scholarly journals Dynamics of Primary and Secondary Infection in Take-All Epidemics

1999 ◽  
Vol 89 (1) ◽  
pp. 84-91 ◽  
Author(s):  
D. J. Bailey ◽  
C. A. Gilligan
Keyword(s):  
Winter Wheat ◽  
Initial Phase ◽  
Primary Infection ◽  
Adventitious Roots ◽  
Secondary Infection ◽  
Inoculum Density ◽  
Separate Experiment ◽  
Disease Progress ◽  
Seminal Roots ◽  
Take All

Using a combination of experimentation and mathematical modeling, the effects of initial (particulate) inoculum density on the dynamics of disease resulting from primary and secondary infection of wheat by the take-all fungus, Gaeumannomyces graminis var. tritici, were tested. A relatively high inoculum density generated a disease progress curve that rose monotonically toward an asymptote. Reducing the initial inoculum density resulted in a curve that initially was monotonic, rising to a plateau, but which increased sigmoidally to an asymptotic level of disease thereafter. Changes in the infectivity of particulate inoculum over time were examined in a separate experiment. Using a model that incorporated terms for primary and secondary infection, inoculum decay, and host growth, we showed that both disease progress curves were consistent with consecutive phases dominated, respectively, by primary and secondary infection. We examined the spread of disease from a low particulate inoculum density on seminal and adventitious root systems separately. Although seminal roots were affected by consecutive phases of primary and secondary infection, adventitious roots were affected only by secondary infection. We showed that the characteristic features of disease progress in controlled experiments were consistent with field data from crops of winter wheat. We concluded that there is an initial phase of primary infection by G. graminis var. tritici on winter wheat as seminal roots grow through the soil and encounter inoculum, but the rate of primary infection slows progressively as inoculum decays. After the initial phase, there is an acceleration in the rate of secondary infection on both seminal and adventitious roots that is stimulated by the increase in the availability of infected tissue as a source of inoculum and the availability of susceptible tissue for infection.

scholarly journals An Epidemiological Analysis of the Role of Disease-Induced Root Growth in the Differential Response of Two Cultivars of Winter Wheat to Infection by Gaeumannomyces graminis var. tritici

2006 ◽  
Vol 96 (5) ◽  
pp. 510-516 ◽  
Author(s):  
D. J. Bailey ◽  
A. Kleczkowski ◽  
C. A. Gilligan
Keyword(s):  
Winter Wheat ◽  
Root Growth ◽  
Primary Infection ◽  
Secondary Infection ◽  
High Density ◽  
Inoculum Density ◽  
Root Production ◽  
Epidemiological Modeling ◽  
High Inoculum ◽  
Take All

Epidemiological modeling combined with parameter estimation of experimental data was used to examine differences in the contribution of disease-induced root production to the spread of take-all on plants of two representative yet contrasting cultivars of winter wheat, Ghengis and Savannah. A mechanistic model, including terms for primary infection, secondary infection, inoculum decay, and intrinsic and disease-induced root growth, was fitted to data describing changes in the numbers of infected and susceptible roots over time at a low or high density of inoculum. Disease progress curves were characterized by consecutive phases of primary and secondary infection. No differences in root growth were detected between cultivars in the absence of disease and root production continued for the duration of the experiment. However, significant differences in disease-induced root production were detected between Savannah and Genghis. In the presence of disease, root production for both cultivars was characterized by stimulation when few roots were infected and inhibition when many roots were infected. At low inoculum density, the transition from stimulation to inhibition occurred when an average of 5.0 and 9.0 roots were infected for Genghis and Savannah, respectively. At high inoculum density, the transition from stimulation to inhibition occurred when an average of 4.5 and 6.7 roots were infected for Genghis and Savannah, respectively. Differences in the rates of primary and secondary infection between Savannah and Genghis also were detected. At a low inoculum density, Genghis was marginally more resistant to secondary infection whereas, at a high density of inoculum, Savannah was marginally more resistant to primary infection. The combined effects of differences in disease-induced root growth and differences in the rates of primary and secondary infection meant that the period of stimulated root production was extended by 7 and 15 days for Savannah at a low and high inoculum density, respectively. The contribution of this form of epidemiological modeling to the better management of take-all is discussed.

scholarly journals Epidemiology and Chemical Control of Take-All on Seminal and Adventitious Roots of Wheat

2005 ◽  
Vol 95 (1) ◽  
pp. 62-68 ◽  
Author(s):  
D. J. Bailey ◽  
N. Paveley ◽  
C. Pillinger ◽  
J. Foulkes ◽  
J. Spink ◽  
...  
Keyword(s):  
Primary Infection ◽  
Seed Treatment ◽  
Adventitious Roots ◽  
Compartmental Model ◽  
Secondary Infection ◽  
Field Trials ◽  
Root Production ◽  
Epidemiological Modeling ◽  
Composite Curve ◽  
Take All

Epidemiological modeling is used to examine the effect of silthiofam seed treatment on field epidemics of take-all in winter wheat. A simple compartmental model, including terms for primary infection, secondary infection, root production, and decay of inoculum, was fitted to data describing change in the number of diseased and susceptible roots per plant over thermal time obtained from replicated field trials. This produced a composite curve describing change in the proportion of diseased roots over time that increased monotonically to an initial plateau and then increased exponentially thereafter. The shape of this curve was consistent with consecutive phases of primary and secondary infection. The seed treatment reduced the proportion of diseased roots throughout both phases of the epidemic. However, analysis with the model detected a significant reduction in the rate of primary, but not secondary, infection. The potential for silthiofam to affect secondary infection from diseased seminal or adventitious roots was examined in further detail by extending the compartmental model and fitting to change in the number of diseased and susceptible seminal or adventitious roots. Rates of secondary infection from either source of infected roots were not affected. Seed treatment controlled primary infection of seminal roots from particulate inoculum but not secondary infection from either seminal or adventitious roots. The reduction in disease for silthiofam-treated plants observed following the secondary infection phase of the epidemic was not due to long-term activity of the chemical but to the manifestation of disease control early in the epidemic.

