Is strongyloidiasis a zoonosis from dogs?

Abstract

Strongyloides stercoralis infection remains a major veterinary and public health challenge globally. This chronic and potentially lifelong disease has fatal outcomes in immunosuppressed people and dogs. Currently, the role of dogs in the transmission cycle of human strongyloidiasis remains enigmatic. While zoonotic transmission to humans from companion animals has been proposed, this has not been confirmed. Modern molecular methods have allowed greater opportunity to explore the genotypes of S. stercoralis in dogs and humans. Work thus far has demonstrated that at least two distinct lineages exist, one apparently confined to canine hosts and one found in canine, feline, human and non-human primate hosts. Although genotyping of dog and human isolates from the same village has demonstrated identical genotypes in both species, coprophagia of human waste by dogs confounds interpretation. It remains unclear if dogs act as a zoonotic reservoir for human infection, or vice versa, or if this occurs only in some regions of the world and not in others. These questions must be answered before effective control strategies for strongyloidiasis can be instituted. This review explores the evidence for and against cross-species transmission of S. stercoralis between dogs and humans and summarizes future directions for research in this area.

This article is part of the Theo Murphy meeting Issue ‘Strongyloides: omics to worm-free populations’.

1. Introduction

Parasitic nematodes of the genus Strongyloides spp. remain a major veterinary and public health challenge globally [1–7]. Human strongyloidiasis is in most cases caused by infection with Strongyloides stercoralis. It is a chronic and potentially lifelong disease with potentially fatal outcomes in immunosuppressed dogs [7,8] and people [1,6,9]. Strongyloides stercoralis are spread by exposure to larvae deposited in soil following defaecation. Infective larvae pass through the exposed skin of the host and migrate via the lungs, or through the organs, to the small intestine. Within the intestine, they develop into female parasitic adults which reproduce through parthenogenesis [9]. Current global estimates indicate that approximately 600 million people [2] and 6% of dogs [3,5] are infected with S. stercoralis. Infection is more common in tropical, sub-tropical regions but the prevalence in both dogs and humans may vary widely in different geographical locations [2,3]. Marginalized and resource-poor communities, where the accessibility of adequate sanitation facilities and both human healthcare and canine veterinary care may be sparse, are disproportionately affected [10–13].

Since the very early days of S. stercoralis research there has been a debate if dogs carry the same or just a similar species of Strongyloides as humans [14–16] and, as a consequence, if dogs are a putative source of zoonotic human infection with S. stercoralis (or vice versa). Although knowing this would be of great importance for devising effective strongyloidiasis control and prevention measures in animals or people, so far, this question cannot be conclusively answered. There are major gaps in our knowledge of S. stercoralis and its zoonotic potential. For this article, we limit ourselves to S. stercoralis, well knowing that similar problems exist with other parasites, for example, Ascaris spp. in pigs and humans [17–19].

2. Historical background

Strongyloides stercoralis is the most studied Strongyloides species and has been found infecting domestic and wild canids (dogs), cats, non-human primates (NHPs) and people [7,20–22]. It was first discovered as a parasite of humans by Louis Alexis Normand, with the assistance of Arthur Réné Jean Baptiste Bavay in 1876 [23]. Friedrich Fülleborn first reported S. stercoralis as a natural infection of dogs in China and Japan in 1911 and 1914 [14,24]. Frank and Mary Ware later reported natural infections from dogs in India in 1925 [25]. Initially, there was confusion over the taxonomic status of human and dog strains. Although morphologically identical, Emile Brumpt considered S. stercoralis in dogs and humans to be distinct taxa owing to the apparent differences in geographical range for dog and human strongyloidiasis, a reported difference in the direct or indirect life cycle in dog and human strains, and the difficulties in establishing lasting infection in dogs with human strains [16]. He proposed that dog infecting strains be named ‘Strongyloides canis’ [16].

3. Cross-infection studies

Cross-infection experiments between dogs and people in several parts of the world during the late nineteenth and throughout the twentieth century yielded variable results which did not assist in clarifying the host specificity of S. stercoralis (table 1; [15,16,27,29,30,32,33,35,37,38,40,41,43,44]). These experiments used S. stercoralis isolates from humans from several regions of the world. In most of these experiments, the experimental animals were exposed to unnaturally large doses (1000–430 000 individuals) of infective filariform larvae (iL3). In some cases, dogs were refractory to infection with human strains or self-cured within 3–13 weeks of inoculation. In other cases, patent infection lasting more three months or more was established [33]. Immunosuppression of dogs increased the likelihood of patent infection, and the duration of larval passage [36,39–42]. Reviewing the available data, there appears to be a trend towards dogs inoculated with human strains which had been passaged through another dog maintaining longer durations of larval excretion than those directly inoculated with infective larvae taken from human hosts (table 1). This might be explained by the physiological adaptation of strains during passage in the new host. However, this hypothesis is speculative owing to the non-comparable nature of the historical experimental data and that many dogs died or were sacrificed within two months of infection. In other cases, passage through multiple dogs appeared to reduce virulence to the point where dogs became refractory to infection [35]. Studies on the capacity of canine and human strains to physiologically adapt to other hosts are warranted.

Table 1.

A summary of human/dog cross-species transmission studies performed to date from the scientific literature. (Year: year/s experiments conducted; geographical origin of infection: country or region where the donor host was infected; origin host: the donor host species; passage host: the species of host that the worms were passaged through prior to inoculation into the final recipient (if this occurred); recipient host/s: species of the final recipient host or hosts; wks: weeks; mo: months; n.s.: not stated; n.a.: not applicable.)

