Purpose: To study the characteristics of dry eye disease (DED) secondary to ocular or systemic infections. Methods: PubMed, Scopus, and Cochrane databases were systematically reviewed for DED development after systemic and ocular infections. The severity of DED symptoms and signs, type of infection, and management outcomes were analyzed. Results: Of the 28 included studies, eight were related to HIV infection, five had hepatitis C, four to COVID-19, and 11 studies had DED secondary to herpes keratitis, Mycoplasma pneumoniae , viral conjunctivitis, Chlamydia infection, Mycobacterium leprae , and Chikungunya infections. The organisms implicated in conjunctivitis associated with DED were Coxsackie A24virus, S taphylococcus , and Mycoplasma . There were no immunocompromised patients in any of the studies except HIV. Nine studies established DED diagnosis based on symptoms alone, seven on signs alone, and 12 on symptoms and signs (at least abnormal Schirmer or tear break-up time, but not DEWS II criteria). The severity of DED symptoms was usually mild. HIV and hepatitis C showed no difference in tear volume and stability between cases and healthy controls. Advanced stages of hepatitis (stage 4 to stage 6) showed worse tear film parameters than the initial stages. Tear volume and stability were affected in 1/5 th of patients post-COVID-19. Absolute tear deficiency (zero Schirmer) was reported in two patients after Epstein–Barr virus and HIV infection that improved with intravenous acyclovir, cyclosporin A, and prednisolone in EBV infection only. Very few studies reported the management of postinfectious DED with artificial tears and had fair outcomes. Conclusion: Bacterial and viral infections can have DED as sequelae, although the infectious agent has not been isolated from the ocular surface in reported studies. DED is usually mild to moderate symptomatically, and tear film parameter levels do not meet DEWS II diagnostic criteria. The nonuniformity in reporting disease duration, tear film changes, and DED symptoms makes it difficult to understand the role of infection in causing DED.
Kothandan et al. (Fri,) studied this question.