ANTHRAX (Spleenic Fever)

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.