Een treinkaartje regelen in Kolkata is pittig. Eerst bracht de Uber ons naar het station. Bij een loket vulden we op aanraden van behulpzame Indiërs een formulier in; de beambten waren voor onbepaalde tijd met pauze. Na hun terugkomst bleken we in de verkeerde rij te staan. Bij het andere loket keek een bebrilde Indiër ons aan en concludeerde: buitenlanders. Die horen hun kaartje te kopen in een heel ander station. Daar kregen we een nieuw formulier. Wij waren nummer 125 van die dag; nummer 101 was in behandeling. Het was inmiddels al halverwege de middag en op een bordje stond duidelijk dat men hier om 5 uur ophield met werken.
Dan krijg je een oefening in gelatenheid. Wat valt er te doen? Wachten en hopen. Het verdragen van de gestolde gang van zaken. Zo gaat dit hier nu eenmaal. De klok tikt. Een treinkaartje verstrekken duurt minstens tien minuten, ook al werken er twee beambten tegelijk aan. Een simpele rekensom leert dat we het in dit tempo nooit gaan halen. Wacht: er komen een paar nummers niet opdagen! Wie weet… en ja, we worden opgeroepen. Een dame schrijft het formulier over dat wij ingevuld hebben, waarna haar collega die gegevens nogmaals intikt in de computer. Zo bemachtigen we het laatste treinkaartje dat die dag wordt uitgegeven. Het Nepalese stel met nummer 126 heeft het nakijken.
Zodra iets tegen de verwachting in toch lukt, gebeurt er veel in een mens. Een tergende middag wordt plotsklaps een verhaal waarin wij figureren als de bijzondere hoofdpersonen die dit natuurlijk moest overkomen. Iets valt je toe en binnen een mum van tijd denk je: ik zal het wel verdiend hebben. Zo’n verhaal laat geen ruimte voor het Nepalese stel, of voor toeval, of voor reflecties over rechtvaardigheid of efficiëntie. Verhalen zijn geen analyses. Verhalen zijn in hun aard egocentrische constructen waarin de wereld draait rond de verteller.
Veel rijke Amerikanen schijnen te beweren dat hun rijkdom bewijst dat God van hen houdt. Dus hoeven ze in principe geen poot uit te steken naar arme Amerikanen van wie God – om ondoorgrondelijke maar dus wel goddelijke redenen – kennelijk minder houdt. Zou het niet juist hovaardig zijn om tegen Gods oordeel in te gaan? Om de wereld anders te maken dan God haar bedoeld heeft? Het is deze manier van redeneren die ik hier in India te veel om me heen voel. Sommige mensen bezingen de spiritualiteit van dit land, maar het is net of ik er geen toegang toe krijg. Ik voel me vooral opstandig.
Ik weet dat religie mensen kan helpen om de schoonheid van het leven te ervaren. Daar wil ik niets aan afdoen, en ik wens dat vooral de Indiërs in benarde omstandigheden van harte toe. Maar verder gaat mijn eerbied voor religie niet. Al die aandacht voor het hogere, voor de verticale lijn, leidt tot een soort mechanisch wereldbeeld, waarin mensen volgens een gegeven orde om elkaar heen draaien zonder zich werkelijk met elkaar te hoeven engageren, want alles ligt toch al vast. Die houding leidt ertoe dat mensen wel kansen pakken, maar geen alternatieven zoeken. Het staat waarlijk burgerschap in de weg. Die nadruk op de godgegeven orde maakt India tot de droom van Thatcher: there is no such thing as society.
Je verbinden met een maatschappij vraagt iets moeilijks en tegennatuurlijks van de menselijke psychologie: het waarlijk accepteren van het idee van willekeur. We maken liever een spannend verhaal van onze voor- of tegenspoed dan dat we het toevallige van ons eigen plekje onder ogen zien. Want toeval gooit ons uit het centrum van het verhaal.
De filosofie heeft een woord voor het besef dat de wereld om je heen net zo goed anders had kunnen zijn dan hij feitelijk is: radicale contingentie. Het begrip vraagt van je om toeval en willekeur te accepteren en biedt bar weinig troost, want er is nergens voorzien in een vast plekje voor jou. Maar het schept wel ruimte voor verandering. Voor opstand in plaats van lijdzaamheid. Voor betrokkenheid in plaats van acceptatie.
Anders gezegd: ik kan ze even niet meer zien, die heilige mannen met hun eeuwenoude teksten en hun kosmische orde. Ze doen me aan Thatcher denken.
Toen in mei 1940 de bezetting aanbrak, wist Betty wat haar te doen stond: níet tegemoet komen aan de eisen van de bezetter. Dat betekende: zich niet laten registreren als Jood, geen fiets inleveren, de radio verstoppen. En later: geen jodenster dragen. „Ik dacht: ze moeten maar zien dat ze me te pakken krijgen.”
Honderd is Betty Bausch-Polak dit jaar geworden. Maar het had meer in de rede gelegen als ze gestorven was op haar drieëntwintigste. Of vierentwintigste.
Meer dan twintig onderduikadressen had ze nodig om de oorlog te overleven, als Joodse uit Amsterdam. En een flinke dosis geluk. Haar ouders en oudste zus hadden dat geluk niet: ze stierven in de kampen. Haar echtgenoot Philip werd door de Duitsers gefusilleerd.
Toch kun je gerust zeggen dat Betty Bausch haar leven te danken heeft aan meer dan alleen mazzel. Ze doorstond de oorlogsjaren met een portie gogme, creativiteit en vastberadenheid die vijfenzeventig jaar na dato nog altijd ontzag inboezemen.
„Ik heb levensgevaarlijke dingen gedaan,” zegt ze over de telefoon vanuit haar woonplaats Kfar Saba, in Israël. „Maar daar stond ik op dat moment niet bij stil. Pas later heb ik gedacht: belachelijk, hoe heb je dat kunnen doen?”
Ze groeide op als Betty Polak, de derde van vier kinderen in een welgesteld, sociaal bewogen Joods gezin in Amsterdam. Ze woonden in de Plantagebuurt; vanuit huize Polak keek je recht in de tuin van de Hollandsche Schouwburg – de plek van waaruit later driekwart van de Amsterdamse Joden op transport gezet zou worden.
