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Blackleg in ruminants

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DOI: 10.1079/PAVSNNR20061040

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 CAB Reviews: Perspectives in Agriculture, Veterinary Science, Nutrition and Natural Resources 2006 1, No. 040

Review

Blackleg in ruminants
N. M. Useh1,*, A. J. Nok2 and K. A. N. Esievo1

Address: 1 Department of Veterinary Pathology and Microbiology, Faculty of Veterinary Medicine, Ahmadu Bello University, Zaria,
Nigeria. 2 Department of Biochemistry, Ahmadu Bello University, Zaria, Nigeria.

*Correspondence: N. M. Useh. Email: nickuseh@yahoo.com

Received: 2 August 2006

Accepted: 5 October 2006

doi: 10.1079/PAVSNNR20061040

The electronic version of this article is the definitive one. It is located here: http://www.cababstractsplus.org/cabreviews

g CABI Publishing 2006 (Online ISSN 1749-8848)

Abstract

Blackleg is a per acute or acute and fatal disease of cattle and sheep caused by Clostridium chauvoei
Jakari, Vom and K76 strains in Nigeria, strains NCTC 8070 and 8361 in UK, strain 49 in India and
other parts of Asia, strain NC08596 in Germany and other parts of Europe and America, strains
ch.16 and ch.22 in Mozambique and Tanzania and strain Awasa in Ethiopia, respectively. The
haematological and biochemical changes observed in ruminants with blackleg include haemo-
concentration (increased packed cell volume, haemoglobin concentration, red blood cell counts,
and total plasma protein concentration), increased erythrocyte sedimentation rate (ESR), decrease
in total and differential leucocyte counts (leucopaenia, panleucopaenia i.e. lymphopaenia, neu-
tropaenia, eosinopaenia and monocytopaenia), thrombocytopaenia, increased plasma neur-
aminidase activity, increased erythrocyte surface and plasma sialic acid concentration, increased
levels of serum lactate dehydrogenase (LDH), alanine aminotransferase (ALT), aspartate amino-
transferase (AST) and increased creatine kinase (CK) activity. The leucopaenia and decrease in
differential leucocyte counts, increase in plasma sialic acid concentration and decrease in ery-
throcyte surface sialic acid levels were attributed to the action of neuraminidase, whose activity is
increased in the plasma in clinical blackleg. The neuraminidase produced by C. chauvoei is reported
to possibly play a significant role in the inflammation and vascular permeability which are observed
in blackleg. The pathological changes observed in cattle, sheep and deer with blackleg are
essentially similar and are discussed. Some herbal remedies (Tamarindus indicus and Combretum
fragrans) have been used by the transhumance (nomadic) Fulani pastoralists of rural Nigeria to
successfully treat the disease. The economic losses of ruminants to the disease have not been
quantified in most countries of the world, but in Nigeria, annual losses of cattle to it have been
estimated at US$4.3 million. Vaccination has remained the best control strategy against the disease,
which is endemic in Africa, USA, Central and Southern America, Asia and Europe.

Keywords: Blackleg, Ruminants, Clostridium chauvoei

Introduction 1929 [6] and has remained a major problem of cattle in

Blackleg is a fatal disease of cattle and sheep mainly (but
has also been reported in deer and other animal species),
caused by Clostridium chauvoei, and was first reported in
1870 [1]. Other synonyms of the disease are: black-
quarter, emphysematous gangrene, symptomatic anthrax,
quarter ill [2], gangrenous myositis [3], clostridial myositis
of ruminants [4] and clostridial myocarditis (blackleg of
the heart) [5]. In Nigeria, the disease was first reported in
the country. Although vaccination against it has been
carried out since 1930, sporadic outbreaks are recorded
annually.
C. chauvoei ( Jakari strain), which causes blackleg in
indigenous Nigerian cattle, has been found to produce
neuraminidase [7]. Studies on this enzyme have not been
carried out in the Vom and K76 strains, which have also
been isolated in clinical cases of blackleg in the country.
Neuraminidases (sialidases, EC 3.2.1.18) are involved in

