11. spirochetes

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11. spirochetes

  1. 1. SpirochetsSpirochetsARUNI.I.S,ReaderDept of MicrobiologyNoorul Islam Institute of Medical ScienceTrivandum
  2. 2. Spirochetes are elongated, motile, flexibleSpirochetes are elongated, motile, flexiblebacteria twisted spirally alone the long axis.bacteria twisted spirally alone the long axis.Motile withMotile with endoflagellaendoflagella..Human pathogens are found in 3 genera:Human pathogens are found in 3 genera:TreponemaTreponemaBorreliaBorreliaLeptospiraLeptospiraSpirochetesSpirochetes
  3. 3. TreponemaTreponema
  4. 4.  Some of theSome of the Treponema speciesTreponema species are pathogensare pathogenswhile others occur as commensals in thewhile others occur as commensals in themouth, intestine and genitalia.mouth, intestine and genitalia. Causes the following diseases in humans:Causes the following diseases in humans:1.1. Venereal syphilis by T.pallidumVenereal syphilis by T.pallidum2.Endemic syphilis T.pallidum(T.endemicum)2.Endemic syphilis T.pallidum(T.endemicum)3.Yaws by T.pertenue3.Yaws by T.pertenue4. Pinta by T.carateum4. Pinta by T.carateumTreponemaTreponema
  5. 5. Treponema pallidumTreponema pallidum Causative agent ofCausative agent of SyphilisSyphilis.. Name pallidum refers to it’s pale staining.Name pallidum refers to it’s pale staining. Delicate spirochete withDelicate spirochete with active motilityactive motility.. Thin with tapering ends.10 mm long & 0.1-0.2 mm wide.Thin with tapering ends.10 mm long & 0.1-0.2 mm wide. Morphology and motility can be seen under theMorphology and motility can be seen under the darkdarkground or phase contrast microscopeground or phase contrast microscope.. Can be stained by Silver impregnation methodCan be stained by Silver impregnation method Very delicateVery delicate and highly susceptible to heat.and highly susceptible to heat. Do not grow in artificial culture media, but possible byDo not grow in artificial culture media, but possible by co-co-cultivationcultivation with tissue culture cells.with tissue culture cells. Natural infection occur only inNatural infection occur only in human beingshuman beings..
  6. 6.  Antigenic structure:Antigenic structure: 3 types of antigens are seen in3 types of antigens are seen in TreponemaTreponema::a)a) Cardiolipin antigenCardiolipin antigen present inpresent in T.pallidumT.pallidum againstagainstwhich reagin Abs are producedwhich reagin Abs are producedb)b) AA group specific antigengroup specific antigen present inpresent in T.pallidumT.pallidum asaswell as non-pathogenic Reiter strain of Treponema.well as non-pathogenic Reiter strain of Treponema.c)c) AA species specific polysaccharidespecies specific polysaccharide present inpresent inpathogenic strain ofpathogenic strain of TreponemaTreponema..
  7. 7. SYPHILISSYPHILISCaused by Treponema pallidumCan enter any mucous membrane or break in the skin,can be spread by kissing and close contact
  8. 8. SYPHILISSYPHILISNONOSYMPTOMSSYMPTOMSUp to 50% of people don’t know they have it.Symptoms may be mild or painless ornearly invisible.
