Leptospira (from Ancient Greekλεπτός (leptós)'fine, thin, narrow, etc.' and Latinspira'coil')[1] is a genus ofspirochaete bacteria, including a small number ofpathogenic andsaprophytic species.[2]Leptospira was first observed in 1907 inkidney tissue slices of aleptospirosis victim who was described as having died of "yellow fever".[3] In 1917,Hideyo Noguchi named the genusLeptospira after witnessing it in the kidneys of American rats seemingly producing the same disease in Guinea pigs as in European rats.[4][5]
Leptospira, together with the generaLeptonema andTurneria, is a member of the familyLeptospiraceae. The genusLeptospira is divided into 20 species based on DNA hybridization studies.[6][7]
PathogenicLeptospira
Leptospira alstoniiSmythe et al. 2013 ["Leptospira alstoni"Haake et al. 1993]
Leptospira biflexa(Wolbach and Binger 1914) Noguchi 1918emend. Faine and Stallman 1982 ["Spirochaeta biflexa"Wolbach & Binger 1914]
Leptospira idoniiSaito et al. 2013
Leptospira meyeriYasuda et al. 1987
Leptospira wolbachiiYasuda et al. 1987
Leptospira vanthieliiSmythe et al. 2013
Leptospira terpstraeSmythe et al. 2013
Leptospira yanagawaeSmythe et al. 2013
Members ofLeptospira are also grouped intoserovars according to their antigenic relatedness. There are currently over 200 recognized serovars. A few serovars are found in more than one species ofLeptospira.
At its 2002 meeting, the Committee on the Taxonomy of Leptospira of the International Union of Microbiological Societies approved the following nomenclature for serovars of Leptospira. Genus and species names are italicized as usual, with the serovar name not italicized and with an upper case first letter.
Although over 200 serotypes ofLeptospira have been described, all members of the genus have similar morphology.Leptospira are spiral-shaped bacteria that are 6-20 μm long and 0.1 μm in diameter with a wavelength of about 0.5 μm.[20] One or both ends of the spirochete are usually hooked. Because they are so thin, liveLeptospira are best observed bydarkfield microscopy.
The bacteria have a number of degrees of freedom; when ready to proliferate viabinary fission, the bacterium noticeably bends in the place of the future split.
Leptospira have aGram-negative-like cell envelope consisting of a cytoplasmic andouter membrane. However, thepeptidoglycan layer is associated with the cytoplasmic rather than the outer membrane, an arrangement that is unique tospirochetes. The twoflagella ofLeptospira extend from the cytoplasmic membrane at the ends of the bacterium into theperiplasmic space and are necessary for the motility ofLeptospira.[21]
The outer membrane contains a variety oflipoproteins and transmembraneouter membrane proteins.[22] As expected, the protein composition of the outer membrane differs when comparingLeptospira growing in artificial medium withLeptospira present in an infected animal.[23][24][25] Several leptospiral outer membrane proteins have been shown to attach to the hostextracellular matrix and tofactor H. These proteins may be important foradhesion ofLeptospira to host tissues and in resistingcomplement, respectively.[26][27][28]
The outer membrane ofLeptospira, like those of most other Gram-negative bacteria, containslipopolysaccharide (LPS). Differences in the highly immunogenic LPS structure account for the numerous serovars ofLeptospira.[20] Consequently, immunity is serovar specific; current leptospiral vaccines, which consist of one or several serovars ofLeptospira endemic in the population to be immunized, protect only against the serovars contained in the vaccine preparation. Leptospiral LPS has low endotoxin activity.[20] An unusual feature of leptospiral LPS is that it activates host cells viaTLR2 rather thanTLR4.[29] The unique structure of thelipid A portion of the LPS molecule may account for this observation.[30] Finally, the LPSO antigen content ofL. interrogans differs in an acutely infected versus a chronically infected animal.[31] The role of O antigen changes in the establishment or maintenance of acute or chronic infection, if any, is unknown.
Leptospira, both pathogenic and saprophytic, can occupy diverse environments, habitats, and life cycles; these bacteria are found throughout the world, except in Antarctica. High humidity and neutral (6.9–7.4) pH are necessary for their survival in the environment, withstagnant water reservoirs—bogs, shallow lakes, ponds, puddles, etc.—being the natural habitat for the bacteria.
