Strongyloides fuelleborni fuelleborni

Strongyloides fuelleborni fuelleborni is a common parasite of NHPs (Al-Jawabreh et al, Reference Al-Jawabreh, Anderson, Atkinson, Bickford-Smith, Bradbury, Breloer, Bryant, Buonfrate, Cadd, Crooks, Deiana, Grant, Hallem, Hedtke, Hunt, Khieu, Kikuchi, Kounosu, Lastik, van Lieshout, Liu, McSorley, McVeigh, Mousley, Murcott, Nevin, Nosková, Pomari, Reynolds, Ross, Streit, Suleiman, Tiberti and Viney2024). Human infection with S. f. fuelleborni was first reported in 1932 in Zimbabwe, Southern Africa (Blackie, Reference Blackie1932). Wallace et al (Reference Wallace, Mooney and Sanders1948) documented the first human case from Asia in 1948. Between 1968 and 1972, Pampiglione and Ricciardi (Reference Pampiglione and Ricciardi1972b) conducted a survey of S. f. fuelleborni infections in 4577 individuals across 13 nations, spanning the breadth of West to East Africa. Infection was detected in 13% (606/4577) of individuals, with prevalence by locality ranging from 0% to 78% (Pampiglione and Ricciardi, Reference Pampiglione and Ricciardi1972b). Prevalence was higher in children compared to adults, and infection was endemic in tropical rainforest localities, but only sporadic in Savannah environments (Pampiglione and Ricciardi, Reference Pampiglione and Ricciardi1972b). Subsequent examination of diagnostic specimens in two Zambian communities found S. f. fuelleborni prevalence of 10% (13/131) (Hira and Patel, Reference Hira and Patel1977) and 31% (138/448) (Hira and Patel, Reference Hira and Patel1980), respectively.

Since then, no active surveillance for S. f. fuelleborni in humans have been undertaken. However, over the past decade, human infections have been increasingly reported in sub-Saharan Africa (Hasegawa et al, Reference Hasegawa, Sato, Fujita, Nguema, Nobusue, Miyagi, Kooriyama, Takenoshita, Noda and Sato2010, Reference Hasegawa, Kalousova, McLennan, Modry, Profousova-Psenkova, Shutt-Phillips, Todd, Huffman and Petrzelkova2016; Barratt et al, Reference Barratt, Lane, Talundzic, Richins, Robertson, Formenti, Pritt, Verocai, Nascimento de Souza and Mato Soares2019; Potters et al, Reference Potters, Micalessi, Van Esbroeck, Gils and Theunissen2020), Southeast Asia (Labes et al, Reference Labes, Wijayanti, Deplazes and Mathis2011; Thanchomnang et al, Reference Thanchomnang, Intapan, Sanpool, Rodpai, Tourtip, Yahom, Kullawat, Radomyos, Thammasiri and Maleewong2017; Janwan et al, Reference Janwan, Rodpai, Intapan, Sanpool, Tourtip, Maleewong and Thanchomnang2020), and South Asia (Barratt et al, Reference Barratt, Lane, Talundzic, Richins, Robertson, Formenti, Pritt, Verocai, Nascimento de Souza and Mato Soares2019; de Ree et al, Reference de Ree, Nath, Barua, Harbecke, Lee, Rödelsperger and Streit2024). While most reports involve isolated cases, a genotyping survey in Bangladesh identified S. f. fuelleborni infections in 3% (4/134) of people from four communities (de Ree et al, Reference de Ree, Nath, Barua, Harbecke, Lee, Rödelsperger and Streit2024). Most recently, S. f. fuelleborni was molecularly detected in 37% (7/19) of infant stool samples collected from the Eastern Highlands Province of PNG (Zhao et al, Reference Zhao, Haidamak, Noskova, Ilik, Pafčo, Ford, Masiria, Maure, Kotale, Pomat, Gordon, Navarro, Horwood, Constantinoiu, Greenhill and Bradbury2025). These findings suggest that S. f. fuelleborni may be far more prevalent and geographically widespread in human populations than currently recognized (Figure 1). Microscopy may misidentify S. f. fuelleborni eggs as morphologically similar embryonated hookworm eggs and hatched larvae are indistinguishable from those of S. stercoralis (Speare, Reference Speare1986). Additionally, the lack of targeted control strategies for strongyloidiasis globally may contribute to sustained transmission (Lo et al, Reference Lo, Addiss, Buonfrate, Amor, Anegagrie, Bisoffi, Bradbury, Keiser, Kepha and Khieu2025). In regions where mass drug administration (MDA) with ivermectin, the most effective chemical against S. stercoralis, has been implemented for the control of onchocerciasis or lymphatic filariasis, S. f. fuelleborni prevalence may have been incidentally reduced, as has been observed for S. stercoralis (Stroffolini et al, Reference Stroffolini, Tamarozzi, Fittipaldo, Mazzi, Le, Vaz Nery and Buonfrate2023). Nonetheless, without targeted surveillance, the true distribution and burden of S. f. fuelleborni remain unknown and likely underestimated.

