anthrax (spleenic fever)
DESCRIPTION
a comprehensive and precise review of a zoonotic disease of significant importance to public healthTRANSCRIPT
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.