Background: Despite reports of malaria and coronavirus diseases 2019 (COVID-19) co-infection, malaria-endemic regions have so far recorded fewer cases of COVID-19 and deaths from COVID-19, indicating a probable protection from the poor outcome of COVID-19 by malaria. On the contrary, other evidence suggests that malaria might contribute to the death caused by COVID-19. Hence, this paper reviewed existing evidence hypothesizing poor outcome or protection of COVID-19 patients when co-infected with malaria. Methods: PRISMA guidelines for systematic review were employed in this study. Published articles from December 2019 to May 2021on COVID-19 and malaria co-infection and outcome were systematically searched in relevant and accessible databases following a pre-defined strategy. Studies involving human, in vivo animal studies, and in vitro studies were included. Results: Twenty three (23) studies were included in the review out of the 3866 records identified in the selected scientific databases. Nine (9) papers reported on co-infection of COVID-19 and malaria. Five (5) papers provided information about synergism of malaria and COVID-19 poor prognosis, 2 papers reported on syndemic of COVID-19 and malaria intervention, and 7 studies indicated that malaria protects individuals from COVID-19. Conclusions: Low incidence of COVID-19 in malaria-endemic regions supports the hypothesis that COVID-19 poor prognosis is prevented by malaria. Although further studies are required to ascertain this hypothesis, cross-immunity and common immunodominant isotopes provide strong evidence to support this hypothesis. Also, increase in co-inhibitory receptors and atypical memory B cells indicate synergy between COVID-19 and malaria outcome, though, more studies are required to make a definite conclusion.

Apicomplexan parasites have challenged researchers for nearly a century. A major challenge to developing efficient treatments and vaccines is the parasite’s ability to change its cellular and molecular makeup to develop intracellular and extracellular niches in its hosts. Ca²⁺ signaling is an important messenger for the egress of the malaria parasite from the infected erythrocyte, gametogenesis, ookinete motility in the mosquito, and sporozoite invasion of mammalian hepatocytes. Calcium-dependent protein kinases (CDPKs) have crucial functions in calcium signaling at various stages of the parasite’s life cycle; this therefore makes them attractive drug targets against malaria. Here, we summarize the functions of the various CDPK isoforms in relation to the malaria life cycle by emphasizing the molecular mechanism of developmental progression within host tissues. We also discuss the current development of anti-malarial drugs, such as how specific bumped kinase inhibitors (BKIs) for parasite CDPKs have been shown to reduce infection in Toxoplasma gondii, Cryptosporidium parvum, and Plasmodium falciparum. Our suggested combinations of BKIs, artemisinin derivatives with peroxide bridge, and inhibitors on the Ca(2+)-ATPase PfATP6 as a potential target should be inspected further as a treatment against malaria.

Pathogenic bacteria, viruses, fungi, parasites, and other microbes constantly change to ensure survival. Several pathogens have adopted strict and intricate strategies to fight medical treatments. Many drugs, frequently prescribed to treat these pathogens, are becoming obsolete and ineffective. Because pathogens have gained the capacity to tolerate or resist medications targeted at them, hence the term antimicrobial resistance (AMR), in that regard, many natural compounds have been routinely used as new antimicrobial agents to treat infections. Thus, plant lectins, the carbohydrate-binding proteins, have been targeted as promising drug candidates. This article reviewed more than 150 published papers on plant lectins with promising antibacterial and antifungal properties. We have also demonstrated how some plant lectins could express a synergistic action as adjuvants to boost the efficacy of obsolete or abandoned antimicrobial drugs. Emphasis has also been given to their plausible mechanism of action. The study further reports on the immunomodulatory effect of plant lectins and how they boost the immune system to curb or prevent infection.