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2 Perspectives in Agriculture, Veterinary Science, Nutrition and Natural Resources
the pathogenesis of infectious diseases, whose aetiologic
agents produce the enzyme [8–13]. The use of neur-
aminidase inhibitors to manage blackleg is a potential
therapeutic strategy that is currently being assessed [14].
This review article provides detailed background infor-
mation on the aetiology, susceptible hosts, epidemiology,
haematology and biochemical changes, pathogenesis,
pathological findings, differential diagnosis, diagnosis,
management, prevention and control of the disease.
Aetiology
Blackleg is caused by C. chauvoei. The organism was named
after Professor J. A. B. Chauveau, a French bacteriologist
[15], and 23 strains of the bacterium have been described
[16]. In Nigeria, Jakari, Vom and K76 strains have been
incriminated as the aetiologic agents of the disease [17,
18], while NCTC 8076 and 8361 [19], strain 49 [20],
strain NC 08596 [19], strains ch.16 and ch.22, strain
Tukyu and strain Awasa [21] have been reported to cause
blackleg in UK, India and other parts of Asia, Germany,
other parts of Europe and the Americas, Mozambique,
Tanzania and other parts of east Africa and Ethiopia,
respectively. These strains are also responsible for the
disease in both the natural and accidental hosts [22].
Susceptible Hosts
Blackleg is a fatal disease of cattle and sheep, but out-
breaks have been reported in deer [1], pig [23], horse
[24] and ostrich [25]. C. chauvoei has been isolated
from hens with a disease of complex aetiology [26] and
wounds of dogs and cats [27]. Another report suggests
that horses, rabbits, mice and pigeons are resistant to
the disease [28]. In cattle, the disease mostly affects
young stock between the ages of 6 months and 2 years
[29, 30].
Epidemiology
Blackleg is an endemic disease in both developed and
developing countries of the world and is a well-known
cause of financial loss to cattle raisers in many parts of
the world [30]. The economic losses of ruminants to the
disease have not been quantified in most parts of the
world, but in Nigeria, the losses of Zebu cattle alone to
the disease have been estimated at US$4.3 million annually
(600 million naira) [31]. In USA, Latin America, India and
other parts of Asia and Europe, the economic losses of
ruminants to blackleg have not been estimated, but it has
been reported that the disease causes major economic
losses in cattle and minor losses in sheep [30, 32–35]. The
disease is enzootic in areas associated with flooding and
the case fatality rate of blackleg may at times approach
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Figure 1. A Zebu calf with blackleg on sternal recum-
bency
100% [29, 30]. C. chauvoei has been isolated in 30% of
postmortem specimens in Nigeria [6].
The incubation period of blackleg may either be 1–5
days [2] or 2–5 days [28]. The clinical signs in the per
acute form of the disease are so short-lived that they are
usually not observed [20]. The acute form of the disease is
the most commonly reported [3]. The observable clinical
signs associated with blackleg in cattle (see Figure 1)
include marked lameness with pronounced swelling of
the affected limbs, marked depression, anorexia, ruminal
stasis, high pulse rate (100–120/min), acute rumen tym-
pany, high temperature (41 C) [36], protruding tongue,
tongue and throat swelling; oedema, emphysema and
crepitation of affected heavy muscles, marked respiratory
distress, stiffness of thigh muscles and reluctance to move;
and discoloured, dry and cracked skin [37]. The clinical
signs of the disease in sheep are the same as in cattle,
except that crepitation may not be palpable in the swelling
during life [22, 36].
The clinical signs observed in hill bulls experimentally
infected with C. chauvoei [20] are similar to those report-
ed by other authors [36, 37] in natural infections. The
course of disease was acute, and per acute cases were not
encountered. The authors were of the view that the
factors responsible for determining the course of infec-
tion in blackleg need to be investigated further. It has been
suggested that acquired immunity, nutritional status and
age, besides other undetermined factors may be respon-
sible for the course of the disease [38]. The clinical pre-
sentation of blackleg in deer [1] and horse [24] is similar
to the clinical picture reported in cattle, while in sheep,
subcutaneous oedema is not common and gaseous cre-
pitation is usually not observed before death [22, 36]. The
clinical presentation of clostridial myocarditis (also known
as myocarditis due to C. chauvoei or blackleg of the heart)
has been described in cattle [5, 39–42] and sheep [42] and
is usually not pathognomonic for the disease, except for
the short duration from onset to death. Depression,
dyspnoea and recumbency of approximately 81 h are