year/s	geographical origin of infection	origin host	passage host	recipient host/s (number, age)	no. larvae inoculated and mode of infection	immunosuppression	diagnostic method/s	prepatent period	duration of larval excretion	notes	reference
1899	—	human	—	dog (n = 1, age n.s.)	‘numerous’ larvae orally administered in milk	none	microscopy	refractory	refractory	dog developed diarrhoea, but no larval passage identified. Dog recovered while donor host died of heavy S. stercoralis infection	[26]
1914	‘exotic’ origin	human	—	dogs (n = n.s., age n.s.)	n.s.	none	n.s.	n.s.	2–3 weeks	a strain from a laboratory assistant of ‘exotic origin’. Fűlleborn revisits these experiments and notes that infection with the human-derived strain lasted less time than the dog-derived strain in canine recipient hosts	[14,15]
1922	Africa (Democratic Republic of Congo)	human	—	dogs (n = n.s., age n.s.)	n.s.	none	n.s.	n.s.	n.s.	patent infection, duration n.s.	[16]
1925	North America (Georgia)	human	—	dog (n = 1, age n.s.)	‘many thousands’ iL3 percutaneous on abdomen, reinfected at 7 days, reinfected at 3 weeks	none	charcoal culture	7 days	8 weeks (ongoing at sacrifice)	‘very large numbers’ of S. stercoralis found throughout small intestine on necropsy	[27]
1925	North America (Georgia)	human	—	dog (n = 1, age n.s.)	800 iL3 percutaneous on abdomen	none	charcoal culture	n.s.	>301 days		[27]
1925	North America (Georgia)	human	—	dog (n = 1, age n.s.)	500 iL3 percutaneous on abdomen	none	charcoal culture	n.s.	>20 weeks (ongoing at sacrifice)	large numbers of larvae in intestine on necropsy	[27]
1925	North America (Georgia)	human	passage through one dog	human (n = 1, age n.s.)	20 iL3 percutaneous, site n.s.	none	charcoal culture	8 days	3 days	no larvae recovered after 3 days	[27]
1926	North America (Georgia)	human	—	dogs (n = 14, ‘young and healthy, many between 2 and 3 years’)	iL3 percutaneous, site n.s.	none	Baermann sedimentation	n.s.	2 mo –> 10 mo	initial mucoid diarrhoea in all dogs, with blood in two dogs, for 2–5 days. Five dogs progressed to chronic diarrhoea. Three dogs died of chronic diarrhoea, another two died of lobar pneumonia	[28]
1926	North America (Georgia)	human	—	dogs (n = 1, ∼6 mo)	5000 iL3 and a further 10 000 iL3 1 week later, percutaneous on the abdomen	none	Baermann sedimentation	n.s.	n.s.	chronic diarrhoea and emaciation despite being well-fed. ‘Countless’ parasitic females recovered upon necropsy at 9 weeks, fibrous thickening of the intestinal mucosa, extensive multi-lobar pneumonia	[28]
1925	Caribbean (Puerto Rico)	human	—	dog (n = 1, age n.s.)	6500 iL3 percutaneous, site n.s., reinfected with 6500 iL3 6 weeks later	none	charcoal culture	n.s.	n.s.	patent infection, duration n.s.	[29]
1926	Caribbean (Puerto Rico)	human	—	dog (n = 1, age n.s.)	800–900 iL3 percutaneous, site n.s.,	none	charcoal culture	n.s.	n.s.	‘light’ patent infection, duration n.s.	[29]
1926	Caribbean (Puerto Rico)	human	passage through one dog	dog (n = 1, age n.s.)	2000 iL3 percutaneous, site n.s.,	none	charcoal culture	n.s.	n.s.	patent infection, duration n.s.	[29]
1926	Caribbean (Puerto Rico)	human	passage through two dogs	dog (n = 1, age n.s.)	600 iL3 percutaneous, site n.s.,	none	charcoal culture	n.s.	n.s.	patent infection, duration n.s.	[29]
1927	Africa (East Africa)	human	—	dog (n = 1, age n.s.)	n.s.	none	Baermann sedimentation	n.s.	n.s.	experimental transfer ‘almost always’ resulted in patent infection, duration n.s.	[15]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼8 mo)	2900+ iL3 percutaneous on the abdomen, reinfected with a total of 89 000 larvae at intervals up to the 32nd week	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	7 days	6–10 weeks	no larvae recovered after 7 weeks. Attempts at reinfection failed	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼3 mo)	210 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	9 days	‘many months’		[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼5 mo)	900 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	n.s.	‘many months’		[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼4 mo)	4600 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	n.s.	8 weeks (until death)	dog died 8 weeks after infection, heavy infection seen on necropsy	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼10 mo)	450 iL3 percutaneous on the abdomen reinfected with 3500 iL3 after 3 weeks	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	7 days	6 weeks (until death)	dog died 6 weeks after infection, heavy infection seen on necropsy	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼15 mo)	10 000 iL3 percutaneous on the abdomen reinfected with 3000 iL3 after 5 weeks	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	8 days	n.s.	dog died 6 weeks after infection, heavy infection seen on necropsy	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, 30+ mo)	20 000 iL3 percutaneous on the abdomen reinfected with 12 000 iL3 after 3 weeks	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	9 days	n.s.	dog died 6 weeks after infection, heavy infection seen on necropsy	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼3 mo)	20 000 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	7 days	>4 weeks (until death)	dog died during time when observations were suspended owing to vacation	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, 24+ mo)	8000 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	n.s.	15 weeks (until death)	dog died 15 weeks after infection, heavy infection seen on necropsy	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, 18+ mo)	6000 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	7 days	>4 weeks	larval output peaked at 4 weeks and reduced to nil thereafter. Attempts at reinfection failed	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼120 mo)	6500 iL3 percutaneous on the abdomen, reinfected with 20 000 iL3 after 8 weeks, reinfected with 35 000 iL3 after 17 weeks	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	7 days	7 weeks	first reinfection (8 weeks) did not result in larval output, second reinfection (17 weeks) resulted in ongoing light infection. Animal escaped and was lost before end of experiment	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼24 mo)	17 000 iL3 percutaneous on the abdomen, reinfected with 28 000 iL3 after 12 weeks, reinfected with 16 200 iL3 after 35 weeks, reinfected with 25 000 iL3 after 37 weeks	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	7 days	7 weeks	no larvae recovered after 7 weeks. Attempts at reinfection failed	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼12 mo)	52 000 iL3 percutaneous on the abdomen, reinfected with 403 000 iL3 after 4 weeks via sub-cutaneous injection, reinfected with 87 000 iL3 after 11 weeks by oral administration	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	6 days	7 weeks	no larvae recovered after 7 weeks. Attempts at reinfection failed	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼18 mo)	430 000 iL3 percutaneous on the abdomen reinfected with 24 000 iL3 after 3 weeks, reinfected with 19 000 iL3 after 23 weeks	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	5 days	11 weeks	no larvae recovered after 11 weeks. Further attempt at reinfection failed	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼30 mo)	8100 iL3 percutaneous on the abdomen reinfected with 14 000 iL3 after 3 weeks, reinfected with 121 000 iL3 after 26 weeks	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	n.s.	12 weeks	no larvae recovered after 12 weeks. Attempts at reinfection failed	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼5 mo)	5000 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	7 days	17 weeks (ongoing at sacrifice)	‘massive infection’ seen at necropsy	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼5 mo)	8000 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	5 days	18 weeks (ongoing at sacrifice)	‘massive infection’ seen at necropsy	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, ∼18 mo)	8000 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	7 days	12 weeks (ongoing at sacrifice)	‘massive infection’ seen at necropsy	[30]
