Marwa Omar

Background/Objectives: The coccidian protozoan Toxoplasma gondii (T. gondii) is among the most prevalent zoonotic parasites worldwide. Nitric oxide (NO) production by macrophages is considered a critical microbicidal mechanism against various intracellular pathogens, including T. gondii. While the role of the inducible nitric oxide synthase isoenzyme (iNOS) has been widely investigated in both acute and chronic T. gondii infections, the specific functions of the neuronal (nNOS) isotype in the antiparasitic immune response, particularly during chronic toxoplasmosis, remain largely uncovered. Hence, this report seeks to bridge the gap regarding the potential participation of nNOS in experimental chronic T. gondii infection. Methods: The study included 56 Swiss albino mice, equally allocated into four experimental groups: (G1) negative control, (G2) infected control, (G3) infected-L-arginine-treated, and (G4) infected-7-Nitroindazole-treated. All groups except (G1) were orally infected with the avirulent (ME49) T. gondii strain. Nine weeks post-infection, all mice were euthanized for parasitological, histopathological, immunohistochemical, and biochemical analyses. Results: The NO donor, L-arginine, induced a significant reduction in the number of T. gondii cysts, together with strong nNOS immunoreactivity in the brain sections of the treated mice. Conversely, the highest parasitic burden was observed following selective nNOS inhibition with 7-Nitroindazole, exacerbating parasite-induced pathology. Conclusions: The neuronal isotype serves as a critical source of NO production during the chronic stage of T. gondii infection, thereby enhancing parasite elimination and contributing to host tissue protection.

The exact role of nitric oxide (NO) in the complex interplay between the host and Trichinella spiralis (T. spiralis) parasite remains uncovered. While much has been revealed about the role of the inducible isoenzyme (iNOS) in different parasitic infections, research is slowly progressing toward understanding the neuronal enzyme (nNOS)-derived impacts on trichinosis. This study aims to clarify the dual nature of (NO) during the enteral phase of experimental trichinosis by examining the participation of both iNOS and nNOS in T. spiralis-infected mice. The experimental design included 48 male Swiss albino mice divided into six groups: (G1) negative control, (G2) infected control, (G3) infected–Albendazole-treated, (G4) infected-infected–L-arginine-treated, (G5) infected–Aminoguanidine-treated, and (G6) infected–7-Nitroindazole-treated. On the seventh day post-infection, the study groups underwent parasitological (adult worm count), histopathological, immunohistochemical, and biochemical assessments. Our results showed that (nNOS) predominance during the enteral phase of trichinosis enhanced parasitic clearance. Conversely, NO produced by iNOS was not essential for worm expulsion but contributed to T. spiralis-mediated enteropathy. Nitric oxide seems to play a puzzling role in T. spiralis infection. While (iNOS) is known for eliminating numerous infections, this is the first example we are aware of where the activity of the neuronal isoform (nNOS) is required in trichinosis.

Background: Trichinella spiralis (T. spiralis) is an important zoonotic parasitic worm that is distributed all over the world. Unlike other parasites, it develops in a single host throughout the whole of its life cycle. Humans develop the infection through ingestion of raw or insufficiently cooked meat of pigs or other animal hosts containing Trichinella spiralis encysted larva. Trichinella spiralis is unique among helminthes by its intriguing abilities not only live and thrive inside the skeletal muscle tissues but have also evolved complex mechanisms for remodeling that niche. T. spiralis triggers a complicated and multidimensional immunological response that includes both innate and adaptive immune systems. During the intestinal phase of infection, the Th1 and Th2 immune responses are both involved in the immunological response to trichinosis. Th1 responses are initially produced, followed by a dominating Th2 response, which is characterized by the production of high amounts of cytokines IL-4, IL-5, IL-9, IL-10, and IL-13. Conclusion: Apart from its significant role in causing sickness and mortality, trichinosis is also thought to be a source of income loss for farmers and meat processors. Consequently, public health officials around the world are concerned about trichinosis. It is necessary to raise awareness of the intricate biology and morphology of trichinosis to create successful prevention and control programs. Hence, in this article, we aspire to provide detailed insights into the morphological, biological and immunological aspects of Trichinella spiralis infection.

Background: Trichinosisis a food borne zoonotic disease caused by parasitic nematode species belonging to the genus Trichinella. Trichinella spiralis (T. spiralis) is the most virulent pathogenic species affecting humans. Human hosts acquire the infection through ingestion of raw or insufficiently cooked meat of pigs or other animal hosts containing Trichinella spiralis encysted larvae. Following ingestion of the infected meat, larvae are released upon gastric digestion in the new host, and the first-stage larval parasites reach the intestinal tract and develop into adult worms. After mating, adult females shed larvae that migrate to other organs through vascular system. The developing larvae invade skeletal muscles forming nurse cell complexes. In addition to the importance of trichinosis as a cause of morbidity and mortality, it is also regarded as a cause of income loss for farmers and meat processors. Therefore, trichinosis is a concern for public health authorities worldwide. To establish effective prevention and control programmes, awareness of the complex morphology and biology of trichinosis must be increased. Hence, this article aims to provide updated insights into the morphological, pathological and diagnostic aspects of Trichinella spiralis infection.

