{"id":2396,"date":"2022-02-09T14:02:31","date_gmt":"2022-02-09T13:02:31","guid":{"rendered":"https:\/\/www.newslab.sk\/mikrobialne-spolocenstva-a-ich-vplyv-na-liecbu-diabetickej-nohy\/"},"modified":"2022-02-10T02:20:44","modified_gmt":"2022-02-10T01:20:44","slug":"microbial-communities-and-their-influence-on-the-treatment-of-diabetic-foot","status":"publish","type":"post","link":"https:\/\/www.newslab.sk\/en\/microbial-communities-and-their-influence-on-the-treatment-of-diabetic-foot\/","title":{"rendered":"Microbial communities and their influence on the treatment of diabetic foot"},"content":{"rendered":"

*A rare case of autochthonous human dirofilariasis with the manifestation of pseudotumor of the epididymis caused by helminth Dirofilaria repens<\/strong><\/span><\/p>\n

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\u00davod<\/h3>\n

K dlhodob\u00fdm komplik\u00e1ci\u00e1m diabetu mellitu patr\u00ed perif\u00e9rna neuropatia s rizikom vzniku vredov na noh\u00e1ch. Tieto ulcer\u00e1cie ozna\u010dujeme pojmom \u201esyndr\u00f3m diabetickej nohy\u201c (SDN)(1). Riziko vzniku diabetick\u00e9ho vredu na nohe pacientov je 19 \u2013 34 %. Vysok\u00e1 je v\u0161ak miera recid\u00edvy vredov, ktor\u00e1 dosahuje a\u017e 40 % do jedn\u00e9ho roka po uzdraven\u00ed a 65 % do piatich rokov(2). Bez poskytnutej v\u010dasnej a vhodnej starostlivosti vedie ulcer\u00e1cia k infekcii, ku gangr\u00e9ne, k amput\u00e1cii a dokonca a\u017e k smrti. Celkovo je amput\u00e1cia doln\u00fdch kon\u010dat\u00edn u pacientov s diabetom 15\u00d7 vy\u0161\u0161ia ako u pacientov bez cukrovky. Odhaduje sa, \u017ee pribli\u017ene 50 \u2013 70 % v\u0161etk\u00fdch amput\u00e1ci\u00ed doln\u00fdch kon\u010dat\u00edn je sp\u00f4soben\u00fdch diabetick\u00fdmi vredmi. Na vzniku vredov sa podie\u013ea mnoho faktorov. Medzi najz\u00e1va\u017enej\u0161ie rizikov\u00e9 faktory patr\u00ed perif\u00e9rna neuropatia, ochorenie perif\u00e9rnych ciev a sprievodn\u00e1 bakteri\u00e1lna infekcia, ktor\u00e1 komplikuje hojenie vredov(3). Pod\u013ea epidemiologick\u00fdch \u00fadajov je asi 50 % pr\u00edpadov SDN sp\u00f4soben\u00fdch v\u00fdlu\u010dne neuropatiou, ktor\u00e1 nar\u00fa\u0161a norm\u00e1lne ochrann\u00e9 reflexn\u00e9 mechanizmy, \u010do m\u00e1 za n\u00e1sledok v\u00e1\u017enu traumu alebo opakovan\u00e9 nepozorovan\u00e9 poranenie sp\u00f4sobuj\u00face otvoren\u00e9 rany. Senzorick\u00e1 neuropatia takisto vedie k vzniku abnormal\u00edt v propriocepcii, ktor\u00e9 sp\u00f4sobuj\u00fa chybn\u00fa z\u00e1\u0165a\u017e pri ch\u00f4dzi, \u010do podporuje tvorbu kalusu alebo vredov(4). Druhou \u010dastou pr\u00ed\u010dinou ulcer\u00e1ci\u00ed s\u00fa ochorenia perif\u00e9rnych ciev (PVD), ktor\u00e9 s\u00fa zodpovedn\u00e9 za 15 % pr\u00edpadov, zatia\u013e \u010do 35 % pr\u00edpadov ulcer\u00e1cie n\u00f4h sa vyv\u00edja ako kombi-n\u00e1cia neuropatie a angiopatie. Ischemick\u00e9 a neuropatick\u00e9 dystrofick\u00e9 tkanivo je citliv\u00e9 na infekcie a poranenia. \u0160truktur\u00e1lne zmeny ve\u013ek\u00fdch a mal\u00fdch ciev spolu s hyperglyk\u00e9miou m\u00f4\u017eu zv\u00fd\u0161i\u0165 vazokonstrikciu a faktory agreg\u00e1cie krvn\u00fdch do\u0161ti\u010diek v cievach. To sp\u00f4sobuje zn\u00ed\u017eenie prekrvenia chodidiel a nervov, \u010do m\u00f4\u017ee v kone\u010dnom d\u00f4sledku vies\u0165 ku gangr\u00e9ne a k infekcii. Sp\u00fa\u0161\u0165ac\u00edmi faktormi s\u00fa v\u0161ak \u010dasto ban\u00e1lne poranenia poko\u017eky sp\u00f4soben\u00e9 obuvou alebo poranenia, ktor\u00e9 vznikaj\u00fa pri strihan\u00ed nechtov(5).<\/p>\n

