Cutaneous Manifestations,Gestational Timing,and Fetal Effects of Infectious Dermatoses in Pregnancy: A Narrative Review

Disseminated gonococcal infection (Neisseria gonorrhoeae)

Pregnancy is a risk factor for disseminated gonococcal infection (DGI). ⁴ All pregnant patients <25 years, as well as patients 25+ years at high risk, should be screened for N. gonorrhoeae at the first prenatal visit. Patients who remain at high risk should be retested in the third trimester. ⁵

Most gonococcal infections in pregnant patients are asymptomatic or limited to the urogenital tract. Dermatologic manifestations are only present in DGI, which is classically associated with a triad of dermatitis, tenosynovitis, and polyarthralgia. ⁶ Typical skin findings, which occur in ∼75% of cases, include 5–50 painless pustular or vesiculopustular lesions on a purpuric base found on the distal extremities lasting 3–4 days.^7,8

Pregnancy complicated by gonorrhea is associated with increased risk of chorioamnionitis and fetal growth restriction. Patients with positive gonorrheal cultures at delivery carry an elevated risk of premature rupture of membranes and prematurity.^9,10 Any neonate whose birthing parent has untreated gonorrhea is at high risk for infection. ¹¹ Neonatal gonococcal infection most commonly presents with conjunctivitis, potentially leading to blindness. ¹²

Syphilis (Treponema pallidum)

All pregnant individuals should be screened for syphilis at their first prenatal visit. Dermatologic presentation of syphilis does not differ between pregnant and nonpregnant individuals.^5,13 In patients without HIV, primary syphilis may present with one or more indurated, painless chancres, often on the genitalia, occurring within 3 weeks of exposure. Secondary syphilis has variable presentations, including condyloma lata (Fig. 1A), papulosquamous lesions (Fig. 1B) that may involve the palms and soles, morbilliform eruption, mucosal lesions including mucous patches and split papules (Fig. 1C), and generalized nontender lymphadenopathy.^5,14,15

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FIG. 1.

(A) Secondary syphilis presenting as condyloma lata on the genitalia. (B) Secondary syphilis presenting as papulosquamous lesions on the neck. (C) Secondary syphilis presenting with mucosal lesions including a mucous patch and split papule. (D) Chronic reddish, hyperpigmented leprosy lesions on the upper back. (E) Large condyloma acuminata from human papilloma virus (HPV) infection. (F) Primary varicella infection with pruritic vesicles erupting into ulcers and crusted sores at different stages of healing. (G) Primary varicella infection with classical “dew drop on a rose petal” lesions. (H) Vulvar zoster infection with linear vesicular outbreak along a nerve distribution.

Syphilis during pregnancy is associated with prematurity, spontaneous abortion, stillbirth, and perinatal death. ¹⁶ Transplacental transmission may occur at any time during pregnancy, and the risk increases with duration of gestational exposure.^17–21 Newborn transmission may also occur intrapartum by contact with maternal genital lesions. ²² Fetal syphilis is associated with elevated liver transaminases early in the disease course, as well as anemia, thrombocytopenia, and hydrops fetalis later in the disease course. Early congenital syphilis (presenting within 2 years of age) is associated with hepatosplenomegaly, skin eruption (oval and maculopapular but becomes copper-colored with desquamation mostly on the palms and soles), rhinitis, thrombocytopenia, and anemia. ²² Of note, Jarisch–Herxheimer reaction presents with cramping, pyrexia, and myalgias in up to 40% of individuals treated with penicillin for syphilis during pregnancy.^23,24

Group A Streptococcus

Group A Streptococcus is commonly associated with impetigo, which presents as honey-colored crusted erosions. Skin findings associated with invasive GAS include cellulitis and necrotizing fasciitis. The risk of invasive GAS is 2× higher in pregnant individuals and 20× higher in postpartum individuals compared with nonpregnant individuals.^25,26 GAS is the leading cause of death in pregnant and recently postpartum patients with sepsis.^27,28 Onset of GAS infection in the antepartum/intrapartum period constitutes 7%–15% of reported pregnancy-related GAS infections, whereas onset in the postpartum period constitutes 85%–92%.^29,30 While fetal demise in the setting of maternal GAS infection has been recorded, it is unclear whether the underlying mechanisms are maternal instability and/or fetal infection.^27,30

