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Ndo, C.

Publications and source records attributed to Ndo, C..

4 recordsLinked to original sources

Larvicidal Potential of Cola nitida Endophytic Bacteria Against Insecticide-Resistant Anopheles gambiae

BackgroundInnovative vector control strategies are urgently needed to combat malaria transmission by Anopheles gambiae, given the limitations of current insecticides--namely resistance, human toxicity, environmental damage, and high costs. This study evaluated the larvicidal efficacy of endophytic bacteria isolated from Cola nitida against third-instar larvae of Anopheles gambiae. MethodsEndophytic bacteria were isolated from nine Cola nitida plant parts (leaves, roots, stems, fruits, flowers, stem bark, branches, root bark, whole plant extracts) using standard surface sterilization and culturing protocols. Thirty-two morphologically distinct strains were purified and screened for larvicidal activity against third-instar An. gambiae larvae using the WHO-recommended turbidity method at McFarland 4 standard. Six active isolates underwent dose-response testing (McFarland 0.5-4) with mortality recorded at 24 and 48 hours. Environmental safety was assessed via Lemna minor growth inhibition, and molecular identification employed the API 20E biochemical gallery. ResultsScreening identified six strains with significant larvicidal activity (LC < McFarland 2). At McFarland 2 concentration, all six strains achieved >50% mortality within 24-48 hours, with Lemna minor EC >100% indicating minimal phytotoxicity. API 20E identification (96-99.99% similarity) revealed three strains (6164, 6211, 6501) matching Photobacterium damselae, two (6186-1, 6512-1) matching Salmonella enterica subsp. arizonae, and one (6600) matching Pseudomonas sp., confirmed by distinctive biochemical profiles. ConclusionThis study provides the first evidence of potent, environmentally safe larvicidal activity from Cola nitida endophytic bacteria against Anopheles gambiae. These strains represent promising biocontrol candidates to address insecticide resistance, offering a sustainable alternative for malaria vector management in endemic regions.

microbiology↗

Transcriptomic profile of Anopheles gambiae Kisumu mosquitoes infected by neglected malaria parasite Plasmodium ovale from gametocyte-carriers in Cameroon

Successful transmission of malaria depends on the complex interactions between the Anopheles mosquito vector and the Plasmodium parasites. Plasmodium ovale, a neglected malaria parasite, successfully develops from ookinete to sporozoite within the Anopheles vector. To elucidate the molecular mechanisms underlying this interaction, we compared RNA-seq-based gene expression profiles of Anopheles gambiae infected with P. ovale and uninfected mosquitoes at 24 hours, 9 days, and 17 days post-infection. The results showed that 2,885 P. ovale transcripts were present only 24 hours after infection. During ookinete invasion (24 h post-infection), differential gene expression analyses revealed the up-regulation of genes related to metabolic processes and the down-regulation of genes associated with cytoskeletal activity in the mosquito. Notably, the non-immune genes with unspecific function AGAP003776, (Fold Change, FC 132.0), AGAP003777, (FC 88.3), and AGAP003778, (FC 104.1), Troponin C (Fold Change, FC 85) and Myofilin (FC 33.3) exhibited the most significant overexpression. Among the immune genes that were upregulated CTL3 (FC 55.9), CLIPB12 (FC 49.4), CTLMA5 (FC 14.5), TRYP7 (FC 24.4), CLIP C9 (FC 12.1) TRYP5 (FC 12.2), LRIM10 (FC 11.2), PPO6 (FC 7.7). This initial analysis of the interaction between P. ovale and An. gambiae identified several well-known candidates for transmission-blocking strategies, including LRIM1, APN1, and D7 family proteins. In addition, new potential candidates, including AGAP003776, AGAP003777, and AGAP003778 cluster, CLIPB12, LRIM10, the APN cluster, AGAP004860, ABCC9, CYP9K1 and GSTD3 were identified. These potential new candidate genes could play a significant role in the development of transmission-blocking strategies for An. gambiae infected with Plasmodium, particularly P. ovale. The urgent functional validation of these genes is required.

