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Animal Trypanosomiasis in Kazakhstan: Epidemiological Burden and One Health Considerations

Submitted:

22 September 2025

Posted:

23 September 2025

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Abstract
Animal trypanosomiasis, primarily caused by Trypanosoma evansi (surra) and related species, represents a neglected but economically significant disease of livestock in Central Asia. In Ka-zakhstan, infections in camels, horses, and cattle contribute to productivity losses and undermine rural livelihoods. Although Human African Trypanosomiasis (HAT) has not been reported in the country, climate change and increased livestock mobility raise concerns about future risks of exotic introductions. This review synthesises current knowledge on the epidemiology, diagnosis, and control of animal trypanosomiasis in Kazakhstan within a regional and global context. Particular attention is given to diagnostic approaches: while conventional parasitological and serological methods remain in use, molecular tools are underdeveloped and inconsistently applied in vet-erinary settings. We highlight gaps in surveillance, the lack of species-specific diagnostic proto-cols, and the need to distinguish clearly between techniques for human versus animal trypano-somes. Framed within a One Health perspective, we argue that addressing animal trypanosomiasis is critical not only for protecting livestock productivity but also for strengthening regional pre-paredness against potential zoonotic threats.
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1. Introduction

Vector-borne diseases are among the most serious threats to global health. According to the World Health Organization (WHO), these infections—caused by parasites, viruses, and bacteria transmitted by arthropod vectors—account for nearly 17% of the global burden of infectious diseases and claim more than 700,000 lives every year [1]. Their capacity for rapid international spread, high transmissibility, and pandemic potential underscores the urgency of addressing them. The burden is especially heavy in tropical and subtropical regions, where favorable environmental conditions for vectors coincide with vulnerable populations [1].
The distribution of vector-borne diseases is determined by a complex interplay of demographic, environmental, and social factors. Morbidity and mortality rates are often disproportionately high in affected populations, while the economic toll is equally devastating. Beyond human health, vector-borne diseases cause direct losses in livestock production and compromise the viability of wild animal populations, collectively limiting the development of both rural and urban areas [1].
Within the WHO’s priority list of vector-borne diseases, trypanosomiases occupy a unique position. Human African trypanosomiasis (HAT, or sleeping sickness) and Chagas disease (American trypanosomiasis) are regionally restricted but highly impactful, exerting profound effects on human health and socioeconomic stability in endemic communities [1].
The challenge is further intensified by climate change. Climate scientists warn that gradual global warming is altering rainfall patterns, enabling monsoon activity in once-arid zones, and expanding vegetation cover [2,3]. These ecological changes shape the “microcosm” of pathogens—viruses, bacteria, fungi [4]—and their carriers such as midges and insects [5]. Consequently, tropical and exotic vector-borne diseases can appear suddenly in regions where they were previously unknown, reshaping epidemiological landscapes and testing the resilience of public health and veterinary systems.
In recent years, diseases such as African swine fever, lumpy skin disease, and trypanosomiasis have been recorded in the Republic of Kazakhstan. Environmental changes, including repeated river flooding in formerly arid regions, create favourable ecological conditions for the proliferation of vectors and the establishment of tropical and exotic infectious and parasitic diseases.
This review aims to provide a critical analysis of trypanosomatid infections of various etiologies, with particular attention to their high transmissibility, zoonotic potential, and broad host range. Special emphasis is placed on assessing the impact of climate change on vector distribution, and on comparing classical versus modern diagnostic methods for protozoa of the genus Trypanosoma, with distinctions drawn according to the type of pathogen.

