leptospirosis 2003

8/3/2019 Leptospirosis 2003

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Dr Vemuri Chaitanya


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It is a bacterial zoonotic disease caused byspirochaetes of the genus Leptospira that affectshumans and other animals

It was described by Adolf Weil in 1886

Also known as Weils disease Swineherds disease Sugarcane growers disease Swamp fever Mud fever Canicola fever


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Broad spectrum of clinical manifestations varyingfrom inapparent infection to fulminant fatal disease.

Mild form : influenza like illness withheadache and myalgia

Severe form : characterized by jaundice,

renal dysfunction &hemorrhagic diathesis Weils syndrome


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Causative organisms : Leptospires Leptospires belong to Order : Spirochaetales Family : Leptospiraceae Genus : Leptospira Pathogenic : Leptospira interrogans

Non pathogenic : Leptospira biflexa(saprophytic) Leptospira interrogans has over 20

serogroups & > 200 serotypes.


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The Leptospira appeartighly coiled thin flexibleSpritochetes 5 15microns long.

Fine spiral of 0.1 0.2microns

One end appears bentforms a hook.

Actively motile Seen best with dark field

Microscopy.


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Electron Microscopyshow thin axialfilament and a delicate

membrane In dark field it may

appear as chain ofminiature cocci.


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Rodents, domestic & wild animals form thereservoir of infection

Temporary carriers : domestic animals like

cattle, dogs & pigs Permanent carriers : rodents

Leptospires are excreted in the urine of theseanimals .

Apart from humans, at least 160 mammalianspecies are infected rats, cattle, pigs, dogs,cats, squirrels, raccoons, bandicoots.


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Transmitted via infected urine. Leptospires infect humans by invasion across

mucous surfaces of eye, throat & gut or nonintact skin . Infection may occur via direct contact with

urine or contact with contaminated water /soil following monsoon rains.


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Occurs both in urban & rural areas. Urban areas of developing countries d/t to

overcrowded slums, inadequate drainage andsanitary facilities, presence of stray dogs,cattle, pigs, domestic rats, poor condition ofslaughter houses.


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In rural areas, high risk groups are workers inrice fields, cane fields & other agricultural

crops & animal husbandry staff In addition sewer workers , miners, fishermen

& those involved in water sports are at risktoo.


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All age groups & races Adult men are at higher risk

More common in tropics , rainy season Number of cases vary every year due to

factors like rainfall, floods & animal infections


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It is endemic in Kerala, Tamil Nadu, Gujarat,Andamans, Karnataka, Maharashtra.

Also reported from Andhra Pradesh, Orissa,West Bengal, Uttar Pradesh, Delhi &Puducherry.


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In Kolencherry, a study of 976 cases confirmed byculture/serology, a mortality rate of 5.32 % isobserved. Autumnalis, Australis & Icterohemorrhagiae

common serogroups isolated. In Calicut, in a study of 282 cases hepatic(69.8%),

renal(56.3%), thrombocytopenia(65.8%). Mortality 6.03% Pomona, Shermani, Canicola commonlyisolated.

In Kottayam, 9000 cases over 10 yrs Jaundice(80%),renal failure(59%), hypotension(20%). Common inagricultural workers, fishermen & oyster shellcatchers.


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It has been reported from Chennai since1980s.

Incidence has been dramatically increasing . In 2006 2765 cases were reported. Autumnalis most common sero group

isolated.

YEAR 2004 2005 2006

LEPTOSPIROSIS 963 1724 2765


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In a study of 33 icteric patients fromPuducherry, 22 had altered sensorium & 20

had multiorgan failure & thrombocytopenia. Mortality 39.3%


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Outbreaks have been reported from 15districts of Karnataka.

Highest incidence have occurred inBangalore, Shimoga, Bidar, Gulbarga, Udipi. In a study of 733 patients suspected of

leptospirosis, 84 were found positive byELISA. Complications Hepatic ( 65% ) &Renal Failure (63% )


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Incompletely understood. Leptospires enter the host through abrasions

in skin or intact mucous membranes(conjunctiva or oro- & nasopharynx)

After entry of organisms , leptospiremiadevelops, with subsequent spread to all

organs. Multiplication takes place in blood & tissues,

leptospires can be isolated from blood & CSFduring first 4 10 days of illness.


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Damage the wall of small blood vesselsleading to vasculitis with leakage &

extravasation of cells, including Hemorrhage. Mainly affect kidneys & liver.


