Neglected Tropical Diseases: The Global Burden of Overlooked Infections
Posted on 2025-02-06
Neglected Tropical Diseases (NTDs) are a diverse group of infectious diseases that disproportionately affect impoverished communities in tropical and subtropical regions (1). Despite their significant health and socioeconomic impact, NTDs receive limited attention from global health initiatives, often overshadowed by high-profile diseases such as malaria, tuberculosis, and HIV/AIDS. These diseases can be caused by a range of pathogens, such as bacteria, viruses, and fungi, resulting in chronic morbidity, disability and social stigma, exacerbating cycles of poverty (2). According to the World Health Organisation (WHO), over 1.7 billion people are at risk of NTDs, with the highest burden observed in low-resource settings (3).
NTDs are transmitted through various mechanisms, including vector-borne transmission (mosquitoes, sandflies, among others), direct human-to-human contact, and ingesting contaminated food and water (4). Once inside the human body, these pathogens invade specific tissues and organ systems, leading to chronic inflammation, immune evasion and progressive tissue damage. Many NTDs result in severe disabilities, blindness and disfigurement, significantly impacting quality of life and economic productivity (5). Even though many NTDs are treatable or preventable through mass drug administration, vector control, and improved hygiene practices, they remain unfunded, leaving millions vulnerable to their devastating effects (6).
Abbexa facilitates the progression of research initiatives by providing high-quality and reliable products for studying NTDs and their molecular mechanisms.
- Bacterial-Neglected Tropical Diseases
Leprosy (Mycobacterium leprae)
Leprosy, caused by Mycobacterium leprae, is a chronic infectious disease that primarily affects the skin, peripheral nerves, and mucous membranes. The bacterium targets Schwann cells, leading to demyelination and axonal degeneration, resulting in peripheral neuropathy, sensory loss, and characteristic skin lesions (7). The ability of M. leprae to evade host immunity is facilitated by phenolic glycolipid-1 (PGL-1), which promotes adhesion to laminin and entry into macrophages via complement receptors. Chronic infection leads to immune-mediated granuloma formation, progressively damaging peripheral nerves and resulting in irreversible deformities (8,9). The treatment for leprosy involves multidrug therapy (MDT) combining dapsone, rifampicin, and clofazimine, administered over 6 to 12 months, effectively curing the disease and preventing transmission (10).
M. leprae Products |
P69 Peptide |
P61 Peptide |
P62 Peptide |
P38 Peptide |
ELISA Kits | Proteins | Antibodies |
Human Chlamydia Trachomatis ELISA Kit (abx053004) | Chlamydia Trachomatis (C. trachomatis) Protein (abx670256) | Chlamydia Trachomatis Antibody (abx021588) |
Human Chlamydia Trachomatis IgM ELISA Kit (abx055439) | Chlamydia Trachomatis Serovar L2 Major Outer Membrane Porin (ompA) Protein (abx600041) | Chlamydia Trachomatis (MOMP) Antibody (abx022948) |
Human Chlamydia Trachomatis IgG ELISA Kit (abx055440) | Chlamydia Trachomatis Probable Outer Membrane Protein PmpD (abx600041) | Chlamydia Trachomatis Major Outer Membrane Protein (C. trachomis) (MOMP) Antibody (abx021596) |
- Fungal-Neglected Tropical Diseases
C. neoformans Products |
Cryptococcus Neoformans Antibody (abx021645) |
Cryptococcus Neoformans Plysaccharide Rapid Test Kit (abx092262) |
- Parasitic-Neglected Tropical Diseases
Chagas disease (Trypanosoma cruzi)
Chagas disease, caused by Trypanosoma cruzi, is transmitted by triatomine bugs. Upon entering the bloodstream, T. cruzi undergoes intracellular differentiation into amastigotes, which invade cardiac myocytes and smooth muscle cells (16). The parasite's trans-sialidase enzymes facilitate immune evasion by altering host cell surface glycoproteins, allowing persistence in tissues (17). Chronic infection leads to inflammatory cardiomyopathy, characterised by fibrosis, arrhythmias, and progressive heart failure. Gastrointestinal complications such as megaoesophagus and megacolon occur due to autonomic nerve damage caused by persistent parasitic invasion (18). Antiparasitic treatment with benznidazole or nifurtimox is most effective during the acute phase of Chagas disease, aiming to eliminate the parasite and prevent chronic complications (10).
ELISA Kits | Proteins | Antibodies |
Human Trypanosoma cruzi ELISA Kit (abx055910) | Trypanosoma cruzi 1F8 (Chagas 1F8) Protein (abx061397) | Trypanosoma cruzi Lipophosphoglycan (T. cruzi LPG) Antibody (abx415773) |
Our full range of T. cruzi products can be found here.
