bluuebunny/crossref_metadata_2025_split huggingface dataset:
Xanthomonas pruni
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Hayward A. C. , Waterston J. M. 
Published: July 2021

Abstract

A description is provided for
Xanthomonas pruni
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Prunus amygdalus, P. armeniaca, P. avium, P. cerasus, P. davidiana, P. domestica, P. japonica, P. mume, P. persica, P. salicina
and other species of
Prunus
(30: 48; Elliott, 31: 105, p. 114). DISEASE: Bacterial leaf spot on leaves, twigs and fruit of plum, peach, apricot and cherry; black spot of plum and peach; bacterial shot-hole of leaves. Previously referred to in earlier literature as bacterial canker of stone fruits, name now reserved for the disease caused by
Pseudomonas morsprunorum
and
P. syringae
. Shot-hole on the leaves of trees infected by
X. pruni
differs from that of fungal origin by the presence of bacterial ooze and in the shape of the leaf perforations which are generally irregular or elongated instead of round (35: 530). Atypical symptoms have been reported on peach leaves (19: 292). Symptoms on cherry fruit differ from those on peach and plum (14: 178). Branch cankers on peach are shallow and do not become perennial as on plum. On peach they were not observed to girdle the stem (10: 224). GEOGRAPHICAL DISTRIBUTION: Africa (Southern Rhodesia, South Africa); Asia (China, India, Japan, Korea, U.S.S.R.): Australasia (Australia, New Zealand), Europe (Cyprus, Italy, Romania); North America (Bermuda, Canada, U.S.A.): South America (Argentina, Brazil, Uruguay). In the U.S.A. the disease occurs on stone fruits in at least 26 States (30: 48; CMI Map 340, Ed. 2, 1964). TRANSMISSION:
Xanthomonas pruni
is disseminated by wind and rain (29: 218). The pathogen enters leaves through the stomata, and fruit infection appears to follow that of the leaves, probably as a result of leaf drop during rainy spells (7: 76). Primary leaf infection on peach originates in twigs with spring cankers (Thornberry & Anderson, 1933) or terminal die-back in which the pathogen overwinters (39: 600). Summer cankers on peach are only important under certain conditions for initiating spring infection (34: 732, 379), but on plum and apricot they play a more permanent role since the infection originating in the current season's twigs continues to develop in them during the following spring (Anderson, 1956). Overwintering on plum buds and fallen leaves has also been reported (41: 608). Species of
Cicada
may damage the bark of plum in New Zealand and thus provide points of entry (32: 322). The chief means of transmission of the pathogen in New Zealand is in budwood and root-stocks (42: 202).
Puccinia allii
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Laundon G. F. , Watenton J. M. 
Published: July 2021

Abstract

A description is provided for
Puccinia allii
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Allium ampeloprasum, A. ascalonicum, A. cepa, A. chinense, A. fistulosum, A. porrum, A. sativum, A
.
schoenoprasum, A. tuberosum, A. ursinum
and many other species of
Allium
. DISEASE: Rust on leaves and stems of chives, garlic, Japanese bunching or Welsh onion, leek, onion, rakkyo and shallot. Leaves may be killed in severe infections. GEOGRAPHICAL DISTRIBUTION: Africa, Asia, Australasia, Europe, North and South America (CMI Map 400, 1963 and Herb. IMI). TRANSMISSION: The pathogen may overwinter in the uredio stage on wild plants in America. There is also a record of interception in the United States on garlic imported from Israel (37: 760). Records of seed transmission on leek and garlic have been made (11: 255; 30: 401) but this is thought to be of minor importance (Noble
et al.
, 1958).
Puccinia asparagi
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Waterston J. M. 
Published: July 2021

