Gibberella xylarioides (coffee wilt)
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- Risk of Introduction
- Hosts/Species Affected
- Host Plants and Other Plants Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Seedborne Aspects
- Plant Trade
- Detection and Inspection
- Similarities to Other Species/Conditions
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Gibberella xylarioides R. Heim & Saccas
Preferred Common Name
- coffee wilt
Other Scientific Names
- Fusarium oxysporum forma xylarioides (Steyaert) Deassus
- Fusarium xylarioides Steyaert
International Common Names
- English: sudden death of coffee; tracheomycosis of coffee; vascular wilt of coffee
- Spanish: fusariosis vascular del cafe
- French: carbunculariose; fusariose du caféier; trachéomycose du caféier
Local Common Names
- Germany: Tracheomykose: Kaffee
- GIBBXY (Gibberella xylarioides)
Taxonomic TreeTop of page
- Domain: Eukaryota
- Kingdom: Fungi
- Phylum: Ascomycota
- Subphylum: Pezizomycotina
- Class: Sordariomycetes
- Subclass: Hypocreomycetidae
- Order: Hypocreales
- Family: Nectriaceae
- Genus: Gibberella
- Species: Gibberella xylarioides
Notes on Taxonomy and NomenclatureTop of page
Steyaert (1948) described Fusarium xylarioides as a new species causing wilt of coffee, Coffea excelsa [C. liberica]. Based on ascomatal and ascospore morphology, Heim and Saccas (1950) later concluded that the teleomorph of F. xylarioides should be referred to Gibberella. Deassus (1954) studied the morphology and biology of the fungus and concluded that the anamorph agreed with previous descriptions of F. xylarioides and Fusarium oxysporum, and proposed that it be named F. oxysporum f. xylarioides. Earlier concepts of variation in G. xylarioides may have led to confusion with other Fusarium species, such as F. stilboides, causing disease on coffee.
DescriptionTop of page
Cultures of the anamorph on potato sucrose agar (pH 6.5) are pale beige with sparse white mycelium; purple discoloration later develops, accompanied by dark bluish-black, discrete stromata, some of which represent ascomatal initials. Microconidia unicellular, allantoid, curved, 5-10 x 2.5-3 µm. Macroconidia fusoid, falcate, 2-3 septate, 20-25 x 4-5 µm. Chlamydospores oval to globose, smooth or roughened, 10-15 x 8-10 µm.
Ascomata perithecioid, violaceous, embedded, single or in groups, in dark purple stromata; globose with a flattened base, 200-400 x 180-300 µm. Asci cylindrical, thin-walled, shortly pedicellate, 90-110 x 7-9.5 µm with 8 monostichous ascospores. Ascospores hyaline to straw-coloured, fusoid, 1-3 septate, finely roughened, 12-14.5 x 4.5-6 µm (Booth and Waterston, 1964).
Cultural, morphological and genetic variability have been described by Rutherford et al. (2009).
DistributionTop of page
Records of the G. xylarioides in Angola, Burkina Faso, Congo, Ghana, Guinea, Gabon, Gambia, Guinea Bissau, Niger and Togo are unconfirmed and, without further surveys to confirm the absence or presence of the pathogen, should be viewed with caution. It is highly likely that there has been considerable misidentification of the causal agents of coffee diseases, including confusion with other Fusarium species (J Flood, CABI, personal communication, 2009).
A record of G. xylarioides isolated from rotting tomatoes in Nigeria (Onesirosan and Fatunla, 1976) may be a misidentification and requires confirmation.
In Rwanda, coffee wilt disease, caused by G. xylarioides, was not found on either Coffea arabica or C. canephora in 2002 (Odour et al., 2003).
A record for El Salvador (Abrego, 1965) requires confirmation due to its geographic isolation and lack of subsequent reports (CABI/EPPO, 2005).
A record of G. xylarioides in Kenya (EPPO, 2009) published in previous versions of the Compendium is erroneous and has been removed.
