Background: Measles can cause miscarriages and preterm birth in nonimmune pregnant women. During the 2018–2019 measles outbreak in New York, a woman with measles delivered an extremely low birth weight preterm infant at our Women and Children’s Hospital. We describe our measles preparedness strategies and infection prevention and control (IPC) management relevant to congenital measles. Methods: Because of the measles outbreak, in Q4 2018, IPC verified measles immunity in all obstetric and pediatric staff, per state regulations, and recommended determining the measles immune status of all pregnant women. To prevent measles exposure, visitor restrictions for the neonatal intensive care unit (NICU) were implemented (May 2019); only 3 visitors were permitted for each infant, including parents. All visitors had to provide written documentation of immunity to measles, regardless of epidemiologic risk factors or receive an MMR vaccine prior to visiting. New York state and New York City health departments performed measles diagnostic testing for maternal and infant specimens. Results: Our hospital was informed of the imminent transfer of a woman in preterm labor with suspected measles. To avoid any exposure, the mother was masked in the ambulance bay and taken by commandeered elevator to the obstetrical operating room suite, which was cleared of other patients. She delivered by C-section and was transferred to an airborne infection isolation (AII) room. The 25-week-gestation infant was transported by isolette to the NICU and was placed on AII. Testing confirmed measles in the mother (measles PCR- and IgM-positive) and congenital measles in the infant (Table 1). The mother was allowed to visit the NICU when her respiratory symptoms and rash resolved, as confirmed by her provider, ~10 days after discharge. The infant never developed a rash, pneumonia, or neurologic findings. AII was discontinued on day of life 61 in consultation with the health departments. The infant was discharged at ~36 weeks gestation. No secondary cases of measles occurred among patients, visitors, or staff. Conclusions: We safely cared for an extremely preterm infant with congenital measles. Laboratory testing suggested prolonged presence of measles virus, but it is unknown how long an infant in the NICU should remain on AII. The current Council of State and Territorial Epidemiologists case definition for measles requires the presence of rash. This case provides support to revise this case definition if laboratory findings are consistent with congenital measles.

Funding: None

Disclosures: None

Caffeine and caffeinated coffee (CC) elicit acute insulin insensitivity when ingested before a carbohydrate load. The effects of CC on glucose tolerance and insulin sensitivity when co-ingested with a high carbohydrate meal and on postprandial metabolism of a subsequent (second) carbohydrate load have not been studied. In a randomised, crossover design, ten healthy males ingested either CC (5 mg caffeine/kg body weight), decaffeinated coffee (DC) or water (W; equal volume) co-ingested with a high glycaemic index cereal followed 3 h later by a 75 g oral glucose tolerance test. After the initial meal, insulin area under the curve (AUC) and insulin sensitivity index did not differ between treatments, although glucose AUC for CC (107 (sem 18) mmol/l × 3 h) and DC (74 (sem 15) mmol/l × 3 h) was greater than W ( − 0·2 (sem 29) mmol/l × 3 h, P < 0·05). After the second carbohydrate load, insulin AUC for CC was 49 % and 57 % greater (P < 0·01) than for DC and W, respectively. Despite the greater insulin response, glucose AUC for CC (217 (sem 24) mmol/l × 2 h) was greater than both DC (126 (sem 11) mmol/l × 2 h, P = 0·01) and W (55 (sem 34) mmol/l × 2 h, P < 0·001). Insulin sensitivity index after the second meal was lower after CC (8·2 (sem 0·9)) compared with both DC (12·4 (sem 1·2), P < 0·01) and W (13·4 (sem 1·4), P < 0·001). Co-ingestion of CC with one meal resulted in insulin insensitivity during the postprandial phase of a second meal in the absence of further CC ingestion. Thus, CC may play a role in daily glycaemic management.

Nine enzyme activity variants of liver/erythrocyte pyruvate kinase have been found amongst laboratory and wild mice. Four of these variants have been shown by biochemical and immunological criteria to be mutations of the structural gene, Pk-1s. These four structural gene mutations, and two regulatory gene mutations, define the gene complex, [Pk-1]. One allele of the structural gene, Pk-1sl, found in the inbred strain C57BL, has an unusual phenotype and affects the expression of pyruvate kinase in the liver but not erythrocyte. A possible mechanism for this tissue-specific structural gene mutation is suggested.

Nine enzyme activity variants and one charge variant of liver/erythrocyte pyruvate kinase have been found amongst laboratory and wild mice. Four of the enzyme activity variants were previously reported to be caused by allelic differences in the structural gene, Pk-ls. Analysis of two putative regulatory gene mutations is now reported, both of which map at, or close to, the structural gene on chromosome 3. One of these mutations, in the inbred strain SWR, is tissue specific, affecting enzyme concentration in the liver but not the erythrocyte the other, which arose in a mutation experiment, doubles the enzyme concentration in both tissues. The organization and the nomenclature in the [Pk-1] gene complex are discussed and are compared with the organization of other comprehensively analysed gene complexes in the mouse.