Abstract

A description is provided for
Puccinia asparagi
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Asparagus officinalis
(cult.), also on a few other species, including
A. maritimus, A. plumosus
and
A. scaber
; slight infections can be obtained on
Allium cepa
(see CMI Descript. 52). DISEASE: Asparagus rust. Causing lesions on asparagus stems, either oval yellowish spots (aecia and pycnia) or blister-like pustules (uredia and telia), and producing premature desiccation with subsequent weakening of roots and crowns which reduces the yield of edible shoots in the following season. May also attack onion, shallot and chives. GEOGRAPHICAL DISTRIBUTION: Occurs in Africa, Asia, Australasia, Europe and North America wherever asparagus is grown (CMI Map 216, Ed. 2, 1950). TRANSMISSION: Spore dissemination mainly by wind with rain contributing to spread on individual plants (33: 333). Also believed to be transmitted in shipments of contaminated plants or packing material and soil accompanying roots (Arthur 1929). Volunteer and wild plants may serve as sources of infection (32: 58).
Uromyces viciae-fabae
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Laundon G. F. , Waterston J. M. 
Published: July 2021

Abstract

A description is provided for
Uromyces viciae-fabae
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Lathyrus, Lens, Orobus, Pisum
and
Vicia
species. DISEASE: Rust on leaves and stems of broad-bean, pea, vetch and lentil, causing partial defoliation of susceptible varieties. GEOGRAPHICAL DISTRIBUTION: World-wide (CMI Map 200, Ed. 2, 1964). TRANSMISSION: Recorded seed-borne on broad-bean (11: 222) and in infected plant debris mixed with seed of
Lens culinaris
in India by Prasada & Verma (1948), who found infection disseminated chiefly by aecidiospores at temperatures below 25°C. At Delhi, aecidiospores and urediospores die after harvest but the teleutospores resist high temperatures and remain viable for 2 yr. when stored at 3-18°C, germinating in January to initiate fresh outbreaks of infection. Studies by Kispatic (1949) in Yugoslavia suggested that aecidiospores probably remain viable in Mediterranean climates, though unable to survive severe winters experienced in Northern regions. The uredio mycelium was found very resistant to both heat and sunlight and survived the winter in leaves and stems of autumn-sown broad-bean, producing new spores as an early source of infection in spring. Urediospores showed 30% germination after 5 months storage at 1°C.
Microsporum audouinii
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Stockdale P. M. 
Published: July 2021

Abstract

A description is provided for
Microsporum audouinii
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Primarily a pathogen of man. Also recorded on the dog, gibbon, guineapig and monkey. Most strains are not pathogenic for experimental animals. DISEASE: Ringworm (dermatophytosis, tinea). Infected hairs usually fluoresce bright green under Wood's light and are surrounded by an ectothrix sheath of small spores in a mosaic arrangement. In man, the scalp (tinea capitis) and less frequently the glabrous skin (tinea corporis) may be infected. Children are most susceptible, and in adults infection is usually confined to the glabrous skin, although a few scalp infections have been reported. Rothman
et al.
(RMVM 1, 614) noted that fatty acids from adult hair fat inhibited
M. audouinii in vitro
and suggested that this was the reason for lower incidence of infection in adults, but Kligman & Grinsberg (RMVM 1, 1800) found that adult sebum was not more fungistatic than that of children. Scalp lesions are usually circular, scaling areas of alopecia and, in contrast to
M. cants
infections, there is generally very little inflammatory reaction. Skin lesions are usually circulate scaling areas with clearing centres. Kligman (RMVM 1, 2510; 2, 2484) studied the pathogenesis of tinea capitis due to
M. audouinii
. GEOGRAPHICAL DISTRIBUTION: Africa (Algeria, Chad Republic, Cameroons, Congo, Egypt, French West Africa, Guinea Republic, Madagascar, Morocco, Mozambique, Nigeria, South Africa, Tunisia); Asia (India, Java, Palestine, Persia, Turkey), Australasia & Oceania (Australia (New South Wales, Western Australia), New Zealand), Europe (Austria, Belgium, Czechoslovakia, Denmark, France, Germany, Great Britain and Ireland, Hungary, Italy, Netherlands, Poland, Portugal, Romania, Spain, Sweden, Switzerland, U.S.S.R., Yugoslavia), North America (Canada, U.S.A.), Central America and West Indies (Cuba, Jamaica, Puerto Rico); South America (Argentina, Brazil, Chile, Ecuador, Venezuela).
Microsporum distortum
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Stockdale P. M. 
Published: July 2021

