Pasteurella multocida infections
- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Pasteurella multocida infections
International Common Names
- English: atropic rhinitis in pigs; fowl cholera; haemorrhagic septicaemia in cattle, sheep and goats; hemorrhagic septicemia in cattle; pneumonic pasteurellosis; progressive atropic rhinitis in pigs; rhinitis in pigs; septicaemic pasteurellosis of cattle; snuffles in rabbits
Local Common Names
- India: galaghotu; ghatsarp
- Italy: barbone
- UK: hippopotamus head
- USA: enzootic pneumonia; shipping fever; stockyard disease
OverviewTop of page
Pasteurella multocida is a cause of haemorrhagic septicaemia in cattle, fowl cholera in poultry and a contributor to progressive atrophic rhinitis in pigs. Infections are characterized by fever, depression and the presence of multiple haemorrhages, and signs of pneumonia, pleuritis, pericarditis and arthritis.
Pasteurellosis of cattle was first described in 1878 by Bollinger in Germany and the causative agent was isolated by Kitt in 1885. This period also saw the discovery of the microorganisms causing fowl cholera (Pasteur, 1880) rabbit septicaemia (Gaffky, 1881) and swine plague (Loeffler, 1886). A German pathologist, Ruappe, noting similarities in these diseases and in the causative organisms, proposed the collective names, haemorrhagic septicaemia and Bacillus septipaemiae haemorrhagicae, respectively. The disease of buffaloes, barbone, described in Italy by Oreate and Armanni, was added to the list in 1887. In 1896, Kmae introduced the binomial Bacillus bovispotlous and in 1900 Ligniers described the whole group more fully than before using the generic name Pasteurella, which had been suggested in 1887 by Trevisan. The specific name Bacterium multocidum (Lehown and Neumann) did not appear in regular binomial form until 1899, so that some points of priorities in nomenclature still have to be defined. Rosenbusch and Merchant (1937) used the name Pasteurella multocida, and this found worldwide usage.
Pasteurella multocida was extensively investigated in 1880 by Pasteur as a cause of fowl cholera and was subsequently identified in association with rabbit septicaemia, swine plague, bovine pneumonia and haemorrhagic septicaemia. Now it is known to infect virtually all species of animals, including humans. It has been isolated as part of normal oral and pharyngeal flora of many species of animals including dogs, cats, wild and domestic ruminants, horses, pigs, rabbits, opossums, rodents, birds and reptiles. Often infection results from invasion of this commensal organism during stress. However, exogenous transmission may occur by aerosol or contact exposure. Haemorrhagic septicaemia causes heavy losses, particularly in low-lying areas of South East Asia.
Pasteurella multocida is a Gram-negative, non-motile, fermentative, facultative anaerobic coccobacilus or rod that shows bipolar staining, particularly as fresh isolates stained with Romoanovsky stain like Wright’s or Giemsa (Kilian and Frederiksen, 1981). P. multocida is classified into 3 subspecies based on DNA-DNA hybridization, namely P. multocida subsp. gallicida, P. multocida subsp. multocida and P. multocidasubsp. septica. Five capsular serogroups and 16 somatic serotypes are currently used to differentiate the organism (Heddleston et al., 1972).
Entry of P. multocida is through the tonsils. Later there is septicaemia, which affects the respiratory tract, heart and gastrointestinal tract. Animals die suddenly or develop warm, painful swelling on the throat or dewlap, and often develop severe dyspnoea. Death is due to respiratory failure. Factors such as stress and minor infections have been postulated as predisposing factors.
Pasteurella multocida is considered a zoonotic agent; occasional infecting people, usually after being bitten by animals. Haemorrhagic septicaemia and fowl cholera cause serious losses. In the Western world, haemorrhagic septicaemia is not common and fowl cholera is controlled with vaccine and antibiotics. In developing countries, pasteurellosis is a very serious problem that should be addressed as a high priority.
Pasteurella multocida infection can be diagnosed by observing clinical signs, isolation and identification of the pathogen, several immunological tests and molecular techniques. The disease in the field is adequately controlled by vaccines directed solely against the appropriate organism. Clinical cases, if treated in time, may be cured by chemotherapy aimed at the pathogen. Vaccines have been used from many years to protect susceptible livestock. Immunity after vaccination protects for at least 6 to 12 months. The disease can be controlled by good management practices. Vaccination is recommended as a preventive measure in extensive management systems.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Anas platyrhynchos||Domesticated host, Wild host|
|Anser (geese)||Domesticated host, Wild host|
|Bos grunniens (yaks)||Domesticated host|
|Bos indicus (zebu)||Domesticated host||Cattle & Buffaloes: All Stages|
|Bos mutus (yaks, wild)||Domesticated host|
|Bos taurus (cattle)||Domesticated host||Cattle & Buffaloes: All Stages|
|Bubalus bubalis (Asian water buffalo)||Domesticated host||Cattle & Buffaloes: All Stages|
|Camelus bactrianus (Bactrian camel)||Domesticated host|
|Camelus dromedarius (dromedary camel)||Domesticated host|
|Canis familiaris (dogs)||Domesticated host|
|Capra hircus (goats)||Domesticated host||Sheep & Goats: All Stages|
|Cercopithecidae (Old World monkeys)||Wild host|
|Equus caballus (horses)||Domesticated host|
|Felis catus (cat)||Domesticated host|
|Gallus gallus domesticus (chickens)||Domesticated host||Poultry: Young poultry|Poultry/Mature female|Poultry/Cockerel|Poultry/Mature male|
|Meleagris gallopavo (turkey)||Domesticated host||Poultry: Young poultry|Poultry/Mature female|Poultry/Cockerel|Poultry/Mature male|
|Muridae||Experimental settings, Wild host|
|Oryctolagus cuniculus (rabbits)|
|Ovis aries (sheep)||Domesticated host||Sheep & Goats: All Stages|
|Phasianidae||Domesticated host, Wild host|
|Sus scrofa (pigs)||Domesticated host||Pigs: All Stages|
Hosts/Species AffectedTop of page
Diseases attributed to Pasteurella multocida occur worldwide in virtually all species of animals. They include cattle, buffaloes, pigs, domestic and wild birds, rabbits and wound infections in dogs, cats and humans (Biberstein, 1981). The disease is also reported from the wild animals like bison (USA). The disease is more common in buffaloes in South East Asian countries, including India. The disease is more common in wet and humid climates. Buffaloes have close habitat with water or mud so the disease is prominent in these animals. There is no breed predisposition for the disease. The disease affects livestock in all types of husbandry practices. However, diseases caused by this organism are seen more often in intensive husbandry practices. Infections caused by P. multocida include fowl cholera of poultry, progressive atrophic rhinitis of pigs, pneumonia of cattle, sheep and pigs, and haemorrhagic septicaemia of cattle and water buffaloes. The organism has also been associated with atrophic rhinitis and septicaemia of sheep. In addition, P. multocida is responsible for snuffles in rabbits, infections in deer, and is associated with human infections resulting from cat and dog bites. A case of bronchitis in a dog and septicaemia pasteurellosis in a Nile crocodile (Crocodylus niloticus) has also been reported (Mohana et al., 1994).
