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

Abstract

Pregnancy introduces physiological changes that can alter the presentation, progression, and treatment considerations of infectious skin diseases. While noninfectious dermatoses during pregnancy have been extensively studied, the impact of various bacterial, viral, fungal, and parasitic dermatoses on maternal and fetal health remains less well characterized. The gestational timing of infection plays a critical role in determining potential risks to both the pregnant patient and fetus, with certain infections leading to complications such as preterm birth, congenital anomalies, or neonatal morbidity. This narrative review consolidates current knowledge on the diagnosis, clinical presentation, and management of infectious dermatoses in pregnancy, with an emphasis on their cutaneous manifestations and potential fetal effects. By enhancing awareness of these conditions, health care providers can improve early recognition, ensure appropriate treatment, and mitigate adverse pregnancy outcomes.

Introduction

Pregnancy introduces physiological changes that can influence the presentation, course, and management of various skin conditions. Dermatoses in pregnancy can be broadly categorized as infectious or noninfectious. While noninfectious dermatoses are caused by autoimmune or inflammatory processes, infectious dermatoses arise from bacterial, viral, fungal, or parasitic agents. Although these infections do not occur solely in pregnancy and/or the immediate postpartum, timely diagnosis and management are critical in obstetric practice given their significant potential risk to both the pregnant patient and fetus.

Infectious dermatoses have received less comprehensive coverage in the literature than noninfectious dermatoses.^1–3 Accordingly, this narrative review aims to summarize the diagnosis and treatment of infectious dermatoses in pregnant individuals, primarily within the tables and figures. Within the main text, we emphasize the cutaneous manifestations, potential effects of gestational timing of disease onset, and associated fetal risks to guide the obstetrician’s clinical practice.

Methods

We performed a PubMed search using relevant search terms, including “infectious dermatoses,” “cutaneous manifestations,” “gestational timing,” “pregnancy,” and “postpartum” across bacterial, viral, fungal, and parasitic infections, limited to English-language articles. Given the scope of this review, infections meeting the following criteria were excluded from the main text and summarized only in the table: (1) minimal or no impact on maternal or fetal health; (2) minimal or no differences in presentation, clinical course, treatment, or outcomes between pregnant and nonpregnant individuals; (3) limited dermatologic manifestations; or (4) clinical relevance primarily in severe immunosuppression. Infections excluded on this basis (lymphogranuloma venereum, Lyme disease, scabies, and Mpox) were retained in the table to preserve completeness and to assist clinicians’ differential diagnosis.

Clinical images were obtained from a hospital database and included only female-identifying patients of childbearing age who provided written informed consent, with documentation maintained in accordance with institutional policies.

Bacterial dermatoses

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

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

Viral dermatoses

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

Fungal dermatoses

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

Parasitic dermatoses

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

Conclusion

Throughout this narrative review, we discuss infectious dermatoses caused by bacteria, viruses, fungi, and parasites that carry important maternal and fetal implications during pregnancy. Because some infections present differently or more severely in pregnancy and carry varying fetotoxic risks depending on the gestational timing of infection, timely diagnosis and management are critical. Cutaneous findings are a prominent and informative indicator of infection in many of these diseases. Thus, obstetrical providers must understand the cutaneous morphologies, associated symptoms, diagnostic techniques, and management options for these infectious dermatoses throughout pregnancy (Table 1).

Table 1.

Summary of the Skin Findings, Diagnosis, and Treatments (Safe During Pregnancy) Associated with Various Bacterial, Viral, Fungal, and Parasitic Infectious Dermatoses, Highlighting Key Considerations Relevant to the Management of Pregnant Patients as well as Congenital and Neonatal Disease Manifestations

