ANTHRAX

(Spleenic Fever)

Etiology

Bacillus anthracis

pathogenic strains ---- plasmid-encoded virulent

factors: a poly-D-glutamic acid capsule--resistance to phagocytosis

tripartite toxin --- edema (factor I) lethal (factor II)

and protective antigen (factor III)

Etiology

Both plasmids ---- full virulence

avirulent strains occur

spores persist in the environment for decades

Epidemiology
Occurrence
originated in sub-Saharan Africa

spread worldwide distribution

area prevalence varies

restricted to particular areas ---- anthrax belts

Epidemiology
Source of Infection
soil

fodder grown on infected soil

contaminated bone meal
infected excreta

Epidemiology

discharges from infected animals

initial source ---- old soil graves

Spread within an area ---streams, insects, dogs,

and other carnivores

Avian scavengers ---- long distances

Epidemiology
Transmission of the infection

ingestion, inhalation or skin

exact mode of infection in doubt
most animals are infected by the ingestion of
contaminated food or water.
Biting flies, mosquitoes, ticks, and other insects
transmission is mechanical only

Zoonotic potential

important cause of fatal human illness

developed world --- appropriate control measures

important zoonosis in developing countries

agent of bio-terrorism

Pathogenesis

ingestion of the spores

infection through intact mucous membrane

defect in the epithelium around erupting teeth

scratches from tough, fibrous food materials

organism resistant to phagocytosis

Pathogenesis
due to poly-D-glutamic acid capsule

proliferate in regional draining lymph nodes

passes via lymphatic vessels into the blood
stream.
.

Pathogenesis

Septicemia with massive invasion of all body

tissues
lethal toxin --- edema and tissue damage
Death --- shock, acute renal failure, terminal
anoxia

Clinical Findings

incubation period ----1-2 weeks

Two forms ----- per-acute and acute

Per-acute form ---common at the beginning of an

outbreak

animals found dead without premonitory signs

Clinical Findings

course ----- 1-2 hours

fever, muscle tremor, dyspnea and congestion of

the mucosae

. Collapses and dies after terminal convulsions

discharges of blood from natural openings

Clinical Findings
Acute form

course --- 48 hours

Sever depression and listlessness
High fever --- 107F
respiration rapid and deep
mucosae congested and hemorrhagic

Clinical Findings

heart rate increased.

Abortion
Reduce milk yield
milk may be blood stained or deep yellow in color
diarrhea and dysentery
edema of tongue
edematous lesions in throat, sternum, perineum
and flank regions.

Clinical
pathology/Diagnosis

Hematology and blood chemistry ----- No

living animal the organism may be detected in a

stained smear of peripheral blood

local edema is evident---- smear from aspirated

edema fluid or lymph node

Clinical
pathology/Diagnosis

Fluorescent antibody techniques

Monoclonal antibodies

Ascoli test and PCR

Necropsy Findings

absence of rigor mortis

carcass undergoes gaseous decomposition

dark tarry blood ---natural openings---fail to clot

Do not open the carcass

Necropsy Findings
If necropsied
failure of blood to clot ,
Ecchymoses
blood stained serous fluid in body cavities
sever enteritis
spleenomegally
reportable disease

Sample for
confirmation of
diagnosis
Bacteriology unopened carcass: blood or edema

in sealed leakproof containers; opened carcass:

spleen in sealed leakproof containers.

Histology: spleen/lymph nodes if carcass has been

opened

zoonotic potential

Differential Diagnosis

Lightening stroke

Per-acute blackleg

Malignant edema

Bacillary hemoglobinurea

Hypomagnesemic tetany

Treatment

Severely ill animals are unlikely to recover

Penicillin @ 20000 IU/kg BW twice daily

streptomycin @ 8-10 gm/day in two doses IM

Oxytetracycline @ 5 mg/kg BW per day

Antiserum @ 100-250mL 5 day -- expensive.

Control

control of meat and milk producing animals in

infected herds to avoid any risk to the human
population

outbreak ----quarantine

destruction of discharges

vaccination survivors

Control
Disposal of anthrax carcass

most important for prevention of spread

carcass should not be opened
immediately burned in situ or buried
together with bedding and soil
contaminated with discharges

Control

Burning is the preferred

Burial should be at least 2 m deep with an ample

supply of quicklime

Control

Disinfection of the premises, hides, bone meal,

fertilizer, wool and hair

Strong solution of formalin or NaOH (5-10%) are

most effective.