Anthrax

Prepared by Dr. Ghalib S. Ridha Visiting Assistant professor of Internal medicine & Infectious diseases. Dept. of Internal Medicine Faculty of Veterinary Medicine Al-Fateh university Tripoli, LIBYA
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Anthrax
Synonyms: Splenic fever, Charbon, Milzbrand, Woolsorters disease.
Anthrax is an peracute, contagious, and usually rapidly fatal septicemia affecting wide range of mammals including humans.

Most commonly affected are cattle & sheep, less commonly, horse & goats. Although all ages are susceptible, older ages are more commonly affected. Bulls are more at risk than cows.

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Anthrax is characterized by sudden death and exudation of tarry blood from natural body orifices of cadaver.

The most important necropsy findings are failure of the blood to clot, absence of rigor mortis, and the presence of splenomegaly

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Etiology

The causative bacterium, Bacillus anthracis, is a Gram-positive, non-motile, capsulated, spore-forming, aerobic bacilli. When bacilli discharged from an infected animal or exposed to free oxygen from an opened carcass, they form spores that are resistant to extreme temperature, chemical disinfectants, and desiccation.

Anthrax bacilli can remain viable in the soil for more than 30 years. In an unopened carcass, the vegetative organisms are rapidly destroyed (1 to 2 hr) at ambient temperature often during the summer. For this reason, the carcass of an animal dead from anthrax should not be necropsied.
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Epidemiology

It is distributed worldwide with incidence varies with soil and climate. The disease is enzootic and restricted in particular areas, the so called anthrax belt. Animals can get spores directly from; The soil or Pasture grown on infected soil, from contaminated bone or meat meal from excretion, blood or other materials from infected animal Contaminated water Contaminated animal products such as hides, fertilizers, hair & wool. Infection gain entrance to the body by ingestion, inhalation or through the skin.
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It is considered that most animals are infected by ingestion of contaminated food or water. Injury to the mucous membrane of digestive tract will facilitate infection. Inhalation is of minor importance in animals but workers in the wool and hair industries (woolsorters disease in humans) can get infection by inhalation. Biting flies and insects have been found to harbor anthrax, but the incidence of this mode of mechanical vector transmission is of minor importance. Outbreaks commonly are associated with neutral or alkaline, calcareous soils. When environmental conditions of soil (moisture, temperature, and nutrition) are optimal, the spores revert to the vegetative and multiply to infectious levels.
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Typically anthrax occurs during the warm, dry summer months, in some African countries, when grasses are short & dusty, although it may occur in cold climates. Epidemics originating from soil-borne infections tend to follow periods of marked climatic and ecologic changes such as heavy rainfall or flooding preceded by drought or dusty conditions and always in seasons of warm weather when the minimal daily environmental temperature is over 15C. Even in endemic areas, anthrax occurs irregularly often with many years between occurrence.

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The zoonotic potential of anthrax is that man may develop;

localized cutaneous lesion (malignant carbuncle) from contact of broken skin with infected blood or tissues or man may acquired a highly fatal hemorrhagic mediastinitis. (woolsorters disease) from spore inhalation when handling contaminated wool or hair. man may also acquire intestinal anthrax from consumption of uncooked meat.

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Pathogenesis

After entry of spores by ingestion, the most common route of infection which may be facilitated by grazing of abrasive forages allowing penetration of the spores through the breaks in the oral mucosa.
The bacteria are moved to local lymph nodes, proliferate & pass via lymphatic vessels into blood and septicemia with massive invasion of all body tissues. B. anthracis possess 2 primary virulence factors which are associated with the presence of 2 plasmids that carry the genes coding for toxin and capsule production. B. anthracis produces an edema toxin and a lethal toxin.
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Both toxins and the capsule are the primary virulence factors of the anthrax bacillus.

The toxins cause wide spread damage to reticuloendothelial system and vasculature.
Death results from secondary changes, including diffuse edema, tissue damage, acute renal failure, shock, and terminal anoxia mediated by the CNS.

