Pakistan Veterinary Journal
ISSN: 0253-8318 (PRINT), 2074-7764 (ONLINE)
Accessible at: www.pvj.com.pk
Enteric Diseases of Poultry with Special Attention to Clostridium perfringens
Hafez Mohamed Hafez*
Institute of Poultry Diseases, Faculty of Veterinary Medicine, Free University Berlin, Königsweg, 14163 Berlin, Germany
*Corresponding author: email@example.com
October 10, 2010
April 18, 2011
April 21, 2011
The enteric health of growing poultry is imperative to success of the production.
The basic role of poultry production is turning feed stuffs into meat. Any changes in
this turning process, due to mechanical, chemical or biological disturbance of
digestive system (enteric disorders) is mostly accompanied with high economic
losses due to poor performance, increased mortality rates and increased medication
costs. The severity of clinical signs and course of the disorders are influenced by
several factors such as management, nutrition and the involved agent(s). Several
pathogens (viruses, bacteria and parasites) are incriminated as possible cause of
enteric disorders either alone (mono-causal), in synergy with other micro-organisms
(multi-causal), or with non-infectious causes such as feed and /or management
related factors. In addition, excessive levels of mycotoxins and biogenic amines in
feed lead to enteric disorders. Also factors such as high stocking density, poor litter
conditions, poor hygiene and high ammonia level and other stressful situation may
reduce the resistance of the birds and increases their susceptibility to infections.
Under field conditions, however, it is difficult to determine whether the true cause
of enteric disorders, is of infectious or non-infectious origin. In recent years and
since the ban of use of antimicrobial growth promoters in several countries the
incidence of intestinal disorders especially those caused by clostridial infection was
drastically increased. The present review described in general the several factors
involved in enteric disorders and summarized the available literatures about
Clostridium perfringens infection in poultry.
©2011 PVJ. All rights reserved
To Cite This Article: Hafez HM, 2011. Enteric diseases of poultry with special attention to Clostridium perfringens.
Pak Vet J, 31(3): 175-184.
The basic role of poultry production is turning feed
stuffs into meat. Broilers and meat turkeys are very
efficient at both growth and feed conversion rate. Any
slight alteration from the optimal condition is mostly
accompanied by disruption of the growth process and all
over performance. To reach the maximal potential of
development, considerable demands should be placed on
good intestinal health.
Enteric disorders are one of the most important
groups of diseases they affect poultry and are continuing
to cause high economic losses in the many areas world-
wide due to increased mortality rates, decreased weight
gain, increased medication costs, and increased feed
conversion rates. Several pathogens (viruses, bacteria and
parasites) are incriminated as possible causes of enteric
disorders either alone (mono-causal), in synergy with
different other microorganisms (multi-causal) or with
non-infectious causes such as feed and /or management
related factors (Table 1). Under field conditions, however,
it is difficult to determine weather the true cause of enteric
disorders in poultry is of infectious or non-infectious
origin (Hafez, 2001).
Since the first report of Moore et al. (1946), it is
generally known, that supplementation of poultry feed
with antibiotic growth promoters (AGPs) improves
performance of livestock. The effect of AGP on gut flora
results in improvement of digestion, better absorption of
nutrients, and a more stable balance in the microbial
population. As consequence this is accompanied with
reduced intestinal disorders. However, AGP can also
increase the prevalence of drug-resistant bacteria.
Based on “Precautionary Principle” and experiences
made in Sweden, Denmark, Germany and the
Netherlands, the EU has decided to ban the use of growth-
promoting antibiotics in feed of food producing animals
completely by January 2006. The first step was taken in
Pak Vet J, 2011, 31(3): 175-184.
1997 by the ban of avoparcin, followed by spiramycin,
tylosin phosphate, zinc bacitracin and virginiamycin in
1998 and carbadox and olaquindox in 1999. Field
observations in several countries in Europe showed that
poultry industry faced several problems after the ban of
AGPs. The impact of the ban has been seen on the
performances (body weight and feed conversion rate) as
well as on the rearing husbandry (wet litter and ammonia
level), animal welfare problem (foot pad dermatitis) and
general health issues on the birds (enteric disorders due to
dysbacteriosis and clostridial infections) (Hafez, 2008).
