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The Journal of Infectious Diseases | 2004

Avian Influenza A Virus (H7N7) Epidemic in The Netherlands in 2003: Course of the Epidemic and Effectiveness of Control Measures

Arjan Stegeman; A. Bouma; A.R.W. Elbers; Mart C.M. de Jong; G. Nodelijk; Fred de Klerk; G. Koch; Michiel van Boven

An epidemic of high-pathogenicity avian influenza (HPAI) A virus subtype H7N7 occurred in The Netherlands in 2003 that affected 255 flocks and led to the culling of 30 million birds. To evaluate the effectiveness of the control measures, we quantified between-flock transmission characteristics of the virus in 2 affected areas, using the reproduction ratio Rh. The control measures markedly reduced the transmission of HPAI virus: Rh before detection of the outbreak in the first infected flock was 6.5 (95% confidence interval [CI], 3.1-9.9) in one area and 3.1 in another area, and it decreased to 1.2 (95% CI, 0.6-1.9) after detection of the first outbreak in both areas. The observation that Rh remained >1 suggests that the containment of the epidemic was probably due to the reduction in the number of susceptible flocks by complete depopulation of the infected areas rather than to the reduction of the transmission by the other control measures.


Preventive Veterinary Medicine | 1999

The classical swine fever epidemic 1997–1998 in the Netherlands: descriptive epidemiology

A.R.W. Elbers; Arjan Stegeman; Hans Moser; H.Mark Ekker; Jan A Smak; Frits H Pluimers

The objective of this paper is to describe the severe epidemic of classical swine fever (CSF) in The Netherlands in 1997-1998 under a policy of non-vaccination, intensive surveillance, pre-emptive slaughter and stamping out in an area which has one of the highest pig and herd densities in Europe. The primary outbreak was detected on 4 February 1997 on a mixed sow and finishing pig herd. A total of 429 outbreaks was observed during the epidemic, and approximately 700,000 pigs from these herds were slaughtered. Among these outbreaks were two artificial insemination centres, which resulted in a CSF-suspect declaration of 1680 pig herds (mainly located in the southern part of The Netherlands). The time between introduction of CSF virus (CSFV) into the country and diagnosis of CSF in the primary outbreak was estimated to be approximately 6 weeks. It is presumed that CSFV was spread from The Netherlands to Italy and Spain via shipment of infected piglets in the beginning of February 1997, before the establishment of a total stand-still of transportation. In June 1997, CSFV is presumed to be introduced into Belgium from The Netherlands. Pre-emptive slaughter of herds that had been in contact with infected herds or were located in close vicinity of infected herds, was carried out around the first two outbreaks. However, this policy was not further exercised till mid-April 1997, when pre-emptive slaughter became a standard operational procedure for the rest of the epidemic. In total, 1286 pig herds were pre-emptively slaughtered. (approximately 1.1 million pigs). A total of 44 outbreaks (10%) was detected via pre-emptive slaughter. When there were clinical signs, the observed symptoms in infected herds were mainly atypical: fever, apathy, ataxia or a combination of these signs. In 322 out of 429 outbreaks (75%), detection was bases on clinical signs observed: 32% was detected by the farmer, 25% by the veterinary practitioner, 10% of the outbreaks by tracing teams and 8% by screening teams of the veterinary authorities. In 76% of the outbreaks detected by clinical signs, the farmer reported to have seen clinical symptoms for less than 1 week before diagnosis, in 22% for 1-4 weeks before diagnosis, and in 4 herds (1%) the farmer reported to have seen clinical symptoms for more than 4 weeks before diagnosis. Transportation lorries played a major role in the transmission of CSFV before the primary outbreak was diagnosed. It is estimated that approximately 39 herds were already infected before the first measures of the eradication campaign came into force. After the first measures to stop the spread of CSFV had been implemented, the distribution of the most likely routes of transmission markedly changed. In most outbreaks, a neighbourhood infection was indicated. Basically, there were two reasons for this catastrophe. Firstly, there was the extent of the period between introduction of the virus in the region and detection of the first outbreak. As a result, CSFV had opportunities to spread from one herd to another during this period. Secondly, the measures initially taken did not prove sufficient in the swine- and herd-dense region involved.