Abstract

A description is provided for
Microsporum distortum
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Recorded on man, monkey, dog and horse. Some human infections have been in children with a history of contact with cats with skin lesions but these animals were not examined by culture. Rats, guineapigs, rabbits and cats have been experimentally infected. DISEASE: Ringworm (dermatophytosis tinea). Similar to
M. canis
infections. Infected hairs fluoresce pale to bright green under Wood's light and are encrusted with ectothrix sheaths of small spores in a mosaic arrangement. In man, the scalp (tinea capitis) and glabrous skin (tinea corporis) may be infected. Most reported infections have been in children under 7 years old. Scalp lesions have been reported only in children, and usually consist of scaling patches of alopecia, with some erythema at the margin. Skin lesions are usually small, circular, with erythematous borders and dry, scaling centres. In animals scaling patches of alopecia are the usual symptom. GEOGRAPHICAL DISTRIBUTION: Australia (New South Wales), New Zealand (apparently restricted to Otago), U.S.A. (Iowa, Ga). All cases reported from U.S.A. have been in pet monkeys probably recently imported from Central America, and in humans and dogs which had been in contact with the monkeys.
Nannizzia fulva
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Stockdale P. M. 
Published: July 2021

Abstract

A description is provided for
Nannizzia fulva
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Recorded only from man (but see NOTES). Guinea-pigs have been experimentally infected. DISEASE: Ringworm (dermatophytosis, tinea).
Nannizzia fulva
is present in the soil and apparently only rarely pathogenic. The scalp (tinea capitis) and glabrous skin (tinea corporis) may be infected. Skin lesions are inflammatory. The only proved case of scalp infection is that recorded by Uriburu (1909); according to Sabouraud (
Les Teignes
, 1910, p. 241) in this case there was a light inflammatory reaction and infected hairs were indistinguishable from those in
M. audouinii
infections. In experimental inoculations of guineapigs (Rdzanek, pers. comm.)
N. fulva
was slightly less virulent than
N. gypsea
and
N. incurvata
, the reaction varying from negative to strongly inflammatory. A few ectothrix hyphae breaking up into arthrospores were seen on some hairs, and infected hairs did not fluoresce under Wood's light. GEOGRAPHICAL DISTRIBUTION: Africa (Tanzania), Europe (Great Britain, Hungary, Yugoslavia), South America (Argentina). Probably world-wide in distribution in the soil, but there may be local limiting factors (e.g., in Great Britain it has been recorded only for Bristol, Somerset, and Wiltshire).
Nannizzia gypsea
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Stockdale P. M. 
Published: July 2021

Abstract

A description is provided for
Nannizzia gypsea
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Recorded only from man (but see NOTES). Guinea-pigs have been experimentally infected. DISEASE: Ringworm (dermatophytosis, tinea).
Nannizzia gypsea
is apparently widespread in soil and only rarely pathogenic. The scalp (tinea capitis) and glabrous skin (tinea corporis) may be infected. Skin lesions are inflammatory, but details of only two scalp infections are known. In both the lesions were inflammatory; in one favus-like crusts were also found and in the other hair invasion was of the large-spored ectothrix type. In experimental inoculations of guineapigs (Rdzanek, pers. comm.)
N. gypsea
was slightly more virulent than
N. incurvata
and
N. fulva
, the reaction varying from negative to strongly inflammatory, a few ectothrix hyphae breaking up into arthrospores were seen on some hairs, and infected hairs did not fluoresce under Wood's light. GEOGRAPHICAL DISTRIBUTION: Asia (Japan), Australasia and Oceania (Australia (New South Wales), New Zealand, Raratonga, Cook Island), Europe (France, Great Britain, Italy); North America (Tenn.). Probably of world-wide distribution in the soil.
Sphacelotheca cruenta
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Ainsworth G. C. 
Published: July 2021

