing Sick Plants
  • 20 Questions on Plant Diagnosis
  • Keeping Plants Healthy: An Overview of Integrated Plant Health Management
  • Viral Diseases of Plants
  • Bacterial Diseases of Plants
  • Fungal and Fungal-like Diseases of Plants
  • Nematode Diseases of Plants
  • Parasitic Higher Plants
  • Sanitation and Phytosanitation (SPS): The Importance of SPS in Global Movement of Plant Materials

These fact sheets can be found at OSU Extension’s Ohioline website: ohioline.osu.edu.

For detailed information on each of the IPM strategies, see the fourth fact sheet in this series, “Keeping Plants Healthy: An Overview of Integrated Plant Health Management.”

Search for these virus disease fact sheets on Ohioline:

  • Mosaic Virus Diseases of Vine Crops
  • Virus Diseases of Greenhouse Floral Crops
  • Wheat Yellow Mosaic
  • Barley Yellow Dwarf of Wheat, Oats and Barley
  • Tobacco Mosaic Virus

“Since there is no documented harm from eating blight-infected fruit, it may be tempting to simply cut off the infected portion. But the fruit will taste bitter and may be harboring other organisms that could cause food-borne illness.”

Ingham also notes that diseased fruit, even with the infected portion removed, should not be canned or frozen.

What if you have unblemished tomatoes growing on plants with leaves, stems or adjacent fruit showing signs of infection? These can be safely eaten, and even preserved, Ingham states.

“Don’t be tempted to can or preserve infected tomatoes,” says Ingham. “The virus can cause changes in the acidity of tomato fruit which is critical in safely preserving tomatoes. However, unblemished tomatoes can safely be canned, or even frozen,” she says.

According to Ingham, tomatoes are the most commonly home-canned item. “It’s important to use up-to-date, research-tested recipes to avoid the risk of botulism poisoning from home-canned tomatoes,” she says.

The University of Wisconsin-Extension offers the following tips for safe canning of tomatoes.

–Always add acid to tomato products. Whether pressure canning or boiling-water canning, research published in the 1990s shows that tomatoes may not have sufficient acid to avoid botulism toxin from forming, so a small amount of acid is always added.

–Add acid to tomatoes in the proper form. When adding acid, use bottled lemon juice because it has a standard level of acidity. Add 2 tablespoons bottled lemon juice per quart and 1 tablespoon per pint. Another option is to add citric acid, ½ teaspoon per quart or ¼ teaspoon per pint. Citric acid is less widely available, but is used mainly by large commercial canneries. Other acids such as ascorbic acid (vitamin C; Fruit Fresh) or acetic acid (vinegar) are not recommended.

–Avoid canning tomatoes that are diseased, harvested from dead vines, or damaged by frost. According to the USDA, diseased tomatoes, or those that are frost-damaged or harvested from dead vines may not develop the proper level of acidity for safe home canning.

–Always follow a research-tested, up-to-date recipe. The University of Wisconsin-Extension publication Tomatoes Tart and Tasty (B2605) was updated in 2008 to incorporate recent changes in the USDA Complete Guide to Home Canning. It is available online at http://learningstore.uwex.edu/pdf/B2605.PDF

And what about potatoes? “Use firm, disease-free potatoes for canning or freezing,” says Ingham.

Potatoes showing signs of late blight infection should not be used for home canning. Discard the whole potato rather than cutting off diseased portions since the fungus may spread to the interior. Since potatoes are a low-acid food, they should be pressure processed. Up-to-date recipes for vegetable canning in Wisconsin can be found in the UW-Extension publication Canning Vegetables Safely (B1159) and online at http://learningstore.uwex.edu/pdf/B1159.PDF

For complete food preservation information, visit http://www.foodsafety.wisc.edu

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The fungus is dispersed by wind-borne sporangia, which are produced on branched hyphae (sporangiophores) that emerge from the stomata of infected leaves in humid conditions (see diagram). When the sporangia land on a new leaf surface they usually undergo internal cleavage of the protoplasm to produce motile, uninucleate zoospores, which locate the leaf stomata, where they encyst and germinate to initiate infection.Within the leaf, the hyphae produce haustoria in the individual host cells. So P. infestans grows initially as a biotroph. However, the infected tissues soon die, and the fungus then spreads through the leaf as a necrotroph.