Infection	Skin findings	Diagnosis	Treatment	Key considerations in pregnancy	Congenital and neonatal disease
BACTERIAL
Disseminated gonococcal infection (DGI)	Pustular or vesiculopustular lesions on purpuric base, found on distal extremities7,8	Nucleic acid amplification testing (NAAT) or culture in a specimen of blood, synovial fluid (from joint aspiration) or tissue, skin lesion (from biopsy), or other nonmucosal sites 5	Ceftriaxone 5 Coadministration of treatment for chlamydia Consult infectious disease expert 5	Increased risk in pregnancy 4 Prenatal screening Increases risk of chorioamnionitis, intrauterine growth restriction, premature rupture of membranes, and prematurity9,10	Neonatal disease: conjunctivitis (most common), consider use of empirical erythromycin ointment in newborns 12 Scalp abscesses, other wound infections, and systemic disease (sepsis, meningitis) may also occur 12
Lymphogranuloma venereum (LGV)	Genital ulcer or mucosal inflammatory reaction at the site of inoculation 140	Presumptive: risk factors and positive NAAT 141 Definitive: LGV-specific molecular testing, such as with polymerase chain reaction (PCR) genotyping (not widely available in the United States) 141	Azithromycin or erythromycin preferred during pregnancy (whereas doxycycline used in nonpregnant patients) 5 Pregnant individuals with rectal LGV should also receive a test of cure with NAAT four weeks after the initial positive test, and undergo retreatment with a second course of antibiotics if test positive again 5	While LGV is most prevalent in men who have sex with men, women and pregnant individuals, especially those who are coinfected with HIV, are susceptible142,143	No adverse fetal effects 142
Syphilis	Primary syphilis: indurated, painless chancres, often on genitalia5,15 Secondary syphilis: condyloma lata, papulosquamous lesions that may involve palms and soles, morbilliform eruption, or mucosal lesions, including mucous patches and split papules5,14,15	Presumptive: nontreponemal and treponemal serologic tests 5 Definitive: darkfield examinations and molecular tests from lesion exudate or tissue 5	IM penicillin G benzathine (some recommend that pregnant patients receive a second dose about 1 week later) 5 Jarisch–Herxheimer reaction in up to 40% of treated pregnant individuals23,24	Prenatal screening 5 Risk of fetal transmission increases with duration of gestational exposure17–21,144,145 Associated with prematurity, spontaneous abortion, stillbirth, nonimmune hydrops, and perinatal death 16 All patients with signs of secondary syphilis should be monitored for headaches, neck pain, and vision changes (potential signs of neurosyphilis; requires treatment with IV penicillin)	Congenital disease: hepatosplenomegaly, rash, rhinitis, thrombocytopenia, anemia 22
Group A Streptococcus (GAS)	Impetigo, cellulitis, necrotizing fasciitis 25	Gram stain or culture from suspected infection site (e.g., blood, throat)30,146	Empirical treatment for toxic shock: fluids, antibiotics, intravenous immune globulin (IVIG) 147 Definitive treatment: penicillin G (or another beta-lactam) and clindamycin (or linezolid if clindamycin is unavailable) 146 Source control with vulvar debridement and/or hysterectomy may be necessary in necrotizing GAS infections recalcitrant to antibiotic therapy 147	Increased risk in pregnancy and especially postpartum25,26 Leading cause of death in pregnant and recently postpartum patients with sepsis27,28	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 infection27,30
Staphylococcus aureus and methicillin-resistant S. aureus (MRSA)	Folliculitis, furunculosis, impetigo, cellulitis 31	Presumptive: clinical 148 Definitive: culture of purulent exudate or blood culture (if systemic) 148	Incision and drainage 149 Debridement 149 Trimethoprim–sulfamethoxazole, clindamycin, or vancomycin 150 First-generation cephalosporin may be used if methicillin-susceptible S. aureus (MSSA) is confirmed 150	More common in multiparous patients and patients with history of cesarean delivery (CD) 31	Fetal transmission and neonatal disease are rare 33–35