Lie\u010dba syndr\u00f3mu diabetickej nohy<\/h3>\n

Konven\u010dn\u00e1 lie\u010dba diabetickej nohy zah\u0155\u0148a vy\u010distenie rany, lie\u010dbu infekcie antibiotikami a revaskulariza\u010dn\u00e9 proced\u00fary. Debridement podporuje rast granula\u010dn\u00e9ho tkaniva, zni\u017euje riziko infekcie a eliminuje z\u00e1pach. \u010cast\u00e9 komplik\u00e1cie s hojen\u00edm v\u0161ak viedli k pou\u017e\u00edvaniu pr\u00eddavn\u00fdch terapi\u00ed, ako je hyperbarick\u00e1 kysl\u00edkov\u00e1 terapia, terapie s negat\u00edvnym atmosf\u00e9rick\u00fdm tlakom v oblasti rany alebo vyu\u017eitie steriln\u00fdch lariev. Tie nielen eliminuj\u00fa nekrotick\u00e9 tkanivo, ale vlastn\u00fdmi v\u00fdlu\u010dkami pom\u00e1haj\u00fa bojova\u0165 s infekciou(6). Lie\u010dba SDN je \u010dasto komplikovan\u00e1 sprievodnou infekciou, ktor\u00e1 sa vyskytuje a\u017e v 60 % pr\u00edpadov(7). \u0160t\u00fadie opisuj\u00face vyu\u017eitie nov\u00fdch pr\u00edstupov lie\u010dby s\u00edce reportovali zn\u00ed\u017eenie po\u010dtu ulcer\u00e1ci\u00ed so sepsou, nedok\u00e1zali v\u0161ak infekciu eliminova\u0165 \u00faplne(8). Rany na noh\u00e1ch u pacientov s cukrovkou stratili mnoh\u00e9 obrann\u00e9 mechanizmy intaktnej ko\u017ee, ktor\u00e9 tak nepredstavuj\u00fa z\u00e1branu pre inv\u00e1zne mikroorganizmy(9). D\u00f4vody zv\u00fd\u0161en\u00e9ho rizika a z\u00e1va\u017enosti infekci\u00ed u os\u00f4b s diabetom nie s\u00fa \u00faplne jasn\u00e9. Zd\u00e1 sa, \u017ee cukrovka m\u00e1 multifaktori\u00e1lne \u00fa\u010dinky na r\u00f4zne \u010dasti imunitn\u00e9ho syst\u00e9mu, najm\u00e4 na bunky, ktor\u00e9 sprostredk\u00favaj\u00fa vroden\u00fa imunitu. T\u00e1to imunitn\u00e1 odpove\u010f pozost\u00e1va predov\u0161etk\u00fdm z lok\u00e1lnych vazoakt\u00edvnych a proz\u00e1palov\u00fdch cytok\u00ednov, komplementov\u00e9ho syst\u00e9mu a buniek schopn\u00fdch fagocyt\u00f3zy, t. j. polymorfonukle\u00e1rnych buniek (PMN) a monocytov. Lok\u00e1lne vazoakt\u00edvne cytok\u00edny sp\u00f4sobuj\u00fa vazodilat\u00e1ciu cez reakciu oxidu dusnat\u00e9ho. Pri hyperglyk\u00e9mii v\u0161ak m\u00f4\u017ee d\u00f4js\u0165 k dysregul\u00e1cii tejto reakcie, \u010do m\u00f4\u017ee, naopak, vies\u0165 k vazokonstrikcii, ktor\u00e1 n\u00e1sledne sp\u00f4sobuje hypoxiu a zhor\u0161en\u00fd pr\u00edliv fagocytov. Takisto sa uk\u00e1zalo, \u017ee u os\u00f4b s diabetom maj\u00fa PMN a monocyty viacer\u00e9 poruchy vr\u00e1tane chemotaxie, adherencie, fagocyt\u00f3zy a intracelul\u00e1rneho zab\u00edjania(10).<\/p>\n

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Met\u00f3dy charakteriz\u00e1cie mikrobi\u00f3mu pri ulcer\u00e1ci\u00e1ch<\/h3>\n