  9. 9.  Organism enters the body through cuts or abrasion on the skinOrganism enters the body through cuts or abrasion on the skinor mucosa during sexual contact.or mucosa during sexual contact. IP is about a month(range 10-90 days)IP is about a month(range 10-90 days) 3stages of venereal syphilis3stages of venereal syphilis Primary:Primary: chancre, disappears spontaneously.chancre, disappears spontaneously. Secondary:Secondary: penetrate mucus membranes, enter blood-stream,penetrate mucus membranes, enter blood-stream,fever, rash.fever, rash. Tertiary:Tertiary: invade heart, musculoskeletal system, CNS, relativelyinvade heart, musculoskeletal system, CNS, relativelynoninfectious.noninfectious.PathogenesisPathogenesis
  10. 10. 11ststStage SYPHILIS(Primary)Stage SYPHILIS(Primary)10 to 90 days after contact, painless, avascular, induratedsuperficially ulcerated lesion may appear, called hard chancres.It occurs at the site of entry of the bacteria – genital organs,mouth , nipples- and heals spontaneously after 10-40 days.They can appear ANYWHERE that the spirochetesentered a mucous membrane or break in the skin.penisfingertonguecervixvulva
  11. 11.  The chancre is covered by a thick ,glairyThe chancre is covered by a thick ,glairyexudate ,rich in spirochetesexudate ,rich in spirochetes The regional lymph nodes are swollenThe regional lymph nodes are swollen Even before the chancre appears, theEven before the chancre appears, thespirochetes spread from the site of entry in tospirochetes spread from the site of entry in tolymph & blood streamlymph & blood stream So the patient may be infectious during the lateSo the patient may be infectious during the lateincubation periodincubation period The chancre heals in 10-40 days ,even with outThe chancre heals in 10-40 days ,even with outtreatment, leaving a thin scartreatment, leaving a thin scar Persistent or multiple chancre may be seen inPersistent or multiple chancre may be seen inHIV & othe immunodeficient patiensHIV & othe immunodeficient patiens
  12. 12. 22ndndStage SYPHILIS(Secondary)Stage SYPHILIS(Secondary)Symptoms appear 2 weeks to 6 months after primary lesion.Characterized by papular skin rashes, mucous patches inoropharynx and condylomata at the mucocutaneous junctions.Patient is highly infectious and these signs disappear withouttreatment.• Rash on hands• Rash over entire body • Lesions of tongue• Rash on feet•Lesions around mouth
  13. 13. ORAL MANIFESTATIONSORAL MANIFESTATIONSThe oral lesions are usuallyThe oral lesions are usuallymultiple,painless. Greenish white plaguesmultiple,painless. Greenish white plaguesoverlying an ulcerated surfaceoverlying an ulcerated surfaceThese are called mucous patchesThese are called mucous patchesThey occur mostly on the tongue, buccalThey occur mostly on the tongue, buccalmucosa or gingivamucosa or gingivaThese lesions are highly infectious as theyThese lesions are highly infectious as theycontain a large number of microorganismscontain a large number of microorganisms
  14. 14. Oral lesion in Secondary SyphilisOral lesion in Secondary Syphilis
  15. 15.  Spirocetes are abundant in the lesions & the patient isSpirocetes are abundant in the lesions & the patient ismost infectious during the secondary stage.most infectious during the secondary stage. The lesions undergo spontaneous healing ,in someThe lesions undergo spontaneous healing ,in someinstances taking as long as 4 or 5 yearsinstances taking as long as 4 or 5 years After the secondary lesion disappears, there is a periodAfter the secondary lesion disappears, there is a periodof quiescence known as latent syphilis.of quiescence known as latent syphilis. Diagnosis during this period is possible only by serologyDiagnosis during this period is possible only by serology In many cases this is followed by natural cure, but inIn many cases this is followed by natural cure, but inothers after several years, manifestations of Tertiaryothers after several years, manifestations of Tertiarysyphilis appearssyphilis appears
  16. 16. 33rdrdStage SYPHILIS(Tertiary)Stage SYPHILIS(Tertiary)The period after the healing of the 2ry lesions- latent syphilis.Occur after several years and diagnose serologically.Damages heart and aorta, causeshardening, distortion, ulceration….canlead to rupture, hemorrhaging and death.Brain damage and infection, causesheadaches, dizziness, blurred vision,paralysis, and can lead to insanity.Skin Damage, causes “gummata”, largeopen sores which are slow to heal.Syphilis can also damage the bones.