Staphylococcus aureus and methicillin-resistant S. aureus

The most common presentation of Staphylococcus aureus and methicillin-resistant S. aureus (MRSA) is skin or soft tissue infection in the form of folliculitis, furunculosis, impetigo, and cellulitis. In a study of 57 pregnant patients diagnosed with MRSA, skin and soft tissue infections accounted for 96% of cases, and 58% of patients had recurrent episodes. ³¹ The most common lesion sites were the extremities, buttocks, and breast (mastitis). Patients with MRSA were more likely to be multiparous and to have a history of cesarean delivery (CD). Maternal systemic illness and bacteremia are important causes of maternal morbidity but are not major causes of fetal infection. ³² While vaginal MRSA colonization has been associated with high rates of transmission to neonates, early-onset neonatal disease is rare.^33–35

Leprosy (Mycobacterium leprae, M. lepromatosis)

Leprosy is an infection of the skin and peripheral nerves by Mycobacterium leprae or M. lepromatosis that should be suspected in the setting of chronic hypopigmented or reddish skin lesions (Fig. 1D) unresponsive to standard treatment, and/or sensory loss within the lesions or extremities. ³⁶ Leprosy can be exacerbated during pregnancy due to hormonal changes and immunosuppression, particularly in the third trimester.^37–39 Type 1 (reversal) reactions characterized by acute inflammation of existing skin lesions tend to occur postpartum, whereas type 2 reactions (erythema nodosum leprosum) tend to occur late in pregnancy. ⁴⁰ These reactions also depend on the type of leprosy initially present, as type 1 reactions tend to occur with the borderline forms of leprosy, while type 2 reactions more commonly occur with borderline lepromatous and lepromatous leprosy. ⁴¹

Fetal transmission of leprosy is possible but rare. ⁴² Most reported cases of leprosy in newborns are attributed to airborne infection. ⁴³ In a sample of 38 pregnant individuals with biopsy-proven leprosy, 5% of neonates developed self-healing indeterminate leprosy younger than 2 years, as well as anti-M. leprae IgA, IgG, and IgM antibodies, likely from airborne exposure. ⁴⁴

Chikungunya

Chikungunya is a mosquito-borne virus presenting with fever, headache, myalgias, arthralgias, conjunctival injection, and skin eruption. ⁴⁵ The skin eruption typically begins as a flushing erythema on the face and upper chest, evolving into maculopapular lesions with or without petechiae on the trunk and extremities. Chikungunya infection during pregnancy may actually protect against long-term joint pain sequelae. ⁴⁶

While some studies show no significant maternal complications, others have demonstrated a possible association with preeclampsia, hemorrhage, and sepsis.^46–48 Several studies suggest that Chikungunya may only pose an elevated risk for pregnancy complications or neonatal toxicity when maternal infection occurs just before delivery. ⁴⁶ In one study of 150 pregnant patients with Chikungunya, 20% developed adverse pregnancy outcomes, including preterm delivery, premature rupture of membranes, decreased fetal movements, intrauterine death, and oligohydramnios. ⁴⁹ Neonatal transmission occurs almost exclusively in the setting of intrapartum maternal viremia.^50,51 In these cases, neonatal sequelae include seizures, encephalitis, neurocognitive delays, or postnatal onset of microcephaly.^51,52

Condyloma acuminata (human papilloma virus)

Condyloma acuminata (genital warts) is caused by human papilloma virus (HPV) types 6 and 11. ⁵³ In pregnant and nonpregnant individuals, condyloma acuminata present as flesh-colored or hyperpigmented papules with an irregular surface (Fig. 1E). During pregnancy, especially at 12–14 weeks of gestation, genital warts may grow more rapidly and become much larger than those in nonpregnant individuals.^54,55 In addition, warts become more friable during pregnancy, leading to irritation and bleeding. ⁵³ Condyloma acuminata can also cause bacterial trapping, which can lead to chorioamnionitis, fetal infection in utero, and premature rupture of membranes in cases of ascending infection. ⁵⁶

HPV transmission to the placenta and newborn is possible but rare. In a study of 1050 pregnant individuals (40.3% HPV-positive), the most frequent neonatal HPV detection sites at birth and/or 3 months were the conjunctiva, mouth, genitalia, and pharynx. Importantly, all HPV detected in neonates cleared before the age of 6 months. ⁵⁷ For pregnant individuals with condyloma acuminata at delivery, CD may be considered to avoid the risk of perinatal transmission or the rare complication of juvenile laryngeal papillomatosis. ⁵³ A CD is particularly recommended if the patient has a large, obstructive condyloma.

