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Supplement bij veertiende jaargang, april 2006 - NVMM

Supplement bij veertiende jaargang, april 2006 - NVMM

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De eerste twee studies concluderen, nogal somber,<br />

respectievelijk:<br />

1) The analysis indicates that the Dutch prevention strategy<br />

fails to stop transmission of hepatitis B from persistently<br />

infected individuals originating from hepatitis B endemic<br />

countries. 2) It must be realised that, after 20 years of<br />

vaccination of at-risk groups, HBV still circulates in the<br />

at-risk groups and Dutch blood donors acquire the HBV<br />

strains involved.<br />

Kan de vorderende, landelijke typering van acute HBVisolaten<br />

[3] nuttig licht op deze zaak werpen? Of is deze<br />

exercitie symptomatisch voor een steeds ingewikkelder,<br />

mogelijk inefficiënt risicogroepenbeleid?<br />

References<br />

1. Steenbergen JE van, Niesters HG, et al. Molecular epidemiology<br />

of hepatitis B virus in Amsterdam 1992-1997. J<br />

Med Virol 2002;66:159-65.<br />

2. Koppelman MH, Zaaijer HL. Diversity and origin of<br />

hepatitis B virus in Dutch blood donors. J Med Virol<br />

2004;73:29-32.<br />

3. Boot H. Workshop moleculaire typering HBV in<br />

Nederland: inzicht in transmissie en epidemiologie van<br />

HBV. Infectieziektenbulletin 2005;16:280-1.<br />

09.02<br />

Tracking hepatitis A virus within and among risk groups<br />

S.M. Bruisten1 , G.M.S. Tjon1 , R.A. Coutinho2 1GGD, Public Health laboratory, Department of Infectious<br />

Diseases, Amsterdam, 2Centre for Infectious Diseases, RIVM,<br />

Bilthoven<br />

In the Netherlands the incidence of infection with hepatitis<br />

A virus (HAV) is decreasing due to high hygienic standards<br />

and vaccination of targeted risk groups. As a consequence<br />

the susceptibility to HAV is increasing with a potential<br />

of larger outbreaks and higher morbidity among adults.<br />

In Amsterdam, we identified an association of groups at<br />

risk for HAV infection and (sub)genotypes of the virus.<br />

Travel to Morocco resulted mainly in infections of the<br />

1B genotype, whereas among men having sex with men<br />

(MSM) exclusively genotype 1A was found.[1] During four<br />

years, with the cooperation of 8 GGDs, we established a<br />

national HAV database containing epidemiological data<br />

combined with phylogenetic analysis. It reinforced our<br />

findings that the correlation risk to genotype was valid all<br />

over the Netherlands.[2,3] Moreover, in other European<br />

countries the same MSM strains were identified during<br />

outbreaks, suggesting endemic transmission among MSM.<br />

Travel associated introductions generally appeared in<br />

small clusters, disappearing soon after introduction.<br />

This suggests that travel related HAV introductions are<br />

effectively recognized and stopped.<br />

Ned Tijdschr Med Microbiol <strong>2006</strong>; 4:<strong>Supplement</strong><br />

S4<br />

Among drug users a major outbreak occurred in Rotterdam<br />

in spring 2004. With molecular epidemiology all cases<br />

with the genotype 3A outbreak strain could be distinguished<br />

from sporadic cases with other genotypes. This<br />

was helpful to assess the efficacy of the mass vaccination<br />

campaign.[4] For public health purposes it is of major<br />

importance to know the period of infectivity. We therefore<br />

followed 27 acute HAV patients for 26 weeks, measuring<br />

viral load in blood and faeces. We found a significant<br />

correlation of HAV and ALT levels in serum. However,<br />

the acute load in faeces was not related to genotype, nor to<br />

duration of excretion. High loads in faeces were found for<br />

81 days, suggesting that transmission may still occur when<br />

adhering to the current policy of 2 weeks of infectiousness<br />

after symptoms.<br />

HAV typing is of use to aid establishig epidemiological<br />

links. Thus the national HAV database should be kept<br />

updated.<br />

References<br />

1. Bruisten SM, et al. JMV 2001;63:88.<br />

2. Steenbergen JE van, et al. JID 2004;189:471.<br />

3. Tjon GMS, et al. JCV 2005;32:128<br />

4. Tjon GMS, et al. JMV 2005;77:360.<br />

09.03<br />

Moleculaire epidemiologie en tuberculosebestrijding, toy<br />

and tool<br />

M. Šebek<br />

KNCV Tuberculosefonds, Den Haag<br />

Achtergrond: In 1994 ging de Mycobacterium tuberculosis<br />

DNA en resistentiesurveillance van start, een co-project<br />

van KNCV Tuberculosefonds en het Rijksinstituut voor<br />

Volksgezondheid en Milieu (RIVM) in samenwerking met<br />

de GGD’en. Het doel is de transmissie van de M. tuberculosis-stammen<br />

in kaart te brengen en daarmee inzicht te<br />

krijgen in de verspreiding van de verschillende stammen<br />

onder de bevolkingsgroepen in Nederland; het traceren<br />

van bronnen en hun contacten en van onvermoede latente<br />

tuberculoseinfecties (LTBI).<br />

Methode: Nadat op het RIVM onderscheid is gemaakt<br />

tussen materiaal van patiënten met een uniek (d.w.z.<br />

niet eerder gevonden) DNA-fingerprintpatroon en 100%<br />

identieke patronen (de zogenaamde clusters), meldt de<br />

verpleegkundig consulent surveillance de geclusterde<br />

patiënten aan de afdeling tuberculosebestrijding van<br />

de GGD’en. De sociaalverpleegkundigen trachten<br />

vervolgens epidemiologische verbanden aan te tonen<br />

samen met de sociaalverpleegkundigen van GGD’en<br />

waar andere patiënten in de clusters zijn gevonden aan<br />

de hand van de sociale anamnese van de patiënt(en).<br />

Over iedere geclusterde patiënt worden de bevindingen

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