Figure 1. Global distribution of Strongyloides fuelleborni fuelleborni in humans and non-human primates (NHPs). African and Asian-Pacific clades of S. f. fuelleborni, inferred from available genbank sequences of cox1, 18S rrna HVR-IV and mitochondrial genome regions, are shown in yellow and pink, respectively. Strongyloides f. fuelleborni infecting St. Kitts vervet monkeys (Chlorocebus aethiops sabaeus), indicated by a red asterisk, were introduced from Africa in the 17th century (RICHINS et al., Reference Richins, Sapp, Ketzis, Willingham, Mukaratirwa, Qvarnstrom and Barratt2023). The distribution of S. fuelleborni on the Island of New Guinea, marked with a green box, remains unresolved (see Figure 2).

There is limited understanding of the clinical presentation of S. f. fuelleborni infections. Most clinical insights come from a historical human experimental infection, which showed a broad spectrum of clinical signs, some resembling those seen in S. stercoralis infection (Pampiglione and Ricciardi, Reference Pampiglione and Ricciardi1972a). These included localized dermatologic manifestations (such as urticaria and/or ground itch) at the onset, followed by transient, non-productive cough and gastrointestinal symptoms (epigastric burning, abdominal pain and diarrhea) in later stages. Marked eosinophilia (up to 48%) was observed 3–4 weeks post-infection (Pampiglione and Ricciardi, Reference Pampiglione and Ricciardi1972a). It should be noted that this study used a human strain of S. f. fuelleborni, which had previously been inoculated into the same participant at a lower dose in a preliminary experiment (Pampiglione and Ricciardi, Reference Pampiglione and Ricciardi1972a). Therefore, the observed symptoms may have been influenced by prior sensitization and/or immune response mounted to S. f. fuelleborni antigens. As this species is passed in the environment as eggs, it has been assumed that an internal autoinfective cycle does not occur (Centers for Disease Control and Prevention, 2019); however, this assumption has not been experimentally confirmed. It remains possible that small numbers of eggs could hatch in the gut or perianal folds and develop into filariform larvae and reinfect the host, although existing epidemiologic data do not support this hypothesis (Pampiglione and Ricciardi, Reference Pampiglione and Ricciardi1972b).