Systems AffectedTop of page blood and circulatory system diseases of large ruminants
blood and circulatory system diseases of pigs
blood and circulatory system diseases of poultry
blood and circulatory system diseases of small ruminants
bone, foot diseases and lameness in large ruminants
bone, foot diseases and lameness in pigs
bone, foot diseases and lameness in small ruminants
digestive diseases of large ruminants
digestive diseases of pigs
digestive diseases of poultry
digestive diseases of small ruminants
mammary gland diseases of large ruminants
mammary gland diseases of pigs
mammary gland diseases of small ruminants
muscular skeletal diseases of poultry
reproductive diseases of large ruminants
reproductive diseases of pigs
reproductive diseases of poultry
reproductive diseases of small ruminants
respiratory diseases of large ruminants
respiratory diseases of pigs
respiratory diseases of poultry
respiratory diseases of small ruminants
skin and ocular diseases of large ruminants
skin and ocular diseases of pigs
skin and ocular diseases of poultry
skin and ocular diseases of small ruminants
DistributionTop of page
Pasteurella multocida has worldwide distribution. Haemorrhagic septicaemia, an OIE listed disease, is endemic in most countries of Asia and sub-Saharan Africa.
Within Asia, countries can be classified into three categories, on the basis of incidence and distribution of the disease; these are respectively countries where the disease is endemic or sporadic, clinically suspected but not confirmed, or free.
During 2013, haemorhagic septicaemia and other pasteurellosis outbreaks were reported to AU-IBAR by 10 countries (see table below), with a total of 1211 outbreaks, 14,122 cases and 2530 deaths. This is a decline from 18 countries that reported 1257 outbreaks, 23,219 cases and 4845 deaths in 2012. Ethiopia recorded the highest number of outbreaks (1063) followed by Niger (81) and Zambia (22), a pattern similar to that of the previous year. Outbreaks occurred most often in January and February (AU-IBAR, 2013).
Countries reporting haemorrhagic septicaemia and other pasteurellosis to AU-IBAR in 2013
NS: Not specified
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Bangladesh||Widespread||Rhoades and Rimler, 1987; Ahmed, 1996|
|China||Present||Zhang et al., 2004|
|India||Present||Present based on regional distribution.|
|-Assam||Localised||Kumar et al., 2004|
|-Goa||Localised||Kumar et al., 2004|
|-Gujarat||Localised||Kumar et al., 2004|
|-Haryana||Localised||Kumar et al., 2004|
|-Himachal Pradesh||Localised||Kumar et al., 2004|
|-Indian Punjab||Localised||Kumar et al., 2004|
|-Jammu and Kashmir||Localised||Kumar et al., 2004|
|-Karnataka||Localised||Kumar et al., 2004|
|-Kerala||Localised||Kumar et al., 2004|
|-Madhya Pradesh||Localised||Kumar et al., 2004|
|-Maharashtra||Localised||Kumar et al., 2004|
|-Odisha||Localised||Kumar et al., 2004|
|-Tamil Nadu||Localised||Kumar et al., 2004|
|-Tripura||Localised||Kumar et al., 2004|
|-Uttar Pradesh||Localised||Kumar et al., 2004|
|-West Bengal||Localised||Kumar et al., 2004|
|Indonesia||Widespread||Mariana and Hirst, 2000; Jonas et al., 2001|
|Japan||Present||Kawamoto et al., 1990; Arashima et al., 1993; Hirose et al., 2003|
|Korea, DPR||Present||Kwon and Kang, 2003|
|Malaysia||Chandrasekaran et al., 1981|
|Pakistan||Widespread||Sheikh et al., 1996|
|Saudi Arabia||Localised||Yaneza et al., 1992; Elfaki et al., 2002|
|Singapore||Present||Rhoades and Rimler, 1987; Tay et al., 1992|
|Taiwan||Present||Wu et al., 2003|
|Thailand||Widespread||Unchitti et al., 1992|
|Vietnam||Widespread||Gunawardana et al., 2000; Townsend et al., 2000|
|Namibia||Present||Voigts et al., 1997|
|Nigeria||Widespread||Odugbo et al., 2004|
|Senegal||Widespread||Dehoux et al., 1996|
|South Africa||Widespread||Bastianello and Jonker, 1981|
|Sudan||Localised||Hassan and Mustafa, 1985|
|Tanzania||Widespread||Muhairwa et al., 2001|
|Tunisia||Present||Bekir et al., 1994|
|Zambia||Widespread||Francis et al., 1980|
|Zimbabwe||Localised||Lane et al., 1992; Dziva et al., 2000|
|Canada||Present||Bhasin, 1982; Percy et al., 1984; Rhoades and Rimler, 1987|
|-Quebec||Present||Harel et al., 1990|
|Mexico||Present||Blanco-Viera et al., 1995|
|USA||Present||Present based on regional distribution.|
|-Alaska||Present||Jaworski et al., 1998|
|-Arizona||Present||Jaworski et al., 1998|
|-Arkansas||Present||Rimler and Rhoades, 1987; Hopkins et al., 1990|
|-California||Present||Rimler and Rhoades, 1987; Botzler, 2002|
|-Colorado||Present||Jensen et al., 1976|
|-Georgia||Present||Waltman and Horne, 1993|
|-Idaho||Present||Rudolph et al., 2003|
|-Indiana||Present||Rimler and Rhoades, 1987; Aye et al., 2001|
|-Iowa||Rimler and Rhoades, 1987|
|-Kansas||Present||Williams et al., 2000|
|-Maine||Present||Korschgen et al., 1978|
|-Michigan||Dabo et al., 1999; Einum et al., 2003|
|-Minnesota||Dabo et al., 1999|
|-Mississippi||Windingstad et al., 1983|
|-Missouri||Rimler and Rhoades, 1987; Olson and Wilson, 2001|
|-Montana||Rhyan et al., 1997|
|-New Jersey||Rimler and Rhoades, 1987|
|-New York||Itoh et al., 1980|
|-Ohio||Present||Aye et al., 2001|
|-Oklahoma||Dabo et al., 1999; Welsh et al., 2004|
|-Oregon||Present||Dunbar et al., 2000; Rudolph et al., 2003|
|-Pennsylvania||Present||Aye et al., 2001|
|-South Carolina||Present||Derieux, 1974|
|-Texas||Present||Lu et al., 1983; Dabo et al., 1999|
|-Utah||Present||Rhoades et al., 1992|
|-Virginia||Present||Rimler and Rhoades, 1987|
|-Washington||Present||DiGiacomo et al., 1983; Rudolph et al., 2003|