The present paper reviews the currently most
important causes of enteric disorders of poultry and their
economic impacts with special attention to clostridial
Table 1: Some possible causes of enteric disorders in poultry
Non - Infectious Infectious
Feed Viral agents
Structure Reo, Astro, Entero, Rota,
Palatability Coronavirus enteritis, HE
Energy content ND, Influenza A
Pellet quality Bacterial agents
Management Salmonellas, E. coli,
Available feed space Clostridia
Available water space Mycotic agents
Distribution of feeders Candida
Distribution of waterers Parasites
Air quality Coccidia, Histomonas,
Temperature Hexamitia, Ascaridia
Non-infectious factors involved in intestinal disorders
Enteric health and nutrition are closely related. Poor
enteric health can adversely affect food digestion, gut
motility and nutrient absorption by several means.
Likewise, poor nutrition and feed quality can either
increase the bird’s susceptibility to enteric disorders or
directly cause them (Ferket, 1996; Hafez, 1998).
Nutritional factors that influence gut health include feed
intake, palatability, feed ingredient quality, feed
formulation and pellet quality. In addition, mistakes in
feeding technique, the amount of fibre in the feed, the
content and quality of the raw materials as well as sudden
feed changes or restriction, can result in changes in the
intestinal flora and/or in the enzymatic activity which lead
to digestive disorders (Nixey, 1989; Kaldhusdal and
Skjerve, 1996; D’Mello, 1997; Corless and Sell, 1999;
Annett et al., 2002; Batal and Parsons, 2002; Kocher,
2003; McReynolds et al., 2004). Also, excessive levels of
mycotoxins and biogenic amines in feed lead to enteric
disorders (Smith and Hamilton, 1970; Burditt et al., 1983;
Brown et al., 1992; Dwivedi and Burns, 1986; Hoerr,
Feed contains a little dust; however, excess dust can
adversely affect the palatability and lead to reduction of
feed intake. Badly stored feed can contain fungal spores,
and fat may go rancid which results in reduction of the
feed intake and may negatively affect the content of some
vitamins in the feed (Dhand et al., 1998; FAO, 2004).
Inadequate feeder space and false distribution can result in
competition and stronger birds dominating the feeder with
a consequent variation in feed intake within the flock.
Feed can contain undesirable substances such as
mycotoxins, which adversely affect the immune system,
increase the susceptibility of the birds to infectious
diseases and cause poor response to vaccine (Uraguchi
and Myamazaki, 1978; Campbell et al., 1981; Burns and
Dwivedi, 1986; El-Karim et al., 1991; D’Mello et al.,
1993, D’Mello and MacDonald, 1998; Devegowda et al.,
1998). Proper adjustment of feeder is a factor that should
receive constant attention (Hafez, 1998).
Management and environmental factors
Good rearing management is the starting point for
healthy, productive and profitable poultry production in
agreement with animal welfare. Rearing management
mean all factors which influence the birds health include
several factors such as house structure, climatic conditions
(ventilation, temperature, litter condition), stocking
density, feed and water supply, hygienic condition as well
as the knowledge’s and qualification of the stockman.
These factors affect each other and can promote or inhibit
the health condition of the flock. In aim to achieve desired
performance results, managers of turkey flocks should
integrate good environment, husbandry, nutrition and
disease control programmes (Sundrum, 1995; Hafez,
1996; 1998). The rearing management must be directed to
satisfy the bird’s requirements, to promote the production
and to prevent diseases condition (Morgen and Avens,
1985). Any disturbance will cause stress, which will
reduce the resistance of the birds, increase their
susceptibility to infections and reduce their immune-
response to vaccines (Sainsbury, 1992; Hafez, 1998).
Several infectious agents such as viruses, bacteria,
fungus and parasites are involved in intestinal disorders
(Fig. 1). These infectious agents can introduce and spread
in poultry farms by different routes. It occurs by vertical
and/or horizontal route. At early days of age the main
disease problems are related to vertically transmitted
infections such as salmonella, E. coli and improper
hatchery management (Hafez, 1999; Hafez, 2005;
Bermudez and Stewart-Brown, 2008). Those and other
infectious agents can also be transmitted horizontally
(laterally) by direct contact between infected and non-
infected susceptible birds, and through indirect contact
with contaminated feed, water, equipment, environment
and dust through ingestion or inhalation (Hafez, 1996;
Bermudez and Stewart-Brown, 2008).