  17. 17. CONGENITSAL SYPHILISCONGENITSAL SYPHILISSyphilis is transmitted fromthe mother to the baby troughthe placenta.The more recent the infection,especially during the pregnancy, themore damaging to the baby.COMPLICATIONS:Miscarriage Enlarged liver and spleenStillbirth HydrocephalusMeningitis Mental RetardationConvulsions Sever Skin RashesBlindness DeafnessDeformities of face, nose, teeth, jaw, leg bones
  18. 18. Laboratory DiagnosisLaboratory Diagnosisa)a) Microscopy:Microscopy: wet films of exudates examinedwet films of exudates examinedunder the dark ground microscope.under the dark ground microscope.b)b) Serology:Serology:1)1) Reagin antibody test: tests for antibodiesReagin antibody test: tests for antibodiesreacting with cardiolipin antigen and arereacting with cardiolipin antigen and areknown asknown as standard test for syphilis (STS).standard test for syphilis (STS).i.i. Wasserman complement fixation testWasserman complement fixation testii.ii. Khan flocculation testKhan flocculation testiii.iii. VDRL / RPR testVDRL / RPR test
  19. 19. 2)2) Group specific treponemal tests - Here cultivableGroup specific treponemal tests - Here cultivabletreponems (Reiter strain) used as antigen.treponems (Reiter strain) used as antigen.Reiter Protein Complement Fixation Test(RPCF)Reiter Protein Complement Fixation Test(RPCF)3)3) SpecificSpecific T.pallidumT.pallidum test - Here virulent Nichol’s strainstest - Here virulent Nichol’s strainsofof T.pallidumT.pallidum is used as antigen.is used as antigen.i.i. T.pallidumT.pallidum immobilization (TPI) testimmobilization (TPI) testii.ii. Fluorecent treponemal antibody (FTA) testFluorecent treponemal antibody (FTA) testiii.iii. T.pallidumT.pallidum Haemagglutination (TPHA) testHaemagglutination (TPHA) test EIA for Treponemal antibody detectionEIA for Treponemal antibody detection CSF VDRL is used for neurosyphilisCSF VDRL is used for neurosyphilis
  20. 20. Prophylaxis & TreatmentProphylaxis & TreatmentAvoid sexual contact with an infectedAvoid sexual contact with an infectedindividual.individual.Use of physical barriers, antiseptics orUse of physical barriers, antiseptics orantibiotics may minimise the risk.antibiotics may minimise the risk.Chemoprophylaxis by penicillin.Chemoprophylaxis by penicillin.No vaccine is available.No vaccine is available.Treatment by Penicillin G, Erythromycin,Treatment by Penicillin G, Erythromycin,
  21. 21. Non-venereal TreponemesNon-venereal Treponemes Organisms closely resemblesOrganisms closely resembles T.pallidumT.pallidum but do not causesbut do not causesVD.VD. Transmission occurs through direct body to body contactTransmission occurs through direct body to body contactamong people of unhygienic practices.among people of unhygienic practices. Important non-venereal infections include:Important non-venereal infections include:Endemic syphilisEndemic syphilisYawsYawsPintaPinta
  22. 22. Endemic SyphilisEndemic Syphilis Causative agent isCausative agent is T.endemicum.T.endemicum. Common in children of poor personal hygiene.Common in children of poor personal hygiene. Infection can also be seen on the nipples of the mother infected byInfection can also be seen on the nipples of the mother infected byher children.her children. Usually seen with the manifestations of secondary syphilis such asUsually seen with the manifestations of secondary syphilis such asmucous patches & skin eruptionsmucous patches & skin eruptions The disease may progress to gummatous lesions on the skin, boneThe disease may progress to gummatous lesions on the skin, boneand nasopharynyx.and nasopharynyx. Laboratory diagnosis and treatment are same as venereal syphilis.Laboratory diagnosis and treatment are same as venereal syphilis.
  23. 23. YawsYawsIn India, it has been reported from Orissa,In India, it has been reported from Orissa,Andra Pradesh and Madhya Pradesh.Andra Pradesh and Madhya Pradesh.Like in syphilis, the primary lesion isLike in syphilis, the primary lesion isfollowed by secondary and tertiaryfollowed by secondary and tertiarymanifestations.manifestations. Causative agent isCausative agent is T.pertenue.T.pertenue. The primary lesion in yaws is anThe primary lesion in yaws is anextra-genital papula which breaksextra-genital papula which breaksdown to form an ulceratingdown to form an ulceratinggranuloma.granuloma.
