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Review

Autochthonous Leishmaniasis in the United States of America

by
Chaoqun Yao
1,2,*,
Yi Yang
3,4 and
Aifang Du
3,4
1
Department of Biomedical Sciences, Ross University School of Veterinary Medicine, Basseterre P.O. Box 334, Saint Kitts and Nevis
2
One Health Center for Zoonoses and Tropical Infectious Diseases, Ross University School of Veterinary Medicine, Basseterre P.O. Box 334, Saint Kitts and Nevis
3
Institute of Preventive Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China
4
Zhejiang Provincial Key Laboratory of Preventive Veterinary Medicine, College of Animal Sciences, Zhejiang University, Hangzhou 310058, China
*
Author to whom correspondence should be addressed.
Microorganisms 2025, 13(11), 2485; https://doi.org/10.3390/microorganisms13112485
Submission received: 12 September 2025 / Revised: 24 October 2025 / Accepted: 27 October 2025 / Published: 30 October 2025
(This article belongs to the Section Public Health Microbiology)
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Abstract

Leishmaniasis is endemic in 99 countries worldwide, including the USA where it has low endemicity. The disease is emerging but likely underdiagnosed due to its historical absence in the diagnostic differentials of American physicians. Additionally, the public seems to have little knowledge about this disease. Here, a comprehensive literature review was carried out on autochthonous leishmaniases in humans in the USA, including their associated Leishmania spp., capable sand fly vector, transmission route, and risk to the parasitic infection. All 89 cases were cutaneous leishmaniasis reported in Texas, Oklahoma, Arizola, and North Dakota. The collective information should serve to mitigate both autochthonous and imported leishmaniasis by expanding reservoir and vector surveillance and improving physician training in diagnosis in the USA.

1. Introduction

Leishmaniasis is an emerging/re-emerging parasitic disease caused by over 20 Leishmania spp. protozoa. It clinically manifests in three major forms, i.e., cutaneous leishmaniasis (CL), visceral leishmaniasis (VL), and mucocutaneous leishmaniasis [1,2]. Among them, CL is the most benign, often displaying chronic skin lesions on the frequently exposed body parts such as the head and extremities. This form is known to last several months to over a year, followed by self-healing even without proper treatment. In contrast, VL is the most severe form of the disease, usually resulting in the death of more than 90% of patients if left untreated [3,4,5]. Annually, there are approximately 0.6−1.0 million new CL cases and 50−90 thousand VL cases worldwide across 99 endemic countries according to the World Health Organization (WHO, https://www.who.int/news-room/fact-sheets/detail/leishmaniasis, accessed on 24 October 2025). The USA is among the 99 endemic countries and has a few species of wild mammals serving as reservoirs including Neotoma micropus (Southern Plains woodrats), N. floridana (eastern woodrat), N. albigula (White-throated woodrat), and Peromyscus attwateri (Texas deermice) [6,7]. Leishmaniasis has been a notifiable disease since 2007 in Texas (https://www.dshs.texas.gov/2007-annual-report, accessed on 24 October 2025).
The rareness of leishmaniasis in the USA makes a timely diagnosis very challenging. Autochthonous leishmaniases in humans have been reported infrequently. In addition, U.S. residents, just like those in non-endemic countries, may acquire infections internationally when they travel to highly endemic areas such as South America, the Indian subcontinent, and Mediterranean regions [8,9,10]. Furthermore, considering the effects of climate change, there is a trend for the disease to spread to more northern latitudes [11]. Consequently, there needs to be a pivotal effort to draw medical doctors’ attention to include this disease in their clinical differential list as well as to educate general populations. Here, we comprehensively review autochthonous leishmaniasis in humans, in aspects of its distribution within the USA, routes of transmission, various parasite species, sand fly vector, and risk to infection.

2. Case Identification

2.1. Identification of Leishmania spp.

The gold standard for the diagnosis of leishmaniasis is the microscopic finding of amastigotes within macrophages in biopsied tissues/organs/aspirates. Positive in vitro culture of promastigotes from these biological materials is also considered a confirmed diagnosis no matter whether a positive microscopic finding is obtained. Molecular techniques for positive identification of Leishmania spp. are preferred, as the morphologic similarity of both amastigotes and promastigotes makes discrimination between species difficult, even by electron microscopy (EM). Isoenzyme profile analysis, PCR, and DNA sequencing are useful techniques to identify Leishmania spp. PCR and DNA sequencing have become increasingly popular since the 2000s and have almost completely replaced isoenzyme profiling that was widely used since the 1980s. Lately, metagenomic next-generation sequencing has been applied in diagnosing various pathogens including Leishmania spp. [12,13].

