Infektsioonhaigused

Eesti Arst 2016; 95(3):186–18

Puukentsefaliidi mitu palet

Puukentsefaliidi viirusnakkus (PE) on äge varieeruva kuluga nakkushaigus, mis levib kesknärvisüsteemi vaid 20–30%-l juhtudest. Enamasti on tegemist kergelt kulgeva haigusega, mis väljendub üldistes infektsiooninähtudes. Haiguse diagnoos kinnitatakse laboratoorselt. Artiklis on antud ülevaade puukentsefaliidist ning analüüsitud kesknärvisüsteemi haaravate PE-vormide esinemissagedust, haiguse kulgu ning diagnostika põhimõtteid TÜ Kliinikumis ravitud patsientidel. Eesti Arst 2013; 92(3):134–13

COVID-19 aktiivravi tulemused Tartu Ülikooli Kliinikumis 2021. aastal

Taust. Koroonaviirusnakkuse ulatuslik levik oli tõsine proovikivi paljude riikide, sealhulgas ka Eesti tervishoiusüsteemile. Uuringu eesmärk oli saada ülevaade kliinikumi koroonapatsientide demograafilistest näitajatest, ravitulemustest ning võrrelda seda rahvusvaheliste andmetega.Metoodika. Tegemist on kliinikumi 2021. aasta ravitöö retrospektiivse analüüsiga, millesse on kaasatud kõik aasta jooksul statsionaarsel aktiivravil viibinud patsiendid. Esmaselt õendusabi osakonda hospitaliseeritud on analüüsist välja jäetud. Koroonahaigetena identifitseeriti patsiendid, kelle elektroonilises haigusloos (eHL) oli lõplikus kliinilises diagnoosis põhi- või kaasuva haigusena märgitud RHK-10 kood U07.1.Tulemused. 2021. aastal hospitaliseeriti kliinikumi 1819 COVID-19-diagnoosiga patsienti, mis on 4,8% kõigist statsionaaris ravitud haigetest. COVID-19-haigete voodipäevad moodustasid 10,3% kõikidest aktiivravi voodipäevadest. Intensiivravi päevadest oli vastav osakaal 23,4%. Koroonahaigetest 50% olid mehed, mediaanvanus 64 aastat. Ligi kolmandik haigetest olid vähemalt 75aastased. Ainult tavaosakonna tingimustes raviti 1475 (81,1%) patsienti, haiglaravi mediaankestus oli 7 päeva. Selles kohordis esines 100 surmajuhtumit (letaalsus 6,8%), neist 79 patsienti olid vähemalt 75aastased. Intensiivravi vajas 344 (18,9%) patsienti. Intensiivravi mediaankestus oli 9 päeva, kogu haiglaravi kestus selles rühmas 21 päeva. 233 patsienti (67,7% intensiivravi haigetest) vajasid kopsude kunstlikku ventilatsiooni (KKV), ekstrakorporaalset membraanoksügenisatsiooni (EKMO) rakendati 26 haigel (7,5%). Suremus intensiivravi, KKVd ja EKMOt vajanute hulgas oli vastavalt 25,4%, 28,3% ja 44,4%.Kokkuvõte. Kliinikumi kõigist aktiivravi haigetest moodustasid 2021. aastal koroonapatsiendid märkimisväärse osa. Nende patsientide ravi kestis kolm korda kauem ning suremus oli ligi viis korda suurem võrreldes tavapäraste aktiivravi haigetega. Kliinikumi ravitulemused olid rahvusvahelisel tasemel

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

Autoantibodies against type I IFNs in patients with life-threatening COVID-19

Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-w (IFN-w) (13 patients), against the 13 types of IFN-a (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men

A first update on mapping the human genetic architecture of COVID-19

peer reviewe

Long COVID and Biomarker Dysregulation—A Shift Toward Immune Exhaustion?

Background: SARS-CoV-2 infection can lead to persistent or newly emerging symptoms lasting for months, a condition known as long COVID (LC). The pathophysiology of LC remains poorly understood, with cytokine dysregulation proposed as a key mechanism, although findings across the studies have been inconsistent. Patients and methods: We conducted a longitudinal study using the Olink® Target 96 Inflammation Panel to assess cytokines in COVID-19 (COV) patients at three months and six months post-infection. These profiles were compared with those of individuals recovering from other upper respiratory tract infections (non-COV). Additionally, we analyzed differences between individuals with LC and those who recovered from COVID-19. Predictive models for LC at three months and sixth months post-infection were developed using inflammatory markers and relevant clinical cofactors, including gender, age, BMI, hemogram, Β2-microglobulin, D-dimers, LDH, AST, ALT, Ferritin, vitamin D, CRP, and the severity of acute COVID-19 infection as classified by WHO criteria. Results: We observed a general decline in inflammatory biomarkers in post-COVID-19 patients over time, with only a few cytokines elevated (CCL4 at month 3 and CST5 at month 6) compared to non-COV controls. In LC patients, an early phase of low-grade inflammation transitioned into significant reduction in proinflammatory biomarkers compared to recovered individuals. Rather than indicating immune normalization, this pattern suggests a possible suppression or exhaustion of the immune response in the months following acute infection. Importantly, our predictive modeling demonstrated that this specific cytokine signature, in combination with acute disease severity and clinical cofactors, described well the presence of LC. Conclusions: Our findings suggest that inflammation-related biomarker dysregulation following acute SARS-CoV-2 infection evolves dynamically over a six-month period. By the sixth month, compared to the third month, the presence of LC is more accurately predicted by a combination of persistent biomarker alteration and the severity of the initial infection, as defined by WHO criteria. This represents a novel insight, as previous studies have primarily associated LC with elevated proinflammatory markers, whereas our results suggest that immune suppression or exhaustion may play a more prominent role in the later stages

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