Inligting

9.8: Infeksies in plante - Biologie

9.8: Infeksies in plante - Biologie


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Die produksie van voldoende gewasse van goeie gehalte is noodsaaklik vir menslike bestaan. Byvoorbeeld, die swam Claviceps purpurea veroorsaak ergot, 'n siekte van graangewasse (veral van rog). Smuts, roes en poeieragtige of donsagtige skimmel is ander voorbeelde van algemene swampatogene wat gewasse beïnvloed.

Aflatoksiene is giftige, kankerverwekkende verbindings wat deur swamme van die genus vrygestel word Aspergillus. Oeste van neute en korrels word periodiek deur aflatoksiene besmet, wat lei tot massiewe herroeping van produkte. Dit ruïneer produsente soms en veroorsaak voedseltekorte in ontwikkelende lande.

Nederlandse Iepsiekte

Vraag: Skei bome wat bestand is teen Hollandse iepsiekte antifungale verbindings af?

Hipotese: Konstrueer 'n hipotese wat hierdie vraag aanspreek.

Agtergrond: Hollandse iepsiekte is 'n swambesmetting wat baie spesies iep aantas (Ulmus) in Noord-Amerika. Die swam besmet die bloedvatstelsel van die boom, wat watervloei binne die plant blokkeer en droogtestres naboots. Dit is per ongeluk in die vroeë 1930's aan die Verenigde State bekendgestel, en het skadubome oor die hele vasteland vernietig. Dit word deur die swam veroorsaak Ophiostoma ulmi. Die elmbaskewer dien as 'n vektor en dra die siekte van boom tot boom oor. Baie Europese en Asiatiese elms is minder vatbaar vir die siekte as Amerikaanse elms.

Toets die hipotese: 'n Navorser wat hierdie hipotese toets, kan die volgende doen. Ent verskeie Petri plate wat 'n medium bevat wat die groei van swamme ondersteun met fragmente van Ophiostoom miselium. Sny (met 'n metaalpons) verskeie skywe uit die vaskulêre weefsel van vatbare variëteite van Amerikaanse elms en weerstandbiedende Europese en Asiatiese elms. Sluit kontrole Petri plate ingeënt met miselia sonder plantweefsel om te verifieer dat die medium en inkubasie toestande nie inmeng met swamgroei nie. As 'n positiewe kontrole, voeg papierskywe wat met 'n bekende swamdoder geïmpregneer is by Petri-plate wat met die miselium geënt is.

Inkubeer die plate vir 'n vasgestelde aantal dae om swamgroei en verspreiding van die miselium oor die oppervlak van die plaat moontlik te maak. Teken die deursnee van die sone van skoonmaak, indien enige, rondom die weefselmonsters en die swamdoderbeheerskyf aan.

Teken jou waarnemings in die volgende tabel aan.

Resultate van Antifungale Toetsing van Vaskulêre Weefsel van Verskillende Spesies van Elm
SkyfSone van inhibisie (mm)
Gedistilleerde water
Swamdoder
Weefsel van vatbare iep #1
Weefsel van vatbare iep #2
Weefsel van Resistant Elm #1
Weefsel van Resistant Elm #2

Ontleed die data en rapporteer die resultate. Vergelyk die effek van gedistilleerde water met die swamdoder. Dit is negatiewe en positiewe kontroles wat die eksperimentele opstelling bekragtig. Die swamdoder moet omring word deur 'n duidelike sone waar die swamgroei geïnhibeer is. Is daar 'n verskil tussen verskillende spesies elm?

Maak 'n gevolgtrekking: Was daar antifungale aktiwiteit soos verwag van die swamdoder? Het die resultate die hipotese ondersteun? Indien nie, hoe kan dit verduidelik word? Daar is verskeie moontlike verklarings vir weerstand teen 'n patogeen. Aktiewe afskrikking van infeksie is slegs een van hulle.


Tekens en simptome van plantsiekte: Is dit swam, viraal of bakteries?

Bekendheid met die manier waarop plantsiektes visueel geïdentifiseer word, kan jou help om probleme te diagnoseer.

Die meeste plantsiektes &ndash ongeveer 85 persent &ndash word deur swam- of swamagtige organismes veroorsaak. Ander ernstige siektes van voedsel- en voergewasse word egter deur virale en bakteriese organismes veroorsaak. Sekere aalwurms veroorsaak ook plantsiekte. Sommige plantsiektes word geklassifiseer as &ldquoabioties,&rdquo of siektes wat nie-aansteeklik is en skade van lugbesoedeling, voedingstekorte of toksisiteite insluit, en groei onder minder as optimale toestande. Vir eers kyk ons ​​na siektes wat veroorsaak word deur die drie hoofpatogene mikrobes: swam, bakterieë en virus. Indien plantsiekte vermoed word, kan noukeurige aandag aan plantvoorkoms 'n goeie leidraad gee oor die tipe patogeen wat betrokke is.

A teken van plantsiekte is fisiese bewyse van die patogeen. Swamvrugliggame is byvoorbeeld 'n teken van siekte. As jy na poeieragtige skimmel op 'n seringblaar kyk, wil jy eintlik na die parasitiese swamsiekte-organisme self kyk (Microsphaera alni). Bakteriese kanker van steenvrugte veroorsaak gummosis, 'n bakteriese ekssudaat wat uit die kankers kom. Die dik, vloeibare ekssudaat bestaan ​​hoofsaaklik uit bakterieë en is 'n teken van die siekte, hoewel die kanker self uit plantweefsel bestaan ​​en 'n simptoom is.

A simptoom van plantsiekte is 'n sigbare effek van siekte op die plant. Simptome kan 'n waarneembare verandering in kleur, vorm of funksie van die plant insluit soos dit op die patogeen reageer. Blaarverwelking is 'n tipiese simptoom van verticilium-verwelk, wat deur die swamplantpatogene veroorsaak word Verticillium albo-atrum en V. dahliae. Algemene bakteriële roes simptome sluit in bruin, nekrotiese letsels omring deur 'n heldergeel stralekrans by die blaarrand of binnekant van die blaar op boontjieplante. Jy sien nie eintlik die siektepatogeen nie, maar eerder 'n simptoom wat deur die patogeen veroorsaak word.

Hier is 'n paar voorbeelde van algemene tekens en simptome van swam-, bakteriële en virale plantsiektes:

  • Blaarroes (gewone blaarroes in mielies)
  • Stamroes (koringstamroes)
  • Sclerotinia (wit skimmel)
  • Poeieragtige skimmel
  • Voël-oog kol op bessies (antraknose)
  • Demp van saailinge (phytophthora)
  • Blaarvlek (septoria-bruinvlek)
  • Chlorose (vergeling van blare)

Streeproespustels op 'n winterkoringblaar is 'n simptoom. Fotokrediet: Fred Springborn, MSUE

Bakteriese siektetekens (moeilik om waar te neem, maar kan insluit):

  • Bakteriese vloei
  • Water-deurdrenkte letsels
  • Bakteriële stroom in water vanaf 'n afgesnyde stam

Simptome van bakteriese siektes:

  • Blaarvlek met geel stralekrans
  • Vrugtevlek
  • Kanker
  • Kroongal
  • Sheperd&rsquos kromstam eindig op houtagtige plante

Donkerrooi nierboontjieblaar wat bakteriese blaarvlek simptoom toon (bruin blaarvlek met geel stralekrans). Fotokrediet: Fred Springborn, MSUE

Jy kan sien dat daar baie oorvleueling is tussen swam-, bakteriële en virussiekte simptome. Ook moet abiotiese siektes, onkruiddoderbeserings en aalwurmprobleme as moontlikhede beskou word wanneer 'n onbekende plantprobleem voorkom. Hierdie lyste is nie volledig of volledig, slegs voorbeelde.