  24. 24. PintaPinta Causative agent isCausative agent is T.carateum.T.carateum. Disease is seen mainly in central and south America.Disease is seen mainly in central and south America. Infection occurs by direct person to person contact.Infection occurs by direct person to person contact. The primary lesion is an extra-genital papule.The primary lesion is an extra-genital papule. Hypopigmentation or hyperpigmentation is seen.Hypopigmentation or hyperpigmentation is seen. Laboratory diagnosis and treatment are similar asLaboratory diagnosis and treatment are similar asT.pallidum.T.pallidum.
  25. 25. BorreliaBorrelia
  26. 26. BorreliaBorreliaMicroaerophilic-to-anaerobicMicroaerophilic-to-anaerobic Loose, irregular coilsLoose, irregular coils In vitroIn vitro cultivation is difficultcultivation is difficult Visualization byVisualization byGiemsa stainGiemsa stainGram staining-Gram negativeGram staining-Gram negativeSilver stainingSilver stainingDark field microscopyDark field microscopy Highly adapted to arthropod transmissionHighly adapted to arthropod transmission
  27. 27.  Antigenic variationBorrelia undergoes antigenic variations in vivoand is found to be the cause of relapses in thediseases.Recovery from the disease is believed to be dueto the development of immunity to thesesantigenic variants.
  28. 28.  Species of medical importance:Species of medical importance:B.recurrentisB.recurrentis – Relapsing fever– Relapsing feverB.vincentiB.vincenti – Fusospirochetosis(Vincent’s– Fusospirochetosis(Vincent’sangina)angina)B.burgdorferiB.burgdorferi – Lyme disease– Lyme disease
  29. 29.  This Acute infection is caused byThis Acute infection is caused by B.recurrentisB.recurrentis.. Sudden onset with fever, septicemia, headache, muscle pain.Sudden onset with fever, septicemia, headache, muscle pain. After 3-5 days, fever subsides and during this afebrile period ofAfter 3-5 days, fever subsides and during this afebrile period of4-19 days borreliae are not found in the blood.4-19 days borreliae are not found in the blood. After a afebrile period when another bout of fever sets in,After a afebrile period when another bout of fever sets in,borreliae reappear in blood.borreliae reappear in blood. Patient returns to normal, after 4-10 relapses.Patient returns to normal, after 4-10 relapses. Sporadic in US, distributed worldwide.Sporadic in US, distributed worldwide.Relapsing Fever
  30. 30. Transmitted animal-to-animal, animal-to-Transmitted animal-to-animal, animal-to-human by ticks, human-to-human by bodyhuman by ticks, human-to-human by bodylice.lice.Causative agents:Causative agents:Louse borne diseaseLouse borne disease :: B. recurrentisB. recurrentisTick borne diseaseTick borne disease :: B.duttonii, B.hermsii,B.duttonii, B.hermsii,B.parkeriB.parkeri etc.etc.
  31. 31. Relapsing fever- 2 types:Relapsing fever- 2 types:Tickborne RFTickborne RFTransmitted by soft ticks (genusTransmitted by soft ticks (genusOrnithodorosOrnithodoros))O. turicatae, O. parkeri, O. hermsiO. turicatae, O. parkeri, O. hermsi in US,in US,15 others worldwide15 others worldwideLouseborne RFLouseborne RFBody / head / pubic lice (Body / head / pubic lice (Pediculus humanusPediculus humanuscorporis / capitis / pubiscorporis / capitis / pubis))Also by bed bugs.Also by bed bugs.
  32. 32.  Laboratory diagnosis:Laboratory diagnosis: Microscopy:Microscopy:Light microscopy- Giemsa / Leishman stain.Light microscopy- Giemsa / Leishman stain.Silver stainingSilver stainingDark ground microscopy.Dark ground microscopy. Culture:Culture: too difficult to grow.too difficult to grow. Animal inoculationAnimal inoculation: into white mouse.: into white mouse. Serology:Serology: not reliable.not reliable.
