South African Avocado Growers’ Association Yearbook 1987. 10:117-119

Proceedings of the First World Avocado Congress

 

Avocado fruit diseases and their control in South Africa

 

JM DARVAS¹ and JM KOTZE²

¹Letaba Estates, PO Box 6, Letaba 0870, RSA

²Department of Microbiology and Plant Pathology,

University of Pretoria, Pretoria 0002, RSA

 

 

 

 

INTRODUCTION

A five-year investigation was conducted at Westfalia Estate to determine the major pre- and post-harvest fruit diseases of avocados (Persea americana Mill) and to devise effective control measures. Westfalia Estate is the largest single avocado grower in South Africa, with about 600 hectares planted mainly with the cultivars Fuerte, Hass, Edranol and Ryan. The estate is situated in the North-Eastern Transvaal and the average annual rainfall is 1 300 mm, most of which falls in summer. The warm and humid climate of the estate creates conditions conducive to a wide variety of disease problems on avocados.

 

The pre-harvest fruit disease, Cercospora spot, was first described in South Africa by Brodrick, Pretorius & Frean (1974), but was incorrectly identified as Phomopsis spot. It spread rapidly and it is now found in all avocado centres of the Lowveld and occurs in Natal as well.

 

In South Africa, stem-end rot was reported by Jacobs (1974), who believed that it was mainly a problem on irradiated fruit and by Gorter (1977), who stated that it was caused by Botryodiplodia theobromae Pat. Doidge (1924) described Colletotrichum gloeosporioides (Penz) Sacc for the first time in this country as the cause of anthracnose. Gorter (1977) reported Botryosphaeria ribis from avocado fruit spot.

 

RESULTS AND DISCUSSION

Pre-harvest fruit diseases

Cercospora spot disease was the most important pre-harvest avocado fruit disease at Westfalia Estate. Losses were appreciable even in commercially treated fruit (up to 12 per cent); losses up to 69 per cent were recorded for unsprayed fruit. Fuerte and Ryan cultivars were considerably more susceptible to the disease than Edranol and Hass. The pathogen causing Cercospora spot disease is Pseudocercospora purpurea (Cke) Deighton (syn Cercospora purpurea Cke). Inoculated Fuerte produced typical symptoms, which agree with descriptions given by earlier workers (Stevens, 1922; Zentmyer, 1953; Brodrick et al, 1974). Two distinct disease stages were recorded. At first, the green epidermis of the fruit became slightly darker at the site of infection and a swelling of the underlying tissues caused the spot to rise above the level of the epidermis. As the epidermis cells were killed and the tissues dried out, the spot became sunken and darker with horizontal cracks. Leaf symptoms were common on mature Fuerte leaves. Most of the fresh P. purpurea isolates produced conidia on artificial media when kept continuously under near-ultra-violet light. Sporulation began ca 10 days after inoculation and a fair amount of conidia was produced for about another 10 days, after which the fungus became sterile. These cultures regained the ability to sporulate if transferred to sterile, freshly-cut avocado pieces, but again only for a limited period. The incidence of P. purpurea did not differ significantly in the two types of lesions (Table 1). The occurrence of C. gloeosporioides was considerably higher in sunken lesions and these spots also contained more secondary fungi.

 

 

 

A highly significant correlation (R² = 0,8754) was found between the spores trapped daily in the orchard and rainfall, and temperature figures. The model to forecast the number of conidia in the atmosphere of an established Fuerte orchard at Westfalia Estate was: Z (number of conidia) = 24,8 (constant) -- 0,93 X (X is temperature in °C) + 0,25 Y (Y is rainfall in mm). In practice, the number of conidia first reached significant proportions with the onset of the warm, rainy summer period and often great numbers of conidia were detected even as late as March, when harvesting of Fuerte had already started. A significant correlation was found between the number of Cercospora spots on the fruit exposed to natural infections and the exposure periods. Fuerte fruit exposed early in summer, were more severely infected than fruit exposed later in the growing season (Figure 1).

