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Apa itu penyakit Kencing Tikus(Pathogenic Leptospires)

Penyakit kencing tikus atau Leptospirosis (juga dikenali sebagai, penyakit/sindrom Weil, demam canicola, demam ladang tebu, demam 7-hari  merupakan penyakit berjangkit zoonosis yang berpunca daripada spirochaete dalam genus Leptospira yang menjejaskan manusia dan sejumlah besar haiwan, termasuk mamalia, burung, afimbia, dan reptilia. Penyakit ini pertama kali digambarkan oleh Adolf Weil pada tahun 1886 apabila dia melaporkan “penyakit jangkitan akut dengan bengkak spleen (“splenomegaly”), penyakit kuning dan nephritis”. Leptospira pertama kali dilihat pada 1907 dari hirisan buah pinggang bedah siasat. Pada 1908, Inada dan Ito pertama kali mengenal pasti ia sebagai organisma penyebab  dan pada 1916 menyedari kehadirannya pada tikus.

Sungguhpun diakui sebagai antara zoonosis paling biasa di dunia, leptospirosis merupakan jangkitan bakteria jarang berlaku pada manusia. Jangkitan biasanya dipindahkan kepada manusia apabila air yang dicemari dengan air kencing haiwan menyentuh bukaan pada kulit, mata, atau dengan selaput lendir. Di luar kawasan tropika, kes leptospirosis berlaku mengikut musim dan kebanyakannya berlaku sekitar bulan Ogos–September/Februari–March.

Punca

Leptospirosis disebabkan oleh bakteria spirochaete yang dikenali sebagai Leptospira yang sekurang-kurangnya terdapat dalam 5 serovar kepentingan di Amerika Syarikat dan Kanada menyebabkan penyakit pada anjing (Icterohaemorrhagiae, Canicola, Pomona, Grippotyphosa, dan Bratislava)[5]. Terdapat jangkitan jenis lain (yang jarang). Secara genetik organisma leptospira berlainan boleh dikenal pasti secara serologi dan sebaliknya. Dengan itu, pertelingkahan wujud berkenaan asas mengenal pasti jenis. Sistem serologi tradisi kelihatannya lebih berguna dari segi diagnostik dan epidemiologi pada masa ini (yang mungkin berubah dengan pembangunan lanjut dan perkembangan teknologi seperti PCR – polymerase chain reaction).

Leptospirosis disebarkan melalui kencing haiwan yang dijangkiti dan berjangkit selagi ia masih lembab. Sungguhpun tikus, dan mondok merupakan hos utama, sejumlah besar mamalia lain termasuk anjing, rusa, arnab, landak, lembu, biri-biri, rakoon, possum, skunk, dan mamalia laut tertentu mampu membawa dan menyebarkan penyakit sebagai hos kedua. Anjing mungkin menjilat kencing haiwan yang dijangkiti dari rumput atau tanah, atau minum dari lopak yang dijangkit. Terdapat laporan “anjing rumah” dijangkiti leptospirosis kelihatannya kerana menjilat kencing tikus yang dijangkiti yang memasuki rumah. Jenis habitat yang berkemungkinan membawa bacteria berjangkit adalah tebing sungai berlumpur, terusan, longkang, dan kawasan peliharaan ternakan berlumpur di mana terdapat laluan biasa bagi samaada mamalia liar atau ladang. Terdapat kaitan langsung antara jumlah air hujan dan kejadian leptospirosis, menjadikannya bermusim di kawasan serdahana dan sepanjang tahun di kawasan bercuaca tropika.

Leptospirosis turut disebarkan melalui air mani haiwan dijangkiti.Pekerja rumah penyembelihan boleh dijangkiti melalui sentuhan dengan cecair badan dan darah.

