BACKGROUND: Exposure of critically ill patients to antibiotics lead to intestinal dysbiosis, which often manifests as antibiotic-associated diarrhoea. Faecal microbiota transplantation restores gut microbiota and may lead to faster resolution of diarrhoea. METHODS: Into this prospective, multi-centre, randomized controlled trial we will enrol 36 critically ill patients with antibiotic-associated diarrhoea. We will exclude patients with ongoing sepsis, need of systemic antibiotics, or those after recent bowel surgery or any other reason that prevents the FMT. Randomisation will be in 1:1 ratio. Patients in the control group will receive standard treatment based on oral diosmectite. In the intervention group, patients will receive, in addition to the standard of care, faecal microbiota transplantation via rectal tube, in the form of a preparation mixed from 7 thawed aliquots (50 mL) made from fresh stool of 7 healthy unrelated donors and quarantined deep frozen for 3 to 12 months. Primary outcome is treatment failure defined as intervention not delivered or diarrhoea persisting at day 7 after randomisation. Secondary outcomes include safety measures such as systemic inflammatory response, adverse events, and also diarrhoea recurrence within 28 days. Exploratory outcomes focus on gut barrier function and composition of intestinal microbiota. DISCUSSION: Faecal microbiota transplantation has been effective for dysbiosis in non-critically ill patients with recurrent C. difficile infections and it is plausible to hypothesize that it will be equally effective for symptoms of dysbiosis in the critically ill patients. In addition, animal experiments and observational data suggest other benefits such as reduced colonization with multi-drug resistant bacteria and improved gut barrier and immune function. The frozen faeces from unrelated donors are immediately available when needed, unlike those from the relatives, who require lengthy investigation. Using multiple donors maximises graft microbiota diversity. Nonetheless, in vulnerable critically ill patients, Faecal microbiota transplantation might lead to bacterial translocation and unforeseen complications. From growing number of case series it is clear that its off label use in the critically ill patients is increasing and that there is a burning need to objectively assess its efficacy and safety, which this trial aims. TRIAL REGISTRATION: www.clinicaltrials.gov (NCT05430269).

• MeSH
• antibakteriální látky * škodlivé účinky   terapeutické užití   MeSH
• dysbióza terapie   mikrobiologie   MeSH
• feces mikrobiologie   MeSH
• fekální transplantace * metody   škodlivé účinky   MeSH
• klinické zkoušky, fáze II jako téma MeSH
• kritický stav * MeSH
• lidé MeSH
• multicentrické studie jako téma MeSH
• prospektivní studie MeSH
• průjem * terapie   mikrobiologie   MeSH
• randomizované kontrolované studie jako téma MeSH
• střevní mikroflóra * účinky léků   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• protokol klinické studie MeSH

MEDNIK syndrome is a rare autosomal recessive disease characterized by mental retardation, enteropathy, deafness, peripheral neuropathy, ichthyosis, and keratoderma, and caused by variants in the adaptor-related protein complex 1 subunit sigma 1 (AP1S1) gene. This gene encodes the σ1A protein, which is a subunit of the adaptor protein complex 1 (AP-1), a key component of the intracellular protein trafficking machinery. Previous work identified three AP1S1 nonsense, frameshift and splice-site variants in MEDNIK patients predicted to encode truncated σ1A proteins, with consequent AP-1 dysfunction. However, two AP1S1 missense variants (c.269 T > C and c.346G > A) were recently reported in patients who presented with severe enteropathy but no additional symptoms of MEDNIK. This condition was described as a novel non-syndromic form of congenital diarrhea caused specifically by the AP1S1 missense variants. In this study, we report two patients with the same c.269 T > C variant, who, contrary to the previous cases, presented as complete MEDNIK syndrome. These data substantially revise the presentation of disorders associated with AP1S1 gene variants and indicate that all the identified pathogenic AP1S1 variants result in MEDNIK syndrome. We also provide a series of functional analyses that elucidate the impact of the c.269 T > C variant on σ1A function, contributing to a better understanding of the molecular pathogenesis of MEDNIK syndrome. KEY MESSAGES: A missense AP1S1 c.269 T > C (σ1A L90P) variant causes full MEDNIK syndrome. The σ1A L90P variant is largely unable to assemble into the AP-1 complex. The σ1A L90P variant fails to bind [DE]XXXL[LI] sorting motifs. The σ1A L90P variant results in loss-of-function of the protein.