Abstract

A description is provided for
Sphacelotheca cruenta
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Sorghum bicolor (S. vulgare
) (sorghum),
S. sudanense
(Sudan grass),
S. halepense
(lohnson grass), and other
Sorghum
spp., and (in India, fide Chona & Munjal; 31: 400)
Saccharum officinarum
(sugarcane). DISEASE: Loose smut of sorghum. In addition to the grain being replaced by smut spores the plants are markedly stunted and their forage value reduced while infected heads are looser, bushier and darker green than healthy ones due to hypertrophy of the glumes; for further details see Tarr, 1962. GEOGRAPHICAL DISTRIBUTION: Africa, Asia, Europe, N., C. and S. America; see CMI Map 408, 1965. TRANSMISSION: Infection of the seedlings occurs from seed contaminated with spores (Noble
et al, An annotated list of seed-borne diseases
, 1958, p. 66). Spores remain viable for four years in the laboratory but as they germinate readily in water soil transmission is unimportant. Spread within the crop by floral infection by air-borne spores has been observed.
Tilletia barclayana
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Ainsworth G. C. 
Published: July 2021

Abstract

A description is provided for
Tilletia barclayana
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Oryza sativa
(rice) and species of
Brachiaria, Digitaria, Eriochloa, Panicunr
and
Pennisetum
. DISEASE: Rice smut (black smut, kernel smut, bunt of rice). A disease of variable incidence but at times responsible for economically important losses. GEOGRAPHICAL DISTRIBUTION: Africa (Sierra Leone), Asia (widespread in India and the Far East), N. (Mexico), C. (Trinidad) and S. (British Guiana, Venezuela, British Honduras) America, Pacific (Fiji, Norfolk lsl.); see CMI Map 75, 1945 (as N.
horrida
). TRANSMISSION: Infection occurs via the opening flowers and the disease is seed borne (Noble
et al., An annotated list of seed-borne diseases
, 1958, p. 54). It can survive for several years in soil or seed (40: 465).
Tolyposporium ehrenbergii
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Ainsworth G. C. 
Published: July 2021

Abstract

A description is provided for
Tolyposporium ehrenbergii
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Sorghum bicolor
(
S. vulgare
) (sorghum) and other
Sorghum
spp. DISEASE: Long smut of sorghum. Losses are usually slight. GEOGRAPHICAL DISTRIBUTION: Africa (widespread), Asia (China, India, Iraq, Israel, Pakistan, Turkey, U.S.S.R.); see CMI Map 377, 1960. TRANSMISSION: Floral infection is believed to occur and the infection is transmitted by seed (Noble
et al., An annotated list of seed-borne diseases
, 1958, p. 66) and soil. See Tarr (1962, p. 250) for a discussion.
Ustilago crameri
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Ainsworth G. C. 
Published: July 2021

Abstract

A description is provided for
Ustilago crameri
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Setaria italica
(Italian or foxtail millet) and its varieties and
S. riridis
. DISEASE: Head smut of millet. A major disease of
Setaria italica
wherever the crop is grown. GEOGRAPHICAL DISTRIBUTION: Africa (Kenya, S. Africa), Asia (widespread), Europe (widespread in S.E.), N. America (general), S. America (Argentina), Australia (N.S.W.); see CMI Map 239, 1951. TRANSMISSION: The disease is seed borne with infection at seedling stage. Spores at least 62 years old were found to be viable by Wang (1936).
Guignardia citricarpa
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Sutton B. C. , Waterston J. M. 
Published: July 2021

