Browsing by Author "Lukwago, Luswa"

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    Ebola Hemorrhagic Fever Associated with Novel Virus Strain, Uganda, 2007–2008
    (Emerging infectious diseases, 2010) Wamala, Joseph F.; Lukwago, Luswa; Malimbo, Mugagga; Nguku, Patrick; Yoti, Zabulon; Musenero, Monica; Amone, Jackson; Mbabazi, William; Nanyunja, Miriam; Zaramba, Sam; Opio, Alex; Lutwama, Julius J.; Talisuna, Ambrose O.; Okware, Sam I.
    During August 2007–February 2008, the novel Bundibugyo ebola virus species was identified during an outbreak of Ebola viral hemorrhagic fever in Bundibugyo district, western Uganda. To characterize the outbreak as a requisite for determining response, we instituted a caseseries investigation. We identified 192 suspected cases, of which 42 (22%) were laboratory positive for the novel species; 74 (38%) were probable, and 77 (40%) were negative. Laboratory confirmation lagged behind outbreak verification by 3 months. Bundibugyo ebola virus was less fatal (case fatality rate 34%) than Ebola viruses that had caused previous outbreaks in the region, and most transmission was associated with handling of dead persons without appropriate protection (adjusted odds ratio 3.83, 95% confidence interval 1.78–8.23). Our study highlights the need for maintaining a high index of suspicion for viral hemorrhagic fevers among healthcare workers, building local capacity for laboratory confirmation of viral hemorrhagic fevers, and institutionalizing standard precautions.
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    Epidemiology and Surveillance of Influenza Viruses in Uganda between 2008 and 2014
    (PLoS ONE, 2016) Wabwire-Mangen, Fred; Mimbe, Derrick E.; Erima, Bernard; Mworozi, Edison A.; Millard, Monica; Kibuuka, Hannah; Lukwago, Luswa; Bwogi, Josephine; Kiconco, Jocelyn; Tugume, Titus; Mulei, Sophia; Ikomera, Christine; Tsui, Sharon; Malinzi, Stephen; Kasasa, Simon; Coldren, Rodney; Byarugaba, Denis K.
    Influenza surveillance was conducted in Uganda from October 2008 to December 2014 to identify and understand the epidemiology of circulating influenza strains in out-patient clinic attendees with influenza-like illness and inform control strategies. Methodology Surveillance was conducted at five hospital-based sentinel sites. Nasopharyngeal and/or oropharyngeal samples, epidemiological and clinical data were collected from enrolled patients. Real-time reverse transcription polymerase chain reaction (RT-PCR) was performed to identify and subtype influenza strains. Data were double-entered into an Epi Info 3.5.3 database and exported to STATA 13.0 software for analysis. Results Of the 6,628 patient samples tested, influenza virus infection was detected in 10.4% (n = 687/ 6,628) of the specimens. Several trends were observed: influenza circulates throughout the year with two peaks; the major one from September to November and a minor one from March to June. The predominant strains of influenza varied over the years: Seasonal Influenza A(H3) virus was predominant from 2008 to 2009 and from 2012 to 2014; Influenza A (H1N1)pdm01 was dominant in 2010; and Influenza B virus was dominant in 2011. The peaks generally coincided with times of higher humidity, lower temperature, and higher rainfall. Conclusion Influenza circulated throughout the year in Uganda with two major peaks of outbreaks with similar strains circulating elsewhere in the region. Data on the circulating strains of influenza and its patterns of occurrence provided critical insights to informing the design and timing of influenza vaccines for influenza prevention in tropical regions of sub-Saharan Africa.
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    A Large Outbreak of Typhoid Fever Associated With a High Rate of Intestinal Perforation in Kasese District, Uganda
    (Clinical infectious diseases, 2012) Neil, Karen P.; Lukwago, Luswa; Mukobi, Peter; Kweyamba, Vianney; Asiimwe, Frank; Wefula, Edward
    Salmonella enterica serovar Typhi (Salmonella Typhi) causes an estimated 22 million typhoid fever cases and 216 000 deaths annually worldwide. In Africa, the lack of laboratory diagnostic capacity limits the ability to recognize endemic typhoid fever and to detect outbreaks. We report a large laboratory-confirmed outbreak of typhoid fever in Uganda with a high proportion of intestinal perforations (IPs). A suspected case of typhoid fever was defined as fever and abdominal pain in a person with either vomiting, diarrhea, constipation, headache, weakness, arthralgia, poor response to antimalarial medications, or IP. From March 4, 2009 to April 17, 2009, specimens for blood and stool cultures and serology were collected from suspected cases. Antimicrobial susceptibility testing and pulsed-field gel electrophoresis (PFGE) were performed on Salmonella Typhi isolates. Surgical specimens from patients with IP were examined. A community survey was conducted to characterize the extent of the outbreak.
