Late-onset Cytomegalovirus Infection Associated With Gastric Outlet Obstruction in a Preterm Twin

**Background:** Cytomegalovirus (CMV) is the most common cause of congenital and postnatal viral infection. While congenital CMV often causes severe neurological disease, postnatal infection is typically mild in term infants but poses significant risks to preterm infants (<32 weeks gestation) and those with very low birth weight (<1500 g). Known manifestations in this vulnerable population include pneumonia, thrombocytopenia, hepatitis, colitis, and hearing impairment. Gastric outlet obstruction had not previously been described in association with CMV in neonates.

**Methods:** This is a single case report of a preterm twin born at 28+2 weeks gestation with a birthweight of 1325 g to a 26-year-old woman (G1/P0) via delivery due to preeclampsia. The infant developed nonbilious vomiting at 6 weeks of age while on full enteral feeds without respiratory support. Diagnostic workup included ultrasound, functional x-ray swallow examination, esophagogastroduodenoscopy (EGD), and histology. CMV infection was confirmed by polymerase chain reaction (PCR) on tissue, blood, and urine samples. A dry blood sample from day 3 of life was tested for CMV to rule out congenital infection. The infant underwent surgical intervention including resection of a submucous fibrotic ring and pyloroplasty according to Heineke-Mikulicz.

**Key Results:** Ultrasound revealed hypertrophy and stenosis of the proximal pylorus, though without the classic appearance of pyloric hypertrophy. Initial pyloromyotomy at the peripheral hospital did not improve symptoms. Upon transfer at 9 weeks of age, EGD showed severely inflamed gastric and esophageal mucosa with a non-passable pylorus. Histology demonstrated giant cells typical of CMV infection, confirmed by PCR. Quantitative PCR results showed: urine CMV >900,000 IU/ml (normal <200), EDTA-blood 1249 IU/ml (normal <200), gastric/esophageal tissue positive, and spinal fluid <100 IU/ml (normal <200). The dry blood sample from day 3 of life was negative for CMV, ruling out congenital infection. Brain ultrasound, ophthalmological assessment, and brainstem evoked response audiometry showed no cerebral involvement. Electrolytes, transaminases, complete blood count, coagulation, and albumin were within normal limits. Intraoperatively, a submucous fibrotic ring extending into the proximal one-third of the pylorus was found and resected. Histopathology of the resected tissue showed giant cells and CMV-DNA was amplified via nested multiplex-PCR. Continuous enteral feeding via duodenal tube began on postoperative day 2, with full enteral feeding achieved by day 12. The patient was discharged home on day 26 after surgery at a gestational age of 41 weeks with a weight of 3410 g (26th percentile). Treatment included intravenous ganciclovir switched to oral valganciclovir (continued for 3 months) and omeprazole (continued for 6 weeks).

**Clinical Implications:** This is the first reported case of noncongenital neonatal gastric outlet obstruction associated with intestinal CMV infection in a preterm infant. The case is notable because: (1) oral feeding was tolerated well until 6 weeks of age, making congenital malformation unlikely; (2) breastmilk pasteurization (due to maternal CMV-IgG seropositivity) was stopped only 2 weeks before symptom onset; (3) congenital infection was ruled out by negative day-3 dry blood sample; (4) pathology showed fibrous tissue with active CMV replication rather than muscular hypertrophy; and (5) no common systemic signs of CMV (e.g., elevated liver enzymes) were present, suggesting infection was mainly restricted to the intestine. This case expands the known spectrum of CMV presentations in preterm infants and underscores the importance of considering CMV as a potential cause of intestinal symptoms, including gastric outlet obstruction, in neonatal and gastroenterological practice.