Leprosy	Chronic hypopigmented or reddish skin lesions 36	At least one of three signs are present: (i) loss of sensation in a hypopigmented or reddish patch, (ii) thickened or enlarged peripheral nerve with loss of sensation and/or weakness in the associated muscle, or (iii) presence of acid-fast bacilli from a biopsy of the leading edge of the skin lesion 36	Dapsone, clofazimine (causes reddening of neonate’s skin), rifampin36,39,151	Symptom exacerbation in third trimester 37–39 Type 1 reactions (RR) characterized by acute inflammation of existing skin lesions tend to occur postpartum, whereas type 2 reactions (ENL) characterized by painful erythematous nodules tend to occur late in pregnancy 40	Fetal transmission rare 42
Lyme disease (LD)	Erythema migrans (EM) 152	Early stage: characteristic EM rash (poor serology sensitivity at this stage) 153 Late stage: serology 153	Prevention in endemic areas: apply insect repellant such as N,N-diethyl-meta-toluamide (DEET) or picaridin to exposed skin and clothing to prevent tick bites 153 Prophylaxis after tick bite: Doxycycline 153 Early-stage treatment: amoxicillin or cefuroxime153,154 Late-stage treatment: cater to specific organ systems involved153,154	Lower risk in pregnancy 155 Smaller proportion of patients with annular EM and extracutaneous symptoms, as well as lower number of truncal lesions 156	Limited evidence of fetal transmission153,157,158
VIRAL
Chikungunya	Initially face and upper chest erythema, then maculopapular lesions with or without petechiae on the trunk and extremities 45	Acute phase: NAAT 159 After first week: serology 159	Supportive care only	Possible association with preeclampsia, hemorrhage, sepsis, preterm delivery, premature rupture of membranes, decreased fetal movements, intrauterine death, and oligohydramnios 46–49 May only increase risk for pregnancy complications or neonatal toxicity if infection occurs just before delivery 46	Neonatal transmission: almost exclusively in the setting of intrapartum maternal viremia50,51 Neonatal disease: seizures, encephalitis, neurocognitive delay, postnatal onset of microcephaly51,52
Condyloma acuminata	Flesh-colored or hyperpigmented papules with rough surface 53	Physical examination 53 Biopsy if uncertain	Surgical (preferred): electrocautery, tangential excision with fine scissors or scalpel, cryotherapy, or carbon dioxide laser53,58 Nonsurgical: trichloroacetic acid (other topical agents including podophyllotoxin, imiquimod 5% cream, and sinecatechin ointment are contraindicated in pregnancy)53,58	Genital warts may be more friable and larger than those in nonpregnant individuals54,55 Increased risk of chorioamnionitis and premature rupture of membranes 56 CD may be recommended for individuals with condyloma acuminata at the time of delivery, rupture of membranes, or high viral load 53	Fetal transmission rare 57 Human papilloma virus (HPV) detected in children at birth usually clears before the age of 6 months 57
Cytomegalovirus (CMV)	Possible morbilliform drug eruption after penicillin 60	IgM and IgG assays used to determine whether CMV was contracted before or after conception; in some cases, IgM can quickly become undetectable, or it may persist up to 7 months after the initial infection; therefore, the only way to reliably diagnose primary maternal infection is with seroconversion from IgG negative to positive58,109 IgG avidity testing and amniotic fluid testing for CMV DNA	No approved maternal treatment for primary CMV infection 58 Antivirals such as ganciclovir, valganciclovir, or valacyclovir may be effective in preventing congenital infection 58	Most common cause of congenital viral infection in the United States 58 Risk of intrauterine transmission is higher in patients who contract primary CMV after conception 58 Primary infection during first 20 weeks of gestation is most likely to cause symptomatic disease in newborn 58	Fetal transmission if parent reactivates or becomes infected with new variant 58 Neonatal disease: petechiae, rashes, jaundice, microcephaly, retinitis, myocarditis, splenomegaly, thrombocytopenia, hearing loss 58