|-Wyoming||Windingstad et al., 1988; Rhyan et al., 1997|
Central America and Caribbean
|Jamaica||Present||Chen et al., 1976|
|Croatia||Present||Bilic et al., 1996|
|Czech Republic||Present||Jaglic et al., 2004|
|Denmark||Present||Eriksen et al., 1999; Pedersen et al., 2003|
|Finland||Present||Hartel et al., 2004|
|France||Present||Kobisch and Tillon, 1985; Donnio et al., 1994|
|Germany||Present||Bisgaard et al., 1991; Wallmann et al., 2004|
|Hungary||Present||Native||Rusvai and Fodor, 1998; Stipkovits et al., 2000|
|Italy||Present||Casolari and Fabio, 1988; Guasticchi, 1989|
|Netherlands||Present||Kouwenhoven et al., 1976; Yadin and Moraal, 1978; Bisgaard et al., 1991|
|Norway||Present||Baalsrud, 1987; Falk et al., 1991|
|Spain||Present||Ferrer et al., 1999; Felix et al., 2003|
|Switzerland||Present||Boerlin et al., 2000|
|UK||Present||Curtis, 1979; Bisgaard et al., 1991; Davies, 2004|
|Australia||Present||Fegan et al., 1995; Bowles et al., 2000|
|-New South Wales||Present||Blackall et al., 1995|
|-South Australia||Present||Gardner et al., 1989; Djordjevic et al., 1998|
PathologyTop of page
In cattle, postmortem examination reveals pronounced hyperaemia of the internal organs and multiple haemorrhages in serous membranes, mucous membranes and different organs, especially the lungs and muscles. The kidney and liver show cloudy swellings. In sub-acute cases, the subcutaneous tissue of head, neck and throat is infiltrated with gelatinous material and is studded with haemorrhages with serous infiltration between deeper layers of muscle. Tongue is more or less enlarged and is dark brown. The retropharyngeal and cervical lymphatic glands show acute swelling. In enteric forms of disease, acute haemorrhagic inflammation in the abomasums and small intestine and, less often, in the colon, is observed. Intestines contain fluid, which is yellowish -grey or reddish from admixture with blood. The plural cavity contains serous or serofibrinous exudation. The pleura is inflamed and studded with blood spots and the visceral layer is covered with fibrinous membrane. One or both lungs are hepatized and friable. On section lungs have a dark, reddish-brown or grey surface. The unconsolidated part is hyperaemic and oedematous. In buffaloes and sheep the interlobular septa is greatly thickened with multiple small haemorrhages. The pericardium may also contain exudation with fibrin. The peri-bronchial lymph glands are swollen (Hutryra et al, 1949).
A patchy to confluent bronchopneumonia in calves following infection of P. multocida characterized by abscess formation, haemorrhage, oedema and suppurative consolidation have been recorded (Mathy et al., 2002). In an experimental study on the pathogenesis of P. multocida, 4 days after infection, lung lesions, mainly in the apical lobes, were found in all challenged calves (Dowling et al., 2002). Histopathologically, areas of purulent pneumonia with a tendency to abscessation and inflamed interlobular septa characterized by accumulation of neutrophils and oedema were seen. Histologically the lung lesions comprized a fibrinous bronchopneumonia with variable sized areas of coagulative necrosis. Extensive deposition of fibrin and massive dilatation and oedema of the interlobular and pleural lymphatics was also reported in calves experimentally infected with P. multocida Gourlay et al., 1989).
Cellular analysis following infection of naïve animals was characterized by an influx of neutrophils in the bronchi-associated lymphoid tissue, with macrophages and dendritic cells observed in the lesion perimeter. A significant increase in the number of CD8+ blasts expressing MHC (major histocompatibility complex) II was also observed in the bronchi-associated lymphoid tissue of infected calves. Decreased expression of interleukin (IL)-1 beta and increased expression of IL-8 compared to naïve unchallenged controls was apparent in lung lymph node (Mathy et al., 2002).
The ultrastructural changes recorded in rabbits after experimental infections are deciliation or clumping of cilia of ciliated epithelium, cellular swelling, vacuolation and sloughing. The subepithelial capillaries showed congestion, intravascular fibrin deposition, platelets aggregation and endothelial injury. P. multocida was observed attached to the injured endothelial cells. Heterophils, mast cells, vacuolated monocytes and macrophages infiltrated the lamina propria and between the degenerated epithelial cells (Al-Haddawi et al., 2001).
Atrophic rhinitis is characterized by distortion of the face and atrophy of the nasal turbinates. The mucous membrane changes from ciliated pseudostratified columnar epithelium to stratified squamous epithelium, and the lamina propria is reduced in amount and vascularity. Anosmia results, and epistaxis may be recurrent and severe.
In the acute types of infection, few clinical signs are observed before death and the lesions will be dominated by general septicaemia lesions. In chronic forms of P. multocidainfections, suppurative lesions may be widely distributed, often involving the respiratory tract, conjunctiva and adjacent tissues of the head (Christensen and Bisgaard, 2000). Increased spleen and liver weights were observed during the acute phase of septicaemia in broilers. Airsacculitis, pericarditis, and perihepatitis were also observed. These macroscopic lesions are sufficient to identify infected septicaemic broiler carcasses before the onset of changes in the skeletal muscle of the carcass (Fisher et al., 1998).