Ulcer\u00e1cie s\u00fa kolonizovan\u00e9 spektrom r\u00f4znych bakt\u00e9ri\u00ed, ktor\u00fdch vplyv na postup infekcie nepozn\u00e1me. Klasick\u00e9 met\u00f3dy zalo\u017een\u00e9 na kultiv\u00e1cii s\u00fa orientovan\u00e9 na tie mikroorganizmy, ktor\u00fdm sa dar\u00ed r\u00e1s\u0165 v\u00a0 laborat\u00f3rnych podmienkach a\u00a0 nedostato\u010dne reprezentuj\u00fa ples\u0148ov\u00e9, kvasinkov\u00e9 a ostatn\u00e9 bakteri\u00e1lne spolo\u010denstv\u00e1(11). Z toho d\u00f4vodu sa za\u010dali vyu\u017e\u00edva\u0165 met\u00f3dy nez\u00e1visl\u00e9 od kultiv\u00e1cie. Tie s\u00fa zalo\u017een\u00e9 na vysokoparalelnom sekvenovan\u00ed a n\u00e1slednej bioinformatickej anal\u00fdze. V\u00e4\u010d\u0161ina vedeck\u00fdch skup\u00edn vyu\u017e\u00edva amplik\u00f3nov\u00e9 sekvenovanie 16S rRNA regi\u00f3nu, 28S rRNA, pr\u00edpadne ITS sekvenci\u00ed, ktor\u00e9 predstavuj\u00fa konzervat\u00edvne sekvencie obsiahnut\u00e9 vo v\u0161etk\u00fdch prokaryotick\u00fdch alebo eukaryotick\u00fdch organizmoch. Napriek nesporn\u00fdm v\u00fdhod\u00e1m n\u00e1m met\u00f3da pon\u00faka len slab\u00e9 taxonomick\u00e9 rozl\u00ed\u0161enie na \u00farovni rodov a v niektor\u00fdch pr\u00edpadoch aj druhov. Najviac \u0161t\u00fadi\u00ed vyu\u017e\u00edva sekvenovanie 16S rRNA regi\u00f3nu, ktor\u00fd pozost\u00e1va z 9 hypervariabiln\u00fdch \u00fasekov (V1-V9), medzi ktor\u00fdmi sa nach\u00e1dzaj\u00fa konzervovan\u00e9 sekvencie vhodn\u00e9 pre dizajn amplifika\u010dn\u00fdch primerov(12). Vzh\u013eadom na efektivitu met\u00f3dy sa neanalyzuje cel\u00e1 oblas\u0165 g\u00e9nu 16S rRNA, ale iba jednotliv\u00e9 \u00faseky. Naj\u010dastej\u0161ie sa vyu\u017e\u00edva \u00fasek V4, pr\u00edpadne \u00faseky V1 a\u017e V3. Vyu\u017eitie len jednotliv\u00fdch \u00fasekov v\u0161ak sp\u00f4sobuje niektor\u00e9 nedostatky v presnom zaraden\u00ed do taxonomick\u00fdch jednotiek, napr\u00edklad rozl\u00ed\u0161enie jednotliv\u00fdch druhov \u010de\u013eade Enterobacteriaceae alebo druhov rodu Staphylococcus. V\u00e1\u017enym nedostatkom sekvenovania regi\u00f3nu V4 z poh\u013eadu stanovenia mikrobi\u00f3mu ko\u017ee je zna\u010dn\u00e1 nepresnos\u0165 pri detekcii komenz\u00e1lov Propionibacterium acnes, Staphylococcus a Corynebacterium(13). Pre lep\u0161ie ch\u00e1panie vplyvu mikrobi\u00f3mu na hojenie je v\u0161ak potrebn\u00e9 uvies\u0165 bakteri\u00e1lne zlo\u017eenie na \u00farovni kme\u0148a. Z\u00e1rove\u0148 z amplik\u00f3nov\u00e9ho sekvenovania nez\u00edskame \u017eiadne inform\u00e1cie o ostatnom genetickom vybaven\u00ed mikroorganizmov a jeho vplyve na progres infekcie(13,14). Alternat\u00edvou je pou\u017eitie celogen\u00f3mov\u00e9ho shotgun sekvenovania, ktor\u00e9 je s\u00edce n\u00e1ro\u010dnej\u0161ie na \u010das aj zdroje, ale poskytuje viac potrebn\u00fdch inform\u00e1ci\u00ed o taxon\u00f3mii mikroorganizmov aj ich rezistencii proti antibiotik\u00e1m(13). Na druhej strane, aj ke\u010f s\u00fa tieto techniky ove\u013ea citlivej\u0161ie ako kultiv\u00e1cia, kvalita extrakcie DNA sa l\u00ed\u0161i v\u00a0z\u00e1vislosti od druhu, a\u00a0tak m\u00f4\u017ee st\u00e1le nies\u0165 ur\u010dit\u00fa chybovos\u0165 v\u00a0ur\u010den\u00ed kvantity. Ne-rozli\u0161uj\u00fa ani medzi \u017eiv\u00fdmi a\u00a0m\u0155tvymi bakt\u00e9riami a\u00a0vy\u017eaduj\u00fa si n\u00e1kladn\u00e9 vybavenie(15).<\/p>\n