Infections with Clostridium perfringens
Infections with Clostridium perfringens in poultry
can cause several clinical manifestations and lesions
include necrotic enteritis, necrotic dermatitis,
cholangiohepatitis as well as gizzard erosion. However,
subclinical infection can take place too. In addition, C.
perfringens type A has been showed to cause food
poisoning in humans (Løvland and Kaldhusdal, 2001;
McClane et al., 2006; Novoa-Garrido et al., 2006).
Clostridium perfringens is a Gram-positive, non-
motile, spore-forming anaerobic bacterium which is
widespread in soils, feed, litter and the intestinal tract of
Pak Vet J, 2011, 31(3): 175-184.
diseased and healthy birds (Char et al., 1986; Frame and
Bickford, 1986; Gazdzinski and Julian, 1992; Branton et
al., 1997). The optimum growth occurs within
temperature range of 12-50°C and pH between 6.0 and 7.0
(Adams and Moss, 1995). Under optimal conditions,
43−47°C, C. perfringens grows extremely rapidly, with a
generation time of 8-10 min, and growth is accompanied
by abundant gas production (Bryant and Stevens, 1997).
The bacterial spores are very resistant to heat, desiccation,
acids and many chemical disinfectants (Willis, 1977).
C. perfringens is divided into 5 biotypes A, B, C, D,
and E based on the synthesis of four major lethal toxins:
alpha, beta, epsilon, and iota. Along with these four major
toxins, enterotoxin (CPE) and beta2 (CPB2) toxins
produced by C. perfringens are considered as important
toxins for enteric diseases (McDonel, 1986; Songer, 1996;
Waters et al., 2003, Smedley et al., 2004, McClane et al.,
2006). However, it is not clear whether CPE and CPB2
are involved in C. perfringens-associated avian enteric
diseases (Crespo et al., 2007).
The infections in poultry are mostly caused by C.
perfringens type A, and to a lesser extent by type C
(Songer and Meer, 1996; Engström et al., 2003). Because
C. perfringens type A is highly prevalent in the intestines
of healthy animals, controversy exists about its real
pathogenic role (Smedley et al., 2004; McClane et al.,
2006). Additionally, it was shown that strains isolated
from necrotic enteritis outbreaks did not produce more
alpha toxin compared to isolates from the gut of clinically
healthy broilers (Gholamiandehkordi et al., 2006).
Timbermont et al. (2009) examined the ability of C.
perfringens isolates from both healthy and diseased
poultry, and from calf hemorrhagic enteritis cases,
producing different concentrations of alpha toxin in vitro,
to induce necrotic enteritis in broilers. The obtained
results revealed that induction of necrotic lesions in the
broiler gut is not associated with the ability to produce
alpha toxin in vitro. Moreover, the results also suggest
that the virulence of C. perfringens strains is to some
extent host specific since two C. perfringens strains
isolated from calf hemorrhagic enteritis were not able to
produce necrotic lesions in chickens.
Keyburn et al. (2008) were able to identify a novel
toxin (netB) in a C. perfringens type A strains isolated
from chickens suffering from necrotic enteritis. According
to the authors this novel toxin is the first definitive
virulence factor to be identified in avian C. perfringens
strains capable of causing necrotic enteritis. However,
netB strain could be also found in healthy chickens and
turkeys (Gad et al., 2011a) as well as in other animal
species such bovine (Martin, 2010). On the hand, Martin
(2010) reported that the majority (58%) of chickens with
NE were caused by C. perfringens isolates that were NetB
positive. Under experimental condition they found that
only strains that possess NetB were capable of producing
NE regardless of the source of the isolate. NetB negative
strains including those isolated from cases of NE were
unable to produce NE in the disease model. Martin and
Smyth (2009) also found a strong correlation between the
detection of the cpb2 gene and netb gene. However, when
interpreting the results it has to be kept in mind that the
presence of the gene of a toxin does not necessarily mean,
that the toxin is produced, as it was shown for netb toxin
(Abildgaard et al., 2010) or cpb2 (Crespo et al.,2007).