• MeSH
• adaptorový proteinový komplex - sigma-podjednotky * genetika   MeSH
• adaptorový proteinový komplex 1 * genetika   MeSH
• genetická predispozice k nemoci MeSH
• lidé MeSH
• mentální retardace genetika   MeSH
• missense mutace * MeSH
• průjem genetika   MeSH
• syndrom MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• kazuistiky MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Intramural MeSH

V této kazuistice se budeme věnovat případu 14letého chlapce, který byl přivezen zdravotnickou záchrannou službou (ZZS) na dětské oddělení naší nemocnice pro dva dny trvající horečky, dehydrataci a celkové vyčerpání. Kromě horeček se u chlapce za hospitalizace postupně rozvíjely příznaky respiračního infektu, objevily se průjmovité stolice a makulózní exantém s bílým dermografismem. Z anamnézy bylo při příjmu zjištěno, že se chlapec před dvěma dny vrátil z pobytu v tropické oblasti.

In this article we present a case of a fourteen-year-old boy who was transported via ambulance to our Pediatric Ward due to a two-day-lasting fever, dehydration and total exhaustion. Additionally, the patient progressively developed respiratory symptoms, diarrhoea and rash with white dermographism during hospitalization. The medical history revealed that the boy had been visiting a tropical destination two days prior to hospital admission.

• MeSH
• cestovní nemoci * MeSH
• dengue diagnóza   přenos   virologie   MeSH
• diferenciální diagnóza MeSH
• horečka * diagnóza   etiologie   klasifikace   mikrobiologie   MeSH
• koinfekce etiologie   klasifikace   mikrobiologie   MeSH
• lidé MeSH
• mladiství MeSH
• průjem diagnóza   etiologie   mikrobiologie   MeSH
• Salmonella enterica klasifikace   patogenita   MeSH
• tracheitida diagnóza   etiologie   farmakoterapie   mikrobiologie   MeSH
• tropické lékařství MeSH
• Check Tag
• lidé MeSH
• mladiství MeSH
• mužské pohlaví MeSH
• Publikační typ
• přehledy MeSH

• MeSH
• farmakokinetika MeSH
• lidé MeSH
• nemoci jater farmakoterapie   patofyziologie   MeSH
• průjem etiologie   farmakoterapie   MeSH
• pyróza etiologie   farmakoterapie   MeSH
• střevní mikroflóra MeSH
• syndrom krátkého střeva * farmakoterapie   komplikace   patofyziologie   MeSH
• týmová péče o pacienty MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy MeSH

