Blackleg Disease in Cattle and Sheep
BLACK LEG
By
Dr. Hussein Al Naji
ETIOLOGY
Presentation title
Blackleg, or clostridial myositis of skeletal and/or heart muscle
tissue, is associated with Clostridium chauvoei (feseri), a gram
positive, spore-forming, rod-shaped bacterium. The spores are
normally found in soil.
Blackleg is an acute febrile disease primarily affecting cattle and
sheep, with worldwide occurrence.
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Transmission
1.
In cattle the disease usually occurs without a history of trauma
2.
In sheep, skin wounds from shearing, docking, fighting and
vulvar or vaginal lacerations from parturition or the fresh
navel at birth are the most common routes through which C.
chauvoei penetrates and infects muscle tissue to cause clinical
disease.
3.
Occasional out breaks have occurred in sheep after vaccination
against enterotoxemia.
3
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Spores of C. chauvoei have
been found normally in the
soil, digestive tract, spleen and
liver healthy animals
cause severe necrotizing
myositis locally in skeletal
muscles and a systemic
toxemia that is usually fatal.
C. chauvoei produces a number
of toxins, such as
1- oxygen-stable
2-oxygen-labile
3-hemolysins,DNase,
4-hyaluronidase,
5-neuramidase,.
In sheep the disease related to tissue
laceration and trauma, the stimulus
growth of the latent bacterial spores
but in cattle is unknown.
Pathogenesis
CLINICAL
FINDING
Presentation title
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In cattle
1.
In the early stages, the swelling is hot and painful to the touch but
soon becomes cold and painless, and edema and emphysema can
be felt.
2.
The skin is discolored and soon becomes dry and cracked.
3.
The animal will be found to be very depressed, have complete
anorexia and ruminal stasis, and have a high temperature (41
°
C).
The animal is observed before death there is severe lameness,
usually with pronounced swelling of the upper part of the affected
leg.
CLINICAL
FINDING
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In Sheep
1.
A stiff gait, and the sheep is disinclined to move because
of severe lameness in one limb or, more commonly, in
several limbs. The lameness may be severe enough to
prevent walking.
Clinical
pathology
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1.
Culture from needle biopsy.
2.
No diagnostic change in hematology or serum biochemistry.
Necropsy findings
Myositis; dark, rancid odor, metallic sheen on the cut surface.
Diagnostic confirmation
1.
Fluorescent antibody identification of C. chauvoei in lesion.
2.
PCR
DIFFERENTIAL DIAGNOSIS
1- Malignant edema
2-
Anthrax
3-
Lightning strike
4-
Bacillary hemoglobinuria
4-
Other causes of sudden
unexpected death
TREATMENT AND CONTROL
1.
Treatment Penicillin G sodium/potassium
(44,000 IU/kg IV q6–8h).
2.
Clostridium chauvoei antitoxin (only in early
stages, but doubtful efficacy)
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Control
1-
Multivalent
clostridial vaccine including at least C.
chauvoei, C. septicum, and C. novyi (R-2)
2-
Penicillin (44,000 IU/kg IM q24 for 3 days for animals at risk) (R-2)
Thank you
Presentation title
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Blackleg, caused by Clostridium chauvoei, is an acute disease affecting cattle and sheep globally. This article discusses its etiology, transmission, pathogenesis, clinical findings, and diagnostic confirmation methods.
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Presentation Transcript
BLACK LEG By Dr. Hussein Al Naji
ETIOLOGY This Photo by Unknown Author is licensed under CC BY-NC-ND Blackleg, or clostridial myositis of skeletal and/or heart muscle tissue, is associated with Clostridium chauvoei (feseri), a gram positive, spore-forming, rod-shaped bacterium. The spores are normally found in soil. Blackleg is an acute febrile disease primarily affecting cattle and sheep, with worldwide occurrence. 20XX Presentation title 2
Transmission 1. In cattle the disease usually occurs without a history of trauma 2. In sheep, skin wounds from shearing, docking, fighting and vulvar or vaginal lacerations from parturition or the fresh navel at birth are the most common routes through which C. chauvoei penetrates and infects muscle tissue to cause clinical disease. 3. Occasional out breaks have occurred in sheep after vaccination against enterotoxemia. 3
Pathogenesis In sheep the disease related to tissue laceration and trauma, the stimulus growth of the latent bacterial spores but in cattle is unknown. Spores of C. chauvoei have been found normally in the soil, digestive tract, spleen and liver healthy animals C. chauvoei produces a number of toxins, such as 1- oxygen-stable cause myositis locally in skeletal muscles and toxemia that is usually fatal. severe necrotizing 2-oxygen-labile a systemic 3-hemolysins,DNase, 4-hyaluronidase, 5-neuramidase,. 20XX Presentation title 4
In cattle 1. In the early stages, the swelling is hot and painful to the touch but soon becomes cold and painless, and edema and emphysema can CLINICAL FINDING be felt. 2. The skin is discolored and soon becomes dry and cracked. 3. The animal will be found to be very depressed, have complete anorexia and ruminal stasis, and have a high temperature (41 C). The animal is observed before death there is severe lameness, usually with pronounced swelling of the upper part of the affected leg. 20XX Presentation title 5
CLINICAL FINDING In Sheep 1. A stiff gait, and the sheep is disinclined to move because of severe lameness in one limb or, more commonly, in several limbs. The lameness may be severe enough to prevent walking. 20XX Presentation title 6
1. Culture from needle biopsy. 2. No diagnostic change in hematology or serum biochemistry. Clinical pathology Necropsy findings Myositis; dark, rancid odor, metallic sheen on the cut surface. Diagnostic confirmation 1. Fluorescent antibody identification of C. chauvoei in lesion. 2. PCR 20XX Presentation title 7
DIFFERENTIAL DIAGNOSIS TREATMENT AND CONTROL 1- Malignant edema 2- Anthrax 1. Treatment Penicillin G sodium/potassium 3- Lightning strike (44,000 IU/kg IV q6 8h). 4- Bacillary hemoglobinuria 2. Clostridium chauvoei antitoxin (only in early 4- Other causes of sudden stages, but doubtful efficacy) unexpected death Control 1- Multivalent clostridial vaccine including at least C. chauvoei, C. septicum, and C. novyi (R-2) 2- Penicillin (44,000 IU/kg IM q24 for 3 days for animals at risk) (R-2) 20XX Presentation title 8
Thank you 20XX Presentation title 9