  33. 33.  It is an ulcerativeIt is an ulcerative gingivostomatitisgingivostomatitis oror oropharyngitisoropharyngitiscaused bycaused by Borrelia vincentiBorrelia vincenti.. B.vincentiB.vincenti is a normal mouth commensal motileis a normal mouth commensal motilespirochete, about 5-20spirochete, about 5-20 μμm wide, with 3-8 coils ofm wide, with 3-8 coils ofvariable size.variable size. It is a normal mouth commensal ,but under certainIt is a normal mouth commensal ,but under certainpre disposing condition(malnutrition ,viral infection)pre disposing condition(malnutrition ,viral infection)give rise to ulcerative gingivo stomatitis orgive rise to ulcerative gingivo stomatitis ororophangitis(Vincent’s angina)orophangitis(Vincent’s angina) In this infection,In this infection, B.vincentiB.vincenti is associated withis associated withfusiform bacilli and this symbitic infection is knownfusiform bacilli and this symbitic infection is knownasas fusospirochetosisfusospirochetosis..Vincent’s AnginaVincent’s Angina
  34. 34. DiagnosisDiagnosis may be made by demonstratingmay be made by demonstratingspirochetes and fusiform bacilli in stainedspirochetes and fusiform bacilli in stainedsmears of exudates form the lesions.smears of exudates form the lesions.TreatmentTreatment-- Penicillin & metronidazolePenicillin & metronidazole
  35. 35. Lyme DiseaseLyme Disease First observed in 1975, in Old Lyme, USA.First observed in 1975, in Old Lyme, USA. Caused byCaused by Borrelia burgdorferiBorrelia burgdorferi.. Incubation period: 7 - 14 days (range 3 - 30 days).Incubation period: 7 - 14 days (range 3 - 30 days). Infection may be sub-clinical, manifest onlyInfection may be sub-clinical, manifest onlynonspecific symptoms: fever, headache, myalgia.nonspecific symptoms: fever, headache, myalgia. Most prevalent human tick-borne disease in theMost prevalent human tick-borne disease in theUS, Europe, parts of Asia.US, Europe, parts of Asia.
  36. 36. EpidemiologyEpidemiologyHuman encroachment into habitat of white-Human encroachment into habitat of white-tailed deer.tailed deer.Spread from deer, mice to humans by theSpread from deer, mice to humans by the bitebiteof soft ticksof soft ticks (genus(genus Ixodes)Ixodes)
  37. 37.  First stage:First stage: Erythema migransErythema migrans spirochetes multiply in skin, quickly enter circulationspirochetes multiply in skin, quickly enter circulation rashrash appears days-to-weeks after tick biteappears days-to-weeks after tick bite surround site of inoculation, expand insurround site of inoculation, expand in concentric ringsconcentric rings disappear spontaneously after several weeksdisappear spontaneously after several weeks
  38. 38. Second stage:Second stage: disseminated infectiondisseminated infectionassociated with fever, headache, myalgia,associated with fever, headache, myalgia,arthralgia and lymphadenopathy.arthralgia and lymphadenopathy.Musculoskeletal signs (migratory joint, muscleMusculoskeletal signs (migratory joint, musclepains), CNS signs, cardiac damage may alsopains), CNS signs, cardiac damage may alsoappear.appear.
  39. 39. Third stageThird stage of persistent infection,of persistent infection, occurringoccurringmonths or years latermonths or years later..Develops chronic arthritis, polyneuropathy,Develops chronic arthritis, polyneuropathy,encephalopathy, etc.encephalopathy, etc.Symptoms include arthritis, facial palsy andSymptoms include arthritis, facial palsy andmeningitis.meningitis.
  40. 40. 45Borrelia burgdorferiBorrelia burgdorferi
  41. 41. 46Ixodes scapularis, tick vector for Lyme disease.
