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Prečo sa nemôžeme zabiť zadržaním dychu?

Prečo sa nemôžeme zabiť zadržaním dychu?


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Je možné zabiť sa zadržaním dychu?

Táto otázka je očividne skopírovaná z Quory, ale počul som to ako fakt, že sa nemôžeme zabiť zadržaním dychu a hľadám odkazovanú odpoveď.


Stručná odpoveď
Zdraví ľudia nedokážu zadržať dych až do bezvedomia, nieto ešte spáchať samovraždu.

Pozadie
Normálny človek podľa Parkesa (2005) nedokáže ani len zadržať dych do bezvedomia, nieto ešte smrť. Parkes hovorí:

Zadržanie dychu je dobrovoľný čin, ale zdá sa, že normálne subjekty nie sú schopné zadržať dych až do bezvedomia. Výkonný mimovoľný mechanizmus zvyčajne prepíše dobrovoľné zadržanie dychu a spôsobí dych, ktorý definuje bod zlomu.

Parkes vysvetľuje, že dobrovoľné zadržanie dychu nezastaví centrálny respiračný rytmus. Namiesto toho zadržiavanie dychu iba potláča jeho prejav tým, že dobrovoľne drží hrudník pri určitom objeme. V čase písania tohto článku neexistovalo žiadne jednoduché vysvetlenie bodu zlomu. Je známe, že je spôsobená parciálnymi tlakmi krvných plynov aktivujúcich chemoreceptory karotických tepien. Sú to periférne senzorické neuróny, ktoré detegujú zmeny v chemických koncentráciách, vrátane nízkeho kyslíka (hypoxia) a vysokého oxidu uhličitého (hyperkapnia). Hypoxia aj hyperkapnia sú príznakmi zadržiavania dychu a obe sú detekované chemoreceptormi. Tieto receptory vysielajú nervové signály do vazomotorického centra drene, ktoré nakoniec prekoná vedomé zadržiavanie dychu.

Bod zlomu sa dá oddialiť veľkým nafúknutím pľúc, hyperoxiou a hypokapniou a skráti ho zvýšený metabolizmus.

Odkaz
- Parkes, Exp Physiol (2006); 91(1): 1-15


Protipríklad: Niektorí ľudia sa aspoň dokážu naučiť zadržať dych, kým neomdlia, a ak k tomu dôjde pod vodou, takmer určite zomrú utopením.

Keď som bol vo vojenskej službe, spriatelil som sa s niektorými príslušníkmi US Navy SEAL. Prechádzajú notoricky náročným tréningovým a výberovým procesom (BUDS), ktorý bol dobre zdokumentovaný. Medzi "evolúcie" programu patria testy, v ktorých musia kandidáti vyriešiť problémy s prístupom k potápačským jednotkám, keď sú ponorení v bazénoch alebo vodných nádržiach (a keď sú obťažovaní inštruktormi). Je bežné, že kandidáti počas týchto testov prepadnú, pretože ak sa vynoria na vzduch, v teste neuspejú. (A to sú ľudia, ktorí sa sami vyberajú ako veľmi motivovaní nezlyhať za žiadnu cenu.) Testy zjavne vyraďujú kandidátov, ktorí sú náchylní na paniku, pretože strácajú kyslík a nedokážu potlačiť svoj fyziologický inštinkt dýchania.

Hovoril som s jedným absolventom, ktorý počas jednej takejto evolúcie omdlel (ale na druhý pokus uspel). Poznamenal, že po tomto incidente stratil akýkoľvek strach z utopenia, pretože si uvedomil, že ak by sa niekedy ocitol v situácii, keď by mu dochádzal kyslík, nepocítil by paniku a pred utopením by upadol do bezvedomia.


Ignorovanie emócií je zlé pre vaše zdravie. Tu je to, čo s tým robiť

Moderný život je plný emocionálnych výziev. Tlak na úspech, potreba držať krok, strach z premeškania a túžba po dobrých vzťahoch a pracovnej spokojnosti, to všetko môže vyvolať prchavé kombinácie emócií.

V našej spoločnosti sa však neučíme, ako s emóciami pracovať, ale ako ich blokovať a vyhýbať sa im. Robíme to celkom dobre: ​​Medzi pitím alkoholu, užívaním liekov na predpis a časom stráveným pred obrazovkou existuje množstvo spôsobov, ako sa vyhnúť našim pocitom. Keď ich uznáme, zasypeme ich mantrami naučenými od detstva. (“Mysli na hmotu,” “uchopte” a “nasajte to” sú známe.) Brnenie emócií nie je dobré pre duševné ani fyzické zdravie. Je to ako stlačenie plynu a bŕzd vášho auta súčasne, čím sa vytvorí vnútorný tlakový hrniec.

Získajte náš zdravotný bulletin. Prihláste sa a získajte najnovšie správy o zdraví a vede, ako aj odpovede na otázky týkajúce sa wellness a odborné tipy.


Čo sa stane, keď príliš dlho zadržíte dych?

Keď človek zadrží dych príliš dlho, množstvo oxidu uhličitého sa v jeho tele začne hromadiť, uvádza The Science Creative Quarterly. Môže začať cítiť pálenie v pľúcach.

Keď je hladina oxidu uhličitého príliš vysoká, začnú bolestivé kontrakcie v rebrách a v bránici. Bolesť je signálom, že človek potrebuje vydýchnuť. Telo a mozog začnú trpieť nedostatkom kyslíka. Kritická línia sa vzťahuje na moment, keď sa človeku v tele nahromadí toľko oxidu uhličitého, že začne pociťovať bolesť. Hyperventilácia je jedným zo spôsobov, ako oddialiť kritický moment, ale hyperventilácia je tiež nebezpečná, poznamenáva The Science Creative Quarterly. Hyperventilácia môže viesť k bezvedomiu, pretože podkopáva signály tela na dýchanie.

Účinky zadržiavania dychu na mozog zatiaľ nie sú podľa The New York Times jasné. Vedci z University of Queensland vykonali neuropsychologické testy na voľných potápačoch, aby preskúmali spôsob, akým sa správali ich mozgy v porovnaní s ľuďmi, ktorí sa nepotápali. Zistili, že mozgy voľných potápačov reagovali normálne vo vizuálnych, jazykových a pamäťových testoch. Skenovanie mozgu SPECT ukázalo určité abnormality v mozgoch piatich voľných potápačov, ale vedci si neboli istí významom zistení.


ELI5: Prečo sa nemôžeš udusiť zadržaním dychu?

Nemal som v úmysle zabiť sa zadržaním dychu. Ale každý sa to snažil udržať čo najdlhšie, no bez ohľadu na to, ako dlho to robíme, vždy sa zrazu nadýchneme. Je to nejaký druh reflexnej akcie?

Ak to budete robiť dostatočne dlho, omdliete a začnete znova dýchať (za predpokladu, že si cestou dole neudriete hlavu), ale väčšinou sa vaša Británia jednoducho „nie“ a prinúti vás dýchať

Automatické opravy! Váš MOZOR nie Británia.

Nakoniec upadnete do bezvedomia a vaše telo bude v tej chvíli dýchať samo, ako keby ste spali. Stále dýchaš.

Funguje tu niekoľko mechanizmov. Keď na určitý čas zadržíte dych, vaše telo sa nedokáže zbaviť oxidu uhličitého, ktorý je prirodzeným vedľajším produktom metabolizmu. Niektoré zmyslové bunky v krčných tepnách detegujú túto zvýšenú hladinu CO2 a posielajú impulzy do vášho mozgového kmeňa (oblasť mozgu, ktorá reguluje dýchanie). Váš mozgový kmeň vám dáva impulz na dýchanie. Čím vyššia je koncentrácia CO2 vo vašej krvi, tým silnejší je dýchací impulz. Väčšina ľudí podľahne tomuto impulzu a pred nádychom vydýchne. Výdychom sa zbavíte určitého množstva CO2 a po niekoľkých nasledujúcich nádychoch a výdychoch sa dýchací impulz zníži na normálnu hodnotu.

Ak ste dostatočne odhodlaní odolať dychovému impulzu, je možné pokračovať v zadržiavaní dychu, kým koncentrácia kyslíka vo vašej krvi nebude dostatočne vysoká na to, aby váš mozog správne fungoval. V tomto bode stratíte vedomie. Akonáhle omdliete, už nemôžete vedome zadržať dych a vaše telo automaticky reguluje dýchanie a všetok CO2 sa vyfúkne a hladiny O2 sa opäť normalizujú.

Je však veľmi ťažké nechať sa omdlieť. Vaše telo je veľmi citlivé na hladiny CO2 v porovnaní s hladinami O2. Osobne som mal na prste pulzný oxymeter a zadržiaval som dych tak dlho, ako som to dokázal. Po asi 50 sekundách nedýchania bola moja saturácia kyslíkom stále na 99%, ale nutkanie dýchať ma premohlo a musel som sa nadýchnuť.


