Quince

Olive-green, velvety, blurred spots appear on the leaves and gradually darken and turn brown; heavily infected leaves turn yellow and drop prematurely. Dark, corky spots form on the fruit and crack as the fruit grows, producing the characteristic fissures and deformations. Infected fruit stay small, store poorly and lose market value. The first spots are usually seen on the youngest, developing leaves and on the sepals of the flowers; at first they are poorly delimited, later taking on a distinctly dark-olive to blackish-brown colour with a velvety sporulating coating. The primary spring infections are caused by ascospores discharged during rain from the fruiting bodies overwintering in the fallen leaves; the resulting spots in turn produce conidia responsible for numerous secondary infections through the summer. Early infection of the fruitlets leads to one-sided growth and severe fruit deformation, and the cracks in the corky tissue become entry points for rot fungi and storage rots. On especially susceptible cultivars the disease also produces crusty lesions and cracks on the young shoots and twigs, which become an additional source of spores the following season. A separate form is the so-called storage scab - small, pinpoint spots that only show up in cold storage when the fruit was infected just before harvest.

On pome and stone fruit, brown, enlarging rot spots appear, on which concentrically arranged, grey-beige cushions of spores form. Infected fruit rot, dry out and mummify, often remaining on the tree until the next season. In spring the fungus also infects blossoms and short shoots, causing them to die back and killing the branch tips. The disease has two distinct phases. Spring blossom and twig blight (most often Monilinia laxa on stone fruit — sour cherry, sweet cherry, plum, apricot) begins on the blossoms, which turn brown, wilt and dry out without dropping; the infection enters through the stigma and style into the short shoot, girdles it and causes whole shoots to die back, with withered leaves hanging as if scorched — hence the misleading resemblance to frost damage. On stone fruit, infected shoots often exude gum (gummosis) and develop small, cracked bark cankers. The summer-to-autumn brown rot of the fruit (mainly Monilinia fructigena on apple and pear) develops on ripening fruit: the rot spot quickly engulfs the whole fruit, the flesh turns brown and softens, and characteristic, concentrically arranged rings of cream-beige cushions of conidial spores grow out on the surface. In cool conditions (including in storage), the fruit may take the form of hard, black glossy mummies lacking sporulation (so-called black rot). Mummified fruit hanging on the tree and Monilinia cankers on the shoots are the main source of spores in the following season.

Blossoms and young shoots suddenly turn brown and then black, looking as if scorched by fire — hence the name of the disease. The tips of infected shoots bend downwards into a characteristic hook resembling a shepherd's crook. In humid conditions a milky, sticky bacterial ooze seeps from the infected tissue, and the infection spreads rapidly down the shoot, killing whole branches. Infected leaves and fruit dry out but remain attached to the tree for a long time. Pear and quince are the most severely affected, followed by apple, and among ornamental and wild plants — hawthorn, cotoneaster, firethorn (Pyracantha) and rowan, which can be a dangerous reservoir of infection. On the bark of the branches and trunk, sharply delimited, sunken necroses (bark canker) form with cracking bark; when the bark is cut, the tissue beneath is discoloured reddish-brown, often with marbled streaks. The drop of bacterial ooze eventually turns amber and dries, and the presence of the bacterium can be confirmed by the so-called streaming test — from freshly cut infected tissue immersed in water, threads of a cloudy bacterial suspension flow out. Infected fruit turns black and mummifies, remaining on the tree, which distinguishes fire blight from ordinary wilting caused by water shortage.

Small (1–3 mm) soft-bodied insects, green, black or pink, feeding in clusters on young shoots and the underside of leaves. They excrete sticky honeydew. The diagnostic feature that distinguishes aphids from other small sucking insects is the pair of siphunculi (tubular projections) at the rear of the abdomen together with a tail-like cauda; a single colony usually holds wingless forms (parthenogenetic females) alongside winged migrants that fly onto new plants in summer. In summer aphids reproduce parthenogenetically and viviparously over many generations, so the population builds up explosively; in autumn many species produce a sexual generation that lays overwintering eggs on the host, and host-alternating species move between a winter host (often a tree or shrub) and a summer host (a herbaceous plant). Feeding symptoms include curling, crinkling and distortion of young leaves, stunted growth, yellowing, and the shedding of buds and fruitlets. Abundant honeydew coats the leaves, and the sooty mould fungus that develops on it forms a black film which limits photosynthesis; the honeydew is fed on by ants, which in return defend the colony against predators. Aphids are also important vectors of plant viruses (mosaics among them), transmitting them from plant to plant even during a brief probing puncture.