Around 1960 some disorders which initially were considered to be of a physiological nature were found in tomato plants grown in glasshouses in the Netherlands. One complex of symptoms was a brown rot of the lateral roots and the tap root, often followed by decomposition of the stem base tissue and death of the plant. A second group of symptoms was the sudden death of plants within three days after planting on sunny days in June or July due to a rot of the stem base only, the root system itself staying in good order.
In 1964 and 1965 two Phytophthora
spp. were isolated from such tissues and were identified as P.nicotianae
Breda de Haan var. nicotianae
Pethybr. & Laff. Later on the first mentioned pathogen was found to be also the cause of a rot of tomato stems, leaf petioles, leaf blades and fruits. This pathogen is considered identical with the P.parasitica
Dast., known for over 50 years to be the cause of 'buckeye' rot or wet fruit rot. Fruits thus infected do not always demonstrate the 'buckeye' symptom, which therefore is considered of limited diagnostic value.
The main difference in symptoms between tomato fruits infected by P. infestans
and P. nicotianae
was the dry and the very wet consistency of the infected fruits respectively, for which as trivial names 'dry (Phytophthora)
fruit rot' and 'wet (Phytophthora)
fruit rot' are suggested. Other differences in symptoms were the absence of infection of the roots, the stem bases and the stem pith by P. infestans,
parts which were frequently infected by P.nicotianae.
Whereas the first mentioned pathogen entered the glasshouses through the open ventilators infecting firstly the plants immediately beneath, the last mentioned occurred throughout the whole glasshouse as, usually, did the infected plants.P. nicotianae
were isolated by plating out infected plant tissue on pea dextrose agar supplemented with 30 ppm pimaricin and 10-20 ppm oxytetracyclin-HCl. The pathogen could be obtained from soil by adding a chilled I % glucose solution or distilled water to the soil and using green tomato fruits as bait in the supernatant. Zoosporangia of P.nicotianae
were produced abundantly by culturing the mycelium in V8 juice/CaCO 3
medium and, after rinsing with water, by subsequent incubation under moist, sterile conditions. Indirect germination of zoosporangia was obtained by chilling in water to 10-12°C. Addition of cholesterol to glucose nitrate agar or to pea dextrose agar as culture medium for P. nicotianae
improved the shape and the content but very little the number of the zoosporangia formed.
The lesions of wound inoculated stems and leaf petioles extended much faster than those resulting from inoculations without wounding.P. nicotianae
remained virulent for at least four years in sandy border soil kept moist under glasshouse conditions. In the fourth year the inoculum potential seemed to decline.
Screening all phases of the process of propagation showed the top soil of the propagation beds to be the most important source of infection for planting material.
At the same soil moisture content root infection developed more quickly at soil temperatures between 17 and 27°C than at temperatures below and above. Ample soil moisture reduced the incidence of aerial symptoms, as plants were enabled to form new roots which replaced those lost by infection. With subsequent growth the plants proceeded to a more resistant stage. This effect was more pronounced at 25°C than at 14°C.
The incidence of stem base rot seemed to depend on suitable conditions for zoospore liberation in the soil. In the presence of free water these zoospores could infect vigourously. At soil temperatures of less than 20°C this infection hardly occurred.
The nitrogen and potassium nutrition of the host plants was found to have little influence on infection by the pathogen, except that ample nitrogen was found to reduce stem lesion development and to retard the abscission of infected leaf petioles.
The thermal death-point of P.nicotianae was
found to be between 50 and 55°C. Root infection could be largely avoided, when before planting the soil was disinfected by means of steam, chloropicrin (35 ml/m 2
) or methyl bromide (50 g/m 2
). Such disinfection was also necessary for propagation beds in order to be able to produce diseasefree planting material.
Soil treatment by means of dithiocarbarnates or chlorophthalonil at or after planting reduced the activity of the pathogen sufficiently to allow the tomato plants to overcome the susceptible juvenile period. Captan, captafol, folpet, triphenyltin compounds, fenaminosulf and triarimol gave sufficient fungal control, but the level of phytotoxicity at the dosages to be applied was too great to allow their use in normal commercial practice.
When wettable powders of maneb or zineb were applied as a suspension around the stems of the plants or as a dust to the whole soil surface, the controlling effects were the same, provided equal quantities of active ingredient per planting hole were applied and the dusted fungicides were drenched into the soil with water. A quantity of 200 mg maneb (active ingredient) per planting hole thus required a dust of 5 g of an 80 % commercial product per ml; likewise a quantity of 325 mg zineb required dusting at a rate of 13 g of a 65 % commercial product per m 2
. A dose of 2 g of maneb per m 2
, which is often applied in normal commercial practice, was not effective enough to control Phytophthora
Treating the propagation beds regularly with wettable powder formulations of maneb or zineb appeared a practical way of keeping this disease in planting material under control. However, a short steam treatment of these beds in February or early March would go a long way to eradicate the sources of infection during propagation.
No root resistance was found in young root stock material from Lycopersicum hirsutum
. Resistance of the tap root of L. esculentum
increased with age and so the death-rate decreased. The same was true for Nicotiana
spp. (N. clevelandii, N. glutinosa
, N. rustica
and N. tabacum
'White Burley mosaic').
The increase of the incidence of the disease in the Netherlands in the 1960's could be attributed to modification of the growing methods leading to higher levels of infestation in the glasshouse soils and to the delivery of infected transplants. The better growing conditions, the lower levels of soil infestation and the lower forcing temperatures probably brought about the lower incidence of this disease in England and Guernsey.