Virulence of<i>Pasteurella multocida</i>subsp.<i>multocida</i>isolated from outbreaks of fowl cholera in wild birds for domestic poultry and game birds

Petersen, Kamille Dumong; Christensen, Jens Peter; Permin, A.; Bisgaard, Magne

doi:10.1080/03079450020023168

Cited by 38 publications

(30 citation statements)

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“…Culture technique especially detecting bacteria in the lungs, trachea and liver, and this may indicate that these organs carry the highest bacterial load; however, we did not quantify bacteria in the current study. The low recovery is a general P. multocida re-isolation trend, which has also been reported for commercial birds, where recovery after 48 h is usually scanty (Christensen & Bisgaard, 2000;Petersen et al, 2001).…”

Section: Discussionsupporting

confidence: 53%

Time-course investigation of infection with a low virulentPasteurella multocidastrain in normal and immune-suppressed 12-week-old free-range chickens

et al. 2011

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Twelve-week-old indigenous chickens, either immune-suppressed using dexamethasone (IS) or non-immunesuppressed (NIS), were challenged with a low virulent strain, Pasteurella multocida strain NCTC 10322 T , and developed clinical signs and pathological lesions typical of chronic fowl cholera. NIS birds demonstrated much more severe signs of fowl cholera than IS birds. With few exceptions, signs recorded in IS and NIS birds were of the same types, but significantly milder in the IS birds, indicating that immune suppression does not change the course of infection but rather the severity of signs in fowl cholera. P. multocida signals by fluorescent in situ hybridization (FISH) were observed between 1 h and 14 days in the lungs, trachea, air sacs, liver, spleen, bursa of Fabricius and caecal tonsils, while signals from other organs mostly were observed after 24 h. More organs had FISH signals in NIS birds than in IS birds and at higher frequency per organ. Many organs were positive by FISH even 14 days post infection, and it is suggested that these organs may be likely places for long-term carriage of P. multocida following infection. The present study has demonstrated the spread of P. multocida in different tissues in chickens and distribution of lesions associated with chronic fowl cholera, and pointed to a decrease of pathology in IS birds. Since dexamethasone mostly affects heterophils, the study suggests that these cells play a role in the development of lesions associated with chronic fowl cholera in chickens. IntroductionPasteurella multocida subspecies multocida of capsular type A is the cause of different diseases in animals, including fowl cholera in chickens (Christensen & Bisgaard, 2000). This is a severe, systemic condition with sudden onset of clinical signs and high mortality (Glisson et al., 2008). However, in certain production systems, such as the common free-range scavenging poultry production systems in developing countries, the bacterium may be endemic present (Muhaiwa et al., 2001). Under such circumstances, outbreaks of acute fulminating disease are rare, and infected birds show more chronic clinical signs (Mbuthia et al., 2008).During fowl cholera infections, P. multocida is believed to enter primarily through the lungs (Christensen & Bisgaard, 2000), even though it has also been shown to invade the intestinal wall in an in vivo chicken loop model (Christensen et al., 2002). The bacterium probably adheres to the epithelial lining and subsequently associates with resident macrophages (Matsumoto et al., 1991), and, through a yet to be understood mechanism, it translocates to the bloodstream and from there to internal organs. Polymorphonuclear neutrophils (PMNs) (heterophils) are considered the first line of defence against the bacterium, but the role of this cell type seems dual, since selective removal of these have been shown to diminish pathological changes (Bojesen et al., 2004). Bacteria have been reported to be detectable in the blood as soon as 6 to 12 h post infection (p.i.) (Rhodes & ...

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Section: Discussionsupporting

confidence: 53%

Time-course investigation of infection with a low virulentPasteurella multocidastrain in normal and immune-suppressed 12-week-old free-range chickens

et al. 2011

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“…P. multocida is a common commensal or opportunistic pathogen found in the upper respiratory tracts of most livestock, domestic, and wild animals (34), including chickens (126)(127)(128)(129)(130)(131), turkeys (132,133), and other wild birds (123,(134)(135)(136)(137)(138)(139)(140)(141)(142)(143)(144), cattle and bison (121,(145)(146)(147), swine (34, 148-151), rabbits (152)(153)(154), dogs (41, [155][156][157], cats (domestic house cats as well as large wild cats, such as tigers, leopards, cougars, and lions) (39, 42-46, 49, 157-166), goats (125,139,167,168), chimpanzees (169), marine mammals (seals, sea lions, and walruses) (170), and even komodo dragons (171,172). The manifestation and pathological symptoms associated with Pasteurella infection, or "pasteurellosis," range from asymptomatic or mild chronic upper respiratory inflammation to acute, often fatal, pneumonic and/or disseminated disease.…”