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Centrilobular necrosis with proliferation ofkupffer cells


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Pulmonary involvement is as a result ofhemorrhage but not of inflammation.

Invasion of skeletal muscles results inswelling, vacuolation of myofibrils & focalnecrosis.

In severe infection, vasculitis impairs themicrocirculation & increased capillarypermeability results in fluid leakage &hypovolemia.


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When antibodies are formed, leptospires areeliminated from all sites except eye, proximal

renal tubules & brain where they persist fromweeks to months. Persistence in aqueous humour leads to

recurrent uveitis.


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Many remain asymptomatic. In symptomatic cases, clinical manifestations

vary from mild to serious or even fatal. >90% of symptomatic have mild, anicteric

form of leptospirosis with / withoutmeningitis.

5-10% - Weils syndrome Incubation period : 7-12 days, can vary from

2 30 days.


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Typically characterized by

Acute leptospiremic phase Immune leptospiruric phase.

Distinction between the 2 phases is notalways clear and milder cases do not alwaysinclude the 2nd phase.


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Acute febrile, influenza like illness with chills,sore throat, headache, myalgia, back pain,

anorexia, nausea & vomiting , sometimesherpes labialis. When acute phase is severe, pt is prostate &

has persistently high fever with tendermuscles, cough, dyspnea, hemoptysis,vomiting & abdominal pain.


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During this phase, leptospires may be cultured from blood & CSFand other tissues, but not from urine.

Serological tests are negative until at least 5 days after the onsetof symptoms.

This phase lasts for around 4 -7 days.

Wide spread dissemination meningeal invasion. There may betransient rash.

Myalgia with raised CPK & Conjunctival suffusion arecharacteristic.

Moderate hepatomegaly Splenomegaly is rare. Thrombocytopenia Proteinuria Normal creatinine clearence until tubular necrosis /

glomerulonephritis ensues.


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After the initial illness, a second phasebegins, characteristically the pt havingdeveloped antibodies, predominantly of IgMclass.

In mild cases the 2nd phase is associated withminimal signs & symptoms.

Severe infections meningeal & hepatorenalmanifestations predominate. Important feature of immune phase is

development ofASEPTIC MENINGITIS.


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Fever with chills Frontal headache / retroorbital pain

Nausea, vomiting Myalgia ( calves, back, abdomen ) Sore throat Cough, occasionally hemoptysis.


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Fever with conjunctival suffusion Muscle tenderness

Lymphadenopathy Throat congestion Macular, maculopapular, erythematous,

utricarial & hemorrhagic rash Hepatomegaly Rarely splenomegaly


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Most become asymptomatic within 1 week. After 1-3 days , illness reccurs the start of

this immune phase & symptoms are morevariable.


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Characterized by jaundice, renal dysfunction &hemorrhagic diathesis

Pulmonary involvement in many cases

Mortality 5 -15 % Commonly due to serovar icterohaemorrhagiae Onset same as anicteric leptospirosis After 4-9 days, jaundice, renal & vascular

dysfunction develop.

Hepatomegaly Tenderness Right Upper quadrant Splenomegaly 20 % cases


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Renal failure often in 2nd week Hypovolemia & decreased renal perfusion

acute tubular necrosis with oliguria or anuria. Pulmonary involvement : cough, dyspnea,

chest pain & blood stained sputum . Sometimes hemoptysis / resp failure / ARDS

Hemorrhagic : epistaxis, petechiae, purpura,ecchymosis, rarely SAH & GI bleed.


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Rhabdomyolysis Hemolysis

Myocarditis Pericarditis CHF ARDS Necrotizing Pancreatitis Multi organ dysfunction


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Serovar L.lai was the first recognized inassociation with pulmonary hemorrhagic

syndrome. Serovar Canicola CANICOLA FEVER more

likely to cause lymphocytic meningitis thanhepatorenal syndrome & is rarely fatal.