Trypanosoma

Trypanosomiasis is a tropical, vector-borne disease caused by protozoan parasites of the genus Trypanosoma (class Kinetoplastea, family Trypanosomatidae), which infect both humans and animals [6]. The genus belongs to a monophyletic group of flagellated protozoa, characterised by a distinctive kinetoplast DNA structure and a corkscrew-like motility, reflected in the Greek etymology trypaô (“to bore”) and soma (“body”) [6].
To date, approximately 125 species of Trypanosoma have been described in mammals, of which about 10% are pathogenic to humans and/or domestic animals [7]. These parasites are widely distributed in Africa, the Americas, Latin America, and Asia, where they contribute to severe human disease, major epizootics in livestock, and substantial economic losses in animal production [8,9,10,11,12,13].
Figure 1 shows the map that highlights the distinct yet overlapping geographic distribution of Trypanosoma infections. Human African Trypanosomiasis (HAT) remains confined to sub-Saharan Africa, Chagas disease is mainly endemic in Latin America, while animal trypanosomiases (e.g., surra, nagana, dourine) extend into Africa, Asia, and beyond. This visualisation underlines the global nature of trypanosomiasis, contrary to the perception of it as a strictly regional problem. Figure 1 also demonstrates the dual burden of trypanosomiasis. Human cases are geographically restricted, but animal infections are more widely distributed, causing significant economic losses in livestock production. The largest endemic zones coincide with regions of high dependence on livestock. This amplifies the financial burden of animal trypanosomiasis while raising concern about the zoonotic potential of species such as T. evansi and T. vivax. It also provides a platform for discussing climate-driven expansion of vector habitats, which could blur current geographic boundaries. Trypanosomiasis should be prioritised as a neglected tropical disease (NTD). It provides evidence that coordinated international action is required, not only to control human trypanosomiasis in its remaining foci, but also to strengthen surveillance of animal trypanosomes, which remain underdiagnosed and underreported despite their wide distribution.
In humans, two primary forms of disease are recognised: Human African trypanosomiasis (HAT, or sleeping sickness) and American trypanosomiasis (Chagas disease) [14]. HAT is caused by Trypanosoma brucei gambiense (T. b. g.) and T. b. rhodesiense (T. b. r.), while Chagas disease is caused by T. cruzi [14]. Despite differences in geographic distribution and clinical presentation, these pathogens share morphological similarities that complicate diagnosis and species-specific identification [15,16,17,18,19].
Trypanosoma brucei is the causative agent of Human African Trypanosomiasis (HAT, or sleeping sickness), a neglected parasitic disease that affects both humans and animals [21,22,23,24,25]. Two subspecies are pathogenic to humans: T. b. gambiense (T.b.g.) and T. b. rhodesiense (T.b.r.), first described by David Bruce. These are commonly referred to as West African (Gambian) HAT and East African (Rhodesian) HAT, respectively. Among reported human cases, T. b. gambiense accounts for more than 98%, reflecting its dominance in endemic regions [20].
Transmission occurs primarily through the bite of an infected tsetse fly (Glossina spp.), which is widespread in rural sub-Saharan Africa. Three major groups of tsetse flies are responsible for parasite transmission: the morsitans group (Glossina morsitans), which inhabits open savannah and woodland; the palpalis group (G. palpalis), which thrives along rivers and lakes; and the fusca group (G. fusca), which is associated with forested ecosystems [20].
Although vector-borne transmission remains the primary route, other forms have been documented. These include vertical transmission from mother to child, mechanical transmission by other blood-sucking insects, transmission through contaminated needles, and even sexual transmission. Sporadic cases of congenital and transfusion-associated infections further highlight the adaptability of the parasite and the challenges of controlling its spread [21,22,23,24,25].
American trypanosomiasis (Chagas disease), caused by Trypanosoma cruzi, was first described in South America by the Brazilian physician Carlos Chagas, who identified both the parasite and its insect vector in the early 20th century [26,27,28]. The parasite was named T. cruzi in honor of Oswaldo Cruz. Locally, the triatomine vector is commonly referred to as the “kissing bug” (chupão) or “barber bug” (barbeiro), reflecting its nocturnal habit of feeding on human blood while people sleep [26,27,28].
Although the disease was initially thought to be restricted to the Americas, evidence from archaeological remains of 4,000–9,000-year-old mummies suggests that T. cruzi has been infecting humans for millennia [26,27,28]. Furthermore, studies by Coura, Viñas, and Junqueira emphasize that the sylvatic cycle of Chagas disease has existed for millions of years, maintained in diverse wild reservoirs long before human settlements emerged [26,27,28]. With increasing encroachment of human activity into wildlife habitats and the expansion of travel to remote areas, the risk of human contact with infected vectors and the potential for parasite adaptation or zoonotic spillover is heightened.
Over the past decades, the epidemiological profile of Chagas disease has shifted from a rural to an urban setting. Factors such as population displacement, urbanization, and migration have facilitated its spread beyond endemic regions. Cases have now been documented not only in the Americas—including Canada and the United States—but also in Europe, Africa, the Eastern Mediterranean, and the Western Pacific due to human mobility [29]. According to WHO, an estimated 75 million people remain at risk of infection, with many cases undiagnosed or untreated, particularly in areas where vector transmission persists [29].
Cases of Chagas disease are no longer confined to Latin America. Reports now document infections in Europe, Africa, the Eastern Mediterranean, and the Western Pacific, reflecting the global spread of the parasite through migration and travel [29]. The World Health Organization (WHO) estimates that nearly 75 million people remain at risk of infection, mainly due to the high proportion of undiagnosed or untreated cases, as well as the persistence of active vector transmission in endemic regions [29].
Transmission is primarily associated with blood-sucking insects of the subfamily Triatominae (family Reduviidae), whose natural habitat includes Mexico, Central, and South America [20,25]. In the work of Schmunis, human infection with T. cruzi was reported across 21 countries in North, Central, and South America, highlighting its wide geographic distribution [30]. Most infections in the Western Hemisphere occur through direct contact with infected vectors. However, T. cruzi can persist in the blood of untreated individuals for decades, enabling additional transmission routes such as blood transfusion and organ transplantation, now recognized as the second most common mode of spread [30]. Congenital transmission from mother to child represents a third important pathway.
Socioeconomic factors strongly influence disease risk. Poverty, combined with political and economic instability, has fueled migration from endemic countries to developed regions such as Australia, Canada, Spain, and the United States. Consequently, cases of transfusion-related, transplant-related, and congenital Chagas disease have been documented in non-endemic countries, including Spain and the United States [31].
Taken together, these findings emphasize the parasitic aggressiveness and adaptability of trypanosomatids. Their broad host range, diverse transmission routes, and growing international footprint highlight the urgent need for enhanced surveillance and monitoring of Chagas disease—a neglected vector-borne infection with profound social and economic consequences, now posing risks beyond traditionally endemic regions [29,30,31].