When P. infestans sporangia are studied in laboratory conditions, they are found to germinate either by releasing zoospores or by producing a hyphal outgrowth. The type of germination is governed by environmental conditions, especially temperature. As shown in the table below, the sporangia release zoospores at low temperatures (4 – 12 oC) but by hyphal outgrowth at higher temperatures (20 – 27oC).

Temperature
oC

Percent direct
germination

Percent zoospore production

The image below shows two sporangia of P. infestans germinating by hyphal outgrowth at 20oC. The sporangia have a typical lemon-shape, with a papilla at their tip (arrowheads). We see that germination has not occurred from the papilla (a region of thickened wall) but from just around it. At the opposite end of each sporangium we see a short stalk where the sporangium was detached from the supporting hypha.

The sequence below shows germination by production of zoospores at 12oC (but for a related fungus, Phytophthora palmivora). In this type of germination the multinucleate protoplasm of the sporangium undergoes cleavage to form several zoospores, then the papilla is digested enzymatically and the individual zoospores squeeze through the opening.

Control of potato blight

Potato blight has been a problem for over 150 years, and many approaches have been developed to control it. However, in the brief account below we shall see that the search for effective control measures is a continuing challenge – the fungus still poses a major threat, and it has evolved to overcome most of the control measures that were introduced over the years.

Fungicidal control

Control of potato blight traditionally relied on copper-based fungicides such as Bordeaux mixture (consisting of copper sulphate and calcium oxide). However, copper is potentially phytotoxic, so disease forecasting was developed to enable growers to predict when the environmental conditions were highly conducive to spread of the pathogen and thus when the growers needed to spray to protect their crops. Forecasting methods for blight epidemics differ in different countries but in Britain they are based on the “temperature-humidity rule” devised by Beaumont (1947). After a certain date (depending on locality) blight was found to develop within 15-22 days following a period when the temperature was not less than 10oC and the relative humidity was over 75% for 2 consecutive days. Radio stations now broadcast warnings of the Beaumont periods or updated versions of these in the early-morning farming programmes.

Copper is a broad-spectrum fungicide which acts as a protectant – it must be applied to prevent disease. It has been superseded by modern systemic fungicides, which move within the plant and can both protect and eradicate existing infections. These fungicides are much more specific in their mode of action. Chief among these for control of potato blight are the acylalanine fungicides such as metalaxyl and furalaxyl. They act specifically on the RNA polymerase of Phytophthora and closely related fungi. However, resistance to them can develop quickly in the pathogen population – it requires only a single gene mutation leading to a minor change in the RNA polymerase molecule. In many parts of the world, P. infestans is now resistant to these fungicides.

Haulm destruction

If P. infestans gets established on the potato foliage then sporangia can be washed down into the soil to infect the tubers, or the tubers can be contaminated with sporangia during crop harvesting. This can lead to rotting of the tubers during storage, and carry-over of inoculum from one season to the next. In order to minimise these problems it is common practice to destroy the foliage (the haulm) with sprays of sulphuric acid or herbicide 2-3 weeks before the tubers are lifted.

