Jens Peter Peter Christensen

Prof. Jens Peter Peter Christensen


Research Focus & Metrics

Academic Career Length

34Years (1993-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2013 in Frontiers in Microbiology
Verified
Journal Article
Open access
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SHSimon Le Hello
Simon Le Hello
ABAmany Bekhit
Amany Bekhit
SGSophie A. Granier
Sophie A. Granier
HBHimel Barua
Himel Barua
JBJanine Beutlich
Janine Beutlich
FWFrançois-Xavier Weill
François-Xavier Weill
While the spread of Salmonella enterica serotype Kentucky resistant to ciprofloxacin across Africa and the Middle-East has been described recently, the presence of this strain in humans, food, various animal species (livestock, pets, and wildlife) and in environment is suspected in other countries of different continents. Here, we report results of an in-depth molecular epidemiological study on a global human and non-human collection of S. Kentucky (n = 70). We performed XbaI-pulsed field gel electrophoresis and multilocus sequence typing, assessed mutations in the quinolone resistance-determining regions, detected β-lactam resistance mechanisms, and screened the presence of the Salmonella genomic island 1 (SGI1). In this study, we highlight the rapid and extensive worldwide dissemination of the ciprofloxacin-resistant S. Kentucky ST198-X1-SGI1 strain since the mid-2000s in an increasingly large number of contaminated sources, including the environment. This strain has accumulated an increasing number of chromosomal and plasmid resistance determinants and has been identified in the Indian subcontinent, Southeast Asia and Europe since 2010. The second substitution at position 87 in GyrA (replacing the amino acid Asp) appeared helpful for epidemiological studies to track the origin of contamination. This global study provides evidence leading to the conclusion that high-level resistance to ciprofloxacin in S. Kentucky is a simple microbiological trait that facilitates the identification of the epidemic clone of interest, ST198-X1-SGI1. Taking this into account is essential in order to detect and monitor it easily and to take rapid measures in livestock to ensure control of this infection.

1 December 2008 in Emerging Infectious Diseases
Verified
Journal Article
Open access
PBParitosh K. Biswas
Paritosh K. Biswas
JCJens Peter Peter Christensen
Jens Peter Peter Christensen
Syed Sayeem Uddin AhmedSyed Sayeem Uddin Ahmed
Syed Sayeem Uddin Ahmed
HBHimel Barua
Himel Barua
Ashutosh DasAshutosh Das
Ashutosh Das
NDNitish C. Debnath
Nitish C. Debnath
To determine the epidemiology of outbreaks of avian influenza A virus (subtypes H5N1, H9N2) in chickens in Bangladesh, we conducted surveys and examined virus isolates. The outbreak began in backyard chickens. Probable sources of infection included egg trays and vehicles from local live bird markets and larger live bird markets.

1 December 2009 in Emerging Infectious Diseases
Verified
Journal Article
Open access
PBParitosh K. Biswas
Paritosh K. Biswas
JCJens Peter Peter Christensen
Jens Peter Peter Christensen
Syed Sayeem Uddin AhmedSyed Sayeem Uddin Ahmed
Syed Sayeem Uddin Ahmed
Ashutosh DasAshutosh Das
Ashutosh Das
MRMohammad H. Rahman
Mohammad H. Rahman
NDNitish C. Debnath
Nitish C. Debnath
To evaluate risk factors for infection with highly pathogenic avian influenza A virus (H5N1) in backyard chickens in Bangladesh, we conducted a matched case–control study. We enrolled 25 case farms (cases March–November 2007) and 75 control farms (June–November 2007). We used a questionnaire to collect farm data, which were analyzed by matched-pair analysis and multivariate conditional logistic regression. Factors independently associated were offering slaughter remnants of purchased chickens to backyard chickens (odds ratio [OR] 13.29, 95% confidence interval [CI] 1.34–131.98, p = 0.027), having a nearby water body (OR 5.27, 95% CI 1.24–22.34, p = 0.024), and having contact with pigeons (OR 4.47, 95% CI 1.14–17.50, p = 0.032). Separating chickens and ducks at night was protective (OR 0.06, 95% CI 0.01–0.45, p = 0.006). Reducing these risks and taking protective measures might reduce the risk for influenza (H5N1) infection in backyard chickens.

1 August 2006 in Veterinary Microbiology
Verified
Journal Article
Closed access
APAndreas Petersen
Andreas Petersen
JCJens Peter Peter Christensen
Jens Peter Peter Christensen
PKPeter Kuhnert
Peter Kuhnert
MBMagne Bisgaard
Magne Bisgaard
JOJohn Elmerdahl Olsen
John Elmerdahl Olsen

1 May 2002 in Veterinary Microbiology
Verified
Journal Article
Closed access
CDC. Dahl
C. Dahl
APA. Permin
A. Permin
JCJens Peter Peter Christensen
Jens Peter Peter Christensen
MBM. Bisgaard
M. Bisgaard
AMA.P. Muhairwa
A.P. Muhairwa
AJAsger Lundorff Jensen
Asger Lundorff Jensen

1 August 2000 in Scientific and Technical Review
Verified
Journal Article
Closed access
JCJens Peter Peter Christensen
Jens Peter Peter Christensen
MBM. Bisgaard
M. Bisgaard
Pasteurella multocida subspecies multocida is the most common cause of fowl cholera, although P. multocida subspecies septica and gallicida may also cause fowl cholera-like disease to some extent. However, the virulence properties of the different subspecies for various hosts have not been elucidated. The severity and incidence of P. multocida infections may vary considerably depending on several factors associated with the host (including species and age of infected birds), the environment and the bacterial strain. No single virulence factor has been associated with the observed variation in virulence among strains. Possible virulence factors include the following: the capsule, endotoxin, outer membrane proteins, iron binding systems, heat shock proteins, neuraminidase production and antibody cleaving enzymes. No RTX toxins (repeats in toxin) appear to be produced by P. multocida, but P. multocida exotoxin (PMT) could contribute to virulence in some avian infections. 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. The site of infection for P. multocida is generally believed to be the respiratory tract. The outcome of infections may range from peracute/acute infections to chronic infections. In the former type of infections, few clinical signs are observed before death and the lesions will be dominated by general septicaemic lesions. In chronic forms of P. multocida infections, suppurative lesions may be widely distributed, often involving the respiratory tract, the conjunctiva and adjacent tissues of the head. Diagnosis is always dependent upon isolation of the organism. For the detection of subclinical infections, mouse passage of relevant samples is recommended, but polymerase chain reaction and isolation attempts on selective media may represent alternatives. 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 to live vaccines.