Trypanosomiasis of Animals: Surra and Dourine

Animal trypanosomiasis is a protozoan disease caused by parasites of the genus Trypanosoma and transmitted by blood-sucking vectors, including the tsetse fly and other biting insects [32]. The principal veterinary species include T. congolense, T. vivax, T. brucei brucei, and T. simiae. At the same time, T. brucei rhodesiense and T. b. gambiense are zoonotic, with humans as their primary hosts [32]. Historically, several animal trypanosomiases were given distinct names—surra (T. evansi), dourine (T. equiperdum), and nagana (caused by T. brucei, T. congolense, and T. vivax)—to distinguish clinical syndromes. However, a critical review of published and unpublished data indicates that clinical signs such as abdominal swelling, emaciation, anaemia, and neurological symptoms are nonspecific and overlapping, making differential diagnosis challenging and often unreliable in the absence of laboratory confirmation [32].
The geographical distribution of camel populations and sampling points across the main camel-breeding regions like Mangystau, Kyzylorda, and Turkestan regions (Figure 2) underscores the epidemiological importance of these areas for trypanosomiasis surveillance. Notably, the regions with the largest camel populations (dark blue zones) coincide with areas of higher sampling density, reflecting the strategic prioritisation of surveillance in zones of intensified animal husbandry. Such mapping is critical, as camel breeding in Kazakhstan is concentrated in desert and semi-desert zones, where environmental and climatic factors favour vector activity and parasite circulation. The data presented in this figure also highlight potential “hotspots” where animal density and movement may enhance transmission risks, reinforcing the need for targeted monitoring, early diagnostics, and preventive measures. These findings align with the One Health perspective, demonstrating how ecological and demographic conditions shape the risk landscape for both veterinary and public health sectors.
In addition to pathogenic species, non-pathogenic trypanosomes such as T. theileri are also widespread. These digenetic blood parasites, transmitted by biting flies, are commonly detected in ungulates including cattle, buffalo, sheep, antelope, and deer [33,34,35,36,37,38]. Although generally regarded as non-pathogenic and of limited economic importance, T. theileri infections may present in a latent form and become clinically relevant under stress or in the presence of coinfections, manifesting with fever, anorexia, or anaemia [33,34,35,36,37,38]. Despite their wide distribution, these species remain neglected, mainly in veterinary research and surveillance.
Genetic studies have provided new insights into the taxonomy of pathogenic trypanosomes. For example, Lai et al. (2008) demonstrated that both T. equiperdum and T. evansi represent T. brucei strains that have lost either part of their kinetoplast DNA (dyskinetoplastic, Dk) or the entire kinetoplast genome (akinetoplastic, Ak), resulting in distinct but related lineages [33].
Among the diseases listed by the World Organization for Animal Health (WOAH) as notifiable infections of international concern are surra (T. evansi) and dourine (T. equiperdum), classified under diseases of multiple species and equidae [34,35,36,37,38]. Their inclusion reflects their:
  • Wide global distribution
  • Zoonotic potential
  • Capacity to spread rapidly in naïve populations, and
  • Severe impact on animal health and productivity.
Of these, T. evansi is considered the most essential veterinary pathogen due to its comprehensive host range, which includes camels, horses, cattle, buffalo, goats, sheep, pigs, dogs, tigers, and Asian elephants [39,40]. Infections cause profound economic losses, high mortality in susceptible hosts, and have been associated with vaccination failure, further exacerbating animal vulnerability [39,40]. While primarily an animal disease, sporadic human cases have been reported in India, Vietnam, and Sri Lanka, raising concern about its zoonotic potential [9,41,42,43].
Analysis of horse population dynamics, based on data as of March 1 for the period 2021–2025 by the Bureau of National Statistics of the Republic of Kazakhstan, shows a steady upward trend. The lowest recorded number of horses was in 2021, with 3.49 million head, whereas in 2025 the population reached its peak at 4.80 million head (Figure 3).
Diagnosis of T. evansi remains problematic. Parasitological methods are field-adaptable and straightforward but lack sensitivity. Improved techniques, such as the hematocrit centrifugation technique (HCT) and the modified miniature anion-exchange centrifugation technique (mAECT), increase detection rates, though they still miss chronic infections [44]. Molecular methods outperform antigen-based assays, enabling detection in both prepatent and chronic stages, but their field implementation remains limited [45].
