Exposure to quinolones, including levofloxacin, during the first-trimester is not associated with an increased risk of stillbirths, premature births, birth defects, or low birth weight.Two small post-marketing epidemiology studies of mostly short-term, first-trimester exposure found that fluoroquinolones did not increase risk of major malformations, spontaneous abortions, premature birth, or low birth weight. The label notes, however, that these studies are insufficient to reliably evaluate the definitive safety or risk of less common defects by ciprofloxacin in pregnant women and their developing fetuses. Breastfeeding
Fluoroquinolones have been reported as present in a mothers milk and thus passed on to the nursing child. The U.S. Food and Drug Administration (FDA) recommends that because of the risk of serious adverse reactions (including articular damage) in infants nursing from mothers taking ciprofloxacin, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother. Children
Oral and intravenous ciprofloxacin are approved by the FDA for use in children for only two indications due to the risk of permanent injury to the musculoskeletal system:

Inhalational anthrax (postexposure)
Complicated urinary tract infections and pyelonephritis due to Escherichia coli, but never as first-line agents.Current recommendations by the American Academy of Pediatrics note the systemic use of ciprofloxacin in children should be restricted to infections caused by multidrug-resistant pathogens or when no safe or effective alternatives are available. Spectrum of activity
Its spectrum of activity includes most strains of bacterial pathogens responsible for community-acquired pneumonias, bronchitis, urinary tract infections, and gastroenteritis.
Nager acrofacial dysostosis, also known as Nager syndrome, is a genetic disorder which displays several or all of the following characteristics: underdevelopment of the cheek and jaw area, down-sloping of the opening of the eyes, lack or absence of the lower eyelashes, kidney or stomach reflux, hammer toes, shortened soft palate, lack of development of the internal and external ear, possible cleft palate, underdevelopment or absence of the thumb, hearing loss (see hearing loss with craniofacial syndromes) and shortened forearms, as well as poor movement in the elbow, and may be characterized by accessory tragi. Occasionally, affected individuals develop vertebral anomalies such as scoliosis. The inheritance pattern is autosomal, but there are arguments as to whether it is autosomal dominant or autosomal recessive. Most cases tend to be sporadic. Nager syndrome shares many characteristics with five other craniofacial syndromes: Miller, Treacher Collins, Pierre Robin, Genee–Wiedemann and Franceschetti–Zwahlen–Klein. Genetics
While Nager syndrome is thought to be most often caused by haploinsufficiency of the spliceosomal factor SF3B4, in over one third of patients tested, the SF3B4 mutation is not found. Genetic sequencing shows that the syndrome can be caused by either autosomal recessive or autosomal dominant inheritance. Treatment
Due to craniofacial development, it is recommended that families work closely with craniofacial specialists as soon as Nager is recognized or suspected. Children born with Nager may need intubation immediately after birth, requiring tube feeding and a tracheotomy tube to help with breathing. Surgical intervention is commonly necessary to increase mandibular mobility.