ARGT is a neurological condition and affects the brain. Sheep may at first appear perfectly normal, but if driven for a hundred metres or so, the slight stress will cause mildly affected animals to lag behind the rest of the flock and exhibit a high-stepping gait. More seriously affected animals may lose co-ordination and stumble, but will usually recover and join the rest of the flock if left quietly alone. The most-severely affected sheep will fall repeatedly and may be unable to get up. These sheep are likely to die, with death sometimes occurring within a few hours of the first symptoms appearing.

Annual ryegrass toxicity (ARGT) is the poisoning of livestock from toxin contained in bacterially infected annual ryegrass ("Lolium rigidum"). The toxin is produced by the bacterium "Rathayibacter toxicus" (formerly "Clavibacter toxicus"), which is carried into the ryegrass by the nematode "Anguina funesta".

Symptoms are neurological and may develop one to two weeks after exposure to infected pasture. Symptoms may include head shaking and irregular eye movements, changes in gait, stiffness, staggering and falling. Recumbent animals may display tetanic spasms and may die through misadventure, dehydration, starvation, loss of rumen function or predation. In the case of horses, the animal may quiver or tremble, be easily startled and be awkward to handle. More severely affected animals may repeatedly nod their head, show a tendency to splay their legs, and stumble and fall. The hind-quarters, moreover, may become paralysed.

Perennial ryegrass staggers is poisoning by peramine, lolitrem B, and other toxins that are contained in perennial ryegrass ("Lolium perenne"), and produced by the endophyte fungus "Neotyphodium lolii" which can be present in all parts of the grass plant, but tends to be concentrated in the lower part of the leaf sheaths, the flower stalks and seeds. This condition can affect horses, cattle, sheep, farmed deer and llamas. It regularly occurs in New Zealand and is known spasmodically from Australia, North and South America, and Europe.

The symptoms of organophosphate poisoning include muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis. Other symptoms include hypertension, and hypoglycemia.

Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur.

The effects of organophosphate poisoning on muscarinic receptors are recalled using the mnemonic SLUDGEM (salivation, lacrimation, urination, defecation, gastrointestinal motility, emesis, miosis) An additional mnemonic is MUDDLES: miosis, urination, diarrhea, diaphoresis, lacrimation, excitation, and salivation.

The onset and severity of symptoms, whether acute or chronic, depends upon the specific chemical, the route of exposure (skin, lungs, or GI tract), the dose, and the individuals ability to degrade the compound, which the PON1 enzyme level will affect.

Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

Cholinergic syndrome occurs in acute poisonings with OP pesticides and is directly related to levels of AChE activity. Symptoms include miosis, sweating, lacrimation, gastrointestinal symptoms, respiratory difficulties, shortness of breath, slowed heart rate, cyanosis, vomiting, diarrhea, trouble sleeping, as well as other symptoms. Along with these central effects can be seen and finally seizures, convulsions, coma, respiratory failure. If the person survives the first day of poisoning personality changes can occur, aggressive events, psychotic episodes, disturbances and deficits in memory and attention, as well as other delayed effects. When death occurs, it is most commonly due to respiratory failure from the combination of central and peripheral effects, paralysis of respiratory muscles and depression of the brain respiratory center. For people afflicted with cholinergic syndrome, atropine sulfate combined with an oxime is used to combat the effects of the acute OP poisoning. Diazepam is sometimes also administered in combination with the atropine and oximes.

The intermediate syndrome (IMS) appears in the interval between the end of the cholinergic crisis and the onset of OPIDP. Symptoms associated with IMS manifest within 24–96 hours after exposure. The exact etiology, incidence, and risk factors associated with IMS are not clearly understood, but IMS is recognized as a disorder of neuromuscular junctions. IMS occurs when a person has a prolonged and severe inhibition of AChE and has been linked to specific OP pesticides such as methylparathion, dichlorvos, and parathion. Patients present with increasing weakness of facial, neck flexor and respiratory muscles.