Resistance breeding

The cultivated potato (Solanum tuberosum) originates from the Andean region of South America, where there are several other species of the genus Solanum. The potato blight fungus also is thought to have its centre of origin in this region, so it is sensible to seek sources of genetic resistance to the pathogen in the wild potato plants of this region. The species Solanum demissum proved to be an important source of resistance, and by conventional plant breeding (crossing and back-crossing) in the 1940s and 1950s this resistance was bred into commercial potato cultivars. Four major resistant genes (termed R genes) were discovered and were introduced successively into commercial cultivars. However, within a few years of each R gene being introduced widely into potato cultivars, the fungus was found to be able to attack these plants – the resistance was overcome by new strains (termed physiologic races) of the pathogen that developed in response to the selection pressure imposed by the specific R genes. Thus, race 1 of the pathogen could cause disease of potato cultivars carrying the R1 gene, and so on. With four R genes there are a possible 16 combinations – you can breed potatoes with, for example, R1 and R2, or R1 and R4, or R1, R2, R3 and R4, etc. But eventually a pathogen race would emerge that had the corresponding virulence genes to overcome all these.

For long-term control, this form of resistance breeding based on a few “major resistance genes” seems destined to fail. So, many plant breeders now prefer to develop cultivars that have “polygenic” or “field resistance” to the pathogen. Such plants have combinations of several “minor” genes, none of which gives absolute resistance, but together they slow the rate of development of the fungus and enable the plant to tolerate infection.

Emergence of new pathogenic strains through sexual crossing.

Like many members of the Oomycota, P. infestans has two mating types, termed A1 and A2. It can undergo sexual reproduction only if both mating types are present in a population. Both mating types occur in Mexico, near the centre of origin of Solanum and thus presumably of its pathogen P. infestans. However, in Europe only the A1 strain was known to occur – presumably because it was introduced by chance on potatoes imported from elsewhere. Then, in 1978, the A2 mating type was discovered in Britain and is now also found commonly in much of continental Europe. How it arrived or originated here is still unclear, but this has the important consequence that the fungus can now generate genetic variation via recombination. The stage is now set for even more rapid emergence of new pathogenic variants, to overcome our continuing attempts to control this disease.

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If the farmer suspects a late blight infection is underway, she can remove a leaf from a living plant and place it in a small, covered glass jar. After the leaf’s volatile compounds have accumulated for 15 minutes or so, the cap is removed and the air is pumped from the jar into a reader device attached to the back of a smartphone.

Inside the smartphone reader is a strip of paper specially treated with organic dyes and nanoparticle sensors developed by the researchers. Upon interacting with the plant’s volatile compounds, the strip changes color to indicate the presence or absence of the pathogen. It’s like a home-pregnancy kit for tomatoes, or a strep test for tubers.

In proof-of-concept testing, Dr. Wei and his team found that the technology could accurately detect changes in 10 different plant odor molecules just two days after plants were inoculated with the pathogen that causes late blight, even before the effects were visible to the eye. The team’s results were published Monday in the journal Nature Plants.

The test can also distinguish between late blight infections and other tomato diseases that appear similar, such as Septoria leaf spot and a fungus that causes “early blight.”

Currently, farmers must send leaf samples to specialized labs if they can’t identify the onset of disease by eye. This costs more and delays identification of the disease, increasing the odds that the pathogen will spread.

EDITORIAL

Year : 2017 | Volume : 7 | Issue : 2 | Page : 21-22

Impact of Plant Diseases on Human Health
Abdullah M Al-Sadi
Department of Crop Sciences, College of Agricultural and Marine Sciences, Sultan Qaboos University, Al-Khod, Oman

Date of Web Publication 27-Apr-2017

Correspondence Address:
Abdullah M Al-Sadi
Department of Crop Sciences, College of Agricultural and Marine Sciences, Sultan Qaboos University, P.O. Box-34, Al-Khod 123
Oman

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/ijnpnd.ijnpnd_24_17

How to cite this article:
Al-Sadi AM. Impact of Plant Diseases on Human Health. Int J Nutr Pharmacol Neurol Dis 2017;7:21-2