The transmission patterns of S. f. fuelleborni in human populations are similarly not fully understood. Both NHP-to-human (Sandground, Reference Sandground1925; Blackie, Reference Blackie1932; Freedman, Reference Freedman1991) and human-to-human (Pampiglione and Ricciardi, Reference Pampiglione and Ricciardi1972a) transmissions have been experimentally demonstrated. Human infections have historically been considered a zoonosis from NHPs. This is supported by molecular evidence showing identical or closely clustered genotypes in worms isolated from humans and NHPs living in close proximity in Tanzania (Hasegawa et al, Reference Hasegawa, Sato, Fujita, Nguema, Nobusue, Miyagi, Kooriyama, Takenoshita, Noda and Sato2010), the Democratic Republic of the Congo (Potters et al, Reference Potters, Micalessi, Van Esbroeck, Gils and Theunissen2020) and Thailand (Thanchomnang et al, Reference Thanchomnang, Intapan, Sanpool, Rodpai, Tourtip, Yahom, Kullawat, Radomyos, Thammasiri and Maleewong2017; Janwan et al, Reference Janwan, Rodpai, Intapan, Sanpool, Tourtip, Maleewong and Thanchomnang2020). However, growing evidence suggests that exclusively interhuman transmission is also possible. Hira and Patel (Reference Hira and Patel1980) found high prevalence in people from urban and peri-urban communities in Zambia, where contact with NHPs was unlikely. Likewise, Hasegawa et al (Reference Hasegawa, Kalousova, McLennan, Modry, Profousova-Psenkova, Shutt-Phillips, Todd, Huffman and Petrzelkova2016) observed marked genetic divergence at the cox1 and 18S rRNA HVR-IV loci in worms from humans (n = 7) and NHPs (n = 18) cohabiting the Dzanga-Sangha Protected Area of the Central African Republic. These findings, together with emerging evidence of human S. f. fuelleborni infections in PNG where NHPs are absent (Zhao et al, Reference Zhao, Haidamak, Noskova, Ilik, Pafčo, Ford, Masiria, Maure, Kotale, Pomat, Gordon, Navarro, Horwood, Constantinoiu, Greenhill and Bradbury2025), suggest that this parasite has adapted to sustained human-to-human transmission in some parts of the world. Brown and Girardeau (Reference Brown and Girardeau1977) noted the transmammary passage of Strongyloides infective filariform larvae (iL3), suspected to be S. f. fuelleborni, from one of 26 African nursing mothers to her infant. This finding requires further confirmation, as only a single larva was morphometrically characterised and found to be relatively small (340 µm) (Brown and Girardeau, Reference Brown and Girardeau1977), so the possibility of this being an autoinfective larva of S. stercoralis cannot be excluded based on the size and morphology alone.

Strongyloides fuelleborni kellyi

Strongyloides fuelleborni kellyi was first reported by Allen Kelly in 1971 during a stool microscopy survey in western PNG (Kelly and Voge, Reference Kelly and Voge1973). Due to its morphological similarity in adult stages to S. fuelleborni von Linstow, 1905, but the absence of a NHP reservoir in New Guinea, it was designated a subspecies of S. fuelleborni and named S. f. kellyi (Viney et al, Reference Viney, Ashford and Barnish1991). A separate isoenzyme electrophoretic analysis grouped African and most PNG S. fuelleborni isolates together; however, 4 PNG isolates clustered with Strongyloides ransomi from local pigs (Viney and Ashford, Reference Viney and Ashford1990). Viney and Ashford (Reference Viney and Ashford1990) speculated that these findings might represent artifact from participants submitting pig faeces in substitution for human samples. Subsequently, phylogenetic analysis of a 330 bp 18S rRNA fragment from a formalin-fixed human isolate from PNG by Dorris et al (Reference Dorris, Viney and Blaxter2002) placed the parasite within a clade containing Strongyloides venezuelensus and S. ransomi, but separate from S. f. fuelleborni. This placement was supported by a recent genotyping analysis of 18S rRNA HVR-IV (252–259 bp) and HVR-I (432 bp) loci. Most importantly, this study demonstrated the co-occurrence, in one of 19 infants, of the genospecies identified by Dorris et al (Reference Dorris, Viney and Blaxter2002) alongside the Asian clade of S. f. fuelleborni in PNG (Zhao et al, Reference Zhao, Haidamak, Noskova, Ilik, Pafčo, Ford, Masiria, Maure, Kotale, Pomat, Gordon, Navarro, Horwood, Constantinoiu, Greenhill and Bradbury2025).

The co-endemicity of two genetically distinct non-S. stercoralis human-infecting Strongyloides nematodes in PNG necessitates a reassessment of historical data previously attributed to S. f. kellyi (Figure 2). The parasite described by Viney et al (Reference Viney, Ashford and Barnish1991) and designated S. f. kellyi may represent the Asian-Pacific clade of S. f. fuelleborni, whereas the genospecies identified by Dorris et al (Reference Dorris, Viney and Blaxter2002) and Zhao et al (Reference Zhao, Haidamak, Noskova, Ilik, Pafčo, Ford, Masiria, Maure, Kotale, Pomat, Gordon, Navarro, Horwood, Constantinoiu, Greenhill and Bradbury2025) may represent an undescribed Strongyloides sp., potentially of animal origin. As there exists no morphological studies of S. f. fuelleborni from Asia, further comparative morphologic and genomic analyses of adult isolates from Africa, Asia and New Guinea are needed to resolve this taxonomic confusion.