Emerging Infectious Diseases | 2013

Schmallenberg Virus in Culicoides spp. Biting Midges, the Netherlands, 2011

A.R.W. Elbers; Rudy Meiswinkel; Erik van Weezep; Marianne M. Sloet van Oldruitenborgh-Oosterbaan; Engbert A. Kooi

To determine which species of Culicoides biting midges carry Schmallenberg virus (SBV), we assayed midges collected in the Netherlands during autumn 2011. SBV RNA was found in C. scoticus, C. obsoletus sensu stricto, and C. chiopterus. The high proportion of infected midges might explain the rapid spread of SBV throughout Europe.


PLOS Computational Biology | 2005

Risk Maps for the Spread of Highly Pathogenic Avian Influenza in Poultry

Gert Jan Boender; T.H.J. Hagenaars; A. Bouma; G. Nodelijk; A.R.W. Elbers; Mart C.M. de Jong; Michiel van Boven

Devastating epidemics of highly contagious animal diseases such as avian influenza, classical swine fever, and foot-and-mouth disease underline the need for improved understanding of the factors promoting the spread of these pathogens. Here the authors present a spatial analysis of the between-farm transmission of a highly pathogenic H7N7 avian influenza virus that caused a large epidemic in The Netherlands in 2003. The authors developed a method to estimate key parameters determining the spread of highly transmissible animal diseases between farms based on outbreak data. The method allows for the identification of high-risk areas for propagating spread in an epidemiologically underpinned manner. A central concept is the transmission kernel, which determines the probability of pathogen transmission from infected to uninfected farms as a function of interfarm distance. The authors show how an estimate of the transmission kernel naturally provides estimates of the critical farm density and local reproduction numbers, which allows one to evaluate the effectiveness of control strategies. For avian influenza, the analyses show that there are two poultry-dense areas in The Netherlands where epidemic spread is possible, and in which local control measures are unlikely to be able to halt an unfolding epidemic. In these regions an epidemic can only be brought to an end by the depletion of susceptible farms by infection or massive culling. The analyses provide an estimate of the spatial range over which highly pathogenic avian influenza viruses spread between farms, and emphasize that control measures aimed at controlling such outbreaks need to take into account the local density of farms.


Veterinary Microbiology | 2001

Herd level husbandry factors associated with the serological Salmonella prevalence in finishing pig herds in The Netherlands

P.J. van der Wolf; W.B. Wolbers; A.R.W. Elbers; H.M.J.F. van der Heijden; J.M.C.C. Koppen; W.A. Hunneman; F.W. van Schie; M.J.M. Tielen

A national program to reduce Salmonella in pork and pork products should include monitoring and intervention at farm level. To develop an adequate intervention strategy at farm level, risk factors for Salmonella infections in finishing pigs have to be determined. In this study, blood samples were collected randomly at two slaughterhouses from slaughter pigs. Samples were tested by the Dutch Salmonella ELISA, based on the O-antigens 1, 4, 5, 6, 7 and 12, using a cut-off of OD%=10. This ELISA has been calibrated against the Danish ELISA to give comparable results. Workers from herds from which at least forty blood samples had been collected, were asked to participate in a questionnaire. In total, 353 questionnaires were obtained and analysed. Significant risk factors associated with the proportion of seropositive samples were identified by multiple linear logistic regression. The feeding of a complete liquid feed containing fermented by-products and the omission of disinfection after pressure washing a compartment as part of an all-in/all-out procedure, were both associated with a lower Salmonella seroprevalence. A small to moderate herd size (<800 finishing pigs), a previous diagnosis of clinical Salmonella infection in the herd, the use of tylosin as an antimicrobial growth promoter in finishing feed, or herds which had more than 16% of the livers of their pigs condemned at the slaughterhouse as a result of white spots were associated with a higher Salmonella seroprevalence. Hypothetical intervention strategies based on these risk factors can be studied for their effect on the Salmonella seroprevalence and practical applicability in field studies.


