Pyrenophora teres. [Descriptions of Fungi and Bacteria].

1973 ◽  
Author(s):  
M. B. Ellis
Keyword(s):  
Geographical Distribution ◽  
Primary Infection ◽  
Secondary Infection ◽  
Growing Season ◽  
Pyrenophora Teres ◽  
Net Blotch ◽  
Floral Bracts

Abstract A description is provided for Pyrenophora teres. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Primarily barley, but also occurs sporadically on wheat, oats and many other Gramineae. DISEASE: Causes net blotch of barley. Primary infection occurs from seed-borne inoculum and produces lesions on the first leaves, which are at first pale but develop into dark spots or streaks later. Secondary infection on older leaves produces pale brown blotches, in which is a network of dark brown lines; these may later coalesce to form irregular leaf stripes. Lesions also occur on the floral bracts. On other hosts the reticulate pattern of the lesions is usually absent. GEOGRAPHICAL DISTRIBUTION: Worldwide; occurs in most barley-producing countries (CMI Map 364, ed. 2, 1968). TRANSMISSION: The disease can be seed-borne as mycelium or conidia, but can also over-winter on crop debris. Perithecia are common on old barley stubble in the spring and ascosporic inoculum can produce much infection (49, 116). Secondary infection by air-borne conidia occurs throughout the growing season.

Venturia pirina. [Descriptions of Fungi and Bacteria].

1974 ◽  
Author(s):  
A. Sivanesan
Keyword(s):  
Leaf Litter ◽  
Geographical Distribution ◽  
Primary Infection ◽  
Secondary Infection ◽  
Apple Scab ◽  
Black Spot ◽  
Eriobotrya Japonica ◽  
Venturia Pirina ◽  
Young Growth

Abstract A description is provided for Venturia pirina. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Principally on pear (Pyrus communis) and other Pyrus spp., also recorded from Eriobotrya japonica (loquat) (Herb. IMI). DISEASE: Causes scab or black spot of pear, which results in loss of quantity and quality of fruit. The disease attacks shoots, buds, leaves and fruit, symptoms and aetiology being very similar to those of apple scab caused by V. inaequalis on Malus spp. (CMI Descript. 401). Dark, more or less circular scabs are produced on leaves and fruit, often with some growth distortion. Infection of young wood is more common than with apple scab and causes pale brown blister-like lesions which burst to release conidia in the following year. GEOGRAPHICAL DISTRIBUTION: Worldwide in temperate and subtropical regions wherever pears are grown (see CMI Map 367, ed. 2, 1968). TRANSMISSION: Epidemiology is similar to that of apple scab. The overwintering saprophytic perithecial stage on leaf litter releases airborne ascospores in spring which infect young growth, and secondary infection by conidia dispersed during wet summer weather also occurs. Overwintering lesions on young wood are more frequent than with apple scab and conidia produced by these in the spring can be an important source of primary infection (46, 2061; 47, 849).

Pyrenophora avenae. [Descriptions of Fungi and Bacteria].

1973 ◽  
Author(s):  
M. B. Ellis
Keyword(s):  
Geographical Distribution ◽  
Primary Infection ◽  
Secondary Infection ◽  
Seedling Blight ◽  
Secondary Spread ◽  
Leaf Stripe ◽  
Blight Of Oats

Abstract A description is provided for Pyrenophora avenae. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Oats (Avena spp.). DISEASE: Leaf stripe, blotch or spot and seedling blight of oats. Seed-borne infection produces a range of seedling symptoms from pre-emergence death to slight spotting or streaking of coleoptiles. Mycelial infection of emerging leaves causes distortion and spotting. Inoculum from primary leaves causes secondary spread to upper leaves, producing light reddish-brown irregular streaks or blotches. Spikelet drop (42, 543) and stem-break (36, 641) may also occur when the disease is severe. GEOGRAPHICAL DISTRIBUTION: Widespread; occurs throughout most oat-growing areas. CMI Map 105, ed. 2, 1966, and in addition in Queensland, Egypt, Angola and Colombia. TRANSMISSION: Primary infection appears to be entirely by seed-borne inoculum, either as conidia or more particularly as mycelium in the outer layers of the seed. Secondary infection is by air-borne conidia. Soil-borne inoculum appears to be unimportant.