Figure 2. Human infections with S. fuelleborni in New Guinea. The data presented may also include infections caused by an undescribed strongyloides sp. genetically distinct from S. fuelleborni, as molecularly demonstrated by Dorris et al. (Reference Dorris, Viney and Blaxter2002) and Zhao et al. (Reference Zhao, Haidamak, Noskova, Ilik, Pafčo, Ford, Masiria, Maure, Kotale, Pomat, Gordon, Navarro, Horwood, Constantinoiu, Greenhill and Bradbury2025). Sites of confirmed SBS outbreaks are indicated by green triangleS. Sporadic SBS cases have also been reported elsewhere in Papua New Guinea (data not shown).

Historical epidemiologic and clinical data on S. f. kellyi, generated prior to the molecular era, also warrant re-evaluation (Speare, Reference Speare1986; Viney et al, Reference Viney, Ashford and Barnish1991). Faecal microscopy surveys conducted between 1976 and 1997 in PNG reported S. f. kellyi prevalence ranging from 20% to 93% in children and 5% to 20% in adults (Ashford and Babona, Reference Ashford and Babona1980; Ashford et al, Reference Ashford, Vince, Gratten and Bana-Koiri1979; Barnish and Ashford, Reference Barnish and Ashford1989a, Reference Barnish and Ashfordb; Barnish and Harari, Reference Barnish and Harari1989; Kelly et al, Reference Kelly, Little and Voge1976; King and Mascie-Taylor, Reference King and Mascie-Taylor2004; Shield et al, Reference Shield, Hide, Harvey, Vrbova and Tulloch1987; Shield and Kow, Reference Shield and Kow2013). Infections were detected in children as young as 18 days, with prevalence peaking between 30 and 60 months of age and declining after 5 years (Ashford et al, Reference Ashford, Barnish and Viney1992; Barnish and Ashford, Reference Barnish and Ashford1989a, Reference Barnish and Ashford1989b). Faecal egg count could reach up to 100 000 epg in late infancy (Barnish and Ashford, Reference Barnish and Ashford1989a). Human infections have also been reported in Deiyai Regency, in the Indonesian province of Central Papua (Muller et al, Reference Muller, Lillywhite, Bending and Catford1987). No faecal surveys for Strongyloides have been conducted in New Guinea since 1997. However, two community-based serosurveys reported Strongyloides seroprevalence of 22.5% (27/120) (Scott et al, Reference Scott, Emeto, Melrose, Warner and Rush2022) in Western Province by a S. stercoralis L3 crude antigen ELISA, and 68% (192/283) in Madang Province by a dual NIE and SsIR recombinant antigen ELISA (Tobon Ramos et al, Reference Tobon Ramos, Maure, Carias, Lew, Goss, Samuel, Tavul, Fischer, Weil and Laman2025). In the absence of cross-reactivity data for these assays, the proportion of seropositivity attributable to S. f. kellyi remains unknown.

Uncertainty also surrounds the transmission pattern of S. f. kellyi. Ashford et al (Reference Ashford, Barnish and Viney1992) postulated that heavy infections in infancy may result from repeated exposure to iL3 within soiled straw bags (bilums) used to carry infants. Transmammary transmission has also been suspected; however, a survey of breastmilk from lactating women in a PNG community did not detect any larvae, although the infection status of the mothers and their infants was not assessed (Barnish and Ashford, Reference Barnish and Ashford1989a). No zoonotic reservoir has been identified, despite investigations into local pigs, chickens and dogs (Kelly and Voge, Reference Kelly and Voge1973; Viney and Ashford, Reference Viney and Ashford1990).

