ANTHRAX

Jeevan Ghimire(1629)
khusbu(1630)
 Contents
• Introduction
• Epidemilogy
• Etiology
• Pathophsiology
• Clinical forms
• Diagnosis
• Treatment
 Also known as
• Malignant pustule
• Ragpickers disease
• Black baine
• Siberian plague
• Woolsorters disease
 INTRODUCTION
A zoonotic disease caused by bacillus
anthracis.Greek;Anthrakis-coal
Primarily affect herbivores; goat ,sheep,horse.
Prototypic disease of bioterrorism.
 Epidemiology
• World
 Anthrax case in Nepal
• First confirmed in 1992 in four cattle near
Kathmandu.
• Galdha vdc-7 of palpa district,in dead cattle
 Agent
• Bacillus anthracis.
• Gram positive,spore forming, non-
motile,capsulated.
• Sporesremain viable for decades.
• LD50=10000
 Spores
• Heat resistant spores
• Formed in soil or culture
• Survive in soil for decades
• Never formed in animal body
• Forms under unfavourable condition
• Resistant to drying
 Host
• Primary Host: Cattle ,sheep goat. Spores in soil
contaminate hide of hervivores
• Wild animals: carnivores when they feed
infected herbivores
• Accidental host: Human , farmers animal
product handlers ,lab personnel
• Common man: threat of bioterrorism
 Environment
• Favourable factors for spore formation and
survival:
-abundant rainfall following period of
drought
-soil pH>6
- Improper disposal of animal
carcasses
-Poor nutrient condition
 Mode of Transmission
Direct transmission -through cutaneous contact
with infected animals or contaminated animal
products
Indirect transmission – through ingestion of
contaminated meat
Airborne transmission – through inhalation of
air contaminated by spores
Life cycle
 Three major clinical forms
• Inhalational Anthrax(Wool sorter disease)
• Cutaneous Anthrax (hide porters diosease)
• Gastrointestinal anthrax
 Pathophysiology of inhalational
Once the spores are inhaled, they are transported
through the air passages into the tiny air particles
sacs (alveoli) in the lungs.

The spores get picked up in the lungs

by macrophages. Most of the spores are
killed. Unfortunately, some survive and are
transported to the lymph nodes in the central chest
cavity (mediastinum).
Once in the lymph nodes, the spores germinate
into active bacilli that multiply and eventually
burst the macrophages, releasing many more
bacilli into the bloodstream to be transferred
to the entire body.
Once in the blood stream, these bacilli release
three proteins named lethal factor, edema
factor, and protective antigen.
These toxins are the primary agents of tissue
destruction, bleeding, and death of the host.
 Clinical Features
• Incubation: 1 to 7 days
• Initial phase
– Nonspecific (mild fever, malaise)
• Second phase
– Severe respiratory distress
– Dyspnea, stridor, cyanosis, mediastinal widening,
death in 24 to 36 hours
• Case fatality: 75 to 90% (untreated)
Bacterial toxins released during replication
result in mediastinal widening and pleural
effusions (accumulation of fluid in the
pleural space).
 Cutaneous anthrax
• Spore enter through opening in skin usually via
preexisting skin lesions,abrasions and skin mucus
membranes.
• A pruritic papule develops 1–7 days after entry of
the organisms or spores through a scratch.
Initially it resembles an insect bite.
• The papule rapidly changes into a vesicle or small
ring of vesicles that coalesce, and a necrotic ulcer
develops. The lesions typically are 1–3 cm in
diameter and have a characteristic central black
eschar.
• Papules vesicle ulcer eschar
Endospores are often phagocytosed by
macrophages and carried to lymph nodes
which can result in painful lymphadenopathy
and lymphangitis
Hematogenous spread with resultant toxemia
can occur with symptoms such as headache,
fever,meningitis and even death.
 Gastrointestinal
• Pathogenesis and statistics are unclear due to
rarity of this form
• Transmission is due to vegetative cells from
uncooked meat rather than spores
• Cause severe gastroenteritis
• Two forms recognized:
-Oropharyngeal:bacteria enters via oral or
pharyngeal mucosa. Mucosal ulcer can occur
initially.Symptoms include sore throat, dysphagia,
fever, hoarseness, and swelling of the neck
 -Abdominal anthrax: entrance occurs through
ileum or cecum mucosa. Intestinal lesions
,regional lymphadenopathy,edema of bowel,
ascites can occur.