Kyslík a oxid uhličitý

Počas zadržiavania dychu, arteriálny alebo koncový dychový parciálny tlak kyslíka P klesne pod svoju normálnu hladinu ~100 mmHg a hladinu oxidu uhličitého P stúpne nad svoju normálnu hladinu ~40 mmHg. V bode zlomu od maximálnej inflácie vo vzduchu, P je typicky 62 ± 4 mmHg a P je typicky 54 ± 2 mmHg (n= 5 riadkov a kol. 1974) a čím dlhšie je zadržanie dychu, tým viac sa menia. Je pozoruhodné, že dospelí normálne nedokážu dôsledne zadržať dych až do bezvedomia, dokonca ani pod laboratórnym dohľadom. Nunn (1987) odhaduje, že vedomie u normálnych dospelých je stratené P hladiny pod ~27 mmHg a P hladiny medzi 90 a 120 mmHg. Boli hlásené hraničné hladiny blízke týmto hodnotám, napr. P hladiny až 24 mmHg, P hladiny až 91 mmHg a doba zadržania dychu 14 minút alebo viac (Schneider, 1930 Ferris a kol. 1946 Klocke & Rahn, 1959). Pre porovnanie Schneider (1924, 1930) mimoriadne opisuje tajné prepínanie dýchania subjektov na inšpiráciu zo spirometra N2 (a vydýchnuť do vzduchu v miestnosti) a meranie (obr. 1b) rozsah dychových časov do hroziaceho bezvedomia (cyanóza, maskový výraz tváre, rozšírenie zreníc, konvergencia očí, klesajúci systolický tlak Schneider & Truesdell, 1923). Tento rozsah je podobný jeho rozsahu trvania zadržania dychu (obr. 1a), ale takéto symptómy nie sú charakteristické pre bod zlomu zadržiavania dychu.

Jedna zrejmá hypotéza na vysvetlenie bodu zlomu je, že raz P klesne pod resp P stúpne nad určitú prahovú hodnotu parciálneho tlaku alebo rýchlosť zmeny parciálneho tlaku dosiahne prahovú hodnotu, potom stimulácia chemoreceptora spôsobí mimovoľný nádych. Vždy sa predpokladalo, že by to boli karotické chemoreceptory [aortálne chemoreceptory nemajú preukázateľný vplyv na dýchanie u ľudí ( Lugliani a kol. 1971 Wasserman a kol. 1975)]. Ako ukazujú nasledujúce odseky, túto „hypotézu arteriálneho chemoreceptora“ podporujú výrazné účinky zmeny zloženia vdychovaného plynu na trvanie zadržania dychu. Je to však zmätené nedostatkom konzistentného vzoru arteriálnych tlakov plynu v bode zlomu, denerváciou karotických chemoreceptorov, ktoré nedokážu predĺžiť zadržanie dychu až do bezvedomia, a schopnosťou opakovane zadržať dych po vdýchnutí dusivých zmesí plynov.

Trvanie zadržania dychu sa takmer zdvojnásobí pri zadržaní dychu s hyperoxickými zmesami plynov (obr. 5c), alebo predchádzajúcim zadržaním dychu dobrovoľnou alebo mechanickou hyperventiláciou na zníženie P úrovne (obr. 5a). Mimochodom, preoxygenácia má veľa praktických výhod pri štúdiu zadržiavania dychu. Nielenže to predlžuje trvanie, ale tiež vedie k tomu, že srdcová frekvencia sa počas zadržania dychu takmer nezmení (Gross a kol. 1976) a v bodoch zlomu, ktoré sa nevyskytujú pri P úrovne dostatočne nízke na to, aby ohrozovali mozog. [Prísne existuje riziko atelektázy so zadržaním dychu, keď pľúca obsahujú 100 % O2 (Campbell a kol. 1967), takže je vhodnejšie nejaké riedenie dusíkom.]

Alternatívne je trvanie zadržania dychu takmer na polovicu skrátené zadržaním dychu z hypoxie (obr. 5c), alebo z hyperkapnie, napr. pozdvihnutie inšpirovaného P na 65 mmHg (Godfrey & Campbell, 1969 Kelman & Wann, 1971).

Hypotéza arteriálneho chemoreceptora však nie je podporovaná známymi tlakmi krvných plynov v bode zlomu. Preoxygenácia teda nepredĺži trvanie zadržania dychu až do priemeru P padá na cca. 62 mmHg. Namiesto toho bod prerušenia nastane, kým P je stále pozoruhodne zvýšená, napr. 553 ± 16 mmHg, n= 5 ( Lin a kol. 1974). Naopak, hypoxia neskracuje trvanie zadržania dychu do r P klesne na 62 mmHg. Namiesto toho sa bod zlomu vyskytuje ešte nižšie P hodnoty 24–43 mmHg (Ferris a kol. 1946). Podobne hyperkapnia neskracuje trvanie zadržania dychu do P stúpa na 54 mmHg (Kelman & Wann, 1971) a P môže dosiahnuť 70 mmHg (Godfrey & Campbell, 1969). Okrem toho bod zlomu zadržaní dychu z hypokapnie nastáva pri P úrovne medzi 48 ± 3 (Cooper a kol. 2003) a 71 ± 3 mmHg (Klocke & Rahn, 1959). Ani bod zlomu nie je pri nejakej jedinečnej kombinácii nízkych P a vysoké P (Klocke & Rahn, 1959). Dokonca aj po najdlhších možných zadržaniach dychu z hypokapnie s preoxygenáciou sú hladiny krvných plynov v bode zlomu pozoruhodne benígne.

U ľudí sú krčné telieska jediným známym prostriedkom na detekciu arteriálnej hypoxie (Lugliani a kol. 1971 Wasserman a kol. 1975) a rýchlej detekcie arteriálnej hyperkapnie. Proti hypotéze arteriálnych chemoreceptorov ďalej stojí fakt, že po chemodenervácii karotídy (resekcii) stále nastáva bod zlomu, teda denervácia nepredlžuje zadržiavanie dychu až do bezvedomia. Davidson a spolupracovníci (Davidson a kol. 1974 Gross a kol. 1976) porovnávali trvanie zadržania dychu pri inspiračnej kapacite u piatich pacientov po bilaterálnej resekcii karotického tela s resekciou normálnych jedincov (obr. 5b). Priemerná dĺžka trvania zadržania dychu v 100 % O2 sa takmer nelíšili a neboli v ich priemere žiadne funkčne dôležité rozdiely v bode zlomu P úrovne [362 ± 20 proti 425 ± 12 mmHg (priemer ± smerodajná odchýlka) u kontrol], ani v priemere P úrovne [59 ± 2 proti 56 ± 4 mmHg (priemer ± smerodajná odchýlka)]. Interpretácia týchto údajov o trvaní zadržania dychu však môže byť nejednoznačná, pretože sa dajú použiť aj na preukázanie, že denervácia karotického tela spôsobuje malé predĺženie trvania zadržania dychu, čo potvrdil ( Honda a kol. 1988). Obrázok 5b ukazuje, že priemerné trvanie zadržania dychu u denervovaných pacientov u 21 % O2 je o 54 % dlhší (P < 0,05) ako u intaktných jedincov a to u 12 % O2 je o 65% dlhšia (P < 0,05). Ak sú však karotické chemoreceptory jediným prostriedkom na detekciu hypoxie, aký mechanizmus vysvetľuje, ako hypoxia naďalej skracuje trvanie zadržania dychu u denervovaných pacientov? Je možné, že k tomuto skráteniu stále dochádza, pretože dôležitý účinok hypoxie nie je na karotických chemoreceptoroch, ale na chemoreceptoroch bránicových svalov (Road, 1990 Jammes & Speck, 1995), ktorých stimulácia môže namiesto toho významne prispieť k bodu zlomu (pozri časť s názvom Paralýza bránice).

Sprostredkúvajú centrálne chemoreceptory bod zlomu? Ich úloha pri zadržaní dychu je stále nejasná. Rovnako ako PaCO2 odráža ich úroveň stimulácie počas zadržiavania dychu, nedostatok konzistentného PaCO2 úroveň v bode zlomu naznačuje, že nie. Fakty, že trvanie zadržania dychu u 5 pacientov zjavne bez funkčnej periférnej alebo centrálnej chemoreceptivity (vrodený centrálny hypoventilačný syndróm – Shea a kol., 1993) je takmer dvojnásobný v porovnaní s 5 vekovo a rodovo zodpovedajúcimi kontrolnými skupinami a že 4/5 museli experimentátori povedať, aby porušili, naznačuje opak.


Smrteľné huby sú najnovšou hrozbou mikróbov na celom svete

Maryn McKenna je novinárka špecializujúca sa na verejné zdravie, globálne zdravie a potravinovú politiku a vedúci pracovník Centra pre štúdium ľudského zdravia na Emory University. Najnovšie je autorkou Veľké kura: Neuveriteľný príbeh o tom, ako antibiotiká vytvorili moderné poľnohospodárstvo a zmenili spôsob, akým sa svet stravuje (Národné geografické knihy, 2017).
Poďakovanie: Nick Higgins

AUTOR

Maryn McKenna je novinárka špecializujúca sa na verejné zdravie, globálne zdravie a potravinovú politiku a vedúci pracovník Centra pre štúdium ľudského zdravia na Emory University. Najnovšie je autorkou Veľké kura: Neuveriteľný príbeh o tom, ako antibiotiká vytvorili moderné poľnohospodárstvo a zmenili spôsob, akým sa svet stravuje (Národné geografické knihy, 2017).

Bol štvrtý júnový týždeň v roku 2020 a uprostred druhej vlny pandémie COVID v USA Počet úmrtí na nový koronavírus presiahol 2,4 milióna, čím sa blížilo 125 000. Vo svojej domácej kancelárii v Atlante Tom Chiller zdvihol oči od svojich e-mailov a poutieral si ruky po tvári a oholil hlavu.