1928	North America (Georgia)	human	passage through multiple puppies	dogs (n = 1, 60+ mo)	16 600 iL3 percutaneous on the abdomen	none, but poor nutrition owing to poor diet	charcoal culture, followed by Baermannisation	8 days	5 weeks (ongoing at sacrifice)	‘many thousands’ of parasites seen at necropsy	[30]
1933	North America (Louisiana), isolate A	human A	—	dog (n = 1, age n.s.)	500 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	10 days	13 days (until death)	‘bronchial involvement’ on necropsy	[31]
1933	North America (Louisiana), isolate A	human A	passage through one dog	dog (n = 1, age n.s.)	2000 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	9 days	105 days (ongoing at sacrifice)	‘heavy infection’ on necropsy	[31]
1933	North America (Louisiana), isolate A	human A	passage through two dogs	dog (n = 1, age n.s.)	2000 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	15 days	>4 months	profound dyspnoea and rales at 2 weeks 27 following incoculation (treated with gentian violet, recovered). Dog still passing larvae when published	[31]
1933	North America (Louisiana), isolate A	human A	passage through two dogs	dog (n = 1, age n.s.)	1000 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	—	—	died 3 days after inoculation, prior to patency ‘metamorphosing filariform larvae and immature adults in the lungs and trachea’ on necropsy	[31]
1933	North America (Louisiana), isolate B	human B	—	dog (n = 1, age n.s.)	100 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	14 days	>1 month (actual duration n.s.)		[31]
1933	North America (Louisiana), isolate B	human B	passage through one dog	dog (n = 1, age n.s.)	1000 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	19 days	3 weeks (sparse larvae passed)	3 months after stools became negative, 12 live and active but barren parasitic females were recovered from duodenum and jejunum upon necropsy	[31]
1933	North America (Louisiana), isolate C	human C	—	dog (n = 1, age n.s.)	2000 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	17 days	4 months	stools consistently negative after 4 months	[31]
1933	North America (Louisiana), isolate C	human C	—	dog (n = 1, age n.s.)	1000 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	9 days	10 days (until death)	died at day 21 post-inoculation, ‘profound haemorrhagic congestion for the lungs…from several dozen immature parasitic worms were recovered’ parasitic adults in jejunum and duodenum on necropsy	[31]
1933	North America (Louisiana), isolate C	human C	—	dog (n = 1, age n.s.)	2000 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	5 days	8 months (intermittent larval shedding)	dog still infected and shedding larvae in ‘arrhythmic showers’ 8 months after infection	[31]
1933	North America (Louisiana), isolate C	human C	passage through one dog	dog (n = 1, age n.s.)	500 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	refractory	refractory		[31]
1933	North America (Louisiana), isolate F	human F	—	dog (n = 1, age n.s.)	500 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	12 days	44 days (until death)	dog died of respiratory involvement after 1.5 months	[31]
1933	North America (Louisiana), isolate F	human F	passage through one dog	dog (n = 1, age n.s.)	2000 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	1 L1 larva on day 3, 1 L1 larva on day 7	11 days (until death)	dog died of ‘overwhelming Strongyloides infection for the small and large bowels, superimposed on a haemorrhagic pneumonitis’	[31]
1933	North America (Louisiana), isolate F	human F	passage through two dogs	dog (n = 1, age n.s.)	500 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	13 days	1 month	dog alive at >5 months after inoculation and still no longer shedding larvae	[31]
1933	North America (Louisiana), isolate G	human G	—	dog (n = 1, age n.s.)	500 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	no larval shedding	no larval shedding	diarrhoea from from day 3, ‘profound dyspnoea’ and death on day 9. Pneumonitis but no Strongyloides in lungs, two immature parasitic adults in the colonic wall on necropsy	[31]
1933	North America (Louisiana), isolate H	human H	—	dog (n = 1, age n.s.)	100 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	1 egg on day 13, L1 larvae passed from day 16	1 month (sparse larval shedding)	dog alive at >4 months after inoculation and still no longer shedding larvae	[31]
1933	North America (Louisiana), isolate J	human J	—	dog (n = 1, age n.s.)	500 iL3 percutaneous, site n.s.	none	culture (method n.s.) and microscopy	no larval shedding	no larval shedding	animal sacrificed owing to marked constipation at day 15. Moderate parasitization of the duodenal wall on necropsy	[31]
1938	North America (Massachusetts)	5 week old puppy	—	human (n = 1, ‘adult’)	n.s.	none	n.s.	refractory	refractory	refractory to infection	[32]
1938	southeast Asia (Vietnam)	human	—	dogs (n = n.s., 4 mo)	‘dermal route’ a few by oral route. Number of larvae inoculated n.s., but probably very high based on results described	none	Baermann culture	7 days	n.s.	those with massive infections died within 10–12 days of patency, those with moderate infections survived up to 20 days. Ulceration and necrosis of the duodenum on necropsy. Oral infection led to very light infections	[33]
1938	southeast Asia (Vietnam)	human	—	dogs (n = n.s., ‘older’)	‘dermal route’	none	Baermann culture	7 days	4 months	‘older’ dogs do not die of infections. Larval passage is only detectable on culture or necropsy, and not by direct microscopy. Virulence did not attenuate upon passage through six separate dogs	[33]
1938–1945	southeast Asia (Vietnam), North Africa and Caribbean (Antilles)	human	passage through multiple dogs	dog s (n = many, 4 mo)	percutaneous, some possibly sub-cutaneous	none	charcoal culture	n.s.	n.s.	passage of human strains through multiple dogs over more than a decade. Older dogs survived up to 220 days. Although larval output may be low, all dogs remained infected upon necropsy	[34]
1938–1945	Caribbean (Antilles)	human		dog (n = 1, n.s.)	100 iL3 percutaneous, site n.s.	none	necropsy	n.a.	n.a.	necropsy at 15 days demonstrated no infection	[35]
1938–1945	Caribbean (Antilles)	human		dog (n = 1, n.s.)	2000 iL3 percutaneous, site n.s.	none	necropsy	n.a.	n.a.	necropsy at 14 days demonstrated no infection
