Background SARS-CoV-2 predisposes patients to secondary infections; however, a better understanding of the impact of coinfections on the outcome of hospitalized COVID-19 patients is still necessary. Aim To analyse death risk due to coinfections in COVID-19 patients. Methods We evaluated the Odds of death of 212 severely ill COVID-19 patients, with detailed focus on the risks for each pathogen, site of infection, comorbidities and length of hospitalization. Findings The mortality rate was 50.47%. Fungal and/or bacterial isolation occurred in 89 patients, of which 83.14% died. Coinfected patients stayed hospitalized longer and had an increased Odds of dying (OR = 13.45, R 2 =0.31). The risk of death was increased by bacterial (OR=11.28) and fungal (OR=5.97) coinfections, with increased levels of creatinine, leukocytes, urea and C-reactive protein. Coinfections increased the risk of death if patients suffer from cardiovascular disease (OR= 11.53), diabetes (OR=6.00) or obesity (OR=5.60) in comparison with patients with these comorbidities but without pathogen isolation. The increased risk of death was detected for negative-coagulase Staphylococcus (OR=25.39), Candida non- albicans (OR=11.12), S. aureus (OR=10.72), Acinetobacter spp. (OR=6.88), Pseudomonas spp. (OR=4.77) and C. albicans (OR=3.97). The high-risk sites of infection were blood, tracheal aspirate and urine. Patients with coinfection undergoing invasive mechanical ventilation were 3.8 times more likely to die than those without positive cultures. Conclusions Severe COVID-19 patients with secondary coinfections required longer hospitalization and had higher risk of death. The early diagnosis of coinfections is essential to identify high-risk patients and to determine the right interventions to reduce mortality.

Storage of acetylcholine in synaptic vesicles plays a key role in maintaining cholinergic function. Here we used mice with a targeted mutation in the vesicular acetylcholine transporter (VAChT) gene that reduces transporter expression by 40% to investigate cognitive processing under conditions of VAChT deficiency. Motor skill learning in the rotarod revealed that VAChT mutant mice were slower to learn this task, but once they reached maximum performance they were indistinguishable from wild-type mice. Interestingly, motor skill performance maintenance after 10 days was unaffected in these mutant mice. We also tested whether reduced VAChT levels affected learning in an object recognition memory task. We found that VAChT mutant mice presented a deficit in memory encoding necessary for the temporal order version of the object recognition memory, but showed no alteration in spatial working memory, or spatial memory in general when tested in the Morris water maze test. The memory deficit in object recognition memory observed in VAChT mutant mice could be reversed by cholinesterase inhibitors, suggesting that learning deficits caused by reduced VAChT expression can be ameliorated by restoring ACh levels in the synapse.These data indicate an important role for cholinergic tone in motor learning and object recognition memory.

Sporotrichosis is a fungal disease that causes symptoms similar to those of other infectious and non-infectious diseases, making diagnosis difficult and challenging. Here, we report a case of an HIV-negative patient presenting disseminated sporotrichosis with widespread cutaneous lesions mimicking pyoderma gangrenosum, with bone marrow infection, pancytopenia, and hemophagocytic syndrome. However, all the clinical manifestations and a bacterial coinfection delayed the request for a fungal diagnosis. Therefore, sporotrichosis should always be investigated in patients from endemic areas presenting with widespread cutaneous lesions associated with pancytopenia.