Michigan State University Extension bied publikasies en aanlyn inligting aan om produsente te help om ernstige plantsiektes te identifiseer en te beheer. Daarbenewens bied MSU Diagnostiese Dienste aanlyn feiteblaaie wat baie algemene plantsiektes in Michigan dek, en kan siek plantmonsters teen 'n bekostigbare koste diagnoseer. Die laboratoriumwebwerf het indieningsvorms en besonderhede oor monstervoorlegging en koste.

Vir meer basiese inligting oor plantsiekte, besoek Ohio State University & rsquos Inleiding tot Plant Disease Series webblad.

Hierdie artikel is gepubliseer deur Michigan State University Uitbreiding. Vir meer inligting, besoek https://extension.msu.edu. Besoek https://extension.msu.edu/newsletters om 'n opsomming van inligting reguit by jou e-pos inkassie af te lewer. Om 'n kenner in jou area te kontak, besoek https://extension.msu.edu/experts, of bel 888-MSUE4MI (888-678-3464).

Het jy hierdie artikel nuttig gevind?

Vertel ons asseblief hoekom

Veldgewasse virtuele ontbyt: 'n Gratis weeklikse reeks oor plaag- en gewasbestuuronderwerpe

Die verkennerskool bestaan ​​uit 22 webinars van gewasbeskermingspesialiste by 11 Midwest-universiteite en word deur die CPN aangebied.


Suksesverhale van bevolkingsisolate

Een van die mees indrukwekkende voorbeelde van die vindingryke gebruik van bekende genealogie, groot uitgebreide families en groot hoeveelhede mediese data in genetiese studies word verskaf deur die maatskappy deCODE genetics in Ysland, waar meer as 50% van die volwasse bevolking vrywillig hul mediese en genetiese inligting om in genetiese navorsing gebruik te word [4, 5]. Alhoewel die Yslandse bevolking nie 'n bevolkingsisolaat verteenwoordig soos konvensioneel gedefinieer nie, het genetiese drywing oor generasies die hoeveelheid variasie binne dit verminder relatief tot die res van Europa [6]. Dit, onder andere voordele van 'n geografies geïsoleerde bevolking, het die identifikasie moontlik gemaak deur middel van koppeling, en meer onlangs deur genoomwye assosiasie (GWA) studies, van 'n indrukwekkende aantal variante wat bydra tot die ontwikkeling van algemene/komplekse siektes [5 ]. Onder hierdie is geen lokusse vir miokardiale infarksie en beroerte (ALOX5AP en chromosomale streek 9p21) [7, 8], tipe 2-diabetes (TCF7L2 en CDKAL1) [9, 10], boezemfibrilleren (4q25) [11] en prostaatkanker (2p15 en Xp11.22) [12]. Benewens siektegene, het die Yslandse bevolking gene onthul wat bydra tot 'n aantal komplekse eienskappe, soos volwasse statuur (verskeie lokusse, insluitend ZBTB38) [13] sowel as vel- en haarpigmentasie (SLC24A4, KITLG, TYR, OCA2, MC1R en 6p25.3) [14, 15]. Die voortgesette werk deur deCODE genetika oor 50 algemene siektes sal sekerlik 'n rits bykomende geenbevindinge tot gevolg hê en help om die alleliese spektrum van siekte-predisponerende variante te karakteriseer. Die verstandig ontwerpte strategie om die unieke bevolking volledig te oes en die gekombineerde krag van koppeling en assosiasie was die basis van die sukses van genetiese navorsing in Ysland.

Nog 'n bevolkingsisolaat met bewese waarde in geenkartering is die bevolking van Finland, waar gene vir 35 monogene siektes wat meer gereeld as in ander bevolkings voorkom, geïdentifiseer is [16]. Kenmerke van die Finse bevolking was ook 'n voordeel in studies van skisofreniespektrumafwykings: 'n gebalanseerde translokasie (111)(q42.1q14.3) wat met skisofrenie segregeer is die eerste keer beskryf in 'n groot Skotse familie [17] en bewyse vir assosiasie van die geen SKYF1 met die versteuring is daarna verkry in Finse gesinne met gediagnoseerde skisofrenie [18, 19]. Groot stambome van die Finse bevolking is ook suksesvol gebruik in 'n studie van familiale gekombineerde hiperlipidemie wat die geen vir stroomop stimulatoriese faktor 1 (USF1) as 'n risikofaktor vir hierdie komplekse siekte [20]. Hierdie assosiasie is daarna in ander populasies herhaal, en bewyse van die funksionele betekenis van die geenvariante en hul assosiasie met kardiovaskulêre siekte en dislipidemie op bevolkingsvlak is ook verkry [21-23]. Nog 'n uitstekende voorbeeld uit Finland is 'n geen wat vatbaarheid vir asma verleen (NPSR1), ontdek in Kainuu en Noord-Karelia subbevolkings van Oos-Finland wat streke van die laat-nedersetting verteenwoordig [24].

Die gemeenskaplike leefstyl en genetiese isolasie van die Hutteriete, wat in die noorde van die Verenigde State en Wes-Kanada woon, het veral studies van asma en verwante eienskappe aangehelp [25]. Onlangs is die chitinase 3-agtige 1-geen geïdentifiseer as 'n asma-gevoeligheidsgeen in Hutterites, en die bevinding is daarna in twee bevolkingsgroepe van Europese afkoms herhaal [25]. Studies van tipe 2-diabetes en vetsug het Pima-Indiane [26] gebruik, sowel as ander genetiese isolate, soos Finland en Sardinië [27, 28]. Gene wat bydra tot neuropsigiatriese versteurings word gesoek, en vorige gene-ontdekkings word bevestig, in studies van spesiale bevolkings, soos mense van die Antioquia in Colombia en die Sentrale Vallei van Costa Rica [29], Baske van Spanje [30], die Mikronesiese bevolking van die eilande Kosrae [31] en Palau [32], Bulgaarse Sigeuners [33], en sub-isolate van Swede [34] en Israel [35]. Ander spesiale populasies wat in onlangse genetiese studies van komplekse siektes gebruik is, sluit in Franse Kanadese [36], Ashkenazi-Jode [37], Mennoniete [38], Newfoundlanders [39], sub-isolate van Nederland [40] en die Amish [41].

Die belangrike waarneming van al hierdie studies is dat die genetiese variante wat geïdentifiseer is binne isolate en/of uitsonderlike families wat oënskynlik 'n algemene siekte op 'n byna-Mendeliaanse wyse afsonder, nie daarin beperk word nie, maar in grootskaalse bevolkingsmonsters gerepliseer word en nuwe weë ontbloot. agter hierdie siekteprosesse.


1. Inleiding

SynBio is 'n interdissiplinêre veld op die koppelvlak van ingenieurswese en biologie wat daarop gemik is om nuwe biologiese stelsels te ontwikkel en nuwe funksies aan lewende selle oor te dra. Dit gebruik ingenieursbeginsels soos standaardisering, modulariteit, modellering en rekenaargesteunde ontwerp om die voorspelbaarheid van die bio-ingenieursproses te verbeter. Standaardisering en modulariteit versnel die ingenieursproses deur toe te laat dat onderdele maklik uitgeruil kan word en iteratiewe ingenieursiklusse van 'ontwerp-bou-toets-leer' om die funksionaliteit te verbeter. Terselfdertyd lig en voorspel die toepassing van modellering en rekenaargesteunde ontwerp die uitkomste van verskillende ingenieurstrategieë en verbeter dit die ontwerp deur kwantitatiewe data in te sluit wat uit die 'ontwerp-bou-toets-leer'-siklusse gegenereer word (Figuur 1). ). Deur ingenieurswese, lewenswetenskappe en rekenaarmodellering te kombineer, brei SynBio die reeks toepassings en produkte uit wat ontwikkel word.