Abstract

A description is provided for
Guignardia citricarpa
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Citrus
spp. Also recorded in a non-pathogenic form on many other hosts in the following families:
Anacardiaceae, Aquifoliaceae, Bignoniaceae, Burseraceae, Cunoniaceae, Dioscoreaceae, Gramineae, Lauraceae, Leguminosae, Liliaceae, Lythraceae, Magnoliaceae, Myrtaceae, Orchidaceae, Passifloraceae, Proteaceae, Rosaceae, Rutaceae, Solanaceae, Sterculiaceae, Theaceae
(29: 208; 43: 1922a; Herb. IMI). DISEASE: Black spot of citrus. Kiely (1949) described 3 types of fruit lesion:
Hard spot and shot-hole spot
numerous, at first circular, brown with slight depressions, later more depressed in the centre which turns grey-white, margin black and surrounded by a ring of green rind tissue;
Freckle spot
develops after hard spot phase with abundant lesions, small, deep organge to brick red, finally brown, lacking a green ring,
Virulent spot
, irregular, confluent, rapidly spreading, black in the centre where pycnidia are produced, brown nearer the edge, finally brick red at the periphery forming the margin of the sunken lesion. McOnie found field temperatures affected symptom expression (44: 1556b). Also occurs on leaves, twigs and flowers of citrus and other hosts, often as latent infections. GEOGRAPHICAL DISTRIBUTION: Widely distributed on a large number of hosts. Countries where the fungus has been reported as a pathogen of citrus fruit in the field are designated below with an asterisk: Africa (? Egypt, Kenya, Mozambique, Nigeria, *Rhodesia, *South Africa, Uganda), Asia (Ceylon, *China, *Formosa (Taiwan), Hong Kong,? India, *Indonesia, Iran, Israel, *Japan, Korea,? Malaya, Okinawa,? Pakistan,? Philippines,? Singapore,? Thailand,? Vietnam); Australasia & Oceania, (*Australia,? Fiji Islands,? Hawaii, New Hebrides), Europe (Sicily, Spain, U.S.S.R. (Republic of Georgia)); North America (United States (Florida)); Central America and the Caribbean (Honduras, Jamaica, Trinidad); South America (*Argentine, *Brazil, *Peru, Venezuela). (CMI Map 53, ed. 3, 1961; 29: 208; 44, 701; Herb. IMI). TRANSMISSION: By air-borne ascospores from perithecia produced on cirrus leaf litter (43, 1922b). Conidia produced from pycnidia require water droplets for emergence and dispersal. They play a minor role by contributing to the infection of low hanging fruit. Mycelium in latent infections of citrus leaves remains viable up to 18 days and may be detected when the leaves are incubated at 30°C (Kiely, 1949). Nursery trees may also carry latent infection into other citrus growing areas (Kiely, 1949; Wager, 1953). Wounds on fruit made by insects may also provide infection courts (16: 247, 22: 19).
Leptosphaeria nodorum
. [Descriptions of Fungi and Bacteria].
Authors: UK, CAB International  , Sutton B. C. , Waterston J. M. 
Published: July 2021

Abstract

A description is provided for
Leptosphaeria nodorum
. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On
Triticum
spp. Also on many other genera in the
Gramineae
including
Agropyron, Cinna, Dactylis
,
Deschampsia, Elymus, Festuca, Glyceria, Hordeum, Hystrix, Lepturus, Melica, Poa, Psamma, Secale, Stipa
(Sprague, 1950). DISEASE: Glume blotch of wheat. Causes discoloured to brown lesions on glumes, culms and leaves. Leaf lesions are 1 cm long, elongated, elliptical, golden brown, surrounded by a diffuse, lighter margin becoming darker and bearing pycnidia. Similar brown lesions occur on glumes where they spread from the apices downwards, and bear pycnidia and perithecia. Perithecia are also formed on dead glumes and culms. The heads of wheat may become blackened, producing shrivelled kernels of abnormal structure. Germinating seedlings may also be attacked with subsequent loss of vigour. GEOGRAPHICAL DISTRIBUTION: Africa (Ethiopia, Kenya, Malawi, Morocco, Rhodesia, South Africa, Tanzania, Uganda, Zambia); Asia (China, Formosa (Taiwan), India, Japan, U.S.S.R.); Australasia (Australia, New Zealand); Europe (Austria, Belgium, Bulgaria, Czechoslovakia, Denmark, France, Germany, Great Britain, Greece, Ireland, Italy, Latvia, Netherlands, Norway, Poland, Portugal, Rumania, Spain, Sweden, Switzerland, U.S.S.R., Yugoslavia); North America (Canada, U.S.A.); South America (Argentina, Bolivia, Brazil, Uruguay). (CMI Map 283, ed. 2, 1954; Herb IMI.) TRANSMISSION: Frequently seed-borne (Noble
et al.
, 1958; Hewett, 1965), persisting in a viable condition in seed up to 7 yr. in Canada (31: 596). Also surviving in wheat stubble and crop residues and after 1 yr. in straw kept in dry storage (43, 4g, 2589). Conidia have remained viable in pycnidia after 18 months in the open (Weber, 1922).