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Spontaneous bacterial peritonitis (SBP) is a bacterial infection in the peritoneum commonly seen in the setting of cirrhosis and ascites. SBP is typically caused by gram-negative bacteria. Pasteurella is an organism typically associated with skin and soft tissue infections secondary to bites or scratches from domestic animals. We performed a literature review of all cases of Pasteurella-associated SBP to date. Due to the rarity of this clinical finding, there are a limited number of reported SBP cases due to Pasteurella. Our review showed that most associated cases are secondary to an animal wound and often present with hemodynamic instability. Furthermore, Pasteurella SBP has a high mortality rate when compared to the typical causative organisms. Herein, we present a case of septic shock secondary to spontaneous bacterial peritonitis caused by Pasteurella multocida in a patient with no evidence of dog or cat wounds. The patient was treated with antibiotics, but unfortunately required multiple pressors while in the hospital and he ultimately succumbed to his disease. This case not only demonstrates the importance of avoiding risk factors associated with Pasteurella SBP due to its high mortality rate, but also to maintain a high clinical suspicion for the infection in patients with seemingly no risk factors to initiate prompt treatment.

Patient: Female, 74 Final Diagnosis: Acute drug-induced liver failure Symptoms: Anorexia • fatigue • nausea • vomiting Medication: — Clinical Procedure: — Specialty: Gastroenterology and Hepatology Objective: Challenging differential diagnosis Background: Ciprofloxacin is a commonly used fluoroquinolone antibiotic. It is occasionally associated with benign elevations in liver enzymes. Few reports in the literature correlate ciprofloxacin with significant liver injury. We present a fatal case of ciprofloxacin-induced liver failure. Case Report: A 74-year-old female was successfully treated with ciprofloxacin for a urinary tract infection (UTI), but immediately began having new-onset symptoms, including fatigue and nausea. This continued for two months, at which time she presented to the hospital; she was found to have elevated liver enzymes and another UTI. She was treated with ciprofloxacin again for UTI and discharged three days later, following mild improvement. One week later, she returned to another hospital and was found to have more significantly elevated liver function tests and jaundice. Extensive viral and autoimmune panels were unremarkable. Liver biopsy showed cholestatic hepatitis of unclear etiology. The patient was discharged again following a mild decline in liver enzymes. Soon after, the patient was admitted to our institution with similar complaints. Serum transaminases remained elevated, with an increase in alkaline phosphatase and bilirubin. The Council for International Organizations of Medical Sciences/the Roussel Uclaf Causality Assessment Method (CIOMS/RUCAM) scale was found to be 8, outlining a high or definite probability that the ciprofloxacin was the cause of the patient’s hepatotoxicity. A one-week course of prednisone for possible hypersensitivity reaction was tried; however, it proved unsuccessful. Palliative care was consulted, and the patient passed away shortly thereafter. Conclusions: This case demonstrates the potential for liver failure from ciprofloxacin. Clinicians should evaluate the possibility of ciprofloxacin-induced hepatotoxicity in a patient presenting with liver injury of unknown etiology. Similarly, it is important to consider this significant effect when a practitioner considers antibiotic choice.

No abstract available. Article truncated after first 150 words. History of Present Illness: A 50-year-old African American woman presented with weakness, altered mental status and constipation of 12 days duration. She was complaining of abdominal distension with diffuse pain and bloating. She denied melena, hematochezia or hematemesis. She had a history weight loss, anorexia and fatigue which had evolved over the past few months leading to recent severe weakness and inability to get out of bed. Past Medical History, Social History and Family History: Her past medical history included HIV infection with AIDS and noncompliance with her antiretroviral medications. Her most recent CD4 count was

No abstract available. Article truncated at 150 words. History of Present Illness: A 39-year-old Hispanic woman was admitted complaining of shortness of breath and bilateral lower extremity edema. She was felt to be in acute hypoxic respiratory failure. Past Medical History: Systemic lupus erythematosus; Congestive heart failure with an ejection fraction of 40%; End-stage renal disease on dialysis secondary to lupus nephritis. Medications: Rituximab 550 mg once a week; Prednisone 40 mg daily; Plaquenil 200 mg twice a day. Physical Examination: The patient was tachypneic in obvious respiratory distress. She was afebrile. Crackles at the bases. Heart was tachycardic. There was 3+ bilateral pitting pretibial edema. Laboratory: CBC: Hemoglobin 7.8 g/dL, WBC 11 X 109 cells per liter, differential: neutrophils 98%, eosinophils 0%, lymphocytes 1%. Electrolytes: Potassium 5.8 mEq/L, sodium 143 mEq/L, creatinine 3.3 g/dL, BUN 98 mg/dL. Brain naturetic peptide: 4055 pg/ml. Imaging: Admission chest x-ray showed cardiomegaly and bilateral interstitial prominence suggestive of congestive heart failure ...

Background Coccidioidal meningitis (CM), a common cause of chronic meningitis in endemic area, is usually diagnosed by detection of anti-Coccidioides antibodies in cerebrospinal fluid (CSF), and findings may be negative in up to one-third of cases. CSF cultures and cytology are infrequently positive. Antigen detection has been used for the diagnosis of other forms of coccidioidomycosis and meningitis caused by other mycoses. The purpose of this study was to assess the diagnostic utility of CSF Coccidioides antigen (CAg) detection for the diagnosis of CM. Methods The medical records of patients with clinically suspected meningitis, in whom CSF was tested for Coccidioides antibodies and CAg, were retrospectively reviewed, and CSF CAg testing was prospectively conducted in patients with CM. All specimens were submitted for CAg testing. Results Thirty-six patients with 42 episode of CM were studied. The sensitivity and specificity of CAg were 93% and 100%, respectively. Cultures of CSF were positive in 7%, antibodies were demonstrated by immunodiffusion in 67% and complement fixation in 70%, and immunoglobulin M and G antibodies were demonstrated by enzyme immunoassay in 8% and 85%, respectively. Conclusions Testing CSF for CAg is a useful addition to diagnostic methods in suspected CM and complements testing with CSF antibodies and culture.