2.2. Criteria for Autochthonous Leishmaniasis

A confirmed case of human leishmaniasis described in the literature must meet at least one of three criteria to have been considered USA-autochthonous, i.e., locally acquired in the USA, and thus included in the current study: (1) a confirmed case of patients who did not, in the course of their lifetime, travel outside of the USA; (2) a confirmed case of patients who did not travel to an endemic foreign country in the immediate 5 years prior to leishmaniasis onset; (3) a confirmed case of a military personnel or veteran who had not been deployed to Iraq, Kuwait, or Afghanistan since Operation Desert Storm in 1990.

3. Autochthonous Leishmaniasis

Until now, all autochthonous leishmaniases recorded in humans in the USA are CL. A typical CL case clinically manifests as an ulcerated skin lesion that is often located on exposed body parts such as the head and extremities (Figure 1). The first undisputable autochthonous leishmaniasis that meets the criteria outlined in the Section 2 was reported by Stewart and Pilcher in 1945. The patient was a six-year-old boy who presented to a doctor on 10 October 1942, with ulcerated skin lesions on the dorsum of both feet, right knee, and right buttock. A biopsy of these lesions revealed amastigotes microscopically, which confirmed the diagnosis of leishmaniasis. The boy was born in Alice, Texas and had never traveled out of Texas prior to the onset of the disease [10]. Since then, 89 autochthonous cases in total have been reported (Table 1). The patients originated from four different U.S. states. The states and case numbers are Texas—84, Oklahoma—2, Arizona—2, and North Dakota—1.
Table 1. Autochthonous human leishmaniasis in USA (open cells indicate no data available).
Table 1. Autochthonous human leishmaniasis in USA (open cells indicate no data available).
YearStateAgeSexClinical Signs and SymptomsDiagnostic Methods *Leishmania spp.Treatment (/F/H/LTF/NR) ‡References
1942TX6MChronic ulcers on the dorsum of both feet, right knee, and right buttockM [10]
1967TX64FNumerous nodules and plaques over extremities and buttocks for yearsC, M Camolar (F)[14]
1972TX74FHard plaque on right eyelid, left cheek, and left earlobeAI, M Surgery (H)[15] €
1974TX56MCrusting and superficial ulceration of the left cartilaginous septumAI, C, M, S, VIPentostam (F)
1980TX11MRed papule on the left cheekC, IP, ML. mexicanaSodium stibogluconate (H)[16,17]
1982TX56FCrusted plaque on left earlobeM, SAntimony potassium tartrate (H)
1982TX5MPapule on left front thighM, SSurgery (H)
1983TX10MPapules on faceC, M, SNo treatment (H)
1986TX46FNodules on right arm and wristM, C, IPL. mexicanaKetoconazole (H)[18]
1986TX13MUlcer on right earM Antimony tartrate (H)[19]
1986TX28FUlcerating papule on right cheekMUnknown (LTF)
1988TX52MCrusted lesion on right earMIsoniazid (H)
1988TX37FUlcerating nodule on right lower legMNo treatment (H)
1988TX3MPapule on noseM, CCryotheropy (LTF)
1988TX4MNodule on left lower eyelidM, CNo treatment (H)
1988TX50FUlcerating papule on noseMNo treatment (H)
1988TX2MPlaque on left cheekM, CNo treatment (LTF)
1989TX28FUlcerating nodule on right cheekM, CKetoconazole (H)
1989TX20FUlcerating nodule on right angleMAntimony tartrate (H)
1989TX86FUlcer on right cheekMKetoconazole (H)
1989TX2MUlcer on right earMAntimony tartrate (H)
1989TX62MNodule on right ear, right cheek, forehead and right elbow; plaque on right thighM, CSodium stibogluconate (F); Sodium stibogluconate + Ketoconazole (H)
1989TX67MUlcer on left earMNo treatment (H)
1990TX81FUlcerating papule on right cheekMElectrodesiccation + curettage (H)
1992TX15MLesion on faceMIsoniazid + Rifampin (H)
1993TX51FUlcerating nodule on left wristM, CKetoconazole (H)
1987TX62MCutaneous lesions on the extremitiesM, C [20]
2002 +TX78FErythematous plaque on right forearmM No treatment (LTF)[21]
2003OK26MSkin lesion on right cheekM No treatment (H)[22]
2005OK73MSkin lesions on right forearmMHeat (LTF)
2005TX74FNodule on left eyelidMNo treatment (LTF)
2005TX70MSkin lesion on right armM Amphotericin + Fluconazole (NR)[11,22] #
2005TX8FSkin lesions on face and left upper armM, C, PCR #L. mexicanaAmphotericin B + Fluconazole (NR)
2006TX60FSkin lesion on noseM Ketoconazole + Cryotherapy (NR)
2006TX76FSkin lesion on foreheadM Cryotherapy (NR)
2006TX80MSkin lesion on left armM
2006TX64MSkin lesion on right abdomenM
2007TX57MSkin lesion on left backM Diflucan + Surgery (NR)
2007TX82FSkin lesion on left cheekM Fluconazole (NR)
2007TX64FSkin lesion on right chestM
2006TX MSkin lesion on right abdomenM [23]
2007TXFSkin lesion on upper armM, PCRL. mexicana
2007TXFSkin lesions on chin and neckM
2007TXFSkin lesions on forearm and wristM, PCRL. mexicana
2010TXMSkin lesion on left wristM
2011TXFSkin lesions on face, left elbow, and buttockM, PCRL. mexicana
2011TXFSkin lesion on upper armM
2012TXMSkin lesion on faceM, PCRL. mexicana
2013TXFSkin lesion on right wristM, PCRL. mexicana
2013TXFSkin lesion on upper armM
2013TXFSkin lesion on right foreheadM, PCRL. mexicana