SynBio het potensiële toepassings in die voedsel- en voerketting wat onder huidige wetgewing 'n voorafmarkmagtiging in Europa sal vereis. Sommige van daardie toepassings kan die doelbewuste vrystelling van sulke geneties gemodifiseerde organismes in die omgewing insluit (bv. SynBio-plante of SynBio-mikro-organismes vir plantgroeibevordering of plantbeskerming) en sal dus onderhewig wees aan 'n omgewingsrisiko-evaluering (ERA). Dit word ook gerapporteer deur die Scientific Advice Mechanism (SAM) verduidelikende nota van April 2017 oor nuwe tegnieke in landboubiotegnologie,4 4 https://ec.europa.eu/info/publications/new-techniques-agricultural-biotechnology_en
'n uiteensetting van die landboutoepassing van nuwe tegnieke in die velde van SynBio en geenaandrywing. Voorheen, in 2014 en 2015, het die Europese Kommissie se Wetenskaplike Komitee oor Opkomende en Nuut Geïdentifiseerde Gesondheidsrisiko's (SCENIHR), die Wetenskaplike Komitee vir Gesondheid en Omgewingsrisiko's (SCHER) en die Wetenskaplike Komitee oor Verbruikersveiligheid (SCCS) drie menings gepubliseer (SCENIHR, SCCS, en SCHER, 2014, 2015a, 2015b) op SynBio,1 1 SCENIHR, SCCS en SCHER, 2014. Synthetic Biology I Definition, Opinion, September 2014. Aanlyn beskikbaar: http://ec.europa.eu/healthic_committ/health /emerging/docs/scenihr_o_044.pdf SCENIHR, SCCS en SCHER (2015) Sintetiese Biologie II – Risikobepalingsmetodologieë en veiligheidsaspekte, Opinie, Mei 2015. Aanlyn beskikbaar: http://ec.europa.eu/health/scientific_committees/emerging /docs/scenihr_o_048.pdf SCENIHR, SCCS en SCHER, 2015. Sintetiese Biologie III – Navorsingsprioriteite, Opinie, Desember 2015. Aanlyn beskikbaar: http://ec.europa.eu/health/scientific_committees/emerging/docs_050hrpofd.scenihrpof.
wat ses SynBio-ontwikkelings aanspreek: (1) genetiese deelbiblioteke en metodes (2) minimale selle en ontwerperonderstel (3) protoselle en kunsmatige selle (4) xenobiologie (5) DNA-sintese en genoomredigering en (6) burgerwetenskap (Doen-Dit) -Jyself biologie). Die menings het die definisie van SynBio, risikobepalingsmetodologieë en veiligheidsaspekte, risiko's vir die omgewing en biodiversiteit en navorsingsprioriteite in die veld van SynBio aangespreek. Hierdie nie-voedselwetenskaplike komitees het in hul menings tot die gevolgtrekking gekom dat nuwe SynBio-toepassings geassesseer kan word deur gebruik te maak van huidige risikobepalingsmetodologie vir geneties gemodifiseerde organismes (GMO's) en dat die vinnig ontwikkelende SynBio-tegnologieë moontlik vereis dat bestaande metodologieë met gereelde tussenposes hersien en verbeter word wanneer nodig. om voort te gaan om hul veiligheid te verseker.

Daarom, as 'n proaktiewe maatreël, het die Europese Kommissie die Europese Voedselveiligheidsowerheid (EFSA) versoek vir 'n mening oor GMO's wat ontwikkel is met SynBio-benaderings en die implikasies, indien enige, vir risiko-assesseringsmetodologieë. EFSA het 'n totaal van ses menings geïdentifiseer wat ontwikkel moet word, volgens organismegroep- en risikobepalingsaspekte.

1.1 Definisies vir SynBio vir die Verwysingsbepalings

SynBio is voorheen soos volg gedefinieer deur die nie-voedselwetenskaplike komitees op versoek van die Europese Kommissie5 5 https://ec.europa.eu/research/sam/index.cfm?pg=agribiotechnology
, 6 6 SCENIHR, SCCS, SCHER (2014) Synthetic Biology I Definition, Opinion, September 2014. Aanlyn beskikbaar: http://ec.europa.eu/health/scientific_committees/emerging/docs/scenihr_o_044.pdf
: 'Sintetiese biologie is die toepassing van wetenskap, tegnologie en ingenieurswese om die ontwerp, vervaardiging en/of modifikasie van genetiese materiale in lewende organismes te fasiliteer en te versnel'. Hierdie definisie word gebruik as 'n beginpunt vir die huidige mening as gevolg van die versoek van die Europese Kommissie om voort te bou op die menings van die nie-voedselwetenskaplike komitees.

Die Konvensie oor Biologiese Diversiteit7 7 Die Konvensie oor Biologiese Diversiteit is 'n multilaterale verdrag onder die beskerming van die Verenigde Nasies se Omgewingsprogram. Die hoofdoelwitte daarvan is die bewaring van biodiversiteit, volhoubare gebruik van die komponente van biodiversiteit, en regverdige en regverdige verdeling van voordele voortspruitend uit genetiese hulpbronne wat voortspruit uit biodiversiteit Sien: https://www.cbd.int/doc/meetings/cop/cop -12/information/cop-12-inf-11-en.pdf
verder verduidelik dat 'Terwyl daar geen internasionaal ooreengekome definisie van "sintetiese biologie" is nie, sluit sleutelkenmerke van sintetiese biologie die "de novo" sintese van genetiese materiaal en 'n ingenieursgebaseerde benadering om komponente, organismes en produkte te ontwikkel' in.

Hierdie verdere verduideliking vestig die skakel vir die versoek om die Europese Unie (EU) te ondersteun in die werk onder die Konvensie oor Biologiese Diversiteit en die Cartagena-protokol oor bioveiligheid.8 8 Die Cartagena-protokol oor bioveiligheid tot die konvensie oor biologiese diversiteit is op 29 aangeneem. Januarie 2000, en het op 11 September 2003 in werking getree. Die Cartagena-protokol het tans 171 kontrakterende partye, uitgesluit groot LMO-uitvoerders soos Argentinië, Kanada en die Verenigde State. Sien: https://www.cbd.int/doc/legal/cartagena-protocol-en.pdf

1.2 Agtergrond en Opdragte soos verskaf deur die versoeker

  1. EFSA is gevra om te oorweeg of en watter nuwer sektore/vooruitgang moet onder SynBio-ontwikkelings oorweeg word, benewens die ses wat deur die Wetenskaplike Komitees (ToR1) geïdentifiseer is.
  2. EFSA is versoek om, waar moontlik, te identifiseer potensiële risiko's in terme van impak op mense, diere en die omgewing wat huidige en nabye toekoms SynBio-ontwikkelings in hierdie opsig kan inhou, word EFSA ook gevra om potensiële nuwe gevare te identifiseer vergelyk met gevestigde tegnieke van genetiese modifikasie11 11 Vir die doel van hierdie mandaat verwys die terme 'gevestigde tegnieke van genetiese modifikasie' na verskeie genetiese ingenieurstegnieke wat aansienlik gebruik is oor die afgelope 30 jaar om geneties gemodifiseerde organismes te produseer, soos dié wat gemagtig is kragtens Richtlijn 2001/18/EG en Regulasie (EU) No 1829/2003.
    (ToR2).
  3. EFSA is versoek om vas te stel of die bestaande riglyne vir risiko-assessering voldoende en voldoende is vir huidige en nabye toekomstige SynBio-ontwikkelings of of daar 'n behoefte is aan opgedateerde leiding (ToR3).
  4. In laasgenoemde geval is EFSA versoek om die spesifieke gebiede te identifiseer waar so opgedateerde leiding is nodig (ToR4).

