Traditionally, surfactant has been administered to preterm infants with respiratory distress syndrome via an endotracheal tube and in conjunction with mechanical ventilation. However, negative consequences of mechanical ventilation such as pneumothorax and bronchopulmonary dysplasia are well known. In order to provide the benefits of surfactant administration without the negative effects of mechanical ventilation, several methods of less invasive surfactant administration have been developed. These methods include InSurE (intubate, surfactant, extubate), pharyngeal administration, laryngeal mask administration, aerosolized surfactant administration, and thin catheter administration (TCA). Of these, TCA has been studied most extensively and holds the most promise as a less invasive and effective mode of surfactant administration to preterm infants. Further studies will aid in determining which patients would benefit most from less invasive surfactant administration.

The inner membrane complex (IMC), a series of flattened vesicles at the periphery of apicomplexan parasites, is thought to be important for parasite shape, motility and replication, but few of the IMC proteins that function in these processes have been identified. TgPhIL1, a Toxoplasma gondii protein that was previously identified through photosensitized labeling with 5-[125I] iodonapthaline-1-azide, associates with the IMC and/or underlying cytoskeleton and is concentrated at the apical end of the parasite. Orthologs of TgPhIL1 are found in other apicomplexans, but the function of this conserved protein family is unknown. As a first step towards determining the function of TgPhIL1 and its orthologs, we generated a T. gondii parasite line in which the single copy of TgPhIL1 was disrupted by homologous recombination. The TgPhIL1 knockout parasites have a distinctly different morphology than wild-type parasites, and normal shape is restored in the knockout background after complementation with the wild-type allele. The knockout parasites are outcompeted in culture by parasites expressing functional TgPhIL1, and they generate a reduced parasite load in the spleen and liver of infected mice. These findings demonstrate a role for TgPhIL1 in the morphology, growth and fitness of T. gondii tachyzoites.

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