Case Presentation: A 35-year-old male with a history of HIV (on Biktarvy), Kaposi sarcoma s/p chemotherapy, hypertension, and tobacco use presented to the ER with a syncopal episode. The patient reported sharp chest and abdominal pain, shortness of breath, fever, chills, tremors, and bloody stools over the past week. On admission, his vital signs revealed fever (102.3°F), sinus tachycardia, tachypnea, and hypotension. Examination showed facial and periorbital edema, coarse breath sounds bilaterally, abdominal tenderness, violaceous papules on the upper extremities, and non-tender cervical lymphadenopathy. Labs revealed hemoglobin of 5.0 g/dL, hematocrit 17.1%, White blood cell count 9.9 K/µL, platelets 13,000/µL, metabolic acidosis (lactic acid 15.3 mmol/L), elevated BUN (82 mg/dL), creatinine (2.8 mg/dL), and large blood with trace bacteria in urine. The HIV viral load was undetectable prior to admission, but repeat studies showed CD4% of 7% and an absolute CD4 count of 43 cells/µL. Imaging showed right basilar pneumonia, cervical lymphadenopathy, small abscess near the tongue, cellulitis, and severe proctocolitis. Blood and stool cultures were obtained, and the patient was started on Zosyn. On day three, his chest and abdominal pain persisted, and imaging revealed worsening bilateral pneumonia. Stool culture tested positive for Shigella and CMV DNA, while blood cultures grew Parvimonas micra, likely from buccal infection. A bronchoscopy was negative. Despite escalated treatment, the patient’s respiratory and mental status worsened, and developed throat edema, requiring a tracheostomy. Throughout the hospitalization, the patient received multiple transfusions and escalation to broad-spectrum antibiotics. Laboratory and physical findings suggested hemolytic uremic syndrome (HUS), and the diagnosis was confirmed to be HUS secondary to Shigella infection. Despite supportive care and discussions with the family, the patient’s condition continued to deteriorate, and care was withdrawn. The patient passed away shortly thereafter.
Discussion: Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy (TMA) characterized by thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury. The most common cause is infection with Shiga toxin-producing bacteria. HUS typically develops 5 to 13 days after diarrhea onset, with symptoms including renal dysfunction, anemia, and bleeding from thrombocytopenia. Worse outcomes are linked to cardiac and neurologic complications. Diagnosis requires a high index of suspicion, supported by CBC, metabolic panel, stool testing, and exclusion of other causes. Management is supportive, with careful fluid resuscitation, blood transfusions, and cautious platelet transfusions. Dialysis is indicated for standard renal failure, and the role of therapeutic plasma exchange remains unclear. Early recognition and targeted care improve outcomes.
Conclusions: This case highlights the severe complications of Shigella infection in an immunocompromised patient, leading to HUS and encephalopathy. In HIV-positive individuals with low CD4 counts, Shigellosis can cause significant morbidity and mortality. The patient’s condition was further complicated by CMV co-infection, respiratory failure, and septic shock. HUS, though rare in Shigella infection, requires intensive care and possibly plasmapheresis. This case underscores the need for a multidisciplinary approach to managing complex, multi-organ infections.