The lesions found on postmortem examination of birds dying of fowl cholera are not specific. In acute fowl cholera, haemorrhages are always present. Acute haemorrhagic inflammation of intestine and lungs together with fibrinous exudation on serous membranes are the common findings. Pneumonia is common in turkeys. Intestinal content mainly of duodenum is red-grey. The pericardial fluid is often turbid and contains flakes of fibrin. Lungs are congested and show croupous pneumonia. Liver in acute cases reveals a parenchymatous hepatitis. In less acute cases the liver is studded with pinhead sized necrotic foci. Necrotic foci are small, irregular shaped, and yellow or yellow-grey. Extensive necrosis of liver is also seen in some cases.
Histologically, hypertrophic infiltration and fibrin deposition are usually observed in air spaces. Multinodular giant cells are often associated with necrotic masses in air spaces of turkeys (Oleson, 1966). Livers of acutely infected birds usually contain multiple small focal areas of coagulative necrosis and heterophilic infiltration. Less virulent P. multocida do not produce necrotic lesions in liver. Heterophilic infiltration also occurs in lungs and certain parenchymatous organs (Rhoades, 1964).
In chronic cases of fowl cholera the pathology is limited to the subcutaneous tissue of head, particularly to comb and wattles. Oedematous infiltration is followed by necrosis of connective tissue and is transformed into a caseous, brittle mass.
DiagnosisTop of page
A clinical, provisional diagnosis of haemorrhagic septicaemia is based on a combination of clinical signs, gross pathological lesions and a consideration of relevant epidemiological parameters and other similar diseases prevalent in the local region.Diagnosis can be made from clinical signs. In cattle, buffaloes and small ruminants, disease is characterized by fever, subcutaneous oedema in the submandibular/brisket region, diarrhoea and sudden death. Fowl cholera is characterized by facial swelling, swelling of wattles and cyanosis of comb. Atrophic rhinitis is characterized by atrophy of nasal bone. Confirmatory diagnosis is made by isolation and identification of the aetiological agent.
Fixed smears of blood from sick and throat swelling from dead animals, smears from heart blood and liver, in sterile containers, lymph nodes and spleen maintained on ice, and long bones can be collected for direct microscopy and isolation of the aetiological agent. Disease can also be diagnosed in the field by staining smears with Leishman’s or Giemsa stains. Typical bipolar organisms are seen. Dowling et al. (2002) recorded increased plasma haptoglobin concentrations (P<0.05) in calves given a high-volume challenge infection.
Postmortem diagnosis can be made by observing typical lesions, which includes petechial haemorrhages, haemorrhagic tracheitis, fibrinous pericarditis and pneumonia. In birds, pneumonia with multiple necrotic foci on the liver are the important lesions for diagnosis.Isolation
Pure cultures of P. multocida can usually be grown in blood cultures from mice, even when the original samples come from relatively old carcasses. The organisms can be identified by its morphological and cultural characteristics, biochemical reactions and serological tests. A suitable medium for the growth of Pasteurella is casein/sucrose/yeast (CSY) agar containing 5% blood. Freshly isolated P. multocida forms smooth, greyish, glistening translucent colonies, approximately 1 mm in diameter, on blood agar after 24 h of incubation at 37°C. Colonies grown on CSY agar are larger. P. multocida does not grow on MacConkey agar.Serology
Several immunological tests are used for the identification of serotypes of P. multocida. These consist of a rapid slide agglutination test (Namioka and Murata, 1961a), an indirect haemagglutination test (IHA) test for capsular typing (Carter, 1955), an agglutination test using hydrochloric acid-treated cells for somatic typing (Namioka and Murata, 1961b), the AGID test (Wijewardena et al., 1982), and the counter immunoelectrophoresis test (CIEP) (Carter and Chengappa, 1981).
An ELISA test has recently been developed in Australia, however it fails to differentiate between the Asian (B:2) and African (E:2) types. This is not a serious limitation in Asia as only B:2 type of P. multocida has been so far found there. Thus ELISA can be a good test for screening a large number of cultures from a collection in a laboratory where the turnover is high (Benkirane and Alwis, 2002). ELISA was found to be at least twice as sensitive as IHA (Solano et al., 1983).Polymerase chain reaction
A number of different methods such as bacteriophage typing, acriflavine flocculation test, plasmid profiling, restriction endonuclease analysis, ribotyping, analysis of outer membrane proteins, capsular PCR typing and multilocus sequence analysis (Davies, 2004) are employed for characterization of P. multocida strains.
Random amplified polymorphic DNA (RAPD) analysis offers better discrimination of Pasteurella strains than ribotyping. No phenotype characteristics were directly related to the genotype clusters (Dziva et al., 2004).
Application of PCR to support diagnosis of haemorrhagic septicaemia will greatly improve accuracy, laboratory response time, and will facilitate rational deployment of resources for controlling this disease (Brickella et al., 1998). PCR methods are employed for rapid and specific detection of P. multocida. Species-specific PCR assays for detection of P. multocidain mixed culture or clinical samples involve the use of oligonucleotide primers constructed to amplify the psl gene encoding the P6 protein (psl) of P. multocida (Kasten et al., 1997a). To date, the HSB- PCR developed by Townsend et al. (1998) has been found to be specific for haemorrhagic septicaemia-causing P. multocida serogroup B. Amplification of toxA gene has formed the basis for detection of toxigenic P. multocida (Nagai, 1994; Kamp et al., 1996; Lichtensteiger et al., 1996). Similarly, a colony lift- hybridization assay (Register et al., 1998) is also useful for detection of toxigenic P. multocida.Differential diagnosis
Anthrax, blackquarter, leptospirosis, death due to lightening strike and, more importantly rinderpest (due to its possible implications in international animal health) should always be considered when investigating sudden deaths in cattle and buffaloes.
Atrophic rhinitis is differentiated from other forms of chronic rhinitis by the abnormal patency of the nasal cavities, caused by atrophy of the blood vessels and the seromucinous glands in the lamina propria. Sneezing in the farrowing area may be due to a range of other organisms, in particular, uncomplicated Bordetella bronchiseptica and porcine cytomegalovirus, which should be differentiated from atrophic rhinitis.
In birds, cases of swelling on face should be differentiated from infectious coryza.Immunology
Strains of certain capsular serogroups are associated with specific diseases and animal species, suggesting that the capsular polysaccharide type plays a role in host and disease specificity (Davies, 2004).
Mechanisms of immunity to P. multocida have been difficult to determine, and efficacious vaccines have been a challenge to develop and evaluate. Important immunogens have not been characterized for P. multocida infection in cattle.