Plant diseases have always been a challenge to plant growth and crop production in several parts of the world. Plant diseases can affect plants by interfering with several processes such as the absorbance and translocation of water and nutrients, photosynthesis, flower and fruit development, plant growth and development and cell division and enlargement. Plant diseases can be caused by different types of fungi, bacteria, phytoplasma, viruses, viroids, nematodes and other agents. The severity of diseases caused by these pathogens varies from mild symptoms to decline of the infected plants, depending on the aggressiveness of the pathogen, host resistance, environmental conditions, duration of infection and other factors. Plant disease symptoms vary with the infecting pathogen and the infected part and can include leaf spots, leaf blights, root rots, fruit rots, fruit spots, wilt, dieback and decline.
Although infection of plants by pathogens can have serious consequences on plant health, human health can be affected by one of the several ways. Viruses, bacteria and fungi that infect plants do not usually cause infection in humans. However, a study reported that Pepper mild mottle virus may react with the immune system of humans and induce a clinical symptom, but the study did not provide a clear evidence on the pathogenic role of this plant virus in humans. Despite the question about the possible direct effect of plant pathogens on humans, several plant pathogens can affect humans by reducing the available food or by contaminating human food with toxic compounds. Human health can also be affected by bacterial species living in agricultural soils and used as biocontrol agents for plant diseases.
Plant diseases are well known to reduce the food available to humans by ultimately interfering with crop yields. This can result in inadequate food to humans or lead to starvation and death in the worst cases. For example, late blight disease of potato, which is caused by Phytophthora infestans, destroyed potatoes which were the main crop in Ireland during 1845–1850. This resulted in the Great Famine (or Great Hunger), where about one million people died and another million emigrated to Canada, the USA and other countries. Rust is another example of a disease that threatens several crops, including wheat which is known to be one of the three most important crops in the world. Plant diseases continue to be a challenge to crop production in different countries, not only through reductions of crop yields, but indeed through reduction of fruit quality and nutritional value.
One of the most common ways by which plant diseases can affect humans is through the secretion of toxic metabolites ’mycotoxins’ by fungi infecting plant products. Although the fungi producing these mycotoxins infect plants but not humans, these mycotoxins can have direct effects on humans and animals, resulting in diseases and death. Examples of fungal species producing mycotoxins include Aspergillus flavus, Fusarium spp. and Penicillium spp. There are several groups of mycotoxins under which several types are included. Aflatoxins are one of the most common and serious groups (types = B1, B2, G1 and G2), which are produced by some Aspergillus species. Aflatoxin B1 is one of the most serious mycotoxins, because it is lethal at high doses and is carcinogenic to humans at low doses and can result in reduced liver function, vomiting and abdominal pain. Annual deaths in some parts of Africa due to the effect of aflatoxin have been reported to reach 250,000 annually. Mycotoxins can be found in several products, especially peanuts, pistachios and maize. Infection of these products by mycotoxin-producing fungi can occur in the field or during storage. In addition, mycotoxins can be consumed indirectly by humans through the consumption of meat from animals fed on food contaminated with mycotoxins.
Ergot is also a disease of several cereals including bread wheat. It is caused by some fungi belonging to the Claviceps genus. Consumption of bread produced from contaminated flour can result in ergotism disease in humans. Ergotism has been reported to result in death, loss of peripheral sensation or hallucinations.
Although most plant pathogens do not infect humans, it is advised to avoid consuming rotted or mouldy fruits and vegetables or food contaminated by toxin-producing fungi. Removing diseased parts of fruits may help reduce pathogen inoculum and rotted fruit parts. However, it may not ensure that all contamination has been excluded as some fungi and their toxins can diffuse into symptom-less parts of fruits. Although cooking may result in the decomposition of some mycotoxins, some mycotoxins are not destroyed by high heat. The effects of some mycotoxins can be reduced through the addition of some mycotoxin-binding agents or through deactivation.
More research is required on the direct effects of plant pathogens and diseases on humans. Special attention should be given to mycotoxin-producing fungi and their presence in human food. Efforts should be directed towards avoiding plant disease epidemics similar to the late blight disease of potatoes in Ireland through food diversification and the development of effective plant disease management strategies. Awareness of community about the ways by which plant diseases can affect human health is also important.
Acknowledgements
Thanks are due to Sultan Qaboos University and Oman Animal and Plant Genetic Resources Center for the support of the studies on fungi (EG/AGR/CROP/16/01).
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.

