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<title xml:lang="en">What has “Karonga” taught us? Tuberculosis studied over three decades</title>
<author>
<name sortKey="Crampin, Amelia C" sort="Crampin, Amelia C" uniqKey="Crampin A" first="Amelia C." last="Crampin">Amelia C. Crampin</name>
<affiliation>
<nlm:aff id="A1">London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A2">Karonga Prevention Study, PO Box 46, Chilumba, Malawi</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Glynn, Judith R" sort="Glynn, Judith R" uniqKey="Glynn J" first="Judith R." last="Glynn">Judith R. Glynn</name>
<affiliation>
<nlm:aff id="A1">London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Fine, Paul E M" sort="Fine, Paul E M" uniqKey="Fine P" first="Paul E. M." last="Fine">Paul E. M. Fine</name>
<affiliation>
<nlm:aff id="A1">London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK</nlm:aff>
</affiliation>
</author>
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<idno type="wicri:source">PMC</idno>
<idno type="pmid">19146741</idno>
<idno type="pmc">3272402</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3272402</idno>
<idno type="RBID">PMC:3272402</idno>
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<title xml:lang="en" level="a" type="main">What has “Karonga” taught us? Tuberculosis studied over three decades</title>
<author>
<name sortKey="Crampin, Amelia C" sort="Crampin, Amelia C" uniqKey="Crampin A" first="Amelia C." last="Crampin">Amelia C. Crampin</name>
<affiliation>
<nlm:aff id="A1">London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A2">Karonga Prevention Study, PO Box 46, Chilumba, Malawi</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Glynn, Judith R" sort="Glynn, Judith R" uniqKey="Glynn J" first="Judith R." last="Glynn">Judith R. Glynn</name>
<affiliation>
<nlm:aff id="A1">London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Fine, Paul E M" sort="Fine, Paul E M" uniqKey="Fine P" first="Paul E. M." last="Fine">Paul E. M. Fine</name>
<affiliation>
<nlm:aff id="A1">London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK</nlm:aff>
</affiliation>
</author>
</analytic>
<series>
<title level="j">The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease</title>
<idno type="ISSN">1027-3719</idno>
<idno type="eISSN">1815-7920</idno>
<imprint>
<date when="2009">2009</date>
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<div type="abstract" xml:lang="en">
<p id="P1">This paper summarises tuberculosis (TB) research over almost 30 years in Karonga District, northern Malawi, an area typical of much of rural Africa. The dominant factor has been HIV, which arrived in the district about 1980, leading to an increase in TB incidence to a peak of approximately 65 smear-positive pulmonary cases/100,000 in 2000. Tuberculin surveys indicate annual risks of
<italic>M. tuberculosis</italic>
infection of approximately 1%, thus most of the population is uninfected and at risk of primary infection and disease. Molecular epidemiological studies demonstrate that about two thirds of TB arises from recent infection, but recognisable recent contact is responsible for only about 10 % of disease. By 2001, 57% of TB was directly attributable to HIV, implying that it would have declined were it not for HIV. HIV infection increases the risk of TB most among young adults, and greatly increases the risk of recurrence from new infection after treatment. Mortality rates in the HIV-infected are high, but there is no association of HIV with drug resistance. Other risk factors with relatively smaller effects include age and sex, contact, several genetic polymorphisms and area.</p>
<p id="P2">Neither one nor two doses of BCG provides protection against adult pulmonary tuberculosis, despite protecting against leprosy. Skin test surveys, cohort studies and comparative immunological studies with the UK suggest that exposure to environmental mycobacteria provides some protection against TB and that BCG’s failure is attributable partly to this widespread heterologous exposure masking effects of the vaccine.</p>
<p id="P3">Drug resistance has remained constant (<10%) over more than 20 years. Immunotherapy with
<italic>Mycobacterium vaccae</italic>
provided no benefit, but treatment of HIV-positive patients with cotrimoxazole reduced mortality. The Karonga programme illustrates the value of long-term population-based studies to investigate the natural history of TB and to influence TB control policy. Current studies focus on immunological markers of infection, disease and protection, and on elucidating the impact of anti-retroviral therapy on TB incidence at population level.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article">
<pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-journal-id">9706389</journal-id>
<journal-id journal-id-type="pubmed-jr-id">20773</journal-id>
<journal-id journal-id-type="nlm-ta">Int J Tuberc Lung Dis</journal-id>
<journal-id journal-id-type="iso-abbrev">Int. J. Tuberc. Lung Dis.</journal-id>
<journal-title-group>
<journal-title>The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease</journal-title>
</journal-title-group>
<issn pub-type="ppub">1027-3719</issn>
<issn pub-type="epub">1815-7920</issn>
</journal-meta>
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<article-id pub-id-type="pmid">19146741</article-id>
<article-id pub-id-type="pmc">3272402</article-id>
<article-id pub-id-type="manuscript">UKMS40325</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
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<title-group>
<article-title>What has “Karonga” taught us? Tuberculosis studied over three decades</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Crampin</surname>
<given-names>Amelia C.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
<xref ref-type="corresp" rid="CR1">*</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Glynn</surname>
<given-names>Judith R.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Fine</surname>
<given-names>Paul E.M.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
</contrib-group>
<aff id="A1">
<label>1</label>
London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK</aff>
<aff id="A2">
<label>2</label>
Karonga Prevention Study, PO Box 46, Chilumba, Malawi</aff>
<author-notes>
<corresp id="CR1">
<label>*</label>
Corresponding author London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK
<email>mia.crampin@lshtm.ac.uk</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted">
<day>9</day>
<month>1</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="ppub">
<month>2</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>05</day>
<month>2</month>
<year>2012</year>
</pub-date>
<volume>13</volume>
<issue>2</issue>
<fpage>153</fpage>
<lpage>164</lpage>
<abstract>
<p id="P1">This paper summarises tuberculosis (TB) research over almost 30 years in Karonga District, northern Malawi, an area typical of much of rural Africa. The dominant factor has been HIV, which arrived in the district about 1980, leading to an increase in TB incidence to a peak of approximately 65 smear-positive pulmonary cases/100,000 in 2000. Tuberculin surveys indicate annual risks of
<italic>M. tuberculosis</italic>
infection of approximately 1%, thus most of the population is uninfected and at risk of primary infection and disease. Molecular epidemiological studies demonstrate that about two thirds of TB arises from recent infection, but recognisable recent contact is responsible for only about 10 % of disease. By 2001, 57% of TB was directly attributable to HIV, implying that it would have declined were it not for HIV. HIV infection increases the risk of TB most among young adults, and greatly increases the risk of recurrence from new infection after treatment. Mortality rates in the HIV-infected are high, but there is no association of HIV with drug resistance. Other risk factors with relatively smaller effects include age and sex, contact, several genetic polymorphisms and area.</p>
<p id="P2">Neither one nor two doses of BCG provides protection against adult pulmonary tuberculosis, despite protecting against leprosy. Skin test surveys, cohort studies and comparative immunological studies with the UK suggest that exposure to environmental mycobacteria provides some protection against TB and that BCG’s failure is attributable partly to this widespread heterologous exposure masking effects of the vaccine.</p>
<p id="P3">Drug resistance has remained constant (<10%) over more than 20 years. Immunotherapy with
<italic>Mycobacterium vaccae</italic>
provided no benefit, but treatment of HIV-positive patients with cotrimoxazole reduced mortality. The Karonga programme illustrates the value of long-term population-based studies to investigate the natural history of TB and to influence TB control policy. Current studies focus on immunological markers of infection, disease and protection, and on elucidating the impact of anti-retroviral therapy on TB incidence at population level.</p>
</abstract>
<funding-group>
<award-group>
<funding-source country="United Kingdom">Wellcome Trust : </funding-source>
<award-id>079828 || WT</award-id>
</award-group>
</funding-group>
</article-meta>
</front>
</pmc>
</record>

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