Browsing by Author "Mutoloki, Stephen"
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Item Antimicrobial susceptibility of flavobacteriaceae isolates from nile tilapia (oreochromis niloticus) in Tanzania(African Journal of Microbiology Research, 2020) Mwega, Elisa; Chengula, Augustino; Colquhoun, Duncan; Mutoloki, Stephen; Mdegela, Robinson; Evensen, Øystein; Wasteson, YngvildThis study aimed to assess antimicrobial susceptibility of members of the family Flavobacteriaceae isolated from Nile tilapia (Oreochromis niloticus). Antimicrobial susceptibility of 67 Flavobacteriaceae isolates originating mainly from ponds and Lake Victoria against 19 antimicrobial agents was determined by the broth micro dilution method. Overall, most isolates were susceptible to enrofloxacin (97%; MIC 90 2 μg/ml) followed by novobiocin (85%, MIC 90, 4 μg/ml) and the aminoglycoside streptomycin (85%; MIC 90 , 128 μg/ml). Some isolates were also susceptible towards trimethoprim/sulfamethoxazole (77.6%), neomycin and florfenicol both at 62.7%. Susceptibility levels were low for tylosin tartrate (32.8%), clindamycin and sulphathiazole both at (23.9%), ceftiofur (6%), spectinomycin (6%) and tetracyclines/oxtetracyclines (4.5%). In contrast, β-Lactams (amoxicillin, penicillin), gentamycin and erythromycin exhibited very poor activity against Flavobacteriaceae isolates. The extent of antimicrobial susceptibility did not vary significantly among isolates from farmed and wild fish isolates (P > 0.01). The highest Multiple Antimicrobial Resistance (MAR) index was observed in Chryseobacterium indologenes (0.89) and the lowest in Chaetoderma indicum isolates (0.32). Our results indicate that most of Flavobacteriaceae isolates are multidrug resistance, and this may be associated with intrinsic resistance mechanisms to a broad range of antimicrobial agents. However, the need remains to carryout in-depth study to understand better the underlying genetic mechanisms given that the magnitude and trend for susceptibility was comparable between isolates from aquaculture and fisheries. The findings from this study give us insight into appropriate choice of antimicrobial agents for effective treatment of infections caused by these isolates.Item Tilapia lake virus does not hemagglutinate avianand piscine erythrocytes and nh 4 cl does not inhibit viral replication in vitro(MDPI, 2019) Chengula, Augustino Alfred; Mutoloki, Stephen; Evensen, Øystein; Munang’andu, Hetron MweembaTilapia lake virus (TiLV) is a negative-sense single-stranded RNA (-ssRNA) icosahedral virus classified to be the only member in the family Amnoonviridae. Although TiLV segment-1 shares homology with the influenza C virus PB1 and has four conserved motifs similar to influenza A, B, and C polymerases, it is unknown whether there are other properties shared between TiLV and orthomyxovirus. In the present study, we wanted to determine whether TiLV agglutinated avian and piscine erythrocytes, and whether its replication was inhibited by lysosomotropic agents, such as ammonium chloride (NH 4 Cl), as seen for orthomyxoviruses. Our findings showed that influenza virus strain A/Puerto Rico/8 (PR8) was able to hemagglutinate turkey (Meleagris gallopavo), Atlantic salmon (Salmo salar L), and Nile tilapia (Oreochromis niloticus) red blood cells (RBCs), while infectious salmon anemia virus (ISAV) only agglutinated Atlantic salmon, but not turkey or tilapia, RBCs. In contrast to PR8 and ISAV, TiLV did not agglutinate turkey, Atlantic salmon, or tilapia RBCs. qRT-PCR analysis showed that 30 mM NH 4 Cl, a basic lysosomotropic agent, neither inhibited nor enhanced TiLV replication in E-11 cells. There was no difference in viral quantities in the infected cells with or without NH 4 Cl treatment during virus adsorption or at 1, 2, and 3 h post-infection. Given that hemagglutinin proteins that bind RBCs also serve as ligands that bind host cells during virus entry leading to endocytosis in orthomyxoviruses, the data presented here suggest that TiLV may use mechanisms that are different from orthomyxoviruses for entry and replication in host cells. Therefore, future studies should seek to elucidate the mechanisms used by TiLV for entry into host cells and to determine its mode of replication in infected cells.