  42. 42. 47Lyme DiseaseLyme Diseaseerythematous rasherythematous rash
  43. 43. DiagnosisDiagnosis made be isolating the organismsmade be isolating the organismsform skin lesions, CSF, blood or by serology.form skin lesions, CSF, blood or by serology.Treatment:Treatment: Amoxycillin, doxycycline andAmoxycillin, doxycycline andcefuroxime.cefuroxime.Tick control important forTick control important for prevention.prevention.
  44. 44. LeptospirLeptospiraa
  45. 45. Leptospira are actively motile, delicateLeptospira are actively motile, delicatespirochetes, which can causespirochetes, which can cause Leptospirosis orLeptospirosis orWeil’s diseasesWeil’s diseases..
  46. 46. Leptospirosis is an acute zoonotic infection ofLeptospirosis is an acute zoonotic infection ofworldwide significance caused by spirochaeteworldwide significance caused by spirochaeteLeptospira interrogansLeptospira interrogans ..Various factors influencing the animal activity,Various factors influencing the animal activity,suitability of the environment for the survivalsuitability of the environment for the survivalof the organism and behavioral andof the organism and behavioral andoccupational habits of human beings can beoccupational habits of human beings can bethe determinants of incidence and prevalencethe determinants of incidence and prevalenceof the disease.of the disease.
  47. 47.  Leptospirosis, also known as canicola fever,Leptospirosis, also known as canicola fever,hemorrhagic jaundice, , mud fever, spirochetalhemorrhagic jaundice, , mud fever, spirochetaljaundice, swamp fever, swineherds disease, caversjaundice, swamp fever, swineherds disease, caversflu or sewermans flu.flu or sewermans flu. There is an acute form of human infection known asThere is an acute form of human infection known asWeils diseaseWeils disease, where the patient suffers from, where the patient suffers fromjaundice.jaundice. This condition is usually caused byThis condition is usually caused byL.L.icterohaemorrhagiaeicterohaemorrhagiae serogroup of L.serogroup of L.interrogansinterrogans
  48. 48. Leptospira interrogansLeptospira interrogans Leptospira appear tightly coiled thinLeptospira appear tightly coiled thinflexible Spirochetes with 5 – 15flexible Spirochetes with 5 – 15microns x 0.1 micron size.microns x 0.1 micron size. One end appears bent forms a hook.One end appears bent forms a hook. Actively motile.Actively motile. Seen best with dark fieldSeen best with dark fieldMicroscopy.Microscopy. 13 serogroups, >200 serovars13 serogroups, >200 serovars
  49. 49. Cultivation of LeptospiraCultivation of Leptospira Leptospira grows best underLeptospira grows best underaerobic conditions at 28aerobic conditions at 2800to 30to 3000ccand pH 7.2 – 7.5.and pH 7.2 – 7.5. EMJHEMJH (Ellinghausen,(Ellinghausen,McCullough, Johnson, Harris)McCullough, Johnson, Harris)mediamedia is commonly used.is commonly used. Other MediaOther Media Fletchers MediaFletchers Media..Optimal growth after 1 – 2 weeksOptimal growth after 1 – 2 weeks ..
  50. 50. എലിപ്പനിഎലിപ്പനി PathogenesisPathogenesis Rats, Mice, Wild Rodents, Dogs, Swine, Cattle areRats, Mice, Wild Rodents, Dogs, Swine, Cattle areprincipleprinciple source of infectionsource of infection.. The animals excrete Leptospira both in active infectionThe animals excrete Leptospira both in active infectionand Asymptomatic stage through urine.and Asymptomatic stage through urine. The Leptospira survive and remain viable for severalThe Leptospira survive and remain viable for severalweeks in stagnant water.weeks in stagnant water. Enter through cuts and abrasionsEnter through cuts and abrasions in the skin andin the skin andmucous membranes or through mouth, nose ormucous membranes or through mouth, nose orconjunctive.conjunctive.
  51. 51.  Man is the end host, and there is no evidence ofMan is the end host, and there is no evidence ofhuman to human infection.human to human infection. Incubation periodIncubation period 1 – 2 weeks1 – 2 weeks.. Multiplication of leptospires inMultiplication of leptospires in blood streamblood streamproducesproduces feverfever.. Establish organ involvement inEstablish organ involvement in Kidney and LiverKidney and Liver.. May produceMay produce hemorrhage and necrosishemorrhage and necrosis in the tissuesin the tissuesand initiatesand initiates dysfunctiondysfunction of these organs.of these organs.