Section: Pasteurella Disease In Animals Pasteurellosis Prevalencementioning

confidence: 99%

Pasteurella multocida: from Zoonosis to Cellular Microbiology

2013

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SUMMARY In a world where most emerging and reemerging infectious diseases are zoonotic in nature and our contacts with both domestic and wild animals abound, there is growing awareness of the potential for human acquisition of animal diseases. Like other Pasteurellaceae , Pasteurella species are highly prevalent among animal populations, where they are often found as part of the normal microbiota of the oral, nasopharyngeal, and upper respiratory tracts. Many Pasteurella species are opportunistic pathogens that can cause endemic disease and are associated increasingly with epizootic outbreaks. Zoonotic transmission to humans usually occurs through animal bites or contact with nasal secretions, with P. multocida being the most prevalent isolate observed in human infections. Here we review recent comparative genomics and molecular pathogenesis studies that have advanced our understanding of the multiple virulence mechanisms employed by Pasteurella species to establish acute and chronic infections. We also summarize efforts being explored to enhance our ability to rapidly and accurately identify and distinguish among clinical isolates and to control pasteurellosis by improved development of new vaccines and treatment regimens.

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“…The small difference between the isolates seen by REA still allows the conclusion that the isolates belong to the same clonal lineage (Tenover et al ., 1995). The original clone was only moderately virulent in chickens (Petersen et al, 2001b), whereas the clone on farm A seemed more virulent, resulting in higher mortality.…”

Section: Discussionmentioning

confidence: 93%

“…This clone was also detected in wild birds in Sweden in 1998 (Bisgaard, unpublished data). These observations seem to indicate a significant risk for transmission of P. multocida between wild birds and free-range poultry, especially as the original outbreak clone has been shown to be highly virulent for poultry (Petersen et al ., 2001b). However, the genetic stability of P. multocida associated with outbreaks of fowl cholera needs to be investigated in further detail to allow meaningful epidemiological interpretations to be made.…”

Section: Introductionmentioning

confidence: 99%

Clonal stability ofPasteurella multocidain free-range layers affected by fowl cholera

et al. 2006

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Detailed longitudinal studies of the genetic stability of Pasteurella multocida ssp. multocida, the cause of fowl cholera, have not previously been carried out. Consequently, the aim of the present study was to provide detailed information on the genetic stability and diversity of P. multocida ssp. multocida in poultry flocks over time, enabling new insights into the molecular epidemiology of this important poultry pathogen. Longitudinal investigations of the rate and causes of mortality were carried out on two free-range layer farms (A and B) over a period of 11 months. The total mortality of two flocks, A 1 and A 2 , on farm A were 62 and 91%, respectively, while the total mortality of a single flock B 1 on farm B was 6%. Postmortem examinations were performed on 708 layers from flocks A 1 and A 2 and in 159 from flock B 1 . Fowl cholera was the main cause of mortality on both farms. Pasteurella multocida isolates recovered from layers on both farms were characterized phenotypically and genotypically, and 322 isolates were identified as P. multocida ssp. multocida. The genetic diversity of 99 isolates from farm A and 31 from farm B was characterized by restriction endonuclease analysis and amplified fragment length polymorphism analysis. The isolates on each farm had a unique restriction endonuclease analysis and amplified fragment length polymorphism analysis type, suggesting a

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Virulence ofPasteurella multocidasubsp.multocidaisolated from outbreaks of fowl cholera in wild birds for domestic poultry and game birds

Cited by 38 publications

References 27 publications

Time-course investigation of infection with a low virulentPasteurella multocidastrain in normal and immune-suppressed 12-week-old free-range chickens

Time-course investigation of infection with a low virulentPasteurella multocidastrain in normal and immune-suppressed 12-week-old free-range chickens

Pasteurella multocida: from Zoonosis to Cellular Microbiology

Clonal stability ofPasteurella multocidain free-range layers affected by fowl cholera

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