Chiller je lekár a epidemiológ a za normálnych okolností vedúci pobočky v Centrách pre kontrolu a prevenciu chorôb v USA, zodpovedný za sekciu, ktorá monitoruje zdravotné ohrozenia hubami, ako sú plesne a kvasinky. Túto špecialitu odložil v marci, keď si USA začali uvedomovať veľkosť hrozby nového vírusu, keď sa New York City uzavrelo a CDC povedalo takmer všetkým svojim tisíckam zamestnancov, aby pracovali z domu. Odvtedy bol Chiller súčasťou frustrujúceho a brzdeného úsilia agentúry verejného zdravotníctva proti COVID. Jej zamestnanci spolupracovali so štátnymi zdravotníckymi oddeleniami, sledovali správy o prípadoch a úmrtiach a čo jurisdikcie museli urobiť, aby zostali v bezpečí.

Chiller pokrčil vyčerpaním plecami a opäť sa sústredil na svoju schránku. Bol v ňom pochovaný bulletin, ktorý poslal jeden z jeho zamestnancov, ktorý ho prinútil posadiť sa a zaťať zuby. Nemocnice neďaleko Los Angeles, ktoré zvládali nápor COVID, hlásili nový problém: U niektorých z ich pacientov sa vyvinuli ďalšie infekcie s hubou tzv. Candida auris. Štát bol v stave najvyššej pohotovosti.

Chiller o všetkom vedel C. auris&mdash možno viac ako ktokoľvek iný v USA. Takmer presne pred štyrmi rokmi on a CDC poslali nemocniciam urgentný bulletin, v ktorom im povedali, aby sa mali na pozore. Huba sa ešte neobjavila v USA, ale Chiller sa rozprával s rovesníkmi v iných krajinách a počul, čo sa stalo, keď mikrób napadol ich systémy zdravotnej starostlivosti. Odoláva liečbe väčšinou z mála liekov, ktoré sa proti nej dali použiť. Darilo sa mu na studených tvrdých povrchoch a smialo sa z čistenia chemikálií, v niektorých nemocniciach, kde pristálo, museli roztrhať vybavenie a steny, aby ho porazili. Spôsobil rýchlo sa šíriace ohniská a zabil až dve tretiny ľudí, ktorí sa ním nakazili.

Krátko po tomto varovaní, C. auris vstúpilo do USA Pred koncom roka 2016 sa ním nakazilo 14 ľudí a štyria zomreli. Odvtedy CDC sledovalo jeho pohyb a klasifikovalo ho ako jednu z mála nebezpečných chorôb, o ktorých museli lekári a zdravotnícke oddelenia informovať agentúru. Do konca roka 2020 bolo v USA v 23 štátoch vyše 1 500 prípadov. A potom prišiel COVID, zabíjal ľudí, zahltil nemocnice a presmeroval všetko úsilie v oblasti verejného zdravia na nový vírus a preč od iných nečestných organizmov.

Od začiatku pandémie sa však Chiller cítil znepokojený možným prienikom plesňových infekcií. Prvé správy o kazuistike COVID, publikované čínskymi vedcami v medzinárodných časopisoch, popisovali pacientov ako katastrofálne chorých a odoslaných na intenzívnu starostlivosť: farmaceutický paralyzovaní, zapojení do ventilátorov, so závitom s I.V. línie, nabité liekmi na potlačenie infekcie a zápalu. Tieto zbesilé zásahy by ich mohli zachrániť pred vírusom, ale lieky na tlmenie imunity by znemožnili ich vrodenú obranu a širokospektrálne antibiotiká by zabili prospešné baktérie, ktoré držia inváziu mikróbov pod kontrolou. Pacienti by zostali mimoriadne zraniteľní voči akémukoľvek inému patogénu, ktorý by mohol číhať v blízkosti.

Chiller a jeho kolegovia začali potichu oslovovať kolegov v USA a Európe a žiadali ich o akékoľvek varovné signály, že COVID umožňuje smrteľným hubám oporu. Údaje o infekciách sa vrátili z Indie, Talianska, Kolumbie, Nemecka, Rakúska, Belgicka, Írska, Holandska a Francúzska. Teraz sa tie isté smrtiace huby objavili aj u amerických pacientov: prvé príznaky druhej epidémie, vrstvené na vrchole vírusovej pandémie. A nebolo to len tak C. auris. Ďalšia smrteľná huba tzv Aspergillus si tiež začínala vyberať daň.

&ldquoToto bude rozšírené všade,&rdquo hovorí Chiller. &ldquoNemyslíme si, že to zvládneme.&rdquo

Huby, ak o nich vôbec uvažujeme, budeme pravdepodobne považovať za drobné nepríjemnosti: pleseň na syre, pleseň na topánkach odstrčených vzadu do skrine, huby vyrastajúce v záhrade po silných dažďoch. Všimneme si ich a potom ich zoškrabeme alebo oprášime, pričom nikdy nevnímame, že sa stretávame s krehkými okrajmi siete, ktorá spája planétu. Huby tvoria svoju vlastnú biologickú ríšu asi šiestich miliónov rôznych druhov, od bežných spoločníkov, ako sú kvasnice na pečenie, až po divokú exotiku. Od ostatných kráľovstiev sa líšia zložitými spôsobmi. Na rozdiel od zvierat majú na rozdiel od rastlín bunkové steny, nedokážu si vyrobiť vlastnú potravu na rozdiel od baktérií, svoju DNA držia v jadre a nabaľujú bunky organelami a vlastnosťami, vďaka ktorým sú na bunkovej úrovni čudne podobné nám.* Huby lámu kamene, vyživujú rastliny, vysievajú oblaky, zahaľujú našu pokožku a balia naše vnútornosti, väčšinou skrytý a nezaznamenaný svet žijúci vedľa nás a v nás.

V septembri 2018 mal Torrence Irvin z Pattersonu v Kalifornii pocit, že prechladol. O sedem mesiacov neskôr stratil 75 percent kapacity pľúc. Irvin mal údolnú horúčku, plesňovú infekciu, a život mu zachránil experimentálny liek. Poďakovanie: Timothy Archibald

To vzájomné spolužitie sa teraz vychýli z rovnováhy. Huby sa vzmáhajú za klimatické zóny, v ktorých dlho žili, prispôsobujú sa prostrediam, ktoré by kedysi boli nepriateľské, učia sa novému správaniu, ktoré im umožňuje preskakovať medzi druhmi novými spôsobmi. Pri vykonávaní týchto manévrov sa stávajú úspešnejšími patogénmi, ktoré ohrozujú ľudské zdravie takým spôsobom, akým sa im to nepodarilo.

Dohľad, ktorý identifikuje vážne plesňové infekcie, je nejednotný, a preto je akýkoľvek počet pravdepodobne podhodnotený. Jeden široko zdieľaný odhad však naznačuje, že na celom svete je možno 300 miliónov ľudí infikovaných plesňovými chorobami a 1,6 milióna úmrtí každý rok – viac ako malária, toľko ako tuberkulóza. Len v USA CDC odhaduje, že viac ako 75 000 ľudí je ročne hospitalizovaných kvôli plesňovej infekcii a ďalších 8,9 milióna ľudí vyhľadá ambulantnú návštevu, čo stojí približne 7,2 miliardy dolárov ročne.

Pre lekárov a epidemiológov je to prekvapujúce a znepokojujúce. Dlhodobá lekárska doktrína zastáva názor, že pred plesňami nás chráni nielen vrstvená imunitná obrana, ale aj preto, že sme cicavce s teplotou jadra vyššou, než uprednostňujú huby. Chladnejšie vonkajšie povrchy nášho tela sú ohrozené menšími útokmi – napríklad mykóza nôh, kvasinkové infekcie, lišaj, no u ľudí so zdravým imunitným systémom boli invazívne infekcie zriedkavé.

To v nás možno zanechalo prílišnú sebadôveru. &ldquoMáme obrovský slepý bod,&rdquo hovorí Arturo Casadevall, lekár a molekulárny mikrobiológ na Johns Hopkins Bloomberg School of Public Health. &ldquoChoďte na ulicu a opýtajte sa ľudí, čoho sa boja, a oni vám povedia, že sa boja baktérií, vírusov, ale neboja sa umierania na plesne.&rdquo.

Je iróniou, že práve naše úspechy nás urobili zraniteľnými. Huby využívajú poškodený imunitný systém, ale pred polovicou 20. storočia ľudia s oslabenou imunitou nežili príliš dlho. Odvtedy je medicína veľmi dobrá v udržiavaní takýchto ľudí nažive, aj keď ich imunitný systém je ohrozený chorobou alebo liečbou rakoviny alebo vekom. Vyvinula tiež celý rad terapií, ktoré zámerne potláčajú imunitu, aby udržali príjemcov transplantátu zdravých a liečili autoimunitné poruchy, ako je lupus a reumatoidná artritída. V súčasnosti žije obrovské množstvo ľudí, ktorí sú obzvlášť zraniteľní voči hubám. (Bola to plesňová infekcia, Pneumocystis carinii zápal pľúc, ktorý upozornil lekárov na prvé známe prípady HIV pred 40 rokmi tento rok v júni.)