Enteroaggregative Escherichia coli (EAEC) strains including those of serogroup O111 are important causes of diarrhea in children. In the Czech Republic, no information is available on the etiological role of EAEC in pediatric diarrhea due to the lack of their targeted surveillance. To fill this gap, we determined the proportion of EAEC among E. coli O111 isolates from children with gastrointestinal disorders ≤ 2 years of age submitted to the National Reference Laboratory for E. coli and Shigella during 2013-2022. EAEC accounted for 177 of 384 (46.1 %) E. coli O111 isolates, being the second most frequent E. coli O111 pathotype. Most of them (75.7 %) were typical EAEC that carried aggR, usually with aaiC and aatA marker genes; the remaining 24.3 % were atypical EAEC that lacked aggR but carried aaiC and/or aatA. Whole genome sequencing of 11 typical and two atypical EAEC O111 strains demonstrated differences in serotypes, sequence types (ST), virulence gene profiles, and the core genomes between these two groups. Typical EAEC O111:H21/ST40 strains resembled by their virulence profiles including the presence of the aggregative adherence fimbriae V (AAF/V)-encoding cluster to such strains from other countries and clustered with them in the core genome multilocus sequence typing (cgMLST). Atypical EAEC O111:H12/ST10 strains lacked virulence genes of typical EAEC and differed from them in cgMLST. All tested EAEC O111 strains displayed stacked-brick aggregative adherence to human intestinal epithelial cells. The AAF/V-encoding cluster was located on a plasmid of 95,749 bp or 93,286 bp (pAAO111) which also carried aggR, aap, aar, sepA, and aat cluster. EAEC O111 strains were resistant to antibiotics, in particular to aminopenicillins and cephalosporins; 88.3 % produced AmpC β-lactamase, and 4.1 % extended spectrum β-lactamase. We conclude that EAEC are frequent among E. coli O111 strains isolated from children with gastrointestinal disorders in the Czech Republic. To reliably assess the etiological role of EAEC in pediatric diarrhea, a serotype-independent, PCR-based pathotype surveillance system needs to be implemented in the future.

• MeSH
• antibakteriální látky farmakologie   MeSH
• Escherichia coli * genetika   izolace a purifikace   patogenita   klasifikace   MeSH
• faktory virulence genetika   MeSH
• gastrointestinální nemoci mikrobiologie   MeSH
• genom bakteriální MeSH
• infekce vyvolané Escherichia coli * mikrobiologie   epidemiologie   MeSH
• kojenec MeSH
• lidé MeSH
• multilokusová sekvenční typizace MeSH
• novorozenec MeSH
• předškolní dítě MeSH
• proteiny z Escherichia coli genetika   MeSH
• průjem * mikrobiologie   MeSH
• sekvenování celého genomu * MeSH
• séroskupina MeSH
• trans-aktivátory MeSH
• Check Tag
• kojenec MeSH
• lidé MeSH
• mužské pohlaví MeSH
• novorozenec MeSH
• předškolní dítě MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Geografické názvy
• Česká republika MeSH

Průjmy jsou častým zdravotním problémem u dětí, zejména mladších 2 let, a jsou zodpovědné za 13,2 % celosvětových dětských úmrtí. Převážná většina průjmů je akutních, 3-20 % je chronických, tj. trvající déle než 2 (až 4) týdny. Ve většině případů je etiologie chronických průjmů infekční. V rozvinutých zemích a s klesajícím věkem dítěte stoupá, zejména u novorozenců a kojenců, riziko průjmů z genetických nebo vrozených příčin. U dětí starších věkových kategorií je nutno zvážit i alergické a imunitně mediované etiologie. Při vyšetření dítěte s chronickým průjmem je klíčová anamnéza a podrobné klinické zhodnocení. Laboratorní a další vyšetřovací metody se odvíjí od zvažované diferenciální diagnózy, a mohou zahrnovat i endoskopická a genetická vyšetření. Terapie záleží na etiologii obtíží. Při intractable diarrhoea of infancy, neboli neustupujícímu průjmu kojenců, je často nutná parenterální výživa a ani indikace transplantace tenkého střeva není výjimkou.

Diarrhoea is a frequent health problem in children, mainly in those younger than 2 years of age, and is responsible for up to 13,2% of international child mortality. Majority of diarrhoea is acute and 3-20% are chronic, lasting for more than 2 (to 4) weeks. In most cases, infectious causes are responsible for chronic diarrhoea. In developed countries and with the decreasing age of the child, mainly in newborns and infants, the risk of congenital and genetic causes is increasing. In older children, allergies and immune mediated aetiologies should be considered. History and a detailed physical examination are key in evaluating a child with chronic diarrhoea. Laboratory work and other diagnostic methods evolve from the considered differential diagnosis and may include endoscopies and genetic testing. Therapy depends on the aetiology of diarrhoea. In intractable diarrhoea of infancy, parenteral nutrition is often required, and small intestine transplantation is not an exception.