Dengue	24–48 hours after symptom onset: transient flushing erythema64,65 3–6 days after fever onset: asymptomatic maculopapular or morbilliform eruption64,65	NAAT or non-structural protein 1 (NS1) ELISA testing, both in combination with an IgM antibody test 67 Tourniquet test: positive result is indicated by numerous petechiae appearing below the blood pressure cuff, signifying increased capillary fragility	Supportive care only	Pregnancy is risk factor for severe infection 66 Infection increases risk of preeclampsia, gestational hypertension, anemia, organ dysfunction, stillbirth, preterm birth, low birthweight, and neurological congenital anomalies 67–70 Infections in first and second trimesters carry greater risk of fetal harm than infections in third trimester 67	Neonatal disease: fever, rash, bleeding, hepatosplenomegaly 71
Herpes simplex virus (HSV1, HSV2)	Painful vesicles on erythematous base; ultimately rupture and progress into crusted ulcers 58 Oral (HSV1) or genital (HSV2)	Viral culture or PCR of vesicle fluid 160	Oral acyclovir is given for primary infection and may also be considered in patients with a history of recurrent genital HSV starting at 36 weeks of gestation 161 IV acyclovir is approved only for life-threatening maternal herpetic infection 161	Monitor closely for genital herpetic lesions throughout pregnancy 161 Increased symptom severity during pregnancy 72 If active lesions are present, CD is recommended; if no lesions or prodromal symptoms are present, CD is not indicated 161	Fetal transmission is rare but occurs more frequently in the first 20 weeks of gestation, potentially resulting in abortion, stillbirth, or congenital anomalies 58 Intrapartum transmission is common, especially if primary infection 58 Congenital disease: skin/eye/mucous membrane disease (vesicular lesions, conjunctivitis), isolated central nervous system disease, or disseminated disease (often accompanied by liver failure and death) 58
Human immunodeficiency virus (HIV)	Seborrheic dermatitis, oral hairy leukoplakia, bacillary angiomatosis, Kaposi sarcoma, acute retroviral syndrome 75–79	Fourth-generation immunoassay; if positive, confirm with antibody differentiation immunoassay; if positive fourth-generation immunoassay but negative or indeterminate antibody differentiation immunoassay, RNA 162	Combined antiretroviral therapy (ART): triple drug therapy for all pregnant and breastfeeding individuals with HIV, regardless of CD4 count, viral load, or clinical stage 163 Drug choice depends on prior treatment history, drug-resistance, toxicity, comorbidities, and ability to cross the placenta 85	Pregnancy does not increase the prevalence of skin disease in HIV-infected individuals, but HIV is associated with higher rates of spontaneous abortion, stillbirths, perinatal mortality, intrauterine growth restriction, low birth weight, and chorioamnionitis 81–83 If viral load is <50 HIV RNA copies/mL at 36 weeks of gestation: vaginal delivery should be offered 85 If viral load is ≥400 HIV RNA copies/mL at 36 weeks of gestation: planned CD should be offered 85	Without intervention, there is a high risk of fetal transmission with active or advanced disease 83
Measles	Koplik spots on buccal mucosa, followed by maculopapular lesions appearing 7–18 days after exposure that spread from head to trunk to lower extremities 86	Measles-specific IgM antibodies 86 PCR 86	Supportive care only 86	Nonimmune individuals planning to become pregnant: get MMR vaccine and defer conception for at least 4 weeks 86 Nonimmune individuals who are already pregnant: Defer MMR vaccine until after delivery 86 Pregnancy increases risk of measles-associated complications88,89 Increased rates of low birth weight, preterm delivery, admissions to neonatal intensive care unit, spontaneous abortion, intrauterine fetal demise, neonatal mortality 88–90	Congenital disease: maculopapular rash at birth or within first 10 days of life, fever, cough, coryza, conjunctivitis 91 Neonates with maternal measles exposure should receive IM measles immune globulin 91