1938–1945	Caribbean (Antilles)	human		dog (n = 1, n.s.)	100 iL3 percutaneous, site n.s.	none	necropsy	<13 days	13 days (ongoing at sacrifice)	necropsy at 13 days demonstrated 12 adult parasitic females	[35]
1938–1945	Caribbean (Antilles)	human		dog (n = 1, n.s.)	2000 iL3 percutaneous, site n.s.	none	necropsy	<15 days	15 days (ongoing at sacrifice)	necropsy at 15 days demonstrated 53 adult parasitic females	[35]
1938–1945	Caribbean (Antilles)	human	passage through one dog	dog (n = 1, n.s.)	10 000 iL3 sub-cutaneous injection, site n.s.	none	necropsy	n.a.	n.a.	necropsy at 4 days demonstrated no parasites in trachea, lungs or duodenum	[35]
1938–1945	Caribbean (Antilles)	human	passage through one dog	dog (n = 1, age n.s.)	10 000 iL3 sub-cutaneous injection, site n.s.	none	necropsy	n.a.	14 days (ongoing at sacrifice)	necropsy at 14 days, 20 adult parasitic females in duodenum	[35]
1938–1945	North Africa	human		dog (n = 3, age n.s.)	500 iL3 (500 direct, 500 indirect and 500 mixed cycle to 1 dog each), percutaneous, site n.s.	none	necropsy	n.a.	40 days (ongoing at sacrifice)	necropsy at 40 days, adult parasitic females recovered from all	[35]
1938–1945	North Africa	human	passage through multiple dogs	dog (n = 12, age n.s.)	500 iL3 (500 direct, 500 indirect and 500 mixed cycle to 1 dog each), percutaneous, site n.s.	none	necropsy	n.a.	40 days (ongoing at sacrifice)	necropsy at 40 days, adult parasitic females recovered. All dogs were refractory to the fifth passage of larvae (indicating loss of virulence in passage)	[35]
1938–1945	North Africa	human	? passage through multiple dogs	dog (n = 1, age n.s.)	20 000 iL3, percutaneous, site n.s.	none	necropsy	refractory	refractory		[35]
1938–1945	southeast Asia (Vietnam)	human	? passage through multiple dogs	dog (n = 1, age n.s.)	10 000 iL3, percutaneous, site n.s.	none	necropsy	n.a.	<17 days (until death)	same individual as above, refractory to infection with 20 000 iL3 of the North African strain. Was superinfected 40 days later with a Vietnamese strain and died 17 days afterwards of massive infection	[35]
1951–1952	Africa (Guinea)	human	—	dog (n = 1, 3 mo)	20 000 iL3 percutaneous, site n.s.	cortisone, adrenocorticotropic hormone	charcoal culture	14 days	180 days	no larvae detectable after 180 days post infection	[36]
1951–1952	Africa (Guinea)	human	—	dog (n = 1, 3 mo)	10 000 iL3 percutaneous, site n.s.	cortisone, adrenocorticotropic hormone	charcoal culture	<16 days	34 days	dog dies of pneumonia 80 days after infection, necropsy reveals no S. stercoralis remaining	[36]
1951–1952	Africa (Guinea) and southeast Asia (Vietnam)	human	—	dog (n = 1, 3 mo)	10 000 iL3 of Guinea strain percutaneous, site n.s. 10 000 iL3 of Vietnamese strain percutaneous, site n.s. 10 days after above Guinea strain inoculation	cortisone, adrenocorticotropic hormone	charcoal culture	<16 days	32 days	no culturable larvae at 32 days	[36]
1951–1952	Africa (Guinea)	human	passage through one dog	dog (n = 1, 3 mo)	10 000 iL3 percutaneous, site n.s.	cortisone, adrenocorticotropic hormone	charcoal culture	<17 days	120 days		[36]
1951–1952	southeast Asia (Vietnam)	human	—	dog (n = 1, ‘elderly’)	‘massive inoculations’ twice over 2 years	none	charcoal culture	—	—	refractory to infection	[36]
1951–1952	southeast Asia (Vietnam)	human	—	dog (n = 1, ‘elderly’)	26 000 iL3 percutaneous, site n.s.	cortisone, adrenocorticotropic hormone	charcoal culture	15 days	40 days	same individual as above. Cortisone begun 8 days prior to infection and continued 4 days afterward. Dog self-cured at 40 days. No necropsy reported	[36]
1952	southeast Asia (Myanmar/Thailand)	human	—	dog (n = 1, 7 wks)	10 000 iL3 percutaneous inguinal skin exposure	none	culture	22 days	5 days	very few larvae excreted, very low intensity infection	[37]
1974	North America (New York)	dog	human	dogs (n = 6, 3 mo)	1250 iL3 by oral administration	none		9–11 days	n.s.	parasitic females recovered from one dog on necropsy, no data on date of euthanasia, nor if necropsy was performed on the other five dogs	[38]
1981	S.E. Asia (Myanmar/Thailanda)	humana	nil	dog (n = 1, ‘puppy’)	2000 iL3 percutaneous anterior abdominal wall	prednisolone (recipient)	microscopy in Sedgewick-Rafter type chambers	3 weeks	15 months (ongoing at sacrifice)		[39]
1982	S.E. Asia (Myanmar/Thailand)	humana	passage through one dog	dog (n = 4, 6–8 wks)	1500 iL3 percutaneous inguinal skin exposure and 1500 iL3 sub-cutaneous injection	none	microscopy in Sedgewick-Rafter type chambers	2 weeks	12 weeks		[40]
1982	southeast Asia (Myanmar/Thailand)	humana	passage through multiple dogs	dogs (n = 4, 7 mo)	500 iL3 (mode unstated)	none	microscopy in Sedgewick-Rafter type chambers	refractory	refractory		[40]
1982	southeast Asia (Myanmar/Thailand)	humana	passage through multiple dogs	dogs (n = 4, 7 mo)	500 iL3 (mode unstated)	none	microscopy in Sedgewick-Rafter type chambers	2.5 weeks	n.s.		[40]
1982	southeast Asia (Myanmar/Thailand)	humana	passage through multiple dogs	dog (n = 1, ‘puppy’)	400 iL3 (mode unstated) followed by 4000 iL3 at 6 weeks, then monthly challenges with 2000, 8000 and 5000 larvae	none	microscopy in Sedgewick-Rafter type chambers	<6 weeks	20 weeks (ongoing at sacrifice)		[40]
1983	southeast Asia (Myanmar/Thailand)	humana	passage through multiple dogs	dogs (n = 2, ‘adults’)	5000 iL3 percutaneous inguinal skin exposure	prednisolone 4 weeks after infection	microscopy in Sedgewick-Rafter type chambers	3 weeks	9 and 14 weeks (ongoing at sacrifice)		[40]
1983	southeast Asia (Myanmar/Thailand)	humana	passage through multiple dogs	dog (n = 1, ‘adult’)	5000 iL3 percutaneous inguinal skin exposure	prednisolone 4 weeks after infection + azathioprine at 10 weeks	microscopy in Sedgewick-Rafter type chambers	3 weeks	24 weeks (ongoing at sacrifice)		[41]
1983	southeast Asia (Myanmar/Thailand)	humana	passage through multiple dogs	dog (n = 1, ‘adult’)	5000 iL3 percutaneous inguinal skin exposure	none	microscopy in Sedgewick-Rafter type chambers	3 weeks	13 weeks		[41]
1983	southeast Asia (Myanmar/Thailand)	humana	passage through multiple dogs	dog (n = 1, 9 wks)	5000 iL3 percutaneous inguinal skin exposure	prednisolone + azathioprine from 3 days prior to infection	microscopy in Sedgewick-Rafter type chambers	2 weeks	20 days (ongoing at sacrifice)	dog euthanized owing to severe strongyloidiasis	[41]
1983	southeast Asia (Myanmar/Thailand)	humana	passage through multiple dogs	dog (n = 1, age n.s.)	6000 iL3 percutaneous inguinal skin exposure	prednisolone + azathioprine from 3 days prior to infection	microscopy in Sedgewick-Rafter type chambers	n.s.	3 weeks (until death)	animal died during course of experiment, cause of death not stated, no necropsy was performed	[41]
1996	southeast Asia (Thailand)	human	passage through one dog	dogsb (n = 2, 6 mo)	3000 iL3 sub-cutaneous injection into nape of the neck	initially none. Methylprednisone was administered for 1 mo at 6 mo post-infection	Baermann sedimentation	0.5 and 1 mo	2 mo and 3.5 mo Recrudescence on immunosuppression of 0.75 mo and 2.8 mo duration	despite absence of larvae in faeces, gravid parasitic females were recovered from both dogs upon necropsy at 12 mo after initial infection	[42]