Symptoms progresses from initial

nausea,vomiting to bloody diarrhoea,acute
abdomen or sepsis
• Incubation: 2 to 5 days
• Severe gastroenteritis common
– Consumption of undercooked or contaminated
meat
• Case fatality rate: 25 to 75%
 Diagnosis
• Occupational and exposure history is
important
• Gram stain and culture
• Direct fluorescent antibody (DFA) test and
polymerase chain reaction (PCR) assay
• Chest Xray,CT
• LP
• ELISA
 Lab Diagnosis
Samples:
Cutaneous:fluid or pus from the lesion

Gastrointestinal anthrax: stool ,blood, peritoneal

fluid, splenic and lymph node aspirate

Inhalational: Pleural fluid, sputum

CSF if signs of meningeal irritation
 Microscopy
• Stain: Gram staining is done.
In Gram stain chain of bacilli presents as a
bamboo stick appearance.
• Mac fadyean stain is done on blood aspirate of
animal for bacilli
• Spores: stained by Sudan black B
• Culture:Good growth occurs on ordinary
media.
• Blood agar: non hemolytic grey to white
colonies with rough texture and ground glass
appearance.
• Comma shaped outgrowth may be seen to
project from colony resembling matted hair
,medusa head appearance
• Gelatin stab culture: Inverted fir tree
appearance
• ELISA:Detects antibodies against the anthrax
toxin
• Molecular technique: PCR ,DFA
• Anthrax can be identified in dried smears by
immunofluorescence staining techniques
C Xray
 Treatment
• Antibiotics
• Cutaneous anthrax without significant edema
or systemic symptoms is treated with one of
the following antibiotics:
• Ciprofloxacin
• Levofloxacin
• Doxycycline
• Amoxicillin may still be used if the infection is
thought to have been naturally acquired.
• Inhalation and other forms of
anthrax,including cutaneous anthrax with
significant edema or systemic symptoms,
require therapy with 2 or 3 antibiotics.
Antibiotic therapy should include ≥1 antibiotic
with bactericidal activity, and ≥1 should be a
protein synthesis inhibitor, which may block
toxin production
(eg, ciprofloxacin plus clindamycin).
 Other drugs
• Corticosteroids
• Raxibacumab and obiltoxaximab
 Vaccine
• An anthrax vaccine, composed of a cell-free
culture filtrate, is available for people at high
risk (eg, military personnel, veterinarians,
laboratory technicians, employees of textile
mills processing imported goat hair).
 Post-exposure Prophylaxis
Postexposure measures include
• Antibiotics
• Vaccination
• Asymptomatic people (including pregnant women and
children) exposed to inhaled anthrax require
prophylaxis with one of the following oral antibiotics,
given for 60 days:
• Ciprofloxacin
• Doxycycline
• Levofloxacin
• Moxifloxacin
 Prevention
o Humans are protected by preventing disease
in animals
o Veterinary supervision
o Trade restrictions
o Improved industry standards
o Safety practices in laboratories
o Post-exposure antibiotic prophylaxis
• Sterilize hair, wool or hides, bone meal or
other feed of animal origin prior to processing.
• Avoid working with raw animal hides, fur or
skin, especially those of goats, sheep, or cows.
• Do not eat meat that has not been properly
slaughtered and cooked.
• Immunization of high risk individuals usually
laboratoryworkers who are liable to handle B.
anthracis
• Anyone working with anthrax in a suspected
or confirmed victim should wear respiratory
equipment.
 Anthrax as a bioweapon
Because it is deadly, contagious, and dispersed
by spores, anthrax has always been considered a
good candidate for a bioweapon .

In 2001, this possibility became a reality. Letters

containing anthrax spores were sent to several
news reporters and two United States Senators.
Five people died of inhalational anthrax as a result
of exposure to these spores.
Anthrax containing Envelope
 Bibliography
• Text Book Of Microbiology ,Ananthanarayan