Mpox	Painful macules evolving into umbilicated papules, vesicles, pseudo-pustules, and then pruritic crusted-over lesions164,165	PCR 166 Serology 166 Consult public health authorities 166	Antiviral (tecovirimat; limited data have not shown adverse maternal or fetal effects) 167–169	Increased risk of neonatal intensive care unit admission, pediatric death, preterm labor, pregnancy loss, maternal hospitalization, maternal death, prematurity, small-for-gestational age, low birthweight, microcephaly, congenital anomalies 167 Pregnant individuals exposed to mpox should receive postexposure vaccination with the modified vaccinia Ankara (MVA) if certain indications based on public health authorities and exposure risk are met 168	Can be vertically transmitted across the placenta to the fetus (congenital mpox) or to the neonate through close contact during or after birth117,169,170 Congenital disease: prematurity, small-for-gestational age, low birthweight, microcephaly, and structural anomalies 167
Parvovirus B19	Papular, purpuric eruption on the hands and feet in a “gloves and socks” distribution 93 Erythema infectiosum (“slapped cheek”)	Immunocompetent: serology93,171 Immunocompromised or aplastic crisis: viral DNA titers93,171	Supportive care Potentially blood transfusions, IVIG 58	Early detection of maternal infection is critical so that the fetus can be monitored for hydrops fetalis 97 Pregnant individuals diagnosed with parvovirus B19 should receive serial ultrasonography weekly or biweekly for 10–12 weeks 97	∼30% risk of fetal transmission, resulting in fetal anemia, myocarditis, cardiac failure, liver damage, hydrops fetalis, and fetal loss 94 Highest risk to fetus in second trimester, lowest in first 93
Rubella	Fine pink maculopapular lesions spreading from face to trunk and extremities 58	Serology 99	Supportive care	Prenatal screening 99 Nonimmune individuals planning to become pregnant: get MMR vaccine and defer conception for 3 months 99 Nonimmune individuals who are already pregnant: defer MMR vaccine until after delivery 99 Increased risk of intrauterine growth retardation, spontaneous abortion 98 Risk of congenital disease decreases with gestational age 99	Congenital disease: deafness, heart defects, retinopathy, anemia, microcephaly, psychomotor retardation 98 Diagnosis of fetal rubella syndrome can be made using ultrasound (to detect physical abnormalities) or amniocentesis (to detect rubella DNA) 109
Varicella and herpes zoster	Varicella: intensely pruritic, maculopapular eruption with vesicles that erupt into ulcers and crusted sores 58 Herpes zoster: linear vesicular outbreak along nerve distribution 53	Clinical If uncertainty: PCR 172	Uncomplicated: oral acyclovir173,174 Varicella pneumonia: IV acyclovir173,174	Prenatal screening for varicella Varicella has a higher risk of severe maternal and fetal complications in pregnancy than herpes zoster 101 Varicella has not been associated with higher spontaneous abortion, premature birth, or intrauterine death rates103,104	Congenital varicella syndrome: cicatricial (scarring), depressed lesions in dermatomal pattern, central nervous system abnormalities, ocular abnormalities, musculoskeletal abnormalities 106 Risk of severe neonatal infection is higher if maternal infection with varicella occurs between 5 days before and 2 days after delivery 107 Varicella acquired between 10 and 28 days after birth tends to be mild 11
Zika	Diffuse, fine, mildly pruritic, maculopapular eruption; lesions often follow symmetrical pattern involving face, neck, trunk, palms, and soles111,112	NAAT 112	Supportive care 112	Pregnancy does not increase maternal susceptibility to or severity of infection 117–119 Earlier infection during gestation may increase risk of birth defects 120	Congenital disease: microcephaly, brain atrophy, ventricular enlargement, intracranial calcifications 118
FUNGAL
Candida vulvovaginitis	Vulvar erythema, introital pruritis, irritation 121	Microscopy, pH, and NAAT of vaginal discharge 175	First line: antifungal (clotrimazole, miconazole) 53 Second line: nystatin cream 53	Pregnancy is one of the most important risk factors (up to 50% of pregnant individuals infected) and may increase symptom severity 121–123 Increased risk of infection with duration of gestation and gravidity 124–126 Increased risk of preterm delivery and low birth weight 124–126	Neonatal disease: oral thrush, cutaneous candidiasis 53