Preventive Veterinary Medicine | 2008

Field observations during the Bluetongue serotype 8 epidemic in 2006: II. Morbidity and mortality rate, case fatality and clinical recovery in sheep and cattle in the Netherlands

A.R.W. Elbers; A. Backx; Koen Mintiens; Guillaume Gerbier; Christoph Staubach; Guy Hendrickx; Arco van der Spek

Data collected in the Netherlands during the Bluetongue serotype 8 (BTV-8) epidemic indicated that in outbreak cattle herds, predominantly dairy and nursing cows were clinically affected and not young stock, beef cattle, beef calves, or breeding animals. In outbreak sheep flocks, mainly ewes and--if present--rams, were clinically affected and not the lambs. Median morbidity rate in outbreak herds was 1.85 per 100 sheep-month at risk and 0.32 per 100 cattle-month at risk for sheep and cattle, respectively. The mean proportion of BT-affected animals in outbreak herds that recovered from clinical disease was approximately eight times higher for cattle compared to sheep in the Netherlands. Median mortality rate in outbreak herds was 0.5 per 100 sheep-month at risk of dying and 0 per 100 cattle-month at risk of dying for sheep and cattle, respectively. Median recovery time of both sheep and cattle that recovered from clinical disease in outbreak herds was 14 days. Median case fatality was 50% in sheep outbreak flocks and 0% in outbreak cattle herds. It is concluded that morbidity and mortality in outbreak cattle herds was very limited during the BTV-8 epidemic in the Netherlands in 2006. In outbreak sheep flocks, morbidity was limited, with exceptions for a few flocks. However, almost 50% of the clinically sick sheep died in outbreak sheep herds.


Preventive Veterinary Medicine | 2008

Field observations during the bluetongue serotype 8 epidemic in 2006: I. Detection of first outbreaks and clinical signs in sheep and cattle in Belgium, France and the Netherlands

A.R.W. Elbers; A. Backx; E. Méroc; Guillaume Gerbier; Christoph Staubach; Guy Hendrickx; Arco van der Spek; Koen Mintiens

Starting August 2006, a major epidemic of bluetongue (BT) was identified in North-West Europe, affecting The Netherlands, Belgium, Germany, Luxembourg and the North of France. It was caused by BT virus serotype 8 (BTV-8), a serotype previously unknown to the European Union (EU). In this outbreak, the virus caused clinical disease in a few individual animals within cattle herds, whereas overt clinical disease was usually restricted to sheep. Investigations in Belgium suggested that the first clinical signs of BTV-8 appeared mid July 2006 in a cattle herd, while the first suspicion of a BT-outbreak in Belgium was reported on 17 August 2006. In the first 10 BTV-8 outbreaks in the Netherlands, the owners indicated that the first clinical signs started approximately 12-17 days before a suspicion was reported to the veterinary authorities via a veterinary practitioner. In BTV-8 affected sheep flocks, erosions of the oral mucosa, fever, salivation, facial and mandibular oedema, apathy and tiredness, mortality, oedema of the lips, lameness, and dysphagia were among the most frequent clinical signs recorded. The most prominent clinical signs in BTV-8 affected cattle herds were: crusts/lesions of the nasal mucosa, erosions of lips/crusts in or around the nostrils, erosions of the oral mucosa, salivation, fever, conjunctivitis, coronitis, muscle necrosis, and stiffness of the limbs. Crusts/lesions of nasal mucosa, conjunctivitis, hyperaemic/purple coloration and lesions of the teats, and redness/hypersensitivity of the skin were relatively more seen on outbreak farms with cattle compared to sheep. Mortality, oedema of the head and ears, coronitis, redness of the oral mucosa, erosions/ulceration of tongue mucosa, purple coloration of the tongue and tongue protrusion and dyspneu were relatively more seen on outbreak farms with sheep compared to cattle.


Veterinary Microbiology | 1999

Salmonella infections in finishing pigs in The Netherlands: bacteriological herd prevalence, serogroup and antibiotic resistance of isolates and risk factors for infection

P.J. van der Wolf; J.H. Bongers; A.R.W. Elbers; F.M.M.C. Franssen; W.A. Hunneman; A.C.A. van Exsel; M.J.M. Tielen