EFSA word ook versoek om tegniese en wetenskaplike kundigheid te verskaf oor die risikobepaling van GMO's wat deur SynBio verkry is om die EU te ondersteun in die werk onder die Konvensie oor Biologiese Diversiteit en die Cartagena-protokol oor bioveiligheid.

1.3 Interpretasie van die Opdrag en Bestek

  1. Mikrobiese karakterisering en ERA van geneties gemodifiseerde mikroörganismes (GMM's) (WP1)
  2. Molekulêre karakterisering en ERA van geneties gemodifiseerde plante (GMP's) (WP2)
  3. Voedsel- en voerrisikobepaling van GMM's (WP3)
  4. Voedsel- en voerrisikobepaling van GMP's (WP4)
  5. Molekulêre karakterisering en ERA van geneties gemodifiseerde diere (WP5)
  6. Voedsel- en voerrisikobepaling van geneties gemodifiseerde diere (WP6)

Die huidige mening spreek WP2 aan.

Die omvang van hierdie plantspesifieke opinie oorweeg twee uit die ses SynBio-kategorieë wat voorheen deur die nie-voedselwetenskaplike komitees geïdentifiseer is, naamlik genetiese deelbiblioteke en metodes, en DNA-sintese en genoomredigering dus uitgesluit minimale selle en ontwerperonderstel, en protoselle en kunsmatige selle per definisie, xenobiologie en burgerwetenskap. Daarbenewens word ontwikkelings rakende geteikende mutasies aangespreek in die EFSA GMO Paneel se mening oor 'Toepasbaarheid van die EFSA-opinie oor terreingerigte nukleases tipe 3 vir die veiligheidsbeoordeling van plante wat ontwikkel is deur gebruik te maak van plekgerigte nukleases tipe 1 en 2 en oligonukleotiedgerigte mutagenese '.12 12 http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2020.6299/full

  • Nie al die ses ontwikkelings wat voorheen deur die nie-voedselwetenskaplike komitees geïdentifiseer is, is as relevant beskou nie.
  • 'Nabye toekoms': vir hierdie mandaat word dit geïnterpreteer as produkte met die potensiaal om die EU-mark in die volgende dekade te bereik. Dit word weerspieël in Afdeling 2.3 wanneer hipotetiese gevallestudies gekies word.
  • 'Agri-voedselgebruike': Op voetnoot 5 van die mandaat 'Vir die doel van hierdie mandaat beteken landbouvoedselgebruike landbou-/voedsel-/voerprodukte wat binne die bevoegdheid van EFSA val’, was verdere verduidelikings nodig om te bepaal watter aansoeke binne die bevoegdheid van EFSA en hierdie mandaat val, en die beskikbare tydsraamwerk. Die beperkte tydsraamwerk beskikbaar om hierdie mening te voltooi, het gelei tot die uitdruklike uitsluiting van bio-remediëring aansoeke van hierdie mandaat. Die volgende gebruike is ook uitgesluit van hierdie mandaat: uitwissing, bio-wapens/bio-paraatheid, mediese gebruik en biobrandstof (sien Afdeling 2.2 en die EFSA Eksterne Wetenskaplike Verslag13 13 https://efsa.onlinelibrary.wiley.com/ doi/abs/10.2903/sp.efsa.2020.en-1687
    ).
  • Vir die doel van hierdie mening is ToR2 beperk tot doelbewuste vrystelling slegs in die omgewing (insluitend wild). Die blootstelling aan mense en plaasdiere (toevallig of opsetlik) sal spesifiek in WP4 aangespreek word, wat die voedsel-/voeraspekte van GM plante dek wat verkry is deur SynBio-benaderings (SynBio GMP).
  • ‘Bestaande riglyne vir risikobepaling’: sien Afdeling 2.1

Die mening word nie net geproduseer om die Europese Kommissie te ondersteun nie, maar is ook bedoel vir die publiek, wetenskaplike gemeenskap en belanghebbendes, maatskappye en instellings wat belangstel in of handel oor die veiligheid van SynBio-aanlegontwikkelings.


Inhoud

Legionella word tradisioneel opgespoor deur kultuur op gebufferde houtskoolgisekstrak-agar. Dit vereis die teenwoordigheid van sisteïen en yster om te groei, dus groei nie op gewone bloedagar-media wat gebruik word vir laboratorium-gebaseerde totale lewensvatbare tellings of on-site dipslides nie. Algemene laboratoriumprosedures vir die opsporing van Legionella in water [7] konsentreer die bakterieë (deur sentrifugering en/of filtrasie deur 0.2-μm filters) voor inenting op 'n houtskool gis ekstrak agar wat selektiewe middels (bv. glisien, vankomisien, polimixien, sikloheksamied, GVPC) bevat om ander flora in die monster. Hitte- of suurbehandeling word ook gebruik om interferensie van ander mikrobes in die monster te verminder.

Na inkubasie vir tot 10 dae, word verdagte kolonies bevestig as Legionella as hulle groei op gebufferde houtskool-gisekstrak-agar wat sisteïen bevat, maar nie op agar sonder dat sisteïen bygevoeg is nie. Immunologiese tegnieke word dan algemeen gebruik om die spesies en/of serogroepe bakterieë wat in die monster teenwoordig is, te bepaal.

Alhoewel die plateringsmetode redelik spesifiek is vir die meeste spesies van Legionella, het een studie getoon dat 'n saamkultuurmetode wat die noue verwantskap met amoebes verantwoord, meer sensitief kan wees, aangesien dit die teenwoordigheid van die bakterieë kan opspoor selfs wanneer dit gemasker word deur hul teenwoordigheid in die amoebes. [8] Gevolglik sal die kliniese en omgewingsvoorkoms van die bakterieë waarskynlik onderskat word weens die huidige laboratoriummetodologie.

Baie hospitale gebruik die Legionella urinêre antigeen toets vir aanvanklike opsporing wanneer Legionella longontsteking word vermoed. Sommige van die voordele wat hierdie toets bied, is dat die resultate in ure verkry kan word eerder as die etlike dae wat benodig word vir kultuur, en dat 'n urinemonster oor die algemeen makliker verkry kan word as 'n sputummonster. Nadele is dat die urine-antigeentoets slegs antigeen van opspoor Legionella pneumophila serogroep 1 (LP1) slegs 'n kultuur sal infeksie deur nie-LP1 stamme of ander opspoor Legionella spesies en wat isolate van Legionella verkry word nie, wat openbare gesondheidsondersoeke van uitbrekings benadeel. [9]

Nuwe tegnieke vir die vinnige opsporing van Legionella in water is monsters ontwikkel, insluitend die gebruik van polimerase kettingreaksie en vinnige immunologiese toetse. Hierdie tegnologieë kan tipies baie vinniger resultate lewer.

