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LEPTOSPIROSIS
UPDATE
Dr Vasif MC
GMKMCH
• Zoonotic disease
• Caused by the spirochete Leptospira
• Historically known as Weil’s disease
• Described in 1885 by Adolf Weil with clinical hallmarks of
 splenomegaly
 jaundice
 nephritis
INTRODUCTION
SYNONYMS
THE CAUSATIVE BACTERIUM
Order Spirochaetales – Treponema, Borrelia, Leptospira
Family – Leptospiraceae, susceptible to heat, acid
Genus – Leptospira, 26 serogroups, 250 serovars
Pathogenic: Interrogans, Nonpathogenic: biflex
Corkscrew shaped, delicate, flexible spirochete, Gram -ve
thick, coiled, flagellate, actively motile
EPIDEMIOLOGY
• Incidence of Leptospirosis in developing countries is 10 - 100/1,00,000 cases/year
• Only four states (Kerala,Gujarat, Tamilnadu & Maharashtra) report more than
500 cases per year
• Incidence of Leptospirosis is 50 – 65 cases /100,000 per year in Andaman and
Nicobar Islands
• Prevalence rate of Leptospirosis reported
• 38.1% from Calicut
• 52.7% from Andaman and Nicobar Islands
• 32.9% from Chennai (data from asymptomatic persons detected during sero surveys)
• Leptospirosis is grossly under reported because of lack of awareness of the disease
and non availability of diagnostic tests
• Last outbreak reported in Mumbai during 2015
Organism disappears from blood but remains in
organs including brain , liver, lung, heart and
kidneys
Development of antibodies(5-7 days)
Proliferate in bloodstream and disseminate
hematogenously
Infects through mucosa ( conjunctival , oral) or
through punctured or abraded skin
PATHOGENESIS
Excreted in urine
Adhere to proximal tubule epithelial cells
Penetrate basement membrane of PCT
Traverse interstitial spaces of kidney
Hypovolaemic shock and vascular collapse
Loss of fluids into the third space
Vasculitis and leakage : petechiae , intra parenchymal
bleeding and bleeding along serosa and mucosa
Capillary vasculitis (endothelial necrosis and lymphocytic
infiltration)
Attach onto the endothelial cells
Produces endotoxin
•Clinical expression can be
Subclinical infection
Undifferentiated febrile illness
Weil’s disease
•Incubation period 2-30 days (average 5-14 days)
CLINICAL FEATURES
• The most severe form of leptospirosis
• Monophasic and fulminant
• Variable combinations of jaundice, acute kidney injury,
hypotension and hemorrhage
• Pulmonary hemorrhage is the most common
• Multisystem involvement occurs
WEIL’S DISEASE
• High index of suspicion is critical in a setting of
An appropriate exposure history
Infection’s protean manifestations
• Biochemical, hematological and urinalysis may suggest but
are not specific for diagnosis
DIAGNOSIS
LABORATORY TESTS
• TC / DC / ESR / Hb / Platelet count LEUCOCYTOSIS/THROMBOCYTOPENIA
• Serum Bilirubin / SGOT/ SGPT / SAP
• Blood Urea, Creatinine & Electrolytes HYPOKALEMIA/HYPOMAGNESEMIA
• Chest X-Ray; ECG
• Tests for diagnosis of Leptospirosis
• Culture for Leptospira
• MAT; Sero conversion or 4 fold rise/ high titer
• ELISA / MSAT
• PCR
• MAT: Microscopic agglutination test
• (M)SAT: Microscopic slide agglutination Test
Dark field microscopy showing Leptospira spp.