Leptospira are cultivated at 30 °C in Ellinghausen-McCullough-Johnson-Harris (EMJH) medium, which can be supplemented with 0.21% rabbit serum to enhance growth of fastidious strains.[32] Growth of pathogenicLeptospira in an artificial nutrient environment such as EMJH becomes noticeable in 4–7 days; growth of saprophytic strains occur within 2–3 days. The minimal growth temperature of pathogenic species is 13–15 °C. Because the minimal growth temperature of the saprophytes is 5–10 °C, the ability ofLeptospira to grow at 13 °C can be used to distinguish saprophytic from pathogenicLeptospira species.[32] The optimal pH for growth ofLeptospira is 7.2–7.6.
Leptospira are aerobes whose major carbon and energy source duringin vitro growth is long-chain fatty acids, which are metabolized by beta-oxidation.[33][34] Fatty acids are provided in EMJH in the form ofTween.[32] Fatty acid molecules are bound byalbumin in EMJH and are released slowly into the medium to prevent its toxic accumulation.
Like most bacteria,Leptospira require iron for growth.[35]L. interrogans andL. biflexa have the ability to acquire iron in different forms.[36] ATonB-dependent receptor required for utilization of the ferrous form of the iron has been identified inL. biflexa, and anortholog of the receptor is encoded in the genome ofL. interrogans.L. interrogans can also obtain iron fromheme, which is bound to most of the iron in the human body. The HbpA hemin-binding protein, which may be involved in the uptake ofhemin, has been identified on the surface ofL. interrogans[37] Although other pathogenic species ofLeptospira andL. biflexa lack HbpA, yet another hemin-binding protein, LipL41, may account for their ability to use hemin as a source of iron.[37] Although they do not secretesiderophores,L. biflexa andL. interrogans may be capable of obtaining iron from siderophores secreted by other microorganisms.[36]
The genome of pathogenicLeptospira consists of two chromosomes. The size of the genomes ofL. interrogans serovars Copenhageni and Lai is approximately 4.6 Mb.[38][39] However, the genome ofL. borgpetersenii serovar Hardjo is only 3.9 Mb in size with a large number of pseudogenes, gene fragments, andinsertion sequences relative to the genomes ofL. interrogans.[40]L. interrogans andL. borgpetersenii share 2708 genes from which 656 are pathogenic specific genes. Theguanine plus cytosine (GC) content is between 35% and 41%.[41]L. borgpetersenii serovar Hardjo is usually transmitted by direct exposure to infected tissues, whereasL. interrogans is often acquired from water or soil contaminated by the urine of carrier animals harboringLeptospira in their kidneys. The high number of defective genes and insertion sequences inL. borgpetersenii Hardjo together with the poor survival outside of the host and difference in transmission patterns compared toL. interrogans suggest thatL. borgpetersenii is undergoing insertion-sequence mediated genomic decay, with ongoing loss of genes necessary for survival outside of the host animal.[40]
Genome sequence determination several strains ofLeptospira lead to the development of multilocusVNTR (Variable Number of Tandem Repeats) typing andmultilocus sequence typing (MLST) for species level identification of pathogenicLeptospira species.[42] Both methods hold the potential to replace the highly ambiguousserotyping method currently in vogue for leptospiral strain identification.[42]
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^Stimson AM (1907). "Note on an organism found in yellow-fever tissue".Public Health Reports.22 (18): 541.doi:10.2307/4559008.JSTOR4559008.
^Bharti AR, Nally JE, Ricaldi JN, Matthias MA, Diaz MM, Lovett MA, Levett PN, Gilman RH, Willig MR, Gotuzzo E, Vinetz JM (2003). "Leptospirosis: a zoonotic disease of global importance".The Lancet Infectious Diseases.3 (12):757–71.doi:10.1016/S1473-3099(03)00830-2.PMID14652202.
^Levett PN, Morey RE, Galloway RL, Steigerwalt AG (2006). "Leptospira broomii sp. nov., isolated from humans with leptospirosis".Int. J. Syst. Evol. Microbiol.56 (Pt 3):671–3.doi:10.1099/ijs.0.63783-0.PMID16514048.
^Leptospira inLPSN;Freese, H. M.; Meier-Kolthoff, J. P.; Sardà Carbasse, J.; Afolayan, A. O.; Göker, M. (29 October 2025). "TYGS and LPSN in 2025: a Global Core Biodata Resource for genome-based classification and nomenclature of prokaryotes within DSMZ Digital Diversity".Nucleic Acids Research.53:D1–D12.doi:10.1093/nar/gkaf1110.
Data related toLeptospira at Wikispecies