OPIDP occurs in a small percentage of cases, roughly two weeks after exposure, where temporary paralysis occurs. This loss of function and ataxia of peripheral nerves and spinal cord is the phenomenon of OPIDP. Once the symptoms begin with shooting pains in both legs, the symptoms continue to worsen for 3–6 months. In the most severe cases quadriplegia has been observed. Treatment only affects sensory nerves, not motor neurons which may permanently lose function. The aging and phosphorylation of more than 70% of functional NTE in peripheral nerves is one of the processes involved in OPIDP. Standard treatments for OP poisoning are ineffective for OPIDP.

COPIND occurs without cholinergic symptoms and is not dependent on AChE inhibition. COPIND appears with a delay and is long lasting. Symptoms associated with COPIND include cognitive deficit, mood change, autonomic dysfunction, peripheral neuropathy, and extrapyramidal symptoms. The underlying mechanisms of COPIND have not been determined, but it is hypothesized that withdrawal of OP pesticides after chronic exposure or acute exposure could be a factor.

Tin poisoning refers to the toxic effects of tin and its compounds. Cases of poisoning from tin metal, its oxides, and its salts are "almost unknown"; on the other hand certain organotin compounds are almost as toxic as cyanide.

Epidemic dropsy is a form of edema of extremities due to poisoning by "Argemone mexicana" (Mexican prickly poppy).

Epidemic dropsy is a clinical state resulting from use of edible oils adulterated with "Argemone mexicana" seed oil.

Sanguinarine and dihydrosanguinarine are two major toxic alkaloids of argemone oil, which cause widespread capillary dilatation, proliferation and increased capillary permeability. When mustard oil is adulterated deliberately (as in most cases) or accidentally with argemone oil, proteinuria (specifically loss of albumin) occurs, with a resultant edema as would occur in nephrotic syndrome.

Other major symptoms are pitting edema of extremities, headache, nausea, loose bowels, erythema, glaucoma and breathlessness.

Leakage of the protein-rich plasma component into the extracellular compartment leads to the formation of edema. The haemodynamic consequences of this vascular dilatation and permeability lead to a state of relative hypovolemia with a constant stimulus for fluid and salt conservation by the kidneys. Illness begins with gastroenteric symptoms followed by cutaneous erythema and pigmentation. Respiratory symptoms such as cough, shortness of breath and orthopnoea, progressing to frank right-sided congestive cardiac failure, are seen.

Mild to moderate anaemia, hypoproteinaemia, mild to moderate renal azotemia, retinal haemorrhages, and glaucoma are common manifestations. There is no specific therapy. Removal of the adulterated oil and symptomatic treatment of congestive cardiac failure and respiratory symptoms, along with administration of antioxidants and multivitamins, remain the mainstay of treatment.

Epidemic dropsy occurs as an epidemic in places where use of mustard oil, (from the seeds of Brassica "juncea" commonly known as Indian mustard ) as cooking medium is common.

Chronic poisoning usually presents with symptoms affecting multiple systems, but is associated with three main types of symptoms: gastrointestinal, neuromuscular, and neurological. Central nervous system and neuromuscular symptoms usually result from intense exposure, while gastrointestinal symptoms usually result from exposure over longer periods. Signs of chronic exposure include loss of short-term memory or concentration, depression, nausea, abdominal pain, loss of coordination, and numbness and tingling in the extremities. Fatigue, problems with sleep, headaches, stupor, slurred speech, and anemia are also found in chronic lead poisoning. A "lead hue" of the skin with pallor and/or lividity is another feature. A blue line along the gum with bluish black edging to the teeth, known as a Burton line, is another indication of chronic lead poisoning. Children with chronic poisoning may refuse to play or may have hyperkinetic or aggressive behavior disorders. Visual disturbance may present with gradually progressing blurred vision as a result of central scotoma, caused by toxic optic neuritis.

Secondary poisoning is poisoning that can result when one organism comes into contact with or ingests another organism that has poison in its system. It typically occurs when a predator eats an animal, such as a mouse, rat, or insect, that has previously been poisoned by a commercial pesticide. If the level of toxicity in the prey animal is sufficiently high, it will harm the predator.

Mammals susceptible to secondary poisoning include humans, with infants and small children being the most susceptible. Pets such as cats and dogs, as well as wild birds, also face significant risk of secondary poisoning.