Eén ding was de jonge Betty volstrekt duidelijk na de machtsovername van Hitler in 1933: hier dreigde een catastrofe voor de Joden. „Ik luisterde thuis naar zijn toespraken op de radio. Zet dat ding uit, zeiden de anderen in het gezin, we willen er niets van horen. Maar we konden eenvoudigweg niet zeggen: hier hebben we niets mee te maken. Helaas waren er niet veel mensen die er zo over dachten. Dus hield ik ook vaak m’n mond.”
Wie er wel zo over dacht, was Philip de Leeuw, de man met wie Betty in 1939 trouwde in de grote synagoge van Amsterdam. De Leeuw, die als reserve-officier onder de wapenen was geroepen vanwege de dreiging uit het oosten, had Mein Kampf thuis in de kast staan – en helemaal gelezen.
Toen in mei 1940 de bezetting aanbrak, wist Betty wat haar te doen stond: níet tegemoet komen aan de eisen van de bezetter. Dat betekende: zich niet laten registreren als Jood, geen fiets inleveren, de radio verstoppen. En later: geen jodenster dragen. „Ik dacht: ze moeten maar zien dat ze me te pakken krijgen.”
Eerst probeerden Philip en zij weg te komen uit Nederland. Maar hun pogingen om over te steken naar Engeland mislukten: de schepen bleken telkens op het laatste moment vol. „De derde boot waarmee we wilden gaan, is onderweg getorpedeerd en onder water gelopen.”
Dus begonnen Betty en Philip aan een zwervend bestaan door het land – eerst samen, toen gescheiden, later weer samen. Een van hun eerste adressen was het Apeldoornsche Bos, een Joodse psychiatrische inrichting op de Veluwe. Toen de kliniek in januari 1943 ontruimd werd en alle patiënten en personeelsleden op transport werden gesteld, kon het echtpaar op tijd wegkomen. „De arts had ons van tevoren ingelicht. We hadden een afspraak gemaakt met een boer, dat we met onze koffers naar hem toe konden komen en een paar uur op de boerderij verblijven.”
Ik heb het visbestek en een mantel van Juul meegenomen, als enige aandenken
Toen begon de onderduik pas goed. Ze kreeg valse identiteitspapieren. Betty Polak werd Jo Musch. Jo Musch werd Adrie Kool. Adrie Kool werd Ada Koole. Langer dan drie maanden bleef ze nooit op een adres. Haar ouders, broers en zussen bleven waar ze waren: tot haar grote verdriet had Betty ze niet aan hun verstand kunnen brengen dat onderduiken de enige optie was. „Ik zie m’n ouders nog staan, keurig aangekleed. Nee, zeiden ze, dat kunnen we niet doen, de mensen hebben ons nodig. Ze zijn weggehaald en nooit meer teruggekomen.”
Haar oudste zuster Juul was hetzelfde lot beschoren. Ze werd afgevoerd tijdens een grote razzia in 1943. Toen ze het nieuws hoorde, deed Betty een van die gevaarlijke dingen die ze naderhand onbegrijpelijk vond: met een reservesleutel ging ze het verlaten huis binnen. „Op tafel stonden nog de borden met de restanten van een visgerecht. Ik zag dat ze zo, in één keer, waren weggevoerd.” Ze had van alles kunnen meenemen uit het huis, maar ze deed het niet. „Daar kreeg ik ze toch niet mee terug. Ik heb het visbestek en een mantel van Juul meegenomen, als enige aandenken.”
Ze verbleef in die tijd bij de familie Althoff in Amsterdam, waar ze overdag op de baby paste. Op een middag ging de bel: voor de deur van de portiekwoning stonden twee Gestapo-agenten. „Ik dacht: o, mijn God. Mevrouw Althoff was boven, ze gaf Spaanse les aan huis. ‘Heren, wat komt u doen?’ gilde ik zo hard ik kon tegen die mannen. Ik kon nog net naar de kamer van mevrouw rennen en zeggen: denk erom, Gestapo.”
De mannen kwamen boven, maar Betty weigerde mevrouw Althoff in haar les te storen. „Dan word ik er meteen uitgegooid, zei ik tegen ze. Het is mijn taak om te zorgen dat ze ongestoord les kan geven.” Toen ze voet bij stuk hield, vroegen de Gestapo-agenten om haar papieren. „In mijn valse persoonsbewijs stond: litteken aan de keel rechts. Dat had ik speciaal door een bevriende arts laten zetten. Nou, dat litteken heeft mijn leven gered.”
In de zomer van 1944 werd Betty herenigd met haar man Philip. Ze vonden dicht bij elkaar een onderduikadres in Bilthoven. Philip werd actief in het verzet: hij kreeg de leiding over een ‘knokploeg’ van acht man.
Het mocht niet lang duren. Op de avond van 7 november mislukte een aanslag van Philips verzetsgroep op een spoorlijn in de buurt. Hij werd verraden, gevangengezet en kort daarop gefusilleerd in de bossen bij Veenendaal. Ook Betty werd gevangengezet, maar na enige tijd weer vrijgelaten.
Het lot van Philip vernam Betty pas toen ze een bezoek bracht aan het Gestapo-hoofdkwartier aan de Utrechtse Maliebaan. Een krankzinnige actie voor een Jodin met valse papieren, vond ze naderhand ook zelf. „Maar ik móest weten wat er met Philip was gebeurd. En dat kon ik alleen te weten komen bij de Gestapo.” Ze werd ontvangen door een hoge Gestapo-officier, die haar vertelde dat Philip dood was. „Hij ging weg en kwam terug met een horloge en ring. Die waren van Philip. Ik heb gezegd dat ik er geen belangstelling voor had. Daar kreeg ik hem toch niet mee terug. Daarna mocht ik opstaan en weggaan.”
Het waagstuk bij de Gestapo leidde tot achterdocht bij Philips voormalige makkers uit de illegaliteit. Hoe kon zij in hemelsnaam levend naar buiten zijn gelopen? De verzetskring verbrak alle contact, na de bevrijding werd ze zelfs twee dagen door een commissie ondervraagd.
Ik stond er totaal alleen voor, ik kon met niemand contact krijgen
Eenzelfde onverschrokkenheid legde Betty aan de dag bij de voedseltochten die ze ondernam in de hongerwinter. Ze was inmiddels ondergedoken in Oegstgeest, bij een alleenstaande moeder met drie kinderen die in een wolfabriek werkte. Toen het eten op begon te raken, ging Betty op een fiets met houten banden naar het oosten van het land, wol ruilen tegen eten.