2013TXFSkin lesion on foreheadM
2013TXMSkin lesion on forearmM
2013TXFSkin lesion on upper armM, PCRL. mexicana
2013TXFSkin lesion on shoulderM
2013TXMSkin lesion on left armM
2013TXFSkin lesion on right lower eyelidM
2013TXFSkin lesion on left eyelidM
2013TXFSkin lesion on upper shoulderM, PCRL. mexicana
2014TXMSkin lesion on upper eyelidM, PCRL. mexicana
2014TXFSkin lesion on faceM, PCRL. mexicana
2014TXFSkin lesion on left templeM, PCRL. mexicana
2014TXMSkin lesions on armM, PCRL. mexicana
2014TXFSkin lesions on face and eyelidM
2014TXFSkin lesion on right foreheadM
2014TXFSkin lesion on left cheekM, PCRL. mexicana
2014TXMSkin lesion on right earM, PCRL. mexicana
2014TXFSkin lesion on left upper armM
2015TXFSkin lesion on left upper armM
2015TXMSkin lesions on face and cheekM, PCRL. mexicana
2015TXFSkin lesion on right dorsal handM
2015TXFSkin lesion on forearmM, PCRL. mexicana
2015TXFSkin lesion on left earlobeM
2015TXMSkin lesions on elbowsM
2015TXMSkin lesion on left forearmM
2015TXFSkin lesion on faceM
2015TXMSkin lesions on ear and backM, PCRL. mexicana
2016TXFSkin lesion on right anterior upper neckM
2016TXMSkin lesion on right upper armM, PCRL. mexicana
2016TXFSkin lesion on left foreheadM, PCRL. mexicana
2016TXFSkin lesion on right faceM
2012ND2MSingle lesion each on the upper and lower eyelid of right eyePCRL. donovani complexNo treatment (H)[24]
2016TX67MMultiple painless and non-pruritic papules at the anterior surface of the right legM, C, PCR, DL. mexicanaMiltefosine + Ketoconazole (F)[25]
2017AZ72FTwo discrete, edematous, violaceous papules on the low backM, C, PCR, DL. ellisiNo treatment (H)[26,27]
2018–2019TX2FNon-healing nodular lesion on right jawline¥L. mexicanaFluconazole (H)[28]
TX3MNon-healing nodular lesion on left armM, PCR, DL. mexicanaFluconazole (H)
TX0 £MNodular lesion on faceM, PCR, DL. mexicanaFluconazole (F); Paromomycin (F)
2020 +TX65MThree erythematous lesions on the left lateral shoulderM Cryotherapy (H)[29]
2023 +AZ34MSingle ulcerated verruous plague on lower left legM, I Surgery (H)[30]
*: AI: animal infection; C: culture; D: DNA sequencing; I: immunohistochemistry; IP: isoenzyme profile; M: microscopy of amastigotes; PCR: polymerase chain reaction; S: serology; VI: sand fly vector infection; ‡: F: failure; H: healed; LTF: lost to follow; NR: not reported; €: also included an additional asymptomatic case of 16-year-old female identified by serology in 1975 [31]; +: publication year; #: reported by both [22] and [11]; ¥: genetic analysis by the Centers for Disease Control and Prevention (CDC); £: 6 months old.
Microorganisms 13 02485 g001
Figure 1. Typical and atypical gross lesions of autochthonous cutaneous leishmaniasis in the U.S. population caused by Leishmania donovani complex (A) and L. mexicana (B,C). (A) From [24] with permission for reuse. (B) From [25] with permission for reuse; the largest lesion ~4.0 × 4.5 cm. (C) From [28] with permission for reuse; the left arm; scale bar: 1 cm.
Figure 1. Typical and atypical gross lesions of autochthonous cutaneous leishmaniasis in the U.S. population caused by Leishmania donovani complex (A) and L. mexicana (B,C). (A) From [24] with permission for reuse. (B) From [25] with permission for reuse; the largest lesion ~4.0 × 4.5 cm. (C) From [28] with permission for reuse; the left arm; scale bar: 1 cm.
Microorganisms 13 02485 g001
Among eighty-nine cases, only twenty-eight (31.5%) have Leishmania spp. firmly identified by molecular techniques, i.e., PCR and/or DNA sequencing (twenty-six cases) and isoenzyme profiling (two cases). Specifically, all 26 cases in Texas are infected by L. mexicana; the remaining two from Arizona and North Dakota are infected with L. ellisi and L. donovani complex, respectively (Table 1). Leishmania donovani complex consists of L. donovani and L. infantum, which usually causes VL in endemic areas in the Indian subcontinent, Brazil, and the Mediterranean area, respectively. Nevertheless, infection with both species also results in CL [32,33,34]. Therefore, the CL case due to infection of L. donovani complex in North Dakota is not extraordinary.
Sex, age and lesional location on body parts of all reported cases are tabulated in Table 1. Forty (44.9%, n = 89) were male and forty-nine (55.1%) were female. There is no statistical difference between this ratio of 40:49 and the presumed equal ratio of 44.5:44.5 (χ2 = 0.4562, p = 0.50), which suggests both sexes are equally susceptible to the disease without much gender bias. These are similar to the epidemiological data of CL in Iran [35,36], but are different from the epidemiological data of VL in Brazil, which have demonstrated that VL is more common in males than in females after puberty [37,38]. In the latter, such male susceptibility to symptomatic VL has been experimentally confirmed to be biological in murine models [38]. As far as onset age, only 48 cases have recorded ages of patients ranging from infant (few months old) to 86 years old. Specifically, the ages are <10 years–11, ≥10–5, ≥25–18, and ≥65–14. Two thirds (32/48) are 