In acute poisoning, typical neurological signs are pain, muscle weakness, numbness and tingling, and, rarely, symptoms associated with inflammation of the brain. Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms. Lead's effects on the mouth include astringency and a metallic taste. Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Absorption of large amounts of lead over a short time can cause shock (insufficient fluid in the circulatory system) due to loss of water from the gastrointestinal tract. Hemolysis (the rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin in the urine. Damage to kidneys can cause changes in urination such as decreased urine output. People who survive acute poisoning often go on to display symptoms of chronic poisoning.

Various pesticides such as rodenticides may cause secondary poisoning. Some pesticides require multiple feedings spanning several days; this increases the time a target organism continues to move after ingestion, raising the risk of secondary poisoning of a predator.

Tin has no known natural biological role in living organisms. It is not easily absorbed by animals and humans. The low toxicity is relevant to the widespread use of tin in dinnerware and canned food. Nausea, vomiting and diarrhea have been reported after ingesting canned food containing 200 mg/kg of tin. This observation led, for example, the Food Standards Agency in the UK to propose upper limits of 200 mg/kg. A study showed that 99.5% of the controlled food cans contain tin in an amount below that level. However un-lacquered tin cans with food of a low pH for example fruits and pickled vegetables can contain elevated concentrations of tin.

The toxic effects of tin compounds is based on the interference with the iron and copper metabolism. For example, it affects heme and cytochrome P450, and decreases their effectiveness.

Organotin compounds can be very toxic. "Tri-"n"-alkyltins" are phytotoxic and, depending on the organic groups, can be powerful bactericides and fungicides. Other triorganotins are used as miticides and acaricides.

Tributyltin (TBT) was extensively used in marine antifouling paints, until discontinued for leisure craft due to concerns over longer term marine toxicity in high traffic areas such as marinas with large numbers of static boats.

Animal lead poisoning (also known as avian plumbism, or avian saturnism for birds) is a veterinary condition and pathology caused by increased levels of the heavy metal lead in animal's body.

Lead interferes with a variety of body and natural processes.

It is toxic to many organs and tissues including the heart, bones, intestines, kidneys, and reproductive and nervous systems. It mainly affects the haematopoietic system. It also affects the sulfhydryl group containing enzymes and also thiol content of erythrocyte. It inhibits the enzyme delta amino levaminic acid dehydrogenase enzyme(ALA) which is present in the rbc.

It is therefore particularly toxic to young animals, mainly dogs and cattle.

As in humans, "animal lead poisoning" may be acute (from intense exposure of short duration) or chronic (from repeat low-level exposure over a prolonged period). Acute intoxication can quickly lead to death.

The olfactory system is the system related to the sense of smell (olfaction). Many fish activities are dependent on olfaction, such as: mating, discriminating kin, avoiding predators, locating food, contaminant avoidance, imprinting and homing. These activities are referred to as “olfactory-mediated.” Impairment of the olfactory system threatens survival and has been used as an ecologically relevant sub-lethal toxicological endpoint for fish within studies. Olfactory information is received by sensory neurons, like the olfactory nerve, that are in a covered cavity separated from the aquatic environment by mucus. Since they are in almost direct contact with the surrounding environment, these neurons are vulnerable to environmental changes. Fish can detect natural chemical cues in aquatic environments at concentrations as low as parts per billion (ppb) or parts per trillion (ppt).

Studies have shown that exposures to metals, pesticides, or surfactants can disrupt fish olfaction, which can impact their survival and reproductive success. Many studies have indicated copper as a source of olfactory toxicity in fishes, among other common substances. Olfactory toxicity can occur by multiple, complex Modes of Toxic Action.

A toxic heavy metal is any relatively dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts. The term has particular application to cadmium, mercury, lead and arsenic, all of which appear in the World Health Organisation's list of 10 chemicals of major public concern. Other examples include manganese, chromium, cobalt, nickel, copper, zinc, selenium, silver, antimony and thallium.