In PNG, S. f. kellyi infection has been uniquely associated with an acute, fatal infantile protein losing enteropathy known as SBS (Ashford et al, Reference Ashford, Barnish and Viney1992). Clinical features include hypoproteinemia, abdominal distension, respiratory distress, eosinophilia, diarrhea and peripheral oedema (Ashford et al, Reference Ashford, Barnish and Viney1992). A remarkably similar syndrome, characterized by villus atrophy, malabsorption, hypoproteinaemia and sudden death, has been described in newborn piglets infected with S. ransomi (Enigk and Dey-Hazra, Reference Enigk and Dey-Hazra1975). Between 1974 and 1983, SBS cases were predominantly reported from 2 regions of PNG, Kanabea in Gulf Province and Wanuma in Madang Province (Ashford et al, Reference Ashford, Vince, Gratten and Bana-Koiri1979; Vince et al, Reference Vince, Ashford, Gratten and Bana-Koiri2005). Elsewhere in the country, SBS was rare and sporadic (Ashford et al, Reference Ashford, Barnish and Viney1992). In Kanabea, approximately 96 cases were recorded, accounting for 8% of infantile mortality (Ashford et al, Reference Ashford, Vince, Gratten and Bana-Koiri1979). Affected infants often passed large numbers of Strongyloides eggs (Ashford et al, Reference Ashford, Vince, Gratten and Bana-Koiri1979), although some high-intensity infections resulted in malnutrition without SBS (Barnish and Harari, Reference Barnish and Harari1989; King and Mascie-Taylor, Reference King and Mascie-Taylor2004). A co-factor in the pathogenesis of SBS has been suggested (Ashford et al, Reference Ashford, Barnish and Viney1992). Given renewed evidence on the co-endemicity of S. f. fuelleborni (potentially synonymous with S. f. kellyi) and an undescribed genospecies closely related to S. ransomi in PNG (Zhao et al, Reference Zhao, Haidamak, Noskova, Ilik, Pafčo, Ford, Masiria, Maure, Kotale, Pomat, Gordon, Navarro, Horwood, Constantinoiu, Greenhill and Bradbury2025), it remains plausible that the latter may be the true aetiologic agent of SBS. This hypothesis is supported by clinical parallels to S. ransomi-induced disease in piglets. Future investigations into strongyloidiasis and SBS cases in PNG should employ species-specific molecular diagnostics and careful morphological characterization to accurately identify the causative agent and establish the epidemiologic link.

Does ‘Strongyloides canis’ exist?

Friedrich Fülleborn first reported natural S. stercoralis infection in dogs in 1911 (Fulleborn, Reference Fulleborn1914). In the years that followed, debate emerged over the taxonomic identity of this canine parasite. Despite being morphologically indistinguishable from human strains, Brumpt (Reference Brumpt1922) postulated that the dog-derived S. stercoralis may represent a separate species. This was based on observed differences in geographical distribution and some life cycle characteristics between human and canine strains, along with unfruitful experimental attempts to establish persistent infections in dogs using human-derived worms (Braun, Reference Braun1899; Brumpt, Reference Brumpt1922; Sandground, Reference Sandground1925; Fülleborn, Reference Fülleborn1927). He proposed naming the canine parasite ‘Strongyloides canis’ (Brumpt, Reference Brumpt1922). However, this designation was largely disregarded in subsequent decades primarily due to the lack of morphological justification (Speare, Reference Speare1986).

This debate has gained renewed attention in the molecular era. Population genetics studies based on partial regions of cox1, 18S rRNA and whole-genome data support the existence of a dog-only lineage of S. stercoralis (cox1 lineage B), alongside a dog-cat-primate shared lineage (cox1 lineage A) (Jaleta et al, Reference Jaleta, Zhou, Bemm, Schär, Khieu, Muth, Odermatt, Lok and Streit2017; Nagayasu et al, Reference Nagayasu, Mppthh, Hortiwakul, Hino, Tanaka, Higashiarakawa, Olia, Taniguchi, Win and Ohashi2017; Barratt et al, Reference Barratt, Lane, Talundzic, Richins, Robertson, Formenti, Pritt, Verocai, Nascimento de Souza and Mato Soares2019). It has been hypothesized that human-infecting S. stercoralis may be a host-adapted variant of an ancestral canine parasite (Nagayasu et al, Reference Nagayasu, Mppthh, Hortiwakul, Hino, Tanaka, Higashiarakawa, Olia, Taniguchi, Win and Ohashi2017; Liu et al, Reference Liu, Ahmr, Sripa, Tangkawattana, Khieu, Nevin, Paterson and Viney2025). Several researchers suggested that this ancestral dog-restricted population, potentially S. stercoralis cox1 lineage B, may represent ‘S. canis’ as proposed by Brumpt (Jaleta et al, Reference Jaleta, Zhou, Bemm, Schär, Khieu, Muth, Odermatt, Lok and Streit2017; Barratt et al, Reference Barratt, Lane, Talundzic, Richins, Robertson, Formenti, Pritt, Verocai, Nascimento de Souza and Mato Soares2019; Barratt and Sapp, Reference Barratt and Sapp2020; Bradbury et al, Reference Bradbury, Pafčo, Nosková and Hasegawa2021).