Geographically, T. evansi is widely distributed across Asia, North America, Central America, and South America. In unvaccinated horses and camels, surra is frequently fatal [11,46,47]. Across Africa, Asia, and Latin America, surra continues to cause severe disease in livestock and wildlife, with significant economic impacts on rural livelihoods [8,48,49,50,51,52,53].
The European Food Safety Authority (EFSA) has assessed T. evansi (surra) under the Animal Health Law (AHL), applying criteria related to disease profile, impact, prevention, and control [38].
However, consensus remains lacking on whether T. evansi meets the requirements for inclusion in the Union intervention list (Article 5(3)). Ambiguities persist regarding its classification under Annexe IV and the list of affected animal species (Article 8), highlighting ongoing regulatory uncertainty in Europe [38].
Equine trypanosomosis is a complex infectious disease of horses caused by several Trypanosoma species, including T. evansi, T. equiperdum, T. brucei, T. vivax, T. congolense, and occasionally T. cruzi [10,11,12]. The classical syndromes historically described as surra (T. evansi), dourine (T. equiperdum), and nagana (T. brucei, T. congolense, T. vivax) are difficult to distinguish clinically, since common symptoms such as abdominal swelling, emaciation, anaemia, and neurological signs are largely nonspecific [10,11,12].
Instead, the primary differences lie in their epidemiology and transmission routes:
  • T. brucei and T. congolense are transmitted by tsetse flies in sub-Saharan Africa;
  • T. equiperdum is sexually transmitted
  • T. evansi is spread mechanically by biting flies, vampire bats, and possibly through sexual transmission [10,11,12].
Taxonomic classification remains controversial. Many isolates historically identified as T. equiperdum have since been recognised as misidentified strains of T. evansi. However, phylogenetic analyses suggest that T. evansi and T. equiperdum evolved independently from T. brucei [10,11,12,13]. Both species are microheterogeneous populations rather than uniform taxa [14]. Molecular tools, particularly the analysis of kinetoplast DNA (kDNA), can help differentiate them: T. evansi and some T. equiperdum strains lack the maxicircle component of kDNA, which is present in T. brucei [32,54]. However, these distinctions remain debated, underscoring the diagnostic challenges within the Trypanozoon subgenus.
Dourine poses particular challenges for equine health and trade. The parasite infects both domestic and wild ungulates, and the movement of breeding horses facilitates its spread across borders. Historical records show that the peak incidence of dourine in the former Soviet republics—including Russia, the Caucasus, Central Asia, the Baltic States, Moldova, Belarus, and Ukraine—occurred between 1961 and 1965. A later outbreak in Russia during 1998–1999 accounted for 70% of all registered equine diseases [55]. Researchers at that time identified pathogenic isolates representing both surra (T. evansi var. ninaekohlyakimovi) and dourine (T. equiperdum) [55].
For Kazakhstan, monitoring, early diagnosis, and prevention of equine trypanosomosis (surra and dourine) are of strategic importance. The breeding of camels and horses has historically been a cornerstone of traditional animal husbandry and remains economically valuable today, particularly in the country’s extensive desert and semi-desert zones. As highlighted in recent studies (Frontiers in Veterinary Science, 2025), these regions represent epidemiologically significant areas where high-density camel populations overlap with ecological conditions favourable to vector activity and parasite circulation. The persistence of trypanosomiasis therefore represents not only a veterinary challenge but also a substantial threat to rural livelihoods and national economic resilience.
Here, it is important to note that the present work was carried out within the framework of the Scientific Research Project IRN BR218004/0223, «Improving biosafety measures in Kazakhstan: countering dangerous and especially dangerous infections» (2023–2025), funded by the Science Committee of the Ministry of Science and Higher Education of the Republic of Kazakhstan. Within this project, scientists from the Kazakh Scientific Research Veterinary Institute (KazSRVI) are conducting ongoing monitoring studies on animal trypanosomosis, the results of which will be published in future reports and peer-reviewed publications. These efforts build directly on the recent findings published in Frontiers in Veterinary Science [56], thereby strengthening the national research framework for controlling neglected vector-borne zoonoses under the One Health approach.

