Cercospora leaf spot treatment

Creative Commons Flickr photo courtesy of PHOTOFARMER.

Cerospora is known as both Leaf Blight and Leaf Spot. It’s a common fungus that infects many food crops including carrots, grain legumes, peppers, corn, soybeans, and coffee. Many gardeners and farmers are familiar with this disease and with how its sudden appearance can spell doom for a crop.

Host Plants

There are many host plants in the cornucopia to which Cercospora can attach. Those listed above, especially carrots and legumes, are the most common. Eggplants, tomatoes, rice, sorghum, cotton, and others are also susceptible to this blight. It can infect plants at any stage of development, usually targeting leaves, stems, fruits, pods and seeds.


It manifests in much the same way on every plant infected, though some nuances for individual species are also possible. In carrots and other thin-leafed plants, it will cause the leaf margins to curl and move towards the withers and stems. On broader leaves, it will manifest as pale-tan to gray spots in semi-round shape and spread to connect those dots into one large blight.

In darker leaves, it can appear as a purplish color with a lighter-colored center.

In all cases, as the spots elongate and spread to infect most of the leaf and/or stem, they will become gray and “fuzzy” as spores are formed. Plants with a large portion of their leaves covered in gray are considered completely infested and “blighted.” Destruction is often the only recourse.

Life Cycle

Like most fungi, Cercospora will infect a host plant and grow until spores form. These will be transferred to seeds, the ground, mulch, compost, etc. and lie dormant until conditions are ripe (usually late spring) for infestation.

Infected plants can seem perfectly healthy until the right humid, damp, warm conditions occur and then the spores and infection can begin quickly and within days have infested much of the host.

How This Leaf Fungus Impacts the Plant

On most plants, it will spread quickly under good conditions and can severely maim or kill the plant within a week or two. Mild infections can lead to infected seeds and fruits, which spreads the spores of the blight to the next generation.

Fruit production will be stunted as will plant and foliage growth. Some plants, if infected early, will die.

How to Prevent Leaf Spot Diseases

As with most fungi, prevention means allowing good aeration around the plants, proper spacing between plants, hygienic conduct such as using only clean seeds, and careful management of moisture and watering.

Damp, humid conditions are the Cercospora’s preferred habitat, so watering at ground level is a must.

Treating Cercospora Leaf Spot

Once infected, plants can be treated if it’s done early. Fungicides work well with this blight at this stage. If the plant is more than 20% infested, then destruction may be the only choice to keep other plants from succumbing.


New fungicides for Cercospora leaf spot control in sugarbeets

SipcamAdvan announced the release of two new fungicides for the control of Cercospora leaf spot in sugarbeets for 2015. The products are Minerva (tetraconazole 1.0 pound per gallon) and Minerva Duo (tetraconazole 0.73 pounds per gallon plus triphenyltin OH 2 pounds per gallon). The products have been registered for only one application per season.

From the label, “Crops other than sugarbeet must not be grown within 120 days following the last application of Minerva Duo. Small grains can be planted 45 days following last application of this product. Applications may be supplemented by use of other triphenyltin hydroxide-based products provided the total seasonal use rate of triphenyltin hydroxide from all products does not exceed 0.5 pounds per acre. Total seasonal application of triphenyltin hydroxide based products in Michigan cannot exceed 0.75 pounds per acre.”

The labels may be accessed here: Minerva and Minerva Duo

Some results on Minerva have been reported in “Efficacy of application of foliar fungicides for control of Cercospora leaf spot in sugarbeet” (page 67-70) by Michigan State University Extension and MSU’s AgBioResearch.

Dr. Kirk’s work is funded in part by MSU’s AgBioResearch.


This common but overlooked airborne pathogen is known to cause diseases of unknown cause. Some online documents state this cancer-causing, mental illness-inducing microorganism is not zoonotic. That’s wrong! It’s carried and shed by bats in their feces. And healthy people can get it, too.

My coworkers and I, all immunocompetent, got Disseminated Histoplasmosis from roosting bats, that shed the fungus in their feces. The doctors said we couldn’t possibly have it, since we all had intact immune systems. The doctors were wrong.

More than 100 outbreaks have occurred in the U.S. since 1938, and those are just the ones that were figured out, since people go to different doctors. One outbreak was over 100,000 victims in Indianapolis. 80-90+% of people in some areas have been infected, and it can lay dormant for up to 40 years in the lungs and/or adrenals.

This underdiagnosed airborne infectious disease mimics the flu and can cause malignancies, precancerous conditions, rheumatological diseases, connective tissue diseases, heart disease, autoimmune symptoms, inflammation, adrenal insufficiency, seizures, migraines, hydrocephalus, hallucinations, etc. and is often undiagnosed/misdiagnosed in immunocompetent people.