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3. Colson P, Richet H, Desnues C, Balique F, Moal V, Grob J-J et al. Pepper mild mottle virus, a plant virus associated with specific immune responses, fever, abdominal pains, and pruritus in humans. PLoS One 2010;5:e10041.
4. Wagacha JM, Muthomi JW. Mycotoxin problem in Africa: Current status, implications to food safety and health and possible management strategies. Int J Food Microbiol 2008;124:1-12. doi: 10.1016/j.ijfoodmicro.2008.01.008
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Scientists poised to win the race against rust disease and beyond

Damage inflicted by rust fungi is a significant constraint in food production across the globe. Cereals and many other important crops such as coffee, sugarcane, and soybean are impacted by these devastating pathogens. Traditional approaches using fungicides can be expensive and present environmental and health costs. Genetic resistance in crop development is often the best disease management strategy to prevent rust outbreaks. However, genetic resistance in crop varieties is frequently defeated by the emergence of new rust strains, turning what used to be a disease resistant plant variety to one that is completely vulnerable. The joint US and Australian research team has now generated the first haplotype-resolved genome sequences for the rust fungi causing oat crown rust and wheat stripe rust diseases, two of the most destructive pathogens in oat and wheat, respectively.

“Like humans, rust fungi contain two copies of each chromosome, which makes their genetics much more complicated than other types of fungi,” said Assistant Professor Melania Figueroa from the University of Minnesota. Figueroa co-led the sequencing effort for the oat crown rust fungus P. coronata f. sp. avenae along with Shahryar Kianian, research leader at the USDA-ARS Cereal Disease Laboratory and adjunct professor at the University of Minnesota. “A key advance of this work is that for the first time, separate genome assemblies were generated reflecting both of the two chromosome copies in the rust.”

In parallel, Postdoctoral Fellow Benjamin Schwessinger and Professor John Rathjen at the Australian National University applied similar approaches to develop an improved genome assembly of the stripe rust fungus, P. striiformis f. sp. tritici. By working together the two teams were able to combine their techniques and knowledge to achieve these breakthroughs much more rapidly than by working alone.

These studies represent a breakthrough in plant pathology as they now show how genetic diversity between the two chromosome copies can influence the emergence of new virulent pathogen strains.

Both studies uncovered a surprisingly high level of diversity between the two copies, suggesting that such variation likely serves as the basis to rapidly evolve new rust strains. “Reports from growers facing yield losses due to oat crown rust occur during most cropping seasons and the genome assemblies of this pathogen will help us understand the evolution of this pathogen and means to develop more resistant crops,” said Kianian, who coordinates annual rust surveys in the US in order to monitor the pathogen population in oat growing areas. The oat crown rust genomics study compared two strains from North Carolina and South Dakota with different virulent profiles which were obtained in 2012 as part of the routine USDA-ARS Rust Surveys.

The first author of this publication, Marisa Miller, is the awardee of a prestigious USDA-NIFA Postdoctoral Fellow and recently embarked on a study comparing the genomic composition of oat crown rust strains collected in 1990 and 2015. “In the last 25 years the population of oat crown rust has gained additional virulences, and we would like to understand how this has occurred. Miller’s work is essential to answering this question,” commented Figueroa.

“Oat crown rust is one of the most rapidly evolving rust pathogens,” explained University of Minnesota Adjunct Professor Peter Dodds of CSIRO Agriculture and Food. “So this work will really help understand how new rust diseases like the highly destructive Ug99 race of wheat stem rust can overcome resistance in crops.”

The publications describing the work in the oat crown rust and wheat stripe rust pathogens, both released in the current issue of mBio, will serve as a framework for future studies of virulence evolution in these pathogens as well as for applying similar approaches to the rust fungi causing many other major crop diseases.