observed. Clostridial myocarditis is rare in cattle, sheep
and deer all over the world [5].
Haematological and Biochemical Changes
Hypovolaemia occurs in later stages of blackleg [43].
Studies on the haematological and biochemical alterations
in hill bulls experimentally infected with C. chauvoei [20]
showed that such hill bulls developed haemoconcentra-
tion, which was evident by significantly increased ery-
throcyte count (8.661012/l), haemoglobin (150 g/l) and
haematocrit (0.44/l). This was associated with fluid exu-
dation in subcutaneous tissues and muscles and serous
effusions in the body cavities. Thrombocyte and total
leucocyte counts were significantly decreased initially at
1–3 days post-infection (180109/l and 4.91109/l). Lym-
phocytes also correspondingly decreased (4.47109/l).
These findings are in consonance with the findings in
bacterial infections. The fluid exudation in subcutaneous
tissues and serous effusions in the body cavities aggra-
vated the haemoconcentration and hence the elevated
values of the haemogramme. The possible cause of the
thrombocytopaenia could be toxaemia [44], while the
leucopaenia may have occurred as a result of the
destruction of leucocytes by the effusing toxins in tissues.
It was suggested that the effect of toxins on circulating
leucocytes and thrombocytes need to be studied further
[20]. In another study [31], there was increased ery-
throcyte sedimentation rate (ESR) in Zebu cattle experi-
mentally infected with C. chauvoei ( Jakari strain) and peak
values of ESR were attained on day 3 (72 h) post-infection.
The ESR remained significantly higher in the infected than
the control animals from day 7 to day 21 post-infection, at
a time when the oedema and haemoconcentration that
preceded this time had subsided. The statistically sig-
nificantly higher ESR was accompanied by low packed cell
volume from day 7 post-infection, suggesting that anaemia
may have occurred in the early stage of the disease,
especially on day 3 (72 h) post-infection, but was masked
by haemoconcentration. The low mean packed cell
volume persisted up to day 21 (413 h) when the experi-
ment was terminated. Since increased ESR is associated
with anaemia, the author concluded that anaemia may be a
haematological change associated with blackleg, but is
usually not observed clinically because of haemoconcen-
tration which occurs as a result of diarrhoea (dehydra-
tion), oedema and anorexia.
The decrease in total leucocyte (leucopaenia) and dif-
ferential leucocyte counts (lymphopaenia, neutropaenia,
eosinopaenia and monocytopaenia) observed in blackleg
was attributed to the action of neuraminidase, whose
activity was higher in the plasma of blackleg-infected Zebu
cattle, compared with their apparently healthy counter-
parts [31] in both natural and experimental infections.
Leucopaenia has also been linked to the activity of neur-
aminidase produced in vivo by pathogenic trypanosomes
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N. M. Useh, A. J. Nok and K. A. N. Esievo 3
[10, 45] and this report gave credence to the leucopaenia
reported in blackleg.
Serum levels of lactate dehydrogenase (LDH), alanine
aminotransferase (ALT) and aspartate aminotransferase
(AST) are significantly increased during the course of the
disease. The values of creatine kinase (CK; 2800 IU/l), ALT
(66 IU/l), AST (233 IU/l) and LDH (201 IU/l) significantly
increased [43], in agreement with other reports [46, 47].
The increase in CK, AST and LDH were attributed to
skeletal and to some extent cardiac muscle damage, while
the increased ALT values appeared to be due to hepatic
damage [48]. Blood glucose values did not show any
definite pattern, as it increased in some groups of infected
animals (8.1 mmol/l) and decreased in others (4.1 mmol/l).
This agrees with the findings of other authors [49, 50].
The elevated and depleted glucose levels observed in