It’s known to cause hematological malignancies, and doctors claim leukemia patients go into remission when given antifungal. My friend in another state who died from lupus lived across the street from a bat colony. An acquaintance with alopecia universalis and whose mother had degenerative brain disorder has bat houses on their property.

Researchers claim the subacute type is more common than believed. It’s known to at least “mimic” autoimmune diseases and cancer and known to give false-positives in PET scans. But no one diagnosed with an autoimmune disease or cancer is screened for it. In fact, at least one NIH paper states explicitly that all patients diagnosed with sarcoidosis be tested for it, but most, if not all, are not. Other doctors are claiming sarcoidosis IS disseminated histoplasmosis.

What if this infection, that made me and my coworkers so ill, isn’t rare in immunocompetent people? What if just the diagnosis is rare, since most doctors ignore it?

Older documents state people who spend a lot of time in a building with roosting bats, in caves, working as landscapers, construction workers, pest control workers, etc. are known to get Disseminated Histoplasmosis, but the info appears to have been lost, for the most part. And now bat conservationists encourage people to leave bats in buildings/homes. What a terrible mistake they’ve made.

This pathogen parasitizes the reticuloendothelial system/invades macrophages, can infect and affect the lymphatic system and all tissues/organs, causes inflammation, granulomas, and idiopathic (unknown cause) diseases and conditions, including hematological malignancies, autoimmune symptoms, myelitis, myositis, vasculitis, panniculitis, dysplasia, hyperplasia, etc. It causes hypervascularization, calcifications, sclerosis, fibrosis, necrosis, eosinophilia, leukopenia, anemia, neutrophilia, pancytopenia, thrombocytopenia, hypoglycemia, cysts, abscesses, polyps, stenosis, perforations, GI problems, hepatitis, focal neurologic deficits, etc.

Many diseases it might cause are comorbid with other diseases it might cause, for example depression/anxiety/MS linked to Crohn’s.

The fungus is an Oxygenale and therefore consumes collagen. It’s known to cause connective tissue diseases (Myxomatous degeneration?), rheumatological conditions, seizures, and mental illness. Fungal hyphae carry an electrical charge and align under a current. It causes RNA/DNA damage. It’s known to cause delusions, wild mood swings (pseudobulbar affect?), and hallucinations. It’s most potent in female lactating bats, because the fungus likes sugar (lactose) and nitrogen (amino acids, protein, neurotransmitters?), releasing lactase and proteinases to obtain them. What about female lactating humans…postpartum psychosis (and don’t some of these poor women also have trouble swallowing)? The bats give birth late spring/summer, and I noticed suicide rates spike in late spring/early summer. It’s known to cause retinal detachment, and retinal detachments are known to peak around June-July/in hot weather. A map of mental distress and some diseases appear to almost perfectly overlay a map of Histoplasmosis. Johns Hopkins linked autism to an immune response in the womb. Alzheimer’s was linked to hypoglycemia, which can be caused by chronic CNS histoplasmosis. Cancer is known to occur more often near rivers than in mountains or deserts, just like this infection.

The bats eat moths, which are attracted to blue and white city lights that simulate the moon the moths use to navigate. Bats feed up to 500 feet in the air and six miles away in any direction from their roost, but not when it’s raining or when the temperature is less than approximately 56° F. The fungus can grow in bird feces, but birds don’t carry it because their body temperature is too high, killing the fungus.

I believe the “side effects” of Haldol (leukopenia and MS symptoms) might not always be side effects but just more symptoms of Disseminated Histoplasmosis, since it causes leukopenia and MS symptoms. What about the unknown reason why beta receptor blockers cause tardive dyskinesia? The tinnitus, photophobia, psychosis “caused” by Cipro? Hypersexuality and leukemia “caused” by Abilify? Humira linked to lymphoma, leukemia and melanoma in children? Disseminated Histoplasmosis is known to cause enteropathy, so could some people thought to have nonsteroidal anti-inflammatory drug enteropathy have it and taking NSAIDs for the pain/inflammation it causes, and the NSAIDs aren’t the actual culprit?