microbiology↗

Xeno-monitoring of molecular drivers of artemisinin and partner drug resistance in P. falciparum populations in malaria vectors across Cameroon

BackgroundMonitoring of drug resistance in Plasmodium populations is crucial for malaria control. This has primarily been performed in humans and rarely in mosquitoes where parasites genetic recombination occurs. Here, we characterized the Plasmodium spp populations in wild Anopheles vectors by analyzing the genetic diversity of the P. falciparum kelch13 and mdr1 gene fragments implicated in artemisinin and partner drug resistance across Cameroon in three major malaria vectors. MethodsAnopheles mosquitoes were collected across nine localities in Cameroon and dissected into the head/thorax (H/T) and abdomen (Abd) after species identification. A TaqMan assay was performed to detect Plasmodium infection. Fragments of the Kelch 13 and mdr1 genes were amplified in P. falciparum positive samples and directly sequenced to assess their drug resistance polymorphisms and genetic diversity profile. ResultsThe study revealed a high Plasmodium infection rate in the major Anopheles vectors across Cameroon. Notably, An. funestus vector recorded the highest sporozoite (8.02%) and oocyst (14.41%) infection rates. A high P. falciparum sporozoite rate (80.08%) alongside epidemiological signatures of significant P. malariae (15.94%) circulation were recorded in these vectors. Low genetic diversity with six (A578S, R575I, G450R, L663L, G453D, N458D) and eight (H53H, V62L, V77E, N86Y, G102G, L132I, H143H, Y184F) point mutations were observed in the k13 and mdr1 backbones respectively. Remarkably, the R575I (4.44%) k13 and Y184F (64.2%) mdr1 mutations were the predominant variants in the P. falciparum populations. ConclusionThe emerging signal of the R575I polymorphism in the Pfk13 propeller backbone entails the regular surveillance of molecular markers to inform evidence-based policy decisions. Moreover, the high frequency of the 86N184F allele highlights concerns on the plausible decline in efficacy of artemisinin-combination therapies (ACTs); further implying that parasite genotyping from mosquitoes can provide a more relevant scale for quantifying resistance epidemiology in the field.

genomics↗

Influence of GST- and P450-based metabolic resistance to pyrethroids on blood feeding in the major African malaria vector Anopheles funestus

Insecticide resistance genes are often associated with pleiotropic effects on various mosquito life-history traits. However, very little information is available on the impact of insecticide resistance, especially metabolic resistance, on blood feeding process in mosquitoes. Here, using two recently detected DNA-based metabolic markers in the major malaria vector, An. funestus, we investigated how metabolic resistance genes could affect blood meal intake. After allowing both field F1 and lab F8 Anopheles funestus strains to feed on human arm for 30 minutes, we assessed the association between key parameters of blood meal process including, probing time, feeding duration, blood feeding success and blood meal size, and markers of glutathione S-transferase (L119F-GSTe2) and cytochrome P450 (CYP6P9a_R) - mediated metabolic resistance. None of the parameters of blood meal process was associated with L119F-GSTe2 genotypes. In contrast, for CYP6P9a_R, homozygote resistant mosquitoes were significantly more able to blood-feed than homozygote susceptible (OR = 3.3; CI 95%: 1.4-7.7; P =0.01) mosquitoes. Moreover, the volume of blood meal ingested by CYP6P9a-SS mosquitoes was lower than that of CYP6P9a-RS (P<0.004) and of CYP6P9a-RR (P<0.006). This suggests that CYP6P9a gene affects the feeding success and blood meal size of An. funestus. However, no correlation was found in the expression of CYP6P9a and that of genes encoding for salivary proteins involved in blood meal process. This study suggests that P450-based metabolic resistance may increase the blood feeding ability of malaria vectors and potential impacting their vectorial capacity.

molecular biology↗