Leptospirosis, Pes and

Chancroid
Umar Zein

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,
Mus musculus)
Dogs
Wild animals
Domesticated animals
Caged game animals
Leptospira are excreted in the
urine

Modes of Transmission
1. Direct contact with urine or tissue of
infected animal
Through skin abrasions, intact mucus
membrane
2. Indirect contact
Broken skin with infected soil, water or
vegetation
Ingestion of contaminated food & water
3. Droplet infection
Inhalation of droplets of infected urine

Transmission

Natural History

Pathogenesis of Severe Disease

Leptospira

Damage to small
blood vessels

Vasculitis

Direct cytotoxic injury

Massive migration of fluid from
Immunological injury
Intravascular to interstitial compartment
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, Andamans & 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, Andamans & Nicaragua

Atypical Pneumonia

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

MAT; Sero conversion or 4 fold rise/
high titer
ELISA / MSAT : positive
MAT: Microscopic agglutination test
(M)SAT: Microscopic slide agglutination
Test

Problems in Diagnosis

Interpretation of Tests

Interpretation of Tests

Time Relationship of Tests

MAT

ELISA or SAT

WHO Guide - Faines 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

Origins
Originated in Mongolias Gobi desert
Moved along the Silk Road to Black Sea
Bacteria carried by fleas, lived on black rats
Major trade/commercial cities were good hosts
Sicily in 1347, England 1348, culminating in Russia 1352
Unstoppable Force

Victims ate lunch with their friends and dinner with their ancestors
in paradise."

History of Plague
Justinians Plague (541-542) killed pop. of Mediterranean
6th & 8th C. breakouts
16th, 17th, 18th C. Pandemics
Italian, London, Vienna, Marseilles, Russia
3rd Pandemic (Asian Plague) 19th, 20th C.
~15 million dead (India, China, Russia)
Biological Weapon (Japanese, WWII)
Looked at Medieval Styles of Catapulting Infected Bodies into
Castles

Released Infected Fleas in China, Manchuria

Studied Live Subject, Dissecting
WhAt NeXt?

In October of 1347, several Italian

merchant ships returned from the
Black Sea.
Docked in Sicily,
many sailors
were already dying of
the plague. Within
days the disease
spread to the city.
That was the
beginning of the end!

Realizing what a deadly disaster had come to them, the

people quickly drove the Italians from their city. But the
disease remained, and soon death was everywhere.
Fathers abandoned their sick sons. Lawyers refused to
come and make out wills for the dying. Friars and nuns
were left to care for the sick, monastaries and converts
were soon deserted, as they were stricken, too. Bodies
were left in empty houses, and there was no one to give
them a Christian burial.

The Italian writer Boccaccio said its victims

often:
Ate lunch with their friends and dinner with
their ancestors in paradise.
In winter the disease seemed to disappear,
but only because fleas are dormant then.
After Five years 25 million people were
dead- One Third of Europes people!

How Did It Affect So Many People?

Myth or Fact?
(Song)

Ring around the rosie,

A pocket full of posies,
Ashes! Ashes!
We all fall down!

Effect on European
Civilization

DISASTER STRIKES

Estimated population of
Europe from 1000 to
1352.

1000 38
million
1100 48
million
1200 59
million
1300 70
million
1347 75
million
1352 50
million

Black Death
Carried by Ships throughout Europe
Rats infested the goods on board

The burning of Jews in 1349 (from a European chronicle written on

the Black Death between 1349 and 1352)

Early Theories
Some blamed invisible particles in the air.
Some blamed poisoned wells.
Many inevitably and unfairly blamed the Jews.

Will It Ever End?

Bands of hooded men, wearing white
robes marked front and back with a red
cross, moved to and fro across Europe.
They were attempting to atone for the
ravages of the Black Death by whipping
themselves in ritual public ceremonies.
They are known as the Flagellant
Brahren!

The Flagellant Brahren

50 to 500 men in a group
singing hymns and sobbing, the men beat themselves with scourges studded with
iron spikes. Blood gushes from their many wounds, and the spikes embed
themselves in the torn flesh.
The ritual was performed in public twice a day!

WHY?
Ignorance Surrounded Cause and Cure
Europeans were Frantic
Blames
Alignment of Planets
Infected Clothing, Humans
Gods Wrath aimed at Sin
Jews
Cures/Remedies
Pomanders
Mixture of Molasses & Chopped Snake
Repentance
Flagellants

The Flagellant Brahren

Singing hymns and sobbing, the men

beat themselves with scourges studded
with iron spikes. Blood gushes from their
many wounds, and the spikes embed
themselves in the torn flesh. The ritual is
performed in public twice each day.
Such exhibitions are highly influential.
The establishment may focus their
attacks on church corruption and their
promotion of a wave of savage antiSemitism. but the masses worship the
flagellants as living martyrs. Their deeds
are to be admired and their commands
to be carried out.
Many Followers massacred Jews
believing they had poisoned society.