Op haar tochten werd ze regelmatig staande gehouden door Duitse soldaten. „Als ik werd aangehouden, maakte ik in mijn beste Duits een praatje met die soldaten. ‘Och,’ zei ik, ‘wat ben ik blij dat u me aanhoudt. Ik ben zo moe van die fiets met houten banden, kunnen we even gezellig kletsen?’ Daarna reed ik weer vrolijk weg. Die militairen hebben nooit een tas van mij opengemaakt. Nooit.”
Mei 1945, de bevrijding kwam. Nederland vierde feest, maar voor Betty was er weinig reden tot vreugde. Haar ouders, schoonouders en oudste zus waren gedeporteerd, haar man was dood, ze wist niet waar haar broer Jaap was. „Ik stond er totaal alleen voor, ik kon met niemand contact krijgen.”
Jaap en zijn vrouw kwamen terug uit het kamp. Betty trof ze een paar weken na de bevrijding aan in Eindhoven, uitgemergeld, maar in leven. Van haar jongere zus Lies wist Betty al eerder dat ze op onwaarschijnlijke’ wijze aan de dood was ontsnapt: via een gevangenenruil tussen de Duitsers en de Britten kon ze vanuit Bergen-Belsen naar Palestina reizen. „Dat dat is gelukt, is werkelijk een wonder.”
Na de oorlog leverde ze een bescheiden bijdrage aan de publicatie van het dagboek van Anne Frank. Betty werkte inmiddels als ambtenaar op het ministerie van Landbouw, waar ze – uniek voor een vrouw – in de jaren vijftig en zestig carrière zou maken. „Vanuit mijn baan zat ik in de commissie die mocht bepalen wie er papier mocht krijgen.” Op een dag vertelde het bevriende historici-echtpaar Jan en Annie Romein over het dagboek van Anne Frank. Er was een uitgever gevonden, maar nog geen papier. „Ik heb die uitgever gebeld en gezegd: ik ga onmiddellijk zorgen dat jullie papier krijgen. Die man was dolgelukkig.”
Praten over de oorlog deed ze decennialang niet, dat was veel te pijnlijk. Pas in het nieuwe millennium, ze was al in de tachtig, begon Betty haar verhaal te doen, op scholen in Nederland en Duitsland. Ze schreef haar herinneringen op in een boekje, samen met haar zus Lies.
Nu woont ze permanent in Israël, waar ze begin jaren tachtig een huis kocht met haar tweede echtgenoot. Twee keer per jaar probeert ze naar Nederland te komen: rond 4 mei, en in november, voor de herdenking van Philips executie in Veenendaal. „Dat geeft me het gevoel dat zijn leven niet zomaar is weggegooid.”
Haar broer Jaap werd 102 jaar oud. „Dus heb ik tegen mezelf gezegd: ik moet sowieso ouder worden dan hij. Daar ben ik nu hard mee bezig.”
Met dank aan Aline Dijkshoorn. Voor dit artikel werd gebruik gemaakt van Bewogen stilte (2014) van Elisheva Auerbach-Polak, Betty Bausch-Polak en Nanda van der Zee.
Neus Català i Pallejà was born in 1915 in Els Guiamets, a village with 500 inhabitants in Priorat, a mountainous wine-producing region west of Barcelona. She was born in October, but her date of birth was registered as June 15 because her grandfather put the wrong date. She sometimes celebrated both birthdays.
Her father, Baltasar Català, was a barber and her mother, Rosa Pallejà, was a housewife. Her parents liked telling stories to Català and her brother, Lluís. A favourite was about Spartacus, the gladiator who took part in the slave rebellion against the Roman Empire that started in 73BC. It was to prove prophetic because Català, in her own way, challenged the might of the Third Reich.Even as a teenager she was imbued with the spirit of woman-to-woman solidarity that would sustain her through her wartime imprisonment, and took part in a women’s strike. “She was very politically independent. She was a natural feminist before these feminist organisations existed,” said her daughter, Margarita Català.When the Second Spanish Republic was declared in 1931, the ripples caused by the arrival of a socialist government reached Català’s remote village. She joined the youth wing of the United Socialist Party of Catalonia, moved to Barcelona and trained to be a nurse.When the country descended into civil war in 1936, she was caring for orphans and children of political refugees at a home north of Barcelona. Three years later, with Franco’s nationalist forces closing in on victory, she took 182 children across the border into France. They were known as the Children of Negrín, after Juan Negrín, the president of the Second Republic, who was forced into exile. She made sure they were adopted.Like many other Spanish left-wing exiles, she joined the French Resistance, through which she met her first husband, Albert Roger. They married in 1942 and their house was used to pass messages, documents and guns, and for sheltering political refugees. “Our honeymoon was to find a place where the Maquis could meet,” remembered Català.Their luck ran out in 1943 when they were betrayed by a local chemist and were arrested by the Gestapo. Both were tortured. Català was sent to a prison camp and deported the next year to Ravensbrück. Roger was sent to Sachsenhausen camp, but later died in Bergen-Belsen.Neus Català felt she was transformed from a human being into nothing more than a number, in her case 27,534, after entering Ravensbrück, a concentration camp that held only women prisoners.She recalled that her captors treated her as if she was “worth less than a dog or a horse”, yet she refused to let them crush her spirit and lived to be one of the last survivors of the 130,000 French, Polish, Dutch and Russian women who entered the camp. More than half of them died there.Like many women, Català had to undergo humiliating medical checks carried out by the SS medics as she stood naked. They were subjected to gynaecological checks without any of the normal standards of hygiene. She said that if any woman was liked by one of the camp guards, they could end up in the camp brothel, from which no one emerged alive.
When she fell ill, camp medics believed she might have caught tuberculosis. A positive diagnosis would have meant execution. “For a week, before a second check-up, she believed she would die, but other inmates tried to help her pull through by cheering her up,” said a friend who did not want to be named. In the end, it was a false alarm.She had only been in Ravensbrück a month when the camp guards identified her as a “good worker” and sent her to Holleischen camp in the former Czechoslovakia to work in an armaments factory. Eager to sabotage the Nazi war effort, there she formed a group who called themselves the Lazy Commandos. They risked their lives by spitting into the powder used to make bullets and shells, having been told that this would compromise their effectiveness.Català was no stranger to covert operations of this sort, having joined the French Resistance after fleeing Spain when Franco’s nationalist forces won the civil war in 1939. The chance to resume surreptitiously disrupting the Nazi war machine gave her and her fellow inmates the strength to endure their captivity. They were charged with producing 10,000 bullets or shells each month, but claimed to have rendered thousands unusable.By the time the camp was liberated in 1945 she and her comrades were desperately ill. “We were just skulls with eyes,” she later said.