Necrotic enteritis (NE)
NE is an acute disease caused by Clostridium
perfringens when proliferates to high numbers in the
small intestine and produces toxins responsible for
damaging the intestinal lining (Long and Truscott, 1976;
Shane et al., 1985). It was firstly described by Parish
(1961). The disease has been observed in several domestic
and wild birds world wide. Recently several reviews were
published (Van Immerseel et al., 2004; Williams, 2005;
Wilson et al., 2005; McDevitt et al., 2006; Opengart,
2008). Beside clinically manifested disease, subclinical
infections may take place and are mostly accompanied
with reduction of performance.
Mode of infection
The most important source of infection in poultry
appears to be contaminated feed, litter, water and the
environment (Wijewanta and Seneviratna, 1971;
Komnenov et al., 1981; Craven et al., 2001a). In addition,
some reports about the possible vertical transmission have
been published (Köhler et al., 1974a, b; Shane et al.,
1984; Craven et al., 2001b, 2003). Recently, Martin
(2010) were able to demonstrate under experimental
condition, that factors such as co-infection with Eimeria
species, genotype of chicken and the strain of C.
perfringens were the most critical factors involved in
disease development, while other factors such as age of
chickens, contact with litter and protein content of the diet
played a lesser role.
Clinical signs and lesions
After experimental infection, the first mild clinical
signs are evident approximately 24 to 36 hours after
administration of a pure C. perfringens culture to broiler
chickens (Bains, 1968; Helmboldt and Bryant, 1971;
Balauca et al., 1976; Al-Sheikhly and Truscott, 1977;
Balauca, 1978). The clinical signs appear suddenly;
apparently healthy birds may become acutely depressed
and die within hours (Long, 1973; Tsai and Tung, 1981;
Shane et al., 1985). Mortality ranges between 2 and 10%.
Affected birds show ruffled feathers, marked depression,
in-appetence, tendency to huddle, watery droppings and
diarrhoea (Long, 1973; Porter, 1998; Gazdzinski and
The presence of C. perfringens in the intestinal tract
or inoculation of the animals with high doses of C.
perfringens, however, does generally not lead to the
development of necrotic enteritis. One or several
predisposing factors may be required to elicit the clinical
signs and lesions (Shane et al., 1984; Cowen et al., 1987;
Kaldhusdal et al., 1999). It appears that some
dysfunctions of the alimentary tract are necessary
predisposing cause of infection. Intestinal stasis, intestinal
distension, coccidiosis, salmonellosis, crop mycosis and
haemorrhagic enteritis (HE) may predispose the birds to
infection (Al-Sheikhly and Al-Saieg, 1980; Shane et al.,
1985; Baba et al., 1992, Williams, 2005). Factors
predisposing the intestinal tract to overgrowth by
clostridia organisms may also be the consumption of diets
high in energy, protein and fish meal as well as the
Pak Vet J, 2011, 31(3): 175-184.
consumption of high fibre litter and wheat based diet
(Branton et al., 1987; 1997; Kaldhusdal and Skjerve,
1996; Ficken and Wages, 1997; Kocher, 2003). Panneman
(2000) demonstrated that the proximal intestine of normal
birds has very low levels of bacteria, whereas birds
affected with dysbacteriosis have substantially higher
bacterial counts. Clostridium spp. has been shown to
contribute to this overgrowth. Dysbacteriosis is defined as
the presence of a qualitatively and/or quantitatively
abnormal flora in the small intestine causing a clinical
disorder and/or malabsorption. It is seen in broilers after
21 days of age with wet faeces and a reduction in feed
intake (Fabri, 2004). Furthermore, Siegel et al. (1993)
reported that genetic susceptibility could be an additional
factor, which can influence the course of infection, since a
significant difference in mortality rate between different
major histocompatibility complex genotypes was
observed. An outbreak of necrotic enteritis occurred in
chickens that were B13B13 or B21B21 at the MHC in
sublines of lines selected for high (HA) and low (LA)
antibody response to sheep erythrocytes. Percentage
mortality and hen-day egg production, although similar
for both background genomes, were different for MHC
genotypes. Mortality was 6% for B21B21 and 15% for
B13B13 types. Although hen-day egg production for both
types declined from about 76 to 50%, the decrease
occurred earlier but recovery of survivors was faster in
B13B13 than in B21B21 pullets (Siegel et al., 1993).
