Infectious crystalline keratopathy was first reported by Gorovoy and colleagues in 1983 when they identified bacteria colonizing a cornea after a penetrating keratoplasty. Subsequent cases have elaborated on the organisms responsible and the management outcomes. Patients present with a white or gray branching opacity originating from an epithelial defect, commonly after a penetrating keratoplasty. Local immunosuppression contributes to the quiescent nature and the limited inflammatory response associated with infectious crystalline keratopathy. Diagnosis of the infective pathogens may be difficult, with a corneal scraping often being too superficial to obtain an adequate specimen. A biofilm is present that advantages microorganism survival, reduces antibiotic bioavailability, and inhibits diagnostic microbial detection. Treatment begins with topical antimicrobials, initially broad spectrum and then targeted to microorganism sensitivity. Adjunctive therapies to enhance the efficacy of treatment include disruption of the microorganism biofilm by laser, intrastromal antibiotics, and keratectomy. In recalcitrant cases, or where corneal scarring ensues, corneal transplantation is required.
Mice lacking functional neurokinin-1 receptors (NK1R-/-) display abnormal behaviours seen in Attention Deficit Hyperactivity Disorder (hyperactivity, impulsivity and inattentiveness). These abnormalities were evident when comparing the behaviour of separate (inbred: ‘Hom’) wildtype and NK1R-/- mouse strains. Here, we investigated whether the inbreeding protocol could influence their phenotype by comparing the behaviour of these mice with that of wildtype (NK1R+/+) and NK1R-/- progeny of heterozygous parents (‘Het’, derived from the same inbred strains). First, we recorded the spontaneous motor activity of the two colonies/genotypes, over 7 days. This continuous monitoring also enabled us to investigate whether the diurnal rhythm in motor activity differs in the two colonies/genotypes. NK1R-/- mice from both colonies were hyperactive compared with their wildtypes and their diurnal rhythm was also disrupted. Next, we evaluated the performance of the four groups of mice in the 5-Choice Serial Reaction-Time Task (5-CSRTT). During training, NK1R-/- mice from both colonies expressed more impulsive and perseverative behaviour than their wildtypes. During testing, only NK1R-/- mice from the Hom colony were more impulsive than their wildtypes, but NK1R-/- mice from both colonies were more perseverative. There were no colony differences in inattentiveness. Moreover, a genotype difference in this measure depended on time of day. We conclude that the hyperactivity, perseveration and, possibly, inattentiveness of NK1R-/- mice is a direct consequence of a lack of functional NK1R. However, the greater impulsivity of NK1R-/- mice depended on an interaction between a functional deficit of NK1R and other (possibly environmental and/or epigenetic) factors.
HighlightsWe compared the behaviour of NK1R−/− mice and wildtypes in the 5-Choice Continuous Performance Test.NK1R−/− mice did not express excess impulsivity (premature response or false alarms) in this test.NK1R−/− mice expressed excessive perseveration, which is common in ADHD.The findings point to a behavioural phenotype for ADHD patients with polymorphism of the TACR1 gene.
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