Venturia populina. [Descriptions of Fungi and Bacteria].

1976 ◽  
Author(s):  
A. Sivanesan
Keyword(s):  
North America ◽  
Geographical Distribution ◽  
Primary Infection ◽  
Secondary Infection

Abstract A description is provided for Venturia populina. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOST: Populus spp. DISEASE: Blight or dieback of poplars. GEOGRAPHICAL DISTRIBUTION: Europe and North America. TRANSMISSION: By ascospores and conidia (41, 106). Primary infection by ascospores and secondary infection by conidia.

scholarly journals Reinfection as a cause of complications and relapses in scarlet fever wards

1937 ◽  
Vol 37 (2) ◽  
pp. 153-171 ◽  
Author(s):  
V. D. Allison ◽  
W. A. Brown
Keyword(s):  
Scarlet Fever ◽  
Primary Infection ◽  
Secondary Infection ◽  
Clinical Signs ◽  
Late Complications ◽  
Isolation Method ◽  
Fever Patient ◽  
The Third ◽  
Serological Type ◽  
Mode Of Transmission

1. The term “reinfection” has been defined as the secondary infection of a scarlet fever patient during hospitalization withStr. pyogenesbelonging to a serologically different type from that producing the primary infection.2. Of forty-seven scarlet fever patients nursed in a multiple-bed ward and swabbed twice weekly during their period of isolation, thirty-three (70.2 per cent) became reinfected with a serological type ofStr. pyogenesdifferent from that causing the primary disease.3. In fifteen out of the thirty-three patients reinfected, the reinfection was “latent”, i.e. gave rise to no clinical signs, while in the remaining eighteen the reinfection was “manifest”, i.e. was accompanied by clinical signs or complications.4. Patients nursed in cubicles or in a ward confined to infections with a single serological type did not show reinfection; their convalescence was progressive and there were no late complications.5. The majority of complications occurring during the third week of hospitalization and subsequently, in multiple-bed wards devoted to scarlet fever, are due to reinfection.6. Most reinfections occur during the third week in hospital at a time when patients are as a rule convalescent from their primary infection.7. The most frequent mode of transmission of reinfection appears to be by direct contact of patient with patient.8. Ten instances of “relapse” in scarlet fever (only three in the present series) are quoted; in all of them the patients were nursed in multiple-bed wards. In each instance the “relapse” coincided with the isolation of a fresh serological type ofStr. pyogenesfrom the throat, and must therefore be regarded as a second attack of scarlet fever.9. The various systems of nursing patients in isolation hospitals are discussed and it is suggested that scarlet fever patients should be cubicle-nursed if possible. Failing this they should be nursed by the bed-isolation method in multiple-bed wards. By setting aside small wards it might be possible to keep together patients who are all infected by the same serological type ofStr. pyogenes; the number of such wards would vary with the number (usually three or four) of epidemic types current at the time.

Gibberella zeae. [Descriptions of Fungi and Bacteria].

1973 ◽  
Author(s):  
C. Booth
Keyword(s):  
Geographical Distribution ◽  
Secondary Infection ◽  
Brown Rot ◽  
Gibberella Zeae ◽  
Infested Soil ◽  
Foot Rot ◽  
Seedling Blight ◽  
Water Droplets ◽  
Ascospore Discharge ◽  
The Tropics

Abstract A description is provided for Gibberella zeae. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Wheat, maize, barley, carnations and other ornamentals; also reported infecting Lycopersicon, Pisum, Trifolium and Solanum DISEASE: Seedling blight, pre-emergence and post-emergence blight, root and foot rot, brown rot, culm decay, head or kernel blight (scab or ear scab) of wheat, maize, barley and other cereals. Leaf and flower rot of carnations and other ornamentals. Also reported infecting species of Lycopersicon, Pisum, Trifolium and Solanum. GEOGRAPHICAL DISTRIBUTION: Worldwide on maize and rice in the tropics. Wheat, oats, barley and rye in temperate regions. TRANSMISSION: By planting infected or infested seeds or by planting in infested soil. Secondary infection occurs widely by water droplets under moist conditions or by ascospore discharge.

Podosphaera clandestina. [Descriptions of Fungi and Bacteria].