From my experience, I learned that NO doctor, at least in DFW, will suspect subacute and/or progressive disseminated histoplasmosis in immunocompetent people. Some doctors, at least the ones I went to, will actually REFUSE to test for it, even when told someone and their coworkers have all the symptoms and spend a lot of time in a building with bats in the ceiling. Victims will be accused of hypochondriasis. (My doctors told me only farmer’s get it, it’s only in bird feces, and it only infects the lungs…wrong, wrong, and wrong!) In fact, the first doctor to diagnose me was a pulmonologist, and the only reason he examined me was to try to prove that I didn’t have it, when I really did. No doctor I went to realized bats carry the fungus. And NO doctor I went to in DFW, even infectious disease “experts,” understand the DISSEMINATED form, just the pulmonary form, and the only test that will be done by many doctors before they diagnose people as NOT having it is an X-ray, even though at least 40-70% of victims will have NO sign of it on a lung X-ray. It OFTEN gives false-negatives in lab tests (some people are correctly diagnosed only during an autopsy after obtaining negative test results) and cultures may not show growth until after 6-12 weeks of incubation (but some labs report results after 2 weeks).

One disease of unknown cause that could be caused by Disseminated Histoplasmosis: I suspect, based on my and my coworker’s symptoms (during our “rare” infectious disease outbreak) and my research, that interstitial cystitis and its comorbid conditions can be caused by disseminated histoplasmosis, which causes inflammation throughout the body, causes “autoimmune” symptoms, and is not as rare as believed. I read that “interstitial cystitis (IC) is a chronic inflammatory condition of the submucosal and muscular layers of the bladder, and the cause is currently unknown. Some people with IC have been diagnosed with other conditions such as irritable bowel syndrome (IBS), fibromyalgia, chronic fatigue syndrome, allergies, and Sjogren’s syndrome, which raises the possibility that interstitial cystitis may be caused by mechanisms that cause these other conditions. In addition, men with IC are frequently diagnosed as having chronic nonbacterial prostatitis, and there is an extensive overlap of symptoms and treatment between the two conditions, leading researchers to posit that the conditions may share the same etiology and pathology.” Sounds like Disseminated Histoplasmosis, doesn’t it?

My coworkers and I were always most ill around April/May/June, presumably since the Mexican Free-tail bats gave birth in Texas during May (and the fungus was most potent), and fall/Thanksgiving to December, for some unknown reason (maybe migrating bats from the north?). We had GI problems, liver problems, weird rashes (erythema nodosum, erythema multiforme, erythema marginatum/annulare, etc.), plantar fasciitis, etc., and I had swollen lymph nodes, hives, lesions, abdominal aura, and started getting migraines and plantar fasciitis in the building, and I haven’t had them since I left. It gave me temporary fecal incontinence, seizures, dark blood from my intestines, tinnitus, nystagmus, blurry vision/floaters/flashes of light, benign paroxysmal positional vertigo, isolated diastolic hypertension, what felt like burning skin, various aches and pains (some felt like pin pricks and pinches), tingling, tremors, “explosions” like fireworks in my head while sleeping, and temporary blindness. Suddenly I was allergic to Comice pears (latex fruit allergy or oral allergy syndrome?). I had insomnia (presumably from the fungus acidifying the blood, releasing adrenaline) and parasomnias. It felt like strong bursts of electrical shocks or steady electrical currents in my body, which now feel like low electrical currents at times, mostly at night. I suddenly had symptoms of several inflammatory/autoimmune diseases, including Fibromyalgia, Sarcoidosis, ALS, MS, Sjogren’s syndrome, etc. that have disappeared since leaving the area and taking nothing but Itraconazole antifungal.

No one, including doctors (we all went to different ones), could figure out what was wrong with us, and I was being killed by my doctor, who mistakenly refused to believe I had it and gave me progressively higher and higher doses of Prednisone (2 years after I already had Disseminated Histoplasmosis) after a positive ANA titer, until I miraculously remembered that a visiting man once told my elementary school class that bats CARRY histoplasmosis. So much of it that they evolved to deal with the photophobia and tinnitus it causes by hunting at night by echolocation. There’s a lot more. I wrote a book about my experience with Disseminated Histoplasmosis called “Batsh#t Crazy,” because bats shed the fungus in their feces and it causes delusions and hallucinations, I suspect by the sclerotia fungal mycelia can form emitting hallucinogens (like psilocybin and dimethyltryptamine) along with inflammation in the CNS. (Schizophrenics have 2X of a chemical associated with yeast, part of the fungal life cycle.)

Thank you for your time,

Susan McIntyre

P.S. Doesn’t this infection share all the same symptoms with Gulf War Syndrome?

By: Kevin Ong and Ashley Brake

Members of the fungal genus Cercospora are pathogens of many types of plants. On roses, the fungus Cercospora rosicola can cause premature defoliation when infection is severe. Cercospora leaf spot is often mistakenly identified as black spot disease.

Although the symptoms are similar and Cercospora leaf spot is not as well known, it is a fairly common foliar disease of roses in Texas.

