The life cycle of pathogenic leptospires can very in terms of the host species, but usually follows the sequence below:-
Entry to a host
The bacteria enter a host via portals such as damaged skin, certain mucous membranes, the lungs and conjunctival membranes. They are not thought capable of penetrating undamaged skin except where it has been exposed to water and has swollen significantly. Transfer to the portal requires the bacteria to be enveloped in water and so normally involves direct contact with urine or water containing the bacteria in suspension. Entry via the lungs requires inhalation of aerosol droplets and not the bacteria alone. Leptospires cannot exist as spores or reactivate once dessicated in the natural environment.
Once within the host tissues, pathogenic strains can reproduce as they are optimised for metabolism at body temperatures. Their survival depends on the lack of an efective host immune response, but they do not seem to cause an inflammatory reaction and so in a host without adapted immunity the chances of being able to establish a positive growth curve are high. In virulent strains the bacteria are resistant to attack from the innate immune system and so can develop rapidly, until the adaptive system has a change to select and replicate a cognate antibody. Saphrophytes, and the pathogens that are less virulent, seem to be easily targeted by the innate immune system and so are eliminated.
Leptosires that survive entry and the immediate innate response will rapidly migrate to the bloodstream and lymphatic system, so spreading throughout the host body within a very short time. Avirulent strains are rapidly removed by the immune system, but the speed of spread is far higher than in other bacterial infections and a host can show leptospira within blood samples in a matter of minutes from exposure. Pathogenic bacteria reproduce by binary fission, so the colony increases exponentially, and the typical doubling time is 8 hours. The growth continues unchecked until the adaptive immune response develops or the host dies.
A strain is virulent if it is adapted to reproduce rapidly in-vivo and has resistance to the innate immune response. No fully-resistant strains exist, so the adaptive response is always able to select a cognate antibody given ehough time. Virulence is directly related to pathogenicity – the host suffers illness because of the sheer number of leptospires in their body, not to any specifically-developed killing mechanism employed by different strains.
One of more species in the environment will maintain the bacteria as a viable population, via urinary shedding. Reservoir hosts are carrier-state species and so are usually not clinically ill, or have a sufficiently short natural life that the infection has no bearing on host populations. Rats are the main reservoir host but other rodents, marsupials and feral mammals are known to perform the function. Humans are not capable of becoming carrier-state and so are incidental to the bacterial life cycle. Reservoir hosts can cross-infect each other via urine or congenitally. Sexual transmission is known to occur in many species.
These are infected either directly from carrier-state hosts through contact with urine, or via the environment where urine from infected hosts has been able to remain viable in water or soil. Non-carrier hosts are a mistake in the bacterial ecosystem as for genetic dissemination the bacteria of course prefer a host that will survive for as long as possible and shed as many bacteria as possible – non-carrier hosts often die from their illness and tend to be less efficient urinary shedders while they are still alive. However leptospires cannot tell which hosts they are infecting, and so many species pay the price simply by being in the wrong place at the wrong time.
Reservoir hosts for leptospirosis are often non-migratory, and even territorial. This means that leptospiral genetic diversity in a local area can remain static, and this local cultivation is one of the reasons for such a large number of serovars and their frequent localisation. However the acute infection of non-reservoir hosts that do cross territorial boundaries allows for bacterial transfer and the slow migration of serovars across continents. Since birds seem unable to carry leptospirosis the speed of spread is far smaller than with other infections (such as avian infuenza) and for isolated places such as islands the leptospiral diversity can be fixed, or on occasion the bacteria can be completely absent. Since leptospires reproduce via binary fission there is no DNA combination between serovars or the host and the development of new serovars via mutative virulence selection is slow.
Survival outside the host
Pathogenic leptospires will survive in many environments for an extended time, lasting months or years, so allowing reinfection of animal hosts. The environmental conditions for survival are quite narrow and so the bacteria tend not to be as significant a problem ex-vivo as other bacteria or viruses.
Broadly, leptospires are of two types – saphrophytes living in freshwater and using organic material as a food supply but not requiring a host, and pathogens that require a host. The metaphysical reason that pathogens require a host is debatable, as of course the saphrophytes prove that the bacteria can do perfectly well without one, but spread is enhanced by hitching a ride within a host animal, and pathogens have clearly evolved because of a nett benefit to their mode of operation.
In the past it was believed that leptospires ‘switched’ from one form into another, depending on where they found themselves. Saphrophytes entering a host’s tissues became pathogenic, then when excreted back into water they converted to saphrophytes again. This is known not to be true, but there is an important blurring of the line and a conversion process at play in other areas.
Firstly, saphrophytes can enter the body of a host just the same as pathogens, but are unable to exploit the conditions and reproduce rapidly. As such they are removed by the innate immune system within a few minutes and cause no long-term illness – however they can trigger an adaptive immune response and this is believed to be the reason that many aquatic species are immune to pathogenic infection – such as fish and amphibians. Many such species will show antibodies to saphrophyte-sourced antigens that are also cognate with antigens from pathogens.
Secondly, a pathogenic baterium that is cultured outside a host will gradually lose virulence, as genetic mutations alter the colony. Passing the culture through a host will select out the most virulent individuals, using the host’s immune system as a filter, and this is used to preserve and concentrate lab samples. In the natural environment the same process occurs and so a colony of pathogenic bacteria in a body of water will gradually lose their ability to cause disease.