Cases of Human Infection with T. evansi

According to WHO data (2020), deaths from trypanosomiasis in Kazakhstan were 0 or 0.00% of total mortality, with an age-adjusted mortality rate of 0.00 per 100,000 population, ranking Kazakhstan 92nd worldwide [57]. While no human cases are documented locally, sporadic reports of human infections with animal trypanosomes have been described globally. These include T. vivax, T. congolense, T. b. brucei, T. evansi, and T. lewisi or T. lewisi-like parasites, collectively termed atypical human trypanosomiasis (a-HT) [8,58,59,60].
Figure 4 clearly illustrates the rarity yet global distribution of atypical human trypanosomiasis (a-HT) cases, including those caused by T. evansi. While confirmed human infections have been documented in India, Egypt, and Vietnam, alongside sporadic reports elsewhere, the absence of cases in Kazakhstan should not be interpreted as immunity to risk. On the contrary, Kazakhstan’s intensive horse and camel husbandry, active livestock trade, and vulnerability to climate change create conditions that could facilitate zoonotic spillover. The contrast between “zero cases” in Kazakhstan and “sporadic but proven cases” globally underscores two critical points: (i) the underestimated zoonotic potential of animal trypanosomes, and (ii) the urgent need for enhanced surveillance and reliable diagnostic tools to detect emerging infections before they pose wider threats.
The zoonotic potential of animal trypanosomes is linked to socio-economic and environmental conditions, especially in regions with close human–livestock interactions and abundant mechanical vectors [61,62,63]. Experimental studies in India demonstrated that diverse mammals—including albino rats, guinea pigs, bandicoot rats, mongooses, cats, and monkeys—are susceptible to T. evansi following syringe passage, with variable virulence [63]. Notably, rhesus macaques developed severe clinical signs resembling human sleeping sickness, suggesting that primates could serve as potential models of zoonotic infection [64]. Confirmed human infections with T. evansi remain rare but significant. In India (2005), a molecularly confirmed case demonstrated high parasitemia without central nervous system involvement, although T. evansi typically invades the CNS in horses within two weeks [10,39,65,66]. In Egypt (2010), one human sample out of 30 tested positively by ELISA and microscopy, and the patient recovered following treatment [59,60]. In Vietnam (2016), a healthy individual without APOL1 deficiency developed confirmed T. evansi infection, most likely acquired through exposure to infected cattle meat [47]. These cases draw attention to the role of apolipoprotein L1 (APOL1) in human innate immunity. While humans are naturally resistant to T. b. brucei through APOL1-mediated lysis [47], a frame-shift mutation in the APOL1 gene was identified in the Indian patient, explaining the absence of trypanolytic activity [67]. However, no APOL1 mutation was detected in the Vietnamese patient (2015), indicating that other host or parasite factors may facilitate infection [47,68].
Collectively, these findings demonstrate that close contact with infected animals increases the risk of zoonotic spillover of T. evansi and highlight the importance of controlling parasitemia in livestock to prevent atypical human infections across continents [69]. For Kazakhstan, where horses and camels are integral to animal husbandry and are actively traded internationally, the surveillance and prevention of surra are of strategic importance for both veterinary and public health sectors.

Diagnosis of Trypanosomiasis

Despite more than a century of study, dourine diagnosis remains a challenge. Only a small number of T. equiperdum laboratory strains have been characterised, and data on most isolates remain unpublished. Definitive diagnosis is possible only at the serological or molecular level; clinical signs are non-specific, and international screening still relies heavily on the outdated complement fixation test (CFT) developed in 1915, which remains cross-reactive and may produce misleading results [47]. In Abay et al.’s study, large-scale field data from Kazakhstan showed that the formalin gel test (FGT) detected more seropositive camels than the complement fixation test (CFT), supporting a combined FGT+CFT screening algorithm [Frontiers | Serological Surveillance of Trypanosoma evansi in Kazakhstani Camels by Complement Fixation and Formalin Gel Tests [56].
Figure 5 underscores several key points. First, there is no single gold standard capable of meeting the diagnostic demands of both field settings and trade-sensitive surveillance. Parasitological methods remain useful for confirming active infection but systematically miss chronic carriers. Serology fills this gap with higher sensitivity but introduces the risk of false positives due to cross-reactivity, which can be particularly problematic in the context of Kazakhstan’s role as an exporter and importer of thoroughbred horses. Molecular methods provide the highest accuracy and allow early detection. Yet, their dependence on laboratory infrastructure and their current inability to separate closely related subspecies limit practical application in endemic regions.
Taken together, the relative weighting in this pie chart reflects a fragmented diagnostic landscape where each method has strengths but also critical weaknesses. For Kazakhstan and comparable regions, this fragmentation is not merely an academic issue but a strategic vulnerability, since inadequate or misleading diagnostics can undermine disease control, animal husbandry, and international trade certification. The data emphasize that progress depends on an integrated approach—combining the confirmatory role of parasitology, the screening potential of serology, and the precision of molecular tools—alongside sustained investment in accessible, affordable, and species-specific diagnostics. Only then can both local disease control and global biosecurity be ensured
For Kazakhstan, diagnosis of animal trypanosomiasis (surra and dourine) is of strategic importance. The breeding of camels and horses has been a traditional sub-branch of animal husbandry for centuries, particularly in desert and semi-desert regions, where it contributes significantly to the national economy. Camels supply meat, milk, and wool, but yields remain low, mainly due to infectious diseases, among which trypanosomiasis occupies a special place. Kazakhstan’s status as an exporter and importer of thoroughbred horses also increases the risk of introducing or disseminating dourine. While WOAH listed Kazakhstan as free from equine trypanosomosis between 2005 and 2022 [70], earlier studies demonstrated otherwise: infection rates of 16.4% in Almaty horses (2004) [71] and confirmed cases in 2014 [72]. Given the disease’s long incubation period (up to 6 months) and frequent asymptomatic infections, the risk of widespread undetected transmission remains high.
Parasitological methods are the traditional gold standard, relying on direct microscopic observation of motile trypanosomes in blood [54,74,75]. While inexpensive and straightforward, their sensitivity is highly variable, depending on parasitemia levels, which fluctuate cyclically due to antigenic variation of surface glycoproteins [76,77,78,79,80,81,82,83,84,85]. As a result, negative results cannot rule out infection, particularly in chronic or subclinical cases, whereas positive findings confirm active infection in epizootic contexts. Enhanced microscopy (e.g., LED fluorescence, dark-field, phase-contrast) and concentration methods such as the hematocrit centrifugation technique (HCT) and anion exchange chromatography improve sensitivity, but limitations persist [78,79,80,81].
Serological tests improve sensitivity but suffer from cross-reactivity between Trypanosoma species [86]. WOAH recommends: For T. equiperdum: CFT and indirect immunofluorescence assay (IFA); For T. evansi: IFA, ELISA (RoTat 1.2), card agglutination test (CATT/T. evansi), and immune trypanolysis (TL/RoTat 1.2); For T. brucei, T. vivax, T. congolense: IFA and ELISA [89,90,91].
Advanced immunoassays include recombinant ELISA (rELISA), Western blot using FeSOD antigen, and anti-idiotypic antibody approaches [86,87,101]. In Kazakhstan, local researchers have developed diagnostic antigens using infected animals, ultrasound disruption, isoionic fractionation, and enzyme immunoassay systems [98,99,100,101], contributing valuable but still imperfect diagnostic tools.
Molecular methods (PCR, LAMP-LFA) offer higher specificity and can differentiate subgenera or subspecies depending on primers [86]. However, limitations include false positives (DNA contamination), false negatives (very low parasitemia, high primer specificity), and higher costs, restricting their application in field settings [95]. Importantly, there is no single molecular assay that reliably distinguishes T. brucei from T. equiperdum, forcing reliance on epidemiological context [103,104,105].
International frameworks complicate matters further. The WOAH and CDC recommend a combination of microscopy, serology, and molecular assays for diagnosis, but none achieve perfect sensitivity or specificity [105,106]. Serological tests remain mandatory for international horse trade, yet their cross-reactivity undermines species-specific conclusions [107,108,109,110,111].