Zlo\u017eenie mikrobi\u00f3mu syndr\u00f3mu diabetickej nohy<\/h3>\n

V zdravom stave ko\u017en\u00e9 komenz\u00e1lne mikr\u00f3by koexistuj\u00fa so svojimi \u013eudsk\u00fdmi hostite\u013emi a pom\u00e1haj\u00fa predch\u00e1dza\u0165 koloniz\u00e1cii ko\u017ee potenci\u00e1lne patog\u00e9nnymi mikr\u00f3bami. \u0160t\u00fadie v\u0161ak preuk\u00e1zali klinicky relevantn\u00e9 rozdiely v ko\u017enom mikrobi\u00f3me poko\u017eky nohy medzi nediabetick\u00fdmi a diabetick\u00fdmi jedincami, ktor\u00e9 pravdepodobne prispievaj\u00fa k vy\u0161\u0161ej miere ko\u017en\u00fdch infek\u010dn\u00fdch chor\u00f4b u diabetick\u00fdch pacientov(16). Dlhodob\u00e1 \u0161t\u00fadia mikrobi\u00f3mu SDN sledovala zlo\u017eenie mikrobi\u00e1lneho spolo\u010denstva ulcer\u00e1cie v porovnan\u00ed s pacientovou zdravou nohou aj s kontrolnou skupinou zdrav\u00fdch jedincov. Mikrobi\u00f3m rany a nepo\u0161kodenej ko\u017ee diabetick\u00e9ho pacienta sa l\u00ed\u0161ili. Bola takisto pozorovan\u00e1 zn\u00ed\u017een\u00e1 diverzita mikroorganizmov medzi pacientmi s diabetom a zdrav\u00fdmi jedincami. Napriek zn\u00ed\u017eenej diverzite bolo identifikovan\u00fdch 69 taxonomick\u00fdch jednotiek (OTUs) \u0161pecifick\u00fdch pre ko\u017en\u00fd mikrobi\u00f3m pacientov s diabetom(17). V star\u0161ej \u0161t\u00fadii v\u0161ak pozorovali, naopak, vy\u0161\u0161iu diverzitu bakteri\u00e1lnych druhov na ko\u017ei pacientov s diabetom(27). Takto v\u00fdznamn\u00e9 rozdiely nazna\u010duj\u00fa vplyv geografick\u00e9ho a environment\u00e1lneho prostredia, trvania a \u0161t\u00e1dia progresie ochorenia. Okrem toho hospitaliz\u00e1cia pacienta a zvolen\u00e1 antibiotick\u00e1 lie\u010dba m\u00f4\u017eu zmeni\u0165 profil citlivosti, ale aj zast\u00fapenie bakteri\u00e1lnych patog\u00e9nov. Nieko\u013eko vedeck\u00fdch t\u00edmov sa sna\u017eilo identifikova\u0165 jednotliv\u00fdch p\u00f4vodcov komplik\u00e1ci\u00ed. Pomocou klasick\u00fdch kultiva\u010dn\u00fdch met\u00f3d a typiz\u00e1cie pomocou testov ABI20 sa podarilo identifikova\u0165 bakteri\u00e1lne druhy v skor\u00fdch aj neskor\u00fdch ran\u00e1ch. Pri ak\u00fatne infikovan\u00fdch ran\u00e1ch patria medzi be\u017ene izolovan\u00e9 patog\u00e9ny predov\u0161etk\u00fdm Staphylococcus aureus, Staphylococcus epidermidis a\u00a0 \u03b2-hemolytick\u00e9 streptokoky Streptococcus pyogenes a Streptococcus agalactiae. Naproti tomu chronick\u00e9 rany boli \u010dastej\u0161ie polymikrobi\u00e1lne so zmesou aer\u00f3bnych a anaer\u00f3bnych bakt\u00e9ri\u00ed. V chronick\u00fdch vredoch boli naj\u010dastej\u0161ie izolovan\u00fdmi aer\u00f3bnymi grampozit\u00edvnymi bakt\u00e9riami Staphylococcus