Cytomegalovirus

Cytomegalovirus (CMV) is the most common cause of congenital viral infection in the United States. ⁵⁸ While maternal CMV is typically asymptomatic, 15% of women with primary infection develop mononucleosis-like symptoms. ⁵⁹ While CMV is not typically associated with dermatologic manifestations in immunocompetent individuals, patients with CMV may develop a morbilliform drug eruption following aminopenicillin administration. ⁶⁰ Immunocompromised individuals with cutaneous CMV can have varied clinical presentations from localized perioral or perianal ulcers to maculopapular lesions or vesiculobullous eruptions that mimic herpetic infections. ⁶¹

CMV can be transmitted to the newborn when a previously infected birthing parent reactivates the infection or becomes infected with a different viral variant. The risk of fetal transmission depends on the presence of maternal antibodies to CMV. In primary CMV, no antibodies are present. Individuals who experience a primary infection during pregnancy, particularly in the first 20 weeks, are most likely to deliver infants with symptomatic disease. ⁵⁸ A positive serologic test in the first trimester is also strongly associated with stillbirth. ⁶² Symptoms of neonatal infection include petechiae, skin lesions, jaundice, microcephaly, retinitis, myocarditis, splenomegaly, thrombocytopenia, and sensorineural hearing loss. ⁶³

Dengue

Dengue is a mosquito-borne virus with significant morbidity and mortality among pregnant individuals and fetuses. It typically presents with fever, headache, nausea, myalgias, arthralgias, retroorbital pain, and skin eruption. ⁴⁵ The characteristic eruption occurs in 50%–82% of patients with dengue fever.^64,65 Within the first 24–48 hours of symptom onset, patients develop a transient flushing erythema. Approximately 3–6 days after fever onset, the skin findings evolve into an asymptomatic maculopapular or morbilliform eruption. Individual lesions may coalesce into a generalized confluent erythema with petechiae and round islands of sparing. ⁶⁴ The lesions typically start on the dorsal hands and feet, spread to the extremities and torso, and last for several days before subsiding. Hemorrhagic cutaneous manifestations, including petechiae, purpura, or ecchymosis, are commonly seen in dengue hemorrhagic fever and dengue shock syndrome, but rarely in dengue fever. ⁴⁵

Pregnancy is considered a risk factor for serious, symptomatic dengue infection. ⁶⁶ Dengue causes labor and delivery complications in ∼7%–8% of cases. ⁶⁷ Severe dengue in pregnant individuals increases the risk of complications, including preeclampsia, gestational hypertension, anemia, and organ dysfunction. ⁶⁷ While data are limited, symptomatic dengue during pregnancy may be associated with adverse fetal outcomes, including stillbirth, preterm birth, low birth weight, and neurological issues.^68–70 Similar to adult manifestations, neonatal dengue presents with fever, skin eruptions, bleeding risk, and hepatomegaly. ⁷¹ Compared with infections occurring in the third trimester, maternal dengue in the first and second trimesters carries a greater risk of fetal harm. ⁶⁷

Herpes simplex virus

Infections caused by the human Herpesviridae are characterized by periods of latency, as the virus remains dormant in target cells until reactivation, viral replication, and subsequent infection. ⁵⁸ While herpes simplex virus (HSV1) lesions are predominantly oral (75%) and HSV2 lesions are largely genital (75%), both present as extremely painful vesicles on an erythematous base, which ultimately rupture and progress to crusted ulcers. Even in individuals with a nonprimary first episode or recurrent HSV infection, symptoms during pregnancy may be more severe. ⁷²