Staatstoesig oor openbare gesondheid het toenemende proporsies van drinkwaterverwante uitbrake getoon, spesifiek in gesondheidsorgomgewings. [10]

In die natuurlike omgewing, Legionella leef binne amoebes soos Acanthamoeba spp., Naegleria spp., Vermamoeba vermiformis, of ander protosoë soos Tetrahymena pyriformis. [11]

By inaseming kan die bakterieë alveolêre makrofage besmet, waar die bakterieë kan repliseer. Dit lei tot Legioensiekte en die minder ernstige siekte Pontiac-koors. Legionella oordrag is deur inaseming van waterdruppels van 'n besmette bron wat die organisme toegelaat het om te groei en te versprei (bv. koeltorings). Oordrag vind ook minder algemeen plaas deur aspirasie van drinkwater vanaf 'n besmette bron. Persoon-tot-persoon-oordrag is nie gedemonstreer nie [4], maar dit kan in seldsame gevalle moontlik wees. [12]

Sodra dit binne 'n gasheer is, kan die inkubasietydperk tot twee weke wees. Prodromale simptome is griepagtig, insluitend koors, kouekoors en droë hoes. Gevorderde stadiums van die siekte veroorsaak probleme met die spysverteringskanaal en die senuweestelsel en lei tot diarree en naarheid. Ander gevorderde simptome van longontsteking kan ook voorkom. Die siekte is egter oor die algemeen nie 'n bedreiging vir die meeste gesonde individue nie, en is geneig om meer dikwels tot ernstige simptome te lei by immuunonderdrukte gashere en bejaardes. Gevolglik moet die waterstelsels van hospitale en verpleeginrigtings periodiek gemonitor word. Die Texas Departement van Staatsgesondheidsdienste verskaf aanbevelings vir hospitale om die verspreiding van hospitaalverworwe siekte op te spoor en te voorkom a.g.v. Legionella infeksie. [13] Volgens Infeksiebeheer en Hospitaalepidemiologie, hospitaal-verwerf Legionella longontsteking het 'n sterftesyfer van 28%, en die bron is die waterverspreidingstelsel. [14]

Legionella spesies bestaan ​​tipies in die natuur teen lae konsentrasies, in grondwater, mere en strome. Hulle plant voort nadat hulle mensgemaakte toerusting binnegegaan het, gegewe die regte omgewingstoestande. [ aanhaling nodig ] In die Verenigde State raak die siekte tussen 8 000 en 18 000 individue per jaar. [15]

Bronne van Legionella Wysig

Gedokumenteerde bronne sluit in koeltorings, [16] swembaddens (veral in Skandinawiese lande), huishoudelike waterstelsels en storte, ysmaakmasjiene, [17] verkoelde kaste, bubbelbad-spa's, [18] [19] warmwaterbronne, [20] fonteine, [21] tandheelkundige toerusting, [22] grond, [23] motorruitsproeiervloeistof, [24] industriële koelmiddel, [25] en afvalwaterbehandelingsaanlegte.

Lugversending vanaf koeltorings Wysig

Die grootste [26] en mees algemene bron van Legioensiekte-uitbrake is koeltorings (hitteverwerpingstoerusting wat in lugversorging en industriële verkoelingswaterstelsels gebruik word), hoofsaaklik as gevolg van die risiko vir wydverspreide sirkulasie. Baie regeringsagentskappe, koeltoringvervaardigers en industriële handelsorganisasies het ontwerp- en instandhoudingsriglyne ontwikkel vir die beheer van die groei en verspreiding van Legionella binne koeltorings.

Navorsing in die Tydskrif vir aansteeklike siektes (2006) het bewys gelewer dat L. pneumophila, die veroorsakende middel van Legioensiekte, kan ten minste 6 km van sy bron af reis deur die lugverspreiding. Daar is voorheen geglo dat die oordrag van die bakterie tot baie korter afstande beperk is. ’n Span Franse wetenskaplikes het die besonderhede hersien van ’n epidemie van Legioensiekte wat in Pas-de-Calais, Noord-Frankryk, in 2003–2004 plaasgevind het. Van 86 bevestigde gevalle tydens die uitbreking, het 18 tot die dood gelei. Die bron van infeksie is geïdentifiseer as 'n koeltoring in 'n petrochemiese aanleg, en 'n ontleding van diegene wat in die uitbreking geraak is, het aan die lig gebring dat sommige besmette mense so ver as 6–7 km van die aanleg af gewoon het. [27]

As gevolg van hierdie risiko's, vereis 'n Britse wetlike mandaat eienaars om die plaaslike owerhede in kennis te stel van enige koeltorings wat 'n maatskappy bedryf. Koeltoringkennisgewing

Entstofnavorsing Edit

Geen entstof is beskikbaar vir legionellose nie. Inentingstudies met hitte-gedood of asetoon-gedood selle is uitgevoer in proefkonyne, wat dan gegee is Legionella intraperitoneaal of per aërosol. Beide entstowwe is getoon om matige hoë vlakke van beskerming te gee. Beskerming was dosisafhanklik en gekorreleer met teenliggaamvlakke soos gemeet deur ensiem-gekoppelde immunosorbent-toets aan 'n buitenste membraanantigeen en deur indirekte immunofluoressensie na hitte-gedood selle. [ aanhaling nodig ] 'n Gelisensieerde entstof is egter heel waarskynlik nog baie jare weg. [ aanhaling nodig ]

Legionella is ontdek as 'n geneties diverse spesie met 7-11% van gene stamspesifiek. Die molekulêre funksie van sommige van die bewese virulensiefaktore van Legionella ontdek is. [28]

Beheer van Legionella groei kan plaasvind deur chemiese, termiese of ultraviolet behandelingsmetodes.

Hitte wysig

Die duurder [ aanhaling nodig ] opsie is temperatuurbeheer—d.w.s. hou alle koue water onder 25 °C (77 °F) en alle warm water bo 51 °C (124 °F). Die hoë koste wat met hierdie metode aangegaan word, spruit uit die uitgebreide retrofitting wat benodig word vir bestaande komplekse verspreidingstelsels in groot fasiliteite en die energiekoste om die water te verkoel of te verhit en die vereiste temperature te alle tye en by alle distale punte binne die stelsel te handhaaf.

Temperatuur beïnvloed die oorlewing van Legionella soos volg: [3]

  • Bo 70 °C (158 °F) – Legionella sterf byna onmiddellik
  • By 60 °C (140 °F) – 90% sterf binne 2 minute (desimale reduksietyd (D) = 2 minute)
  • By 50 °C (122 °F) – 90% sterf binne 80–124 minute, afhangend van spanning (D = 80–124 minute)
  • 48 tot 50 °C (118 tot 122 °F) – kan oorleef maar nie vermeerder nie
  • 32 tot 42 °C (90 tot 108 °F) – ideale groeigebied
  • 25 tot 45 °C (77 tot 113 °F) – groeireeks
  • Onder 20 °C (68 °F) – kan oorleef, selfs onder vriespunt, maar is dormant

Ander temperatuursensitiwiteit [29] [30]

  • 60 to 70 °C (140 to 158 °F) to 80 °C (176 °F) – Disinfection range
  • 66 °C (151 °F) – Legionella dies within 2 minutes
  • 60 °C (140 °F) – Legionella dies within 32 minutes
  • 55 °C (131 °F) – Legionella dies within 5 to 6 hours

Water can be monitored in real-time with sensors. [ aanhaling nodig ]

Chlorine Edit

A very effective chemical treatment is chlorine. For systems with marginal issues, chlorine provides effective results at 0.5 ppm [ aanhaling nodig ] residual in the hot water system. For systems with significant Legionella problems, temporary shock chlorination—where levels are raised to higher than 2 ppm for a period of 24 hours or more and then returned to 0.5 ppm—may be effective. [ aanhaling nodig ] Hyperchlorination can also be used where the water system is taken out of service and the chlorine residual is raised to 50 ppm or higher at all distal points for 24 hours or more. The system is then flushed and returned to 0.5 ppm chlorine prior to being placed back into service. These high levels of chlorine penetrate biofilm, killing both the Legionella bacteria and the host organisms. Annual hyperchlorination can be an effective part of a comprehensive Legionella preventive action plan. [31]

Copper-silver ionization Edit

Industrial-sized copper-silver ionization is recognized by the U.S. Environmental Protection Agency and WHO for Legionella control and prevention. [ aanhaling nodig ] Copper and silver ion concentrations must be maintained at optimal levels, taking into account both water flow and overall water usage, to control Legionella. The disinfection function within all of a facility's water distribution network occurs within 30 to 45 days. [ aanhaling nodig ] Key engineering features such as 10 amps per ion chamber cell and automated variable voltage outputs having no less than 100 VDC are but a few of the required features for proper Legionella control and prevention, using a specific, nonreferenced copper-silver system. Swimming pool ion generators are not designed for potable water treatment.