aureus, Enterococcus faecalis a\u00a0 Staphylococcus epidermidis. Z\u00a0 aer\u00f3bnych gramnegat\u00edvnych bakt\u00e9ri\u00ed sa vyskytovali predov\u0161etk\u00fdm Escherichia coli, Proteus mirabilis, Klebsiella pneumoniae a Pseudomonas aeruginosa. Hlb\u0161ie chronick\u00e9 vredy os\u00edd\u013eovali preva\u017ene anaer\u00f3bne bakt\u00e9rie Peptococcus, Clostridia, Fusobacterium, Bacteroides, pri\u010dom najroz\u0161\u00edrenej\u0161\u00edm bakteri\u00e1lnym patog\u00e9nom pr\u00edtomn\u00fdm v infikovan\u00fdch vredoch bol Bacteroides fragilis(18) (obr\u00e1zok 1). Komplexnej\u0161\u00ed n\u00e1h\u013ead do zlo\u017eenia mikrobi\u00f3mu poskytuj\u00fa techniky zalo\u017een\u00e9 na vysokoparalelnom sekvenovan\u00ed. V\u00e4\u010d\u0161ina dostupn\u00fdch \u0161t\u00fadi\u00ed stanovovala zlo\u017eenie mikrobi\u00e1lneho spolo\u010denstva pomocou amplik\u00f3nov\u00e9ho sekvenovania 16S rRNA. Wolcott a kolekt\u00edv (19) zistili mas\u00edvnu pr\u00edtomnos\u0165 druhov z rodov Staphylococcus, Pseudomonas, Corynebacterium, Streptococcus a Finegoldia. Gardner a kol.(11) rozdelili diabetick\u00e9 vredy na tri typy v z\u00e1vislosti od dominantn\u00fdch tax\u00f3nov v ran\u00e1ch, ktor\u00fdmi boli Staphylococcus, Streptococcus alebo zmes anaer\u00f3bnych bakt\u00e9ri\u00ed a proteobakt\u00e9ri\u00ed. Podobn\u00e9 v\u00fdsledky boli zisten\u00e9 v neskor\u0161ej \u0161t\u00fadii, kde v dvoch skupin\u00e1ch r\u00e1n dominoval bu\u010f Staphylococcus, alebo Streptococcus a rody Corynebacterium a Finegoldia(20). Tie ist\u00e9 rody boli pozorovan\u00e9 vo v\u00e4\u010d\u0161ine r\u00e1n, zatia\u013e \u010do rody Serratia a Proteus boli \u0161pecifick\u00e9 pre jednotlivcov. V \u0161t\u00fadii McDonald a kol.(21) stanovili vplyv identifikovan\u00fdch bakt\u00e9ri\u00ed na hojenie. Nehojace sa rany obsahuj\u00fa preva\u017ene bakt\u00e9rie zo skup\u00edn Bacteroidales, Streptococcaceae a fakultat\u00edvne anaer\u00f3by, najm\u00e4 druhy rodu Enterobacter. Naopak, rany, ktor\u00e9 sa hojili r\u00fdchlo, \u010dasto obsahovali druhy z Actinomycetales a Staphylococcaceae. Zauj\u00edmav\u00e9 s\u00fa aj zmeny v zlo\u017een\u00ed biofilmu v ran\u00e1ch v z\u00e1vislosti od \u010dasu a lie\u010dby. Stanovenie mikrobi\u00f3mu nov\u00fdch vredov v porovnan\u00ed s opakuj\u00facimi sa viedlo k zisteniu, \u017ee stafylokok bol be\u017en\u00fd pri nov\u00fdch vredoch, ale nie pri chronick\u00fdch ran\u00e1ch(22). Rozdiely vo v\u00fdsledkoch napovedaj\u00fa ve\u013ek\u00fa variabilitu mikrobi\u00f3mov diabetick\u00fdch vredov, pri\u010dom nie je zjavn\u00e1 \u017eiadna typick\u00e1 mikrofl\u00f3ra vyskytuj\u00faca sa u v\u0161etk\u00fdch pacientov.<\/p>\n