25 years or older, which suggests a likelihood of professional/adventure exposure, although this needs to be confirmed. Regarding the location of skin lesions on various body parts, the head (including ears and nose) is the most common, accounting for 53.9% (48/89), followed by the upper limb 32.6% (29/89), lower limb 11.2% (10/89), and trunk 10.1% (9/89), with the least on the neck at 2.2% (2/89) (Figure 2). The total number of body parts affected are more than 89 (the total number of patients) as a few patients had more than one body part affected. These data clearly show that often exposed body parts (such as the head and the upper limb) are more likely to sustain sand fly bites, hence having the greatest chance of being infected by the Leishmania parasites and leading to leishmaniasis. Interestingly, the neck, another often exposed body part, is the least of the lesional locations. The reason why the neck is much less attractive to sand fly bites is unknown at this time. Further studies are warranted and may provide informational clues to develop preventions to minimize sand fly bites on the head and upper limb where almost 90% of the bites occur.
Since 94.4% (84/89) of the confirmed autochthonous cases are in Texas (Table 1), it is worthy of further discussion. An autochthonous case of CL was firmly diagnosed by EM in a 78-year-old woman with a 4-month history of a skin lesion on her right forearm in Washington County, Texas. An additional 29 cases were collected, which were all from south-central Texas [21]. Nevertheless, nine CL cases were later found at the Dallas-Fort Worth metroplex in 2005–2007 [11,22]. The latest cases involving three children occurred between October 2018 and April 2019. Their ages were 2 years, 3 years, and six months old. Two lived in Ellis County and were only 9 miles from one another; the third in Grayson County [28]. These latest cases show an unequivocal trend of the northward spread of the disease in the state, which is a clearly alarming movement which should trigger a response by medical and public health professionals.
In 2007, leishmaniasis became a notifiable disease in Texas. The annually reported cases are as follows: 2007—nine; 2008—zero; 2009—two; 2010—zero; 2011—four; 2012—six; 2013—eleven; 2014—twelve; 2015—six; 2016—thirteen; 2017—eight; 2018—fifteen; 2019—ten; 2020—not available; 2021—nine; 2022—eleven; 2023—ten; and 2024—four (https://www.dshs.state.tx.us/IDCU/data/annual/Texas-Annual-Reports-2000s.aspx, accessed on 24 October 2025). Nevertheless, determining whether all of these were autochthonous cases is very challenging. In 2018, McIlwee BE and colleagues investigated the increasing number of cases in Texas. They used laboratory information systems to find each patient’s travel history for all patients reported from 2007 to 2017. Forty-one out of sixty-nine reported cases (59%) had no history of travel outside the USA. Consequently, they were all considered autochthonous (Table 1) [23].
The case that originated in North Dakota is interesting and worthy of further discussion. First, out of all 89 autochthonous cases, it is the only case that was infected with L. donovani complex (L. donovani and L. infantum) [24] that usually causes VL in humans (although rare, CL cases without a VL history have been reported) [39]. Second, among the four tests performed, only PCR was positive for parasite DNA of L. donovani complex [24], whereas the remaining three were negative. The latter included microscopic findings, parasite cell culture performed by the Center for Disease Control and Prevention (CDC), and antibodies to K-39 antigen using the immunochromatographic strip test. Third, the boy’s family (the parents and older brother) had just immigrated to the USA from Nepal in 2009, which is the year before the boy was born in the USA in March 2010 [24]. It is plausible that the mother was pregnant with the boy prior to immigration to the USA and he acquired the parasite through vertical transmission. Nepal is an endemic country with VL and had recorded over 1000 annual cases before 2009, and 935 cases in 2009 when the family emigrated from the country [40]. A pertinent question to ask is whether the boy was congenitally infected, considering the timing of his birth in relation to family immigration history. Unfortunately, no data on testing the boy’s mother for leishmaniasis are presented in the original publication. There are several reports of such transmission, including cases occurring in non-endemic areas, which will be further discussed later in the section on transmission routes. Fourth, the authors of the reported case speculated that case was transmitted by sand flies, and possibly had a canine origin since leishmaniasis is endemic in Foxhound populations in many U.S. states (although possibly not in North Dakota). It might even be possible that there is an anthroponotic origin of the parasite as the authors also suggested the likelihood of the boy’s parents transporting the infected vector from Nepal to North Dakota [24].