  52. 52. PPaatthhooggeenneessiiss
  53. 53.  Clinical Pictures:Clinical Pictures: JaundiceJaundice HemorrhageHemorrhage Nitrogen retentionNitrogen retention TheThe Illness is BiphasicIllness is Biphasic with initial temperaturewith initial temperaturewhen the second phase comes with raise of IgMwhen the second phase comes with raise of IgMtiters raise.titers raise. Aseptic meingitisAseptic meingitis – initial headache, stiffness of– initial headache, stiffness ofneck, pleocytosis of Cerebro spinal fluid.neck, pleocytosis of Cerebro spinal fluid.
  54. 54.  ComplicationsComplications NephritisNephritis HepatitisHepatitis Manifestations in eyeManifestations in eye Muscular lesionsMuscular lesions Many infections are mild and subclinicalMany infections are mild and subclinical
  55. 55. Weil’s SyndromeWeil’s Syndrome Weils syndrome is a severe form of leptospirosis thatWeils syndrome is a severe form of leptospirosis thatcauses continuouscauses continuous fever, stuporfever, stupor & reduction in the& reduction in thebloods ability to clot, which leads tobloods ability to clot, which leads to bleeding withinbleeding withintissuestissues.. Blood tests reveal anemia.Blood tests reveal anemia. By the third to sixth day, signs ofBy the third to sixth day, signs of kidney damagekidney damage andandliver injuryliver injury appear.appear. Kidney abnormalities may causeKidney abnormalities may cause blood in the urineblood in the urineand painful urinationand painful urination.. Liver injury may be mild & usually heals completely.Liver injury may be mild & usually heals completely.
  56. 56. Hepatitis - LeptospirosisHepatitis - Leptospirosis Hepatitis is the frequent complication.Hepatitis is the frequent complication. Elevation of serum creatine phospholipaseElevation of serum creatine phospholipaseenzyme raise differentiates from Viral hepatitisenzyme raise differentiates from Viral hepatitiswhere the enzyme is not raised.where the enzyme is not raised.
  57. 57. Nephritis - LeptospirosisNephritis - Leptospirosis Kidney involvement in animals produce chronicKidney involvement in animals produce chronicdisease of the kidney and the infected animaldisease of the kidney and the infected animalstartsstarts shedding large number of leptospirashedding large number of leptospira andandmain source of environmental contamination ofmain source of environmental contamination ofbacteria and results in human infections.bacteria and results in human infections. Human urine also contain Spirochetes in theHuman urine also contain Spirochetes in thesecond and third week of infection.second and third week of infection.
  58. 58.  Laboratory diagnosis:Laboratory diagnosis: Specimen:Specimen: Blood, urine, CSF.Blood, urine, CSF. Blood examinationBlood examination is significant only in the early stage of theis significant only in the early stage of thedisease.disease. Urine examinationUrine examination is significant from second week onwardsis significant from second week onwardsup to 6 weeks.up to 6 weeks.Microscopy:Microscopy: Blood film / urine sediments under dark groundBlood film / urine sediments under dark groundmicroscope or by IF.microscope or by IF.Culture:Culture: Blood culture in EMJH medium.Blood culture in EMJH medium.Animal inoculation:Animal inoculation: Blood / urine into guinea pig.Blood / urine into guinea pig.Serology:Serology: Detection of antibodies by ELISADetection of antibodies by ELISA..
  59. 59. Prophylaxis:Prophylaxis: Rodent control, disinfection of water andRodent control, disinfection of water andwearing of protective clothing.wearing of protective clothing. Vaccination on trial basis.Vaccination on trial basis.Treatment:Treatment: Penicillin, Tetracycline, Doxycycline.Penicillin, Tetracycline, Doxycycline.
  60. 60. Thank youThank you
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