infected hill bulls respectively may be due to disturbances
in carbohydrate metabolism caused by C. chauvoei. It was
concluded that more work should be carried out to
explain this finding.
The haematological changes in cattle and sheep with
natural infections of C. chauvoei include haemoconcen-
tration (due to dehydration following oedema and an-
orexia, increases in packed cell volume, haemoglobin
concentration and total erythrocyte counts), and panleu-
copaenia (decreased total leucocyte counts due to
lymphopaenia, neutropaenia, eosinopaenia and mono-
cytopaenia) [22, 31], while the biochemical changes in
cattle with natural infection that have been reported
include increases in plasma neuraminidase activity and
plasma sialic acid and decreased erythrocyte surface sialic
acid concentrations [31]. The changes in serum levels of
LDH, ALT, AST, CK and glucose are similar to those
described in experimental infections [22]. The biochem-
ical changes in sheep with natural blackleg are similar to
the description in cattle [22], while the haematological
and biochemical changes in deer, pig and horse with
blackleg have not been investigated.
Pathogenesis
There is no consensus on the pathogenesis of blackleg
[20]. In the 1960s, some authors believed that C. chauvoei
enters the host animal through the oral route and intes-
tine, mixed with putrefactive material. Thereafter, the
vegetative forms of the organism enter the circulation
before localizing in injured or poorly drained muscles [2].
Another report [36] suggests that the infection is
acquired by ingestion of spores, which are probably taken
across the alimentary mucosa in macrophages and then
distributed to the tissues including muscles. The spores
reside in the muscle as a latent infection and later become
activated and vegetative when the muscle is injured in
some manner with a lowering of its oxidation–reduction
potential. This leads to anaerobiosis and reduced hydro-
gen ion concentration (pH) in the muscles, thus providing
4 Perspectives in Agriculture, Veterinary Science, Nutrition and Natural Resources
a favourable environment for the germination of the
spores to cause blackleg [51]. High rainfall is a known
predisposing factor to blackleg [5, 52], as the spores are
dispersed to far areas to become vegetative and infective
during grazing. Soil excavation has been reported to also
predispose ruminants to blackleg [53]. Vaccination could
also be a source of trauma which may predispose to
infection, by creating a favourable condition for the
growth of latent spores through needle punctures in
muscles [54, 55].
This sequence of events that leads to clinical blackleg as
described previously [36] seems to disagree with the
report of Merchant and Barner [2] who believed that
spores germinate before they reach the muscle. The later
authors are silent on any trigger mechanisms that may
promote or cause the germination of C. chauvoei spores in
the muscles, such as injury. C. chauvoei spores were found
in the livers and spleens of normal cattle [56]. This gave
further credence to the report that there must be injury
for spores to germinate and cause disease. The finding
was collaborated by the report that the mere presence of
C. chauvoei spores in the muscles of animals does not
mean any harm [57]. To become pathogenic, the spores
must be made to germinate during experimental infection
by causing injury in the muscles and liver using calcium
chloride [58], sharp objects [57] or dilute solutions of
saponins [54].
The suggested mechanisms of blackleg as outlined
above are believed to occur in cattle and sheep, including
deer, pig and horse which are unconventional hosts of
C. chauvoei [31, 49].
The Role of Toxins
The role of toxins in the pathogenesis of C. chauvoei
infection in hill bulls has been investigated [20]. It was
reported that the toxins initiated a humoral immune
response in the spleen, leading to hyperplasia of the