An early symptom of Cercospora leaf spot is the appearance on the leaves of tiny maroon to purple spots or lesions (Fig. 1) that vary in size (approximately 1 centimeter). The edges of the lesions are smooth, as opposed to the fringed or feathered look caused by black spot of roses.

As the disease progresses, the center of the spots turns gray or tan while the margins remain maroon to dark purple. Severely infected leaves usually develop chlorosis (yellowing), which leads to premature defoliation. Cercospora leaf spot often begins on the lower leaves and progresses upwards. The severity of the symptoms can vary depending on the resistance of the rose cultivar to this disease.


C. rosicola affects the plant leaves; damage lesions are not often found on other plant parts. Newly developing leaves are the most susceptible to infection. In Texas, Cercospora leaf spot tends to begin in the spring a little earlier or about the same time as black spot disease, although it can occur anytime during the growing season. Wet, mild to warm conditions encourage disease development and the formation of spores that spread through the air. Free moisture (presence of water) on foliage helps initiate spore germination and subsequent infection. Eventually, fruiting bodies (where new spores develop) will appear within the lesions (Fig. 2). Under humid conditions, tufts of spores on these lesions are visible under magnification.


Preventive measures are the best approach to managing Cercospora leaf spot. Cultural practices that help prevent and reduce disease incidence include:

  • Avoid overwatering or watering in the late evening to reduce free moisture.
  • Avoid overhead watering where the water can dislodge and disperse spores to uninfected plants.
  • Space plants to encourage air movement and reduce high humidity levels.

Fungicides are available to manage Cercospora leaf spot. Many of the conventional products used to prevent black spot of roses will also protect against Cercospora leaf spot. These fungicides contain the active ingredient chlorothalonil (OrthoMax Garden Disease Control) and myclobutanil (Immunox).

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Cercospora Leaf Spot: Learn About The Treatment Of Cercospora

Cercospora fruit spot is a common disease of citrus fruits but it also affects many other crops. What is cercospora? The disease is fungal and survives on any affected fruit in soil from the previous season. Read on to learn more.

What is Cercospora?

Fruit and crop management is an ongoing process. One of the key aspects is inspection of fruits and vegetables for disease and preventative measures early in the season to protect the crop. Cercospora leaf spot or fruit spot is a fungus that requires moisture and is wind borne. The disease survives in dormant lesions from previous season fruit. Once warm, wet weather starts, the fungus disseminates condida, which are similar to a spore. These condida transfer from rain splash, mechanical transfer, or wind.

The full name for this fungal disease is Pseudocercospora angolensis. Leaves of affected plants will produce circular spots with light brown to grayish centers. When the rainy season sets in, these spots become dark and almost black with a yellow halo. Leaves generally fall off after a period. Stem lesions are not frequent but you may find twig dieback.

The fruit gets dark spots that may produce a tumor-like growth surrounded by a halo. These will sink in and develop necrosis. Early fruit that is immature will drop. Cercospora fungus in mature fruits will dry up and become tough.

Symptoms are slightly different on various crops. Okra will develop a sooty mold on leaves and carrots get more necrotic spots on young leaves. Roses will develop cercospora leaf spot as lesions and dark sunken areas on the leaves. Other crops affected are:

  • Bean
  • Beetroot
  • Capsicum (peppers)
  • Watercress
  • Avocado
  • Fig
  • Coffee

Cercospora Fungus Damage

In well managed crops, it does not usually run rampant but the disease can produce unsavory fruit and diminish harvest. To preserve the best fruit, treatment of cercospora should start with cleanup of downed fruit at the end of the season and commence with fungicides applied in the spring.

In small infestations, the few fruit affected will not limit crop yield much, but in heavily diseased plants, the entire crop may become useless. Not only are fruits unsightly and unappetizing, but they are not juicy or tasty. The necrotic areas from cercospora fruit spot are dry, tough, and woody in some species, creating a poor eating experience.

These rather ugly fruits are impossible to sell and provide a dilemma as to disposal. In the compost pile, the fungus can survive unless temperatures are hot enough to destroy the condida. Fruit cleanup in affected areas is necessary to prevent the spread of cercospora leaf spot in the next season’s crop.

Treatment of Cercospora

In addition to cleaning up dropped fruit, it may be necessary to destroy heavily infected crops in fall. There are also fungal sprays and dusts recommended for control of cercospora. Treatment must begin in the wet, rainy season when temperatures have warmed.

It is advised to rotate the chemicals used yearly to minimize the chance of resistance. A second application may be required in wet, humid regions. Use all sprays and dusts in a manner consistent with the manufacturer’s instructions. If you are in doubt, use a licensed professional to apply the treatments.

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