4. Leishmania spp. in the USA

As described earlier in the section of case identification, identification of Leishmania spp. almost exclusively depends upon molecular techniques including isoenzyme profile, PCR, DNA sequencing, and metagenomic next-generation sequencing. In all, five Leishmania spp. have been confirmed in the USA, accounting for approximately one fourth of all human-infecting Leishmania spp. worldwide. All human cases in the USA are caused by L. mexicana except two cases—one by L. donovani complex and the other by L. ellisi (Table 1). Leishmania ellisi is the newest member in the genus that causes CL (Table 1) [26]. Interestingly, parasites identified from autochthonous canine cases are exclusively L. infantum [41]; and the parasites infecting horses are L. martiniquensis [42,43], which has been found causing human CL in Martinique and Thailand (1). Geographical distribution of the five Leishmania spp. is presented in Figure 3.
The U.S. isolates of L. mexicana are worthy of a brief discussion since they appear to have a unique genotype. In an early study, 72 L. mexicana isolates from North and Latin America and the Caribbean were analyzed for the profile of 20 isoenzymes. The isolates included were from Texas—eight, Mexico—thirteen, Belize—six, Guatemala—twelve, Ecuador—twelve, Venezuela—five, and the Dominican Republic—eight. It was found that all eight Texan isolates were highly similar to the central American ones [46]. Recently, by means of DNA sequencing, Texan L. mexicana isolates of a unique genotype have been found in ITS2, i.e., A → C647 and T → C649, which is different from the Mexican and South American isolates. The genotype can be a very useful tool for identifying autochthonous L. mexicana infection in the USA [25,28,47].

5. Transmission Routes

Leishmania spp. are vector-borne kinetoplastid protozoa that are naturally transmitted by sand fly vectors [48,49]. Lately, they have been confirmed to be vertically transmitted from mother to offsprings [50]. In addition, they may also be horizontally passed between individuals by blood transfusion. We discuss here the roles that these various transmission routes play in the U.S. endemicity of leishmaniasis.