scholarly journals Epidemiological Analysis of Take-All Decline in Winter Wheat

2009 ◽  
Vol 99 (7) ◽  
pp. 861-868 ◽  
Author(s):  
D. J. Bailey ◽  
N. Paveley ◽  
J. Spink ◽  
P. Lucas ◽  
C. A. Gilligan
Keyword(s):  
Primary Infection ◽  
Seed Treatment ◽  
Secondary Infection ◽  
Disease Suppression ◽  
Root Production ◽  
Wheat Crop ◽  
Epidemiological Analysis ◽  
Infection Disease ◽  
Low Levels ◽  
Take All

Take-all dynamics within crops differing in cropping history (the number of previous consecutive wheat crops) were analyzed using an epidemiological model to determine the processes affected during take-all decline. The model includes terms for primary infection, secondary infection, inoculum decay, and root growth. The average rates of root production did not vary with cropping history. The force of primary infection increased from a low level in 1st wheat crops, to a maximum in 2nd to 4th wheat crops, and then to intermediate levels thereafter. The force of secondary infection was low but increased steadily during the season in first wheat crops, was delayed but rose and fell sharply in 2nd to 4th wheat crops, and for 5th and 7th wheat crops returned to similar dynamics as that for 1st wheat crops. Chemical seed treatment with silthiofam had no consistent effect on the take-all decline process. We conjecture that these results are consistent with (i) low levels of particulate inoculum prior to the first wheat crop leading to low levels of primary infection, low levels of secondary infection, and little disease suppression; (ii) net amplification of inoculum during the first wheat crop and intercrop period; (iii) increased levels of primary and secondary infection in subsequent crops, but higher levels of disease suppression; and (iv) an equilibrium between the pathogen and antagonist populations by the 5th wheat, reflected by lower overall rates of primary infection, secondary infection, disease suppression and hence, disease severity.

Colonization of lateral, seminal and adventitious roots of wheat by the take-all fungus, Gaeumannomyces graminis var. tritici

1980 ◽  
Vol 94 (2) ◽  
pp. 325-329 ◽  
Author(s):  
C. A. Gilligan
Keyword(s):  
Adventitious Roots ◽  
Lateral Roots ◽  
Initial Period ◽  
Hyphal Growth ◽  
Gaeumannomyces Graminis ◽  
Rate Of Growth ◽  
Direct Inoculation ◽  
Seminal Roots ◽  
Gaeumannomyces Graminis Var Tritici ◽  
Take All

SummaryProgressive colonization of adventitious, seminal and lateral roots of wheat by Gaeumannomyces graminis var. triticiwas monitored for 18 days after direct inoculation of roots. Adventitious roots supported greater colonization by superficial runner hyphae above and below inoculation sites than did seminal roots due to more rapid establishment of colonization. Subsequent rates of superficial runner hyphal growth along the two types of root were not significantly different. In contrast with seminal and lateral roots, adventitious roots did not show any dark stelar discoloration during the period of observation. Both the rate of growth of superficial runner hyphae and of advance of dark stelar discoloration were substantially slower on lateral roots than on seminal roots. After an initial period of equal growth above and below inoculation sites, superficial runner hyphae grew more slowly below than above these sites on all three types of root.

Analysis of disease-progress curves for take-all in consecutive crops of winter wheat

1991 ◽  
Vol 40 (1) ◽  
pp. 8-24 ◽  
Author(s):  
A. R. WERKER ◽  
C. A. GILLIGAN ◽  
D HORNBY
Keyword(s):  
Winter Wheat ◽  
Disease Progress ◽  
Take All

scholarly journals Influence of Crop Management on Take-All Development and Disease Cycles on Winter Wheat

1997 ◽  
Vol 87 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Nathalie Colbach ◽  
Philippe Lucas ◽  
Jean-Marc Meynard
Keyword(s):  
Primary Infection ◽  
Plant Density ◽  
Secondary Infection ◽  
Disease Onset ◽  
Gaeumannomyces Graminis ◽  
Growth Stages ◽  
Root Number ◽  
Infection Cycle ◽  
Infection Cycles ◽  
Take All

Wheat was assessed at four crop growth stages for take-all (Gaeumannomyces graminis var. tritici) in a series of field trials that studied the effects of five wheat management practices: sowing date, plant density, nitrogen fertilizer dose and form, and removal/burial of cereal straw. An equation expressing disease level as a function of degree days was fitted to the observed disease levels. This equation was based on take-all epidemiology and depended on two parameters reflecting the importance of the primary and secondary infection cycles, respectively. Early sowing always increased disease frequency via primary infection cycle; its influence on the secondary cycle was variable. Primary infection and earliness of disease onset were increased by high density; however, at mid-season take-all was positively correlated to the root number per plant, which was itself negatively correlated to plant density. At late stages of development, neither plant density nor root number per plant had any influence on disease. A high nitrogen dose increased both take-all on seminal roots and severity of primary infection cycle but decreased take-all on nodal roots and secondary infection cycle. Ammonium (versus ammonium nitrate) fertilizer always decreased disease levels and infection cycles, whereas straw treatment (burial versus removal of straw from the previous cereal crop) had no influence.

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.

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).

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.

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