**3.1 Known virulence factors**

The emergence of the mutagenesis system revealed a small number of *Leptospira* genes that encode the components necessary for the manifestation of pathogenicity. The first leptospiral protein, identified as virulence, is Loa 22, and the outer membrane protein containing the C-terminal OmpA domain

**49**

**Figure 2.**

*Mechanism of Leptospira.*

*Leptospirosis: Rising Nuisance for Cattle and Threat to Public Health*

appears to mediate the connection between the outer membrane and the peptidoglycan layer (mutant hama loa 22). The presence of a homolog of Loa 22 in *L. biflexa* has an indirect effect on pathogenicity. Since lipopolysaccharide (LPS) is a pathogenic factor for all Gram-negative bacteria, it is not surprising that this hypothesis cannot be obtained until a certain mutant is identified in the *Leptospira*, studies eliminate motility by inactivating flagellated structures or genes involved in biosynthesis. Inactivation of fliY-encoding choleretic switching protein reduces toxicity in guinea pigs [29]. Mutations in the gene encoding the sensory protein LB139 reduce motility and down-regulation of a number of chemotactic genes and weaken the mutant for hamsters [30]. The lack of similar genes in vegetative bacilli strongly suggests the survival of mammalian species as well as in nutrition intake. Indeed, studies have shown toxicity related activities of *Leptospira* sphingomyelinase such as pore formation and cytotoxicity [31]. However, the key role of leptospiral sphingomyelinase in the pathogenesis is not genetically established. Recently, it has been shown that *Leptospira*-LruA [48] plays an important role in autoimmune response, which is associated with mam-

Transmission of *Leptospira* occurs often with direct contact with infected urine, placenta, or milk. Transmission through venereal or transplacental route is also possible, whereas the most common route is infected urine. If there are leptospiral infected animals present in a dairy farm, the environment is also contaminated. Dairy feeder calves are probably the largest carriers of *Leptospira* in commercial feed yards. Dairy calves have the habit of sucking the scrotum of other calves in the pen, so this would be direct contamination of infected urine from carriers by

suckling habit. *Leptospira* survives in the moist, damp, and moderately

warm environment and can be easily killed by freezing, dehydration, and direct

*DOI: http://dx.doi.org/10.5772/intechopen.82211*

malian apolipoprotein A1 [49].

**4. Transmission**

sunlight (**Figure 2**).

*Leptospirosis: Rising Nuisance for Cattle and Threat to Public Health DOI: http://dx.doi.org/10.5772/intechopen.82211*

appears to mediate the connection between the outer membrane and the peptidoglycan layer (mutant hama loa 22). The presence of a homolog of Loa 22 in *L. biflexa* has an indirect effect on pathogenicity. Since lipopolysaccharide (LPS) is a pathogenic factor for all Gram-negative bacteria, it is not surprising that this hypothesis cannot be obtained until a certain mutant is identified in the *Leptospira*, studies eliminate motility by inactivating flagellated structures or genes involved in biosynthesis. Inactivation of fliY-encoding choleretic switching protein reduces toxicity in guinea pigs [29]. Mutations in the gene encoding the sensory protein LB139 reduce motility and down-regulation of a number of chemotactic genes and weaken the mutant for hamsters [30]. The lack of similar genes in vegetative bacilli strongly suggests the survival of mammalian species as well as in nutrition intake. Indeed, studies have shown toxicity related activities of *Leptospira* sphingomyelinase such as pore formation and cytotoxicity [31]. However, the key role of leptospiral sphingomyelinase in the pathogenesis is not genetically established. Recently, it has been shown that *Leptospira*-LruA [48] plays an important role in autoimmune response, which is associated with mammalian apolipoprotein A1 [49].
