L Ugboko, V, Olasoji O, Ogunbodede E.
1998.
Cervicofacial actinomycosis after partial mandibular resection: Case report, 1998/03/01. East African medical journal. 75:122-3.
AbstractAn unusual case of cervicofacial actinomycosis in a 60-year old male Nigerian is reported. The patient had had partial mandibular resection for plexiform ameloblastoma one year earlier with insertion of Kirschner wire to serve as a splint. The authors highlight the possible pathophysiology of this condition. It is suggested that clinicians be aware of the various modes of presentation and natural history of the disease to facilitate prompt diagnosis and appropriate treatment. This will assist in forestalling the numerous complications that may result from actinomycosis.
L.J.J, G, W.L A, M E, P.A M, T B, B A, P D, F.K.N A, S.A B, A M, M L, E.A A-A, W D, P T, O J, M D, P A, A.A O, R B, G P-R, M G, S O-Y, G.O O, P.B O, L A-R, F A, T H, P G, M.O O, C.J B, M.L M, A.A A, J.C M, A B.
2016.
Association studies and direct DNA sequencing implicate genetic susceptibility loci in the etiology of nonsyndromic orofacial clefts in sub-Saharan African populations. J Dental Research. 95(11):1245-1256.
L.J.J, G, T.D B, P.A M, M.A E, W.L A, B A, P D, F.K.N A, P A, O J, P T, R B, A.A O, G P-R, S O-Y, F A, P.E H-W, T H, J.C M, A B.
2017.
The prevalence, penetrance and expressivity of etiologic IRF6 variants in orofacial clefts patients from sub-Saharan Africa. Molecular Genetics Genomic Med.. 5(2):164-171.
L.J.J., G, G. O, P.A. M, W.L. A, M.A. E, T.D. B, P. D, S. O-Y, G. P-R, A.A. O, A. O, P.B. O, B.S. A, F.O. O, Bello S.A., R. A, C. O, P. A, M.O. O, L.O. A-R, M.L. M, A.A. A, J.C. M, A. B.
2018.
Novel GREM1 variations in Sub-Saharan African patients with cleft lip and/or cleft palate. The Cleft Palate-Craniofacial Journal. 55(5):736-742.
Lamikanra, A, Crowe JL, Lijek RS, Odetoyin BW, Wain J, Aboderin OA, Okeke IN.
2011.
Rapid Evolution of Fluoroquinolone-Resistant {{Escherichia}} Coli in {{Nigeria}} Is Temporally Associated with Fluoroquinolone Use, dec. BMC Infectious Diseases. 11, Number 1: {BioMed Central}
AbstractBackground: Antibiotic resistance has necessitated fluoroquinolone use but little is known about the selective forces and resistance trajectory in malaria-endemic settings, where selection from the antimalarial chloroquine for fluoroquinolone-resistant bacteria has been proposed. Methods: Antimicrobial resistance was studied in fecal Escherichia coli isolates in a Nigerian community. Quinolone-resistance determining regions of gyrA and parC were sequenced in nalidixic acid resistant strains and horizontally-transmitted quinolone-resistance genes were sought by PCR. Antimicrobial prescription practices were compared with antimicrobial resistance rates over a period spanning three decades. Results: Before 2005, quinolone resistance was limited to low-level nalixidic acid resistance in fewer than 4% of E. coli isolates. In 2005, the proportion of isolates demonstrating low-level quinolone resistance due to elevated efflux increased and high-level quinolone resistance and resistance to the fluoroquinolones appeared. Fluoroquinolone resistance was attributable to single nucleotide polymorphisms in quinolone target genes gyrA and/or parC. By 2009, 35 (34.5%) of isolates were quinolone non-susceptible with nine carrying gyrA and parC SNPs and six bearing identical qnrS1 alleles. The antimalarial chloroquine was heavily used throughout the entire period but E. coli with quinolone-specific resistance mechanisms were only detected in the final half decade, immediately following the introduction of the fluoroquinolone antibacterial ciprofloxacin. Conclusions: Fluoroquinolones, and not chloroquine, appear to be the selective force for fluoroquinolone-resistant fecal E. coli in this setting. Rapid evolution to resistance following fluoroquinolone introduction points the need to implement resistant containment strategies when new antibacterials are introduced into resource-poor settings with high infectious disease burdens.