Vplyv interakcie medzi mikroorganizmami na hojenie ulcer\u00e1cie<\/h3>\n

Vzh\u013eadom na polymikrobi\u00e1lnu povahu SDN je vplyv na v\u00fdvoj rany jednotliv\u00fdch bakteri\u00e1lnych druhov z\u00e1visl\u00fd od partnersk\u00fdch bakt\u00e9ri\u00ed. Napr\u00edklad patog\u00e9nne \u00fa\u010dinky anaer\u00f3bov za zvy\u0161uj\u00fa v pr\u00edtomnosti aer\u00f3bov, preto\u017ee spotreb\u00favaj\u00fa kysl\u00edk, a n\u00e1sledn\u00e1 hypoxia v h\u013abke tkaniva u\u013eah\u010duje rast anaer\u00f3bov. Tak\u00e9to symbiotick\u00e9 vz\u0165ahy s\u00fa definovan\u00e9 ako kooperat\u00edvna interakcia dvoch alebo viacer\u00fdch druhov, \u010do m\u00f4\u017ee vies\u0165 k zv\u00fd\u0161eniu virulencie ved\u00facej k oneskoreniu uzdravenia(23). \u010eal\u0161\u00edm pr\u00edkladom je spolo\u010dn\u00fd v\u00fdskyt Pseudomonas aeruginosa a S. aureus ako dvoch naj\u010dastej\u0161\u00edch pr\u00ed\u010din chronick\u00fdch r\u00e1n. Ich spolo\u010dn\u00e9 infekcie s\u00fa virulentnej\u0161ie ne\u017e jednotliv\u00e9 infekcie a vykazuj\u00fa aj zv\u00fd\u0161en\u00fa rezistenciu proti antibiotickej lie\u010dbe(24). Existuj\u00fa v\u0161ak aj pozit\u00edvne vplyvy interakci\u00ed. Pr\u00edkladom je, \u017ee kompetit\u00edvna interakcia medzi nepatog\u00e9nneho komenz\u00e1la Helcococcus kunzii pr\u00edtomn\u00e9ho v ran\u00e1ch v\u00fdrazne zni\u017euje virulenciu S. aureus bez priamej modifik\u00e1cie obrannej odpovede hostite\u013ea(25). Celogen\u00f3mov\u00e9 sekvenovanie mikrobi\u00f3mu umo\u017enilo identifikova\u0165 nielen taxonomick\u00e9 zlo-\u017eenie, ale aj jednotliv\u00e9 g\u00e9ny obsiahnut\u00e9 v gen\u00f3moch mikroorganizmov. D\u00f4kladnou bioinformatickou anal\u00fdzou mo\u017eno filtrova\u0165 g\u00e9ny zodpovedn\u00e9 za virulenciu bakt\u00e9ri\u00ed. Kalan a kolekt\u00edv(14) pou\u017eit\u00edm tejto met\u00f3dy potvrdili \u010dast\u00fd v\u00fdskyt rezistencie proti antibiotik\u00e1m v ran\u00e1ch s pomal\u00fdm hojen\u00edm. Dok\u00e1zali tie\u017e identifikova\u0165 a celogen\u00f3movo sekvenova\u0165 kme\u0148 S. aureus, ktor\u00fd sa vyskytoval v ran\u00e1ch pacientov s pomal\u00fdm hojen\u00edm. Tento kme\u0148 obsahoval nieko\u013eko g\u00e9nov zabezpe\u010duj\u00facich rezistenciu proti r\u00f4znym antibiotik\u00e1m. V inej \u0161t\u00fadii Sloan a kolekt\u00edv (26) identifikovali rezistencie proti tetracykl\u00ednu a makrolidom v kme\u0148och Streptococcus anginosus a Prevotella. Tetracykl\u00edn ani makrolidy nepatria k aktu\u00e1lne pou\u017e\u00edvan\u00fdm antibiotik\u00e1m na lie\u010dbu diabetickej nohy, no pou\u017e\u00edvaj\u00fa sa v pr\u00edpade pacientov s alergiou na penicil\u00edn. Rezistencia proti antibiotik\u00e1m v\u0161ak nie je jedin\u00fdm faktorom virulencie asociovan\u00fdm s komplikovan\u00fdmi infekciami r\u00e1n. K \u010dast\u00fdm faktorom patr\u00ed aj produkcia biofilmov, ktor\u00e9 zvy\u0161uj\u00fa odolnos\u0165 bakt\u00e9ri\u00ed proti antibiotik\u00e1m, komplikuj\u00fa \u010distenie r\u00e1n, pr\u00edpadne umo\u017e\u0148uj\u00fa anaer\u00f3bnym bakt\u00e9ri\u00e1m efekt\u00edvnej\u0161ie r\u00e1s\u0165. Anot\u00e1ciou g\u00e9nov v minulosti identifikovali agrABCD oper\u00f3n k\u00f3duj\u00faci metabolick\u00fa dr\u00e1hu asociovan\u00fa s produkciou biofilmu(14).<\/p>\n

Z\u00e1ver<\/h3>\n

Mikrobi\u00f3m infikovanej diabetickej nohy predstavuje komplikovan\u00e9 a\u00a0 komplexn\u00e9 spolo\u010denstvo mikroorganizmov. Mnoh\u00e9 vedeck\u00e9 skupiny sa pok\u00fa\u0161ali identifikova\u0165 konkr\u00e9tne bakteri\u00e1lne druhy sp\u00f4sobuj\u00face komplik\u00e1cie, no ich v\u00fdsledky sa \u010dasto nezhoduj\u00fa. Naj\u010dastej\u0161ie sa vyskytuj\u00facimi organizmami s\u00fa S. aureus, Streptococcus alebo Bacteroides. R\u00f4znorodos\u0165 v\u00fdstupov nasved\u010duje, \u017ee p\u00f4vodcov infekci\u00ed je nieko\u013eko a ich v\u00fdskyt je z\u00e1visl\u00fd od mnoh\u00fdch faktorov. Existuje \u010doraz viac d\u00f4kazov, \u017ee p\u00f4vod infekcie je polymikrobi\u00e1lny, pri\u010dom vz\u00e1jomn\u00e9 interakcie m\u00f4\u017eu priebeh hojenia zhor\u0161ova\u0165 alebo, naopak, zlep\u0161ova\u0165 ihib\u00edciou rastu patog\u00e9nov vplyvom nepatog\u00e9nnych komenz\u00e1lov. Je preto d\u00f4le\u017eit\u00e9 smerova\u0165 v\u00fdskum na odha\u013eovanie t\u00fdchto interakci\u00ed a ich vplyvu na hojenie r\u00e1n.<\/p>\n