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Clinical findings

Anthrax can occur as a peracute, acute or chronic disease. The incubation period is 3-7 days but can range from 1-14 days. Peracute form is of sudden onset and rapid fatal course. There may be staggering, dyspnea, trembling, collapse with few convulsive movements and death may occur in cattle, sheep or goats without previous signs of illness. In acute form of anthrax in cattle and sheep, there is a high fever (41.5C), ruminal stasis, hematuria, bloody diarrhea, abrupt decrease in milk production, and possibly blood-tinged or yellow milk. A period of excitement and aggression followed by depression, muscle tremors, cardiac and respiratory distress, staggering, convulsions and death (1-3 days) with bloody discharges exude from natural orifices.
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Chronic anthrax in ruminants is characterized by localized edematous swellings on the shoulder, ventral neck, and thorax.

Horses with acute anthrax may show signs of fever, weakness, depression, severe colic, enteritis with bloody diarrhea, and swellings in the region of neck, sternum, lower abdomen, and external genitalia.
Death usually occurs within 2-4 days.

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Necropsy findings

Carcasses suspected of having anthrax should not be opened for necropsy to reduce environmental contamination and health risk to humans.

The gross lesions of anthrax include, black tarry blood from body orifices (mouth, nostrils, vulva, and anus), failure of blood to clot, incomplete rigor mortis, splenomegaly ( dark red to black, soft, semifluid spleen is common with increased size of 2-4 times), marked bloating and rapid body decomposition.
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The liver, kidneys, and lymph nodes usually are congested and enlarged.

Other findings, Ecchymotic hemorrhages of serosal and mucosal lining on the abdomen, thorax, epicardium, pericardium and GIT. Areas of gelatinous edema in skeletal muscles, organs, subcutis, and lymph nodes. Serosanguinous peritoneal and pericardial effusions may be found

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Diagnosis

It can be determined without necropsy (unopened carcass). Various laboratory tests can be performed to determine the presence of B. anthracis: Bacterial staining and culture, ELISA test, FAT, and mouse and guinea pigs inoculation.

Other specific diagnostic tests include PCR, chromatographic assays, and Western blot
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The organisms can be detected in blood collected by needle puncture of superficial blood vessel, ear or jugular vein or edema fluid & transported to the lab through sealed syringe, sterile swab, or blood smear.

If decomposition of a carcass is advance an ear or section of spleen sealed in a leak-proof bag should be sent to lab to be used for bacterial isolation and for preparation of an Ascoli precipitin test.
P.M materials should be collected from untreated animals dead less than 12 hr because other motile, capsulated bacilli such as Clostridium perfringens and other Bacillus spp. rapidly contaminate the carcass.
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A simple and quick diagnosis of anthrax is through the use of staining techniques in combination with Clinical signs History of endemic areas, and Necropsy findings. Various stains can be used including Giemsa Loefflers methylene blue or Wrights stain.

With a Gram stain, young bacteria will appear Gram-positive, but older organisms may appear Gram-negative.

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Differential diagnosis

Anthrax must be differentiated from other causes of sudden death in cattle and sheep including; Clostridial infection Acute boat Acute leptospirosis Lightning stroke Bacillary hemoglobinuria Anaplasmosis Acute lead poisoning.

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Treatment and control

Because of the rapid death and high mortality rate (90%) associated with anthrax, treatment should be initiated before death and vigorous implementation of a preventive program are essential. If anthrax is suspected, immediate segregation of infected animals is advised with early antimicrobial therapy may be useful. The M.O. is highly susceptible to a wide range of antimicrobials including penicillin, streptomycin, and tetracycline with 1st dose should be administered IV & can be continued IM for at least 5 days.

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When soil-borne outbreak occur, antibiotics for sick animals and immunize all apparently well animals are used in the herd & surrounding premises. If outbreak is due to contaminated bone meal, antibiotic therapy of exposed animals & removal of the source may be more effective than vaccination in reducing losses. In the endemic area, control is largely depend on annual vaccination of all grazing animals and by application of control measures. This can be accomplished through the use of a viable, avirulent, non-capsulated spore vaccine (Stern-strain spore vaccine). It should be done 2-4 wk before the season when outbreaks may be expected.

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Two vaccine doses is recommended to produce more solid immunity in cases of an outbreak. Antibiotics should not administered before and during the 1st wk following vaccination. Immunity is established within 1 wk.

There is 2 mo slaughter withdrawal after administration of live spore vaccines.

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Beside therapy and immunization, specific control procedures to contain the disease and prevent its spread are necessary. These include the following: Official notification Rigid quarantine measures Prompt disposal of dead animals and infected materials Isolation of sick animals & removal of well animals from infected areas. Disinfection of stables, barns, pens, and equipments. Use of insects repellents Control scavengers.

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