The identity of the pathogen in Zimbabwe has been questioned (Ndimande, 1985).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Angola||Absent, unreliable record||CABI/EPPO, 2005; EPPO, 2014|
|Burkina Faso||Absent, unreliable record||CABI/EPPO, 2005; EPPO, 2014|
|Cameroon||Absent, confirmed by survey||CABI/EPPO, 2005; Phiri and Baker, 2009; EPPO, 2014|
|Central African Republic||Present||Guillemat, 1946; Saccas, 1956; CABI/EPPO, 2005; EPPO, 2014|
|Congo||Absent, unreliable record||CABI/EPPO, 2005; EPPO, 2014|
|Congo Democratic Republic||Widespread||Fraselle, 1950; OZACAF, 1995; CABI/EPPO, 2005; Flood, 2009; EPPO, 2014|
|Côte d'Ivoire||Absent, formerly present||Deassus, 1954; Bouriquet, 1959; Porteres, 1959; CABI/EPPO, 2005; Phiri and Baker, 2009; EPPO, 2014|
|Ethiopia||Widespread||Lejeune, 1958; Van and der Graaff Pieters, 1978; Girma et al., 2001; CABI/EPPO, 2005; EPPO, 2014|
|Gabon||Absent, unreliable record||CABI/EPPO, 2005; EPPO, 2014|
|Gambia||Absent, unreliable record||CABI/EPPO, 2005; EPPO, 2014|
|Ghana||Absent, unreliable record||CABI/EPPO, 2005; EPPO, 2014|
|Guinea||Absent, unreliable record||Krantz, 1962; CABI/EPPO, 2005; EPPO, 2014|
|Guinea-Bissau||Absent, unreliable record||CABI/EPPO, 2005; EPPO, 2014|
|Kenya||Absent, invalid record||EPPO, 2014|
|Niger||Absent, unreliable record||CABI/EPPO, 2005; EPPO, 2014|
|Nigeria||Present||Onesirosan and Fatunla, 1976; CABI/EPPO, 2005; EPPO, 2014||Isolated from rotting tomatoes under laboratory conditions.|
|Rwanda||Absent, confirmed by survey||Oduor et al., 2003; Phiri and Baker, 2009; EPPO, 2014|
|Senegal||Present||CABI/EPPO, 2005; EPPO, 2014|
|South Africa||Present||Anon, 1989; CABI/EPPO, 2005; EPPO, 2014|
|Sudan||Present||Lejeune, 1958; CABI/EPPO, 2005; EPPO, 2014|
|Swaziland||Present||Anon, 1989; CABI/EPPO, 2005; EPPO, 2014|
|Tanzania||Restricted distribution||CABI/EPPO, 2005; EPPO, 2014|
|Togo||Absent, unreliable record||CABI/EPPO, 2005; EPPO, 2014|
|Uganda||Widespread||CABI/EPPO, 2005; EPPO, 2014|
|Zimbabwe||Absent, unreliable record||Clowes and Hill, 1981; Ndimande, 1985; CABI/EPPO, 2005; EPPO, 2014|
Central America and Caribbean
|El Salvador||Absent, unreliable record||Abrego, 1965; EPPO, 2014|
Risk of IntroductionTop of page
The re-emergence of this disease in Zaire (Democratic Republic of Congo) and Uganda is a major problem and quarantine facilities in neighbouring countries should be aware of this threat. There have been some unconfirmed reports in West African countries but without independent surveys these reports should be viewed with caution. Nevertheless the quarantine authorities in countries adjacent to DRC, Uganda, Tanzania and Ethiopia (where the disease is confirmed) should be vigilant.
There is only one report of the disease in South Africa and Swaziland (Anon., 1989) which would seem to indicate that G. xylarioides is not common in southern Africa but further surveys are needed to confirm absence or presence and extent of distribution. It is highly likely that there has been considerable mis-identification of the causal agents of coffee diseases including confusion with other Fusarium species.
Hosts/Species AffectedTop of page
Fusarium xylarioides (teleomorph = G. xylarioides) has been reported to be pathogenic to cotton seedlings of IAC 20 cultivar under laboratory conditions; less so under glasshouse conditions (Pizzinatto and Menten, 1991). It has also been isolated from rotting tomatoes in Nigeria (Onesirosan and Fatunla, 1976) but this may be a misidentification.
Host Plants and Other Plants AffectedTop of page
Growth StagesTop of page Flowering stage, Fruiting stage, Pre-emergence, Seedling stage, Vegetative growing stage
SymptomsTop of page
Fraselle (1950) described the disease symptoms fully on C. robusta in the Belgian Congo (formally Zaire and now Democratic Republic of Congo). First symptoms were described as generalized chlorosis of the leaves which became flaccid and curled. Leaves dry up, turn brown and very fragile, and abscise. The crowns of the dead trees are completely defoliated. The branches may turn black-brown or blackish, and dry up. The bark on the trunk is hypertrophied and has numerous vertical or spiral cracks which reveal blue-black streaks in the wood under the bark. In the roots, the black rot becomes moist. Infection may be general or partial. Van der Graaff and Peters (1978), describing the disease in C. arabica in Ethiopia, observed that dieback may start unilaterally and extend to the whole tree.