Manusia boleh dijangkiti melalui hubungan dengan air, makanan, atau tanah yang mengandungi kencing haiwan yang dijangkiti ini. Ini mungkin berlaku dengan menelan makanan atau air yang dicemari, atau melalui sentuhan luka pada kulit. Penyakit ini tidak diketahui berjangkit dari manusia ke manusia dan kes penyebaran bacteria pada mereka yang sedang sembuh amat jarang bagi manusia. Leptospirosis biasa berlaku dikalangan peminat sukan air di kawasan tertentu kerana lama berendam diketahui menggalakkan kemasukan bakteria. Peluncur dan pengayuh air berbuih (“whitewater”) adalah berisiko tinggi di kawasan yang diketahui mempunyai bacteria, dan boleh dijangkit dengan menelan air tercemar Leptospirosis, menyimbah air tercemar Leptospirosis pada mata atau hidung, atau atau luka terdedah kepada air yang dijangkiti. Pekerjaan berisiko termasuk veterinarian, pekerja penyembelihan, petani, pekerja kumbahan, dan mereka yang bekerja di rumah tinggal, pendayung juga kadang-kala diketahui turut dijangkiti penyakit tersebut.

Simptom

Jangkitan Leptospiral pada manusia menyebabkan sejumlah symptom, dan sesetengah mereka yang dijangkiti mungkin tidak menunjukkan sebarang symptom sama sekali. Leptospirosis merupakan penyakit dwifasa (“biphasic”) yang bermula dengan simptom seperti selsema (demam, sejuk, myalgia, sakit kepala yang kuat). Fasa pertama sembuh, dan pesakit tanpa symptom (“asymptomatic”) sehingga fasa kedua bermula. Ini berciri meningitis, kerosakan hati (menyebabkan demam kuning), dan kegagalan buah pinggang. Jangkitan ini sering kali salah diagnosis kerana symptom yang meluas. Ini mendorong kepada jumlah kes berdaftar yang jauh lebih rendah berbanding yang sebenarnya berlaku. Simptom leptospirosis termasuk demam tinggi, askit kepala yang teruk, sejuk, sakik otot, dan muntah-muntah, dan mungkin termasuk demam kuning, mata merah, sakit perut, cirit-birit, dan keradangan. Simptom bagi manusia hadir selepas 4–14 hari tempoh pengeraman.

Tempoh pengeraman (tempoh pendedahan kepada symptom pertama bagi haiwan antara 2 hingga 20 hari. Bagi anjing kerosakan hati dan buah pinggang merupakan paling biasa oleh leptospirosis. Vaskulitis boleh berlaku, menyebabkan lebam/edema dan berkemungkinan pembekuan dalam salur darah tersebar (disseminated intravascular coagulation -DIC). Myocarditis, pericarditis, meningitis, dan uveitis juga turutan yang mungkin.Leptospirosis perlu disyaki dan dimasukkan sebagai sebahagian diagnosis pembezaan sekiranaya mata putih bagi anjing kelihatan jaundice (walaupun sedikit kekuningan). Ketiadaan jaundice tidak menyingkirkan kemungkinan leptospirosis sepenuhnya, dan kehadirannya mungkin menunjukkan hepatitis atau pathologi hati lain dan bukannya leptospirosis. Muntah-muntah, demam, hilang selera makan, kurang kencing, kencing gelap atau perang luar biasa, dan lesu juga merupakan tanda-tanda penyakit.

Komplikasi

Komplikasi termasuk meningitis, kelesuan melampau, kehilangan pendengaran, masaalah pernafasan, azotemia, dan masaalah buah pinggan (“renal interstitial tubular necrosis”, yang menyebabkan kegagalan buah pinggang dan sering kali kegagalan hati (bentuk penyakit ini yang teruk dikenali sebagai Penyakit Weil, sunggupun ia turut dikenali sebagai Sindrom Weil). Masaalah kardiovaskular juga mungkin.

SUMBER DARI WIKIPEDIA

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Life cycle of pathogenic leptospires

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.
Growth

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.


Reservoir hosts

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.
Non-carrier hosts

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.
Colony transfer

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.
Virulence changes

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.