The outer membrane proteins (OMPs) of Gram-negative bacteria are at the interface between pathogens and host and play an essential role in the disease process (Lin et al., 2002). Immune response to P. multocida is mainly antibody mediated. The OMPs of P. multocida function as immunogen and can provide protection as a vaccine component (Confer, 1993; Confer et al.,1996; Dabo et al.,1997). P. multocida express on their cell surface a heat modifiable or OmpA protein (Vasfi Marandi and Mittal, 1996, 1997; Dabo et al., 1997) and a porin or OmpH protein (Lugtenberg et al., 1984,1986; Vasfi Marandi and Mitatl, 1997). There is evidence that OmpH protein is protective and has potential as a vaccine candidate (Luo et al., 1997; 1999; Vasfi Marandi and Mittal, 1997). The molecular mass heterogeneity of the OmpA and OmpH proteins could provide a selective advantage to P. multocida by generating antigenic variation. (Davies et al., 2003b). Antibody responses in cattle are induced by P. multocida IROMPs, and 96-kDa HasR protein is an immunodominant IROMP (Prado et al., 2005). ). The capsular 39-kDa protein was determined to be an adherence factor and a cross-protective antigen of avian P. multocidatype A strains. (Alia et al., 2004a).
Purified P. multocida LPS is antigenic. In general, LPS seems to be a major immunogen in birds (Rhoades and Rimler, 1989). However, LPS-protein complex is essential for induction of immunity in turkeys (Tsuji and Matsumota, 1988). The role of LPS in immunity was studied using monoclonal antibodies (MAbs) and active immunization experiments suggesting that LPS plays a partial role in immunity to infection in cattle (Adler et al., 1996).
P. multocida toxin (PMT) is mainly a virulence factor in atrophic rhinitis of pigs. As an immunogen, inactivated PMT induces protection against lethal effects of PMT in rats and mice (Thurston et al., 1991) and against experimental atrophic rhinitis in pigs (Foged et al., 1989). Monoclonal antibodies against PMT can neutralize its lethal effects in mice (Foged, 1988).
Virulent strains of P. multocida are more resistant to phagocytosis and phagocytic killing by chicken macrophages compared with less virulent strains (Poermadjaja and Frost, 2000). It was suggested that hyaluronic capsule was important for resistance.
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Cattle & Buffaloes:All Stages,Other:All Stages||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Cattle & Buffaloes:All Stages,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male,Other:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Diarrhoea||Cattle & Buffaloes:All Stages,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|Digestive Signs / Difficulty in prehending or chewing food||Cattle & Buffaloes:All Stages,Other:All Stages||Sign|
|Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism||Cattle & Buffaloes:All Stages,Poultry:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Rumen hypomotility or atony, decreased rate, motility, strength||Cattle & Buffaloes:All Stages,Other:All Stages,Sheep & Goats:All Stages||Sign|
|Digestive Signs / Tongue protrusion||Cattle & Buffaloes:All Stages,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|General Signs / Cyanosis, blue skin or membranes||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male,Sheep & Goats:All Stages||Sign|
|General Signs / Dehydration||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|General Signs / Discomfort, restlessness in birds||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Cattle & Buffaloes:All Stages,Poultry:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Diagnosis|
|General Signs / Increased mortality in flocks of birds||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Diagnosis|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Cattle & Buffaloes:Calf,Cattle & Buffaloes:Heifer||Sign|
|General Signs / Lameness, stiffness, stilted gait in birds||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia||Cattle & Buffaloes:Cow||Sign|
|General Signs / Petechiae or ecchymoses, bruises, ecchymosis||Cattle & Buffaloes:All Stages||Diagnosis|
|General Signs / Sudden death, found dead||Cattle & Buffaloes:All Stages,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|General Signs / Swelling of the comb, wattles in birds||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|General Signs / Weakness, paresis, paralysis, drooping, of the wings||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|General Signs / Weight loss||Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Cattle & Buffaloes:All Stages,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male,Other:All Stages,Pigs:All Stages,Sheep & Goats:All Stages||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Cattle & Buffaloes:All Stages,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|Pain / Discomfort Signs / Pain mammary gland, udder||Cattle & Buffaloes:Cow||Sign|
|Pain / Discomfort Signs / Pain, neck, cervical, throat||Cattle & Buffaloes:All Stages,Other:All Stages||Diagnosis|
|Reproductive Signs / Decreased hatchability of eggs||Poultry:Mature female,Poultry:Mature male||Sign|
|Reproductive Signs / Edema of mammary gland, udder||Cattle & Buffaloes:Cow,Other:Adult Female||Sign|
|Reproductive Signs / Fluid in uterus||Other:Adult Female||Sign|
|Reproductive Signs / Mastitis, abnormal milk||Cattle & Buffaloes:Cow,Other:Adult Female||Sign|
|Reproductive Signs / Purulent discharge, vulvar, vaginal||Other:Adult Female||Sign|
|Skin / Integumentary Signs / Ruffled, ruffling of the feathers||Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
Disease CourseTop of page
Pasteurella multocida is transmitted by the faecal-oral route. The transmission is also mediated by ticks and mites from affected and carrier animals to healthy animals. Wild animals also act as carriers. Chronically affected birds and free flying birds having contact with poultry are a major source of infection. In some cases droplet infections are significant. The incubation period of disease is estimated to be 48 h. Large numbers of bacteria are shed in the faeces and nasal discharge, which contaminate the surroundings. The effect of septicaemia is most severe in the respiratory tract, heart and gastrointestinal tract. In acute cases the predominant lesions, widespread haemorrhages and necrotic lesions are presumed to be due to end toxaemia (Collins, 1977). Free endotoxins and large numbers of organisms have been demonstrated in tissues and body fluids of moribund animals.
Pathogenicity is generally related to serogroup of the organism. The pathogenesis is similar in all species. Acute cases of haemorrhagic septicaemia are clinically characterized by sudden onset of fever and death in about 24 h. On rangeland, animals may be found dead without any clinical signs. Affected animals have painful swellings about throat, dewlap and brisket, and have severe dyspnoea. Haemorrhagic septicaemia is the same in both cattle and other species (Murty and Kaushik, 1965). Death in haemorrhagic septicemia is due to respiratory failure and toxaemia.
The pathogenesis of haemorrhagic septicaemia in buffaloes infected with P. multocida is poorly understood. However, the characteristic of sudden onset leading to the rapid death of infected animals is due to endotoxic shock (Horadagoda et al., 2001).
