Case Presentation:

A 26 year old female with a history of morbid obesity status post lap band procedure presented with fevers, bloating, nausea and vomiting for 1 month. CT Abd/Pelvis w/o contrast demonstrated marked ascites intra-abdominally and in the pelvic cavity. Chlamydia/Gonorrhea assays were performed and returned negative. She then had a paracentesis with fluid studies consistent with spontaneous bacterial peritonitis.  She was then started on Vancomycin and Ceftriaxone. Repeat CT Chest/ABD/Pelvis post-paracentesis demonstrated interval decrease in ascites and peritoneal wall thickening. Gastroenterology was consulted, an EGD was performed and noted a tight-appearing gastric lap band. Despite antibiotics the patient’s symptoms and leukocytosis persisted. Her ceftriaxone was switched to pipercillin-tazobactam. Bariatric surgery subsequently released the lap band but the patient’s symptoms persisted. An abdominal U/S demonstrated re-accumulation of ascites and a second paracentesis was performed. Fluid studies now showed macrophage-predominant leukocytosis. Obstetrical and oncological workup ruled out ovarian and uterine malignancy. The patient after several days admitted to possible TB exposure, and a PPD was ordered and found to be positive. A Quantiferon Gold of the ascitic fluid returned positive as well, but a PCR of the ascitic fluid for M. Tuberculosis returned negative as well as the AFB smears and gram stains.  Given a recurrence of the ascites after a lap band release, a peritoneoscopy was performed and there was gross evidence of necrotizing granulomas diffusely in the abdominal and pelvic cavities. The patient was started on Rifampin, Isoniazid, Pyrazinamide, Ethambutol therapy given suspicion of miliary TB. Pathology confirmed necrotizing granulomas from peritoneal biopsies. However, AFB cultures of the peritoneal fluid remained negative. Several days after therapy, the patient’s leukocytosis improved and fever resolved. The patient had 3 AFB sputum stains that returned negative. The patient was discharged home on RIPE therapy. Several days after discharge, the patient’s mycobacterial sputum cultures grew out M. porcinum. Susceptibilities demonstrated that this strain was susceptible to cefoxitin, imipenem, ciprofloxacin, moxifloxacin, amikacin, trimethoprim-sulfamethoxazole, and linezolid.  The patient was informed and appropriate antibiotic therapy was instituted. 

Discussion:

This patient’s case was an unusual presentation of non-TB mycobacterial peritonitis. M. porcinum is a species of rapidly growing mycobacterium. Infection with M. porcinum usually manifests as a pulmonary illness (nodules, bronchiectasis, pneumonitis), soft tissue infections, or central line infections. It is extremely rare to find a reported case of M. porcinum causing peritonitis. Diagnosis is made upon appropriate blood and suspected site mycobacterial cultures. Once Identified as the offending agent M. porcinum is typically treated with aminoglycosides and flouroquinolones. However, individual susceptibility testing will determine final antibiotic therapy. One should always consider non-tuberculosis mycobacterial peritonitis if patients with suspected SBP do not improve with empiric antibiotics after 72 hours.

Conclusions:

In patients with recurrent ascites and clinical signs of peritonitis, with no obvious source of infection, malignancy, and no history of liver abnormalities, one should consider non-TB mycobacterium as a potential source.