MAT INTERPRETATION
• Titres peak late (2nd or 3rd week) but persist longer ( 5 to 10 years)
• Less sensitive,Repeat samples needed
• Single titre 1:100 significant criteria
• Endemic area 1:400
• Non endemic area 1:100, 1:200
• Serosurvey 1:50
• Repeat titre four fold rise / seroconversion
• Leptospires can be cultured from blood and CSF during first
7-10 days
• Urine culture useful beginning in the 2nd week
• May take 2-4 weeks to be positive
• Urine cultures can remain positive for many months/years
despite therapy
ISOLATION
GUIDELINES TO DIAGNOSE
LEPTOSPIROSIS
•INDIAN
GUIDELINES
•WHO
GUIDELINES
• Malaria
• Enteric fever
• Dengue/ chikungunya
• Hanta virus infection
• Viral hepatitis
• Influenza
• Rickettsial diseases
DIFFERENTIAL DIAGNOSIS
TREATMENT
SUPORTIVE TREATMENT
• Methyl Prednisolone at 1 gm daily IV for 3 days, followed by oral prednisolone at
1 mg/kg for 7 days offered benefit if given within 12 h of the onset of pulmonary manifestations
COMPLICATIONS
• Jaundice
• AKI
• Pulmonary hemorrhage
• ARDS
• Neuroleptospirosis
• Hypotension
• Thrombocytopenia
• Myocarditis
• Ocular complications
• Hypokalemic paralysis
LEPTOSPIROSIS IN PREGNANCY
• Fetal loss high in 1st trimester and near term mothers
• Congenital infections are rare and long-term serious effects have not
been documented.
• Hence, leptospirosis acquired in pregnancy is not an indication for its
termination
• AMPICILLIN 500mg 6th hourly should be given
LEPTOSPIROSIS IN HIV
• recovery slower than is usual for leptospirosis
• residual renal impairment likely
LEPTOSPIROSIS WITH CONCOMITANT ILLNESS
• It is important to look for alternative infections in an appropriate setting particularly if the
patient does not show clinical signs of improvement despite pathogen-directed therapy for
leptospirosis as dual infections like
• DENGUE
• HEPATITIS E
• SCRUB TYPHUS
• MALARIA
Can coexist concurrently
PREVENTION
CHEMOPROPHYLAXIS
VACCINE ???
•No vaccine is yet available for use in
humans with proven benefit..
TAKE HOME MESSAGES
• Leptospirosis has a spectrum of clinical presentations, with a biphasic natural history.
• Major systemic complications occur during the immune phase of the disease, which is usually
5–10 days after infection.
• 2 major symptoms : fever and myalgia +/- Jaundice
• 2 major signs : conjunctival suffusion and muscle tenderness
• Choice of diagnostic testing relies on accurate prediction of the infection. Acute disease is best
detected by culture or PCR, and immune phase disease by serology.
• reducing the incidence of leptospirosis can be achieved by promoting the ‘cover-wash-clean up’
strategies to at risk individuals to reduce contact with infected animals or materials
Leptospirosis : update on management

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Leptospirosis : update on management

  • 2. • Zoonotic disease • Caused by the spirochete Leptospira • Historically known as Weil’s disease • Described in 1885 by Adolf Weil with clinical hallmarks of  splenomegaly  jaundice  nephritis INTRODUCTION
  • 4. THE CAUSATIVE BACTERIUM Order Spirochaetales – Treponema, Borrelia, Leptospira Family – Leptospiraceae, susceptible to heat, acid Genus – Leptospira, 26 serogroups, 250 serovars Pathogenic: Interrogans, Nonpathogenic: biflex Corkscrew shaped, delicate, flexible spirochete, Gram -ve thick, coiled, flagellate, actively motile
  • 5. EPIDEMIOLOGY • Incidence of Leptospirosis in developing countries is 10 - 100/1,00,000 cases/year • Only four states (Kerala,Gujarat, Tamilnadu & Maharashtra) report more than 500 cases per year • Incidence of Leptospirosis is 50 – 65 cases /100,000 per year in Andaman and Nicobar Islands • Prevalence rate of Leptospirosis reported • 38.1% from Calicut • 52.7% from Andaman and Nicobar Islands • 32.9% from Chennai (data from asymptomatic persons detected during sero surveys) • Leptospirosis is grossly under reported because of lack of awareness of the disease and non availability of diagnostic tests • Last outbreak reported in Mumbai during 2015
  • 6.
  • 7.
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  • 9.
  • 10. Organism disappears from blood but remains in organs including brain , liver, lung, heart and kidneys Development of antibodies(5-7 days) Proliferate in bloodstream and disseminate hematogenously Infects through mucosa ( conjunctival , oral) or through punctured or abraded skin PATHOGENESIS
  • 11. Excreted in urine Adhere to proximal tubule epithelial cells Penetrate basement membrane of PCT Traverse interstitial spaces of kidney
  • 12. Hypovolaemic shock and vascular collapse Loss of fluids into the third space Vasculitis and leakage : petechiae , intra parenchymal bleeding and bleeding along serosa and mucosa Capillary vasculitis (endothelial necrosis and lymphocytic infiltration) Attach onto the endothelial cells Produces endotoxin
  • 13. •Clinical expression can be Subclinical infection Undifferentiated febrile illness Weil’s disease •Incubation period 2-30 days (average 5-14 days) CLINICAL FEATURES
  • 14.
