BACKGROUND Disseminated Fusarium is rare in healthy children. Children with hematological tumors may have secondary fungal infections, including Fusarium infections , which are due to tumor bone marrow infiltration or prolonged bone marrow suppression after chemotherapy. Because of the lack of typical clinical manifestations and effective antifungal drugs, early diagnosis and treatment of the disease are difficult, and the prognosis is poor. CASE SUMMARY The patient in this case was a 13-year-old female child with rash and fever as the first symptoms. She had the characteristics of the four stages of skin that are typical of Fusarium infection. She was diagnosed with disseminated Fusarium infection through skin biopsy and blood culture and diagnosed with Fusarium solani infection based on the morphological characteristics of the blood culture. After treatment with liposome amphotericin B combined with voriconazole, the child recovered. CONCLUSION This case highlights that for children with secondary agranulocytosis after receiving chemotherapy for hematological malignancies, once typical abnormal skin damage is found, the possibility of Fusarium infection should be considered, and voriconazole alone or in combination with polyenes may be the most effective anti- Fusarium drugs. Amphotericin B, the traditional drug of disseminated Fusarium disease, has a high mortality rate, and it is not recommended to use it alone. Adequate neutrophil counts are essential for the treatment of disseminated Fusarium bloodstream infection.

BACKGROUND Nonketotic hyperglycinemia (NKH) is a rare autosomal recessive genetic disorder of abnormal glycine metabolism caused by insufficient activity of the glycine cleavage enzyme system. Glycine is believed to function mainly as an inhibitory neurotransmitter, but it can also act as a co-agonist of the N-methyl-D-aspartate (NMDA) receptor. The accumulation of a large amount of glycine in the brain leads to neuronal and axonal injury via overactivation of NMDA receptors located in the hippocampus, cerebral cortex, olfactory bulb, and cerebellum and to stimulation of the inhibitory function of glycine receptors located in the spinal cord and brain stem, resulting in central apnea, hiccups, and hypotonia in the early stage of the disease. CASE SUMMARY The child described in this report had typical clinical manifestations of NKH, such as hiccups, disturbance of consciousness, hypotonia, and convulsions, within the first week after birth. Whole-exome genetic testing revealed that the child had a compound heterozygous mutation, namely, c.395C>A (p.S132X) and c.2182G>A (p.G728R), in the GLDC gene, and he was diagnosed with NKH. For treatment, we administered an oral levetiracetam solution and added topiramate and prednisone for epilepsy control, but the epilepsy remained uncontrollable. Ketogenic diet therapy was started at 6 mo of age, his seizures were significantly reduced, and there were no obvious adverse reactions during ketogenic treatment. Furthermore, we found that with the development of the disease, high levels of serum glycine decreased or even disappeared without intervention, and as the disease progressed, the corpus callosum became dysplastic. CONCLUSION This case shows that plasma glycine levels cannot be used to evaluate the prognosis of NKH, that the development of the corpus callosum can be affected by NKH, and that a ketogenic diet may be effective for seizure control in NKH patients.