While HSV is most commonly transmitted through sexual contact (vaginal, anal, or oral intercourse), it can also be transmitted during gestation or delivery. ⁵⁸ Intrauterine transmission is rare, but occurs more frequently in the first 20 weeks of gestation. Congenital HSV infection is not limited to primary maternal infections, although the risk is significantly higher in these cases. Congenital HSV can cause abortion, stillbirth, or congenital anomalies. ⁷³ In newborns, congenital HSV can present as skin/eye/mucous membrane disease (vesicular lesions, conjunctivitis), isolated central nervous system disease, or disseminated disease (often accompanied by liver failure and death). Transmission by contact during delivery is significantly more common, with 90% of newborn infections acquired during birth. ⁵⁸ Primary, first-episode maternal outbreaks of HSV (lesions without HSV antibodies) occurring at birth are most likely to be transmitted to the newborn, with a 30%–50% incidence of newborn infection. ⁵⁸ Because the newborn may not receive maternal HSV antibodies, neonatal infections can have severe manifestations, including skin, eye, and mouth, central nervous system, or disseminated disease. ⁷⁴

Human immunodeficiency virus

Certain dermatologic conditions may manifest in patients with human immunodeficiency virus (HIV) or AIDS exclusively, at increased prevalence or severity, during different disease stages, or in the setting of opportunistic coinfections. ⁷⁵ Affecting up to 85% of patients with HIV, seborrheic dermatitis presents as erythematous macules with white or yellow greasy-appearing scale. ⁷⁶ Oral hairy leukoplakia, bacillary angiomatosis, and Kaposi sarcoma are more common in individuals infected with HIV. ⁷⁵ Oral hairy leukoplakia, caused by the Epstein–Barr virus, typically presents with white, verrucous, confluent plaques on the lateral tongue that cannot be scraped off. ⁷⁷ Bacillary angiomatosis, caused by Bartonella henselae and B. quintana, is typically transmitted via cat scratch/bite and presents with vascular, painful proliferations of the skin. ⁷⁸ Kaposi sarcoma, caused by human herpesvirus type 8, is a cancer often associated with AIDS that presents with multifocal asymptomatic reddish-purple patches which may progress to raised plaques or nodules. ⁷⁹ Many individuals with acute HIV may also experience acute retroviral syndrome, which is a mononucleosis-like illness with characteristic dermatological symptoms including a symmetrical maculopapular erythematous exanthem and possible mucocutaneous ulcerations. ⁸⁰

Pregnancy does not appear to increase the prevalence of skin disease in individuals with HIV.^81,82 However, HIV is associated with higher rates of spontaneous abortion, stillbirths, perinatal mortality, intrauterine growth restriction, low birth weight, and chorioamnionitis. ⁸³ All pregnant patients should be offered HIV testing using an opt-out approach with a strong recommendation for third trimester testing. ⁸⁴ Mode of delivery for HIV patients depends on viral load at 36 weeks of gestation, with considerations of disease trajectory, treatment duration/adherence, and obstetric factors. ⁸⁵

Measles

Measles typically presents with a prodrome of fever, malaise, cough, coryza, and conjunctivitis, followed by a characteristic cutaneous eruption. ⁸⁶ The eruption often begins with Koplik spots (small white lesions on an erythematous base) on the buccal mucosa, followed by maculopapular lesions first appearing ∼7–18 days after exposure that spread from the head to the trunk and lower extremities. ⁸⁷

Pregnant individuals are at an increased risk of measles-associated complications, including hospitalization, pneumonia, and death.^88,89 Measles is also associated with increased rates of adverse pregnancy outcomes, including low birth weight, preterm delivery, spontaneous abortion, intrauterine fetal demise, and neonatal mortality.^89,90 Nonimmune individuals planning to become pregnant should get the MMR vaccine and defer conception for 4+ weeks, whereas nonimmune individuals who are already pregnant should defer this live vaccine until after delivery. ⁸⁶

Congenital measles can occur in neonates born to individuals who develop measles within 10 days of delivery. ⁹¹ Congenital measles presents with characteristic maculopapular lesions at birth or within the first 10 days of life, as well as fever, cough, coryza, and conjunctivitis. To decrease the risk of severe disease such as encephalitis, it is recommended that neonates with maternal measles exposure receive intravenous or intramuscular immune globulin. ⁹²

Parvovirus B19

Most individuals with parvovirus B19 are asymptomatic or have mild, nonspecific, cold-like symptoms. Pregnancy does not alter clinical presentation of this infection. ⁹³ The virus may cause papular, purpuric eruptions on the hands and feet in a “gloves and socks” distribution. Other associated clinical conditions include erythema infectiosum (less common in adults; characteristically presents with “slapped cheek” rash), arthropathy, transient aplastic crisis, and chronic red cell aplasia.