5.1. Sand Fly Vector

Leishmania mexicana parasites were successfully isolated from naturally infected sand flies in the USA for the first time in October 1991. In this study, promastigotes were proliferatively grown from three of the twenty-seven sand flies (Lutzomyia anthophora) collected in Texas; two of them were identified as L. mexicana by isoenzyme profiling [51]. In a separate study, sand flies were collected using a CDC light trap on the personal property of a patient with autochthonous CL in Caldwell County, Texas. Fly species were identified by morphology and PCR followed by DNA sequencing targeting the mitochondrial cytochrome c oxidase subunit I. Bloodmeal sources of engorged sand flies were determined by hemi-nested PCR targeting the 16S rRNA gene. Leishmania spp. infection of the sand flies was determined by PCR targeting the Leishmania spp. rRNA-ITS2 region, followed by DNA sequencing. The fly species identified included Lu. shannoni (n = 1), Lu. texana (n = 3), and Lu. anthophora (n = 188). Two of six Lu. anthophora engorged females with bloodmeal were found to be of human origin. More importantly, 4 out of 138 female flies were PCR positive for Leishmania spp. DNA, one of which was found to be identical to the L. mexicana DNA sequence found in the infected human on the property [25]. However, whether the sand fly infected with the human isolate of L. mexicana was one of two Lu. anthophora that contained human blood was not clear. Lutzomyia anthophora and Lu. vexator were trapped in the residence of a patient in Tarrant County, Texas [22]. Lutzomyia anthophora, Lu. diabolica, and Lu. texana were trapped at leishmaniasis foci in Medina County and Bexar County, TX. A total of 1 out of 347 female Lu. anthophora was found infected with Leishmania sp. promastigotes, whereas none of the 494 Lu. diabolica and 83 Lu. texana were positive [52]. Under laboratory conditions, female Lu. longipalpis sand flies reared in the laboratory were allowed to feed on Foxhound dogs naturally infected with L. infantum. They were then dissected 10 days later. Promastigotes were found in the stomodeal valve of the sand flies. Furthermore, the infected sand flies were allowed to feed on lab-reared hamsters. The blood of these hamsters was tested for leishmanial DNA using qPCR. Four of seven hamsters were positive between two and four months after sand fly blood feeding. Parasite DNA was amplified by the same qPCR in the spleen, bone marrow, and lymph nodes of most of the 15 hamsters at the end of the experiment when they were sacrificed [53]. This experiment clearly shows that L. infantum passed down generations among Foxhounds by congenital transmission is capable of infecting sand flies, and the infected sand flies can infect mammalian hosts. Therefore, those L. infantum-infected Foxhounds in the USA certainly pose some risk to humans.
Collectively, four species of Lutzomyia spp. sand flies in the USA are considered capable vectors of Leishmania parasites. These are Lu. anthophora, Lu. cruciate, Lu. diabolica, and Lu. shannoni (Figure 3) [7,44]. In addition, Lu. vexator’s role as a vector waits to be confirmed and this species has been found in the States of AL, AR, CA, CO, FL, GA, KS, LA, MD, MO, MT, NM, NY, OH, OK, TN, TX, VA, WA, WY [44].

5.2. Vertical Transmission—Congenital Transmission

In 1986, a male infant in Kenya was diagnosed with leishmaniasis at four months of age along with his mother. He was born a premature baby and had been in the hospital all the time prior to diagnosis. Furthermore, he had been sick since day 6 of his birth, suggesting a transplacental transmission [54]. Kenya is an endemic country of leishmaniasis. Similarly, congenital transmission also happens in non-endemic regions. An eight-month-old boy born in Ukraine to a mother who had been treated for leishmaniasis during weeks 28–32 of gestation was also confirmed suffering from the disease. The boy was delivered by cesarean section in Ukraine, which is a non-endemic country for leishmaniasis, and had not traveled outside of the country. The mother had worked in Alicante, Spain, which is a leishmaniasis-endemic region. It is very likely the boy is infected by vertical transmission [55]. A 16-month-old German boy was diagnosed with leishmaniasis by high titer antibodies to Leishmania sp. and positive cell culture from the liver and bone marrow. The boy had never traveled beyond Germany. His mother had been to Portugal, Malta, and Corse—all endemic areas—before giving birth to him. Furthermore, the mother had antibodies to the cultured parasites originated from the boy, suggesting that the mother had been exposed to the same parasite, and that the boy was congenitally infected with the parasite [56]. The second case of congenital transmission in Germany was a 9-month-old girl without a travel history out of the country; she was diagnosed with leishmaniasis by serology, immunoblot, microscopic detection of amastigotes in bone marrow, and molecular techniques. The latter includes PCR and restriction fragment length polymorphism with the parasite being confirmed as L. infantum. The girl’s mother had vacations annually in Spain—an endemic country—and was serologically positive to L. donovani, indicating congenital transmission [57]. The case of a two-year old boy in ND [24] may likely represent an example of vertical transmission in the USA as discussed earlier.