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    Molecular Epidemiology of Influenza A/H3N2 Viruses Circulating in Uganda
    (PLoS ONE, 2011) Byarugaba, Denis K.; Ducatez, Mariette F.; Erima, Bernard; Mworozi, Edison A.; Millard, Monica; Kibuuka, Hannah; Lukwago, Luswa; Bwogi, Josephine; Kaira, Blanche B.; Mimbe, Derrick; Schnabel, David C.; Krauss, Scott; Darnell, Daniel; Webby, Richard J.; Webster, Robert G.; Wabwire-Mangen, Fred
    The increasing availability of complete influenza virus genomes is deepening our understanding of influenza evolutionary dynamics and facilitating the selection of vaccine strains. However, only one complete African influenza virus sequence is available in the public domain. Here we present a complete genome analysis of 59 influenza A/H3N2 viruses isolated from humans in Uganda during the 2008 and 2009 season. Isolates were recovered from hospital-based sentinel surveillance for influenza-like illnesses and their whole genome sequenced. The viruses circulating during these two seasons clearly differed from each other phylogenetically. They showed a slow evolution away from the 2009/10 recommended vaccine strain (A/ Brisbane/10/07), instead clustering with the 2010/11 recommended vaccine strain (A/Perth/16/09) in the A/Victoria/208/09 clade, as observed in other global regions. All of the isolates carried the adamantane resistance marker S31N in the M2 gene and carried several markers of enhanced transmission; as expected, none carried any marker of neuraminidase inhibitor resistance. The hemagglutinin gene of the 2009 isolates differed from that of the 2008 isolates in antigenic sites A, B, D, and to a lesser extent, C and E indicating evidence of an early phylogenetic shift from the 2008 to 2009 viruses. The internal genes of the 2009 isolates were similar to those of one 2008 isolate, A/Uganda/MUWRP-050/2008. Another 2008 isolate had a truncated PB1-F2 protein. Whole genome sequencing can enhance surveillance of future seasonal changes in the viral genome which is crucial to ensure that selected vaccine strains are protective against the strains circulating in Eastern Africa. This data provides an important baseline for this surveillance. Overall the influenza virus activity in Uganda appears to mirror that observed in other regions of the southern hemisphere.
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    Whole-genome analysis of influenza A(H1N1)pdm09 viruses isolated in Uganda from 2009 to 2011
    (Influenza and Other Respiratory Viruses, 2016) Byarugaba, Denis K.; Erima, Bernard; Millard, Monica; Kibuuka, Hannah; Lukwago, Luswa; Bwogi, Josephine; Mimbe, Derrick; Kiconco, Jocelyn B.; Tugume, Titus; Mworozi, Edison A.; Turner, Jasmine; Mckenzie, Pamela P.; Webby, Richard R. J.; Webster, Robert G.; Foret, Charlotte; Ducatez, Mariette F.; Coldren, Rodney; Wabwire-Mangen, Fred; Krauss, Scott
    We report a whole-genome analysis of 19 influenza A(H1N1)pdm09 isolates from four Ugandan hospitals between 2009 and 2011. The isolates differed from the vaccine strain A/California/07/2009 by three amino acid substitutions P100S, S220T, and I338V in the hemagglutinin and by two amino acid substitutions V106I and N248D in the neuraminidase proteins with consistent mutations in all gene segments distinguishing isolates from the 2009/2010 to 2010/2011 seasons. Phylogenetic analysis showed low genetic evolution, with genetic distances of 0%–1.3% and 0.1%–1.6% for HA and NA genes, respectively. The amino acid substitutions did not lead to antigenic differences from the reference strains.