Parvovirus B19 carries an estimated 30% risk of transplacental infection, but the risk of fetal death varies based on gestational age. ⁹⁴ The risk of fetal loss in the first trimester, at 13–20 weeks, and after 20 weeks is 19%, 15%, and 6%, respectively. ⁹⁵ Transplacental transmission of parvovirus B19 is of significant concern given the risk of severe fetal anemia, myocarditis, cardiac failure, and liver damage, potentially leading to hydrops fetalis.^58,96 The most vulnerable period is the second trimester due to increased liver hematopoiesis at this time. ⁹³ Conversely, first trimester is the period of lowest risk due to fetal inability to produce IgM and the difficulty of antibody transfer across the placenta. Nonetheless, early detection of maternal infection is critical so that the fetus can be monitored for hydrops fetalis. Pregnant individuals diagnosed with parvovirus B19 should receive serial ultrasonographies weekly or biweekly for 10–12 weeks. ⁹⁷

Rubella

Rubella presents similarly in pregnant and nonpregnant individuals. Symptoms include fever, malaise, joint pain, and upper respiratory inflammation, followed by development of fine pink maculopapular lesions that start on the face and spread to the trunk and extremities.

Transmission to the fetus can result in congenital rubella syndrome (deafness, heart defects, retinopathy, anemia, microcephaly, and psychomotor retardation), intrauterine growth retardation, or spontaneous abortion. ⁹⁸ Congenital rubella syndrome is unlikely to develop if maternal infection occurs after 20 weeks of gestation. ⁵⁸ Maternal infection before 20 weeks can produce the aforementioned anomalies, although the greatest risk is during the first trimester and decreases with gestational age. The risk of congenital rubella syndrome is about 50%, 25%, and 10% during the first, second, and third month of pregnancy, respectively. ⁹⁹

All patients should be screened for rubella immunity during the preconceptual or first antenatal visit. ⁹⁹ Nonimmune individuals who are planning to become pregnant should receive the vaccine and defer conception for 28+ days, whereas nonimmune individuals who are already pregnant should receive the vaccine postpartum. ¹⁰⁰

Varicella (primary varicella zoster virus; chickenpox) and herpes zoster (varicella zoster virus reactivation; shingles)

Individuals planning to become pregnant should be serologically screened for varicella immunity and vaccinated if not immune. Primary varicella (chickenpox) has a higher risk of severe maternal and fetal complications in pregnancy than herpes zoster (shingles). ¹⁰¹ While varicella incidence is not higher, disease severity appears to be worse in pregnant than nonpregnant individuals.

Primary varicella may present with fever, malaise, myalgias, and an intensely pruritic, maculopapular exanthem with vesicles that erupt into ulcers and crusted sores (Fig. 1F, G). ⁵⁸ Maternal varicella infection may be complicated by pneumonia in 10%–20% of cases. ¹⁰² Varicella has not been associated with higher spontaneous abortion, premature birth, or intrauterine death rates.^103,104 Congenital varicella syndrome (CVS) has been observed in 0.4% of cases, in which maternal varicella infection occurred before 12 weeks of gestation, and in 2% of cases, in which infection occurred between 13 and 20 weeks of gestation. ¹⁰⁵ CVS presents with intrauterine growth restriction, cicatricial (scarring) lesions that may be depressed and distributed in a dermatomal pattern, as well as central nervous system, ocular, and musculoskeletal abnormalities. ¹⁰⁶

Postnatal varicella transmission may occur via vertical or horizontal transmission. The risk of severe neonatal infection is higher if maternal infection occurs between 5 days before and 2 days after delivery. Varicella acquired 10–28 days after birth tends to be mild. ¹⁰⁷ Horizontal transmission is more common in preterm infants in the neonatal intensive care unit. ¹⁰⁸

In contrast to varicella, pregnancy does not appear to affect the presentation of herpes zoster, and herpes zoster does not usually cause transplacental infection or any significant fetal risks.^53,109 It presents as a linear vesicular or pustular outbreak along the nerve’s corresponding dermatome (Fig. 1H). ⁵³

Zika

Zika is a mosquito-borne virus that is usually mild and self-limiting but can have grave fetal consequences when contracted during pregnancy. This infection classically presents as an influenza-like illness with a diffuse, fine, mildly pruritic, maculopapular eruption.^110–112 Lesions commonly follow a symmetrical pattern involving the face, neck, trunk, palms, and soles. ¹¹¹ In 90% of cases, lesions develop within the first 24–48 hours after symptom onset. More atypical cutaneous manifestations of Zika include subcutaneous hematomas, petechiae, oral ulcers, and jaundice.^113–116