5.3. Horizontal Transmission—Blood Transfusion

Another likely route of Leishmania transmission is horizontal transmission through blood transfusion. In the USA, leishmaniases caused by blood transfusion have been reported only in pet dogs. Three of seven recipients of seropositive blood donors developed antibodies to Leishmania sp. One was further confirmed with L. infantum infection by microscopic demonstration of amastigotes, and positive cell culture. In contrast, none of the 25 recipients of seronegative blood donors tested positive [58]. A systematic review on the global prevalence of Leishmania infections among blood donors was carried out, covering databases between 1997 and 2016. Among 13,743 blood donors, the seropositive rate was 7% (95% CI: 5−8%) with the lowest and highest of 0.25% and 16% in Bangladesh and Brazil, respectively. Furthermore, a 2% (95% CI: 1−3%) positive rate was yielded by molecular testing with the lowest and highest of 0.05% and 7% in Iran and Spain, respectively [59]. A total of 500 blood samples from donors in the northeastern region of Brazil were tested for Leishmania DNA by PCR, and 6.2% (95% CI: 4.1−8.3%) were positive. One was further determined to be L. infantum by DNA sequencing, which is the parasite endemic in the region [60]. In north-western Iran, 860 blood donors were tested for Leishmania antibodies and DNA between 2017 and 2018. A total of 2.8% were seropositive and 45% were positive for Leishmania kDNA [61]. In China, metagenomic next-generation sequencing was applied to detect various microbes in 10,720 plasma samples collected from blood donors during 2012−2018; a total of 1.37% were positive for Leishmania spp. [62]. Collectively, blood donors worldwide may carry Leishmania parasites in donated blood and products, which poses some risk to recipients.
Can Leishmania parasites stay viable long enough to be delivered to recipients under the conditions for blood product storage? It has been found that current standard storage conditions for donated blood banks are insufficient to kill Leishmania spp. Live cells of L. tropica and L. donovani were found in blood products under these conditions. The blood products tested included whole blood, packed red blood cells, frozen RBC, and platelet concentrate [63]. In three endemic areas of Brazil, six out of thirteen blood recipients from L. infantum-positive donors were followed up for 60 days, and two converted seropositive [64]. Furthermore, hamsters that were peritoneally injected with whole blood or purified monocytes prepared from clinically asymptomatic donors but serologically positive to Leishmania established infections [65]. Without a doubt, these lines of evidence together confirm that blood donors of Leishmania-positive status, even without clinical manifestations, can transmit the parasites to blood-transfusion recipients.

6. Risks of Leishmania spp. Transmission in the USA

The USA is one of the 99 countries of endemic leishmaniasis according to WHO (https://www.who.int/news-room/fact-sheets/detail/leishmaniasis, accessed on 24 October 2025). In order to maintain endemicity in an area, two components are necessary, i.e., leishmanial parasites and capable sand fly vectors. Figure 3 provides detailed information on both of these components in individual U.S. states. Three states have both necessary factors: Texas, Oklahoma, and Florida. Consequently, the risks for leishmanial transmission are highest among these three U.S. states. Arizona is also facing almost similar levels of risks since autochthonous infections have been found in both humans and wildlife, even though current information on capable sand fly vectors is lacking. Several other states (AL, AR, DE, GA, KY, KS, LA, MD, MO, MS, NC, NJ, OH, SC, TN) have also been confirmed to have capable vectors; however, even though a lower level of risk exists, human travel and animal transporting across state borders must be considered. The sole human case with L. donovani complex in North Dakota apparently indicates transmission from a dog to a human [24]. Therefore, L. infantum-infected Foxhounds should receive appropriate and immediate veterinary treatment with proper biosecurity measures to minimize risk to people, or even be euthanized when treatment fails to minimize any risk of transmission.

7. Conclusion Remarks

Despite being endemic in the USA, leishmaniasis has attracted little attention from medical doctors. It is highly likely that the situation in this country will turn from bad to worse if no urgent actions take place. Several factors are exceedingly important and need to be taken into consideration to mitigate the disease and its spread. First, global warming and climate change are predicted to spread the disease northwards [66]. This trend has already been observed in Texas where the disease is now found in central and northern counties from its earlier limit to southern counties [11]. Second, wild animals are infected with and serve as reservoirs for zoonotic Leishmania spp. [6]. All five Leishmania spp. found in the USA are capable of infecting humans in addition to other mammals. Third, the disease is an emerging infectious disease and a threat to public health in the USA [7]. Capable sand fly vectors exist in various states (Figure 3), which makes the spread of the disease to humans a high probability. Fourth, U.S. populations travel more frequently than ever nationally and internationally to high endemic countries/regions, which greatly increases their risks of infections.
In order to mitigate the spread of leishmaniasis, accurate and timely diagnosis followed by prompt treatment is key. These medical actions should serve to dramatically minimize the source of infections. Reducing exposure to sand fly vectors by wearing insect repellents and covering up body parts when necessary is critical (https://www.cdc.gov/leishmaniasis/hcp/clinical-overview/index.html, accessed on 24 October 2025). Educating general populations about the disease and its prevention should also be a priority. Last but not the least, efforts to combat global warming on a national and international scale should decelerate or even stop the northbound spread of this serious vector-born parasitic disease. In conclusion, there is an urgent need to expand reservoir and vector surveillance and improve physician training in diagnosis in the USA.

