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The purpose of this review is to summarize recent literature on nontuberculous mycobacteria in water of healthcare systems. Despite improvement in identification techniques and emergence of infection prevention and control programs, nontuberculous mycobacteria remain present in hospital water systems, causing outbreaks and pseudo-outbreaks in healthcare settings.Waterborne outbreaks and pseudo-outbreaks of nontuberculous mycobacteria continue to affect hospitals. Improvements in methods of identification and investigation, including MALDI-TOF and whole genome sequencing with evaluation of single nucleotide polymorphisms, have been used successfully in outbreak and pseudo-outbreak investigations. Recent studies have shown control of outbreaks in immunocompromised patients through the use of sterile water for consumption, as well as control of pseudo-outbreaks by using sterile water for procedures. Construction activities have been implicated in outbreaks and pseudo-outbreaks of nontuberculous mycobacteria. Water management programs are now required by the Joint Commission, which will likely improve water risk mitigation.Improvement in detection and identification of nontuberculous mycobacteria has led to increasing recognition of waterborne outbreaks and pseudo-outbreaks. Water management programs are of vital importance in infection prevention.

Patient: Male, 57-year-old Final Diagnosis: Hepatitis • herpes Symptoms: Fever Medication: — Clinical Procedure: — Specialty: General and Internal Medicine Objective: Challenging differential diagnosis Background: Herpes simplex virus-2 (HSV-2) affects nearly 1 in 5 adults in the United States. Complications such as viral hepatitis and dissemination are rare in immunocompetent hosts. In this report, we describe a case of viral hepatitis secondary to disseminated HSV-2 in an immunocompetent patient with recurrent fevers and elevated aminotransferases. Case Report: A 57-year-old man with a history of type 2 diabetes and hypertension was admitted with a right index finger lesion concerning for an abscess. He underwent successful incision and drainage and was started on ampicillin-sulbactam. On Day 2 of hospitalization, he developed recurrent fevers and elevated aminotransferases and inflammatory markers. An extensive infectious, rheumatologic, and malignancy workup were pursued without immediate findings. Imaging demonstrated cirrhotic morphology of the liver and splenomegaly, but lab markers were intact for liver synthetic function. On Day 7 of hospitalization, fever frequency decreased, and HSV-2 titers resulted, with positive IgM and negative IgG. He subsequently developed erythematous, raised lesions in multiple dermatomes. Nucleic acid amplification testing of biopsied lesions was positive for HSV-2, confirming viral hepatitis secondary to disseminated HSV-2. He was started on intravenous acyclovir and discharged on valacyclovir following improvement in symptoms. Conclusions: We report a case of viral hepatitis secondary to disseminated HSV-2 in an immunocompetent host. Up to 25% of cases occur in immunocompetent hosts and many patients do not develop characteristic skin lesions. Early diagnosis and treatment of viral hepatitis secondary to disseminated HSV remains vital to minimize morbidity and mortality.

Background We present a case of a 65-year-old male with a history of acute B-cell lymphoblastic leukemia (ALL) who presented with fevers and skin lesions. The patient achieved remission after induction chemotherapy. Nineteen months after diagnosis, while on maintenance therapy, the patient presented as noted above. He was instructed to hold maintenance therapy and sent to the hospital. Methods Results On examination, the patient was febrile. He had papules present on the forehead, chest, arms, legs, and back. Physical examination was otherwise unremarkable. Labs were notable for a white blood cell count of 3600/uL (absolute neutrophil 3100/uL) and creatine kinase (CK) of 593 U/L. Blood and urine cultures, Histoplasma, Varicella, Toxoplasma, HIV, and an acute hepatitis panel were negative. CT of the chest, abdomen, and pelvis was unremarkable. He was empirically started on micafungin and valacyclovir. However, he continued to have fevers and myalgias. Wound culture was negative for fungus after four weeks of growth. Skin biopsy immunostains were consistent with an unknown protozoan. Specimens were sent to an outside facility and yielded a diagnosis of Anncaliia algerae. Antibiotics were changed to albendazole and voriconazole, with subsequent improvement in all symptoms. Conclusion Microsporidia most commonly infect immunocompromised hosts. Clinical manifestations of microsporidiosis are extremely diverse. Oftentimes, symptoms are not present in those found to be infected with Microsporidia. A disseminated disease has been identified but remains rare. Although Microsporidia have been identified as a cause of infection in immunocompromised patients, there are few reports of infection in those diagnosed with cancer, and only a few cases have been due to Anncaliia algerae. In studies pertaining to ALL patients, roughly one-fifth of patients were identified as being infected with Microsporidia, but most did not have symptoms. This is the first reported case of disseminated Microsporidia in a patient with ALL and the first disseminated infection presenting as a skin manifestation. Of identified cases of disseminated Microsporidial infection, mortality was high. Thus, prompt recognition of Microsporidia as a cause of infection in patients with ALL is of utmost importance. Disclosures All authors: No reported disclosures.