Nie celá naša zraniteľnosť je chybou medicíny, ktorá tak úspešne chráni život. Iné ľudské činy otvorili ďalšie dvere medzi svetom húb a našim vlastným. Čistíme pôdu pre plodiny a osídlenie a narúšame stabilnú rovnováhu medzi hubami a ich hostiteľmi. Prevážame tovar a zvieratá po celom svete a huby na nich stopujú. Plodiny namáčame fungicídmi a zvyšujeme odolnosť organizmov žijúcich v blízkosti. Podnikáme kroky, ktoré otepľujú klímu, a huby sa prispôsobujú, čím sa zmenšuje rozdiel medzi ich preferovanou teplotou a našou, ktorá nás tak dlho chránila.

Ale huby sa na náš trávnik z nejakého cudzieho miesta neprihnali. Boli vždy s nami, pretkali sa našimi životmi, prostredím a dokonca aj našimi telami: každý deň každý človek na planéte vdýchne najmenej 1 000 spór húb. Nie je možné uzavrieť sa pred ríšou húb. Vedci sa však naliehavo snažia pochopiť nespočetné množstvo spôsobov, ktorými sme rozobrali našu obranu proti mikróbom, aby našli lepšie prístupy k ich obnove.

Je mätúce, že my ľudia sme sa cítili tak bezpečne pred hubami, keď sme po stáročia vedeli, že naše plodiny môžu byť zničené ich útokmi. V 40. rokoch 19. storočia hubovitý organizmus, Phytophthora infestans, zničili úrodu írskych zemiakov viac ako jeden milión ľudí, jedna osmina populácie, zomrela od hladu. (Mikrób, predtým považovaný za hubu, je teraz klasifikovaný ako veľmi podobný organizmus, vodná pleseň.) V 70. rokoch 19. storočia hrdza kávových listov, Hemileia vastatrix, vyhladili kávovníky v celej južnej Ázii, úplne zmenili usporiadanie koloniálneho poľnohospodárstva v Indii a na Srí Lanke a presunuli produkciu kávy do Strednej a Južnej Ameriky. Huby sú dôvodom, prečo v 20. rokoch minulého storočia zmizli z Apalačských lesov v USA miliardy amerických gaštanov a v 40. rokoch minulého storočia boli z amerických miest vyrezané milióny umierajúcich holandských brestov. Každoročne zničia na poli jednu pätinu celosvetovej potravinárskej úrody.

Napriek tomu sa medicína roky pozerala na ničivé huby, ktoré spôsobili rastlinnej ríši, a nikdy neuvažovala o tom, že ľudia alebo iné zvieratá môžu byť rovnako ohrozené. &ldquoPatológovia rastlín a farmári berú huby veľmi vážne a vždy ich brali, a agrobiznis to tak robil,“ hovorí Matthew C. Fisher, profesor epidemiológie na Imperial College London, ktorého práca sa zameriava na identifikáciu nových plesňových hrozieb. &ldquoSú však veľmi zanedbávané z hľadiska chorôb voľne žijúcich živočíchov a tiež chorôb ľudí.&rdquo

Takže keď divé mačky v Rio de Janeiro začali ochorieť, nikoho spočiatku nenapadlo pýtať sa prečo. Pouličné mačky majú aj tak ťažký život, hrabú sa, bojujú a rodia nekonečné vrhy mačiatok. Ale v lete roku 1998 začali desiatky a potom stovky mačiek v susedstve vykazovať strašné zranenia: plačúce rany na labkách a ušiach, zakalené opuchnuté oči, niečo, čo vyzeralo ako nádory vyrastajúce z ich tvárí. Mačky z Ria žijú zmiešané s ľuďmi: Deti sa s nimi hrajú a najmä v chudobných štvrtiach ich ženy povzbudzujú, aby zostali blízko domov a vysporiadali sa s potkanmi a myšami. Onedlho začali ochorieť aj niektoré deti a matky. Na rukách sa im otvorili okrúhle rany s chrumkavým okrajom a po rukách sa im ťahali tvrdé červené hrče, akoby sledovali stopu.

V roku 2001 výskumníci z Nadácie Oswalda Cruza, nemocnice a výskumného ústavu so sídlom v Riu, si uvedomili, že za tri roky ošetrili 178 ľudí, väčšinou matky a staré mamy, na podobné hrčky a mokvajúce lézie. Takmer všetci mali každodenný kontakt s mačkami. Pri analýze infekcií a infekcií u mačiek liečených na neďalekej veterinárnej klinike našli hubu tzv Sporothrix.

Rôzne druhy rodu Sporothrix žijú v pôde a na rastlinách. Vnesená do tela rezom alebo škrabancom sa táto huba premení na pučivú formu pripomínajúcu kvasinky. V minulosti kvasinková forma nebola prenosná, ale v tejto epidémii bola. Takto sa mačky nakazili navzájom a ich ošetrovatelia: Kvasinky v ich ranách a slinách lietali z mačky na mačku, keď sa bili, strkali alebo kýchali. Mačky to preniesli na ľudí prostredníctvom pazúrov, zubov a pohladení. Infekcie sa šíria z kože nahor do lymfatických uzlín a krvného obehu a do očí a vnútorných orgánov. V kazuistikách, ktoré zhromaždili lekári v Brazílii, boli záznamy o plesňových cystách rastúcich v mozgoch ľudí.

Huba s touto zručnosťou bola vyhlásená za nový druh, Sporothrix brasiliensis. Do roku 2004 sa v nadácii Cruz liečilo na túto chorobu 759 ľudí, do roku 2011 to bolo až 4 100 ľudí. Do minulého roka diagnostikovali túto chorobu viac ako 12 000 ľuďom v Brazílii v pásme viac ako 2 500 míľ. Rozšíril sa do Paraguaja, Argentíny, Bolívie, Kolumbie a Panamy.

&ldquoTáto epidémia si nedá prestávku,&rdquo hovorí Flávio Queiroz-Telles, lekár a docent na Federálnej univerzite Paraná v Curitibe, ktorý videl svoj prvý prípad v roku 2011. &ldquo sa rozširuje.&rdquo.

Bolo záhadou ako: Divoké mačky sa túlajú, ale nemigrujú tisíce kilometrov. V CDC Chiller a jeho kolegovia tušili možnú odpoveď. V Brazílii a Argentíne bola sporotrichóza zistená u potkanov, ako aj u mačiek. Infikované hlodavce by mohli skákať po tovare, ktorý sa presúva do prepravných kontajnerov. Milióny týchto kontajnerov každý deň pristávajú na lodiach kotviacich v amerických prístavoch. Huba by sa mohla dostať do USA Chorý potkan, ktorý unikol z kontajnera, by mohol zasiať infekciu v meste obklopujúcom prístav.

„V centrách s hustou populáciou, kde je veľa divých mačiek, môžete vidieť nárast extrémne chorých mačiek, ktoré sa potulujú po uliciach,“ hovorí John Rossow, veterinár z CDC, ktorý si možno ako prvý všimol možnú hrozbu. z Sporothrix do USA &ldquoA keďže sa my Američania nemôžeme vyhnúť pomoci zatúlaným zvieratám, myslím si, že budeme svedkami mnohých prenosov na ľudí.&rdquo

Pre mykológa, akým je Chiller, je tento druh šírenia varovaním: Kráľovstvo húb je v pohybe, tlačí na hranice a hľadá akúkoľvek možnú výhodu pri hľadaní nových hostiteľov. A že im možno pomáhame. „Huby sú živé, prispôsobujú sa,“ hovorí. Spomedzi ich niekoľkých miliónov druhov, &doteraz len okolo 300, o ktorých vieme, že spôsobujú ľudské choroby. To je veľký potenciál pre novosť a odlišnosť vo veciach, ktoré existujú už miliardu rokov.&rdquo.

Torrence Irvin mal 44 rokov, keď sa začali jeho plesňové problémy. Veľký zdravý muž, ktorý bol športovcom na strednej a vysokej škole, žije v Pattersone v Kalifornii, pokojnom mestečku v Central Valley pri ceste 5 v USA. O niečo viac ako dva roky predtým Irvin kúpil dom v novú divíziu a presťahoval sa so svojou manželkou Rhondou a ich dvoma dcérami. Bol manažérom skladu pre maloobchodníka Crate & Barrel a hlásateľom miestnych mládežníckych futbalových zápasov.

V septembri 2018 začal mať Irvin pocit, že dostal nádchu, z ktorej sa nevedel striasť. Dávkoval si Nyquil, no ako týždne plynuli, cítil sa slabý a dýchavične. V jeden októbrový deň skolaboval a padol na kolená vo svojej spálni. Našla ho jeho dcéra. Jeho manželka trvala na tom, aby išli na pohotovosť.

Lekári si mysleli, že má zápal pľúc. Poslali ho domov s antibiotikami a pokynmi na užívanie voľnopredajných liekov. Zoslabol a nedokázal udržať jedlo. Chodil k iným lekárom, pričom sa neustále zhoršoval, znášal dýchavičnosť, nočné potenie a chudnutie podobné obeti rakoviny. Z 280 libier sa zmenšil na 150. Nakoniec jeden test ukázal odpoveď: plesňová infekcia nazývaná kokcidioidomykóza, zvyčajne známa ako Valley horúčka. &ldquoKým som to nezískal, nikdy som o tom nepočul,“ hovorí.