The importance of the capsule in virulence has been implicated in a number of studies (Boyce et al., 2000). The outer membrane proteins (OMPs) of Gram-negative bacteria are at the interface between pathogens and host and play essential role in the disease process (Lin et al., 2002). Recent studies have indicated a role for transferrin binding proteins in the pathogenesis of haemorrhagic septicaemia in cattle and buffaloes (Veken et al., 1994).
In birds, signs appear a few hours before death. The severity and incidence of P. multocida infection depends on several factors associated with the host (including age and species), the environment and strain of bacteria. Possible virulence factors are capsule, endotoxin, and outer membrane proteins, iron binding systems, heat shock proteins, neuraminidase production and antibody cleaving enzymes. P. multocida exotoxin could contribute to virulence in some avian infections (Christensen and Bisgaard, 2000). The avian P. multocida capsular type A strains are invasive (Alia et al., 2004b). P. multocida contains multiple immunogenic haemin- and haemoglobin-binding proteins and these iron-dependent outer membrane proteins (IROMPs) play an important role in bacterial pathogenesis and present several attributes of potential vaccine candidates (Bosch etal., 2004). The high degree of strain diversity together with the wide variety of clinical signs indicates that certain avian strains of P. multocida are opportunistic pathogens of relatively low virulence. Strains of capsular types B, D and F, as well as the untypable isolates, are associated exclusively with specific OMP-types and represent distinct and widely disseminated clonal groups.
In rabbits, P. multocida causes snuffles, a disease of varying severity involving respiratory tract and often terminating as a septicaemia. Presence of fimbriae and the absence of capsule seem to enhance the adherence of P. multocida type D strain. The capsular material of P. multocida type A strain influence the adherence to lung tissue in rabbits (Al-Haddawi et al, 2000). Chronic genital infection leading to pyometra and orchitis has also been reported (Shewen and Conlon, 1993).
P. multocida is an aetiological agent of progressive atrophic rhinitis (PAR) of pigs and of considerable economic importance to the pig rearing industry throughout the world. Atrophic rhinitis of piglets results most often from combined infection of the nasal turbinate with Bordetella bronchiseptica and oxygenic strain of P. multocida (DeJong et al., 1980). Infection with respiratory virus or other stress may lead to Pasteurella pneumonia in pigs of all ages. PAR is characterized by atrophy of the nasal turbinate bones, which, in severe cases, can lead to facial distortion. Strains associated with PAR usually produce a 145-kDa DNT toxin, which is encoded by toxA gene (Lax et al., 1990; Buys et al., 1990). This toxin induces osteolysis in the turbinate bones and plays an important role in the pathogenesis of PAR. Toxigenic strains associated with PAR are most frequently of capsular type D (Gardner et al., 1994), and are rarely isolates of capsular type A (Fussing et al., 1999).
Pasteurella multocida is a commonly part of the oral bacterial flora of many animals and frequently contaminates wounds due to animal bites or scratches in humans. Localized suppuration is common, but bacteraemia or endotoxaemia may result in more serious disease.
EpidemiologyTop of page
Pasteurella multocida is part of the healthy oral and pharyngeal flora of a wide variety of animals.
Pasteurella infection mainly results from invasion of commensal organism during a period of stress, but exogenous transmission may occur by aerosol or contact exposure. Septicemia pasteurellosis caused by P. multocida occurs in cattle, water buffalo, yaks, camel and to much smaller extend in pigs and horses. It is a common and serious pathogen of rabbits. In birds, P. multocida causes fowl cholera. This disease is common in southern and South East Asia including India, Indonesia, Malaysia and Thailand. It is also common in Europe, Russia and Africa.
Haemorrhagic septicaemia in cattle
P. multocida causes heavy losses, particularly in low-lying areas and when the animals are exposed to wet, chilly weather or are stressed by heavy work (Benkirane and Alwis, 2002). There is ample evidence that buffaloes are more susceptible than cattle and that, in both species, young and young adult animals are more susceptible than older animals (Alwis,1990b). The two common serotypes of P. multocida associated with disease in these species are types B:2 (in Asia) and E:2 (in Africa). All age groups are affected with P. multocida, but in cattle the most susceptible age group is between 6 months and 2 years. Both morbidity and mortality varies between 50 and 100%, and animals that recover require a long convalescence. Morbidity depends upon the immune status of the herd, either by acquired immunity by natural infection or by vaccination. Incidence of disease is also reduced significantly by vaccination. The phenomenon of naturally acquired immunity resulting from non-fatal infection largely controls the mortality and morbidity patterns. It is, on the other hand the mechanism through which animals that have recovered from haemorrhagic septicaemia acquire a long lasting carrier status, which render the prevention of new outbreaks difficult. The overall case fatality rate of buffaloes is nearly three times higher than that of cattle.
The onset of the monsoon in Asian countries also sets into motion agricultural activities which bring about movements of animals, work stress in traction animals, etc., all of which are risk factors likely to contribute to causing outbreaks (Alwis, 1990a). Infection occurs by inhalation or ingestion of P. multocida bacteria. The outbreaks are more often associated with wet humid whether during the rainy season. During the intervening period, the causative agent persists on the tonsillar and nasopharyngeal mucosa of carrier animals. Approximately 45% of healthy cattle in herds associated with disease carry the organism. The percentage is up to 5% in cattle from herds unassociated with the disease (Mustafa et al., 1978). Spread also occurs by the ingestion of contaminated feed-stuffs. The infection originates from healthy carriers or clinical cases, or possibly from ticks (Radostits et al., 2003) and biting insects. The saliva of affected animals contains large number of Pasteurella during the early stage of the disease. In North American cattle, P. multocida serogroup A is associated mainly with bronchopneumonia (enzootic pneumonia) in young calves; however, it is occasionally isolated from fibrinous pleuropneumonia of feedlot cattle (shipping fever).
Atrophic rhinitis in pigs
Pasteurella multocida is found in the tonsils of pigs and infection spreads by saliva and nasal discharges. Herd infection usually follows the introduction of pigs carrying the disease, many of which have no signs of atrophic rhinitis. Many environmental and management factors contribute to the severity and economic impact of atrophic rhinitis. Factors such as high stocking densities, dusty, poorly ventilated sheds, frequent moving and mixing of pigs, continual pig throughput and large numbers sharing airspace have been associated with greater severity of the disease.