1975 ◽  
Author(s):  
S. M. Khairi
Keyword(s):  
Host Plant ◽  
Geographical Distribution ◽  
Secondary Infection ◽  
Pyrus Communis ◽  
Crataegus Monogyna ◽  
Terminal Buds

Abstract A description is provided for Podosphaera clandestina. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On Crataegus monogyna, C. pentagyna, C. punctata, Mespilus germanica, Cratoegomespilus grandiflora, C. dardari, Pyrus communis, Cydonia vulgaris, Pyrocydonia winkleri and P. danieli. DISEASE: Hawthorn mildew. Severe attacks cause defoliation and death of terminal buds on young seedlings and on soft shoots on hedges and trees. The disease has been recorded on hawthorn fruits. The host plant can be grown only from seeds. GEOGRAPHICAL DISTRIBUTION: Worldwide (Salmon, 1900; 45, 3081). Cleistothecia play no part in the disease in England. The overwintering mycelium, inside infected buds, survives until the following spring. These infected buds are the primary infections found each year. Secondary infection is by air-borne conidia.

Entyloma serotinum. [Descriptions of Fungi and Bacteria].

1988 ◽  
Author(s):  
J. E. M. Mordue
Keyword(s):  
New Zealand ◽  
North America ◽  
Geographical Distribution ◽  
Leaf Spot ◽  
Infected Plant ◽  
Growing Season ◽  
Republic Of Georgia ◽  
Borago Officinalis ◽  
Plant Remains ◽  
Water Splash

Abstract A description is provided for Entyloma serotinum. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Symphytum spp., including S. asperrimum, S. bulbosum, S. cordatum, S. officinale, S. ottomanum and S. tuberosum; Borago officinalis; also recorded on Amsinckia, Lappula and Mertensia spp. (in USA) and Pulmonaria (in Europe, but see 64, 4163). DISEASE: Leaf spot of Symphylum, less frequently (though with similar symptoms) of other members of the Boraginaceae.GEOGRAPHICAL DISTRIBUTION: Africa: Algeria. Asia: Israel, USSR (Republic of Georgia). Australasia: New Zealand. Europe: widespread, including Austria, British Isles, Czechoslovakia, Denmark, France (including Corsica), Germany, Hungary, Italy, Netherlands, Poland, Portugal, Romania, Spain, Switzerland, USSR (Latvia), Yugoslavia. North America: USA. TRANSMISSION: Ustilospores survive on infected plant remains and in soil, and germinate to infect seedlings and the new seasons's leaves. In Europe conidia may also over-winter and initiate new infections in spring (Kaiser, 1936). During the growing season, conidia are disseminated by air currents and water-splash.

scholarly journals Distinct Roles of CD28- and CD40 Ligand-Mediated Costimulation in the Development of Protective Immunity and Pathology during Chlamydia muridarum Urogenital Infection in Mice

2009 ◽  
Vol 77 (7) ◽  
pp. 3080-3089 ◽  
Author(s):  
Lili Chen ◽  
Wen Cheng ◽  
Pooja Shivshankar ◽  
Lei Lei ◽  
Xiaoyun Zhang ◽  
...  
Keyword(s):  
Primary Infection ◽  
Protective Immunity ◽  
Gene Knockout ◽  
Secondary Infection ◽  
Cd40 Ligand ◽  
Wild Type ◽  
Chlamydia Muridarum ◽  
Urogenital Infection ◽  
Costimulatory Signals ◽  
Deficient Mice

ABSTRACT Infection with Chlamydia muridarum in the mouse urogenital tract can induce both protective immunity and inflammatory pathologies, which has been used as a model for understanding the immune and pathogenic mechanisms of C. trachomatis infection. We compared the roles of CD28- and CD40 ligand (CD40L)-mediated costimulation in C. muridarum infection. Mice with CD28 or CD80/CD86 gene knockout (KO) displayed an infection course similar to that of wild-type mice during both primary and secondary infection, suggesting that CD28-mediated costimulation is not required for protection against C. muridarum infection. However, mice deficient in CD40L or CD40 displayed a prolonged infection course after primary or secondary infection, suggesting that CD40-CD40L costimulation plays an essential role in the development of anti-C. muridarum immunity. Interestingly, the CD28- or CD80/CD86-deficient mice displayed significantly lower levels of inflammatory pathologies in the upper genital tracts after primary infection, although the attenuation in inflammation was no longer significant during secondary infection. However, the CD40L or CD40 KO mice developed inflammatory pathologies as severe as those in wild-type mice following either primary or secondary infection despite the obvious deficits in adaptive immunity in these KO mice. The resistance of CD28 or CD80/CD86 KO mice to chlamydial infection correlated with production of gamma interferon, while the development of inflammatory pathologies in CD40L or CD40 KO mice correlated with the production of other proinflammatory cytokines in mouse urogenital tracts during the early stages of the infection. These observations together suggest that C. muridarum-induced protective immunity and inflammatory pathologies can be mediated by distinct costimulatory signals.