Ale iní mali. Irvina poslali na Kalifornskú univerzitu v Davise, 100 míľ od jeho domu, ktorá zriadila Centrum pre údolnú horúčku. Ochorenie sa vyskytuje väčšinou v Kalifornii a Arizone, južnom cípe Nevady, Novom Mexiku a ďalekom západnom Texase. Mikróby za tým, Coccidioides immitis a Coccidioides posadasii, infikovať ročne asi 150 000 ľudí v tejto oblasti a mimo tohto regiónu je infekcia sotva známa. &ldquoIt's not a national pathogen&mdashyou don't get it in densely populated New York or Boston or D.C.,&rdquo says George R. Thompson, co-director of the Davis center and the physician who began to supervise Irvin's care. &ldquoSo even physicians view it as some exotic disease. But in areas where it's endemic, it's very common.&rdquo

Similar to Sporothrix, Coccidioides has two forms, starting with a thready, fragile one that exists in soil and breaks apart when soil is disturbed. Its lightweight components can blow on the wind for hundreds of miles. Somewhere in his life in the Central Valley, Irvin had inhaled a dose. The fungus had transformed in his body into spheres packed with spores that migrated via his blood, infiltrating his skull and spine. To protect him, his body produced scar tissue that stiffened and blocked off his lungs. By the time he came under Thompson's care, seven months after he first collapsed, he was breathing with just 25 percent of his lung capacity. As life-threatening as that was, Irvin was nonetheless lucky: in about one case out of 100, the fungus grows life-threatening masses in organs and the membranes around the brain.

Irvin had been through all the approved treatments. There are only five classes of antifungal drugs, a small number compared with the more than 20 classes of antibiotics to fight bacteria. Antifungal medications are so few in part because they are difficult to design: because fungi and humans are similar at the cellular level, it is challenging to create a drug that can kill them without killing us, too.

It is so challenging that a new class of antifungals reaches the market only every 20 years or so: the polyene class, including amphotericin B, in the 1950s the azoles in the 1980s and the echinocandin drugs, the newest remedy, beginning in 2001. (There is also terbinafine, used mostly for external infections, and flucytosine, used mostly in combination with other drugs.)

For Irvin, nothing worked well enough. &ldquoI was a skeleton,&rdquo he recalls. &ldquoMy dad would come visit and sit there with tears in his eyes. My kids didn't want to see me.&rdquo

In a last-ditch effort, the Davis team got Irvin a new drug called olorofim. It is made in the U.K. and is not yet on the market, but a clinical trial was open to patients for whom every other drug had failed. Irvin qualified. Almost as soon as he received it, he began to turn the corner. His cheeks filled out. He levered himself to his feet with a walker. In several weeks, he went home.

Valley fever is eight times more common now than it was 20 years ago. That period coincides with more migration to the Southwest and West Coast&mdashmore house construction, more stirring up of soil&mdashand also with increases in hot, dry weather linked to climate change. &ldquoCoccidioides is really happy in wet soil it doesn't form spores, and thus it isn't particularly infectious,&rdquo Thompson says. &ldquoDuring periods of drought, that's when the spores form. And we've had an awful lot of drought in the past decade.&rdquo

Because Valley fever has always been a desert malady, scientists assumed the fungal threat would stay in those areas. But that is changing. In 2010 three people came down with Valley fever in eastern Washington State, 900 miles to the north: a 12-year-old who had been playing in a canyon and breathed the spores in, a 15-year-old who fell off an ATV and contracted Valley fever through his wounds, and a 58-year-old construction worker whose infection went to his brain. Research published two years ago shows such cases might become routine. Morgan Gorris, an earth systems scientist at Los Alamos National Laboratory, used climate-warming scenarios to project how much of the U.S. might become friendly territory for Coccidioides by the end of this century. In the scenario with the highest temperature rise, the area with conditions conducive to Valley fever&mdasha mean annual temperature of 10.7 degrees Celsius (51 degrees Fahrenheit) and mean annual rainfall of less than 600 millimeters (23.6 inches)&mdashreaches to the Canadian border and covers most of the western U.S.

Irvin has spent almost two years recovering he still takes six pills of olorifim a day and expects to do that indefinitely. He gained back weight and strength, but his lungs remain damaged, and he has had to go on disability. &ldquoI am learning to live with this,&rdquo he says. &ldquoI will be dealing with it for the rest of my life.&rdquo

Deadly duo of fungi is infecting more people. Coccidioides immitis causes Valley fever, and its range is spreading beyond the Southwest, where it was first identified (top). Aspergillus fumigatus appears in many environments and can be lethal to people suffering from the flu or COVID (dno). Credit: Science Source

S porothrix found a new way to transmit itself. Valley fever expanded into a new range. C. auris, the fungus that took advantage of COVID, performed a similar trick, exploiting niches opened by the chaos of the pandemic.

That fungus was already a bad actor. It did not behave the way that other pathogenic yeasts do, living quiescently in someone's gut and surging out into their blood or onto mucous membranes when their immune system shifted out of balance. At some point in the first decade of the century, C. auris gained the ability to directly pass from person to person. It learned to live on metal, plastic, and the rough surfaces of fabric and paper. When the first onslaught of COVID created a shortage of disposable masks and gowns, it forced health-care workers to reuse gear they usually discard between patients, to keep from carrying infections. A C. auris was ready.

In New Delhi, physician and microbiologist Anuradha Chowdhary read the early case reports and was unnerved that COVID seemed to be an inflammatory disease as much as a respiratory one. The routine medical response to inflammation would be to damp down the patient's immune response, using steroids. That would set patients up to be invaded by fungi, she realized. C. auris, lethal and persistent, had already been identified in hospitals in 40 countries on every continent except Antarctica. If health-care workers unknowingly carried the organism through their hospitals on reused clothing, there would be a conflagration.

&ldquoI thought, &lsquoOh, God, I.C.U.s are going to be overloaded with patients, and infection-control policies are going to be compromised,'&rdquo she said recently. &ldquoIn any I.C.U. kde C. auris is already present, it is going to play havoc.&rdquo

Chowdhary published a warning to other physicians in a medical journal early in the pandemic. Within a few months she wrote an update: a 65-bed I.C.U. in New Delhi had been invaded by C. auris, and two thirds of the patients who contracted the yeast after they were admitted with COVID died. In the U.S., the bulletin that Chiller received flagged several hundred cases in hospitals and long-term care facilities in Los Angeles and nearby Orange County, and a single hospital in Florida disclosed that it harbored 35. Where there were a few, the CDC assumed that there were more&mdashbut that routine testing, their keyhole view into the organism's stealthy spread, had been abandoned under the overwork of caring for pandemic patients.

As bad as that was, physicians familiar with fungi were watching for a bigger threat: the amplification of another fungus that COVID might give an advantage to.

V prírode, Aspergillus fumigatus serves as a clean-up crew. It encourages the decay of vegetation, keeping the world from being submerged in dead plants and autumn leaves. Yet in medicine, Aspergillus is known as the cause of an opportunistic infection spawned when a compromised human immune system cannot sweep away its spores. In people who are already ill, the mortality rate of invasive aspergillosis hovers near 100 percent.

During the 2009 pandemic of H1N1 avian flu, Aspergillus began finding new victims, healthy people whose only underlying illness was influenza. In hospitals in the Netherlands, a string of flu patients arrived unable to breathe and going into shock. In days, they died. By 2018 what physicians were calling invasive pulmonary aspergillosis was occurring in one out of three patients critically ill with flu and killing up to two thirds of them.

Then the coronavirus arrived. It scoured the interior lung surface the way flu does. Warning networks that link infectious disease doctors and mycologists around the globe lit up with accounts of aspergillosis taking down patients afflicted with COVID: in China, France, Belgium, Germany, the Netherlands, Austria, Ireland, Italy and Iran. As challenging a complication as C. auris was, Aspergillus was worse. C. auris lurks in hospitals. The place where patients were exposed to Aspergillus was, well, everywhere. There was no way to eliminate the spores from the environment or keep people from breathing them in.

In Baltimore, physician Kieren Marr was acutely aware of the danger. Marr is a professor of medicine and oncology at Johns Hopkins Medical Center and directs its unit on transplant and oncology infectious diseases. The infections that take hold in people who have received a new organ or gotten a bone marrow transplant are familiar territory for her. When COVID arrived, she was concerned that Aspergillus would surge&mdashand that U.S. hospitals, not alert to the threat, would miss it. Johns Hopkins began testing COVID patients in its I.C.U. with the kind of molecular diagnostic tests used in Europe, trying to catch up to the infection in time to try to treat it. Across the five hospitals the Johns Hopkins system operates, it found that one out of 10 people with severe COVID was developing aspergillosis.

Several patients died, including one whose aspergillosis went to the brain. Marr feared there were many others like that patient, across the country, whose illness was not being detected in time. &ldquoThis is bad,&rdquo Marr said this spring. &ldquoAspergillus is more important in COVID right now than C. auris. Without a doubt.&rdquo

The challenge of countering pathogenic fungi is not only that they are virulent and sneaky, as bad as those traits may be. It is that fungi have gotten very good at protecting themselves against drugs we use to try to kill them.

The story is similar to that of antibiotic resistance. Drugmakers play a game of leapfrog, trying to get in front of the evolutionary maneuvers that bacteria use to protect themselves from drugs. For fungi, the tale is the same but worse. Fungal pathogens gain resistance against antifungal agents&mdashbut there are fewer drugs to start with, because the threat was recognized relatively recently.