After the war, she returned to France and started her psychological recovery. However, Català was so damaged physically, she had to spend time in two medical homes. One compensation was that it was there that she met her second husband, Félix Sancho, who had also fought in the resistance.She presumed that because of what she had been through in the camp she would never be able to have children, but one day, thinking she had a bad stomach, discovered she was in fact pregnant. Her daughter, Margarita, became a psychologist. The couple also had a son, Lluís, who is the director of a library.From her home in Sarcelles, near Paris, she ran the International Committee of Ravensbrück and made it her job to try to collect the testimonies of all those Spanish women who had died in the camp. Her work was made harder because many Spaniards were classed by officials as French, having fled across the border at the end of the Spanish Civil War. She said later in life that her memories of Ravensbrück were always in black and white, never in colour.After years of campaigning, the German government conceded that part of the memorial at the site of the original Ravensbrück camp should be dedicated to the Spanish women who died there. From a grim prison cell, it became a site of remembrance.She remained a member of the Unified Socialist Party of Catalonia and continued her efforts to try to undermine the long dictatorship of Franco, which lasted from the end of the civil war in 1939 until his death in 1975.Sometimes she would flit across the border into Spain undercover and was photographed in Barcelona in 1957, strolling along La Rambla with her daughter. She was able to do this because she had French nationality through her first husband. She returned to Spain in 1978.In 2005 Català gained widespread recognition when she published From the Resistance to the Deportation: 50 Testimonies of Spanish Women. It told the stories of Spaniards who first fought Franco, then the Nazis before being sent to concentration camps. The book came just before Spain’s then Socialist government passed a law to grant greater redress to the victims of Franco.“She spent most of her life fighting against fascism, if not on the barricades, then by keeping alive the memory of those who died at the hands of the Nazis,” recalled Elisenda Belenguer, who wrote a biography of Català.Even as Català lay in her rest home days before her death, her daughter said she could be heard singing Italian and Russian revolutionary songs to celebrate the anniversary of the founding of the Second Spanish Republic on April 14, 1931. Neus Català, Holocaust survivor, was born on October 6, 1915. She died on April 13, 2019 aged 103
In this unpublished essay, the late neurologist and writer discusses his insights and where he felt hope.
Having worked as a neurologist in old-age homes and chronic hospitals for almost 50 years, I have seen thousands of older patients with Alzheimer’s disease or other dementias. One sees a kaleidoscopic array of symptoms and dysfunctions, never exactly the same in any two people. The neurological dysfunctions interact with all that is unique in an individual — their pre-existing strengths and weaknesses, their intellectual powers, their skills, their life experience, their character, their habitual styles, as well as their particular life situations.
Alzheimer’s disease may first present as a full-blown syndrome, but more often it starts as isolated symptoms so focal that one may initially suspect a small stroke or tumour; it is only later that the generalised nature of the disease becomes evident (hence the frequent failure to diagnose Alz- heimer’s at the start). The early symptoms, whether they appear singly or in clusters, are usually subtle. There may be momentary illusions or misperceptions; or difficulties getting jokes or following arguments. But in general it is the most recently evolved functions that are the first to be affected.
In these very early stages, the dysfunctions tend to be momentary. But soon there are grosser disturbances of cognition, memory, behaviour, judgment, and disorientation in space and time, all finally coalescing as profound dementia. As the disease advances it may bring distressing personality changes and even violent behaviour in some people. Finally, every possible cortical disorder may be seen in this devastating disease, even though the paths by which the disease advances are so different in each patient.
Sooner or later patients lose the power to articulate their condition, to communicate in any way, except in so far as tone of voice, touch, or music can briefly reach them. Finally, even this is lost and there is indeed total loss of consciousness, of cortical function, of self-psychic death.
Caring for someone else, especially if that someone is already quite demented and is inexorably going downhill, can involve back-breaking physical exertion as well as a constant, almost telepathic sensitivity to what is going on in a mind now less and less able to communicate its thoughts, less and less able to have clear thoughts. People with dementia may get terrifyingly confused and disoriented. Such a burden can make the caretaker ill with stress. As a physician, I see this all too often.
And yet there are many ways the beleaguered patient may adapt and react, or even help themselves. One of my patients, very early in the course of her disease, suddenly found that she could no longer tell the time when she looked at her watch. She saw the position of the watch hands clearly, but she could not interpret them; for a split second, they made no sense, and then, equally suddenly, they did. The unintelligible periods lengthened to seconds, then minutes, and soon the watch hands were unintelligible all the time.
She was acutely and mortifyingly conscious of this deterioration; it gave her a sharp sense of horror, of the Alzheimer’s process behind it. But she herself was the one to make a crucial therapeutic suggestion: Why don’t I wear a digital watch, she asked, and have digital clocks everywhere? She acted on this, and although her agnosia and other problems continued to increase, she remained able to tell the time and organise her day for another three months.
Another of my patients, who was fond of cooking and whose overall cognitive powers were still very good, found that she could no longer compare the volume of liquids in different containers; an ounce of milk did not look the same if it was poured from a glass into a pan, and ludicrous errors started to occur. The patient herself, a former psychologist, ruefully recognized this as a Piagetian error, a loss of the sense of volumetric constancy that is acquired in early childhood. However, by using graduated vessels and measuring cups instead of trying to guess as she used to, she was able to compensate for the problem and to continue safely in the kitchen.
Such patients may perform badly on formal mental testing and yet be able to describe with clarity, vividness, correctness and humour precisely how one bakes an artichoke or a cake; they may be able to sing a song, tell a story, act a part, play a violin, or paint a painting with remarkably little impairment. It is as if they have lost certain modes of thought while retaining other modes perfectly.
It is sometimes said that people with Alzheimer’s do not realise that they are impaired, that insight is lost from the start. Although this may sometimes be so, it is more common, in my experience, for patients to realize their condition at first. Thomas DeBaggio, a writer and horticulturalist, was even able to publish two insightful memoirs about his own early-onset Alzheimer’s before the disease killed him at the age of 69. Most patients are frightened or mortified by the knowledge of what is befalling them.
Some continue to be severely terrified as they lose their intellectual competences and bearings and find themselves in a world increasingly fragmented and chaotic. But the majority, I think, become calmer with time as they perhaps start to lose the sense of what they have lost and find themselves shifted into a simpler, unreflective world. Such patients might seem to have regressed intellectually, so that they are once again like children. Kurt Goldstein, a neurologist and psychiatrist, would say of such patients that they were now in a lower, more concrete form of consciousness or being.