malphigian corpuscles in the spleen. The congestion,
haemorrhagic and degenerative foci in the liver and kidney
were also attributed to toxins. The toxins also caused
destruction of leucocytes and platelets leading to leuco-
paenia and thrombocytopaenia, respectively.
The role of neuraminidase in the pathogenesis of
blackleg has not been properly researched, although there
is a report that the enzyme assists in spreading the disease
in infected tissues [8]. An in vitro study on the char-
acterization and possible role of neuraminidase in the
pathogenesis of blackleg [7] revealed that C. chauvoei
(Jakari strain) neuraminidase has optimum pH and tem-
perature of 4.5 and 40 C, respectively. The low pH was
thought to be significant in promoting anaerobiosis,
muscle damage, removal of sialic acid from muscles of
infected animals and pathological spread of the disease in
the tissues of infected animals [51]. The optimum tem-
perature of 40 C coincided with the highest temperature
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achieved in the pyrexic phase of the disease [20] and it
was predicted that during the pyrexic phase, the removal
of sialic acid from the muscles by the enzyme may reach
the peak. The neuraminidase at the optimum pH and
temperature desialylated haemoglobin-free erythrocyte
membranes (ghosts) of cattle, sheep, goat and horse at a
statistically significant rate (P < 0.001) in vitro to further
confirm that optimum pH and temperature of the enzyme
are critical parameters required to cause muscle damage
in clinical blackleg [51].
High neuraminidase activity was detected in the
oedema fluid in blackleg and the neuraminidase was
identified as a potent mediator of inflammation and vas-
cular permeability. It cleaved sialic acid from the blood
vessels to cause diapedesis (vascular permeability) and
oedema [31]. Slauson and Cooper [59] and Kumar et al.
[60] had earlier reported other mediators of inflammation
and vascular permeability in some animal and human dis-
eases to include histamine, leukotrienes (C4, D4 and E4),
cytokines (interleukin-1, IL-1; tumour necrosis factor-a,
TNF-a), plasma kinins (bradykinins), serotonin, platelet-
activating factor, interferon, complement fragments
(anaphylatoxins C5a and C3a) and prostaglandins.
Whether these mediators of inflammation and vascular
permeability are produced in blackleg has yet to be
investigated and still remains open to research.
Gross Pathological Picture
The gross pathological changes associated with blackleg in
cattle have been described previously [36]. They include
swollen and bloated carcasses, blood-stained froth in the
nose, blotchy haemorrhages on the conjunctiva, palpable
crepitation of affected muscles, dark-coloured muscles,
haemorrhages in the parietal pleura, blood-stained clots of
fibrin on the ventral mediastinum and epicardium, con-
gested lungs with intestinal oedema and haemorrhages;
pale and friable myocardium, foci of emphysematous
myositis and necrosis and the spleen may be normal or
enlarged with congested mushy pulp. This description
tallies with the report of other authors [37]. The gross
lesions in sheep closely resemble those in cattle, except
that there is less gas and the affected muscles remain
moist rather than dry [22]. The gross lesions in deer [1]
are typically similar to those described in cattle. Pectoral
oedema is observed in horse [24].
The gross pathological changes observed in blackleg of
the heart in cattle and sheep [5, 41, 42] include irregular
dark areas of myocardial necrosis through the full thick-
ness of the atrial and ventricular myocardium, severely
congested and haemorrhagic myocardium, moderate–
excess blood-stained pericardial fluid, congested and
oedematous lung, severely congested liver, excess pleural
and peritoneal fluid, moderately enlarged and pulpy spleen
and no lesions in the skeletal muscles.