&ldquoIn the early 2000s, when I moved from academia to industry, the antifungal pipeline was zero,&rdquo says John H. Rex, a physician and longtime advocate for antibiotic development. Rex is chief medical officer of F2G, which makes the not yet approved drug that Torrence Irvin took. &ldquoThere were no antifungals anywhere in the world in clinical or even preclinical development.&rdquo

That is no longer the case, but research is slow as with antibiotics, the financial rewards of bringing a new drug to market are uncertain. But developing new drugs is critical because patients may need to take them for months, sometimes for years, and many of the existing antifungals are toxic to us. (Amphotericin B gets called &ldquoshake and bake&rdquo for its grueling side effects.) &ldquoAs a physician, you're making a choice to deal with a fungal infection at the cost of the kidney,&rdquo says Ciara Kennedy, president and CEO of Amplyx Pharmaceuticals, which has a novel antifungal under development. &ldquoOr if I don't deal with the fungal infection, knowing the patient's going to die.&rdquo

Developing new drugs also is critical because the existing ones are losing their effectiveness. Irvin ended up in the olorofim trial because his Valley fever did not respond to any available drugs. C. auris already shows resistance to drugs in all three major antifungal classes. Aspergillus has been amassing resistance to the antifungal group most useful for treating it, known as the azoles, because it is exposed to them so persistently. Azoles are used all across the world&mdashnot only in agriculture to control crop diseases but in paints and plastics and building materials. In the game of leapfrog, fungi are already in front.

The best counter to the ravages of fungi is not treatment but prevention: not drugs but vaccines. Right now no vaccine exists for any fungal disease. But the difficulty of treating patients long term with toxic drugs, combined with staggering case numbers, makes finding one urgent. And for the first time, one might be in sight if not in reach.

The reason that rates of Valley fever are not worse than they are, when 10 percent of the U.S. population lives in the endemic area, is that infection confers lifelong immunity. That suggests a vaccine might be possible&mdashand since the 1940s researchers have been trying. A prototype that used a killed version of the form Coccidioides takes inside the body&mdashfungal spheres packed with spores&mdashworked brilliantly in mice. But it failed dismally in humans in a clinical trial in the 1980s.

&ldquoWe did it on a shoestring, and everyone wanted it to work,&rdquo says John Galgiani, now a professor and director of the Valley Fever Center for Excellence at the University of Arizona College of Medicine, who was part of that research 40 years ago. &ldquoEven with [bad] reactions and the study lasting three years, we kept 95 percent of the people who enrolled.&rdquo

Enter dogs. They have their noses in the dirt all the time, and that puts them at more at risk of Valley fever than humans are. In several Arizona counties, close to 10 percent of dogs come down with the disease every year, and they are more likely to develop severe lung-blocking forms than human are. They suffer terribly, and it is lengthy and expensive to treat them. But dogs' vulnerability&mdashplus the lower standards that federal agencies require to approve animal drugs compared with human ones&mdashmakes them a model system for testing a possible vaccine. And the passion of owners for their animals and their willingness to empty their wallets when they can may turn possibility into reality for the first time.

Galgiani and his Arizona group are now working on a new vaccine formula, thanks to financial donations from hundreds of dog owners, plus a boost from a National Institutes of Health grant and commercial assistance from a California company, Anivive Lifesciences. Testing is not complete, but it could reach the market for use in dogs as early as next year. &ldquoI think this is proof of concept for a fungal vaccine&mdashhaving it in use in dogs, seeing it is safe,&rdquo says Lisa Shubitz, a veterinarian and research scientist at the Arizona center. &ldquoI really believe this is the path to a human vaccine.&rdquo

This injection does not depend on a killed Valley fever fungus. Instead it uses a live version of the fungus from which a gene that is key to its reproductive cycle, CPS1, has been deleted. The loss means the fungi are unable to spread. The gene was discovered by a team of plant pathologists and later was identified in Coccidioides by Marc Orbach of the University of Arizona, who studies host-pathogen interactions. After creating a mutant Coccidioides with the gene removed, he and Galgiani experimentally infected lab mice bred to be exquisitely sensitive to the fungus. The microbe provoked a strong immune reaction, activating type 1 T helper cells, which establish durable immunity. The mice survived for six months and did not develop any Valley fever symptoms, even though the team tried to infect them with unaltered Coccidioides. When the researchers autopsied the mice at the end of that half-year period, scientists found almost no fungus growing in their lungs. That long-lasting protection against infection makes the gene-deleted fungus the most promising basis for a vaccine since Galgiani's work in the 1980s. But turning a vaccine developed for dogs into one that could be used in humans will not be quick.

The canine formula comes under the purview of the U.S. Department of Agriculture, but approval of a human version would be overseen by the U.S. Food and Drug Administration. It would require clinical trials that would probably stretch over years and involve thousands of people rather than the small number of animals used to validate the formula in dogs. Unlike the 1980s prototype, the new vaccine involves a live organism. Because there has never been a fungal vaccine approved, there is no preestablished evaluation pathway for the developers or regulatory agencies to follow. &ldquoWe would be flying the plane and building it at the same time,&rdquo Galgiani says.

He estimates achieving a Valley fever vaccine for people could take five to seven years and about $150 million, an investment made against an uncertain promise of earnings. But a successful compound could have broad usefulness, protecting permanent residents of the Southwest as well as the military personnel at 120 bases and other installations in the endemic area, plus hundreds of thousands of &ldquosnowbird&rdquo migrants who visit every winter. (Three years ago the CDC identified cases of Valley fever in 14 states outside the endemic zone. Most were in wintertime inhabitants of the Southwest who were diagnosed after they went back home.) By one estimate, a vaccine could save potentially $1.5 billion in health-care costs every year.

&ldquoI couldn't see the possibility that we'd have a vaccine 10 years ago,&rdquo Galgiani says. &ldquoBut I think it is possible now.&rdquo

I f one fungal vaccine is achieved, it would carve the path for another. If immunizations were successful&mdashscientifically, as targets of regulation and as vaccines people would be willing to accept&mdashwe would no longer need to be on constant guard against the fungal kingdom. We could live alongside and within it, safely and confidently, without fear of the ravages it can wreak.

But that is years away, and fungi are moving right now: changing their habits, altering their patterns, taking advantage of emergencies such as COVID to find fresh victims. At the CDC, Chiller is apprehensive.

&ldquoThe past five years really felt like we were waking up to a whole new phenomenon, a fungal world that we just weren't used to,&rdquo Chiller says. &ldquoHow do we stay on top of that? How do we question ourselves to look for what might come next? We study these emergences not as an academic exercise but because they show us what might be coming. We need to be prepared for more surprises.&rdquo

*Editor&rsquos Note (6/9/21): This sentence was revised after posting to correct the description of how the cells of fungi differ from those of animals.

This article was originally published with the title "Deadly Kingdom" in Scientific American 324, 6, 26-35 (June 2021)


The Ice Bucket Challenge Can Kill. Here's Why You're Doing It Wrong

The Ice Bucket Challenge has raised an impressive amount of money and awareness for motor neuron diseases like Amyotrophic Lateral Sclerosis (Lou Gehrig's Disease). In just one month, the ALS Association has received $80m in donations.

But while the fundraising campaign should be praised, the tragic death of a Scottish teenager reveals that the Ice Bucket Challenge can be dangerous – and potentially deadly.

When you imagine the dangers of cold water, you probably think of hypothermia. "There was a bit of a preoccupation with hypothermia dating right back to the Titanic, and then reinforced during the Second World War," says Professor Mike Tipton, a physiologist at the University of Portsmouth and co-author of Essentials Of Sea Survival.

But fatal hypothermia takes a relatively long time: starting from 37ºC/99ºF, it takes half an hour for your core body temperature to fall below 35ºC/95ºF.

Most deaths in open water occur within minutes, as two-thirds of drowning victims are good swimmers and over half die within 10 feet of safe refuge.

The first thing Ice Bucket challengers and those immersed in cold water experience is a sudden drop in skin temperature, which triggers a reflex called the cold shock response.

"It's basically exactly the same as you would imagine if you stepped or jumped into a pool they said was heated and it wasn't, or stepped under a shower that had just run cold," Tipton explains. "It's a gasp response followed by uncontrollable hyperventilation."

That gasp for air and rapid inhalation completely destroys your ability to hold your breath. Even if you can normally hold your breath for a minute in the bathtub, you would only last a few seconds in cold water. The average volume an adult inhales is 2-3 litres, and the lethal dose for drowning is 1.5 litres of seawater or 3 litres of freshwater.

If you're already underwater or waves are battering your face, the cold shock response could kill you.

There are many reasons why people lose their lives. Some can't swim while others succumb to flash floods, for example. But Tipton believes that many 'drowning' victims are actually being killed from immersion in cold water. He estimates that about 20% succumb to hypothermia, 20% of people die before, during or after being rescued (a phenomenon called circum-rescue collapse) and the remaining 60% are killed by the cold shock response.

The Ice Bucket Challenge has been linked with two deaths so far. The Scottish teenager, 18-year-old Cameron Lancaster, drowned after jumping into a flooded quarry. Another victim, 40-year-old father Willis Tepania from New Zealand, had a heart attack after drinking a bottle of bourbon.

(Although not a consequence of the challenge itself, Corey Griffin, a 27-year-old who raised $100,000 for his friend Pete Frates – the college baseball player with ALS who made the campaign go viral – died after diving into Nantucket Island harbor.)