Questions remain whether the silver and copper ion concentrations required for effective control of symbiotic hosts could exceed those allowed under the U.S. Safe Drinking Water Act's Lead and Copper Rule. In any case, any facility or public water system using copper-silver for disinfection should monitor its copper and silver ion concentrations to ensure they are within intended levels – both minimum and maximum. Further, no current standards for silver in the EU and other regions allow use of this technology.

Copper-silver ionization is an effective process to control Legionella in potable water distribution systems found in health facilities, hotels, nursing homes, and most large buildings. However, it is not intended for cooling towers because of pH levels greater than 8.6, that cause ionic copper to precipitate. Furthermore, tolytriazole, a common additive in cooling water treatment, could bind the copper making it ineffective. Ionization became the first such hospital disinfection process to have fulfilled a proposed four-step modality evaluation by then, it had been adopted by over 100 hospitals. [32] Additional studies indicate ionization is superior to thermal eradication. [33]

Chlorine dioxide Edit

Chlorine dioxide has been approved by the U.S. Environmental Protection Agency as a primary disinfectant of potable water since 1945. Chlorine dioxide does not produce any carcinogenic byproducts like chlorine when used in the purification of drinking water that contains natural organic compounds such as humic and fulvic acids chlorine tends to form halogenated disinfection byproducts such as trihalomethanes. Drinking water containing such disinfection byproducts has been shown to increase the risk of cancer. ClO2 works differently from chlorine its action is one of pure oxidation rather than halogenation, so these halogenated byproducts are not formed. [34] Chlorine dioxide is not a restricted heavy metal like copper. It has proven excellent control of Legionella in cold and hot water systems and its ability as a biocide is not affected by pH, or any water corrosion inhibitors such as silica or phosphate. However, it is 'quenched' by metal oxides, especially manganese and iron. Metal oxide concentrations above 0.5 mg/l may inhibit its activity. [ aanhaling nodig ] Monochloramine is an alternative. Like chlorine and chlorine dioxide, monochloramine is approved by the Environmental Protection Agency [ watter? ] as a primary potable water disinfectant. Environmental Protection Agency registration requires a biocide label which lists toxicity and other data required for all registered biocides. If the product is being sold as a biocide, then the manufacturer is legally required to supply a biocide label, and the purchaser is legally required to apply the biocide per the biocide label. When first applied to a system, chlorine dioxide can be added at disinfection levels of 2 ppm for 6 hours to clean up a system. This will not remove all biofilm, but will effectively remediate the system of Legionella. [ aanhaling nodig ]

Moist heat sterilization Edit

Moist heat sterilization (superheating to 140 °F (60 °C) and flushing) is a nonchemical treatment that typically must be repeated every 3–5 weeks.

Ultraviolet Edit

Ultraviolet light, in the range of 200 to 300 nm, can inactivate Legionella. According to a review by the US EPA, [35] three-log (99.9%) inactivation can be achieved with a dose of less than 7 mJ/cm 2 .

Several European countries established the European Working Group for Legionella Infections [36] to share knowledge and experience about monitoring potential sources of Legionella. The working group has published guidelines about the actions to be taken to limit the number of colony-forming units (that is, live bacteria that are able to multiply) of Legionella per litre:

Legionella bacteria CFU/litre Action required (35 samples per facility are required, including 20 water and 10 swabs)
1000 or less System under control
more than 1000
up to 10,000
Review program operation: The count should be confirmed by immediate resampling. If a similar count is found again, a review of the control measures and risk assessment should be carried out to identify any remedial actions.
more than 10,000 Implement corrective action: The system should immediately be resampled. It should then be "shot dosed" with an appropriate biocide, as a precaution. The risk assessment and control measures should be reviewed to identify remedial actions. (150+ CFU/ml in healthcare facilities or nursing homes require immediate action.)

Monitoring guidelines are stated in Approved Code of Practice L8 in the UK. These are not mandatory, but are widely regarded as so. An employer or property owner must follow an Approved Code of Practice, or achieve the same result. Failure to show monitoring records to at least this standard has resulted in several high-profile prosecutions, e.g. Nalco + Bulmers – neither could prove a sufficient scheme to be in place whilst investigating an outbreak, therefore both were fined about £300,000GBP. Important case law in this area is R v Trustees of the Science Museum 3 All ER 853, (1993) 1 WLR 1171 [37]

Employers and those responsible for premises within the UK are required under Control of Substances Hazardous to Health to undertake an assessment of the risks arising from Legionella. This risk assessment may be very simple for low risk premises, however for larger or higher risk properties may include a narrative of the site, asset register, simplified schematic drawings, recommendations on compliance, and a proposed monitoring scheme. [38]

The L8 Approved Code of Practice recommends that the risk assessment should be reviewed at least every 2 years and whenever a reason exists to suspect it is no longer valid, such as water systems have been amended or modified, or if the use of the water system has changed, or if there is reason to suspect that Legionella control measures are no longer working.

Legionella could be used as a weapon, and indeed genetic modification of L. pneumophila has been shown where the mortality rate in infected animals can be increased to nearly 100%. [39] [40] [41] A former Soviet bioengineer, Sergei Popov, stated in 2000 that his team experimented with genetically enhanced bioweapons, including Legionella. [41] Popov worked as a lead researcher at the Vector Institute from 1976 to 1986, then at Obolensk until 1992, when he defected to the West. He later divulged much of the Soviet biological weapons program and settled in the United States.


Inhoud

Symbiosis spans a wide variety of possible relationships between organisms, differing in their permanence and their effects on the two parties. If one of the partners in an association is much larger than the other, it is generally known as the host. [1] In parasitism, the parasite benefits at the host's expense. [2] In commensalism, the two live together without harming each other, [3] while in mutualism, both parties benefit. [4]

Most parasites are only parasitic for part of their life cycle. By comparing parasites with their closest free-living relatives, parasitism has been shown to have evolved on at least 233 separate occasions. Some organisms live in close association with a host and only become parasitic when environmental conditions deteriorate. [5]

A parasite may have a long-term relationship with its host, as is the case with all endoparasites. The guest seeks out the host and obtains food or another service from it, but does not usually kill it. [6] In contrast, a parasitoid spends a large part of its life within or on a single host, ultimately causing the host's death, with some of the strategies involved verging on predation. Generally, the host is kept alive until the parasitoid is fully grown and ready to pass on to its next life stage. [7] A guest's relationship with its host may be intermittent or temporary, perhaps associated with multiple hosts, making the relationship equivalent to the herbivory of a wild-living animal. Another possibility is that the host–guest relationship may have no permanent physical contact, as in the brood parasitism of the cuckoo. [6]

Parasites follow a wide variety of evolutionary strategies, placing their hosts in an equally wide range of relationships. [2] Parasitism implies host–parasite coevolution, including the maintenance of gene polymorphisms in the host, where there is a trade-off between the advantage of resistance to a parasite and a cost such as disease caused by the gene. [8]

Types of hosts Edit

  • Definitive or primary host - an organism in which the parasite reaches the adult stage and reproduces sexually, if possible. This is the final host.
  • Secondary or intermediate host - an organism that harbors the sexually immature parasite and is required by the parasite to undergo development and complete its life cycle. It often acts as a vector of the parasite to reach its definitive host. Byvoorbeeld, Dirofilaria immitis, the heartworm of dogs, uses the mosquito as its intermediate host until it matures into the infective L3 larval stage.