On autopsy dehydration is the most common finding.
Breast muscles are dark red and gizzards are full of litter.
Severe inflammation in the duodenum and jejunum is the
most predominant finding, but in some instances the entire
length of the intestinal tract is involved (Bains, 1968;
Helmboldt and Bryant, 1971; Long et al., 1974; Tsai and
Tung 1981; Ficken and Berkhoff, 1989). The intestine is
distended thin walled and filled with gas and contains
dark offensive fluid (Broussard et al., 1986). The mucosa
is covered with green or brown diphteroid membrane,
which can be easily separated from the lining (Fig. 1).
Varying degrees of sloughing of the intestinal mucosa
could also be observed (Fig. 2). As the condition
progresses, areas of necrosis can be recognized from
outside of the intestine (Helmboldt and Bryant, 1971;
Long et al., 1974; Balauca, 1978; Shane et al., 1985).
Initial microscopic lesions develop at the apices of
villi and are characterized by sloughing of epithelium and
colonization of the exposed lamina propria with bacilli,
accompanied by coagulation necrosis. Progression of
lesions usually occurs from villi apices to crypts. Necrosis
may extend into the submucosa and muscular layers of the
intestine (Fig. 3) (Nairn and Bamford, 1967; Helmboldt
and Bryant, 1971; Long et al., 1974; Tsai and Tung, 1981;
Opengart, 2008). Large numbers of gram-positive bacilli
can be seen (Fig. 4 and 5) within the necrotic debris
(Randall, 1991). In per acute cases there is little
inflammatory cell infiltrate although, if the animal
survives, there is a progression to heterophil and
mononuclear cell infiltration followed by fibrosis (Shane
et al., 1985; Ficken and Wages, 1997).
Cholangiohepatitis causes severe economic losses
due to high liver condemnation rate on the processing and
downgraded of the slaughtered carcasses. Clostridium
perfringens is usually isolated in association with the
disease. The hepatitis characterized by an enlarged firm
liver sometimes with a slightly knobby surface and a
medium tan colour. Histopathological lesions consist of
hyperplasia of the bile duct, fibrinoid necrosis, cholangitis
and occasionally focal granulomatous inflammation
(Onderka et al., 1990; Løvland and Kaldhusdal, 1999;
Sasaki et al., 2000). Onderka et al. (1990) experimentally
reproduced the condition by either tying off the bile ducts
or injecting C. perfringens into the bile duct. It seems that
the presence of C. perfringens in many of the gall
bladders of affected livers suggested some involvement of
either the bacterium or its toxin which interfere with the
Gizzard erosions has been observed in commercial
broiler chickens and several non-infectious factors such as
mycotoxin-contaminated feed, vitamin B6 and E
deficiency, inadequate levels of sulphur-containing
dietary amino acids, high levels of dietary copper, pelleted
feed as well as inclusion of certain fish meals in the diets
and were discriminated as possible cause. Ono et al.
(2003) reported on Outbreaks of adenoviral gizzard
erosion in slaughtered broiler chickens in Japan and
Novoa-Garrido et al. (2006) found a significant
association between gizzard lesions and increased caecal
C. perfringens counts in broiler chickens.
A presumptive diagnosis may be made from the case
history, clinical signs, lesions and staining fresh smears of
upper part of the intestinal tract with Gram stain showing
an abundant number of clostridia organisms (Ficken and
Wages, 1997; Hafez and Jodas, 1997). This should be
confirmed by the isolation of the causative agent. For
isolation several media are available such as sheep blood
agar supplemented with neomycin or tryptose-sulfite-
cycloserine agar (TSC). The identification can be carried
out using biochemical tests. Most of isolates ferment
lactose, glucose, maltose, hydrolyze gelatin, and reduce
nitrate. This bacterium is non-motile, indole and catalase
negative (Ficken and Berkhoff, 1989). In addition, PCR
was developed to detect of alpha toxin (Heikinheimo and
Korkeala, 2005) as well as a real-time PCR for
quantitative detection of C. perfringens in gastrointestinal
tract of poultry (Wise and Siragusa, 2005). Also ELISAs
for direct detection of C. perfringens major toxins and
enterotoxin are commercially available.