For John Hughlings Jackson, the great English neurologist, there were never just deficits with neurological damage, but “positive” symptoms, as he called them, “releases” or exaggerations of normally constrained neural functions. He spoke of “dissolution”, which was, for him, characterised by regression or reversion to more archaic levels of neural function — the reverse of evolution.
Although Jackson’s notion of dissolution in the nervous system as evolution in reverse can no longer be maintained in so simplistic a fashion, one does see some remarkable behavioural regressions or releases in a disease like Alzheimer’s. I have often seen patients with advanced dementia who show picking, hunting and brushing — a whole range of primitive grooming behaviours that are not seen in normal human development, but are suggestive, perhaps, of a reversion to a primate level. In the final stages of dementia, where no organised behaviours of any sort remain, one may see reflexes that are normally only seen in infancy, including grasping reflexes, snout and sucking reflexes.
Such dissolution was very clear, Jackson thought, in the processes of dreaming, delirium and insanity, and his long 1894 paper The Factors of Insanities is full of fascinating observations and insights in this regard.
One may see remarkable (and sometimes very poignant) behavioural regressions at a more human level too. I had one patient — a very demented woman of 100, who was incoherent, distracted and agitated much of the time — who, if given a doll, would immediately become focused, sharply attentive and take the doll to her breast as if to nurse it, rocking it in her arms, cuddling it, crooning to it. As long as she was occupied by this mothering behaviour, she was perfectly calm; but the moment she stopped, she became agitated and incoherent again.
The sense that everything is lost with a diagnosis of Alzheimer’s is all too common among neurologists, as well as among patients and their families. This may give rise to a premature sense of impotence and doom, whereas in fact all sorts of neurological functions seem remarkably able to persist relatively intact.
In the early part of the 20th century, neurologists started to pay more attention not just to the primary symptoms of neurological disease, but also to the compensations and adaptations to these. Goldstein, studying brain-damaged soldiers during the First World War, was moved from his original, deficit-based point of view to a more holistic one. There were never, he believed, just deficits; there were always reorganisations, and these he saw as strategies (albeit unconscious) by which the brain-damaged organism sought to survive.
People with Alzheimer’s disease may remain intensely human, very much themselves, and capable of normal emotion and relationships until quite late in their illness. (This preservation of self may, paradoxically, be a source of torment for the patient or their families, who see them so painfully eroded in other ways.)
The relative preservation of the personal allows a great range of supportive and therapeutic activities that have in common that they address or evoke the personal. Religious services, theatre, music and art, gardening, cooking, or other hobbies can anchor patients despite their disintegrations and temporarily restore a focus, an island of identity. Familiar melodies, poems, or stories may still be recognised and responded to despite advanced disease.
As Henry James was dying, with pneumonia and a high fever, he became delirious — and it is said, as I wrote in Hallucinations, that though the master was raving, his style was “pure James” and, indeed, “late James”. The neural embodiment of self, it seems, is extremely robust. Every perception, every action, every thought, every utterance seems to bear the mark of the individual’s experience, of his value system, of all that is peculiar to him. If individual experience and experiential selection so determine the developing brain, we should not perhaps be surprised that individuality, self, is preserved for so long even in the face of diffuse neuronal damage.
Aging, of course, does not necessarily entail neurological illness. Working in old-age homes, where people are admitted with a variety of problems (heart ailments, arthritis, blindness, or sometimes just loneliness and a desire to live in a community), I see numbers of old people who are, so far as I can judge, intellectually and neurologically wholly intact. Indeed, several of my patients are bright and intellectually active centenarians who have retained all their zest for life.
One woman, admitted at the age of 109 with diminishing vision, discharged herself once her cataracts had been taken care of and returned home to an independent life. (“Why should I stay here with all these old people?” she asked.) Even in a chronic hospital, there is a sizable proportion of people who can live out a century or more without significant intellectual decline, and this proportion must be considerably greater in the population at large.
So it is not just the absence of disease or preservation of function that we should be concerned with, but the potential for a continuing development throughout life. Cerebral function is not like cardiac or renal function, which proceeds autonomously, almost mechanically, in a fairly uniform way throughout life. The brain/mind, in contrast, is anything but automatic, for it is always seeking to categorise and recategorise the world, to give meaning to its own experience.
It is the nature of living a real life that experience is not uniform, but ever changing and ever challenging and requiring more and more comprehensive integration. It is not enough for the brain/mind simply to tick over (like the heart); it must adventure and advance throughout life. The very concept of health or wellness requires a special definition in relation to the brain.
A distinction must be made in the aging patient between longevity and vitality. A constitutional sturdiness and good luck may make for a long and healthy life. I think here of five siblings I know, all in their nineties or early hundreds, all looking far younger than their age, and all having the physiques, the sexual drives, the behaviours of much younger people. And yet, human beings may be physically and neurologically healthy, but psychically burned out at a relatively early age.
If the brain is to stay healthy, it must remain active, wondering, playing, exploring and experimenting right to the end. Such activities or dispositions may not show up on tests, but they are of the essence in defining the health of the brain and in allowing its development throughout life. This accords well with what Erik and Joan Erikson devoted a lifetime to studying: universal, age-related stages that seem to appear in all cultures. As the Eriksons advanced through their nineties, they added a further stage to the eight stages they originally described: the stage appropriate to old age — wisdom or integrity.
The achievement of this stage involves the synthesis of a long lifetime’s experience, coupled with the lengthening and enlargement of the individual’s perspectives and a sort of detachment or calm. Such a process is entirely individual. It cannot be prescribed or taught; nor is it directly dependent on education or intelligence or specific talents. “We cannot be taught wisdom,” as Proust remarks, “we have to discover it for ourselves by a journey which no one can undertake for us, an effort which no one can spare us.”
Are such stages purely existential or cultural — the behaviours, the perspectives appropriate to various ages and stages — or do they also have some specific neural basis? We know that learning is possible throughout life, even in the presence of cerebral aging or disease, and we can be sure that other processes, at a much deeper level, are continuing, too — a culmination of the ever wider and deeper generalisations and integrations that have been occurring in the brain/mind throughout life.
In the 19th century, when a powerful mind could still take all of nature for its subject, the great naturalist Alexander von Humboldt, after a lifetime of travel and scientific research, embarked in his mid-seventies on a grand synthetic view of the universe, bringing together everything he had seen and thought into a final work, Cosmos. He was well into its fifth volume when he died at 89.