THE TRUE CAUSE OF THE

Yersin discovered the true cause of plague.
The Swiss scientist Alexandre 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.

The Bubonic Plague spreads to

Europe

Fleas spread along trade

routes
Spread along the Silk Road
Also spread to Europe on
ships
First outbreaks of the
Bubonic Plague would
occur in port cities and
towns

Spreading the Plague in Europe

Starts in modern Turkey and Italy
Poor sanitation encouraged the
spread of the Plague
Plague infected rats and fleas feed
on garbage, dead animals, and
human waste
Most people did not change their
clothing
Most people did not bath regularly

People did not know what caused

the Plague, or how it spread

The Black Death,

1348

Impact of the Black Death

Approximately half of the people in China died
24 million Europeans died, about 1/3 of the
population
Trade and The Economy were destroyed
Rebuilt with an emphasis on Common people

Power shifted from the Nobles to the Commoners

So many people had died that workers were in short
supply
Workers could demand more money and more rights
More people moved away from feudal manors and into
towns and cities to look for better opportunities

Peasant rebellions began to break out

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%

The Oriental Rat Flea

Fleas Mouth has two functions:
one for squirting saliva or partly
digested blood into the bite, and one
for sucking up blood
from the host.
This poses a problem!

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

What is the Bubonic Plague?

Most famous form of Plague
Caused by a bacterial infection
Spreads through flea bites, but
can be spread through the air
Without treatment50%100% lethal
Bubonic Plague probably
started in China or Mongolia
Today Bubonic Plague is
curable with the use of proper
antibiotics

Symptoms of the Bubonic

Plague
1st Flu like symptoms
Sneezing, Aches, and Fatigue

2nd Swollen lymph glands

Armpits, Groin, and Neck
Swollen glands develop into Buboes, which eventually
rupture and bleed

3rd Coughing
Once coughing starts the plague has become airborne

4th Pain, Bleeding, Decaying of Tissue and Death.

in 3-7 days

Deat
h

The Plague occurred in 3 Forms

The Whirligig was

PNEUMONIC PHASE

Attacked the Lungs

Caused fierce coughing & sneezing fits
Chest pain, Bloody sputum

not that bad of a

torture. It just
spun the victim
around in circles
until he puked,
mostly all over
himself.

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

The Black Death

Three Forms: The
Bubonic, Pneumonic,
and Septicemic.
Each killed people in
different ways.
Bubonic Plague:
Mortality Rate: 3075%. Symptoms:
Enlarged or inflamed
lymph nodes (Arm
Pit, Neck and Groin).

The Pneumonic Plague was the second most commonly seen form of the Black Death.
Mortality Rate: 90-95%
(Today if Treated 5-10%)
It infected the lungs, and
the symptoms included
slimy snot tinted with blood!
Many times victims choked
on their own Blood (ew).

Septicemic Plague
Most Rare form of all!
Mortality rate was close to 100%(Even today
there is no treatment)
Symptoms: High Fever and
skin turning deep
shades of purple!
Victims usually died
the same day the
symptoms appeared.

Plague (Black Death)

Epidemiology
Endemic on rodent populations in all continents except
Australia
Prairie dogs, rock squirrels and their fleas are main
reservoir
Hundreds of fleas can transmit plague and can remain
infectious for a year
Can spread person to person by household fleas
Organism can remain viable for weeks in dried sputum
and flea feces

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

Chancroid

 Also termed soft chancre or ulcus

molle
Autoinoculable infection caused by
Haemophilus ducreyi characterised by:
painful, necrotizing genital ulcers
painful bubo formation

Chancroid ulcers

Treaatment

Azithromycin 1g stat.
Ciprofloxacin 500 mg (p.o.) b.d. for 3 days
Erythromycin 500 mg (p.o.) q.d.s for 7 days
Ceftriaxone 250 mg (i.m.) stat.
Spectinomycin 2 g (i.m.) stat.
In known low resistance areas:
Trimethoprim 80 mg/Sulphamethoxazole 400 mg
2 tablets (p.o.) b.d. for 7 days
Aspirate fluctuant nodes as required
Chancroid

Chancroid Male - regional

adenopathy

Chancroid - ruptured node

Chancroid - gram stain of H.

ducreyi