Dr. dr. Shahrul Rahman, Sp.

PD, FINASIM

Departemen Ilmu Penyakit Dalam

Fakultas Kedokteran
Universitas Muhammadiyah Sumatera Utara
Synonyms
 Over View
Most common, underdiagnosed zoonosis •
Indonesia – almost area could be endemic •
Source - Animals (rodents and domestic animals) •
Epidemiological factors
Contaminated environment, Rainfall, flood •
High risk groups, endemic in all states of •
Indonesia
First description by Weil in 1886 •
 Over View continued
Rural > Urban •
Male > Female (10 : 1) •
Clinical Features –mild to severe life •
threatening
Mimics many common febrile illnesses •
Diagnosis - difficult to confirm •
Treatment – effective, if started early (<5 days) •
The Causative Bacterium
Leptospira under the Microscope
Dark Field Microscopy FL

Long, Thin, Highly Coiled

 Epidemiology
Rainfall; Contaminated environment •
Poor Sanitation; Inadequate drainage facilities •
Presence of rodents, cattle & stray dogs •
Walking/ working bare foot poses high risk •
Difficult to pinpoint the source of infection •
Any person can get infected, if exposed to •
contaminated and environment
 Risk Groups
Occupational exposure
Farmers – Rice, Sugarcane, Vegetables, Cattle, Pigs•
Sewerage workers; Abattoirs, Butchers•
Vetenarians, Lab staff, Miners, Soldiers•
Fishermen – Inland (not on the sea)•
Recreational activities
Swimming, Sailing, Marathon runners, Gardening•
Reservoirs of Infection
Rodents •
Rattus rattus, Rattus norvegicus, (o
)Mus musculus
Dogs •
Wild animals •
Domesticated animals •
Caged game animals •
Leptospira are excreted in the urine •
 Modes of Transmission
Direct contact with urine or tissue of infected animal .1
Through skin abrasions, intact mucus membrane
Indirect contact .2
Broken skin with infected soil, water or vegetation
Ingestion of contaminated food & water
Droplet infection .3
Inhalation of droplets of infected urine
Transmission
Natural History
 Pathogenesis of Severe Disease
Damage to small
Vasculitis
blood vessels
Leptospira

Massive migration of fluid from Direct cytotoxic injury

Intravascular to interstitial compartment Immunological injury

Renal dysfunction, vascular

Injury to internal organs
Clinical Illnesses
Clinical Presentation
Anicteric Presentation
Icteric Leptospirosis
 Icteric Leptospirosis
KIDNEYS – Mild to Severe
Urinalysis : Hematuria / Pyuria / Proteinuria
Renal Failure: Pre renal azotemia, ATN / AIN
Oliguric / Non Oliguric
Mechanism
Nephrotoxicity – Endotoxin, (Direct )
Bacterial migration, Toxic Metabolites
Hypoperfusion – Hypotension, Fluid loss/ Fluid shift
G.I. Bleed, Myocarditis
 Hemorrhagic
Manifestations
Hemorrhagic Fever - Vascular injury
Respiratory, Alimentary, Renal & Genital tracts•
More common in Icteric & with Renal Failure•
Reported in Korea, Andaman’s & Brazil•
Hemorrhagic Pneumonitis
Hemoptysis / Respiratory failure•
CXR : Single/ Multiple ill defined opacities•
Occurs in 2nd week (as early as 24-48 hours)•
Reported in Korea, Andaman’s & Nicaragua•
 Cardiac Form
Cardiac manifestations
Hemorrhagic Myocarditis•
Cardiomyopathy / Cardiac failure•
Arrhythmias, Hypotension / Death•
Atrial fibrillation / Conduction defects•
ECG changes
Non Specific ST-T changes•
Low voltage complexes•
Reported in Srilanka, Barbados & Portugal
 Other Manifestations
Aseptic Meningo-encephalitis
It is rare; It occurs in the Immune phase•
CSF –­proteins , ­lymphocytes •
Convulsions, Encephalitis, Myelitis & Polyneuropathy•
Ocular manifestations
Late complication; Conjunctival suffusion/hemorrhage•
Anterior uveitis, Iritis, Iridocyclitis, chorioretinitis•
Occurs in 2 weeks to 1 yr. (average 6 months)•
Differential
Diagnosis
 Laboratory Tests
TC / DC / ESR / Hb / Platelet count •
Serum Bilirubin / SGOT/ SGPT •
Blood Urea, Creatinine & Electrolytes •
Chest X-Ray; ECG •
Tests for diagnosis of Leptospirosis •
Culture for Leptospira: Positive o
MAT; Sero conversion or 4 fold rise/ high titer o
ELISA / MSAT : positive o
MAT: Microscopic agglutination test •
SAT: Microscopic slide agglutination Test)M( •
Problems in Diagnosis
Interpretation of Tests
Interpretation of Tests
Time Relationship of
Tests