If we are lucky enough to reach a healthy old age, this sense of wonder can keep us passionate and productive to the end of our lives.
Everything in Its Place: First Loves and Last Tales by Oliver Sacks, is published by Picador on May 2.
Philosopher, corporate lawyer and author known as ‘London’s leading hypochondriac’, who hosted lively salons at his Georgian home
For the past 13 years an eclectic group of writers, academics, philosophers, diplomats, lawyers and others have gathered on a Sunday afternoon every other month at a gorgeous Georgian house in Spitalfields, east London, the home of Oliver Black and his wife, Jenny. After tea and cake there is a 20-minute talk followed by a discussion. Such is the popularity of this salon, with guests sitting on chairs, window ledges, floors and stairs, that on one recent occasion the drawing-room floor began to sag and numbers have had to be limited.
Black was a paradoxical man: serious yet humorous, misanthropic yet sociable. He collected friends with the same enthusiasm a young boy might collect stamps. He loved conversation and dinner parties. Acquaintances would be gathered to read through a play or to listen to a recording of an opera, with Black providing copies of the score.
Despite effortlessly blending his academic studies in philosophy with his “day job” as a lawyer, Black was sometimes introduced to people as “London’s leading hypochondriac”, although he insisted that “valetudinar–ian” was more accurate. “A valetudinarian can always find something on which to hook his anxiety: a tender gland in the neck (sign of mumps), a mild rash (shingles), a dry throat (Ebola), a lack of energy (almost anything),” observed the man who was on first-name terms with his GP, Vera.
This and other subjects were discussed with dry, deadpan humour in his book Shrunk and Other Stories (2016), its title coming from the way in which his bank account was diminished by visits to shrinks. In these autobiographical meanderings, with chapter headings such as DIE-DIY, Road Hogs of the World, and Spotty and Horny, Black describes the pitfalls of arranging DIY funerals for relatives, the delights of driving a black cab as a private car, and how he refused to live in East Anglia for fear that the fallout from a dirty bomb in London would be carried on the prevailing wind.
i love the alarmist tone of this article and i love that ‘nature’ is ‘fighting back’ against the humans and yeah we’re all gonna die sooner or later and with any luck ‘we’ will completely die out because ‘we’ are fuckwits.
Bacteria are rebelling. They’re turning the tide against antibiotics by outsmarting our wonder drugs.
Last May, an elderly man was admitted to the Brooklyn branch of Mount Sinai Hospital for abdominal surgery. A blood test revealed that he was infected with a newly discovered germ as deadly as it was mysterious. Doctors swiftly isolated him in the intensive care unit.
The germ, a fungus called Candida auris, preys on people with weakened immune systems, and it is quietly spreading across the globe. Over the last five years, it has hit a neonatal unit in Venezuela, swept through a hospital in Spain, forced a prestigious British medical center to shut down its intensive care unit, and taken root in India, Pakistan and South Africa.
Recently C. auris reached New York, New Jersey and Illinois, leading the federal Centers for Disease Control and Prevention to add it to a list of germs deemed “urgent threats.”
The man at Mount Sinai died after 90 days in the hospital, but C. auris did not. Tests showed it was everywhere in his room, so invasive that the hospital needed special cleaning equipment and had to rip out some of the ceiling and floor tiles to eradicate it.
“Everything was positive — the walls, the bed, the doors, the curtains, the phones, the sink, the whiteboard, the poles, the pump,” said Dr. Scott Lorin, the hospital’s president. “The mattress, the bed rails, the canister holes, the window shades, the ceiling, everything in the room was positive.”
C. auris is so tenacious, in part, because it is impervious to major antifungal medications, making it a new example of one of the world’s most intractable health threats: the rise of drug-resistant infections.
For decades, public health experts have warned that the overuse of antibiotics was reducing the effectiveness of drugs that have lengthened life spans by curing bacterial infections once commonly fatal. But lately, there has been an explosion of resistant fungi as well, adding a new and frightening dimension to a phenomenon that is undermining a pillar of modern medicine.
“It’s an enormous problem,” said Matthew Fisher, a professor of fungal epidemiology at Imperial College London, who was a co-author of a recent scientific review on the rise of resistant fungi. “We depend on being able to treat those patients with antifungals.”
Simply put, fungi, just like bacteria, are evolving defenses to survive modern medicines.
Yet even as world health leaders have pleaded for more restraint in prescribing antimicrobial drugs to combat bacteria and fungi — convening the United Nations General Assembly in 2016 to manage an emerging crisis — gluttonous overuse of them in hospitals, clinics and farming has continued.
Resistant germs are often called “superbugs,” but this is simplistic because they don’t typically kill everyone. Instead, they are most lethal to people with immature or compromised immune systems, including newborns and the elderly, smokers, diabetics and people with autoimmune disorders who take steroids that suppress the body’s defenses.
Scientists say that unless more effective new medicines are developed and unnecessary use of antimicrobial drugs is sharply curbed, risk will spread to healthier populations. A study the British government funded projects that if policies are not put in place to slow the rise of drug resistance, 10 million people could die worldwide of all such infections in 2050, eclipsing the eight million expected to die that year from cancer.
Yet as the problem grows, it is little understood by the public — in part because the very existence of resistant infections is often cloaked in secrecy.
With bacteria and fungi alike, hospitals and local governments are reluctant to disclose outbreaks for fear of being seen as infection hubs. Even the C.D.C., under its agreement with states, is not allowed to make public the location or name of hospitals involved in outbreaks. State governments have in many cases declined to publicly share information beyond acknowledging that they have had cases.
All the while, the germs are easily spread — carried on hands and equipment inside hospitals; ferried on meat and manure-fertilized vegetables from farms; transported across borders by travelers and on exports and imports; and transferred by patients from nursing home to hospital and back.
C. auris, which infected the man at Mount Sinai, is one of dozens of dangerous bacteria and fungi that have developed resistance. Yet, like most of them, it is a threat that is virtually unknown to the public.
Other prominent strains of the fungus Candida — one of the most common causes of bloodstream infections in hospitals — have not developed significant resistance to drugs, but more than 90 percent of C. auris infections are resistant to at least one drug, and 30 percent are resistant to two or more drugs, the C.D.C. said.
Dr. Lynn Sosa, Connecticut’s deputy state epidemiologist, said she now saw C. auris as “the top” threat among resistant infections. “It’s pretty much unbeatable and difficult to identity,” she said.