^aOriginal source infection was a human infected in the Myanmar/Thailand region 35 years previously (D.I. Grove 5 November 2021, personal communication).

^bDogs had been immunologically challenged three times with 3000 heat killed iL3 at 20 day intervals by sub-cutaneous injection. This experiment began 14 days after the final challenge.

Infection of a human with S. stercoralis derived from a naturally infected dog has, to our knowledge, only been attempted twice, on both occasions with strains acquired in the United States of America (USA). In one case, the human subject was refractory to infection [32], in the other case patency was established 8 days after infection, but larval excretion was short-lived (4 days duration) [27].

All cross-transmission experiments predate the era of molecular genotyping and therefore the genotype of S. stercoralis of the strains used remains unknown. Historical experiments infecting of dogs with human-derived S. stercoralis had varying success at establishing long-term patent infection (table 1). Whether some genotypes of S. stercoralis have better capacity to achieve long-term infection in multiple host species, while others are largely host-restricted, requires exploration. The extensive series of experiments performed by Galliard between the 1930s and the 1950s, would strongly argue in this direction [33–36]. While working in what today is Vietnam, this author described transferring local human-derived S. stercoralis to dogs as easy [33]. He maintained in dogs 19 different human-derived isolates for up to several years and up to more than 80 passages [33]. On the other hand, he found infecting dogs with isolates he had received from Africa and the Caribbean to be far more difficult and only partially successful [33–35]. He described variable responses to infection with the same isolate in different dogs [34–36]. In one case where an individual dog was refractory to infection with a north African isolate, but developed massive infection and died 17 days after infection with a Vietnamese strain 40 days later [35].

It might be suggested that different dog breeds are variably susceptible for human-derived S. stercoralis. It is notable that Galliard found infection of dogs with a human strain from Vietnam easier than human strains from north Africa and the Antilles [33,34]. Despite this, necropsy surveillance of 1676 dogs in Hanoi found only four cases of Strongyloides spp. infection, in contrast to reports of higher canine prevalence from some other areas of Asia [34]. Whether the geographical source (and genotype—refer to below discussion) of human infecting S. stercoralis isolates might influence the cross-infectivity of S. stercoralis isolates between dogs and humans should be explored.