MAT

ELISA or SAT
WHO Guide - Faine’s Criteria
Approach to Diagnosis
 Treatment

Oral Treatment 7 to 10 day IV Treatment 5 to 7 days

Special Measures
Prognosis and Mortality
Prevention
 PES
PLAQUE
SAMPAR
BLACK DEATH
 THE TRUE CAUSE OF THE PLAGUE
.The Swiss scientist Alexandre Yersin discovered the true cause of plague •
The bubonic plague, an infectious disease, are caused by microbes that •
.invade the human body
The microbes that cause the plague are a type of bacteria known as the •
.Yersinia pestis
.The bubonic plague, however, does not start in humans •
Instead it infects only rats and cannot be spread directly from rats to •
.humans
.Fleas, which live on the rats for food, abandon the rat when the rat dies •
If these fleas then find a human the, Yersinia pestis is injected into the •
.bloodstream
.Then the disease can spread from man to man•
 Plague (Black Death)
Symptoms
Develop abruptly 1 – 6 days post infection

Transmission via bite from infected flea

Disease characterized by large tender lymph nodes called buboes
Other symptoms include

High fever
Shock
Delirium
Patchy bleeding under the skin
May also have cough and bloody sputum
Only in lungs infected
Pneumonic plague
 Plague (Black Death)
Causative agent - Yersinia pestis
Facultative intracellular bacteria
Resemble safety pin in stained preparation
Has three plasmids
Smallest is Pla

Causes protective clots to dissolve via activation of

plasminogen activator

Middle plasmid codes Yops (Yersinia outer-membrane

proteins) and regulators of Yops proteins

Yops permits entry of organism into macrophages where

they replicate and interfere with innate immunity

Last is F1
Becomes anitphagocytic capsule

Used in plague vaccine

Not very good and notorious for adverse reactions

 Plague (Black Death)
Pathogenesis
Masses of organism obstruct digestive tract of rat fleas
Flea regurgitates infected material into bite wound
Pla is essential to spread from site of entry
Organisms multiply within macrophages
Produce F1 capsule while in macrophages

Macrophages die and release organism

Organism encapsulated and produces Yops and other mechanisms that
enhance survival

Inflammation in nodes results in characteristic swelling

Nodes become necrotic and spill organisms

Septicemic plague

Mortality rate of untreated reaches between 50% and 80%

 How it was Transmitted

Yersinia pestis seen at 2000x magnification. This

bacterium, carried and spread by fleas, is the cause of the
various forms of the disease plague
 
                                                                                                                        

                 
 SYMPTOMS
painful swellings called buboes which commonly ~
appeared in armpits  and groin area
~dark blisters and purple blotches appeared on skin
~fever
~severe headaches
increasing weakness~
 The Black Death
Three Forms: The Bubonic, •
Pneumonic, and Septicemic.
Each killed people in different
.ways
Bubonic Plague: Mortality •
Rate: 30-75%. Symptoms:
Enlarged or inflamed lymph
nodes (Arm Pit, Neck and
.Groin)
 h
The Plague occurred in 3 Forms •
The Whirligig was
PNEUMONIC PHASE not that bad of a
torture. It just

Attacked the Lungs •

spun the victim
around in circles
until he puked,
Caused fierce coughing & sneezing fits • mostly all over
.himself
Chest pain, Bloody sputum •
SEPTICEMIC PHASE
Rarest and Deadliest •
Traveled thru bloodstream •
Black spots beneath skin •
!Victims choked on own blood, Excruciating Pain •
BUBONIC PHASE
Most Common •
Egg-sized swellings (buboes) •
Neck, armpits, groin (dark blisters) •
Headaches, Weakness, Nausea/Vomiting •
Severe Fever and Delirium •
 Plague (Black Death)
Prevention and Treatment
Prevention directed by rat control
Proper garbage disposal
Rat-proof buildings
Guards on mooring ropes
Extermination programs
Killed vaccine gives short-term partial protection
Treatment via tetracycline for some exposed individuals to
control epidemics
Gentimicin, ciprofloxacin and doxycycline effective on disease
if given early