What is leptospirosis? infectious disease caused by pathogenic bacteria transmitted directly or indirectly from animals to humans. It is therefore a zoonosis.

Human-to-human transmission occurs only very rarely.

Leptospirosis is a potentially serious but treatable disease. Its symptoms may mimic those of a number of other unrelated infections such as influenza, meningitis, hepatitis, dengue or viral haemorrhagic fevers.

In particular dengue, may give rise to large epidemics, and cases of leptospirosis that occur during such epidemics may be overlooked.
For this reason, it is important to distinguish leptospirosis from dengue and viral haemorrhagic fevers, etc.

LEPTOSPIROSIS
Acute febrile illness Zoonotic Worldwide Mud fever, slime fever, swamp fever, field fever, autumnal fever, sugar cane fever, infectious jaundice Usually mild or asymptomatic

ETIOLOGY
Spirochaeta genus Leptospira : Leptospira interrogans (pathogen) Leptospira biflexa (saprophytic) Leptospira parva (apathogen) Fine spiral microorganism Obligate aerob, pH 7.2-7.6, 28-30oC

EPIDEMIOLOGY
Worldwide except Antartica, more prevalent in the tropics Hospes reservoir rat, rodent, cattle, mammals All age groups but primarily in teenage and young adults (10-39 yr), Male > female, occupational disease

How often does leptospirosis occur worldwide? The cases worldwide is not known precisely. incidences range 0.11 per 100 000 per year in temperate climates to 10100 per 100 000 in the humid tropics. During outbreaks and in highexposure risk groups, disease incidence may reach over 100 per 100000

PATHOGENESIS(1)
Leptospira in the urine host enter human through skin abrasion or intake mucous membrane Haematogenic spread all organ most commonly liver, kidneys, striated muscle Cytokine (TNF) & enzymes cellular damage

PATHOGENESIS

..(2)

Immune response (humoral & cellular) cleared and reduced leptospira Persist in the kidney, uvea Liver : centrilobular necrosis, proliferation Kupffer cells, cholestasis Kidney: interstitial nephritis, tubular necrosis

PATHOGENESIS The clinical manifestations are caused by damage to the endothelial lining of smallblood vessels All the internal organs may be affected e.g.interstitial nephritis and tubular, glomerular and vascular kidney lesions lead to uraemia and oliguria/anuria;

PATHOGENESIS Vascular injury to hepatic capillaries, in the absence of hepatocellular necrosis, causes jaundice; Inflammation of the meninges causes headache, neck stiffness, confusion, psychosis, delirium, etc. Thrombocytopaenia may lead to bleeding

PATHOGENESIS ..(3)
Pathogenic leptospires
Direct invasion -Enzymes -Cytotoxic factors

Immunological reactions

Nonspecific inflammatory effects mediators cytokines oxygen radicals complemen activation intravascular haemolysis intravascular coagulation Compromised microcirculation

Tissue injury

CLINICAL MANIFESTATION

(1)

Incubation period : 7 12 days (2-26) Mild (fever) severe (jaundice, renal failure) 80 90 % cases anicteric Leptospiremic phase Immune phase Convalescence

CLINICAL MANIFESTATION(2)
Leptospiremic phase 4 9 days, fever & chills, headache, myalgia, conjunctival injection, muscular tenderness, hepatomegaly, renal involvement, jaundice (severe) Immune phase 4-30 days, circulating IgM, leptospires disappeared from tissue expt. kidney, aqueus humor, rash, secondary fever, meningeal symptoms, uveitis

CLINICAL MANIFESTATION(3)
Weils disease L. icterohaemorrhagica hepatomegaly, jaundice proteinuria, pyuria, hematuria, azotemia haemorrhage

CLINICAL MANIFESTATION

.(4)

Atypical pneumonia syndrome Aseptic meningoencephalitis pleocytosis, L. canicola, L. pomona, L. icterohaemorrhagica Myocarditis Cardiac arrythmias, PAT, VT, atrial flutter, L. icterohaemorrhagica, L. pomona, L gryppotyphosa

Clinical categories: (i) A mild, influenza-like illness; (ii) Weil's syndrome characterized by jaundice, renal failure, haemorrhage and myocarditis with arrhythmias; (iii) meningitis/meningoencephalitis; (iv) pulmonary haemorrhage with respiratory

LABORATORY FINDINGS
Blood: leucocytosis, BUN, creatinin, bilirubin, CPK elevated Urine : albuminuria, hematuria, bilirubinuria Serologic : IgM Bacteriologic : blood (1st week), urine (2nd week), LCS

COMPLICATION
Renal failure : 44 67 % cases Cholestatic jaundice Respiratory : haemoptysis, ARDS, pneumonia, respiratory failure, 12 % cases Hypotension : 12 % cases jaundice, adrenal insuffisiensi Cause of death : respiratory failure, pancreatitis, renal failure, myocarditis, deep jaundice

Cause of death?

Renal failure, Cardiopulmonary failure Widespread haemorrhage. Liver failure is rare, despite the presence of jaundice

Treatment for leptospirosis Antibiotics should be initiated as soon as the diagnosis of Leptospirosis is suspected and preferably before the fifth day after the onset of illness. The benefit of antibiotics after the fifth day of the disease is controversial..

Treatment for leptospirosis Clinicians should never wait for the results of laboratory tests before starting treatment Serological tests do not become positive until about a week After the onset of illness, Cultures may not become positive for several weeks.

Treatment for leptospirosis Severe cases of leptospirosis should be treated with high doses of intravenous penicillin. Less severe cases oral antibiotics such as amoxycillin, ampicillin, doxycycline or erythromycin. Third-generation cephalosporins, such as ceftriaxone and cefotaxime, and quinolone antibiotics also appear to be effective.

TREATMENT
Penicillin G Doxycycline Tetracycline Supportive Dialysis in renal failure Exchange transfusion in severe jaundice

PROGNOSIS & PREVENTION

Prognosis usually recovered mortality is high in severe cases
Prevention avoid contact good sanitation