A problem in interpreting many historical cross-species transmission experiments is the poorly understood phenomenon of S. stercoralis parasitic females entering a barren phase during which very low, or no larval output may be seen, but after which a female may return to fecundity [45]. This appears to have occurred in at least one dog experiment where live, but barren, females were recovered on necropsy three months after larval cultures of stools became negative [31]. Hence, the absence of excreted larvae in the stool of an experimental subject does not necessarily mean the absence of parasitic females in the gut with the capacity to return to patency.

There are also several issues with all historical cross-species transmission experiments that limit the comparability of findings to each other, and to natural infections. First of all, for understandable reasons, they are rather few in number. They were performed using different isolates, following different infection procedures and using different, but compared with natural infections, probably high, infective doses. Some experiments do not clearly report if the test dogs were demonstrably free of Strongyloides infection prior to experimental inoculation [14–16,26–29,34,35]. Great variation in larval inoculation method, diagnostic methods, time to sacrifice and necropsy, and detail in reported experimental outcomes reported further confound comparison of results between these studies.

Another important consideration is that controls using a synonymous host species to the larval donor were never performed. This means that it cannot be determined if the same outcome would have transpired in simultaneous cross-transmission experiments between dogs and dogs, or humans and humans with the same isolates. Furthermore, it remains unclear how often natural exposure to S. stercoralis infection leads to an acute patent infection in humans and dogs, what percentage of acute patent infections become chronic, or how often human infections spontaneously resolve.

Modern ethical limitations would make repeating experimental cross-species infection studies in humans difficult. Although human infection experiments with Necator americanus are being performed [46], the autoinfective nature and potentially life-threatening complications of strongyloidiasis mean that equivalent experimentation using S. stercoralis would require much closer monitoring in experimental volunteers. Despite this obstacle, such experiments, preferably using S. stercoralis of varying genotypes sourced from dogs and humans in different geographical regions of the world and simultaneously infecting human and canine hosts with the same batch of infective larvae, would greatly inform our understanding of the host specificity of this parasite. As a possibly more acceptable alternative one could treat the people in villages with a high incidence of S. stercoralis while simultaneously treating, or not treating, the dogs in those villages. It could then be determined if treating the dogs in the test villages significantly reduced the recovery of S. stercoralis from humans compared to the control (dogs not treated) villages.

4. Genotyping studies

Molecular taxonomy became routine for nematodes approximately 25 years ago and opened new opportunities to detect morphologically inapparent differences between worms [47–50]. To our knowledge, the first group to use such technology to compare S. stercoralis from humans and dogs was Ramachandran et al. [51] who used polymerase chain reaction (PCR) amplification and restriction digestion of a portion of the nuclear ribosomal locus and noted a difference between human and dog derived S. stercoralis. Hasegawa et al. [52,53] developed molecular taxonomic approaches optimized for Strongyloides spp. based on PCR amplification and sequencing of hypervariable regions (HVR I–HVR IV) in the nuclear small ribosomal subunit (SSU), which showed little variability within species of Strongyloides but tends to differ between species, and of a portion of the mitochondrial cytochrome c oxidase subunit I (cox1), which is suitable to detect within species differences [52,53]. Hasegawa and colleagues used these methods to analyse S. stercoralis isolated from different hosts (humans, dogs and NHPs) and from different geographical locations in Asia, the USA and Africa [53]. These authors found that the S. stercoralis they investigated fell into phylogenetic groups according to the host (primates, including humans, versus dogs) and not according to geographical location. Based on this finding, Hasegawa et al. [53] suggested that S. stercoralis in humans and in dogs belong to separate sub-clades, which, if true, would make transmission between these species rather unlikely. While the molecular markers used in these studies have proved useful for a first assessment, their short length and very limited number of polymorphic sites restricts their discriminatory power. The fact that the SSU and the cox1 locus exist in multiple copies, which may slightly vary in the genome (noted for example for the SSU in S. stercoralis by Zhou et al. [54]) may further confound the interpretation. Also, while the studies mentioned above covered a large geographical range, the number of worms investigated was rather small and no dog and human-derived worms originating from the immediate vicinity of each other were analysed.

In 2017, Nagayasu et al. [55] and Jaleta et al. [56] almost simultaneously published studies of much larger numbers of S. stercoralis individuals isolated from humans and dogs in more narrow geographical areas. Nagayasu et al. [55] worked in southeast Asia and Japan while Jaleta et al. [56] concentrated on two neighbouring villages in northern Cambodia. Both studies defined two groups of S. stercoralis, one found only in dogs and the other found in humans and dogs. Both studies based their conclusions on multiple nuclear and mitochondrial sequences (the SSU HVR I, the 28S ribosomal DNA sequence, the sequence of the major sperm protein and cox1 in the case of Nagayasu et al. [55] and the SSU HVR I and HVR IV, cox1 and, for a selection of the worms, whole genome sequence in the case of Jaleta et al. [56]. Jaleta et al. [56] in their sample, found the sequence of the SSU HVR IV to be diagnostic for the type. The haplotype they refer to as B was found only in dog-derived S. stercoralis while haplotype A was found in worms from humans and dogs. There was diversity among the cox1 sequences but upon phylogenetic analysis, the different sequences grouped according to the nuclear SSU HVR IV haplotype in the same worm and not according to the host this worm was isolated from. Later, evidence for a dog-specific type and one found in humans and dogs, distinguishable based on the same SSU HVR IV haplotypes, was also found in Australia [57]. It should be noted that the reference isolate of S. stercoralis, which is a dog-derived isolate from the USA, is, based on its sequence, also of the ‘human and dog’ type [58]. Later, a few studies found the ‘human and dog’ type in dogs in Thailand [59] and Switzerland [60] from a cat from St Kitts in the Caribbean [22]. Thus far, the ‘dog specific’ type has only been reported from dog hosts in southeast Asia and Australia [55–57,61].

Overall, the picture the molecular-genetic work provides is still rather patchy and not straightforward to interpret. A number of additional, slightly different HVR IV haplotypes have been found [61,62]. The number of dog-derived sequences from locations other than southeast Asia or Australia is very small and also for human-derived S. stercoralis there is a strong bias towards these geographical regions [61,62]. A further problem is that the different studies frequently analysed different sequences, making cross-study comparisons difficult.