Treatment with antibiotics such as penicillin,
amoxicillin, ampicillin, erythromycin, dihydrostrepto-
mycin and tetracyclin provided a satisfactory clinical
response. Penicillin’s are known to be particularly active
against C. perfringens. Resistance to penicillin is very rare
and β-lactamase has not been demonstrated. Three days is
the minimum duration of treatment, however longer
applications may be required. Recently, Gad et al. (2011b)
were determined the minimum inhibitory concentrations
of 16 antibiotics for 100 Clostridium perfringens isolates
collected between 2008 and 2009 from commercial turkey
Pak Vet J, 2011, 31(3): 175-184.
flocks using a commercially available broth micro-
dilution test kit. No isolates were resistant against β-
lactam antibiotics (amoxicillin, oxacillin, and penicillin),
lincospectin, tylosin, doxycyclin, tetracycline,
enrofloxacin, trimethoprim/sulfamethoxazole, lincomycin,
and tilmicosin. A low frequency of resistance was
detected against erythromycin and tiamulin with 5 and
20%, respectively. Spectinomycin, neomycin and colistin
showed the highest incidence of resistance with 74, 94
and 100%, respectively.
According to Brennan et al. (2000) administration of
dietary Tylan® for seven consecutive days following
Fig. 1: Necrotic enteritis: The mucosa is covered with green or
brown diphtheroid membrane, which can be easily separated
from the lining.
Fig. 2: Severe necrotic enteritis with necrotic pseudomem-
brane covering the intestinal mucosa.
Fig. 3: Severe, acute, necrotizing enteritis with extensive
transmural spreading as well as associated, necrotizing and
granulomatous steatites/serositis; large number of Gram-
Positive bacilli, located multifocal within lesions (H & E 20X)
(Courtesy: Dr. Olivia Kershaw, Berlin).
Fig. 4: Necrotic enteritis: note large number of Gram-Positive
bacilli, located multifocal on the surface as well as within lesions
(Gram X200) (Courtesy: Dr. Olivia Kershaw, Berlin).
Fig. 5: Necrotic enteritis: note large number of Gram-Positive
bacilli, located multifocal on the surface as well as within lesions
(Gram X600) (Courtesy: Dr. Olivia Kershaw, Berlin).
confirmation of an NE field outbreak reduced the NE
mortality and lesion score and improved overall growth as
well as feed conversion in broilers. The optimum dose of
Tylan to control NE was 100 ppm.
No resistance to the ionophorous anticoccidial drugs
such as Narasin has been found (Watkins et al., 1997;
Martel et al., 2004). Brennan et al. (2001) reported that
Narasin, when administrated at 70 ppm in feed from Day
0 to 41 prevents morbidity, mortality and suppression of
growth and feed conversion associated with NE in
For the commercial poultry industry, controlling the
levels of C. perfringens is an important issue because of
the economic cost of infected flocks. It has been estimated
that, worldwide, C. perfringens costs the international
poultry industry in excess of $US 2 billion per year
(Kaldhusdal and Løvland, 2000). In addition, costs to
broiler producers associated with subclinical (mild)
necrotic enteritis (SNE) were estimated recently by
Skinner et al. (2010) using published information on
impacts on body weight and feed conversion rate (FCR)
associated with SNE and costs and revenues associated
with broiler production. SNE was estimated to result in a
12% reduction in body weight and a 10.9% increase in
FCR compared with healthy birds. For the purposes they
considered scenarios involving hypothetical flocks of
Pak Vet J, 2011, 31(3): 175-184.
20,000 birds raised to final body weights ranging from
4.63 to 7.94 lb. The incidence of SNE was assumed to
occur at 20% based on the literature. SNE resulted in a
loss to producers ranging from US$878.19 to US$1480.52
per flock. When feed costs required to obtain SNE flocks
having a total live body weight equal to equivalent healthy
flocks at market age were calculated, the increased cost to
producers ranged from US$370.49 to US$739.38 per
flock (Skinner et al., 2010).