Threats of Vector-Borne Trypanosomiasis and Its Relationship to the Global Crisis

According to the United Nations Environment Programme (UNEP) medium-term strategy for 2022–2025, three interconnected crises—climate change, biodiversity loss, and environmental pollution—pose severe threats to global socio-economic well-being. To address these challenges, UNEP has identified seven interlinked priority programmes, including climate change mitigation, pollution reduction, biodiversity conservation, science-policy integration, sustainable environmental management, financial and economic reform, and digital transformation [78].
Figure 6 highlights the intersection between climate change and vector-borne disease (VBD) risk, with Kazakhstan serving as a critical case study. The steady temperature rise (+0.32 °C per decade) and projected warming of +3.3 to +6.2 °C by 2085 suggest profound ecological shifts that will reshape habitats and disease dynamics [115,116]. The northward migration of wet zones (50–100 km) and reduction of insufficiently humid areas (6–23%) further illustrate how vector habitats are expanding into previously unaffected regions, increasing the likelihood of novel or reemerging zoonotic threats. The finding that 66% of Kazakhstan’s land is already desertified underscores the severity of environmental stressors, which amplify vulnerability to both livestock and human health crises.
Placed against the backdrop of the 2030 WHO/WOAH/UN target to reduce global VBD mortality by 75%, the contrast is stark: while international frameworks aim to curb mortality, local realities reveal accelerating risk factors that may undermine these goals if not urgently addressed [79,115]. Notably, the figure demonstrates that Kazakhstan is not only a regional hotspot for climate vulnerability but also a strategic sentinel for understanding how climate change multiplies zoonotic risk in Central Asia. Without integrated adaptation measures—including improved vector surveillance, sustainable land management, and climate-informed health policy—the gap between global targets and local realities will likely widen, threatening both public health and long-term sustainable development. Evidence increasingly demonstrates that climate-driven environmental change threatens food security and accelerates the spread of infectious diseases, including drug-resistant and vector-borne pathogens [78]. Changes in social, demographic, and ecological conditions alter patterns of transmission, leading to:
  • the intensification and geographical expansion of vector habitats,
  • the reemergence of previously controlled diseases, and
  • the extension of seasonal transmission windows.
Disorderly urbanisation, poor water supply systems, and inadequate waste management heighten the risk of mosquito-borne viral infections in densely populated cities [112,113]. Moreover, the emergence of insecticide resistance and behavioural shifts in vectors further erode the effectiveness of conventional preventive measures [13,40]. In response, the WHO, WOAH, and UN have established targets for 2030: to reduce global mortality from vector-borne diseases by 75%, curb new infections, and prevent epidemics through sustainable, locally adapted vector control strategies. However, the actual burden of vector-borne diseases remains significantly underestimated [114]. Within the European Union (Regulation 2016/429), animal vector-borne diseases are prioritised for monitoring and notification, with periodic reviews and amendments to ensure inclusion of newly recognised high-risk pathogens [114].
For Kazakhstan, climate change represents a critical risk multiplier. The healthcare vulnerability assessment places the country among the most climate-vulnerable nations in Central Asia. Average annual air temperature has increased by 0.32 °C per decade, with projections indicating a rise of 3.3–6.2 °C by 2085, depending on the region [115,116]. Shifts in climate zones are expected, including a northward movement of wet zones (50–100 km) and a 6–23% reduction in insufficiently humid areas [115,116]. Already, 66% of Kazakhstan’s land area (179.9 million ha out of 272.5 million ha) is affected by desertification [115]. These environmental shifts foster conditions for the northward spread of vectors such as ticks and rodents, opening niches for pathogens in previously unaffected areas. As a result, neglected or novel vector-borne diseases may emerge or reemerge. The region most vulnerable to these changes is South Kazakhstan, North Kazakhstan, and Jambyl, which are experiencing increasing human, financial, and environmental losses. These impacts not only exacerbate food insecurity and poverty but also threaten the country’s long-term sustainable development trajectory [115,116].

