Microcephaly Caused by Lymphocytic Choriomeningitis Virus

Maia Delaine; Anne-Sophie Weingertner; Antoine Nougairede; Quentin Lepiller; Samira Fafi-Kremer; Romain Favre; Rémi Charrel


Emerging Infectious Diseases. 2017;23(9):1548-1550. 

In This Article


The prevalence of LCMV appears to be low (LCMV IgG 0.3%) in France.[8] Only 4 cases of LCMV infection have been described in France since 1978.[9–11] The laboratory of clinical microbiology at Public Hospitals of Marseille has received 83 samples for detection of LCMV during 2015–2016. The only other amniotic fluid specimen tested during this period was negative for LCMV by PCR. During 2005–2015, this laboratory has not reported a positive result for LCMV (R. Charrel, Aix-Marseille University, Marseille, France, 2017, pers. comm).

It is difficult to determine whether these findings were caused by low circulation of LCMV or lack of awareness of general practitioners and obstetricians. However, although Zika virus has been recently identified as a cause of microcephaly, physicians should consider other viruses when dealing with signs compatible with congenital infection by Zika virus.

Since 1955, a total of 58 cases of congenital LCMV infections have been reported worldwide; all were diagnosed postnatally.[2,10,12,13] An influenza-like illness was described in 50% of pregnant women, and exposure to rodents was reported by 33%.[2,10,12,13] Chorioretinitis and chorioretinal scars were observed in 89%–100% of infected children, and hydrocephalus (mostly triventricular dilation) in 96%.[2,10,12,13]

There are many prenatal ultrasonic signs of LCMV infection, involving mostly the central nervous system. Of these signs, ventriculomegaly is the most common. Bilateral cataracts are also observed. The estimated mortality rate for infants with prenatal LCMV infection is 30%–35% at the age of 21 months.[14,15] Almost all survivors have neurologic sequelae,[14] of which 67% are severe.[2,13,15]

Differential diagnoses of congenital LCMV infection include testing for TORCH infections (Table). A definitive diagnosis relies on virus identification by serologic analysis or direct evidence, such as virus isolation or detection of LCMV RNA in fetal or maternal samples. For our patient, limited volumes of samples precluded additional serologic analysis; thus we performed testing by PCR. However, a positive PCR result and sequence confirmation are direct evidence for the presence of LCMV.

When ultrasonographic signs suggestive of infection are identified, complete ultrasonography can be performed to identify associated abnormalities and conventional congenital infections. If results of this initial assessment are negative, testing for LCMV is indicated for fetal samples and maternal serum samples. Medical termination of the pregnancy might need to be considered for some cases.

No vaccine or effective treatment is available for infection with LCMV. Ribavirin has been used for some cases of severe infection. However, this drug is contraindicated for pregnant women.[12] For these women, only preventive measures are available.

LCMV infection is not included among occupation-related diseases in France, and there are few case reports of infection with this virus. Large-scale prospective studies are needed to determine the incidence of malformations associated with this virus. Lesions caused by LCMV might cover a broad spectrum, ranging from minor to severe and irreversible manifestations. Thus, LCMV infection should be considered a possible etiology requiring laboratory investigations for cases of evocative neurologic malformations or nonimmunologic anasarca not caused by a TORCH infection or genetic or chromosomal abnormalities.