Coccidioides	Papule or verrucous lesion that may ulcerate, cutaneous granulomatous lesions, subcutaneous soft tissue abscesses 128	Serology 176 Direct visualization 127 Culture 128 Patients with extrapulmonary disease: coccidioidal antigen assay of urine and blood, or cerebrospinal fluid of patients with coccidioidal meningitis	Pregnant individuals with mild to moderate pulmonary disease: may not need to be treated but should be followed closely 133 Pregnant individuals with severe and/or extrathoracic disease: IV amphotericin B in first trimester with possible transition to triazole later 133 Patients already on azoles at the time they become pregnant: switch to amphotericin B in the first trimester, then new baseline serologic testing and close monitoring for 6–12 weeks 133 Nonpregnant individuals on azoles: consider delaying pregnancy while on therapy or stopping therapy before becoming pregnant 133	Pregnant patients who live in endemic regions or have a history of coccidioidomycosis need to be serologically screened regularly 131 Individuals who acquire coccidioidomycosis during the second to third trimester or within 6 weeks postpartum are at increased risk for developing severe or disseminated disease and should thus be followed closely132,133	Fetal transmission and neonatal disease are rare 134
PARASITIC
Scabies	Generalized pruritis, worse at night 177 Papular or eczematous lesions in the finger webs, flexor wrist surfaces, elbows, axillae, buttocks, and genitalia 177	History (close contact with an individual with similar symptoms) 53 Physical examination 154 Definitive diagnosis: Identification of mites, eggs, eggshell fragments, or mite pellets in superficial skin scraping samples under microscope 177	Topical permethrin 178 While the spread of scabies without direct person-to-person contact is rare and data supporting environmental measures in reducing the spread are lacking, laundering clothes and linens is generally recommended 179	Not associated with adverse pregnancy outcomes 53 Must consider scabies in the differential diagnosis for intrahepatic cholestasis of pregnancy (before laboratory confirmation of that diagnosis)	Neonatal disease: Lesions on face, neck, scalp, palms, and soles, poor weight gain, failure to thrive 180
Leishmaniasis	Mucocutaneous leishmaniasis: nasopharyngeal ulcerations 135 Localized cutaneous leishmaniasis: erythematous papule at bite site that evolves into vesicle, pustule, then crusted ulcer 135 Disseminated cutaneous leishmaniasis: hard erythematous nodules and reddish-brown smooth or verrucous plaques that may ulcerate 135	History (travel to endemic region) 181 Physical examination Definitive diagnosis: parasite in clinical specimen (usually skin) by histology, culture, or PCR	Liposomal amphotericin B138,182 Topical paromomycin for mild cutaneous disease Miltefosine and the pentavalent antimonial drugs are contraindicated during pregnancy and breastfeeding 182	Larger exophytic skin lesions in pregnancy 136 Associated with severe anemia, preterm birth, spontaneous abortion, and stillbirth136,137 Higher risk of adverse outcomes if infection occurs earlier in gestation 138	Fetal and neonatal transmission is rare 139

Authors’ Contributions

C.N.L.: Conceptualization, formal analysis, investigation, methodology, project administration, visualization, writing—original draft, and writing—review and editing. E.R.S.: Conceptualization, formal analysis, investigation, methodology, project administration, visualization, writing—original draft, and writing—review and editing. A.K.B.: Investigation, supervision, and writing—review and editing. J.S.B.: Investigation, methodology, supervision, and writing—review and editing. D.R.G.: Supervision and writing—review and editing. M.K.P.: Conceptualization, investigation, methodology, resources, supervision, visualization, and writing—review and editing. G.P.Q.: Investigation, resources, supervision, and writing—review and editing. J.A.P.: Investigation, supervision, and writing—review and editing. A.F.R.: Conceptualization, investigation, project administration, supervision, validation, and writing—review and editing.