Conclusion

This review highlights the complex nosology of neglected endemic diseases and transmissible zoonoses caused by Trypanosoma spp., underscoring their impact on both human and animal health. Framed within the One Health approach, the evidence demonstrates that trypanosomiasis is not only a veterinary problem but also a potential zoonotic and socio-economic threat. For Kazakhstan and other regions where camel and horse breeding remain integral to livelihoods, trypanosomiasis threatens food security, productivity, and rural economies. Although WHO data report no human cases in Kazakhstan, the increasing reports of atypical human infections worldwide highlight the need for vigilance. At the same time, the diagnostic challenges—linked to fluctuating parasitemia, cross-reactivity of serological tests, and limited availability of molecular assays—continue to impede effective surveillance and control. Globally, the expansion of vectors driven by climate change, urbanisation, and trade magnifies the risk of trypanosome transmission to new territories and hosts. This makes trypanosomiasis an exemplar of how environmental, social, and biological drivers interact in neglected tropical and zoonotic diseases. To address these challenges, integrated strategies are required: Improved diagnostics capable of distinguishing species and detecting chronic carriers, strengthened monitoring and notification systems, particularly in trade-sensitive regions, Sustainable vector control and animal health programmes, adapted to local ecological realities, and cross-sectoral collaboration between veterinary, medical, and environmental health services. Ultimately, controlling the spread of trypanosomiasis is not only about safeguarding livestock production but also about protecting human health, ensuring economic resilience, and promoting sustainable development. Tackling this disease through a comprehensive One Health strategy offers the best opportunity to reduce its burden and prevent future outbreaks in both endemic and at-risk regions.
This review was not conducted as a PRISMA systematic review. Instead, it represents a narrative synthesis of published and unpublished data, with particular emphasis on the epidemiological context of Kazakhstan and the One Health framework.

Funding

This research was funded by the Science Committee of the Ministry of Science and Higher Education of the Republic of Kazakhstan, project IRN BR218004/0223 “Improving biosafety measures in Kazakhstan: countering dangerous and especially dangerous infections” (2023–2025).

Acknowledgments

The authors acknowledge the contribution of scientists from the Kazakh Scientific Research Veterinary Institute of (KazSRVI), who are conducting ongoing monitoring studies on animal trypanosomosis within the framework of this project. The results of these studies will be reported in future publications.

