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1ª Parte - El Estudio Inductivo 1. Lee el Salmo 44 en voz alta

Reproducible transfer of the PaLoc has been demonstrated here for the first time.

Although the PaLoc has been hypothesised to be a mobile genetic element or a phage

remnant [32], the transfer events described here are unlikely to be PaLoc specific as

variable amounts of 630 DNA have transferred. Analysing the transconjugants

containing the PaLoc could not indicate a specific MGE with which the PaLoc co-

transfers, although co-transfer of the PaLoc with CTn1, CTn5 and Tn5397 was

demonstrated. Although Tn5397 had transferred on the same transferred fragment as

the PaLoc, CTn1 and CTn5 never transferred on the PaLoc fragment and transfer of

these elements could be a separate event. Because of the presence of CTn4 and CTn7-

like elements in CD37, co-transfer of these two elements cannot be excluded.

The transfer mechanism of the PaLoc was not determined, although a number of

known mechanisms are considered to be highly unlikely. Transformation of free DNA

has never been observed in C. difficile despite multiple attempts in our laboratory and

others [105,107]. However, to rule out this possibility, filter-matings will be repeated in

our lab on agar plates containing DNase.

The PaLoc could have been transferred via transduction however, the size of the DNA

fragments that were shown to transfer makes this unlikely as the transferred DNA is

over three times the size of the phage genomes of C630-1 and C630-2 of strain 630. Furthermore, CD37 was shown not to be susceptible to the two prophages of 630 and

The transfer of the PaLoc could be facilitated by a high frequency recombination (Hfr)-

type mechanism. During Hfr, a conjugative element mobilises the chromosome in cis

by integrating into the chromosome or in trans by mobilising another element within

the chromosome after which (part of) the chromosome is transferred into a recipient

cell [114,115,260]. The transferred fragment of DNA will recombine with the

chromosome of the recipient cell through a double-crossover event replacing part of

the recipient genome, a process which depends on the recombination protein RecA

[104,114,115]. The mechanism has been described in a number of Gram negative

bacteria but in Gram positive bacteria it has only been described in L. lactis [261]. The

L. lactis sex factor is chromosomally located and can mobilise the chromosome but it can also transpose through site-specific recombination into non-conjugative plasmids

in order to mobilise these [120,121] (Chapter 1).

To determine if the transfer event is Hfr, a number of experiments need to be

performed. As Hfr is a RecA dependent event in the recipient strain, a CD37 recA

mutant could be constructed and used as recipient in filter-matings. Hfr in C. difficile

630 would most likely be mobilisation in cis by one of the CTns. In cis mobilisation

would involve using the oriT of the CTn that facilitated the transfer which means the

element rarely comes across completely as part of the element would be the last

sequence to be transferred to the transconjugant. Part of the element that does come

across may be lost during the double crossover event that integrates the transferred

DNA fragment into the chromosome. Furthermore, if the element responsible for

transfer is unique to 630 then recombination would not occur with this sequence and

the transferred fragment of the responsible element would be lost. As the whole

two of the transconjugants, it is unlikely that the oriT of this element is used as the

whole of the chromosome would have to have been transferred into the recipient cell.

However, CTn1 and CTn2 are located close to this element and were not present in any

of the transconjugants on the integrated DNA fragment (Figure 5.5). Therefore, one of

these two elements may facilitate the Hfr transfer. In order to test this hypothesis,

mutants could be made for genes that are essential for conjugative transfer of these

elements. If genes which are essential for one of the elements are also essential for

Hfr, then the element responsible for Hfr is identified. However, more than one of the

CTns may be capable of mobilising the genome in this manner.

The PaLoc contains the two major virulence factors that have been identified in C.

difficile, making transfer of this locus clinically important. C. difficile has been shown here, and in previous studies, to exchange DNA with a number of species including B.

subtilis [164], E. faecalis [163] and S. aureus [170]. Transfer of the PaLoc into any of these species is therefore theoretically possible and when the transfer mechanism of

the PaLoc transfer is determined, experiments should be carried out in order to

determine the host range. If the transfer mechanism is shown to be Hfr, transfer into

unrelated species would be less likely.

The cytotoxicity assay showed that the CD37 transconjugant has the same level of

cytotoxicity as the donor strain. Although horizontally acquired DNA can be silenced

after transfer, the PaLoc encodes two hypothetical regulators, tcdC and tcdD, which

may also regulate toxin expression in transconjugants [52,53]. Furthermore, a recent

paper by Dingle et al. [89] described MLST data which suggests that a toxigenic

the PaLoc. This data suggests that the PaLoc transfer that was described here may

have also occurred in vivo.

Protective colonization with non-toxigenic C. difficile strains is a new strategy to

prevent colonization by toxigenic C. difficile. Protective colonization in hamsters was

shown to lead to colonization resistance of toxigenic strains and to prevent disease

symptoms [262]. Currently, human phase II trials are being conducted [263] however,

if in vivo transfer of the PaLoc can occur, this treatment strategy may be less effective

than expected and the effect on C. difficile epidemiology cannot be predicted.

5.5.2. Conclusions

The data in this chapter describes the transfer of the PaLoc from a toxigenic donor

strain to a non-toxigenic recipient strain. The recipient strain becomes cytotoxic and

produces similar levels of toxin as the wildtype donor strain.

The transfer mechanism of the PaLoc transfer is still unknown although a number of

transfer methods have been ruled out. Transfer via transformation is unlikely due to

the natural inability of C. difficile to take up DNA under laboratory conditions.

Furthermore, the size of the transferred DNA fragment in some of the transconjugants

is more than three times larger than the phage genomes of C630-1 and C630-2 of strain 630, making transduction of the DNA fragment highly unlikely. As the size of the

DNA fragment that was incorporated in the recipient chromosome varies between the

transconjugants, the donor DNA could be incorporated by non-specific recombination.

This leads to the hypothesis that a Hfr-like transfer mechanism could be responsible