A 37 year old male presented in a tertiary care University Hospital with the chief complaint of prolonged fever after return from a business trip to Malaysia. While in Malaysia, the patient developed an episode of diarrhea for 4 days followed by high fever, rigors and malaise. He described a self-resolved similar episode in a co-traveler that lasted for 5 days.
He returned to Greece on the fifth day of his syndrome. Five days later, due to prolonged fever, he was admitted to the department of Medicine at a tertiary care university hospital. He reported no significant medical history and was receiving no medications at the time of evaluation.
The physical exam was unremarkable, except for a temperature of 39  C, a blood pressure of 120/80 mmHg, a heart rate of 88 beats per minute and an oxygen saturation of 97%. The abdominal examination revealed no tenderness or organomegaly. There were no enlarged peripheral lymph nodes, joint findings or rash.
Laboratory work-up at admission revealed polymorphonuclear leukocytosis with 25,800 white blood cells (82% polymorphonuclear cells, 11% lymphocytes, 5% monocytes, eosinophils 2%), Hct: 35.7% and CRP: 198 mg/L (normal < than 6 mg/L). He was admitted to the hospital for investigation and treatment. During his stay he underwent an extensive evaluation including: a) repeat complete blood testing that disclosed persistent leukocytosis, a severe normocytic anemia with a hematocrit as low as 25% (that required administration of 3 packed red blood cell units), thrombocytosis (as high as 594 x 109/L) and an elevated CRP (as high as 234 mg/L) and erythrocyte sedimentation rate of 100-110 mm/hour; b) multiple blood, stool and urine culture sets were taken that were negative for any pathogen; c) repeat stool cultures that were negative for Salmonella spp., Shigella spp., Yersinia spp., Campylobacter spp. and Aeromonas spp.; d) repeat stool ova and parasite testing that was negative for parasites; e) negative stool culture for C. difficile as well as negative C. difficile toxin assay; f) negative Giardia lamblia, cryptosporidium and entamoeba antigen; g) negative interferon gamma release assay; h) negative HIV, HTLV I and II, CMV, EBV, Echinococcus granulosus, Toxoplasma gondii, Brucella melitensis, leishmania spp, syphilis, hepatitis A, B and C serologies and; i) a bone marrow aspirate examination with normal results.
The patient did not respond to several courses of antimicrobials including sequential use of ciproflocacin and metronidazole followed by piperacillin-tazobactan, followed by meropenem with vancomycin, and last a combination of docycycline and gentamycin.
A computed tomography of the abdomen revealed multiple enlarged and necrotic mesenteric lymph nodes, and edema in the wall of the distal ileum and the entire colon. A colonoscopy showed aphthous ulcerations in many parts, especially in the cecum, the ileocecal junction and the first part of the terminal ileum; histology was nonspecific. Twenty days into his course a new CT scan disclosed exacerbation of the disease with a lot of enlarged necrotic mesenteric lymph nodes and 2 focal deformities in the spleen about 1 cm in size. By this time the patient developed arthritis in the left ankle joint and an atypical bilateral rash in the shins resembling nodular panniculitis. At that point a quadruple anti-tuberculous regimen was initiated. Tissue samples obtained during an exploratory laparotomy from the abnormal mesenteric lymph nodes, showed acute purulent and focally granulomatous suppurating lymphadenitis with extension of acute inflammation into the perinodular mesenteric fat adjacent adipose tissue; PAS and Grocott stains disclosed no fungi, whereas PCR for Mycobacterium tuberculosis was negative.
The patient was diagnosed with aseptic abscesses syndrome and was treated with systemic administration of corticosteroids (40 mg of prednisone) together with methotrexate (15 mg/week). After tissue PCR results came back negative for TBc, the anti-TBc regimen was discontinued.
The patient had an excellent response to the immunosuppressive treatment with rapid clinical improvement with restoration of all his abnormal laboratory parameters during a 6 month follow-up. He is followed by a gastroenterologist for the possibility of development of inflammatory bowel disease.