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Figure 1. Global distribution of central trypanosomiasis infections in humans and animals. Shaded regions highlight the primary endemic zones of different Trypanosoma species: Africa (orange), where T. brucei spp. Human African Trypanosomiasis (HAT, sleeping sickness) and animal trypanosomiasis (nagana) are found in Latin America (blue), where T. cruzi is responsible for American trypanosomiasis (Chagas disease), and in Asia (green), where T. evansi (surra) and T. vivax affect livestock and camels. Icons indicate predominant hosts: humans, livestock, and camels. These parasites collectively impact both public health and animal production, underscoring their importance within the One Health framework [6,7,8,9,10,11,12,13,20,25,29,30,31].
Figure 1. Global distribution of central trypanosomiasis infections in humans and animals. Shaded regions highlight the primary endemic zones of different Trypanosoma species: Africa (orange), where T. brucei spp. Human African Trypanosomiasis (HAT, sleeping sickness) and animal trypanosomiasis (nagana) are found in Latin America (blue), where T. cruzi is responsible for American trypanosomiasis (Chagas disease), and in Asia (green), where T. evansi (surra) and T. vivax affect livestock and camels. Icons indicate predominant hosts: humans, livestock, and camels. These parasites collectively impact both public health and animal production, underscoring their importance within the One Health framework [6,7,8,9,10,11,12,13,20,25,29,30,31].
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Figure 2. Map of the camel population in Kazakhstan, highlighting Mangystau, Kyzylorda, and Turkestan regions. Camel population density is shown by a color gradient ranging from light yellow (low density) to dark blue (high density). Statistical data for 2025 were obtained from the Bureau of National Statis-tics (https://stat.gov.kz).
Figure 2. Map of the camel population in Kazakhstan, highlighting Mangystau, Kyzylorda, and Turkestan regions. Camel population density is shown by a color gradient ranging from light yellow (low density) to dark blue (high density). Statistical data for 2025 were obtained from the Bureau of National Statis-tics (https://stat.gov.kz).
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Figure 3. Map of the equine population in Kazakhstan. Equine population density is shown by a color gradient ranging from light yellow (low density) to dark blue (high density). Statistical data for 2025 were obtained from the Bureau of National Statistics (https://stat.gov.kz).
Figure 3. Map of the equine population in Kazakhstan. Equine population density is shown by a color gradient ranging from light yellow (low density) to dark blue (high density). Statistical data for 2025 were obtained from the Bureau of National Statistics (https://stat.gov.kz).
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Figure 4. Reported human cases of atypical trypanosomiasis (a-HT), including T. evansi infections. The bar chart highlights countries where confirmed cases have been reported: India, Egypt, and Vietnam, alongside sporadic reports from other regions. Kazakhstan is included for comparison, where no human cases have been recorded [56,57,58,59], but where livestock trade and climate change may increase future zoonotic risk. The data presented are illustrative and reflect published case reports rather than population-level incidence.
Figure 4. Reported human cases of atypical trypanosomiasis (a-HT), including T. evansi infections. The bar chart highlights countries where confirmed cases have been reported: India, Egypt, and Vietnam, alongside sporadic reports from other regions. Kazakhstan is included for comparison, where no human cases have been recorded [56,57,58,59], but where livestock trade and climate change may increase future zoonotic risk. The data presented are illustrative and reflect published case reports rather than population-level incidence.
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Figure 5. Relative emphasis on diagnostic approaches for animal trypanosomiasis. Parasitological methods (30%) remain the traditional gold standard, offering low-cost and straightforward confirmatory diagnosis but with poor sensitivity in chronic or subclinical infections [54,74,75,76,77,78,79,80,81,82,83,84,85]. Serological methods (35%) provide higher sensitivity but suffer from cross-reactivity between Trypanosoma species, and the complement fixation test (CFT), developed in 1915, remains widely used despite its limitations [86,89,90,91]. Molecular methods (35%) offer the most tremendous potential for specificity and sensitivity, yet remain costly, field-limited, and unable to reliably distinguish T. brucei from T. equiperdum [95,103,104,105]. For Kazakhstan, where WOAH listed the country as free from equine trypanosomosis between 2005 and 2022, local studies nonetheless confirmed significant infection rates (16.4% in Almaty horses, 2004; further cases in 2014) [70,71,72], highlighting the need for more reliable and accessible diagnostic tools.
Figure 5. Relative emphasis on diagnostic approaches for animal trypanosomiasis. Parasitological methods (30%) remain the traditional gold standard, offering low-cost and straightforward confirmatory diagnosis but with poor sensitivity in chronic or subclinical infections [54,74,75,76,77,78,79,80,81,82,83,84,85]. Serological methods (35%) provide higher sensitivity but suffer from cross-reactivity between Trypanosoma species, and the complement fixation test (CFT), developed in 1915, remains widely used despite its limitations [86,89,90,91]. Molecular methods (35%) offer the most tremendous potential for specificity and sensitivity, yet remain costly, field-limited, and unable to reliably distinguish T. brucei from T. equiperdum [95,103,104,105]. For Kazakhstan, where WOAH listed the country as free from equine trypanosomosis between 2005 and 2022, local studies nonetheless confirmed significant infection rates (16.4% in Almaty horses, 2004; further cases in 2014) [70,71,72], highlighting the need for more reliable and accessible diagnostic tools.
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Figure 6. Climate change indicators and vector-borne disease (VBD) risk in Kazakhstan in the global context. The average annual air temperature in Kazakhstan is increasing by 0.32 °C per decade, with projections of +3.3 to +6.2 °C by 2085, depending on the region [114,115]. Climate-driven northward shifts of wet zones by 50–100 km and reductions of insufficiently humid areas by 6–23% are expected [115,116]. Currently, 66% of Kazakhstan’s land area (179.9 million ha) is affected by desertification [115]. These changes create conditions for the expansion of vector habitats, the reemergence of neglected diseases, and the emergence of novel zoonoses. In parallel, the WHO, WOAH, and UN have set global targets to reduce mortality from vector-borne diseases by 75% by 2030 [78,115]. Error bars indicate reported ranges for projected temperature rise, wet-zone shifts, and humid area reductions.
Figure 6. Climate change indicators and vector-borne disease (VBD) risk in Kazakhstan in the global context. The average annual air temperature in Kazakhstan is increasing by 0.32 °C per decade, with projections of +3.3 to +6.2 °C by 2085, depending on the region [114,115]. Climate-driven northward shifts of wet zones by 50–100 km and reductions of insufficiently humid areas by 6–23% are expected [115,116]. Currently, 66% of Kazakhstan’s land area (179.9 million ha) is affected by desertification [115]. These changes create conditions for the expansion of vector habitats, the reemergence of neglected diseases, and the emergence of novel zoonoses. In parallel, the WHO, WOAH, and UN have set global targets to reduce mortality from vector-borne diseases by 75% by 2030 [78,115]. Error bars indicate reported ranges for projected temperature rise, wet-zone shifts, and humid area reductions.
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