Po\u010fakovanie<\/strong>
\nT\u00e1to pr\u00e1ca bola podporen\u00e1 Agent\u00farou na podporu v\u00fdskumu a\u00a0v\u00fdvoja na z\u00e1klade Zmluvy \u010d. APVV-17-0526.<\/p>\n

LITERAT\u00daRA<\/h3>\n

1. Tuttolomondo A, Maida C, Pinto A. Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes. World J Orthop. 2015;6(1):62-76.<\/p>\n

2. Armstrong DG, Boulton AJM, Bus SA. Diabetic Foot Ulcers and Their Recurrence. N Engl J Med. 2017;376(24):2367-2375.<\/p>\n

3. Monteiro-Soares M, Boyko EJ, Ribeiro J, Ribeiro I, Dinis-Ribeiro M. Predictive factors for diabetic foot ulceration: a systematic review. Diabetes\/Metabolism Research and Reviews. 2012;28(7):574-600.<\/p>\n

4. Tresierra-Ayala M\u00c1, Garc\u00eda Rojas A. Association between peripheral arterial disease and diabetic foot ulcers in patients with diabetes mellitus type 2. Medicina Universitaria. 2017;19(76):123-126.<\/p>\n

5. Hazari A, Arun Maiya G. Diabetic Foot Complications: Foot Deform-ities, Peripheral Vascular Disease, Claudication, Foot Ulcers, and Amputation. Clinical Biomechanics and its Implications on Diabetic Foot. Published online 2020:49-58.<\/p>\n

6. Hinchliffe RJ, Valk GD, Apelqvist J, et al. Specific guidelines on wound and wound-bed management. Diabetes\/Metabolism Research and Reviews. 2008;24(S1):S188-S189.<\/p>\n

7. Zubair M, Ahmad J. Potential risk factors and outcomes of infection with multidrug resistance among diabetic patients having ulcers: 7 years study. Diabetes Metab Syndr. 2019;13(1):414-418.<\/p>\n

8. Shi E, Shofler D. Maggot debridement therapy: a systematic review. Br J Community Nurs. 2014;Suppl Wound Care:S6-S13.<\/p>\n

9. Noor S, Khan RU, Ahmad J. Understanding Diabetic Foot Infection and its Management. Diabetes\u2008&\u2008Metabolic Syndrome: Clinical Research\u2008&\u2008Reviews. 2017;11(2):149-156.<\/p>\n

10. Peters EJG, Lipsky BA. Diagnosis and Management of Infection in the Diabetic Foot. The Foot in Diabetes. Published online 2020:265-286.<\/p>\n

11. Gardner SE, Hillis SL, Heilmann K, Segre JA, Grice EA. The neuropathic diabetic foot ulcer microbiome is associated with clinical factors. Diabetes. 2013;62(3):923-930.<\/p>\n

12. Chakravorty S, Helb D, Burday M, Connell N, Alland D. A detailed analysis of 16S ribosomal RNA gene segments for the diagnosis of pathogenic bacteria. J Microbiol Methods. 2007;69(2):330-339.<\/p>\n

13. Meisel JS, Hannigan GD, Tyldsley AS, et al. Skin Microbiome Surveys Are Strongly Influenced by Experimental Design. J Invest Dermatol. 2016;136(5):947-956.<\/p>\n

14. Kalan LR, Meisel JS, Loesche MA, et al. Strain- and Species-Level Variation in the Microbiome of Diabetic Wounds Is Associated with Clinical Outcomes and Therapeutic Efficacy. Cell Host Microbe. 2019;25(5):641-655.e5.<\/p>\n

15. Lavigne J-P, Sotto A, Dunyach-Remy C, Lipsky BA. New Molecular Techniques to Study the Skin Microbiota of Diabetic Foot Ulcers. Adv Wound Care. 2015;4(1):38-49.<\/p>\n

16. Liu C, Ponsero AJ, Armstrong DG, Lipsky BA, Hurwitz BL. The dynam-ic wound microbiome. BMC Med. 2020;18(1):1-12.<\/p>\n

17. Gardiner M, Vicaretti M, Sparks J, et al. A longitudinal study of the diabetic skin and wound microbiome. PeerJ. 2017;5:e3543.<\/p>\n

18. Abdulrazak A, Bitar ZI, Al-Shamali AA, Mobasher LA. Bacteriological study of diabetic foot infections. J Diabetes Complications. 2005;19(3):138-141.<\/p>\n