However, recent genomic analyses have revealed a more complex landscape. Liu et al (Reference Liu, Ahmr, Sripa, Tangkawattana, Khieu, Nevin, Paterson and Viney2025) demonstrated that S. stercoralis infecting humans and dogs in Asia consisted of 2 largely genomically separable but not reproductively isolated populations. This suggests that human and dog lineages may not be taxonomically distinct, as evidenced by occasional introgression between the two (Liu et al, Reference Liu, Ahmr, Sripa, Tangkawattana, Khieu, Nevin, Paterson and Viney2025). Similarly, de Ree et al (Reference de Ree, Nath, Barua, Harbecke, Lee, Rödelsperger and Streit2024) identified S. stercoralis cox1 lineage B in a Bangladesh human. These findings do not rule out the existence of ‘S. canis’, but caution against oversimplifying genotyping results based on single genes or short gene regions. Further whole-genome analysis of worms from a broader geographical range, coupled with detailed morphological analysis, is necessary to confirm or refute the hypothesis of ‘S. canis’ as a distinct species or a subspecies of S. stercoralis.

Canine cryptic strongyloides species

In a faecal metabarcoding survey conducted in remote northern Australia, Beknazarova et al (Reference Beknazarova, Barratt, Bradbury, Lane, Whiley and Ross2019) identified a Strongyloides sp. in 2 dog samples that clustered basally to all known S. stercoralis isolates on a 217 bp cox1 region. One of these dogs also harboured unique 18S rRNA HVR-I and HVR-IV haplotypes (genotype VIII/F) (Beknazarova et al, Reference Beknazarova, Barratt, Bradbury, Lane, Whiley and Ross2019). These findings suggest the possible existence of a novel, undescribed species, or a genetically distinct strain or subspecies of S. stercoralis, in Australian dogs. However, considering that coprophagy is very common in dogs, the possibility that the detected Strongyloides DNA originated from ingested material rather than true infection cannot be ruled out. Further morphological and long-read genetic sequencing analyses are needed to clarify its identity.

Strongyloides felis

Strongyloides felis was first described by Chandler (1925) in cats from India in 1925. Since then, only 3 studies have reported this species (Speare and Tinsley, Reference Speare and Tinsley1986, Reference Speare and Tinsley1987; Jitsamai, Reference Jitsamai2019). In two faecal (Baermann) surveys conducted in North Queensland, Australia, S. felis infection was morphologically confirmed in 41% (83/203) (Speare and Tinsley, Reference Speare and Tinsley1986) and 33.5% (169/504) (Speare and Tinsley, Reference Speare and Tinsley1987) of shelter cats, respectively. A third study in Thailand identified rhabditiform Strongyloides larvae in 1.7% (14/835) of feline faecal samples by PBS–ethyl acetate centrifugal sedimentation microscopy; adults cultured from 6 of these were morphologically identified as S. felis (Jitsamai, Reference Jitsamai2019). However, this morphological identification is dubious, as it described a hexagonal stoma in the free-living female whereas this feature is characteristic of the parasitic female (Speare, Reference Speare1986). Larvae in the remaining positive samples were not identified to species level (Jitsamai, Reference Jitsamai2019) and could represent S. felis or other feline Strongyloides spp.

No other reports of S. felis are available, and its true prevalence and distribution remain obscure. Given its substantial morphological similarity to S. stercoralis (Speare, Reference Speare1986), S. felis is likely underdiagnosed. Both species characteristically shed larvae, rather than eggs, in faeces (Speare, Reference Speare1986; Speare and Tinsley, Reference Speare and Tinsley1986). Differentiation of these two species requires detailed morphological analysis of stomal and tail shape in the parasitic female and vulval morphology in the free-living female. Strongyloides felis is distinguished by a rectangular stoma shape and a more finely tapered tail in the parasitic female, and by the presence of post-vulval narrowing and posterior vulval rotation in the free-living female (Speare, Reference Speare1986). Morphometrics alone cannot reliably differentiate most Strongyloides spp., including S. stercoralis and S. felis (Speare, Reference Speare1986). Accurate identification currently relies on a very advanced level of parasitological expertise, skills which have been largely lost from the parasitology community (Bradbury et al, Reference Bradbury, Sapp, Potters, Mathison, Frean, Mewara, Sheorey, Tamarozzi, Couturier and Chiodini2022). Therefore, the development of species-specific molecular tools is urgently needed to support future studies.