Salmonellae are wide spread in man and animals world wide and are of increasing significance as causative agents of foodborne diseases in man. The European Union, national authorities and the pig industry are therefore more and more interested in the Salmonella status of the pig population. The aim of this study was to estimate the bacteriological prevalence of Salmonella in finishing pig herds, the serogroup and the resistance to antibiotics of the isolated Salmonellae and a preliminary risk analysis of factors associated with infection. For this, 317 finishing pig herds were randomly selected from a database containing 1500 herds in the southern part of the Netherlands. In each herd 24 samples of fresh faeces were collected from two compartments with pigs close to market weight. Per compartment 12 samples of faeces were pooled into one pooled sample. Pooled samples were cultured in duplicate. Salmonella spp. were recovered from 71 out of 306 herds (23%) in which two compartments could be sampled. A total of 108 isolated Salmonellas were serotyped: 71 serogroup B, 3 serogroup C1, 6 serogroup C2, 22 serogroup D1, and 6 isolates neither serogroup B, C or D1. Of a total of 115 Salmonella isolates tested, none were resistant to colistin, enrofloxacin, flumequin or gentamicin. Automated liquid feeding of by-products, and membership of an Integrated Quality Control (IQC) production group were associated with a decreased risk of infection, while use of trough feeding was associated with an increased risk of infection. It is necessary to test these presumed risk factors in intervention studies to evaluate their potency to reduce the Salmonella prevalence in finishing pigs and thereby reduce the risk of Salmonellosis in people consuming pork.


Avian Diseases | 2004

The highly pathogenic avian influenza A (H7N7) virus epidemic in The Netherlands in 2003--lessons learned from the first five outbreaks.

A.R.W. Elbers; T. H. F. Fabri; T. S. de Vries; J. J. de Wit; A. Pijpers; G. Koch

Abstract Clinical signs and gross lesions observed in poultry submitted for postmortem examination (PME) from the first five infected poultry flocks preceding the detection of the primary outbreak of highly pathogenic avian influenza (HPAI) of subtype H7N7 during the 2003 epidemic in the Netherlands are described. The absence of HPAI from the Netherlands for more than 75 yr created a situation in which poultry farmers and veterinary practitioners did not think of AI in the differential diagnosis as a possible cause of the clinical problems seen. Increased and progressive mortality was not reported to the governmental authorities by farmers or veterinary practitioners. It took 4 days from the first entry of postmortem material to notify the governmental authorities of a strong suspicion of an AI outbreak on the basis of a positive immunofluoresence test result. The gross lesions observed at PME did not comply with the descriptions in literature, especially the lack of hemorrhagic changes in tissues, and the lack of edema and cyanosis in comb and wattles is noted. The following lessons are learned from this epidemic: a) in the future, increased and progressive mortality should be a signal to exclude AI as cause of disease problems on poultry farms; b) intensive contact between the veterinary practitioner in the field and the veterinarian executing PME is necessary to have all relevant data and developments at ones disposal to come to a conclusive diagnosis; c) in an anamnesis, reporting of high or increased mortality should be quantified in the future (number of dead birds in relation to the number of birds brought to the farm to start production, together with the timing within the production cycle), or else this mortality cannot be interpreted properly; d) if clinical findings such as high mortality indicate the possibility of HPAI, the pathologist should submit clinical samples to the reference laboratory, even if PME gives no specific indications for HPAI; e) the best way to facilitate early detection of an HPAI outbreak is to have the poultry farmer and/or veterinary practitioner immediately report to the syndrome-reporting system currently in operation the occurrence of high mortality, a large decrease in feed or water intake, or a considerable drop in egg production; f) in order to detect low pathogenic avian influenza infections that could possibly change to HPAI, a continuous serologic monitoring system has been set up, in which commercial poultry flocks are screened for antibodies against AI virus of subtypes H5 and H7.


Emerging Infectious Diseases | 2012

Seroprevalence of Schmallenberg Virus Antibodies among Dairy Cattle, the Netherlands, Winter 2011–2012

A.R.W. Elbers; W.L.A. Loeffen; Sjaak Quak; Els A. de Boer-Luijtze; Arco N. van der Spek; R.J. Bouwstra; Riks Maas; Marcel A.H. Spierenburg; Eric P. de Kluijver; Gerdien van Schaik; Wim H. M. van der Poel

Seroprevalence was highest in the eastern part of the country, bordering Germany, where the virus was first identified.

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G. Koch

Wageningen University and Research Centre

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W.L.A. Loeffen

Wageningen University and Research Centre

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M.C.M. de Jong

Wageningen University and Research Centre

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G. Nodelijk

Wageningen University and Research Centre

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