Heavy metals are found naturally in the earth. They become concentrated as a result of human caused activities and can enter plant, animal, and human tissues via inhalation, diet, and manual handling. Then, they can bind to and interfere with the functioning of vital cellular components. The toxic effects of arsenic, mercury, and lead were known to the ancients, but methodical studies of the toxicity of some heavy metals appear to date from only 1868. In humans, heavy metal poisoning is generally treated by the administration of chelating agents. Some elements otherwise regarded as toxic heavy metals are essential, in small quantities, for human health.

Thallium and its compounds are often highly toxic. Contact with skin is dangerous, and adequate ventilation should be provided when melting this metal. Many thallium(I) compounds are highly soluble in water and are readily absorbed through the skin. Exposure to them should not exceed 0.1 mg per m of skin in an 8-hour time-weighted average (40-hour work week). Thallium is a suspected human carcinogen.

Part of the reason for thallium's high toxicity is that, when present in aqueous solution as the univalent thallium(I) ion (Tl), it exhibits some similarities with essential alkali metal cations, particularly potassium (due to similar ionic radii). It can thus enter the body via potassium uptake pathways. Other aspects of thallium's chemistry differ strongly from that of the alkali metals, such as its high affinity for sulfur ligands. Thus, this substitution disrupts many cellular processes (for instance, thallium may attack sulfur-containing proteins such as cysteine residues and ferredoxins). Thallium's toxicity has led to its use (now discontinued in many countries) as a rat and ant poison.

Among the distinctive effects of thallium poisoning are hair loss (which led to its initial use as a depilatory before its toxicity was properly appreciated) and damage to peripheral nerves (victims may experience a sensation of walking on hot coals), although the loss of hair only generally occurs in low doses; in high doses the thallium kills before this can take effect. Thallium was once an effective murder weapon before its effects became understood and an antidote (Prussian blue) discovered. Indeed, thallium poisoning has been called the "poisoner's poison" since thallium is colorless, odorless and tasteless; its slow-acting, painful and wide-ranging symptoms are often suggestive of a host of other illnesses and conditions.

Flacherie (literally: "flaccidness") is a disease of silkworms, caused by silkworms eating infected or contaminated mulberry leaves. Flacherie infected silkworms look weak and can die from this disease. Silkworm larvae that are about to die from Flacherie are a dark brown.

There are two kinds of flacherie: essentially, infectious (viral) flacherie and noninfectious ("bouffee") flacherie. Both are technically a lethal diarrhea.

Bouffée flacherie is caused by heat waves ("bouffée" means "sudden heat spell" in French).

Viral flacherie is ultimately caused by infection with "Bombyx mori" infectious flacherie virus (BmIFV, Iflaviridae), "Bombyx mori" densovirus (BmDNV, Parvoviridae) or "Bombyx mori" cypovirus 1 (BmCPV-1, Reoviridae). This either alone or in combination with bacterial infection destroys the gut tissue. Bacterial pathogens contributing to infectious flaccherie are "Serratia marcescens", and species of "Streptococcus" and "Staphylococcus" in the form known as thatte roga.

Louis Pasteur, who began his studies on silkworm diseases in 1865, was the first one able to recognize that mortality due to viral flacherie was caused by infection. (Priority, however, was claimed by Antoine Béchamp.) Richard Gordon described the discovery: "The French silk industry was meanwhile plummeting from a 130 million to an 8 million francs annual income, because the silkworms had all caught "pébrine," black pepper disease…He [Pasteur] went south from Paris to Alais, and rewarded them by discovering the silkworm epidemic to be inflicted by some sort of living microbe…Pasteur threw in another disease, "flâcherie," silkworm diarrhoea. The cures for both were culling the insects which showed the peppery spots — the peasants bottled the silkworm moths in brandy, for display to the experts — and rigorous hygiene of the mulberry leaf."

Red thread disease is a fungal infection found on lawns and other turfed areas. It is caused by the corticioid fungus "Laetisaria fuciformis" and has two separate stages. The stage that gives the infection its name is characterised by very thin, red, needle-like strands extending from the grass blade. These are stromata, which can remain viable in soil for two years. After germinating, the stromata infect grass leaf blades through their stomata. The other stage is visible as small, pink, cotton wool-like mycelium, found where the blades meet. It is common when both warmth and humidity are high.