The oat crown rust study was supported by the USDA-ARS-The University of Minnesota Standard Cooperative Agreement (3002-11031-00053115), The University of Minnesota Experimental Station USDA-National Institute of Food and Agriculture Hatch Funds (project MIN-22-058) and the Organization for Economic Co-operation and Development, the USDA-National Institute of Food and Agriculture Postdoctoral Fellowship Award (2017-67012-26117), a CSIRO Office of the Chief Executive Postdoctoral Fellowship, the Australian Grains Research Development Corporation (grant #US00067) and the Northern Research Station of the USDA Forest Service.

Plant disease

Nature and importance of plant diseases

Plant diseases are known from times preceding the earliest writings. Fossil evidence indicates that plants were affected by disease 250 million years ago. The Bible and other early writings mention diseases, such as rusts, mildews, and blights, that have caused famine and other drastic changes in the economy of nations since the dawn of recorded history. Other plant disease outbreaks with similar far-reaching effects in more recent times include late blight of potato in Ireland (1845–60); powdery and downy mildews of grape in France (1851 and 1878); coffee rust in Ceylon (now Sri Lanka; starting in the 1870s); Fusarium wilts of cotton and flax; southern bacterial wilt of tobacco (early 1900s); Sigatoka leaf spot and Panama disease of banana in Central America (1900–65); black stem rust of wheat (1916, 1935, 1953–54); southern corn leaf blight (1970) in the United States; Panama disease of banana in Asia, Australia, and Africa (1990 to present); and coffee rust in Central and South America (1960, 2012 to present). Such losses from plant diseases can have a significant economic impact, causing a reduction in income for crop producers and distributors and higher prices for consumers.

Loss of crops from plant diseases may also result in hunger and starvation, especially in less-developed countries where access to disease-control methods is limited and annual losses of 30 to 50 percent are not uncommon for major crops. In some years, losses are much greater, producing catastrophic results for those who depend on the crop for food. Major disease outbreaks among food crops have led to famines and mass migrations throughout history. The devastating outbreak of late blight of potato (caused by the water mold Phytophthora infestans) that began in Europe in 1845 brought about the Great Famine that caused starvation, death, and mass migration of the Irish. Of Ireland’s population of more than eight million, approximately one million (about 12.5 percent) died of starvation or famine-related illness, and 1.5 million (almost 19 percent) emigrated, mostly to the United States, as refugees from the destructive blight. This water mold thus had a tremendous influence on economic, political, and cultural development in Europe and the United States. During World War I, late blight damage to the potato crop in Germany may have helped end the war.

Diseases—a normal part of nature

Plant diseases are a normal part of nature and one of many ecological factors that help keep the hundreds of thousands of living plants and animals in balance with one another. Plant cells contain special signaling pathways that enhance their defenses against insects, animals, and pathogens. One such example involves a plant hormone called jasmonate (jasmonic acid). In the absence of harmful stimuli, jasmonate binds to special proteins, called JAZ proteins, to regulate plant growth, pollen production, and other processes. In the presence of harmful stimuli, however, jasmonate switches its signaling pathways, shifting instead to directing processes involved in boosting plant defense. Genes that produce jasmonate and JAZ proteins represent potential targets for genetic engineering to produce plant varieties with increased resistance to disease.

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Humans have carefully selected and cultivated plants for food, medicine, clothing, shelter, fibre, and beauty for thousands of years. Disease is just one of many hazards that must be considered when plants are taken out of their natural environment and grown in pure stands under what are often abnormal conditions.

Many valuable crop and ornamental plants are very susceptible to disease and would have difficulty surviving in nature without human intervention. Cultivated plants are often more susceptible to disease than are their wild relatives. This is because large numbers of the same species or variety, having a uniform genetic background, are grown close together, sometimes over many thousands of square kilometres. A pathogen may spread rapidly under these conditions.

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