Onchocerciasis (Onchocerca volvulus)
Onchocerciasis, or river blindness, is caused by Onchocerca volvulus and transmitted by blackflies (Simulium spp.). The infective larvae migrate into the dermis and subcutaneous tissues, where they mature into adult worms that release microfilariae. The host immune response to dying microfilariae triggers intense pruritus, skin atrophy, and progressive ocular damage. Chronic inflammation leads to sclerosing keratitis, optic nerve atrophy, and irreversible blindness (19). Ivermectin is administered annually or biannually to kill microfilariae and reduce skin and eye pathology; however, it does not kill adult worms, necessitating repeated treatments over several years (10).
ELISA Kits | Proteins | Antibodies |
Human Anti-Onchocerca volvulus IgG ELISA Kit (abx055818) | Onchocerca volvulus OV-16 Antigen (OV16) Protein (abx600077) | Onchocerca volvulus OV-16 Antigen Antibody (abx109429) |
Our full range of Onchocerciasis products can be found here.
- Viral-Neglected Tropical Diseases
Dengue Virus (DENV)
Dengue, caused by four serotypes of Dengue virus (DENV-1 to DENV-4), is transmitted by Aedes aegypti and Aedes albopictus mosquitoes (20). The virus enters monocytes and dendritic cells via Fc receptor-mediated endocytosis, triggering a cytokine storm and capillary leakage (21). Dengue haemorrhagic fever is driven by antibody-dependent enhancement, where non-neutralizing antibodies from a prior infection facilitate increased viral replication, leading to vascular permeability, thrombocytopenia, and multi-organ failure (22). Currently, there is no specific antiviral treatment for dengue infection. Management focuses on supportive care, including maintaining adequate hydration, monitoring for signs of haemorrhage, and using acetaminophen for fever and pain relief. Nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin are generally avoided due to the risk of bleeding complications (20).
ELISA Kits | Proteins | Antibodies |
Human Dengue Virus NS1 (DV NS1) ELISA Kit (abx055461) | Polyvalent Dengue Antigen-I for ELISA Protein (abx260216) | Dengue Type 2 Antibody (abx137060) |
Human Dengue Virus IgG (DV-IgG) ELISA Kit (abx055294) | Dengue Type 1 Protein (abx069810) | Dengue 1 NS1 Antibody (abx137189) |
Human Dengue Virus IgM (DV-IgM) ELISA Kit (abx055293) | Dengue Type 2 Protein (abx069811) | Dengue 2 NS1 Antibody (abx137190) |
Our full range of dengue products can be found here.
Zika Virus (ZINV)
Zika virus, also transmitted by Aedes mosquitoes, has neurotropic properties and is capable of crossing the placental and blood-brain barriers. The ZIKV NS1 protein plays a role in immune evasion by disrupting complement activation. The virus preferentially infects neural progenitor cells, leading to microcephaly, neuronal apoptosis, and developmental delays in foetuses (23). In adults, ZIKV infection has been linked to Guillain-Barré syndrome, a post-viral autoimmune neuropathy (24). There is no specific antiviral therapy for Zika virus infection. Treatment is primarily supportive, addressing symptoms such as fever, rash, and arthralgia with rest, fluids, and analgesics like acetaminophen. Aspirin and NSAIDs are typically avoided until dengue co-infection is ruled out, due to its potential risk of haemorrhage (25).
ELISA Kits | Proteins | Antibodies |
Human Zika Virus IgG (ZIKV-IgG) ELISA Kit (abx050301) | Zika Virus Genome Polyprotein (abx620732) | Zika Virus Envelope Domain III (ZIKV ED3) Antibody (abx201403) |
Human Zika Virus IgM (ZIKV IgM) ELISA Kit (abx055830) | Zika Virus Genome Polyprotein (abx620731) | Zika Virus Non-Structural Protein 1 (ZIKV NS1) ANtibody (abx201406) |
Our full range of Zika products can be found here.
Ebola Virus (EBOV)
Ebola virus (EBOV) is a highly lethal filovirus responsible for severe haemorrhagic fever outbreaks. EBOV enters host cells via macropinocytosis and replicates in monocytes, dendritic cells, and endothelial cells, inducing vascular leakage, coagulopathy, and multi-organ failure (26). The VP35 and VP40 proteins play essential roles in immune suppression and viral assembly, while the glycoprotein (GP) mediates endothelial dysfunction, contributing to shock and mortality (27). Management of Ebola primarily involves supportive care, including fluid resuscitation, electrolyte management, and treatment of secondary infections. Recent clinical trials have evaluated investigational therapies, such as monoclonal antibodies and antiviral agents. For instance, a randomized controlled trial conducted in the Democratic Republic of Congo assessed the efficacy of four investigational therapies for Ebola (28).
Proteins | Antibodies |
Ebola Zaire Protein (abx260222) | Ebola Virus Nucleoprotein Antibody (abx023958) |
Ebola Sudan Protein (abx260223) | Ebola Virus Protein 40 (VP40) Antibody (abx023960) |