It is not always easy or even possible to identify which host is definitive and which secondary. As the life cycles of many parasites are not well understood, sometimes the subjectively more important organism is arbitrarily labelled as definitive, and this designation may continue even after it is found to be incorrect. For example, sludge worms are sometimes considered "intermediate hosts" for salmonid whirling disease, even though the myxosporean parasite reproduces sexually inside them. [9] In trichinosis, a disease caused by roundworms, the host has reproductive adults in its digestive tract and immature juveniles in its muscles, and is therefore both an intermediate and a definitive host. [10]

  • Paratenic host - an organism that harbors the sexually immature parasite but is not necessary for the parasite's development cycle to progress. Paratenic hosts serve as "dumps" for non-mature stages of a parasite in which they can accumulate in high numbers. The trematode Alaria americana may serve as an example: the so-called mesocercarial stages of this parasite reside in tadpoles, which are rarely eaten by the definitive canine host. The tadpoles are more frequently preyed on by snakes, in which the mesocercariae may not undergo further development. However, the parasites may accumulate in the snake paratenic host and infect the definitive host once the snake is consumed by a canid. [11] The nematode Skrjabingylus nasicola is another example, with slugs as the intermediate hosts, shrews and rodents as the paratenic hosts, and mustelids as the definitive hosts. [12]
  • Dead-end , incidental , or accidental host - an organism that generally does not allow transmission to the definitive host, thereby preventing the parasite from completing its development. For example, humans and horses are dead-end hosts for West Nile virus, whose life cycle is normally between culicinemosquitoes and birds. [13] People and horses can become infected, but the level of virus in their blood does not become high enough to pass on the infection to mosquitoes that bite them. [13] - an organism that harbors a pathogen but suffers no ill effects. However, it serves as a source of infection to other species that are susceptible, with important implications for disease control. A single reservoir host may be reinfected several times. [14]

Plant hosts of micropredators Edit

Micropredation is an evolutionarily stable strategy within parasitism, in which a small predator lives parasitically on a much larger host plant, eating parts of it. [2]

The range of plants on which a herbivorous insect feeds is known as its host range. This can be wide or narrow, but it never includes all plants. A small number of insects are monophagous, feeding on a single plant. The silkworm larva is one of these, with mulberry leaves being the only food consumed. More often, an insect with a limited host range is oligophagous, being restricted to a few closely related species, usually in the same plant family. [15] The diamondback moth is an example of this, feeding exclusively on brassicas, [16] and the larva of the potato tuber moth feeds on potatoes, tomatoes and tobacco, all members of the same plant family, Solanaceae. [17] Herbivorous insects with a wide range of hosts in various different plant families are known as polyphagous. One example is the buff ermine moth whose larvae feed on alder, mint, plantain, oak, rhubarb, currant, blackberry, dock, ragwort, nettle and honeysuckle. [18]

Plants often produce toxic or unpalatable secondary metabolites to deter herbivores from feeding on them. Monophagous insects have developed specific adaptations to overcome those in their specialist hosts, giving them an advantage over polyphagous species. However, this puts them at greater risk of extinction if their chosen hosts suffer setbacks. Monophagous species are able to feed on the tender young foliage with high concentrations of damaging chemicals on which polyphagous species cannot feed, having to make do with older leaves. There is a trade off between offspring quality and quantity the specialist maximises the chances of its young thriving by paying great attention to the choice of host, while the generalist produces larger numbers of eggs in sub-optimal conditions. [19]

Some insect micropredators migrate regularly from one host to another. The hawthorn-carrot aphid overwinters on its primary host, a hawthorn tree, and migrates during the summer to its secondary host, a plant in the carrot family. [20]

Host range Edit

The host range is the set of hosts that a parasite can use as a partner. In the case of human parasites, the host range influences the epidemiology of the parasitism or disease. For instance, the production of antigenic shifts in Influenza A virus can result from pigs being infected with the virus from several different hosts (such as human and bird). This co-infection provides an opportunity for mixing of the viral genes between existing strains, thereby producing a new viral strain. An influenza vaccine produced against an existing viral strain might not be effective against this new strain, which then requires a new influenza vaccine to be prepared for the protection of the human population. [21]

Mutualistic hosts Edit

Some hosts participate in fully mutualistic interactions with both organisms being completely dependent on the other. For example, termites are hosts to the protozoa that live in their gut and which digest cellulose, [22] and the human gut flora is essential for efficient digestion. [23] Many corals and other marine invertebrates house zooxanthellae, single-celled algae, in their tissues. The host provides a protected environment in a well-lit position for the algae, while benefiting itself from the nutrients produced by photosynthesis which supplement its diet. [24] Lamellibrachia luymesi, a deep sea giant tubeworm, has an obligate mutualistic association with internal, sulfide-oxidizing, bacterial symbionts. The tubeworm extracts the chemicals that the bacteria need from the sediment, and the bacteria supply the tubeworm, which has no mouth, with nutrients. [25] Some hermit crabs place pieces of sponge on the shell in which they are living. These grow over and eventually dissolve away the mollusc shell the crab may not ever need to replace its abode again and is well-camouflaged by the overgrowth of sponge. [26]

An important hosting relationship is mycorrhiza, a symbiotic association between a fungus and the roots of a vascular host plant. The fungus receives carbohydrates, the products of photosynthesis, while the plant receives phosphates and nitrogenous compounds acquired by the fungus from the soil. Over 95% of plant families have been shown to have mycorrhizal associations. [27] Another such relationship is between leguminous plants and certain nitrogen-fixing bacteria called rhizobia that form nodules on the roots of the plant. The host supplies the bacteria with the energy needed for nitrogen fixation and the bacteria provide much of the nitrogen needed by the host. Such crops as beans, peas, chickpeas and alfalfa are able to fix nitrogen in this way, [28] and mixing clover with grasses increases the yield of pastures. [29]

Neurotransmitter tyramine produced by commensal Providencia bacteria, which colonize the gut of the nematode Caenorhabditis elegans, bypasses the requirement for its host to biosynthesise tyramine. This product is then probably converted to octopamine by the host enzyme tyramine β-hydroxylase and manipulates a host sensory decision. [30]

Hosts in cleaning symbiosis Edit

Hosts of many species are involved in cleaning symbiosis, both in the sea and on land, making use of smaller animals to clean them of parasites. Cleaners include fish, shrimps and birds hosts or clients include a much wider range of fish, marine reptiles including turtles and iguanas, octopus, whales, and terrestrial mammals. [4] The host appears to benefit from the interaction, but biologists have disputed whether this is a truly mutualistic relationship or something closer to parasitism by the cleaner. [31] [32]

Commensal hosts Edit

Remoras (also called suckerfish) can swim freely but have evolved suckers that enable them to adhere to smooth surfaces, gaining a free ride (phoresis), and they spend most of their lives clinging to a host animal such as a whale, turtle or shark. [3] However, the relationship may be mutualistic, as remoras, though not generally considered to be cleaner fish, often consume parasitic copepods: for example, these are found in the stomach contents of 70% of the common remora. [33] Many molluscs, barnacles and polychaete worms attach themselves to the carapace of the Atlantic horseshoe crab for some this is a convenient arrangement, but for others it is an obligate form of commensalism and they live nowhere else. [22]