Objective: This study aimed to assess the prevalence of Cryptosporidium genotypes in the canal water bodies of Minya Al-Qamh District in Sharqia Governorate, Northern Egypt. Rural populations in Egypt lack access to clean water. They obtain their water supplies from different drains and canals, which are frequently exposed to contamination by human activities and untreated agricultural waste, introducing Cryptosporidium infection to unprotected waterways. A total of (72) canal water samples served for the molecular detection of Cryptosporidium species by PCR amplification and sequencing. Results: Only one sample 1.4% (1/72) belonging to the village of Al-Aziziyyah was PCR-positive for Cryptosporidium contamination. Based on the (COWP) gene sequencing, this species was identified as Cryptosporidium parvum (C. parvum). The current work’s findings marked the first report on the molecular characterization of Cryptosporidium species in the canal water of Sharqia Province. Our results suggested that the source of C. parvum contamination could be of human and/or animal origin. Therefore, further studies are warranted to track the source of human infection and mitigate contamination for improved water quality.

In September 2024, the Egyptian Health Ministry declared an Escherichia coli (E. coli) outbreak in the southern province of Aswan. The spread of an ambiguous illness erupted in the village of Abu Al-Rish Bahri, 20 kilometers north of Aswan, with hundreds of citizens arriving at the governorate’s local hospitals suffering from severe gastrointestinal infections. The authorities, however, did not trace the outbreak’s most common source nor determine whether it was food- or water-borne. The official explanations for the frequent cases and the reported fatalities were inconclusive. There was an evident lack of comprehensive documentation on the extent of the infection, the exposed population, the prevalence pattern of the pathogen, or the retrieved E. coli isolates. In addition, the Egyptian government denied any possible association between the contamination of drinking water and the recent Aswan crisis. Challenging the official narrative, this article proposes a scientific report based on featuring the status of E. coli infection in Egypt, highlighting the gaps in the announced outbreak claims and adapting water pollution as an alarming hypothesis for the peculiar Aswan disease.

Dengue or dengue fever (DF) is an acute infectious disease of a febrile nature. It is caused by the dengue virus (DENV), which belongs to the family Flaviviridae and has four antigenically distinctive serotypes (DENV-1, DENV-2, DENV-3 and DENV-4). DENV is regarded as one of the most prevalent fast-emerging mosquito-borne viruses, which has a wide distribution in many tropical and subtropical regions worldwide. The virus is typically transmitted following the bite of an infected female mosquito of the species, Aedes (Ae.) aegypti and Ae. albopictus^[1]. According to the World Health Organization (WHO) statistical records, the global spread of dengue has witnessed substantial growth in recent decades, posing an alarming public health challenge. The number of cases expanded from 505430 cases in 2000 to 5.2 million in 2019, documenting a ten-fold surge in the detected worldwide cases^[1,2].

Cryptosporidium species are enteric apicomplexan parasites associated with diarrhoeal disease in humans and animals globally. Waterborne outbreaks resulting from contamination with the infective oocysts are common worldwide. Updated reports on waterborne protozoal infections are needed to identify emerging pathogens and susceptible populations. Therefore, this study aimed to assess the current profile of Cryptosporidium contamination of various water sources in Sharqia Governorate, Northeastern Egypt. For this purpose, eighty samples were collected from five different water types (canal, tap, tank, filtered, and groundwater), distributed in four major cities (El-Hessenia, Fakous, Zagazig, and Belbies) in Sharqia Governorate. All water samples were examined using conventional microscopy, ELISA, and real-time PCR (RT-PCR) techniques. Based on microscopic analysis, the Cryptosporidium protozoan was identified in 25% of the tested water samples. The RT-PCR assay has allowed for the quantification of Cryptosporidium oocysts in different types of water. Canal water exhibited the highest Cryptosporidium contamination levels (mean = 85.15 oocysts/L), followed by water tanks (mean = 12.031 oocysts/L). The study also provided a comparative evaluation of ELISA and RT-PCR for the diagnosis of Cryptosporidium infection. RT-PCR performed better than ELISA in terms of analytical accuracy (97.50% vs. 86.25%) and specificity (100% vs. 83.33%). However, ELISA showed a higher sensitivity (95.00% vs. 90.00%) for Cryptosporidium recovery. Our findings could serve as a platform for further investigations into the potential risks associated with water contamination in Sharqia Governorate.

Neutrophils are the key players in the innate immune system, being weaponized with numerous strategies to eliminate pathogens. The production of extracellular traps is one of the effector mechanisms operated by neutrophils in a process called NETosis. Neutrophil extracellular traps (NETs) are complex webs of extracellular DNA studded with histones and cytoplasmic granular proteins. Since their first description in 2004, NETs have been widely investigated in different infectious processes. Bacteria, viruses, and fungi have been shown to induce the generation of NETs. Knowledge is only beginning to emerge about the participation of DNA webs in the host’s battle against parasitic infections. Referring to helminthic infections, we ought to look beyond the scope of confining the roles of NETs solely to parasitic ensnarement or immobilization. Hence, this review provides detailed insights into the less-explored activities of NETs against invading helminths. In addition, most of the studies that have addressed the implications of NETs in protozoan infections have chiefly focused on their protective side, either through trapping or killing. Challenging this belief, we propose several limitations regarding protozoan-NETs interaction. One of many is the duality in the functional responses of NETs, in which both the positive and pathological aspects seem to be closely intertwined.