Histopathological Picture
In cattle, myonecrosis, oedema, emphysema and neu-
trophilic cellulitis are observed on microscopic examina-
tion of affected muscles [22, 31, 57, 61] both in natural
and experimental infections. Few C. chauvoei rods may be
observed in tissue sections [62]. The histopathological
picture in sheep closely resembles the findings in cattle
both in natural and experimental infections [62]. Fibrinous
pericarditis and meningitis in cattle with natural infections
of blackleg have been reported [63]. The meningitis
was characterized by thickening and cloudy appearance
of brain meninges. The meningitis was speculatively
attributed to sialic acid removal in the brain by the
neuraminidase produced by C. chauvoei [51] and the
demonstration of C. chauvoei in smears from the inflamed
meninges [63] provided strong support for the
speculation.
The microscopic pathology of blackleg of the heart in
cattle and sheep include multifocal areas of acute coagu-
lative myocardial necrosis and the affected areas contain
large numbers of Gram-positive bacterial rods with
straight sides and rounded ends, some of them with a
central or subterminal spore, which may be associated
with intestinal oedema, haemorrhages and moderate
numbers of degenerating neutrophils [5, 42]. The arteri-
oles may undergo fibrinoid degeneration and necrosis
with infiltration by polymorphonuclear leucocytes. They
could be surrounded by large numbers of C. chauvoei. The
gross and histopathological pictures of blackleg of the
heart have not been described in deer.
Differential Diagnoses
The clinical picture of some animal disorders mimics that
in blackleg. These disorders include lightning strike,
anthrax, bacillary haemoglobinuria, lactation tetany, acute
lead poisoning [22] and malignant oedema [4].
Diagnoses
The criteria for diagnosis of clostridial infections have
been outlined [64]. Diagnosis of these infections cannot
be made based on the mere presence of the causative
organism, without due regard to other relevant factors
such as clinical picture, postmortem findings and state
of decomposition. It has been suggested that smears of
affected tissues should be made in suspected post-
mortem cases and samples should be collected for bac-
teriological examination. The presence of Gram-positive
rods compatible with C. chauvoei has been demonstrated
in impression smears made from heart blood, inoculated
muscles and liver samples using Gram’s staining
method [20].
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N. M. Useh, A. J. Nok and K. A. N. Esievo 5
Certain immunodiagnostic tests such as tube aggluti-
nation test, agar gel double immunodiffusion (DID) test
and counter immunoelectrophoresis (CIEP) test have
been used in demonstrating the presence of C. chauvoei
antibodies [65]. DID and CIEP have been used specifically
for demonstrating C. chauvoei antibodies in the serum of
vaccinated animals [65]. Immunofluorescence has been
used to detect the presence of clostridial organisms on
meat from slaughter houses [48] and clinical cases [63].
The use of a fluorescein agent (fluorescein isothiocyanate-
labelled globulin) to diagnose the presence of C. chauvoei,
Clostridium oedematiens and Clostridium septicum has been
reported [63] and positive smears produced a char-
acteristic fluorescence. A good correlation between the
results of cultural examination of clostridia and the
fluorescent antibody technique was established [4]. In the
survey, C. chauvoei was identified by fluorescent antibody
test on 97 occasions and isolated on 89.
In an attempt to develop a more sensitive and reliable
diagnostic technique for blackleg, a study on the phylo-
genetic positions of C. chauvoei and C. septicum based on
16S rRNA (rrs) gene sequences using polymerase chain
reaction (PCR) was carried out [66]. A sequence similarity
analysis of the gene sequences for both bacteria revealed
the close phylogenetic relationship of these bacterial
species. It was found from the study that 99.3% of the
nucleotides in the genes of C. chauvoei and C. septicum are
identical. This identity informs the difficulty in distin-
guishing these bacterial species, either on culture or
biochemical tests.
C. chauvoei was identified in cultures and clinical
material from blackleg using PCR [67]. Specific oligonu-
cleotide primers, which were designed based on the rrs
gene sequences of C. chauvoei were used in the study.