 

Good Cercospora spot control was achieved by the foliar sprays of benomyl, captafol, Cu-oxychloride and Cu-hydroxide (Table 2). The same fungicides (except Cu-hydroxide) were tested and found effective against Cercospora spot in the Nelspruit area by Kotze, Du Toit & Durand (1982).

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Post-harvest diseases

The most common fungus associated with stem-end rot in Fuerte fruit ripened either directly after harvest or after cold storage, was Thyronectria pseudotrichia (Schw) Seeler. The incidence of the second most common stem-end rot pathogen, C. gloeosporioides, increased after cold storage. A similar increased incidence was observed for Phomopsis perseae Zerova following cold storage. Dothiorella aromatica (Sacc) Petr & Syd was isolated relatively infrequently from both cold-stored and directly-ripened fruit. Fusarium decemcellulare Brick, Fusarium sambucinum Fuckel, Fusarium solani (Mart) Sacc, Pestalotiopsis versicolor (Speg) Steyart, B. theobromae and Drechslera setariae (Sawada) Subram. & Jain occurred only sporadically in stem-end rot. The temperature during ripening of avocado fruit also had an important effect on the development of post-harvest diseases, as indicated by experiments done by Fitzell & Muirhead (1983).

 

Pathogenicity of the fungi isolated from stem-end rot was investigated by pre-harvest inoculation of fruit on the trees. C. gloeosporioides and D. aromatica infected uninjured Fuerte fruit and caused both fruit rot and stem-end rot. B. theobromae caused stem-end rot only and F. decemcellulare induced small decay spots on softening fruit. None of the other organisms caused post-harvest diseases after pre-harvest inoculation. However, they were pathogenic in post-harvest inoculation through wounds.

 

No new information regarding the symptoms of stem-end rot and typical anthracnose as described by Horne (1931), Stevens (1922), Ocfemia & Agati (1925), Horne (1934) and Zentmyer (1953), evolved from this investigation. However, the superficial anthracnose caused by C. gloeosporioides had to be classified with Dothiorella fruit rot caused by D. aromatica as Dothiorella/Colletotrichum complex fruit rot (DCC). The difficulty of separating Dothiorella fruit rot from the superficial anthracnose on the basis of symptoms only, has previously been reported by Muirhead (1977).

 

The occurrence of latent skin infections by C. gloeosporioides and D. aromatica best fitted a non-linear regression model (Figure 2). The maximum build-up was recorded during the very rainy months of January and February, with a gradual decrease thereafter.

 

In the pedicel, the infections of D. aromatica reached maximum at a later stage and persisted in high numbers well into the harvesting season (Figure 3).

 

Acceptable control of post-harvest diseases was obtained with some preharvest fungicide sprays, in particular in spray programmes where benomyl and captafol were used in combination with Cu-oxychloride (Table 3). The increased losses encountered with benomyl treatment might have been due to increased tolerance of the postharvest pathogens to this compound. A similar tolerance developed in P. purpurea after prolonged use of benomyl at Westfalia Estate. Reasonable anthracnose control by pre-harvest sprays was also reported from Florida (Ruehle, 1943), Australia (Peterson & Inch, 1980) and from the Nelspruit area (Kotze, Kuschke & Durand, 1981).

 

Stem-end rot and DCC were statistically more severe on fruit harvested wet than on dry fruit. It was found that the rapid drying of wet fruit in the packhouse was not likely to reduce the problem satisfactorily, since moisture was retained in the lenticels of the quick-dried fruit and many latent infections were located in these tissues (Horne & Palmer, 1935).

 

The sealing of the cut-end of the fruit pedicel with wax plus fungicides was an effective means of controlling stemend rot. The usual waxing of export fruit slowed down the ripening process, but there was an increase in the severity of post-harvest diseases on these fruit. These increased pathological losses could only be partially reduced by the addition of fungicides to the wax. A recently tested fungicide, Prochloraz, may be used in the packhouse for a more effective control (Muirhead, Fitzell, Davis & Peterson, 1982; Rowell, 1983; Darvas, 1984; Darvas, 1985).

 

ACKNOWLEDGEMENTS

The authors thank the management of Westfalia Estate and the South African