Environment

"Laetisaria fuciformis", the fungus that causes red thread disease develops more often in cool (59-77°F) and wet conditions. These conditions are more present in the spring and fall when rainfall is higher and temperatures are slightly lower. Turf grass that is poor in nutrition and are slow growing are areas that are more susceptible to red thread disease. The fungus grows from the thread like red webbing structures called sclerotia. The sclerotia can survive in leaf blades, thatch, and soil for months to years. These areas that have been infected spread the disease by water, wind, and contaminated equipment. Since this fungus can survive for long periods of time it is essential to cure the infected area so further spreading of the disease does not occur.

Management

Managing red thread disease first starts by providing conditions that are not favorable for the fungal disease to develop. Having a balanced and adequate nitrogen fertilization program helps suppress the disease. This includes applying mild to substantial amounts of phosphorus and potassium to the turf. Other than properly fertilizing the turf, it is very important to maintain a soil pH between 6.5 and 7. Having a more basic pH creates less favorable conditions for a fungus to form. Reducing shade on turf areas also reduces chances of the fungal disease to form because shaded areas create a higher humidity near the turfs surface. Another technique to suppressing red thread disease is top dressing with compost. Suppression of the disease increases with the increase of compost used on the turf. Fungicides are not recommended to control red thread because the cost of chemical control is expensive and turf grasses usually recover from the disease quickly. If the use of fungicides is necessary, products containing strobilurins can be applied and can be very effective if applied before symptoms occur.

Hosts and symptoms

The hosts of the red thread disease only include turf grass. Turf grass is primarily present on home lawns and athletic fields. Some of these turf grass species include annual bluegrass, creeping bentgrass, Kentucky bluegrass, pereninial ryegrass, fine fescue, and bermudagrass. These species of grass are not the only types of turf that can be diagnosed with red thread disease but are the most common hosts. Noticeable symptoms of red thread disease are irregular yellow patches on the turf that are 2 to 24 inches in diameter. Affected areas are diagnosed with faintly pinkish web like sclerotia on the leaf blades. This sclerotia is the fungus growing on the leaf blades. This sclerotia has a reddish to pink spider web look to it.

Acute mercury exposure has given rise to psychotic reactions such as delirium, hallucinations, and suicidal tendency. Occupational exposure has resulted in erethism, with irritability, excitability, excessive shyness, and insomnia as the principal features of a broad-ranging functional disturbance. With continuing exposure, a fine tremor develops, initially involving the hands and later spreading to the eyelids, lips, and tongue, causing violent muscular spasms in the most severe cases. The tremor is reflected in the handwriting which has a characteristic appearance. In milder cases, erethism and tremor regress slowly over a period of years following removal from exposure. Decreased nerve conduction velocity in mercury-exposed workers has been demonstrated. Long-term, low-level exposure has been found to be associated with less pronounced symptoms of erethism, characterized by fatigue, irritability, loss of memory, vivid dreams, and depression (WHO, 1976).

Effects of chronic occupational exposure to mercury, such as that commonly experienced by affected hatters, include mental confusion, emotional disturbances, and muscular weakness. Severe neurological damage and kidney damage can also occur. Neurological effects include Korsakoff's dementia and erethism (the set of neurological symptoms characteristically associated with mercury poisoning). Signs and symptoms can include red fingers, red toes, red cheeks, sweating, loss of hearing, bleeding from the ears and mouth, loss of appendages such as teeth, hair, and nails, lack of coordination, poor memory, shyness, insomnia, nervousness, tremors, and dizziness. A survey of exposed U.S. hatters revealed predominantly neurological symptomatology, including intention tremor. After chronic exposure to the mercury vapours, hatters tended to develop characteristic psychological traits, such as pathological shyness and marked irritability (box). Such manifestations among hatters prompted several popular names for erethism, including "mad hatter disease", "mad hatter syndrome", "hatter's shakes" and "Danbury shakes".