The clinical picture of S. felis infection in cats is not fully clear. This parasite is considered moderately pathogenic in cats, based on observations from both natural and experimental infections (Speare, Reference Speare1986; Speare and Tinsley, Reference Speare and Tinsley1986). Pathological changes include adenomatous metaplasia of the glandular epithelium in the intestinal crypts, where parasitic females reside. Larval migration may cause pulmonary inflammation, with frequent interstitial changes or focal haemorrhage. Watery diarrhoea has been noted in some high-burden infections, though it is not a consistent feature (Speare and Tinsley, Reference Speare and Tinsley1986).

Strongyloides felis appears to infect adult cats more commonly than kittens. In the study by Speare and Tinsley (Reference Speare and Tinsley1986), prevalence of S. felis was found to be 56% (77/138) in adult cats compared to only 9% (6/65) in kittens. The infection tends to be long-lasting; experimentally infected cats maintained patent infections for over a year (Speare and Tinsley, Reference Speare and Tinsley1986). These epidemiological features resemble those of S. stercoralis in humans and dogs, indicating the likelihood of autoinfection and potential lifelong infections (Buonfrate et al, Reference Buonfrate, Bradbury, Watts and Bisoffi2023; Al-Jawabreh et al, Reference Al-Jawabreh, Anderson, Atkinson, Bickford-Smith, Bradbury, Breloer, Bryant, Buonfrate, Cadd, Crooks, Deiana, Grant, Hallem, Hedtke, Hunt, Khieu, Kikuchi, Kounosu, Lastik, van Lieshout, Liu, McSorley, McVeigh, Mousley, Murcott, Nevin, Nosková, Pomari, Reynolds, Ross, Streit, Suleiman, Tiberti and Viney2024). Transmission of S. felis in cats is thought to occur predominantly via skin penetration by iL3 from the environment. In a survey of 65 kittens, no infection was found in those under 3 months of age, suggesting that transmammary transmission is unlikely (Speare and Tinsley, Reference Speare and Tinsley1986).

Strongyloides tumefaciens

Price and Dikmans (Reference Price and Dikmans1941) first described S. tumefaciens in cats from the USA in 1941. During necropsy, multiple tumour-like lesions, some of which were haemorrhagic, were observed in the colonic wall of infected cats. Adult worms were found within the nodules but not in the colonic lumen. These pathological features were considered unique among feline Strongyloides spp. Based on these, and the apparent larger body length of S. tumefaciens (5000 µm) compared to other known feline Strongyloides spp. (<3330 µm) in the parasitic female, a new species was designated (Price and Dikmans, Reference Price and Dikmans1941).

Remarkably, another necropsy survey of cats from St. Kitts (Wulcan et al, Reference Wulcan, Dennis, Ketzis, Bevelock and Verocai2019) observed similar colonic nodules in cats infected by S. stercoralis. The recovered adult worms were morphologically indistinguishable from S. tumefaciens as described by Price and Dikmans (Reference Price and Dikmans1941); however, phylogenetic analysis of a 522 bp region of cox1 placed them within the S. stercoralis lineage A (Wulcan et al, Reference Wulcan, Dennis, Ketzis, Bevelock and Verocai2019). These findings challenged the taxonomic validity of S. tumefaciens.

Since its original description, S. tumefaciens has been reported in cats from the USA (Malone et al, Reference Malone, Butterfield, Williams, Stuart and Travasos1977; Lindsay et al, Reference Lindsay, Blagburn, Stuart and Gosser1987), Brazil (Moura et al, Reference Moura, Jorge, KKGd, Riet-Correa, Abel, Cavalcante, CAd and Bezerra2016) and India (Dubey and Â, Reference Dubey and Â1964). In all instances, species identification was based solely on the presence of colonic nodules, which Wulcan et al (Reference Wulcan, Dennis, Ketzis, Bevelock and Verocai2019) indicated to be unreliable.