Internally, in the diseased wood, the main tracheids are heavily infected by mycelium. At the limit of spread, the tracheids alone are affected but where the infection is long established, the mycelium is found in the fibres surrounding the vessels and medullary rays (Fraselle, 1950). Wood parenchyma is rarely attacked but primary xylem and pith may be attacked. Tyloses develop and a yellow gum is observed (Fraselle, 1950). Such occlusion of the vessels leads to the characteristic wilting and desiccation of the foliage. Mycelium is rarely present in the bark, reaching only the cortical medullary rays but fungal reproductive structures (fruiting bodies) can sometime be observed on the outside of the bark at the base of infected trees.
Further details of symptoms can be seen in various chapters and plates in Flood (2009).
List of Symptoms/SignsTop of page
|Fruit / discoloration|
|Fruit / extensive mould|
|Fruit / lesions: scab or pitting|
|Leaves / abnormal colours|
|Leaves / abnormal leaf fall|
|Leaves / wilting|
|Roots / rot of wood|
|Roots / soft rot of cortex|
|Seeds / discolorations|
|Seeds / lesions on seeds|
|Stems / dieback|
|Stems / discoloration of bark|
|Stems / gummosis or resinosis|
|Stems / internal discoloration|
|Whole plant / seedling blight|
Biology and EcologyTop of page
Conidia and ascospores are spread by wind, rain and through human activities (harvesting, pruning etc.) (Jacques-Felix, 1954). The pathogen can penetrate through wounds so any agency causing wounds will aid the spread of the fungus. Krantz and Mogk (1973) noted that most dying and dead trees had been wounded during weeding. Insects may also spread the disease from tree to tree (Wrigley, 1988). Seed from infected berries may contain the pathogen and seedborne infection was considered to be the way in which the disease has spread in Zimbabwe (Wrigley, 1988) but there is some uncertainty as to the identification of the pathogen in Zimbabwe and Girma et al. (2001) reported that seeds did not transmit the pathogen in Ethiopia.
The pathogen is considered to be an endemic soil-inhabiting fungus (Jacques-Felix, 1954) which can penetrate through wounds in the aerial parts or superficial roots (Saccas, 1956; Holliday, 1980). However, Van der Graaff and Pieters (1978) considered that the fungus did not persist in soil because it only rarely produces resting structures (chlamydospores) and Rutherford et al. (2009) reported that isolation from soil was problematic.
The incubation period from first symptoms to death of the tree varies from days in young plants to 8 months in trees more than 10 years old (Saccas, 1956) although most affected trees die 2-3 months after initial symptoms are observed.
The disease cycle, epidemiology, colonization and transmission are reviewed by Rutherford et al. (2009).
Seedborne AspectsTop of page
Evidence for the seedborne nature of this pathogen is conflicting. Studies in Zimbabwe suggested that seed from infected berries may contain the pathogen (Wrigley, 1988). However, Girma et al. (2001) found that seeds did not transmit the pathogen in Ethiopia. Studies on the disease in Zimbabwe (Clowes and Hill, 1981) revealed a rather different symptom pattern than observed in Central Africa and Ethiopia, resembling more coffee bark disease caused by the closely related Fusarium stilboides [Gibberella stilboides].The identity of the pathogen in Zimbabwe has been subsequently questioned (Ndimande, 1985).
Effect on Seed Quality
Seed infection causes blue-black discoloration of the parchment, and silverskin (Wrigley, 1988). Seedborne infection is responsible for seedling blight (see Symptoms for further details). However, the identification of the pathogen in Zimbabwe has been questioned (Ndimande, 1985).
Seedborne infection is considered to be the way in which the disease has spread in Zimbabwe (Wrigley, 1988) but the pathogen identity has been questioned (see Incidence).
Treating seeds with benomyl [pesticide restricted under the Rotterdam Convention] before planting reduces the incidence of seedling blight in Zimbabwe (Wrigley, 1988) but the identity of the pathogen in Zimbabwe has been questioned.