There is no evidence to suggest that pregnant individuals are more susceptible to infection or more severely affected.^117–119 The greatest risk lies in maternal–fetal transmission of Zika virus, as congenital infection can result in fetal microcephaly, brain atrophy, ventricular enlargement, and intracranial calcifications. ¹¹⁸ In a study of 442 completed pregnancies, there was a 6% risk of Zika virus-related birth defects (primarily microcephaly) among patients with a third trimester infection, compared with an 11% risk among patients with a first trimester infection, suggesting that earlier infection during gestation may increase the risk of birth defects. ¹²⁰

Candida vulvovaginitis (Candida albicans, C. tropicalis, C. glabrata, C. parapsilosis)

Pregnancy is one of the most important predisposing factors for Candida vulvovaginitis, with up to 50% of pregnant individuals infected.^121–123 Candida vulvovaginitis risk increases with the duration of gestation and gravidity, and is associated with preterm delivery and low birth weight.^124–126 Symptoms of Candida vulvovaginitis, including vaginal discharge, vulvar erythema, introital pruritus, and irritation, may also be more severe during pregnancy. ¹²¹ When vulvovaginitis is suspected, providers should consider other infections with less prominent dermatologic manifestations such as bacterial vaginosis (Gardnerella vaginalis) and trichomoniasis (Trichomonas vaginalis).

Transmission of Candida to the neonate can occur via ascending infection in utero or passage through the infected birth canal. While neonatal infection is generally limited to the skin and mucosa (including oral thrush and cutaneous candidiasis), it may also cause pneumonia and sepsis in low birth weight or immunosuppressed neonates. ⁵³

Coccidioidomycosis (Coccidioides immitis, C. posadasii; valley fever)

Coccidioides, which is endemic to the Southwest and Pacific United States, primarily causes pulmonary infection. ¹²⁷ While still rare, pregnant individuals who are infected with Coccidioides during or after the second trimester are at increased risk of extrathoracic dissemination to skin and soft tissue, genital tract, peritoneum, and central nervous system weeks to months after the initial exposure. ¹²⁸ Skin or soft tissue involvement typically presents with a persistent papule or verrucous lesion that may ulcerate, cutaneous granulomatous lesions, subcutaneous soft tissue abscesses, or extrathoracic lymphadenopathy.^129,130

Pregnant patients who live in endemic regions or have a history of coccidioidomycosis should be serologically screened regularly. ¹³¹ Individuals who acquire coccidioidomycosis during the second or third trimester or within 6 weeks postpartum are at increased risk of developing severe or disseminated disease and should thus be followed closely.^132,133 The fetus and newborn are rarely affected by maternal coccidioidomycosis. ¹³⁴

Leishmaniasis

Leishmaniasis is endemic to tropical and subtropical areas in Northeastern Africa, Southern Europe, the Middle East, Southeastern Mexico, and Central and South America. ¹³⁵ It is transmitted by infected sand fly bites. The main clinical subtypes are visceral (kala-azar), mucocutaneous, and cutaneous (local and disseminated). ¹³⁵ Symptoms of visceral leishmaniasis include fever, hepatosplenomegaly, and lymphadenopathy. Mucocutaneous leishmaniasis initially presents with superficial ulcerations of the nasopharyngeal mucosa, which may invade more deeply over time. ¹³⁵ Localized cutaneous leishmaniasis presents with an erythematous papule at the bite site that evolves into a vesicle then a pustule. When the pustule breaks, a crusted-over ulcer with thick, nodular borders forms. Disseminated cutaneous leishmaniasis presents first on the face, and then progressively spreads to the rest of the skin with hard erythematous nodules and reddish-brown smooth or verrucous plaques that may ulcerate. ¹³⁵

Pregnancy may be associated with larger exophytic lesions. ¹³⁶ Leishmaniasis in pregnancy is associated with severe anemia, preterm birth, spontaneous abortion, and stillbirth.^136,137 Visceral leishmaniasis and infection earlier in gestation are associated with higher risk of adverse outcomes. ¹³⁸ Vertical transmission has been reported but is rare. ¹³⁹