  • 15. • The most severe form of leptospirosis • Monophasic and fulminant • Variable combinations of jaundice, acute kidney injury, hypotension and hemorrhage • Pulmonary hemorrhage is the most common • Multisystem involvement occurs WEIL’S DISEASE
  • 16.
  • 17.
  • 18. • High index of suspicion is critical in a setting of An appropriate exposure history Infection’s protean manifestations • Biochemical, hematological and urinalysis may suggest but are not specific for diagnosis DIAGNOSIS
  • 19. LABORATORY TESTS • TC / DC / ESR / Hb / Platelet count LEUCOCYTOSIS/THROMBOCYTOPENIA • Serum Bilirubin / SGOT/ SGPT / SAP • Blood Urea, Creatinine & Electrolytes HYPOKALEMIA/HYPOMAGNESEMIA • Chest X-Ray; ECG • Tests for diagnosis of Leptospirosis • Culture for Leptospira • MAT; Sero conversion or 4 fold rise/ high titer • ELISA / MSAT • PCR • MAT: Microscopic agglutination test • (M)SAT: Microscopic slide agglutination Test
  • 20. Dark field microscopy showing Leptospira spp.
  • 21. MAT INTERPRETATION • Titres peak late (2nd or 3rd week) but persist longer ( 5 to 10 years) • Less sensitive,Repeat samples needed • Single titre 1:100 significant criteria • Endemic area 1:400 • Non endemic area 1:100, 1:200 • Serosurvey 1:50 • Repeat titre four fold rise / seroconversion
  • 22. • Leptospires can be cultured from blood and CSF during first 7-10 days • Urine culture useful beginning in the 2nd week • May take 2-4 weeks to be positive • Urine cultures can remain positive for many months/years despite therapy ISOLATION
  • 24.
  • 25.
  • 26.
  • 27.
  • 28. • Malaria • Enteric fever • Dengue/ chikungunya • Hanta virus infection • Viral hepatitis • Influenza • Rickettsial diseases DIFFERENTIAL DIAGNOSIS
  • 29.
  • 31. SUPORTIVE TREATMENT • Methyl Prednisolone at 1 gm daily IV for 3 days, followed by oral prednisolone at 1 mg/kg for 7 days offered benefit if given within 12 h of the onset of pulmonary manifestations
  • 32. COMPLICATIONS • Jaundice • AKI • Pulmonary hemorrhage • ARDS • Neuroleptospirosis • Hypotension • Thrombocytopenia • Myocarditis • Ocular complications • Hypokalemic paralysis
  • 33. LEPTOSPIROSIS IN PREGNANCY • Fetal loss high in 1st trimester and near term mothers • Congenital infections are rare and long-term serious effects have not been documented. • Hence, leptospirosis acquired in pregnancy is not an indication for its termination • AMPICILLIN 500mg 6th hourly should be given LEPTOSPIROSIS IN HIV • recovery slower than is usual for leptospirosis • residual renal impairment likely
  • 34. LEPTOSPIROSIS WITH CONCOMITANT ILLNESS • It is important to look for alternative infections in an appropriate setting particularly if the patient does not show clinical signs of improvement despite pathogen-directed therapy for leptospirosis as dual infections like • DENGUE • HEPATITIS E • SCRUB TYPHUS • MALARIA Can coexist concurrently
  • 36.
  • 38. VACCINE ??? •No vaccine is yet available for use in humans with proven benefit..
  • 39.
  • 40.
  • 41. TAKE HOME MESSAGES • Leptospirosis has a spectrum of clinical presentations, with a biphasic natural history. • Major systemic complications occur during the immune phase of the disease, which is usually 5–10 days after infection. • 2 major symptoms : fever and myalgia +/- Jaundice • 2 major signs : conjunctival suffusion and muscle tenderness • Choice of diagnostic testing relies on accurate prediction of the infection. Acute disease is best detected by culture or PCR, and immune phase disease by serology. • reducing the incidence of leptospirosis can be achieved by promoting the ‘cover-wash-clean up’ strategies to at risk individuals to reduce contact with infected animals or materials