Nearly half of patients who contract C. auris die within 90 days, according to the C.D.C. Yet the world’s experts have not nailed down where it came from in the first place.
“It is a creature from the black lagoon,” said Dr. Tom Chiller, who heads the fungal branch at the C.D.C., which is spearheading a global detective effort to find treatments and stop the spread. “It bubbled up and now it is everywhere.”
‘No need’ to tell the public
In late 2015, Dr. Johanna Rhodes, an infectious disease expert at Imperial College London, got a panicked call from the Royal Brompton Hospital, a British medical center outside London. C. auris had taken root there months earlier, and the hospital couldn’t clear it.
“‘We have no idea where it’s coming from. We’ve never heard of it. It’s just spread like wildfire,’” Dr. Rhodes said she was told. She agreed to help the hospital identify the fungus’s genetic profile and clean it from rooms.
Under her direction, hospital workers used a special device to spray aerosolized hydrogen peroxide around a room used for a patient with C. auris, the theory being that the vapor would scour each nook and cranny. They left the device going for a week. Then they put a “settle plate” in the middle of the room with a gel at the bottom that would serve as a place for any surviving microbes to grow, Dr. Rhodes said.
Only one organism grew back. C. auris.
It was spreading, but word of it was not. The hospital, a specialty lung and heart center that draws wealthy patients from the Middle East and around Europe, alerted the British government and told infected patients, but made no public announcement.
“There was no need to put out a news release during the outbreak,” said Oliver Wilkinson, a spokesman for the hospital.
This hushed panic is playing out in hospitals around the world. Individual institutions and national, state and local governments have been reluctant to publicize outbreaks of resistant infections, arguing there is no point in scaring patients — or prospective ones.
Dr. Silke Schelenz, Royal Brompton’s infectious disease specialist, found the lack of urgency from the government and hospital in the early stages of the outbreak “very, very frustrating.”
“They obviously didn’t want to lose reputation,” Dr. Schelenz said. “It hadn’t impacted our surgical outcomes.”
By the end of June 2016, a scientific paper reported “an ongoing outbreak of 50 C. auris cases” at Royal Brompton, and the hospital took an extraordinary step: It shut down its I.C.U. for 11 days, moving intensive care patients to another floor, again with no announcement.
Days later the hospital finally acknowledged to a newspaper that it had a problem. A headline in The Daily Telegraph warned, “Intensive Care Unit Closed After Deadly New Superbug Emerges in the U.K.” (Later research said there were eventually 72 total cases, though some patients were only carriers and were not infected by the fungus.)
Yet the issue remained little known internationally, while an even bigger outbreak had begun in Valencia, Spain, at the 992-bed Hospital Universitari i Politècnic La Fe. There, unbeknown to the public or unaffected patients, 372 people were colonized — meaning they had the germ on their body but were not sick with it — and 85 developed bloodstream infections. A paper in the journal Mycoses reported that 41 percent of the infected patients died within 30 days.
A statement from the hospital said it was not necessarily C. auris that killed them. “It is very difficult to discern whether patients die from the pathogen or with it, since they are patients with many underlying diseases and in very serious general condition,” the statement said.
As with Royal Brompton, the hospital in Spain did not make any public announcement. It still has not.
One author of the article in Mycoses, a doctor at the hospital, said in an email that the hospital did not want him to speak to journalists because it “is concerned about the public image of the hospital.”
The secrecy infuriates patient advocates, who say people have a right to know if there is an outbreak so they can decide whether to go to a hospital, particularly when dealing with a nonurgent matter, like elective surgery.
“Why the heck are we reading about an outbreak almost a year and a half later — and not have it front-page news the day after it happens?” said Dr. Kevin Kavanagh, a physician in Kentucky and board chairman of Health Watch USA, a nonprofit patient advocacy group. “You wouldn’t tolerate this at a restaurant with a food poisoning outbreak.”
Health officials say that disclosing outbreaks frightens patients about a situation they can do nothing about, particularly when the risks are unclear.
“It’s hard enough with these organisms for health care providers to wrap their heads around it,” said Dr. Anna Yaffee, a former C.D.C. outbreak investigator who dealt with resistant infection outbreaks in Kentucky in which the hospitals were not publicly disclosed. “It’s really impossible to message to the public.”
Officials in London did alert the C.D.C. to the Royal Brompton outbreak while it was occurring. And the C.D.C. realized it needed to get the word to American hospitals. On June 24, 2016, the C.D.C. blasted a nationwide warning to hospitals and medical groups and set up an email address, email@example.com, to field queries. Dr. Snigdha Vallabhaneni, a key member of the fungal team, expected to get a trickle — “maybe a message every month.”
Instead, within weeks, her inbox exploded.
Coming to America
In the United States, 587 cases of people having contracted C. auris have been reported, concentrated with 309 in New York, 104 in New Jersey and 144 in Illinois, according to the C.D.C.
The symptoms — fever, aches and fatigue — are seemingly ordinary, but when a person gets infected, particularly someone already unhealthy, such commonplace symptoms can be fatal.
The earliest known case in the United States involved a woman who arrived at a New York hospital on May 6, 2013, seeking care for respiratory failure. She was 61 and from the United Arab Emirates, and she died a week later, after testing positive for the fungus. At the time, the hospital hadn’t thought much of it, but three years later, it sent the case to the C.D.C. after reading the agency’s June 2016 advisory.
This woman probably was not America’s first C. auris patient. She carried a strain different from the South Asian one most common here. It killed a 56-year-old American woman who had traveled to India in March 2017 for elective abdominal surgery, contracted C. auris and was airlifted back to a hospital in Connecticut that officials will not identify. She was later transferred to a Texas hospital, where she died.
The germ has spread into long-term care facilities. In Chicago, 50 percent of the residents at some nursing homes have tested positive for it, the C.D.C. has reported. The fungus can grow on intravenous lines and ventilators.
Workers who care for patients infected with C. auris worry for their own safety. Dr. Matthew McCarthy, who has treated several C. auris patients at Weill Cornell Medical Center in New York, described experiencing an unusual fear when treating a 30-year-old man.
“I found myself not wanting to touch the guy,” he said. “I didn’t want to take it from the guy and bring it to someone else.” He did his job and thoroughly examined the patient, but said, “There was an overwhelming feeling of being terrified of accidentally picking it up on a sock or tie or gown.”
The role of pesticides?
