Chryseobacterium indologenes is a rare non-fermenting gram-negative pathogen that can cause opportunistic infections in humans. Most infections are nosocomial and acquired through contaminated devices such as ventilators, endotracheal tubes, and indwelling catheters. An increasing number of infections have been reported in recent years after the first reported case of ventilator-associated pneumonia in 1993. Blood, lung, ocular, and peritoneal infections, among others, have been reported. The high rate of intrinsic resistance to broad-spectrum antibiotics is a matter of concern since there are no standard guidelines for the management and treatment of this infection. Here, we present the case of a 94-year-old female who was admitted and intubated after a cerebral vascular accident. During her stay, she developed a fever. The deep tracheal aspirate culture was positive for gram-negative bacilli with smooth, circular, and yellow-pigmented colonies that were later identified as C. indologenes. Antimicrobial susceptibility tests done with VITEK 2 and by the Kirby-Bauer disc diffusion method showed susceptibility to ciprofloxacin, minocycline, and trimethoprim-sulfamethoxazole and resistance to all other tested antimicrobials. The infection was successfully treated with ciprofloxacin antibiotic. To the best of our knowledge, this is the first reported case of C. indologenes infection in Lebanon.

Hemophagocytic lymphohistiocytosis (HLH), a hyperinflammatory hyperferritinemic syndrome, is triggered by various etiologies and diseases and can lead to multiorgan dysfunction and death. There are two types of HLH: primary and secondary. Primary HLH (pHLH) is caused by a genetic mutation resulting in dysfunction in cytotoxic T lymphocytes (CTLs), natural killer (NK) cells, hyperactivated immune cells, and hypercytokinemia. In secondary HLH (sHLH), an underlying etiology is the cause of the disease. Infections, malignancy, and autoimmune diseases are well-known triggers for sHLH. Infectious triggers for sHLH are most frequently viruses, where different mechanisms, including dysregulated CTLs and NK cell activity and persistent immune system stimulation, have been reported. Similarly, in severe coronavirus disease 2019 (COVID-19) patients, a hyperinflammatory mechanism leading to hypercytokinemia and hyperferritinemia has been demonstrated. A similar dysfunction in CTLs and NK cells, persistent immune system stimulation with increased cytokines production, and severe end-organ damage have been reported. Therefore, a significant overlap is present between the clinical and laboratory features seen in COVID-19 and sHLH. However, SARS-CoV-2, similar to other viruses, can trigger sHLH. Hence, a diagnostic approach is needed in severe COVID-19 patients presenting with multiorgan failure, in whom sHLH should be considered.