19. Wolcott RD, Hanson JD, Rees EJ, et al. Analysis of the chronic wound microbiota of 2,963 patients by 16S rDNA pyrosequencing. Wound Repair Regen. 2016;24(1):163-174.<\/p>\n

20. Loesche M, Gardner SE, Kalan L, et al. Temporal Stability in Chronic Wound Microbiota Is Associated With Poor Healing. J Invest Dermatol. 2017;137(1):237-244.<\/p>\n

21. MacDonald A, Brodell JD, Daiss JL, Schwarz EM, Oh I. Evidence of differential microbiomes in healing versus non\u2010healing diabetic foot ulcers prior to and following foot salvage therapy. Journal of Orthopaedic Research. 2019;37(7):1596-1603.<\/p>\n

22. Smith K, Collier A, Townsend EM, et al. One step closer to understanding the role of bacteria in diabetic foot ulcers: characterising the microbiome of ulcers. BMC Microbiol. 2016;16:54.<\/p>\n

23. Dalton T, Dowd SE, Wolcott RD, et al. An In Vivo Polymicrobial Biofilm Wound Infection Model to Study Interspecies Interactions. PLoS ONE. 2011;6(11):e27317.<\/p>\n

24. Pastar I, Nusbaum AG, Gil J, et al. Interactions of methicillin resistant Staphylococcus aureus USA300 and Pseudomonas aeruginosa in polymicrobial wound infection. PLoS One. 2013;8(2):e56846.<\/p>\n

25. Essebe CN, Visvikis O, Fines-Guyon M, et al. Decrease of Staphylococcus aureus Virulence by Helcococcus kunzii in a Caenorhabditis elegans Model. Frontiers in Cellular and Infection Microbiology. 2017;7.<\/p>\n

26. Sloan TJ, Turton JC, Tyson J, et al. Examining diabetic heel ulcers through an ecological lens: microbial community dynamics associated with healing and infection. J Med Microbiol. 2019;68(2):230-240.<\/p>\n

27. Oates A, Bowling FL, Boulton AJ, et al. Molecular and culture-based assessment of the microbial diversity of diabetic chronic foot wounds and contralateral skin sites. J ClinMicrobiol. 2012;50:2263-2271.<\/p>\n

 <\/p>\n","protected":false},"excerpt":{"rendered":"

*A rare case of autochthonous human dirofilariasis with the manifestation of pseudotumor of the epididymis caused by helminth Dirofilaria repens   \u00davod K dlhodob\u00fdm komplik\u00e1ci\u00e1m diabetu mellitu patr\u00ed perif\u00e9rna neuropatia s rizikom vzniku vredov na noh\u00e1ch. Tieto ulcer\u00e1cie ozna\u010dujeme pojmom \u201esyndr\u00f3m diabetickej nohy\u201c (SDN)(1). Riziko vzniku diabetick\u00e9ho vredu na nohe pacientov je 19 \u2013 34<\/p>\n","protected":false},"author":7,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_mi_skip_tracking":false,"footnotes":""},"categories":[287],"tags":[734,1300,1854,1301,1328,1325,453,776],"class_list":["post-2396","post","type-post","status-publish","format-standard","hentry","category-uncategorized","tag-diabetes-mellitus","tag-diabetes-mellitus-2-en","tag-diabetic-foot-ulcer","tag-diabeticka-noha-en","tag-microbiome","tag-mikrobiom-en","tag-sepsa-en","tag-sepsis","typ_clanku-review-article"],"acf":{"abstrakt":"

Chronic, difficult-to-treat diabetic foot ulcerations place a massive burden on the patient and the healthcare system. Despite using many conventional and alternative treatments, we cannot reliably prevent the infection that often leads to sepsis or even amputation of the foot. The growing amount of scientific data obtained from the study of infected wounds in patients suggests that microbiome composition plays an essential role in wound healing. The most common bacterial genera identified in wounds include Staphylococcus, Streptococcus and Pseudomonas. However, modern microbiome studies based on methods independent of the cultivation of organisms have enabled us to detect bacteria that are difficult to cultivate and virulence genes that affect wound healing. According to new findings, the increased diversity of the bacterial community increases the likelihood of successful wound healing.<\/p>\n

Keywords:<\/strong> Diabetes mellitus, Diabetic foot ulcer, Microbiome, sepsis<\/p>\n","casopis":[{"ID":2417,"post_author":"7","post_date":"2022-02-08 13:25:20","post_date_gmt":"2022-02-08 12:25:20","post_content":"Druh\u00e9 vydanie \u010dasopisu laborat\u00f3rnej medic\u00edny 2021\/2<\/strong>\r\n

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  • Molekul\u00e1rny mechanizmus karcinogen\u00e9zy indukovanej prostredn\u00edctvom bakt\u00e9ri\u00ed<\/li>\r\n \t
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