The first signs of infection are small irregular patches of brown/yellowing grass. Upon closer inspection, either the tiny red needles or the pink fluffy mycelium will be visible. As the infection spreads, the small patches will join to form large brown areas.

Nitric acid test and paper chromatography test are used in the detection of argemone oil.Paper chromatography test is the most sensitive test.

Metal toxicity or metal poisoning is the toxic effect of certain metals in certain forms and doses on life. Some metals are toxic when they form poisonous soluble compounds. Certain metals have no biological role, i.e. are not essential minerals, or are toxic when in a certain form. In the case of lead, any measurable amount may have negative health effects. Often heavy metals are thought as synonymous, but lighter metals may also be toxic in certain circumstances, such as beryllium and lithium. Not all heavy metals are particularly toxic, and some are essential, such as iron. The definition may also include trace elements when in abnormally high doses may be toxic. An option for treatment of metal poisoning may be chelation therapy, which is a technique which involves the administration of chelation agents to remove metals from the body.

Toxic metals sometimes imitate the action of an essential element in the body, interfering with the metabolic process resulting in illness. Many metals, particularly heavy metals are toxic, but some heavy metals are essential, and some, such as bismuth, have a low toxicity. Most often the definition of toxic metals includes at least cadmium, manganese, lead, mercury and the radioactive metals. Metalloids (arsenic, polonium) may be included in the definition. Radioactive metals have both radiological toxicity and chemical toxicity. Metals in an oxidation state abnormal to the body may also become toxic: chromium(III) is an essential trace element, but chromium(VI) is a carcinogen.

Toxicity is a function of solubility. Insoluble compounds as well as the metallic forms often exhibit negligible toxicity. The toxicity of any metal depends on its ligands. In some cases, organometallic forms, such as methylmercury and tetraethyl lead, can be extremely toxic. In other cases, organometallic derivatives are less toxic such as the cobaltocenium cation.

Decontamination for toxic metals is different from organic toxins: because toxic metals are elements, they cannot be destroyed. Toxic metals may be made insoluble or collected, possibly by the aid of chelating agents, or through bioremediation. Alternatively, they can be diluted into a sufficiently large reservoir, such as the sea, because immediate toxicity is a function of concentration rather than amount.

Toxic metals can bioaccumulate in the body and in the food chain. Therefore, a common characteristic of toxic metals is the chronic nature of their toxicity. This is particularly notable with radioactive heavy metals such as radium, which imitates calcium to the point of being incorporated into human bone, although similar health implications are found in lead or mercury poisoning. The exceptions to this are barium and aluminium, which can be removed efficiently by the kidneys.

ICD-9-CM code 985.8 "Toxic effect of other specified metals" includes acute & chronic copper poisoning (or other toxic effect) whether intentional, accidental, industrial etc.

- In addition, it includes poisoning and toxic effects of other metals including tin, selenium nickel, iron, heavy metals, thallium, silver, lithium, cobalt, aluminum and bismuth. Some poisonings, e.g. zinc phosphide, would/could also be included as well as under 989.4 Poisoning due to other pesticides, etc.

- Excluded are toxic effects of mercury, arsenic, manganese, beryllium, antimony, cadmium, and chromium.

Symptoms include dying growing tips and bushy stunted growth, extreme cases may prevent fruit set. Crop-specific symptoms include;

- "Apple"- interacting with calcium, may display as "water core", internal areas appearing frozen

- "Beetroot"- rough, cankered patches on roots, internal brown rot.

- "Cabbage"- distorted leaves, hollow areas in stems.

- "Cauliflower"- poor development of curds, and brown patches. Stems, leafstalks and midribs roughened.

- "Celery"- leaf stalks develop cracks on the upper surface, inner tissue is reddish brown.

- "Celeriac"- causes brown heart rot

- "Pears"- new shoots die back in spring, fruits develop hard brown flecks in the skin.

- "Strawberries"- Stunted growth, foliage small, yellow and puckered at tips. Fruits are small and pale.

- "Swede (rutabaga)" and "turnip"- brown or gray concentric rings develop inside the roots.

- "Arecaceae" ("Palm Tree") - brown spots on fronds & lower productivity.