Plant TradeTop of page
|Plant parts liable to carry the pest in trade/transport||Pest stages||Borne internally||Borne externally||Visibility of pest or symptoms|
|Bark||fruiting bodies||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|Roots||hyphae; spores||Yes||Yes||Pest or symptoms usually invisible|
|Seedlings/Micropropagated plants||Yes||Pest or symptoms usually invisible|
|Stems (above ground)/Shoots/Trunks/Branches||fruiting bodies; hyphae; spores||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|Wood||fruiting bodies; hyphae; spores||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|Plant parts not known to carry the pest in trade/transport|
|Fruits (inc. pods)|
ImpactTop of page
In the 1940s and 1950s this disease was a serious problem of coffee in several countries in West and East Africa, but was reduced to a relatively minor disease with effective cultural practices and the establishment of breeding programmes in several countries (Zaire, Ivory Coast and Ethiopia). Pieters and Van der Graaff (1980) considered that it was not a problem in areas of Ethiopia under traditional low-management systems, but only reached epidemic proportions where coffee (C. arabica) is grown under intensive cultivation. However, the disease re-emerged in the late 1980s and 1990s causing considerable losses of robusta coffee in Zaire (OZACAF, 1995) and in Uganda (Flood and Brayford, 1997). In the last few decades of the twentieth century, the disease spread in DRC and Uganda and has been detected in northern Tanzania as well as being more widespread in Ethiopia. For details of in country spread, see chapters in Flood (2009). There is a risk of the disease spreading to neighbouring countries and quarantine authorities should be aware.
DiagnosisTop of page
Following surface sterilization, remove bark and plate pieces of infected wood on tap-water agar. Characteristic microconidia and macroconidia of Fusarium xylarioides will be observed in 2-4 days (see Description).
Detection and InspectionTop of page Indicative symptoms include wilting, chlorosis and defoliation of the aerial parts of the crop, and numerous vertical and spiral cracks in the bark of the trunk. Inspection under the bark, especially around the collar, will reveal characteristic blue-black streaks in the wood. Stromata producing perithecia can be observed in the bark. In Ethiopia, ascospores can be found in August-September at the end of the rainy season (Van der Graaff and Pieters, 1978). Infected berries turn red and appear to ripen early. Seed infection causes blue-black discoloration of the parchment and silverskin (see Symptoms).
Similarities to Other Species/ConditionsTop of page
Fusarium solani [Haematonectria haematococca] also causes a wilt of coffee accompanied by a dry root rot. The distinguishing feature of this disease is a purple-brown discoloration of the wood seen in sections of the main roots and collar region. This disease lacks the blackish, darker discoloration seen under the bark in the collar region of trees affected by G. xylarioides and stromata bearing perithecia in bark fissures are also generally absent. F. solani is readily distinguishable from the Fusarium state of G. xylarioides primarily by its abundant microconidia borne on long, branched conidiophores. Fusarium stilboides [Gibberella stilboides] causes coffee bark disease that also causes a discoloration beneath the bark and a progressive decline in vigour of the tree, but not the typical blackish discoloration of the lower vascular tissues associated with G. xylarioides. F. stilboides is very close to Fusarium lateritium [Gibberella baccata], which also occurs on coffee and other perennial crops and can be pathogenic. Previous confusion with some G. xylarioides strains has occurred, but the pronounced curvature of G. xylarioides macroconidia should enable distinction. See Rutherford et al. (2009).
Prevention and ControlTop of page
Several authors have reported varietal differences in resistance to the pathogen, and suggested the use of resistant varieties as a means of control (Fraselle, 1950; Deassus, 1954; Bouriquet, 1959; Porteres, 1959). Cultivars of Coffea canephora (notably Robusta) which were resistant formed the basis of many of the West African breeding programmes. Van der Graaff and Pieters (1978) reported that coffee lines of Coffea arabica in Ethiopia also differed widely in resistance to G. xylarioides and considered that these differences provided an excellent opportunity to control the disease with resistant varieties. They suggested that resistance in C. arabica was quantitative in nature and horizontal; no evidence of vertical resistance was seen. Pieters and Van der Graaff (1980) reported two methods of screening for resistance: a seedling test which involved wounding seedlings with a knife dipped in spore suspension; and a conidial germination test conducted directly on the bark of the tree. Both tests correlated significantly with field scores and with each other, and provided the basis for a screening programme to be used in a more extensive programme involving selection for resistance to coffee berry disease (Colletotrichum kahawae) and F. xylarioides.