Strategies to reduce the incidence of clostridial
infections are necessary help to increase the profitability
of the poultry production and several further approaches
are generally used to combat the infection and as
alternatives to AGPs. Investigations indicate that
competitive exclusion, prebiotics, probiotics, enzymes and
acids can impact the incidence and severity of NE in
poultry (Fukata et al., 1991; Elwinger et al., 1992;
Hofacre et al., 1998; Kaldhusdal et al., 2001). The data
suggest that these products may provide the poultry
industry with an alternative management tool that has the
potential to promote better intestinal health and decrease
monetary losses due to C. perfringens (McReynolds et al.,
According to Langhout (2007), these approaches will
need adaptations in the feeding program and/or feed
production. The practical relevance of these approaches
may vary between the different areas in the world. At this
moment it is difficult to evaluate novel strategies
developed to antibiotic-free feeding concepts.
Combination of different approaches is necessary to
enhance the performance and reduced health status of the
birds such as:
i) Selection of highly digestible feed ingredients to
reduce nutrients for microbial degradation.
ii) Improvement in the balance of the essential amino
acids resulting in lower total dietary protein levels.
This will reduce the risk for clostridium problems,
since this bacterium in particular increases during
iii) Improvement in the physical form of the diet, for
example via the inclusion of coarse particles in the
diet. Coarse particles will improve the passage rate of
the feed through the intestinal tract and as a
consequence increase digestion and reduce bacterial
fermentation in the intestinal tract.
iv) Introduction of a special prestarter diet in the feeding
program. The main objective of this prestarter diet
should be to stimulate the development of the
immune system and the development of an optimal
v) Improvement of climate control in the broiler house
to avoid stress in the animal and keeping litter quality
in optimal condition.
vi) Improvement of disease control in broilers. This
disease control focuses much more on the prevention
of health problems than on treatment of diseases.
Active and passive immunity using vaccination
against C. perfringens and its toxins appears to offer
protection. Heier et al. (2001) found out that broiler flocks
with high titres of maternal antibodies against C.
perfringens alpha-toxin had lower mortality during the
production period than flocks with low tiers. Also
Løvland et al. (2004) use toxoids vaccines based on C.
perfringens type A and C toxoids to vaccinate breeder
flocks. The IgG responses in vaccinated parent hens were
distinct and the levels of antibodies to C. perfringens
alpha - toxin in progeny of the vaccinated hens was high
enough to protect the progeny against subclinical C.
perfringens associated necrotic enteritis. On the other
hand several recent investigations showed that immunity
to NE after oral infection using virulent strain and
subsequent treatment is much better than using avirulent
C. perfringens strains and they identified immunogenic
secreted proteins apparently uniquely produced by
virulent C. perfringens isolates and concluded that there
are certain secreted proteins beside to alpha-toxin, that are
involved in immunity to NE in broiler chickens
(Thompson et al., 2006; Kulkarni et al., 2007). Further
additional study showed the ability of oral immunisation
against C. perfringens in broiler chickens using an
attenuated Salmonella vaccine vector (Kulkarni et al.,
Implementation of several approaches such as
improvement of management, feed formulation and use of
alternative products to modulate the intestinal flora led to
an improvement of the situation. Limiting exposure to
infectious agents through biosecurity, vaccination,
supportive therapy, cleaning and disinfection are essential.
In addition, early recognition in managing the enteric
disorders is very important.
Finally, use of an effective anticoccidial drug in the
ration is helpful to minimise the effect of enteritis. Since,
recent investigations showed that the use of some
alternative products might be able to reduce the intestinal
colonization with pathogenic bacterial agents. This could
be an additional tool to reduce enteric disorders in future.
I would like to thank Dr. Olivia Kershaw, Institute of
Animal Pathology, Faculty of Veterinary Medicine, Free
University Berlin for providing the histopathological
Abildgaard L, TE Sondergaard, RM Engberg, A
Schramm, O Højberg, 2010. In vitro production of
necrotic enteritis toxin B, NetB, by netB-positive and
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