Persistent human leptospirosis – guide for the public

Persistent infection is a situation where the patient has recovered from an acute illness, but shows some long-term health effects caused by the bacteria remaining in isolated areas of the body, long after the immune system has removed them from the bloodstream and general tissues. It is different from a carrier state as the patient is not infectious to others, but persistent human leptospirosis (PHL) is far more common than previously thought.

These long-term issues are not only a factor of leptospirosis – other infections from bacteria in the same order, such as Lyme disease, often show health problems for several years after recovery.
Symptoms of PHL

Symptoms vary a great deal between patients, with some being almost incapacitated and others noticing nothing. The reported symptoms are listed below, with the most common first:-

1. Depression, from mild personality changes to quite severe clinical disorders and suicides.
2. Fatigue, often quite pronounced and debilitating
3. Headaches, resembling migraines but not always particularly severe.
4. Eye pain, with or without any inflammation, sometimes with vision disturbances.
5. Psychological changes, including mood swings, short tempers, rarely OCD.
6. PIEM, parainfectious encephalomyelitis, is seen in quite a few cases. This is damage to the nervous system and manifests in different ways, so patients can show symptoms of meningitis, epilepsy, balance problems, muscle weakness and vision disturbance. It can mimic the symptoms of multiple sclerosis.

Causes of PHL

There are two reasons for ill health following a bacterial infection:-
Tissue damage

During the acute illness, bacteria cause damage to tissues in the patient’s body, by a combination of toxins and damage to the blood supply. This can lead to long-term changes in the function of internal organs but is not directly related to the bacteria, only to the damage they cause. Reduction in function of the liver and kidneys is one such outcome, but where the tissue damage is not too severe the body will heal over time.
Bacterial residency

In the body there are certain places, called immunologically privileged sites (IPSs) where the immune system is not very active, and bacteria can survive long after they have been killed in the rest of the body. These sites are usually places without a direct blood supply, such as the fluids within the eyeball and the structures of the brain and nervous system. In the rest of the body, the patient’s immune system reacts to leptospires and creates antibodies that will ensure they are killed within a few days, however in IPSs the supply of these antibodies, and the white blood cells that do the killing, are reduced. Bacteria can ‘hide’ in these sites but are kept trapped by the active immune system, so the symptoms tend to be concentrated on the same organs. We have very little direct evidence for the time bacteria can survive in this way, but it is certainly several months or years.

While they are present, leptospires in IPSs have two effects – they still leak toxins into the tissues, albeit at a quite low level, and this can cause slight inflammation or reduction in tissue viabililty. More importantly they can continually trigger the immune system at the border of the IPS, and the immune response to this constant prodding of white blood cells can be more severe than is required – in some cases it will cause an autoimmune response where the body’s immune system starts to attack ‘self’. It’s common for patients with PHL to show unexpected severe symptoms when exposed to leptospires a second time, as the autoimmune response is activated. It’s particularly true in the eyes and is the cause of recurrent symptoms in horses.


Treatment

There is no working treatment for PHL at this time which has shown itself to be effective on every patient – research conducted in recent years has shown promise in developing an immunological treatment program, however in the majority of cases supportive care is given. Maintaining a healthy diet with full nutritional balance is very important, and symptoms can be treated in isolation (with painkillers, etc.) but in many cases a repeat program of antibiotics has been able to increase the speed of recovery. The difficulty is that medication will only act on the persistent bacteria, and so any long-term tissue damage caused by the infection will need to heal at a natural rate – this can take several years and in severe infections there can be some permanent damage to tissues. Patients suffering poor helth after a leptospirosis infection should always discuss the issue of PHL with their physician, if necessary via a referral to a specialist in infectious and autoimmune disease. The symptoms are expected to reduce over time even without treatment, and so in many patients with only minor reduction in health it can simply be a waiting game.

sumber : http://www.leptospirosis.org/

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HUBUNGI SAYA UNTUK MAKLUMAT LEBIH LANJUT DI=

0163153132 (Zaidah)

August 4, 2010 - Posted by | 4LIFE, artikel | , , , , , , , , , , , ,

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