Background: Autophagy has a crucial role in the defense against parasites. The interplay existing between host autophagy and parasites has varied outcomes due to the kind of host cell and microorganism. The presence of autophagic compartments disrupt a significant number of pathogens and are further cleared by xenophagy in an autolysosome. Another section of pathogens have the capacity to outwit the autophagic pathway to their own advantage. Result: To comprehend the interaction between pathogens and the host cells, it is significant to distinguish between starvation-induced autophagy and other autophagic pathways. Subversion of host autophagy by parasites is likely due to differences in cellular pathways from those of ‘classical’ autophagy and that they are controlled by parasites in a peculiar way. In xenophagy clearance at the intracellular level, the pathogens are first ubiquitinated before autophagy receptors acknowledgement, followed by labeling with light chain 3 (LC3) protein. The LC3 in LC3-associated phagocytosis (LAP) is added directly into vacuole membrane and functions regardless of the ULK, an initiation complex. The activation of the ULK complex composed of ATG13, FIP200 and ATG101causes the initiation of host autophagic response. Again, the recognition of PAMPs by conserved PRRs marks the first line of defense against pathogens, involving Toll-like receptors (TLRs). These all important immune-related receptors have been reported recently to regulate autophagy. Conclusion: In this review, we sum up recent advances in autophagy to acknowledge and understand the interplay between host and parasites, focusing on target proteins for the design of therapeutic drugs. The target host proteins on the initiation of the ULK complex and PRRs-mediated recognition of PAMPs may provide strong potential for the design of therapeutic drugs against parasitic infections.

The evidence of rising numbers of multidrug-resistant organisms requires the implementation of effective stewardship programs. However, this should be informed by evidence-based knowledge of local antimicrobial resistance patterns. The current study aims to establish the prevalence of common pathogenic microbes including their antimicrobial susceptibility patterns and distribution in the Cape Coast Metropolis. This was a retrospective study where microbial culture and antimicrobial susceptibility records for 331 patients were reviewed from January to December 2019, at a private health centre. All data were analysed using Excel (Microsoft Office, USA), SPSS and GraphPad Prism 8 software programs. Among the samples tested, 125 (37.76%) were positive for microbes with high vaginal swab (HVS) samples recording the highest number of pathogens (44%), followed by urine (40%) and both pleural and semen samples having the least (0.3% each). Again, gram-negative isolates were more prevalent than the gram-positive isolates. The prevalence of antimicrobial resistance was very significant with isolates resistant to more than one antibiotic (P < 0.05). Escherichia coli showed the highest level of resistance, followed by Citrobacter spp. These were followed by Klebsiella spp., Staphylococcus spp., Coliforms, Pseudomonas spp., Commensals and Candida spp. The high resistance pattern suggests an inevitable catastrophe requiring continuous monitoring and implementation of effective antibiotic stewardship.

Background: Cerebral malaria (CM) is a preeminent cause of severe disease and premature deaths in Sub-Saharan Africa, where an estimated 90% of cases occur. The key features of CM are a deep, unarousable coma that persists for longer than 1 h in patients with peripheralPlasmodium falciparumand no other explanation for encephalopathy. Significant research efforts on CM in the last few decades have focused on unravelling the molecular underpinnings of the disease pathogenesis and the identification of potential targets for therapeutic or pharmacologic intervention. These efforts have been greatly aided by the generation and study of mouse models of CM, which have provided great insights into key events of CM pathogenesis, revealed an interesting interplay of host versus parasite factors that determine the progression of malaria to severe disease and exposed possible targets for therapeutic intervention in severe disease.Main Body: This paper reviews our current understanding of the pathogenic and immunologic factors involved in CM. We present the current view of the roles of certain gene products e.g., the var gene, ABCA-1, ICAM-1, TNF-alpha, CD-36, PfEMP-1 and G6PD, in CM pathogenesis. We also present alterations in the blood–brain barrier as a consequence of disease proliferation as well as complicated host and parasite interactions, including the T-cell immune reaction, reduced deformation of erythrocytes and cytoadherence. We further looked at recent advances in cerebral malaria treatment interventions by emphasizing on biomarkers, new diagnostic tools and emerging therapeutic options.Conclusion: Finally, we discuss how the current understanding of some of these pathogenic and immunologic factors could inform the development of novel therapeutic interventions to fight CM.