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Összefoglaló. A fertőző betegségek kóroki hátterének felderítésére irányuló törekvések hosszú időre tekintenek vissza. Fogalmakkal és követelményekkel (posztulátumokkal) igyekeztek körülírni, hogy egy mikroorganizmus mikor tekinthető egy adott fertőző betegség okozójának. Egy patogén rendszertani kategóriába tartozó mikroorganizmus kimutatása a betegből önmagában még nem elegendő bizonyíték arra, hogy a betegségnek valóban az a kórokozója. Igazolni kell a továbbiakban, hogy rendelkezik azokkal a virulenciafaktoroknak nevezett tényezőkkel, amelyek valójában képessé teszik az adott betegség kiváltására. Robert Koch idejében csak fenotípusos ismeretek álltak rendelkezésre, azok figyelembevételével fogalmazta meg posztulátumait. Később, a megszerzett molekuláris ismeretek birtokában, a posztulátumokat molekuláris szinten is értelmezték. A beteg személyét biológiai, szociális és pszichés egységként kezelő holisztikus megközelítésnek is eleget téve, a posztulátumokat a kórokozó mellett az esetben érintett gazdaszervezet egyedi tulajdonságainak figyelembevételével tovább szélesítették. A dolgozat a fenti kérdéseket példákkal illusztrálva tárgyalja, majd kitér a gyakorlati hasznosítás lehetőségeire. Orv Hetil. 2021; 162(50): 1991–1999.

Summary. Efforts to explore the casual background of infectious diseases have been ambitioned for a long time. Terms and requirements (postulates) have been created to describe in which case a microorganism can be regarded as a causative agent of a given infectious disease. Demonstration of a representative of a pathogenic taxonomic category in the patient, however, does not prove its causative role in itself. It should also be verified if the microbe possesses the so-called virulence factors enabling it to trigger the given disease. At the time when Robert Koch formulated his postulates, only phenotypic characters were at his disposal. Later, in possession of a substantial genetic knowledge, the postulates have been adapted to molecular level. For having a holistic approach, the postulates have been extended also to the host’s individual biological, social and psychological attributes. This paper discusses the above issues with examples for illustration, and outlines their practical applicabilities. Orv Hetil. 2021; 162(50): 1991–1999.

Bactericidal effect against non-dividing bacteria is a very advantageous, but rare characteristic among antimicrobial agents, mostly possessed by those affecting the cell membrane. These kinds of agents can kill bacterial cells without lysis. We assessed these characteristics on primycin, a topical anti-staphylococcal agent highly effective against prevalent multiresistant strains, as it also acts on the cell membrane. In time-kill studies, primycin preserved its bactericidal activity against growth-arrested Staphylococcus aureus cultures. The bactericidal action was slower against growth-arrested cultures compared to the exponentially growing ones to different extents depending on the manner of arrest. The bactericidal effect was less influenced by stringent response and by protein synthesis inhibition, proving that it does not depend on metabolic activity. In contrast, uncoupling of the membrane potential predominantly slowed, and low temperature almost stopped killing of bacteria. In consideration of published data, these facts suggest that the antibacterial action of primycin involves disrupting of the membrane potential, and is predominantly influenced by the membrane fluidity. Optical density measurements and transmission electron microscopy verified that primycin kills bacterial cells without lysis. These results reveal favorable characteristics of primycin and point to, and broaden the knowledge on its membrane-targeted effect.

We investigated the molecular epidemiology of extended spectrum β-lactamase (ESBL) producing Klebsiella pneumoniae isolates derived from the teaching hospitals of University of Pécs, Pécs, Hungary in the time period 2004–2008. Molecular typing, antimicrobial susceptibility testing, detection of common β-lactamase genes (bla _CTX-M, bla _TEM and bla _SHV) and virulence associated traits (hypermucoviscosity, magA, k2a, rmpA, siderophores, type 1 and 3 fimbria, biofilm formation, serum resistance) were performed for 102 isolates. The results showed the presence of three major ciprofloxacin resistant CTX-M-15 producing clones (ST15 n = 69, ST101 n = 10, and ST147 n = 9), of which ST15 was predominant and universally widespread. Considering distribution in time and place, ST101 and ST147 were detected at fewer inpatient units and within a narrower time frame, as compared to ST15. Beside major clones, eleven minor clones were identified, and were shown to harbour the following β-lactamase genes: six clones carried bla _CTX-M, four clones harboured bla _SHV-5 and one clone possessed both bla _CTX-M and ESBL type bla _SHV. Among the SHV-5 producing K. pneumoniae clones a novel sequence type was found, namely ST1193, which harboured a unique infB allele. Different virulence factor content and peculiar antimicrobial susceptibility profile were characteristic for each clone. In contrast to major clone isolates, which showed high level resistance to ciprofloxacin, minor clone isolates displayed significantly lower MIC values for ciprofloxacin suggesting a role for fluoroquinolones in the dissemination of the major K. pneumoniae clones. This is the first description of the CTX-M-15 producing K. pneumoniae clone ST101 in Hungary.