Snuffles in rabbits
Pasteurella multocida is a well-known cause of morbidity and mortality in rabbits. The predominant syndrome is upper respiratory disease or ‘snuffles.’ P. multocida is often endemic in rabbit colonies and the acquisition of infection in young rabbits is correlated with the prevalence in adult rabbits (DiGiacomo et al., 1983). If young rabbits are removed early from infected adults, the chance of infection for the young decreases. Transmission is mainly by direct contact with nasal secretions from infected rabbits and may be greatest when rhinitis induces sneezing and aerosolization of secretions (DiGiacomo et al., 1991). The bacteria can survive for days in moist secretions or water. P. multocida gains entry to the respiratory tract primarily through the nares, and once infection is established, may also colonize the paranasal sinuses, middle ears, lacrimal ducts, thoracic organs and genitalia.
The epidemiology of fowl cholera appears complex. Traditional serotyping systems are only of limited use in epidemiological studies. In recent years, molecular typing methods have been applied to avian strains of P. multocida of different origin. The results obtained using these newer methods indicate that wild birds may be a source of infection to commercial poultry. Documentation suggesting that mammals play a similar role is not as comprehensive, but the possibility cannot be excluded. Carrier birds seem to play a major role in the transmission of cholera. Surviving birds from diseased flocks appear to represent a risk, but more recent investigations indicate that carriers of P. multocida may exist within poultry flocks with no history of previous outbreaks of fowl cholera. The significance of this awaits further investigation (Christensen and Bisgaard, 2000). Fowl cholera may occur in free ranging poultry, and dogs and cats kept in contact with them might serve as sources of P. multocida to other chickens and ducks.
Transmission between host species
Comparison of the OMP profiles of bovine isolates with those of avian, ovine and porcine strains showed that a high proportion of the respiratory tract infections in each of these species are caused by different strains of P. multocida. However, the presence of small numbers of closely related strains in more than one host species suggests that transmission of bacteria between different host species is also a factor in the population biology of P. multocida (Davies et al., 2004).
Impact: EconomicTop of page
Haemorrhagic septicaemia is a disease of great economic importance, particularly in Asia and to a lesser extent in Africa. In Asia the susceptible animal population consists of 432 million cattle and 146 million buffaloes, which constitute 30 and 95%, respectively, of the world’s cattle and buffalo populations.
In India, during the past four decades haemorrhagic septicaemia (HS) has been found to account for 46-55% of all bovine deaths. Between 1974 and 1986 it accounted for 58.7% of deaths caused by five endemic diseases including HS (Dutta et al., 1990). In an active surveillance study in Sri Lanka, it was shown that in the 1970’s, around 15% buffaloes and 8% cattle in HS-endemic areas died of the disease annually. During the same period, the passive reporting systems recorded only 1200 to 1500 deaths a year in a cattle and buffalo population of approximately 2.5 million (Alwis and Vipulasiri, 1981). In Pakistan it has been reported that 34.4% of all deaths in susceptible stock are due to HS. With a cattle and buffalo population of 17.7 and 18.8 million, respectively, the annual economic losses have been estimated at PRs 1.89 billion (US $350 million) (Chandry and Khan, 1978; FAO, 1979; Sheikh et al., 1994). In South East Asia, countries such as Indonesia, Malaysia, Thailand, Myanmar, Laos, Cambodia and the Philippines rank HS high among the economically important diseases of cattle and buffaloes (Patten et al., 1993). In Myanmar it is suggested that 50% of the government’s effort in animal disease control is directed towards HS (Patten et al., 1993). In Malaysia, with a relatively small population of 735,000 cattle and 186,000 buffaloes, the animal losses due to HS are estimated to be M$2.25 million (US $0.85 million) (FAO, 1979). Most estimates of loss take into account only direct loss. A true estimate of loss should take into account a variety of factors, which constitute indirect loss, such as loss of productivity; milk, meat, draught power, and cost of alternate sources of draught power, and impairment of the reproductive potential of animals.
In a study in Bangladesh, the direct and indirect economic losses resulting from three important endemic diseases, anthrax, blackquarter and HS, were US $2.3 and US $148 million annually, respectively (Ahmed, 1996). In India, in 2002 haemorrhagic septicaemia ranked fourth as the disease of economic importance as perceived by livestock keepers (8% of keepers). Pneumonia can be a significant cause of loss through downgrading and condemnation of carcasses and offal at slaughter.
The cost to the Georgia (USA) commercial turkey industry in 1986 from preventive measures, treatment of outbreaks, and production losses from fowl cholera was estimated at US $634,545 (Morris and Fletcher, 1988). The cost of fowl cholera per kg of live production was estimated to be US $0.015.
Zoonoses and Food SafetyTop of page
Pasteurella multocida forms part of the normal flora in the nasopharynx of many domestic and wild animals. The majorities of P. multocida infections in man involve skin and soft tissue and result from a complicated bite or scratch. Animal bites are often complicated by severe wound infection due to P. multocida, but systemic infection is rare. Breen et al. (2000) reviewed the 23 clinical cases of P. multocida reported by a major teaching hospital laboratory over a 10 years. The patients comprized of wound infections following animal bites, newborn meningitis and associated maternal vaginal carriage of P. multocida, and sputum isolates of doubtful significance. P. multocida meningitis (O'Neill et al., 2005), peritoneal dialysis-associated peritonitis (Cooke et al., 2004), septicaemia and premature labour in a pregnant veterinarian (Waghorn and Robson, 2003) and ocular lesions secondary to Pasteurella infection (McNamara et al., 1988) have been reported. Haemoptysis as the sole presentation of P. multocida infection (Sazon et al., 1998) and a severe case of materno-fetal infection due to P. multocida have also been reported (Escande et al., 1997).
A case of acute pneumonia due to P. multocida subspecies multocida in a man with AIDS and chronic sinusitis has been reported (Drabick et al., 1993). The pneumonia was diagnosed by bronchoscopy and responded to treatment with aztreonam. Epidemiological investigation revealed the case was temporally related to non-traumatic exposure to cat secretions and that the patient presumably had acquired infection carried by an aerosol. Transmission of Pasteurella through food to man has not been documented. The carcasses from diseased animals should be condemned at postmortem meat inspection.
Disease TreatmentTop of page
Haemorrhagic septicaemia is primarily a bacterial disease and, theoretically, can be effectively treated using a wide range of antibiotics. Oxytetracycline has been shown to be highly effective in pigs, sheep, goats and poultry and sulfadimidine is effective in cattle and buffaloes (Radostitis et al., 2003). However, other antibiotics such as trimethoprim and sulfamethazine are also reported to be effective.