In response to the re-emergence of coffee wilt disease in Central Africa and Ethiopia, screening tests were established and expanded using the methodologies above and breeding programmes were initiated in Uganda and Ethiopia. Some materials with at least partial resistance to the disease have been released (see Girma et al., 2009; Musoli et al., 2009). Some further details on the strategies used for disease resistance approaches are reported in Bieysse (2007). See also Phiri and Baker (2009).
Caffeine, which inhibits the pathogen, has been found in higher concentrations in tissues of C. canephora than in C. liberica (Rabechault, 1954) and a higher content of chlorogenic acid in the wood of resistant material (variety Robusta) has also been reported (Bouriquet, 1959). Girma et al. (2009) reported some experimentation on the host-pathogen interaction but the actual resistance mechanisms remains unclear.
Frequent inspection of the crop, along with burning infected material and spraying the soil surface with 2.5% copper (II) sulphate, was advocated as an effective control measure (Saccas, 1956). Replanting should not be done until 6 months after uprooting infected trees to allow the viability of the soil inoculum to decline (Wrigley, 1988). Removal of bushes to reduce spread between plantations was effective in the Ivory Coast; gaps of a few hundred metres were enough to confine the disease (Deassus, 1954). Grafting of susceptible varieties to a more resistant Robusta variety was effective in French West Africa (Gaudy, 1956). However, much of this early work dealt with a large-scale plantation model of coffee production. With a smallholder system, as seen in much of African coffee production, other approaches were needed (Phiri et al., 2009). Uprooting and burning were recommended but needed to be part of concerted national action as opposed to be the responsibility of individuals. Other measures included the reduction of wounding (when weeding) and use of mulches.
Gaudy (1956) reported that spraying with copper oxychloride was effective in controlling the disease. Phiri et al. (2009) reported some success with the use of copper oxychloride stem paints in participatory on-farm trials.
Rabechault (1954) isolated four actinomycetes, one bacterium and Corticium, Marasmius and Trichoderma spp., all of which were inhibitory to G. xylarioides, but no methods of biological control are currently available.
Phiri et al. (2009) recommended an integrated approach to management of CWD but noted that early detection was important in the management of the disease; a general lack of preparedness in affected countries had led to the disease spreading before the problem was recognised.
Extension and information provision
Any success at management of the disease relies on early diagnosis. Extension approaches such as farmer field schools and information dissemination were key to the Regional Coffee Wilt Disease Programme and allowed raising of awareness of the symptoms of the disease so that prompt action could be taken whilst various management options were trailed through on-farm experimentation (Negussie et al., 2009).
ReferencesTop of page
Abrego L, 1965. Coffee trees killed by stem pitting disease. Nota fitopatologica Bot. Inf. Int salvador. Tropical Abstracts, 21:550.
Anon, 1989. A new disease of coffee in South Africa? Information Bulletin of Citus and Subtropical Fruit Research Institute, No. 205, 13.
Bieysse D, 2007. Development of a long term strategy based on genetic resistance and agro-ecological approaches against coffee wilt disease in Africa. Final Report INCO-DEV Contract ICA4-CT-2001-100006. Montpellier, France: CIRAD-AMIS.
Bouriquet G, 1959. Plant diseases and pests in some African territories. FAO Plant Protection Bulletin, 7:61-63.
Clowes MStJ; Hill RHK, 1981. Coffee Handbook. 2nd edition. Zimbabwe Coffee Growers Association.
Deassus E, 1954. La tracheomycosis de Cafeier. Bull. Sci. Minist.Colon.Sect. Agron. Trop., 5:345-348.
EPPO, 2014. PQR database. Paris, France: European and Mediterranean Plant Protection Organization. http://www.eppo.int/DATABASES/pqr/pqr.htm
Flood J, 2009. Coffee Wilt Disease. Wallingford, UK: CAB International, 199 pp.
Flood J; Brayford D, 1997. Re-emergence of Fusarium wilt of coffee in East and Central Africa. Proceedings of the 17th International Conference on Coffee Science, July, 1997. Paris, France: Association Scientifique Internationale du Cafe (ASIC).
Fraselle J, 1950. Observations preliminaires sur une tracheomycosis de Coffea robusta. Bulletin Agricole du Congo Belge, 41:361-72.
Gaudy MR, 1956. Contribution du techniques, scientifique ou devvelopment de l'agriculture en Afrique Occidentale Francaise. J. W. Afric. Sci. Ass., 2:172-197.