L.autumnalisFORT BRAGG FEVER pretibial, raised 2-4 cm erythematouspatches less tender than erythema nodosum


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Viral hepatitis Hantavirus infection

Dengue Malaria Enteric fever Hemolytic uremic syndrome Shigella , E.coli Meningococcemia


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WBC : leukocytosis ESR : raised Mild thrombocytopenia ( 50 % cases ) Urine r/e : urinary sediment changes

( leukocytes, erythrocytes, hyaline / granular casts )mild proteinuria ( anicteric form )renal failure (severe form )

LFT : raised bilirubinraised alkaline phosphatasemild rise in transaminases ( upto 200 U/L )

Bleeding time prolonged & bleeding is d/t capillary fragility Clotting time normal Later rise in PT Hepatocyte failure


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S.CPK in 1st week of illness ( differentiatefrom viral hepatitis )

Meningeal involvement : initially PMNs &later mononuclear CSF protein elevated Pulmonary : radiographic abnormalities more

than physical findings. CXR : Most common : patchy alveolar pattern Lower lobes in periphery of lung fields.


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Clinical features & laboratory investigations

A definite diagnosis -isolation of organism from the patient or

on seroconversion ora rise in antibody titre in MAT.

TESTS :

Culture PCR SEROLOGY


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Serovar Specific tests : MicroscopicAgglutination Test

Genus Specific tests : ELISAMSATLatex AgglutinationDipstik Tests

Lepto Tek Dri Dot Test


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Cultures : Blood & CSF during first 10 daysUrine for several weeks beginning

after 10 days

Cultures become positive after 2-4 weeks, with range of 1 week to

6 months

Medium : Ellinghausen-McCullough-Johnson-Harris (EMJH)MediumFletcher MediumKorthof Medium

Most definite way of conforming leptospirosis, but they do notcontribute to early diagnosis.


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Promising on both sensitivity & specificitybasis

Disadvantage : expensive Its value in rapid diagnosis is being evaluated Used in research & reference laboratories


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Serovar specific test Gold standard test - because of unsurpassed

diagnostic specificity Identification of serovar is of epidemiological

importance. In cases with strong clinical evidence, a single

antibody titer of 1:200 -1:800 ( depending onendemicity ) in MAT is required but a risingtiter is diagnostic.


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Antibody titers rise & peak only in 2nd or 3rdweek, making it a less sensitive test

A four fold rise in titer or seroconversion is

the most definitive criteria for diagnosis. So,a 2nd sample is mandatory , which is difficultto obtain. In such cases , a single high rise in

titer is taken as diagnostic In non endemic areas 1:100 titer is diagnostic In endemic areas > 1: 400 ,some > 1: 800 or

1: 1600 as diagnostic


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Tests of choice for diagnosis of currentinfection

Simple More sensitive Become positive earlier than MAT ( 5th 6th

day of illness )

Detect genus specific antibodies, which areshared by pathogenic & saprophyticleptospira.

Detect specific IgM antibody


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Clinicalfeatures

Leptospiremicphase 7 days

Rapidtests

Negative

REPEAT

after 3da s

Positive

POSITIVE


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POSITIVE

MAT

POSITIVE

HIGHTITER

REPEAT

( if lowtiter )

RISING

TITER

NEGATIVE

REPEAT

SEROCON-

VERSION


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ConfirmedCulture : positive

MAT : seroconversion / 4 fold rise in titer

ProbableRapid tests : positiveMAT : high titer ( single sample )


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PART A Score Headache 2 Fever 2 Temp >39C 2 Conjunctival 4

suffusion Meningism 4 Myalgia 4 Conj.suffusion, 10

myalgia,meningism

Jaundice 1 Albuminuria/ 2

nitrogen retention

PART B Score Rainfall 5 Contact with 4

contaminatedenvironment

Animal contact 1

PART C ELISA IgM + 15 SAT + 15 MAT- Single +titer 15 MAT rising titer / 25

seroconversion


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Presumptive diagnosis is made of :Part A or Part A & B Score : 26 or more

Part A,B &C ( Total ) : 25 or moreA Score 20-25 suggest leptospirosis aspossible diagnosis.


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Mild leptospirosis

Severe leptospirosis

Doxycycline 100mg BD / Ampicillin

500-750mg QID / Amoxicillin 500mg QID

Penicillin G 1.5 millionuntis IV QID /

Ampicillin 1g IV QID / Amoxicillin 1g IV QID /

Ceftriaxone 1g IV OD / Cefotaxime 1g IV QID / Erythromycin 500 mg IV

QID


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Renal failure hemodialysis Hemorrhagic manifestations : transfusions of

whole blood and or platelets Acute pulmonary syndrome : pulsed

methylprednisolone may be effective Intensive care


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Chemoprophylaxis Doxycycline 200 mgOD once a week


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leptospirosis 2003

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