• MeSH
• chronická nemoc MeSH
• kojenec MeSH
• lidé MeSH
• průjem kojenců * diagnóza   etiologie   terapie   MeSH
• průjem diagnóza   etiologie   terapie   MeSH
• Check Tag
• kojenec MeSH
• lidé MeSH
• Publikační typ
• práce podpořená grantem MeSH

• MeSH
• hospitalizace MeSH
• lidé MeSH
• mladý dospělý MeSH
• parenterální výživa MeSH
• průjem etiologie   patologie   MeSH
• ulcerózní kolitida * komplikace   terapie   MeSH
• Check Tag
• lidé MeSH
• mladý dospělý MeSH
• ženské pohlaví MeSH
• Publikační typ
• kazuistiky MeSH

Clostridioides difficile is a leading cause of healthcare-associated infections. The main objective was to assess the current landscape of CDI infection prevention and control (IPC) practices. An anonymous survey of IPC practices for CDI was conducted between July 25 and October 31, 2022. Precautions for symptomatic patients were applicable for 75.9% and were discontinued 48 h minimum after the resolution of diarrhea for 40.7% of respondents. Daily cleaning of CDI patients' rooms was reported by 23 (42.6%). There was unexpected heterogeneity in IPC practices regarding the hospital management of CDI.

• MeSH
• Clostridioides difficile * MeSH
• Clostridioides MeSH
• infekce spojené se zdravotní péčí * prevence a kontrola   MeSH
• klostridiové infekce * prevence a kontrola   MeSH
• lidé MeSH
• průjem prevence a kontrola   MeSH
• zdravotnická zařízení MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

Enteropathogenic Escherichia coli (EPEC) is a diarrheagenic bacterium that predominantly infects infants in developing countries. EPEC forms attaching and effacing (A/E) lesions on the apical surface of the small intestine, leading to diarrhea. The locus of enterocyte effacement (LEE) is both necessary and sufficient for A/E lesion morphogenesis by EPEC. Gene expression from this virulence determinant is controlled by an elaborate regulatory web that extends beyond protein-based transcriptional regulators and includes small regulatory RNA (sRNA) that exert their effects posttranscriptionally. To date, only 4 Hfq-dependent sRNAs-MgrR, RyhB, McaS, and Spot42-have been identified that affect the LEE of EPEC by diverse mechanisms and elicit varying regulatory outcomes. In this study, we demonstrate that the paralogous Hfq-dependent sRNAs OmrA and OmrB globally silence the LEE to diminish the ability of EPEC to form A/E lesions. Interestingly, OmrA and OmrB do not appear to directly target a LEE-encoded gene; rather, they repress transcription from the LEE1 promoter indirectly, by means of an as-yet-unidentified transcriptional factor that binds within 200 base pairs upstream of the transcription start site to reduce the expression of the LEE master regulator Ler, which, in turn, leads to reduced morphogenesis of A/E lesions. Additionally, OmrA and OmrB also repress motility in EPEC by targeting the 5' UTR of the flagellar master regulator, flhD.

• MeSH
• barvicí látky MeSH
• enteropatogenní Escherichia coli * MeSH
• kojenec MeSH
• lidé MeSH
• promotorové oblasti (genetika) MeSH
• průjem MeSH
• transkripční faktory MeSH
• Check Tag
• kojenec MeSH
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

Brožura a směrnice, které se zaměřily na diagnostiku a léčbu akutního průjmu. Určeno praktickým lékařům.

• MeSH
• akutní nemoc MeSH
• praktické lékařství MeSH
• průjem diagnóza   terapie   MeSH
• Publikační typ
• směrnice pro lékařskou praxi MeSH

• Konspekt
• Patologie. Klinická medicína
• NLK Obory
• gastroenterologie
• všeobecné lékařství
• NLK Publikační typ
• brožury