Most Ice Bucket Challenge participants don't submerge themselves, so how can cold water immersion be dangerous to them? The problem occurs when you're holding your breath and your face gets wet.

Immersing yourself in cold water triggers two powerful physiological responses: cold shock and another reflex, the diving response.

Cold water becomes particularly dangerous when the two coincide. "If you've got those two responses co-activated then you've got a response trying to accelerate the heart – the cold shock response – at the same time as you've got a response trying to slow it down, the diving response," says Tipton.

He calls this 'autonomic conflict' because both the cold shock and diving responses send signals to the heart via nerves that control involuntary body functions (including breathing), the autonomic nervous system.

The diving response is vital to marine mammals such as seals and dolphins, but humans have it too.

It's the reflex that tells your heart to calm down and redirects blood flow to the most crucial organs, like the brain. It's what prompts you to hold your breath underwater and enables you to conserve oxygen.

Both the cold shock and diving responses are triggered by receptors in the skin – nerve endings of the autonomic system.

The diving response is stimulated by receptors on your face (near the eyes, nose and mouth) while cold shock is triggered by thermoreceptors all around the body. Because these nerve endings are 0.2mm below the surface of the skin, body fat – which insulates against hypothermia – won't stop you detecting a temperature drop.

When cold water is sensed by your face and rest of the body simultaneously, autonomic conflict is the result. Both the cold shock and diving responses relay sensory information (via the brain) to the heart, but their messages contradict each other. Submerge your face alone and heart rate should fall from the normal 60-100 to about 40-50 beats per minute, whereas cold water will boost the rate above 100.

To the heart, autonomic conflict is like pushing the gas pedal to accelerate while also vigorously and repeatedly applying the brakes.

Autonomic conflict creates an abnormal heart rhythm – arrhythmia – and can occasionally lead to the most dangerous outcome of cold water immersion: sudden cardiac death.

After releasing a held breath, an arrhythmia will start within 10 seconds, and this can be detected on an electrocardiogram (ECG). "I would be really interested in having an ECG on all these people who are doing the Ice Bucket Challenge because I pretty well guarantee there will be a fairly significant number of them having an arrhythmia while they do it," says Tipton.

Cardiac arrhythmias are common. If you swim or snorkel, you probably experience them regularly.

In Tipton's previous studies, 2% of fit and healthy subjects experienced an arrhythmia when their body was immersed in cold water, but the proportion goes up to 82% when the face is wet too. The problem gets worse in stressful situations: among people who train to escape from submerged helicopters, including those who work on offshore platforms or for the military, 25% have an arrhythmia during a 10-second drill.

On their own, most cardiac arrhythmias won't show symptoms and probably aren't hazardous to health, but other factors can predispose an individual to a lethal rhythm.

People with a pre-existing cardiovascular problems, such as a heart condition or hypertension, are at particular risk from sudden cardiac death – especially if those problems haven't been identified. Medicines (certain antihistamines, antibiotics and antipsychotic drugs) can also increase risk.

Even athletes aren't safe. Figures from 2003 to 2011 show that 30 out of 43 or 70% of fatal incidents during US triathlons occurred during the swim phase of a race. Because strong emotions like anger increase heart rate and athletes have no trouble while training alone, Tipton believes that competition (through mass starts and collisions) also raise the risk of arrhythmia. "These are all relatively young, fit individuals who are also having a problem with sudden cardiac death."

Autonomic conflict between the cold shock and diving responses might also be behind fatalities where cause of death has been misdiagnosed as hypothermia or drowning, because the electrical disturbances that lead to arrhythmia can't be detected in post-mortem examinations.

Sudden cardiac death is impossible to predict, but highlighting the dangers of cold water can help prevent more people dying from the Ice Bucket Challenge.

Most won't suffer from the symptoms of cardiac arrhythmia, but there's still a real risk that some will. All it takes is for one person to die and the money for worthy causes will quickly dry up.

Fundraising campaigns are a fun way to help charities, but some people – especially celebrities – must participate responsibly.

You could argue that rich celebrities should accept a forfeit instead of the dare. Charlie Sheen and Sir Patrick Stewart are great examples of this. On the other hand, the Ice Bucket Challenge probably wouldn't have gone viral if we didn't enjoy seeing others - especially famous people - in discomfort from being drenched by ice-cold water. It's pure Schadenfreude, that pleasure you get from someone else's misfortune.

Not using cold water removes the danger, but who wants to watch the Lukewarm Bucket Challenge?

Making the Ice Bucket Challenge safe is simple. Professor Mike Tipton's advice for minimising the chances of a heart attack is straightforward:

Participants should also avoid total immersion. "If you go into cold water then the physiological responses will be much more profound and prolonged than if you just have a bucket of water thrown over the top of your head."


Practicing breath focus

Breath focus helps you concentrate on slow, deep breathing and aids you in disengaging from distracting thoughts and sensations. It's especially helpful if you tend to hold in your stomach.

First steps. Find a quiet, comfortable place to sit or lie down. First, take a normal breath. Then try a deep breath: Breathe in slowly through your nose, allowing your chest and lower belly to rise as you fill your lungs. Let your abdomen expand fully. Now breathe out slowly through your mouth (or your nose, if that feels more natural).

Breath focus in practice. Once you've taken the steps above, you can move on to regular practice of controlled breathing. As you sit comfortably with your eyes closed, blend deep breathing with helpful imagery and perhaps a focus word or phrase that helps you relax.

Ways to elicit the relaxation response

Several techniques can help you turn down your response to stress. Breath focus helps with nearly all of them:

  • Progressive muscle relaxation , tai chi, and Qi Gong
  • Repetitive prayer
  • Guided imagery

How does soap work?

To fully understand the FDA’s ruling, we should first understand a little about how soaps clean and disinfect. A quick chemistry refresher will remind us that there are two general types of molecules: polar (things that can be mixed into water, like sugar) and nonpolar (things that cannot be mixed into water, like oil).

Soap molecules are amphipathic, meaning they have both polar and non-polar properties. This gives soap the ability to dissolve most types of molecules, making it easier to wash them off your hands (Figure 1). In terms of illness-causing germs, which are mostly bacteria and viruses, soap has a two-fold effect: one chemical and one behavioral. Firstly, the amphipathic nature of soap loosens the bacteria and viruses off your hands so they can be washed away more easily. Secondly, you tend to wash your hands for a longer period when using soap, because you try to rinse all of it away. Thus, regular soaps don’t necessarily kill bacteria and viruses as much as they simply help you wash them off your skin.

Postava 1:The amphipathic nature of soap molecules help lift dirt and bacteria off skin and into water so that they can be washed away.

Antibacterial soaps have all the same properties as regular soap, but with an extra ingredient added that is intended to stop the bacteria remaining on your skin from replicating. The idea is that this additive will further protect the hand-washer from harmful bacteria as compared to regular soap. It is important to mention that these ingredients generally have no effect on viruses, so the focus is to reduce the risk from bacterial germs. The most common antibacterial additive found in consumer hand soaps is a compound called triclosan.


Why Do We Inhale Oxygen And Exhale Carbon Dioxide?

Why do we inhale oxygen and exhale carbon dioxide? pôvodne sa objavil na Quora: miesto na získavanie a zdieľanie vedomostí, ktoré ľuďom umožňuje učiť sa od iných a lepšie porozumieť svetu.

Answer by Fabian van den Berg, Neuropsychologist, on Quora:

Why do we inhale oxygen and exhale carbon dioxide? Short and long answer, you ready?

The short answer is that you inhale oxygen because you need oxygen for some biological processes. A fairly important one is the production of ATP, the energy all of our cells use. In the process, electrons are used and oxygen has a high affinity for electrons. The waste products of this process are Carbon Dioxide and Water, in different steps along the way.

The long answer needs some pictures. This one is a seriously long answer and will explain the production of ATP. CO2 is involved in the citric acid cycle and water is involved in the electron transport chain.

You know how we eat to live? Well that’s where it starts. The major source of energy we get from food is sugar, more specifically glucose. Now things get a bit funky so bear with me. Glucose needs to be broken down in steps. This has to be done slowly because glucose contains plenty of energy and we don’t want to blow stuff up.

Step 1: Glycolysis

The glucose molecules are broken down into two pyruvate molecules. It takes ten steps to go from glucose to pyruvates. This all happens in the cytosol, which is all the fluid inside a cell between the organelles.

The big 6-carbon glucose molecule first needs to be split into two smaller 3-carbon molecules (phosphoglyceraldehyde, PGAL), this split uses ATP. It might sound counterproductive since we are trying to make ATP, but the investment will pay off. One ATP is used by each kinase reaction, and step one and step three require it, so a total of two ATPs are used to split glucose into the smaller PGAL molecules.

These PGAL molecules are then transformed into Pyruvate, and during that process two ADPs are turned into ATP by a kinase reaction (in steps seven and ten). Because we have two PGALs we create four ATPs (so we gain two because we used two before).

The whole process therefore uses glucose and two ATP and then produces two pyruvates, two NADH, and four ATP. The net gain is two ATP, the investment paid off since we doubled it.

Step 2: Pyruvate Oxidation / Decarboxylation / Pyruvate Dehydrogenase

In the last step we were left with pyruvate after breaking apart glucose, in fact we have two pyruvate molecules for each glucose model. The next step is Pyruvate Oxidation, which takes place inside mitochondria. Remember the famous saying: “Mitochondria are the powerhouses of the cell“? We’ll get there soon enough. The transformation takes place in a few steps.