In order to overcome this last problem, Barratt & Sapp [62] developed a machine-learning approach that allows the comparison of individuals for which overlapping but not identical sequence information is available. Using this approach, and all of the S. stercoralis cox1, HVR I and HVR IV marker sequences available at the time, the authors clustered S. stercoralis isolates into seven clusters. Four of the clusters overwhelmingly contained human-derived isolates, with only between 1% and 2% being from dogs. Two clusters contained 10% and 22% human isolates, respectively, showing the most heterogeneous distribution in hosts in the study. The remaining cluster, predominantly containing samples from Myanmar and Cambodia, contained no human isolates at all, and probably represents the ‘dog only’ type reported by Nagayasu et al. [55] and Jaleta et al. [56]. The geographical association was not possible for the other clusters. These data might suggest that what is currently referred to as S. stercoralis might actually be divided into more than only the two to three subtypes proposed by Nagayasu et al. [55] and Jaleta et al. [56], and that in addition to the ‘dog specific’ and the ‘human and dog’ populations also human host specific populations exist. The authors proposed that what is currently referred to as S. stercoralis is actually not one species but a complex of multiple closely related cryptic species.

There are several limitations to the approach used. The machine-learning algorithm was applied only to Genbank database entries. Owing to unequal sampling and reporting, the number of Genbank database entries is not a good proxy for the true prevalence of specific genotypes. Furthermore, many more humans have been sampled than dogs and this is reflected in the Genbank database entries. Finally, some researchers choose to generate Genbank entries for each individual worm genotyped, while others submit unique sequences only once, such that the information on how many times each particular sequence was recovered is not reliably reflected in the database. These factors all may skew the results reported by the machine-learning algorithm.

In spite of all caveats, from all these studies it appears clear that, at least in southeast Asia and Australia, dogs carry one or multiple populations of S. stercoralis that are only very rarely, if at all, present in humans and a second population that, based on the currently available evidence, cannot be distinguished from the population in humans. The crucial question is now if this later population is really the same or nevertheless a separate but genetically most similar population as the one found in humans.

Nagayasu et al. [55] suggested that S. stercoralis originated and genetically diversified in canines and later one genetic type acquired the ability to also infect humans. The fact that the canine molecular type of S. stercoralis has so far not been found outside of southeast Asia and Australia, if confirmed by future studies, would suggest that this occurred in the southeast Asia/Oceania area. Already Hasegawa et al. [53] had suggested that, in contrast to the NHP parasite Strongyloides fuelleborni, which also occasionally infects humans, S. stercoralis spread fairly recently through human activity to acquire a cosmopolitan distribution. However, if this evolutionary scenario is true, the question remains if the human-adapted type has fully specialized on humans as hosts or remains a parasite of humans and dogs.

Even if we accept that some of the S. stercoralis found in dogs are the same as the ones in humans, this does not prove dog-to-human transmission. The results are also consistent with a one-way transmission from humans to dogs. The treatment experiments mentioned above (co-treating dogs or not) and following the genotypes of the S. stercoralis in the dogs and the humans could shed light on this question.

It should be emphasized that the fact that Strongyloides larvae of a ‘human type’ are found in dog faeces does not necessarily mean that the dog has a patent infection. In most studies, cultured L1 larvae [60], iL3 larvae and free-living adults [55,56,59], or free-living adults only [59,63] were genotyped and it was assumed that the genotyped worms were the progeny of parasitic adults residing in the host individual sampled. However, dogs are notorious for coprophagia of human faeces, such that faecal passage of larvae after consumption in human faeces cannot be excluded. While it is difficult to avoid this problem in future field studies, one could confine the dogs for a few days after sampling restricting their access to human faeces. If they still shed S. stercoralis larvae, it is likely that they carry reproducing adults. The experimental infection experiments and the cases in settings like the one described by Basso et al. [60], where the dogs were most unlikely to have had access to S. stercoralis contaminated human stool, argue that, at least occasionally, dogs can develop patent infections with S. stercoralis of what we currently regard as ‘human and dog type’. However, it may well be that coprophagy contributed for example to the relatively high proportion (greater than 20%) of ‘human type worms’, which Jaleta et al. [56] observed in dogs in a setting with a rather high incidence of S. stercoralis in humans and ample access to human stool for dogs to consume.

5. Epidemiological studies and case reports

Perhaps the scientific community has not stepped back from genotyping and considered a more fundamental question. This question is, ‘if strongyloidiasis is a zoonosis from dogs, why do we not see more case reports of infection in humans that are epidemiologically linked to infected dogs?’ Remarkably, there are virtually no such cases reported in the literature.

The only confirmed example of natural S. stercoralis infection of a human from dogs was a laboratory animal carer from New York in 1976 [38]. This case had no history of travel to strongyloidiasis endemic regions and presented with symptoms of three weeks duration, including initial vomiting, followed by sustained abdominal pain and diarrhoea requiring hospitalization. Upon admission to hospital, the patient's blood showed a peripheral eosinophilia of 76% (18.6 × 10⁹ cells l⁻¹) [38].

A case of autochthonous strongyloidiasis in a teenager from Nottingham in the United Kingdom (UK) without significant travel history was reported in 1987. It was assumed that this case was acquired by the patient walking barefoot in parks where dogs had defaecated [64]. In this case, while unlikely, possible exposure to soil contaminated with the faeces of a human (infected outside of the UK) cannot be definitively excluded. These are the only two case reports describing probable, or suggested, acquisition of S. stercoralis from dogs in areas where dogs are infected, but autochthonous human disease is not reported.

Strongyloides stercoralis prevalence in domestic dogs in the USA, the UK and Europe is between 2% and 5% [3]. All dog isolates genotyped thus far from these regions have been identified as belonging to the ‘human and dog’ type [60,61]. At this prevalence, for any zoonotic parasites with transdermal penetration, one should expect to see sporadic human cases, particularly in population-dense areas such as cities, where infected domestic dogs do reside [61].