Girma A; Bieysse D; Musoli P, 2009. Host pathogen interactions in the Coffea-Gibberella xylarioides pathosystem. In: Coffee Wilt Disease [ed. by Flood, J.]. Wallingford, UK: CAB International, 120-136.
Girma A; Hulluka M; Hindorf H, 2001. Incidence of tracheomycosis, Gibberella xylarioides (Fusarium xylarioides), on Arabica coffee in Ethiopia. Zeitschrift fu^umlaut~r Pflanzenkrankheiten und Pflanzenschutz, 108(2):136-142; 16 ref.
Guillemat J, 1946. Quelques observations sur la traceomycose du Coffea excelsa. Revue de Botanique Appliquee & d'Agriculture Tropicale, 26:542-550.
Heim R; Saccas A, 1950. La tracheomycose des Coffea et Robusta des plantations de L'Oubangui-Chari. Revue de Mycologia. Supplement Colonial, 15:97.
Jacques-Felix H, 1954. La carbunculariose. Bull.Sci. Minist. Colon. Sect. Agron. Trop., 5:296-344.
Krantz J, 1962. Coffee diseases in Guinea. FAO Plant Protection Bulletin, 10:107-110.
Lejeune P, 1958. Rapport au Governement Imperial d'Ethiopie sur le production cafeiere. FAO. Rome. FAO /58/3/1881.
Musoli P; Girma A; Hakiza G; Kangire E; Pinard F; Agwanda C; Bieysse D, 2009. Breeding for resistance against coffee wilt disease. In: Coffee Wilt Disease [ed. by Flood, J.]. Wallingford, UK: CAB International, 155-175.
Ndimande BN, 1985. A review of the current knowledge of Fusarium bark disease of coffee in Zimbabwe. In: Clowes M StJ, Logan WJC eds. Advances in Coffee Management and Technology in Zimbabwe 1980-1985. Harare, Zimbabwe: Coffee Grower's Association, 118-119.
Negussie E; Kimani M; Girma A; Phiri N; Teshome D, 2009. Extension approaches and information dissemination for coffee wilt disese management in Africa: experiences from Ethiopia. In: Coffee Wilt Disease [ed. by Flood, J.]. Wallingford, UK: CAB International, 176-195.
Oduor G; Simons S; Phiri N; Njuki J; Poole J; Pinard F; Kyetere D; Hakiza G; Musoli P; Lukwago G; Abebe M; Tesfaye A; Kilambo D; Asiimwe T; Munyankere P, 2003. Surveys to assess the extent and impact of coffee wilt disease in East and Central Africal. Final Technical Report, EU contract No. ASA-RSP/CV-006. Egham, UK: CAB International.
OZACAF, 1995. Project de lutte contre la tracheomycose du Cafeier au Zaire. Report for Office Zairois du Cafe (OZACAF) on coffee wilt in Zaire.
Phiri N; Kimani M; Negussie E; Simons S; Odour G, 2009. Management of coffee wilt disease. In: Coffee Wilt Disease [ed. by Flood, J.]. Wallingford, UK: CAB International, 137-154.
Pieters R; Graff NAVan der, 1980. Resistance to Gibberella xylarioides in Coffea arabica: evaluation of screening methods and evidence for the horizontal nature of the resistance. Netherlands Journal of Plant Pathology, 86(1):37-43
Porteres R, 1959. Valeur agronomique des Cafeiers des types Kouilou et Robusta cultivars en Cote d'Ivoire. Cafe, Cacoa, The, 3:3-13.
Rabechault H, 1954. Sur quelques facteurs de resistance du Cafier a la Tracheomycose. Bull. Sci. Minist. Colon. Sect. Agron.Trop., 5:292-95.
Rutherford M; Bieysse D; Lepoint P; Maraite HMM, 2009. Biology, taxonomy and epidemiology of the coffee wilt pathogen Gibberella xylarioides sensu lato. In: Coffee Wilt Disease [ed. by Flood, J.]. Wallingford, UK: CAB International, 99-119.
Saccas AM, 1956. Recherches experimentales sur la Tracheomycose des Cafeiers en Oubangui-Chari. Agron. Trop. Nogent, 11:7-38.
Wrigley G, 1988. Coffee. London, UK: Longman Press.
ContributorsTop of page
08/07/15 Updated by:
Julie Flood, CABI, UK.
Distribution MapsTop of page
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