As the C.D.C. works to limit the spread of drug-resistant C. auris, its investigators have been trying to answer the vexing question: Where in the world did it come from?
The first time doctors encountered C. auris was in the ear of a woman in Japan in 2009 (auris is Latin for ear). It seemed innocuous at the time, a cousin of common, easily treated fungal infections.
Three years later, it appeared in an unusual test result in the lab of Dr. Jacques Meis, a microbiologist in Nijmegen, the Netherlands, who was analyzing a bloodstream infection in 18 patients from four hospitals in India. Soon, new clusters of C. auris seemed to emerge with each passing month in different parts of the world.
The C.D.C. investigators theorized that C. auris started in Asia and spread across the globe. But when the agency compared the entire genome of auris samples from India and Pakistan, Venezuela, South Africa and Japan, it found that its origin was not a single place, and there was not a single auris strain.
The genome sequencing showed that there were four distinctive versions of the fungus, with differences so profound that they suggested that these strains had diverged thousands of years ago and emerged as resistant pathogens from harmless environmental strains in four different places at the same time.
“Somehow, it made a jump almost seemingly simultaneously, and seemed to spread and it is drug resistant, which is really mind-boggling,” Dr. Vallabhaneni said.
There are different theories as to what happened with C. auris. Dr. Meis, the Dutch researcher, said he believed that drug-resistant fungi were developing thanks to heavy use of fungicides on crops.
Dr. Meis became intrigued by resistant fungi when he heard about the case of a 63-year-old patient in the Netherlands who died in 2005 from a fungus called Aspergillus. It proved resistant to a front-line antifungal treatment called itraconazole. That drug is a virtual copy of the azole pesticides that are used to dust crops the world over and account for more than one-third of all fungicide sales.
A 2013 paper in Plos Pathogens said that it appeared to be no coincidence that drug-resistant Aspergillus was showing up in the environment where the azole fungicides were used. The fungus appeared in 12 percent of Dutch soil samples, for example, but also in “flower beds, compost, leaves, plant seeds, soil samples of tea gardens, paddy fields, hospital surroundings, and aerial samples of hospitals.”
Dr. Meis visited the C.D.C. last summer to share research and theorize that the same thing is happening with C. auris, which is also found in the soil: Azoles have created an environment so hostile that the fungi are evolving, with resistant strains surviving.
This is similar to concerns that resistant bacteria are growing because of excessive use of antibiotics in livestock for health and growth promotion. As with antibiotics in farm animals, azoles are used widely on crops.
“On everything — potatoes, beans, wheat, anything you can think of, tomatoes, onions,” said Dr. Rhodes, the infectious disease specialist who worked on the London outbreak. “We are driving this with the use of antifungicides on crops.”
Dr. Chiller theorizes that C. auris may have benefited from the heavy use of fungicides. His idea is that C. auris actually has existed for thousands of years, hidden in the world’s crevices, a not particularly aggressive bug. But as azoles began destroying more prevalent fungi, an opportunity arrived for C. auris to enter the breach, a germ that had the ability to readily resist fungicides now suitable for a world in which fungi less able to resist are under attack.
The mystery of C. auris’s emergence remains unsolved, and its origin seems, for the moment, to be less important than stopping its spread.
Resistance and denial
For now, the uncertainty around C. auris has led to a climate of fear, and sometimes denial.
Last spring, Jasmine Cutler, 29, went to visit her 72-year-old father at a hospital in New York City, where he had been admitted because of complications from a surgery the previous month.
When she arrived at his room, she discovered that he had been sitting for at least an hour in a recliner, in his own feces, because no one had come when he had called for help to use the bathroom. Ms. Cutler said it became clear to her that the staff was afraid to touch him because a test had shown that he was carrying C. auris.
“I saw doctors and nurses looking in the window of his room,” she said. “My father’s not a guinea pig. You’re not going to treat him like a freak at a show.”
He was eventually discharged and told he no longer carried the fungus. But he declined to be named, saying he feared being associated with the frightening infection.
Matt Richtel is a best-selling author and Pulitzer Prize-winning reporter based in San Francisco. He joined The Times staff in 2000, and his work has focused on science, technology, business and narrative-driven storytelling around these issues.
Andrew Jacobs is a reporter with the Health and Science Desk, based in New York. He previously reported from Beijing and Brazil and had stints as a Metro reporter, Styles writer and National correspondent, covering the American South. @AndrewJacobsNYTThe New York Times · by Matt Richtel · April 6, 2019
Farmers are being blamed for creating a wave of drug-resistant fungi that can infect people’s lungs or blood — and which are appearing in many gardens and compost heaps.
Several forms of the “superfungi” have emerged, often infecting people with weak immune systems. They are also becoming common in hospitals, causing post-operative blood infections.
The rise of the superfungi is strongly linked to farming, where widespread use of antifungal sprays on crops has made ordinary yeasts and moulds evolve resistance to such chemicals.
Farmers use similar compounds to those used in treating humans — so fungi that evolve resistance in the wild cannot be treated when they attack people.
Aspergillus, a mould that rots compost and vegetation, is emerging as a leading killer. It has evolved drug-resistant strains and is linked with up to 400,000 UK asthma cases a year and 3,600 lung infections. The most dangerous form is “invasive aspergillosis” where the fungus enters the blood, with 4,000 cases a year, according to Professor David Denning, head of the National Aspergillosis Centre in Manchester.
“Four or five years ago only 1%-1.5% of strains tested were drug resistant. Now it has reached 13% in London and 6% in south Wales. It seems very likely that resistance is increasing, and we think farmers spraying crops with fungicide is the cause,” he said.
The drug-resistant strains can be found in most gardens. Mother-of-two Karen Hook, 50, a horticulturist from Bishop’s Stortford, Hertfordshire, discovered the fungus growing in her lungs when she started coughing up green lumps of fungus.
“I started feeling really tired and coughing. I also had bad breath. The mould was growing in my lung.” The fungus had to be removed in an operation which also destroyed part of her lung.
Such cases raise fears that the rise in local authority compost heaps, linked to food recycling, could expose residents to surges in fungal spores. Some UK studies carried out downwind of such sites show spore levels 60 times above normal.
When Sandra Hicks was diagnosed with aspergillosis in 2008, doctors prescribed drugs, but her infection has proven resistant.
The pharmacist, 51, from Verwood, Dorset, said the infection would eventually kill her. “It’s destroying my lungs. I used to walk my dog for miles, but now walking up a slight incline is a problem … it’s very scary to be told the treatment isn’t working.”