2009 Pandemic Influenza A (H1N1) Virus Outbreak and Response – Rwanda, October, 2009–May, 2010

BACKGROUND: In October 2009, the first case of pandemic influenza A(H1N1)pdm09 (pH1N1) was confirmed in Kigali, Rwanda and countrywide dissemination occurred within several weeks. We describe clinical and epidemiological characteristics of this epidemic. METHODS: From October 2009 through May 2010, we undertook epidemiologic investigations and response to pH1N1. Respiratory specimens were collected from all patients meeting the WHO case definition for pH1N1, which were tested using CDC's real time RT-PCR protocol at the Rwandan National Reference Laboratory (NRL). Following documented viral transmission in the community, testing focused on clinically severe and high-risk group suspect cases. RESULTS: From October 9, 2009 through May 31, 2010, NRL tested 2,045 specimens. In total, 26% (n = 532) of specimens tested influenza positive; of these 96% (n = 510) were influenza A and 4% (n = 22) were influenza B. Of cases testing influenza A positive, 96.8% (n = 494), 3% (n = 15), and 0.2% (n = 1) were A(H1N1)pdm09, Seasonal A(H3) and Seasonal A(non-subtyped), respectively. Among laboratory-confirmed cases, 263 (53.2%) were children <15 years and 275 (52%) were female. In total, 58 (12%) cases were hospitalized with mean duration of hospitalization of 5 days (Range: 2-15 days). All cases recovered and there were no deaths. Overall, 339 (68%) confirmed cases received oseltamivir in any setting. Among all positive cases, 26.9% (143/532) were among groups known to be at high risk of influenza-associated complications, including age <5 years 23% (122/532), asthma 0.8% (4/532), cardiac disease 1.5% (8/532), pregnancy 0.6% (3/532), diabetes mellitus 0.4% (2/532), and chronic malnutrition 0.8% (4/532). CONCLUSIONS: Rwanda experienced a PH1N1 outbreak which was epidemiologically similar to PH1N1 outbreaks in the region. Unlike seasonal influenza, children <15 years were the most affected by pH1N1. Lessons learned from the outbreak response included the need to strengthen integrated disease surveillance, develop laboratory contingency plans, and evaluate the influenza sentinel surveillance system

Short communication - A Rwandan spirometry and resting ventilation study

To illustrate spirometric population variation and ventilatory adaptation to moderate altitude, we report the spirometric and resting ventilation values observed in a student population in Butare, Rwanda (altitude: 1 768 m; barometric pressure: 629 mm Hg). Spirometry was carried out with a Mijnhardt Volutest VT-3 water-sealed spirometer in students aged between 20 and 30 years. The results (mean ± SD) are as follows: Vital capacity: males: 4 123 ± 537 mL, females: 2 810 ± 393 mL; Vital capacity per m2 body surface area: males: 2 352 ± 245 mL/m2, females: 1 771 ± 219 mL/m2; FEV1: males: 3 576 ± 618 mL, females: 2 347 ± 474 mL; FEV1%: males: 87.8 ± 8.5 %, females: 84.5 ± 7.7 %; tidal volume: males: 540 ± 80 mL, females: 454 ± 66 mL; respiratory frequency: 17 ± 4 both in males and in females; minute volume: males: 9.3 ± 2.7 L/min., females: 7.6 ± 2.0 L/min. The results indicate that the vital capacity and the FEV1 are lower than classical values from white populations, FEV1% is higher. The tidal volume, respiratory frequency and minute volume are increased relative to sea level

A group specific anamnestic immune reaction against HIV-1 induced by a candidate vaccine against AIDS

The first experimental immunization of humans against the AIDS retrovirus, HIV-1, was started in a series of HIV seronegative, healthy volunteers in November 19861. For the primary vaccination recombinant vaccinia virus (V25)2 expressing the complete gp160 env protein3 of the HTLV-IIIB strain4,5 of HIV-1 was introduced by scarification. This elicited a weak primary response which we subseqently attempted to enhance by additional immunizations (boosting), using four different immunization protocols. We report here that intravenous injection of paraformaldehyde-fixed autologous cells infected in vitro with V25 (individual D.Z.) gave the best results. This individual received second and third boosts of intramuscular gp160 derived from an HTLV-IIIB clone using the hybrid vaccinia virus/bacteriophage T7 expression system6. An anamnestic humoral and cellular immune reaction was achieved for over one year after the original vaccination, with high levels of antibodies to the viral envelope, and neutralizing antibodies against divergent HIV-1 strains such as HTLV-III B4,5,7 and HTLV-IIIRF (also called HTLV-III HAT)3,5 after the first boost. In addition, group-specific cell-mediated immunity and cell-mediated cytotoxicity against infected T4 cells were obtained after the primary vaccine and enhanced by the boosts. Finally, skin tests showed both immediate and delayed hypersensitivity to gp160 in vivo. Although this protocol is not practical for a large scale vaccine trial, our results show for the first time that an immune state against HIV can be obtained in man. © 1988 Nature Publishing Group.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Laboratory-confirmed A (H1N1) pdm09 by response phase and collection site in Rwanda from October 2009– May 2010.

*<p>n = 6; Districts with an ISS site;</p>±<p>n = 24; Districts without an ISS site.</p

Clinical characteristics of positive and negative influenza cases during pandemic period in Rwanda from October 2009– May 2010.

<p>Clinical characteristics of positive and negative influenza cases during pandemic period in Rwanda from October 2009– May 2010.</p

Clinical and laboratory testing algorithm used during the mitigation phase.

<p>From November 16, 2009– May 31, 2010.</p

Location of Influenza Surveillance Sentinel sites and documented pH1N1 virus spread in Rwanda.

<p>From October 2009 - May 2010.</p

Demographic and epidemiological characteristics of influenza cases in Rwanda from July 2008– May 2010.

<p>Demographic and epidemiological characteristics of influenza cases in Rwanda from July 2008– May 2010.</p

Case classification and influenza percent positivity by week in Rwanda.

<p>From July 2008– May 2010.</p

A group specific anamnestic immune reaction against HIV-1 induced by a candidate vaccine against AIDS

The first experimental immunization of humans against the AIDS retrovirus, HIV-1, was started in a series of HIV seronegative, healthy volunteers in November 19861. For the primary vaccination recombinant vaccinia virus (V25)2 expressing the complete gp160 env protein3 of the HTLV-IIIB strain4,5 of HIV-1 was introduced by scarification. This elicited a weak primary response which we subseqently attempted to enhance by additional immunizations (boosting), using four different immunization protocols. We report here that intravenous injection of paraformaldehyde-fixed autologous cells infected in vitro with V25 (individual D.Z.) gave the best results. This individual received second and third boosts of intramuscular gp160 derived from an HTLV-IIIB clone using the hybrid vaccinia virus/bacteriophage T7 expression system6. An anamnestic humoral and cellular immune reaction was achieved for over one year after the original vaccination, with high levels of antibodies to the viral envelope, and neutralizing antibodies against divergent HIV-1 strains such as HTLV-III B4,5,7 and HTLV-IIIRF (also called HTLV-III HAT)3,5 after the first boost. In addition, group-specific cell-mediated immunity and cell-mediated cytotoxicity against infected T4 cells were obtained after the primary vaccine and enhanced by the boosts. Finally, skin tests showed both immediate and delayed hypersensitivity to gp160 in vivo. Although this protocol is not practical for a large scale vaccine trial, our results show for the first time that an immune state against HIV can be obtained in man. © 1988 Nature Publishing Group.SCOPUS: ar.jinfo:eu-repo/semantics/publishe