G.HARIPRASAD M.Sc.,(Med micro), M.phil.,Lecturer in Microbiology Department of Microbiology Thoothukudi Govt. Medical College Thoothukudi

• Aerobic,

• Gram positive

• sporulating

• capsulated

• non-motile bacilli.

Cause of anthrax

BACILLUS ANTHRACIS

(GRAM STAIN)

Resistance

• Vegetative forms are destroyed – 600C in 30min.

• Spore form – viable for years in soil

• Autoclaving – kills anthrax spores

• 4% KmNo4 in 15 mts - kills anthrax spores

• Susceptible to many antibiotics like pencillin etc.,

ANTIGENS

Important antigen:

• Capsular antigen

Other antigens:Cell wall polysaccharide antigens Somatic protein antigens

1. Polypeptide capsule – antiphagocytic2. Anthrax toxin

Multicomponent anthrax toxin Factor I – Edema factor Factor II – Protective factor Factor III – Lethal factor Toxin binds with susceptible cells

through factor II Factor I & III enters the cellFactor I – causes edema by rising cAMP levels.Factor III – Kills the cell finally.

Pathogenesis• Animals get infection

rarely by contact with infected animals

• Ingestion of spores – very common.

• Infected animals – discharge more anthrax bacilli from mouth, nose & rectum – sporulation in soil – survive for years – source for other animal

HUMAN ANTHRAX

• Accidental infection• Secondarily infected

from diseased animal• Three clinical types - Cutaneous anthrax –

most common - Pulmonary anthrax –

less common - Intestinal anthrax – very

rare

CUTANEOUS ANTHRAX• Spores enter thro’

abraded skin • Germinate & Multiply at

the site of entry.• Localised lesions - Face,

neck & hand.• Papule – vesicle –

pustular – centrally necrosed – black coloration.

PULMONARY ANTHRAX

• Inhalation of the dust or Inhalation of the dust or filaments of wool from filaments of wool from infected animals, infected animals, particularly in wool particularly in wool factories ( wool sorter’s factories ( wool sorter’s disease)disease)

• Haemotogenous spread Haemotogenous spread – 50% meningitis– 50% meningitis

INTESTINAL ANTHRAX

• Consumption of improperly cooked infected meat.

• Causes violent enteritis with bloody diarrhoea

All clinical conditions lead to septicaemic anthrax if not treated early – Highly fatal!!!

Laboratory diagnosis

• Pus from pustules – cutaneous anthrax

• Sputum – pulmonary anthrax

• Stool / suspected food – intestinal anthrax

• Blood – septicaemic anthrax

Microscopy • Gram stain – for

bacilli demonstration • McFadyean’s

reaction – for capsule demonstration.

• Spore staining – for spore demonstration.

Gram stain

McFadyaen’s reaction

Spore stain

SELECTIVE MEDIA – PLET MEDIUM –POLYMYXIN, LYSOZYME, EDTA & THALLOUS ACETATE

Culture

Culture

• Other non-selective media

• Nutrient agar – colonies – medusa head appearance on low power microscopy

• Blood agar – usually non-haemolytic

Gelatin liquefaction

Maximum liquefaction on the surface than at the bottom

INVERTED FIR TREE APPEARANCE

Nitrate reduction test

Nitrate negative Nitrate positive

ANIMAL INOCULATION

• Mouse/ guinea pigs are injected with specimens.

• Animal dies in 48 hrs

• Examine bacilli in blood of dead animal.

TREATMENT

• Pencillin

• Erythromycin

• Antitoxins – in emergency cases

ANIMAL VACCINE – Sterne vaccine HUMAN VACCINE – Alum Precipitated Toxoid – 3 doses intramuscularly at intervals of 6 weeks and 6 months Booster dose after one year.