  • The first step is breaking off a carbon molecule, this carbon takes two oxygens with it(so CO2 is removed).
  • In the second step the 2-carbon molecule that is left is oxidized (electrons lost), these electrons are picked up by the NAD+ turning it into NADH.
  • The 2-carbon molecule is attached to Coenzyme-A, this turns it into Acetyl CoA. This is just a carrier molecule to bring the 2-carbon group to the next step.

From one glucose molecule two pyruvate molecules are made, these are turned into two acetyl-CoA molecules. Two carbons are released as carbon dioxide, these are two carbons from the original six in glucose. Lastly, two NADH are produced from NAD+.

Step 3: The Citric Acid Cycle / Krebs cycle / Tricarboxylic Acid (TCA)

This cycle (whatever name you choose) is an essential step in the process. It takes the Acetyl-CoA produced in the last step and squeezes out every tiny bit of potential energy it can. Just like the last step this process takes place in the matrix of mitochondria. It’s called a cycle for a reason, the reason being that it is a closed loop. The last part reforms the molecule used in the first step.

  1. In the very first stage acetyl-CoA is combined with oxaloacetate (a 4-carbon molecule) into the 6-carbon molecule citrate (hence the name).
  2. In a two- stage process a water molecule is removed and added again to citrate to turn it into isocitrate.
  3. Then in a series of reactions it breaks of two carbon molecules, these are released as Carbon Dioxide. This happens in a similar manner as in Oxidácia pyruvátu with the help of NAD+. This part of the cycle has a regulatory function, the enzymes doing this can speed up or slow down depending on energy needs. In the third step we are left with a 5-carbon molecule called a-ketoglutarate.
  4. In stage four we have a repeat of stage three, where a 4-carbon molecule is created, which is again hooked up to Coenzyme A to form Succinyl-CoA.
  5. We are now left with the 4-carbon molecule of Succinyl-CoA. The CoA part is replaced by a phosphate group, and the phosphate group then immediately transfers to ADP to make ATP. Some cells also use Guanine instead of Adenosine, turning GDP into GTP. These two are basically the same, energy carriers. What is left of the Succinyl is now Succinate.
  6. We are working with the Succinate now and in stage six it gets oxidized into fumarate, it loses 2 H+. The hydrogen atoms are transferred onto FAD, turning it into FADH2. FAD is used instead of NAD+ because Succinate doesn’t like to give away electrons. FAD has a higher electron affinity and is able to get them from Succinate, NAD+ is not strong enough. FADH2 production is done by an enzyme embedded into the inner membrane of the mitochondria, so the electrons go straight into the electron transport chain.
  7. In stage seven water is added to the fumarate, turning it into malate.
  8. Stage eight Oxidizes the Malate using NAD+ again, this results in Oxaloacetate the molecule we added in the first step.
  • In each cycle two carbons enter with Acetyl-CoA, two molecules of Carbon Dioxide are released in the process (in steps three and four).
  • Three NADH molecules are formed (in steps three, four, and eight), and one molecule of FADH2 (in step six).
  • One molecule of ATP/GTP is produced (in step five).

Per Glucose (two Acetyl-CoA are produced)

Step 4: Oxidative Phosphorylation

From the last step we have quite a lot of NADH and FADH2 molecules, the actual ATP produced by the Citric Acid Cycle isn’t a lot, but the important molecules are in fact this abundance of NADH and FADH2. This is what we are going to use in the last step, Oxidative Phosphorylation. This is actually a two stage process consisting of the Elektrónový transportný reťazec a Chemiosmosis.

Elektrónový transportný reťazec

The Electron Transport Chain is composed of several proteins and organic molecules that are embedded in the membrane of the mitochondria. These proteins are bundled together into komplexy, four of them in this case.

We start with the NADH and FADH2 molecules that were created in the previous step. These are the ones we got via glycolysis, pyruvate oxidation, and then the citric acid cycle.

  1. In complex 1 NADH transfers its electrons, turning back into NAD+ and H+ which is moved to the intermembrane Space. The electrons are transferred to Ubiquinone (Q). FADH2 holds onto its electrons a bit tighter (they are at a lower energy level), so Complex 1 can’t do anything with it but pass it on.
  2. In Complex 2 the same thing happens to FADH2 using the same enzyme that made it during the citric cycle. The electrons are taken and passed onto Ubiquinone (Q) via iron-sulfur proteins.
  3. The electrons are now in Ubiquinone (Q), which in the process has become QH2­­ and travels through the membrane to deliver the electrons to Complex 3. Complex 3 uses the energy to pump more H+ into the intermembrane space.
  4. The electrons are passed on to another carrier: Cytochrome C (Cyt C), transporting them to complex 4. Complex 4 makes good use of the gradient and pumps a few more H+ across the membrane. The electrons eventually end up attached to O2 which splits up into separate oxygen atoms. The separate oxygen atoms then need Hydrogen to share a proton, and as we know oxygen plus hydrogen equals water (good old H2O).

So what happens is that NADH and FADH2 are turned back into NAD+ and FAD, we need this because they are required in glycolysis and the citric acid cycle. If they wouldn’t be turned back there wouldn’t be any available for the former cycles and the whole thing breaks down.

Secondly a gradient is created, H+ is pumped to the intermembrane space changing the concentrations and creating stored energy to be used later. It’s like winding up a toy, the winding stores energy to be released later.

The “waste” product is water Oxygen is used because it has a high affinity for the electrons. This is why we breath, we need the oxygen to take away the electrons at the end. If there is no oxygen to pick up the electrons the chain ends, production stops, and energy production grinds to a halt.

In the first stage protein complex 1, 2, and 3 actively pump H+ to the intermembrane space. With this difference in concentration of H+ a gradient is created, also called the proton-motive force (hydrogen/H+ are called protons). Because of the gradient H+ wants to move back into the matrix, like a ball wants to move downhill. But the membrane won’t allow the H+ to go, there is only one path it can take. A protein called ATP synthase forms a channel across the membrane. Similar to how a hydroelectric dam uses the force of water, the ATP Synthase protein uses the flow of H+. The process of using a proton gradient to do something is called chemiosmosis (hence the name).

When H+ flows through the protein the top part (poking out into the intermembrane space) turns, the base (inside the matrix) stays stationary. Turning the inner part inside the base grabs ADP and adds a Phosphate to it. In a sense the ADP is energized as ATP (you go from di-phosphate to tri-phosphate). For each 4 H+ ions that flows through the channel, a single ADP molecule is turned into ATP.

This is why the mitochondria are called “powerhouses of the cell”, this is almost a quite literal description of what is going on. Just like how a hydroelectric dam generates power for a town, ATP synthase creates the energy used by everything.

ATP Synthase is a true ATP monster, producing more than 80% of the ATP yield collected from breaking down glucose. This way each molecule of glucose yields an additional 26-28 ATP by using the gradient created by NADH and FADH2. The grand total of ATP produced for each glucose molecule is then about 30-32 ATP.

  • Two ATP are made in Glycolysis and two more are made during the Citric Acid Cycle. The rest comes from the NADH and FADH2 converted in the ATP synthase. When NADH moves through the transport chain about 10 H+ ions are pumped through the membrane, so for each NADH 2.5 ATP can be made (10/4=2.5).
  • FADH2 enters the chain a bit later (during complex 2), so they missed the first pump. FADH2 leads to 6 H+ being pumped though the membrane. So for each FADH2 about 1.5 ATP can be made (6/4=1.5).

This is why all that NADH and FADH2 pays off, this is where the majority of the eventual ATP comes from. It drives the proton (H+) pump that establishes the gradient for ATP synthase.

The yield from Glycolysis isn’t exact, it can be either three or five. This is because Glycolysis occurs in the cytosol and NADH can’t pass through the membrane into the mitochondria. Because it can’t deliver the electrons to complex 1 it needs an intermediary, a shuttle system.

  • Some cells hand it over to FADH2 inside the inner mitochondrial membrane, this results in 3 ATP (2 NADH -> 2FADH2 -> 12 H+ -> 3 ATP).
  • Other cells use NADH inside the inner mitochondrial membrane, resulting in 5 ATP (2 NADH -> 2NADH -> 20 H+ -> 5 ATP).

30-32 ATP is the upper bound of the estimate, in reality it is probably lower. Sometimes the intermediates are siphoned off to be used by other biological systems, ATP production is but one process of many.

This is the entire process where glucose is turned into energy that a cell can use. Oxygen is vital since it is the receiver for electrons used in the process. Without oxygen the process halts and you get no energy. The waste product is Carbon Dioxide and Water, where oxygen bonds to either a carbon or two hydrogen (can’t have them flying around on their own can we?)

So you breath to live, because you need the oxygen to turn glucose into energy. Without oxygen the production stops. Carbon Dioxide is the waste product of this process.

Táto otázka sa pôvodne objavila na Quora. the place to gain and share knowledge, empowering people to learn from others and better understand the world. Quora môžete sledovať na Twitteri, Facebooku a Google+. Ďalšie otázky:



Komentáre:

  1. Joselito

    I cannot participate in the discussion now - no free time. Osvobozhus - necessarily their observations.

  2. Fredek

    Tal nepočul

  3. Llyr

    Wacker, it seems to me a brilliant idea

  4. Pallatin

    Výborná veta a načas

  5. Everet

    what would we do without your brilliant idea



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