A study in Minas Gerais state, Brazil in 2007 tested 181 dogs from breeding kennels and 11 dog keepers from five of these kennels by both serological and coprological techniques [65]. Three (27.3%) of the 11 animal keepers were positive by an in-house enzyme-linked immunosorbent assay, but not in-house immunofluorescence antibody test, Baermann sedimentation or Lutz sedimentation [65]. An almost simultaneous survey of the same region found a 23% seroprevalence in diabetics and 7% seroprevalence among healthy controls [66]. Owing to the small sample size, the findings in kennel keepers are difficult to interpret and may represent natural acquisition from human sources.

Another study attempted to determine if cross-infection with S. stercoralis between dogs and humans was occurring in a stable, geographically contained, community on the Amami islands of Japan [67]. Here, 2.8% of people (n = 660) and 10% of dogs (n = 55) were infected. Remarkably, no people owning infected domestic dogs were found to also be infected, and vice versa [67]. If S. stercoralis represents a zoonosis in this region, it seems highly unlikely that no owners should have contracted infection when disposing of faeces from infected dogs or living in contaminated home environments. For this to occur in the context of zoonotic transmission, owners would have to always dispose of dog faeces almost immediately after passage and almost never go barefoot in areas where their dogs defaecate.

Steinmann et al. [68] found no association between S. stercoralis infection status and the ownership of domestic animals, primarily dogs, in Yunnan, China. More recently a study in of Orang Asli school children in Peninsular Malaysia found a high prevalence (15.8%) of strongyloidiasis in people by agar plate culture and PCR, but no statistical association between infection and owning domestic animals, which were also primarily dogs [69].

The fact that in several studies dog ownership and the infection status of these dogs did not correlate with the infection status of the owners [65,67–69] should not be overinterpreted. From faeces deposition to the time the first larvae are infective takes 2–3 days. The putative source of infection is, therefore, old dog faeces, or the environment immediately surrounding that faeces, and not direct contact with an infected dog itself. In settings where dogs defecate in public areas in particular, dog owners might not be exposed to this putative source of infection more often than other people living in the area.

6. Future directions

Below we provide a list with possible studies we think could enhance our understanding of the zoonotic potential of S. stercoralis. The list is subjective and not complete:

• (i) as far as molecular taxonomy is concerned, currently, there is a strong sampling bias towards southeast Asia and Australia. For other places, little to no molecular information is available. Sampling and genotyping of S. stercoralis from various geographical locations and different hosts will reveal if the dog-specific types are indeed geographically limited while the human infective type has spread fairly recently and became cosmopolitan;
• (ii) In order to assess cross-species transmission, S. stercoralis from humans and dogs (and other possible zoonotic hosts such NHPs) need to be sampled from the same locations and their population genetic structure (e.g. the frequencies of particular alleles) compared;
• (iii) controlled treatment experiments, with and without co-treatment of the dogs could be performed and the post-treatment dynamics of S. stercoralis infection in the human and the dog populations could be followed. At the same time worms from humans and dogs should be analysed molecularly. Such experiments could reveal if dogs are really a significant factor in the epidemiology of human strongyloidiasis and could indirectly inform about the direction of the infection; and
• (iv) controlled infection experiments with human and dog-derived S. stercoralis and with simultaneous infection of human and dog hosts would inform us about the infection potential of the different isolates. While, from a solely scientific point of view, such experiments would be desirable, careful ethical evaluations have to be done, in order to decide if such experiments are also ethically justifiable.

7. Conclusion

The currently available data do not provide a clear-cut answer to the question raised in the title of this article and we think that this question is probably not globally answerable with yes or no. Maybe it would be more reasonable to ask ‘how do dogs influence the epidemiology of human strongyloidiasis?’ We believe that, based on the current evidence, any of the two extreme answers, i.e. ‘not at all’ and ‘they are the dominating factor’ is unlikely. Given that in experimental infections at least some genotypes of human infective S. stercoralis can cause patent infections in dogs (table 1) it is feasible that this also does happen in the wild, at least occasionally, leading to contamination of the environment with dog-derived human infective larvae. On the other hand, there is a sparsity of case reports of human strongyloidiasis unequivocally acquired from a dog [38] and dog ownership has not emerged as major risk factor for human infection in several epidemiological studies [67–69]. Transmission of human strongyloidiasis is seen in some regions where dog ownership is rare, such as some parts of the Middle East [2,70]. In other regions, there is an appreciable incidence of the genetically ‘human infecting’ lineage of S. stercoralis in dogs but very few infected people, such as the USA and Europe [3,60,61]. Therefore, it is also most unlikely that human cases are predominantly zoonoses from dogs. However, there is much room in between the two extremes mentioned above and it is to be expected that the contribution of dogs to the overall exposure of people to S. stercoralis differs between locations. In settings with high prevalence in humans, where dogs are exposed regularly and to many human-derived infective larvae, it is conceivable that they do get infected rather frequently and contribute to the number and the distribution of infective larvae and thereby increase the overall exposure of humans to S. stercoralis. It will be important to find out for how long dogs can sustain a population of human infective S. stercoralis. Even if such infections were rather short-lived, they might still be sufficient to bridge a temporary interruption of human-to-human transmission, for example after a mass distribution of anthelmintics in the context of a public health control campaign.

Data accessibility

This article has no additional data.

Declaration of AI use

We have not used AI-assisted technologies in creating this article.

Authors' contributions

R.S.B.: conceptualization, data curation, methodology, project administration, writing—original draft, writing—review and editing; A.S.: data curation, methodology, writing—review and editing.

Both authors gave final approval for publication and agreed to be held accountable for the work performed therein.

Conflict of interest declaration

R.S.B. is Vice President of ‘Strongyloides Australia’, a non-profit organization composed of health practitioners, scientists and community members, which supports efforts to raise awareness about strongyloidiasis within Australia and to lobby State and Federal Governments to make strongyloidiasis a notifiable disease in Australia.

Funding

The work in A.S. laboratory is funded by the Max Planck Society.