Entyloma ficariae. [Descriptions of Fungi and Bacteria].

1991 ◽  
Author(s):  
J. E. M. Mordue
Keyword(s):  
North America ◽  
Geographical Distribution ◽  
Leaf Spot ◽  
Small Area ◽  
Infected Plant ◽  
Growing Season ◽  
Plant Remains

Abstract A description is provided for Entyloma ficariae. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Ranunculus ficaria and other species of Ranunculus; R. acris, R. auricomus, R. bongardii, R. cassubicus, R. eremogenes, R. macounii, R. montanus, R. multifidus, R. nemorosus, R. occidentalis, R. oreophilus, R. pennsylvanicus, R. polyanthemos, R. repens, R. sardous, R. scleratus, R. septentrionalis; there are occasional records for other Ranunculaceae (Anemone, Thalictrum). DISEASE: Leaf spot or white smut of Ranunculus species. Infected plants often show slightly smaller leaves and fewer flowers than uninfected. Although the smut is not systemic, it is common for almost every leaf of a plant to develop spots and for disease to persist within a small area year after year. GEOGRAPHICAL DISTRIBUTION: Widely distributed in north temperate regions. Asia: Japan, Turkey, USSR; Europe: Austria, Belgium, Czechoslovakia, Denmark, Finland, France, Germany, Greece, Hungary, Iceland, Italy, Netherlands, Norway, Poland, Portugal, Romania, Spain, Sweden, Switzerland, UK, USSR; North America: Canada, USA (33: 450 & 634; Vanky, 1985). TRANSMISSION: Ustilospores survive in infected plant remains in soil and germinate, chiefly in spring, to infect the new seasons leaves. Conidia are disseminated by wind and rain and contribute to the spread of disease throughout the growing season.

Peronospora anemones. [Descriptions of Fungi and Bacteria].

1981 ◽  
Author(s):  
S. M. Francis
Keyword(s):  
New Zealand ◽  
Botrytis Cinerea ◽  
Downy Mildew ◽  
Geographical Distribution ◽  
Primary Infection ◽  
Leaf Surface ◽  
Plant Debris ◽  
Lower Leaf Surface ◽  
Glass Slides ◽  
Secondary Infections

Abstract A description is provided for Peronospora anemones. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Anemone coronaria, A. globosa. DISEASE: Downy mildew of anemones. Infected leaves lose their natural bloom, appearing dull green, almost grey in colour and are often down curled giving the plant a rounded appearance. As the disease progresses, leaf colour may change to shades of pink or purple with necrotic areas appearing on the older leaves. Invasion by secondary organisms (e.g. Botrytis cinerea) is common, especially after frost or storm injury, and this accelerates plant death. In favourable conditions conidiophores develop forming a whitish-grey down on the lower leaf surface, on the bracts and, less frequently, on the petioles. It is not uncommon for affected plants to show little or no sporulation and in these cases the presence of extensive intercellular mycelium and, later in the season, oospores in petioles and peduncles helps diagnosis. GEOGRAPHICAL DISTRIBUTION: Australasia (New Zealand); Europe (England, Jersey, France, Italy, Netherlands). TRANSMISSION: Primary infection is caused by oospores in plant debris in the soil. Tramier (1963) was unable to germinate oospores and thus work out precise details of the conditions affecting their germination but he showed evidence that regular and prolonged rain encouraged germination. Conidia, which cause secondary infections, are dispersed by rain and during harvesting of the flowers. Wind is thought to be unimportant in their dissemination as shown by glass slides covered with vaseline and placed near an infected crop (Tramier, 1965).

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