Rowan et al. (2004) recorded more rapid improvement in the clinical response of 178 animals treated with danofloxacin by day 2 than in 90 animals treated with tilmicosin. For both treatments, there were similar significant reductions in the mean rectal temperature and severity of clinical signs of abnormal respiration and depression on days 4 and 10 compared with day 0 after treatment.
Usually, chemotherapy resorts to either streptomycin or oxytetracycline administered by intramuscular route at fairly high dosage. Penicillin and ampicillin are also widely used. Antibiotic resistance of P. multocida may occur and it has been reported for streptomycin and sulfonamides (Abeynayake et al., 1993; Kedrak and Borkowska-Opacka, 2001).
Pigs were treated successfully with Econor (Novartis) and chlortetracycline, followed by Tiamutin (Leo Laboratories), Pulmotil (Lilly Industries Limited), Cyfac (Roche Products), and lincomycin with chlortetracycline (Stipkovits et al., 2001).
A patient with bacteraemic pneumonia was successfully treated with ceftriaxone and ciprofloxacin (Breen et al., 2000).
Prevention and ControlTop of page
Over a century has passed since the first attempts by Louis Pasteur at immunization against the Gram negative facultative bacterium, P. multocida. Current biologicals in use are live P. multocida vaccines, inactivated toxoids and bacterins. Safe and effective vaccines against pasteurellosis are still lacking.
Vaccination is a major control measure in the face of a new epidemic. The three types of vaccines used against haemorrhagic septicaemia are bacterins, alum-precipitated vaccine (APV) and oil-adjuvanted vaccine (OAV). To provide sufficient immunity with bacterins, repeated vaccination is required. Administration of dense bacterins can give rise to shock reactions, which are less frequent with the APV and almost nonexistent with the OAV. A single dose of vaccine administered to young calves of 4-6 months of age will protect susceptible animals for 3 to 4 months when APV is used, and for 6 to 9 months when OAV is used.
A stable vaccine composed of killed organisms in an adjuvant base containing paraffin and lanolin has been found to be highly effective as a prophylactic (Benkirane and Alwis, 2002). The immunity after vaccination appears to be good for a year. Anaphylactic shock may occur in up to 1% of animals after vaccination. A live streptomycin-dependant mutant P. multocida vaccine provides good protection (Wei and Carter, 1978; De Alwis and Carter, 1980). A live vaccine containing P. multocida serotype B:3, 4 isolated from fallow deer in England has been developed (Myint et al., 1987) and is found to be effective (Myint and Carter, 1990). Potency tests for avian P. multocida biologicals are based on bacterial colony counts for vaccines and vaccination and challenge of birds for bacterins.
In mouse model systems, pure toxoid is a more potent immunogen than crude toxoid (Bordinga and Foged, 1991). In pigs, P. multocida-derived toxin (PMT) is poorly immunogenic and does not initiate a specific protective immune response. It has been speculated that PMT modifies the immune response such that the response is not directed towards the toxin but to an unidentified component in the nose of piglets (Dieman et al., 1994). In pigs, only aerogenous immunization with a temperature-sensitive mutant of live P. multocida (serovar A), was found to be capable of reducing the severity of pneumonia induced by intrabronchial infection (Muller et al., 2000).
Rabbits immunized subcutaneously with P. multocida ghosts (bacterial ghosts produced by the expression of phage PhiX174 lysis gene E are empty cells devoid of cytoplasmic and genomic material) developed antibodies reacting with the immunization strain, as well as with other Pasteurella strains. According to these results, ghosts of P. multocida should be explored as new vaccine candidates (Marchart et al., 2003).
Whole cell bacterins can provide some degree of protection, but only against the homologous lipopolysaccharide (LPS) serotype. There is good evidence that cross-protective antigens are expressed only under in vivoconditions. Empirically derived, live, attenuated vaccines can protect against heterologous serotypes, but because the basis for attenuation is undefined, reversion to virulence is not uncommon (Adler et al., 1999). The toxin appears to be the major immunogen for preventing atrophic rhinitis. Genetically modified PMT may represent a good candidate for use in developing a vaccine against progressive atrophic rhinitis in pigs (To et al., 2005).
In poultry, bacterins produced from P. multocida reference strains X-73, P-1059 and P-1662 are used as vaccines in Indonesia (Mariana and Hirst, 2000). Investigation has also shown that idiotypic antibodies to P. multocida were transferred from chicken to egg (Zhang and Anisworth, 1994). The acapsular strain PBA930 was able to induce protection against challenge with wild type X-73 in chickens (Chunga et al., 2005).
Control programmes and disease prevention
During an outbreak, one should resort to immediate whole herd vaccination, irrespective of previous vaccination history. The use of either broth bacterin or oil adjuvant vaccine is recommended. Sanitary measures include early detection and isolation of new cases and their immediate treatment with antibiotics, deep burial of carcasses or incineration, and the prevention of movements of animals to disease-free areas. In endemic areas the prevention measures include, vaccination on a routine prophylactic basis, preferably two to three months before the high-risk season (monsoon), awareness of the disease among farmers backed up by a good disease reporting/disease information system, segregation of animals from endemic and non-endemic areas to avoid contact with carriers (Benkirane and Alwis, 2002).
Whenever animals are exported from haemorrhagic septicaemia-endemic countries, it is important to vaccinate all susceptible stock in the importing country that are likely to come into contact with the imported animals and quarantine them for 2 to 3 weeks on arrival.
The disease can be controlled by good management practices. Confinement is probably the most effective way to prevent introduction of P. multocida. However, extensive management systems dominate in many parts of the world, and under such circumstances vaccination is recommended as a preventive measure. Unfortunately, the development of safe and efficient live vaccines still poses problems. As a result, control remains dependent on bacterins, which exhibit significant disadvantages compared with live vaccines (Christensen and Bisgaard, 2000). Prophylactic vaccination of all susceptible animals of the enzootic area should be made.
Since the eradication of haemorrhagic septicaemia is not a realistic option for the time being (Syamsudin, 1993), mass prophylactic vaccination, combined with treatment where possible, should theoretically suffice to contain mortality associated with the disease. A sound haemorrhagic septicaemia control programme may be adopted at national level provided that the tools used for the diagnosis and control of the disease meet international standards set by the World Organization for Animal Health (OIE, http://www.oie.int).
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