The first host to be noticed in ancient times was human: human parasites such as hookworm are recorded from ancient Egypt from 3000 BC onwards, while in ancient Greece, the Hippocratic Corpus describes human bladder worm. [34] The medieval Persian physician Avicenna recorded human and animal parasites including roundworms, threadworms, the Guinea worm and tapeworms. [34] In Early Modern times, Francesco Redi recorded animal parasites, while the microscopist Antonie van Leeuwenhoek observed and illustrated the protozoan Giardia lamblia from "his own loose stools". [34]

Hosts to mutualistic symbionts were recognised more recently, when in 1877 Albert Bernhard Frank described the mutualistic relationship between a fungus and an alga in lichens. [35]


Investigating the cell and developmental biology of plant infection by the rice blast fungus Magnaporthe oryzae

Magnaporthe oryzae is the causal agent of rice blast disease, the most widespread and serious disease of cultivated rice. Live cell imaging and quantitative 4D image analysis have provided new insight into the mechanisms by which the fungus infects host cells and spreads rapidly in plant tissue. In this video review article, we apply live cell imaging approaches to understanding the cell and developmental biology of rice blast disease. To gain entry to host plants, M. oryzae develops a specialised infection structure called an appressorium, a unicellular dome-shaped cell which generates enormous turgor, translated into mechanical force to rupture the leaf cuticle. Appressorium development is induced by perception of the hydrophobic leaf surface and nutrient deprivation. Cargo-independent autophagy in the three-celled conidium, controlled by cell cycle regulation, is essential for appressorium morphogenesis. Appressorium maturation involves turgor generation and melanin pigment deposition in the appressorial cell wall. Once a threshold of turgor has been reached, this triggers re-polarisation which requires regulated generation of reactive oxygen species, to facilitate septin GTPase-dependent cytoskeletal re-organisation and re-polarisation of the appressorium to form a narrow, rigid penetration peg. Infection of host tissue requires a further morphogenetic transition to a pseudohyphal-type of growth within colonised rice cells. At the same time the fungus secretes an arsenal of effector proteins to suppress plant immunity. Many effectors are secreted into host cells directly, which involves a specific secretory pathway and a specialised structure called the biotrophic interfacial complex. Cell-to-cell spread of the fungus then requires development of a specialised structure, the transpressorium, that is used to traverse pit field sites, allowing the fungus to maintain host cell membrane integrity as new living plant cells are invaded. Thereafter, the fungus rapidly moves through plant tissue and host cells begin to die, as the fungus switches to necrotrophic growth and disease symptoms develop. These morphogenetic transitions are reviewed in the context of live cell imaging studies.

Sleutelwoorde: Actin Appressorium Biotrophy Effectors Necrotrophy Septins.

Copyright © 2021 The Authors. Gepubliseer deur Elsevier Inc. Alle regte voorbehou.


Hoogtepunte

The internalization and transport of the G-protein signaling components to late endosomal compartments play a critical role during appressoria development in rice blast disease.

TOR pathway activation by intracellular glutamine levels negatively regulates appressorium development.

Rice blast fungus has evolved two secretion mechanisms to deliver effector proteins into the host cell during biotrophic growth.

M. oryzae disrupts hormonal homeostasis to evade or suppress host defenses during plant cell invasion.

The rice blast fungus, Magnaporthe oryzae, causes one of the most destructive diseases of cultivated rice in the world. Infections caused by this recalcitrant pathogen lead to the annual destruction of approximately 10–30% of the rice harvested globally. The fungus undergoes extensive developmental changes to be able to break into plant cells, build elaborate infection structures, and proliferate inside host cells without causing visible disease symptoms. From a molecular standpoint, we are still in the infancy of understanding how M. oryzae manipulates the host during this complex multifaceted infection. Here, we describe recent advances in our understanding of the cell biology of M. oryzae biotrophic interaction and key molecular factors required for the disease establishment in rice cells.


9.8: Infections in Plants - Biology

An open access, sound science journal for the plant sciences.

A leading international journal publishing novel research in plant cellular biology, molecular biology, biochemistry, genetics, development and evolution.

The global community and knowledge hub for plant scientists.

ASPB is your professional society devoted to advancing plant science research and education.

Related Titles

  • About Plant Physiology
  • Editorial Board
  • Author Guidelines
  • Recommend to Your Librarian
  • Advertising & Corporate Services
  • ASPB
  • Skenkings
  • Awards & Funding
  • Plant Science Today
  • Plant Biology Meeting
  • Meeting Management Services
  • The Signal
  • Plantae
  • Plant Science Research Weekly
  • Taproot: A Plantae Podcast
  • Online ISSN 1532-2548
  • Print ISSN 0032-0889
  • Copyright © 2021 American Society of Plant Biologists

Connect

Hulpbronne

Verken

Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide

This Feature Is Available To Subscribers Only

This PDF is available to Subscribers Only

For full access to this pdf, sign in to an existing account, or purchase an annual subscription.


Biologie

Several members of the cestode (tapeworm) family Diphyllobothriidae are known to infect humans. These pseudophyllidean cestodes have a scolex bearing bothria (grooves), instead of suckers as in the cyclophyllidean cestodes (the group including nearly all human-infecting species). All species associated with human diphyllobothriid infections have marine or aquatic life cycles and transmission occurs via ingestion of undercooked fish.

Recent research incorporating morphologic and molecular data has led to the re-classification and re-naming of most of the human-infecting diphyllobothriids. Dibothriocephalus latus (=Diphyllobothrium latum), the &ldquobroad fish tapeworm&rdquo, is usually assumed to be the most common agent of human diphyllobothriasis. However, it is possible that many historical cases were falsely attributed to this species. Dibothriocephalus nihonkaiense (=Diphyllobothrium nihonkaiense), Dibothriocephalus dendriticus(=Diphyllobothrium dendriticum), Diphyllobothrium stemmacephalum(=Diphyllobothrium stemmacephalum =Diphyllobothrium yonagoense), Diphyllobothrium balaenopterae (=Diplogonoporus grandis =Diplogonoporus balaenoptera), en Adenocephalus pacificus (=Diphyllobothrium pacificum) are also known to infect humans. Sporadic case reports exist involving several other diphyllobothriid species, although some of the species identifications in these reports are of questionable validity.

Lewens siklus

Eggs are passed unembryonated in feces . Under appropriate conditions, the eggs mature (approximately 18 to 20 days) and yield oncospheres which develop into a coracidia . After ingestion by a suitable crustacean (first intermediate host) the coracidia develop into procercoid larvae . Procercoid larvae are released from the crustacean upon predation by the second intermediate host (usually a small fish) and migrate into the deeper tissues where they develop into a plerocercoid larvae (spargana), which is the infectious stage for the definitive host . Because humans do not generally eat these small fish species raw, the second intermediate host probably does not represent an important source of human infection. However, these small second intermediate hosts can be eaten by larger predator species that then serve as paratenic hosts . In this case, the plerocercoid migrates to the musculature of the larger predator fish humans (and other definitive host species) acquire the parasite via consumption of undercooked paratenic host fish . In the definitive host, the plerocercoid develops into adult tapeworms in the small intestine. Adult diphyllobothriids attach to the intestinal mucosa by means of two bilateral groves (bothria) of their scolex . The adults can reach more than 10 m in length, with more than 3,000 proglottids. Immature eggs are discharged from the proglottids (up to 1,000,000 eggs per day per worm) and are passed in the feces. Eggs appear in the feces 5 to 6 weeks after infection.