Author Contributions

Conceptualization, C.Y.; methodology, C.Y.; formal analysis, C.Y.; investigation, C.Y.; resources, C.Y.; data curation, C.Y.; writing—original draft preparation, C.Y.; writing—review and editing, C.Y., Y.Y. and A.D.; funding acquisition, C.Y. All authors have read and agreed to the published version of the manuscript.

Funding

The study is sponsored by the RUSVM intramural grants (41040-2025 and 41052-2026). The APC was paid for by RUSVM’s Associate Dean of Research and Postgraduate Study.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Acknowledgments

My colleague at Ross University School of Veterinary Medicine (RUSVM), Christa A. Gallagher, is greatly appreciated for her proofreading of the manuscript.

Conflicts of Interest

The authors declare no conflict of interest.

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Microorganisms 13 02485 g002
Figure 2. Distribution of autochthonous cutaneous leishmaniasis in the USA on human body parts. The body parts are categorized into head, neck, trunk, upper limp, and lower limp. Percentage of the body parts affected is presented as shown in the legend from the highest (>50%) on the head to the lowest (<5%) on the neck.
Figure 2. Distribution of autochthonous cutaneous leishmaniasis in the USA on human body parts. The body parts are categorized into head, neck, trunk, upper limp, and lower limp. Percentage of the body parts affected is presented as shown in the legend from the highest (>50%) on the head to the lowest (<5%) on the neck.
Microorganisms 13 02485 g002
Microorganisms 13 02485 g003
Figure 3. Risk levels of individual states for leishmaniasis endemicity in the USA by the distribution of Leishmania parasites and capable sand fly vectors with solid confirmation. Leishmania spp. data are from Table 1 and references [41,42,43]. Sand fly vectors Lutzomyia spp. are from reference [7,44]. L. mexianan in Arizona was identified in white-throated woodrat (Neotoma albigula) [45]. Leishmania spp: L. mexicana: Microorganisms 13 02485 i001; L. infantum: Microorganisms 13 02485 i002; L. donovani: Microorganisms 13 02485 i003; L. ellisi: Microorganisms 13 02485 i004; L. martiniquensis: Microorganisms 13 02485 i005; Sand fly species: Lu. anthophora: Microorganisms 13 02485 i006; Lu. cruciate: Microorganisms 13 02485 i007; Lu. diabolica: Microorganisms 13 02485 i008; Lu. shannoni: Microorganisms 13 02485 i009. Super Teacher Worksheets—www.superteacherworksheets.com.
Figure 3. Risk levels of individual states for leishmaniasis endemicity in the USA by the distribution of Leishmania parasites and capable sand fly vectors with solid confirmation. Leishmania spp. data are from Table 1 and references [41,42,43]. Sand fly vectors Lutzomyia spp. are from reference [7,44]. L. mexianan in Arizona was identified in white-throated woodrat (Neotoma albigula) [45]. Leishmania spp: L. mexicana: Microorganisms 13 02485 i001; L. infantum: Microorganisms 13 02485 i002; L. donovani: Microorganisms 13 02485 i003; L. ellisi: Microorganisms 13 02485 i004; L. martiniquensis: Microorganisms 13 02485 i005; Sand fly species: Lu. anthophora: Microorganisms 13 02485 i006; Lu. cruciate: Microorganisms 13 02485 i007; Lu. diabolica: Microorganisms 13 02485 i008; Lu. shannoni: Microorganisms 13 02485 i009. Super Teacher Worksheets—www.superteacherworksheets.com.
Microorganisms 13 02485 g003
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Yao, C.; Yang, Y.; Du, A. Autochthonous Leishmaniasis in the United States of America. Microorganisms 2025, 13, 2485. https://doi.org/10.3390/microorganisms13112485

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Yao C, Yang Y, Du A. Autochthonous Leishmaniasis in the United States of America. Microorganisms. 2025; 13(11):2485. https://doi.org/10.3390/microorganisms13112485

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Yao, Chaoqun, Yi Yang, and Aifang Du. 2025. "Autochthonous Leishmaniasis in the United States of America" Microorganisms 13, no. 11: 2485. https://doi.org/10.3390/microorganisms13112485

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Yao, C., Yang, Y., & Du, A. (2025). Autochthonous Leishmaniasis in the United States of America. Microorganisms, 13(11), 2485. https://doi.org/10.3390/microorganisms13112485

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