The DNA sequences of the rrs genes of C. chauvoei
were compared with most of its closely related species
(C. septicum and Clostridium carnis). A subsequent restric-
tion digestion of the 960 bp amplification product was
carried out in order to unambiguously identify C. chauvoei.
This identification system was evaluated on clinical
material during an outbreak of blackleg in cattle and
C. chauvoei was identified as the aetiologic agent of the
outbreak, either directly from clinical samples or from
primary cultures made from these materials. A compar-
ison of the PCR method with standard diagnostic tools
for C. chauvoei showed that it had advantages over
immunofluorescence and is therefore a useful option.
Moreover, the test is a valuable tool for the phylogenetic
identification of C. chauvoei, which can assist to substitute
the fastidious traditional identification methods.
Management
Penicillins (10 000 IU/kg) are a drug of choice in the clinical
management of blackleg. A 3–5 days therapy period
is recommended. It is generally advocated that the
6 Perspectives in Agriculture, Veterinary Science, Nutrition and Natural Resources
administration of crystalline penicillin intravenously should
precede the long-acting preparations that should be
administered directly in the affected tissues [22]. The
nomadic Fulani agropastoralists of rural Nigeria, who
own about 70–80% of livestock in Nigeria, have used
Tamarindus indicus and Combretum fragrans to successfully
manage blackleg in cattle [68]. In outbreak situations, they
boil both the roots and stem barks of these plants and
administer to the sick animals. However, the dosage
regiments of these herbs in rational drug administration
remain undefined. It was later found that these medicinal
plants, which are indigenous to Nigeria, inhibited the
neuraminidase produced by C. chauvoei (Jakari strain)
[69]. Based on this finding, it was predicted that the
inhibition of the enzyme may be the possible mechanism
of pharmacological action by which the medicinal plants
ameliorated blackleg. Recently, it was speculated that
neuraminidase inhibitors may be of value in the clinical
management of blackleg [14, 69, 70]. The effect of inhi-
bition of one toxin (alpha, beta, gamma, delta toxins or
neuraminidase) on the others in vitro or in vivo has yet to
be investigated. It was therefore suggested that proper
clinical trials should be carried out to confirm the suit-
ability for use, of neuraminidase inhibitors in the clinical
management of the disease.
Prevention and Control
The first documented evidence of a successful vaccination
against blackleg was in 1882 [71] and since then, vacci-
nation has proved to be the most reliable preventive
measure against the disease [72]. Annual vaccination of
cattle between 6 months and 2 years of age is advocated
in areas where the disease is enzootic, just prior to the
anticipated danger period. In Nigeria, a regime of pre-
ventive vaccination that should be carried out twice
annually at the beginning of the rains with an interval of 10
days before heavy rain begins has been suggested [6].
Vaccination of calves at 3 weeks old has been recom-
mended where the incidence of the disease is very high
[29, 30]. Subsequent revaccination may also be advisable
[30, 37]. Different types of vaccines have been developed
against the disease [21, 72] but, generally, formalized
vaccines have been found to be very effective. Monoclonal
antibodies have been developed against blackleg [73]. The
use of polyvalent vaccines has been recommended [74].
Grazing on soils contaminated with spores should be
avoided and dead carcasses should be properly disposed
of by burning or deep burial.
Conclusion
Blackleg is a fatal disease of ruminants that is endemic in
both developing and developed countries of the world
and vaccination has remained the best control strategy
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against the disease. Annual vaccinations with constant
antibody monitoring will help in identifying animals at risk.
Acknowledgements
We thank Mrs E. O. Ajiboye for typing this paper. Also,
the arrival of Johnmark Kerter Useh brought the peace of
mind, inspiration and academic enthusiasm needed to put
this paper together.
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3. Williams BM, Andrews AH. Bacterial conditions. In: Andrews
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