Strongyloides planiceps

Strongyloides planiceps was initially reported by R.T. Leiper in rusty tiger cats (Prionailurus rubiginosus) from Malaysia and later described in domestic cats by Rogers (Reference Rogers1939). A distinguishing feature of S. planiceps is that larvated eggs, rather than rhabditiform larvae, are shed in faeces (Rogers, Reference Rogers1939; Speare, Reference Speare1986). Morphologically, the parasitic female of S. planiceps has spiralled ovaries and a bluntly rounded tail, contrasting with the straight ovaries and narrowly tapered tail of S. stercoralis and S. felis (Rogers, Reference Rogers1939; Speare, Reference Speare1986). Unlike S. stercoralis, the life cycle of S. planiceps involves multiple free-living generations, up to 9, as demonstrated experimentally (Yamada et al, Reference Yamada, Matsuda, Nakazawa and Arizono1991).

Strongyloides planiceps is believed to primarily infect wild felids and only sporadically occur in domestic cats (Horie et al, Reference Horie, Noda, Noda and Higashino1981; Fukase et al, Reference Fukase, Chinone and Itagaki1983; El-Seify et al, Reference El-Seify, Aggour, Sultan and Marey2017). Reports of S. planiceps have almost exclusively come from Japan (Arizono, Reference Arizono1976; Horie et al, Reference Horie, Noda, Noda and Onishi1980, Reference Horie, Noda, Noda and Higashino1981; Fukase et al, Reference Fukase, Chinone and Itagaki1983, Reference Fukase, Chinone and Itagaki1985; Sato et al, Reference Sato, Suzuki, Osanai, Kamiya and Furuoka2006). Although numerous feline surveys from other countries have reported egg-shedding Strongyloides spp. in cat faeces, none identified the parasites to the species level, so it is unknown whether they represent S. planiceps (Abbas et al, Reference Abbas, Al-Araby, Elmishmishy and El-Alfy2022; Adams et al, Reference Adams, Elliot, Algar and Brazell2008; Adhikari et al, Reference Adhikari, Dhakal, Ale, Regmi and Ghimire2023; Borkataki et al, Reference Borkataki, Katoch, Goswami, Godara, Khajuria, Yadav and Kaur2013; de Sousa¹ et al. Reference de Sousa¹, de Sousa¹ and dos Santos Sousa¹2015; Heidt et al, Reference Heidt, Rucker, Kennedy and Baeyens1988; Monteiro et al, Reference Monteiro, Ramos, Calado, Lima, ICdN, Tenório, MAdG and Alves2016; Nyambura Njuguna et al, Reference Nyambura Njuguna, Kagira, Muturi Karanja, Ngotho, Mutharia and Wangari Maina2017; Solórzano-García et al, Reference Solórzano-García, White-Day, Gómez-Contreras, Cristóbal-Azkárate, Osorio-Sarabia and Rodríguez-Luna2017; Susilowati, Reference Susilowati1985). One study from Egypt found S. planiceps in one of 170 cat faecal samples, but the method for confirming species was not reported (El-Seify et al, Reference El-Seify, Aggour, Sultan and Marey2017). It is likely that this helminth is significantly underreported in cats globally.

Feline cryptic Strongyloides species

Two studies reported molecular evidence of a Strongyloides sp. in cats (Jitsamai, Reference Jitsamai2019; Ko et al, Reference Ko, Suzuki, Canales-Ramos, MPPTH, Htike, Yoshida, Montes, Morishita, Gotuzzo and Maruyama2020). Ko et al (Reference Ko, Suzuki, Canales-Ramos, MPPTH, Htike, Yoshida, Montes, Morishita, Gotuzzo and Maruyama2020) analysed partial cox1 and protein-coding mitochondrial genome sequences of 70 Strongyloides isolates from 19 cats in Myanmar and found that they formed a sister taxon to S. stercoralis. A similar finding was reported by Jitsamai (Reference Jitsamai2019) based on a 708 bp region of 18S rRNA. It has been suggested that the Strongyloides detected in both studies may represent S. felis, but without morphological confirmation, this remains speculative.