Gram-negative bacteria, escapes human TLR4 recognition [15]
and is recognized by TLR2 in human cells [16].
The first leptospiral genome sequence to be determined in
2003, that of L. interrogans serovar Lai, consists of a 4.33-Mb
large chromosome and a 359-kb small chromosome [17]. Today,
the genome sequences of hundreds of Leptospira strains have been
determined, including representative of each of the 64 Leptospira
species [4]. The genome of Leptospira is always composed of two
chromosomes, and some plasmids have been recently identified
[18–21]. Access to large sets of genome sequences has significantly
improved our understanding of the emergence of virulence in
Leptospira. Genomic comparisons between pathogenic and nonpathogenic species have revealed a number of important differences, suggesting that pathogens evolved from free-living
ancestral species by successive gain and loss of genes/functions
associated with the adaptation to new hosts [4, 8, 22]. For instance,
it is possible to observe a gradient in the repertoire of genes
encoding proteins (hemolysins, etc.) or protein domains (leucinerich repeat, peptidases, etc.) known to be associated with virulence,
with the most virulent species of subclade P1 having the most genes
encoding these virulence factors [4].
4 Conclusion
Leptospira was identified as the causative agents of leptospirosis
100 years ago [5]. Despite some recent progress, although the
burden of leptospirosis is comparable or even higher than diseases
that are much better known, such as dengue or rabies [23], there is
a considerable deficit in the understanding of basic aspects of the
epidemiology of the disease and the biology of the bacterium
responsible.
References
1. Trueba G, Zapata S, Madrid K, Cullen P,
Haake D (2004) Cell aggregation: a mechanism of pathogenic Leptospira to survive in
fresh water. Int Microbiol 7:35–40
2. Andre-Fontaine G, Aviat F, Thorin C (2015)
Water borne leptospirosis: survival and preservation of the virulence of pathogenic Leptospira spp. in fresh water. Curr Microbiol
71:136–142
3. Picardeau M (2014) Family Leptospiraceae. In:
Rosenberg E (ed) The prokaryotes. SpringerVerlag Berlin, Heidelberg, pp 711–729
4. Vincent AT, Schiettekatte S, Goarant C, Neela
VK, Bernet E, Thibeaux R et al (2019) Revisiting the taxonomy and evolution of
pathogenicity of the genus Leptospira through
the prism of genomics. PLoS Negl Trop Dis 13
(5):e0007270
5. Inada R, Ido Y, Hoki R, Kakeno R, Ito H
(1916) The etiology, mode of infection and
specific therapy of Weil’s disease (Spirochaeta
icterohaemorrhagiae). J Exp Med 23:377–403
6. Chakraborty A, Miyahara S, Villanueva SY,
Saito M, Gloriani NG, Yoshida S (2011) A
novel combination of selective agents for isolation of Leptospira species. Microbiol Immunol
55:494–501
7. Puche R, Ferre ´s I, Caraballo L, Rangel Y,
Picardeau M, Takiff H et al (2018) Leptospira
venezuelensis sp. nov., a new member of the
274
Mathieu Picardeau
and is recognized by TLR2 in human cells [16].
The first leptospiral genome sequence to be determined in
2003, that of L. interrogans serovar Lai, consists of a 4.33-Mb
large chromosome and a 359-kb small chromosome [17]. Today,
the genome sequences of hundreds of Leptospira strains have been
determined, including representative of each of the 64 Leptospira
species [4]. The genome of Leptospira is always composed of two
chromosomes, and some plasmids have been recently identified
[18–21]. Access to large sets of genome sequences has significantly
improved our understanding of the emergence of virulence in
Leptospira. Genomic comparisons between pathogenic and nonpathogenic species have revealed a number of important differences, suggesting that pathogens evolved from free-living
ancestral species by successive gain and loss of genes/functions
associated with the adaptation to new hosts [4, 8, 22]. For instance,
it is possible to observe a gradient in the repertoire of genes
encoding proteins (hemolysins, etc.) or protein domains (leucinerich repeat, peptidases, etc.) known to be associated with virulence,
with the most virulent species of subclade P1 having the most genes
encoding these virulence factors [4].
4 Conclusion
Leptospira was identified as the causative agents of leptospirosis
100 years ago [5]. Despite some recent progress, although the
burden of leptospirosis is comparable or even higher than diseases
that are much better known, such as dengue or rabies [23], there is
a considerable deficit in the understanding of basic aspects of the
epidemiology of the disease and the biology of the bacterium
responsible.
References
1. Trueba G, Zapata S, Madrid K, Cullen P,
Haake D (2004) Cell aggregation: a mechanism of pathogenic Leptospira to survive in
fresh water. Int Microbiol 7:35–40
2. Andre-Fontaine G, Aviat F, Thorin C (2015)
Water borne leptospirosis: survival and preservation of the virulence of pathogenic Leptospira spp. in fresh water. Curr Microbiol
71:136–142
3. Picardeau M (2014) Family Leptospiraceae. In:
Rosenberg E (ed) The prokaryotes. SpringerVerlag Berlin, Heidelberg, pp 711–729
4. Vincent AT, Schiettekatte S, Goarant C, Neela
VK, Bernet E, Thibeaux R et al (2019) Revisiting the taxonomy and evolution of
pathogenicity of the genus Leptospira through
the prism of genomics. PLoS Negl Trop Dis 13
(5):e0007270
5. Inada R, Ido Y, Hoki R, Kakeno R, Ito H
(1916) The etiology, mode of infection and
specific therapy of Weil’s disease (Spirochaeta
icterohaemorrhagiae). J Exp Med 23:377–403
6. Chakraborty A, Miyahara S, Villanueva SY,
Saito M, Gloriani NG, Yoshida S (2011) A
novel combination of selective agents for isolation of Leptospira species. Microbiol Immunol
55:494–501
7. Puche R, Ferre ´s I, Caraballo L, Rangel Y,
Picardeau M, Takiff H et al (2018) Leptospira
venezuelensis sp. nov., a new member of the
274
Mathieu Picardeau