Journal of the Louisiana State Medical Society
granular lymphocytes. Review of records revealed that her WBC count had decreased over the preceding 15 months from a peak of 11,700/μL to a nadir of 2,700/μL, with a concurrent decrease in granulocytes. Subsequent bone mar- row evaluation was significant for a mildly hypercellular marrow with a polyclonal T-cell proliferation but negative for malignancy. Thorough investigation into other causes, including HIV, were negative. On further questioning, the patient disclosed she had been non-compliant with metho- trexate due to peripheral neuropathy, which she attributed to the drug. The decline in her WBC count and profound neutropenia coincided with cessation of her methotrexate therapy. Given the triad of rheumatoid arthritis, neutrope- nia, and splenomegalywith a negative marrow and no other overt cause, a diagnosis of FS was made. Discussion: FS is a diagnosis of exclusion, and it is important to rule out other causes of neutropenia even in the presence of splenomegaly and RA. Ultimately, the goal of treatment is to prevent serious infection by augmenting granulocytosis. Methotrexate is considered superior to other agents as illustrated by our patient who saw a precipitous decline in her WBC count and ANC with its cessation, de- spite the continuation of plaquenil and adalimumab. Rat Catching Fellow Without the Yellows D. Lovre, S. Ahmed, M. Varghese, and S.M. Gupta Leonard J. Chabert Medical Center, Houma Case: A 42-year-oldman with a history of hypertension and hyperlipidemia was admitted to surgery for right up- per quadrant (RUQ) pain and found to have cholelithiasis without cholecystitis; surgery was not necessary. The pa- tient complained of body aches and flu like symptoms of two weeks duration, as well as dark and decreased urine output for one week. He was taking eight Tylenols and ibuprofens for four days. On physical exam, he was febrile and tachycardic. He had mild tenderness to palpation in the RUQ and bilateral lower extremity muscles. His serum chemistries revealed elevated liver enzymes, creatine kinase, and blood urea nitrogen/creatinine. He had negative blood cultures and urine culture. Urinalysis demonstrated blood and protein without red blood cells on micro. Vancomycin and pipercillin-tazobactam were initiated, and he became afebrile with normalized WBCs and liver function test but worsening acute kidney injury. All of his medications were stopped. Despite 8-10 liters of intravenous normal saline, his blood urea nitrogen (BUN)/creatinine continued to rise; glomerulonephritis workup was negative. After more his- tory, the patient reported killing a rodent in his house a few weeks prior. Leptospirosis-induced acute interstitial nephri- tis (AIN) was considered. After renal biopsy, the patient was started on doxycycline and prednisone. His renal function improved, and he was discharged home on doxycycline and prednisone. Renal biopsy showed interstitial nephritis. Serum antigen was diagnostic for leptospirosis. Discussion: Often misdiagnosed secondary to an array of symptoms, Leptospirosis is a biphasic disease. The disease
begins with flu-like symptoms followed by an asymptomatic period, then a more severe second phase characterized by meningitis, liver, and kidney damage (also called Weil’s disease). The incubation period is 7-29 days. The bacteria spreads through infected rodent urine, contaminating wa- ter/soil, often surviving there for months. Humans become infected through direct urine contact or through contami- nated water/soil/food. Bacteria enters the body through skin or mucus membranes, especially if cut or scratched. Other names for Leptospirosis include: Weil’s syndrome, canicola fever, canefield fever, swamp fever, nanukayami fever, 7-day fever, Rat Catcher’s Yellows, Fort Bragg fever, black jaundice, and Pretibial fever. Not Your Ordinary Sore Throat M.J. Katz and M.N. Peters Tulane University Health Sciences Center, New Orleans Case: A 19-year-old man presented with a one-week history of sore throat and cough. Seven days earlier he had been prescribed oral penicillin; however, his symptoms continued toworsen. Initial vital signs revealed temperature 99.7 o F, heart rate 126 beats/min, blood pressure 107/62 mmHg, respiratory rate 26/min, and room air oxygen satu- ration 97%. Examination showed tender right posterolateral neck lymphadenopathy and crackles at the left lung base. White blood cell count was 40.9 x10 3 /μL with 73% neutro- phils and 15% bands. Chest radiograph revealed left-lower lobe airspace disease. Intravenous piperacillin-tazobactam was initiated for suspected pneumonia. His throat pain persisted, and a neck CT revealed right palatine tonsil en- largement with diffuse inflammatory lymphadenopathy. A subsequent chest CT showed numerous pulmonary nodules withmultiple areas of consolidation, some of which demonstrated cavitation. Transesophageal echocardiogram revealed no vegetations. Given the concern for embolic phe- nomenon on CT scan, a Doppler ultrasound of the internal jugular veins was ordered and revealed a partially occlusive thrombus in the right internal jugular vein consistent with Lemierre’s Syndrome (LS). All blood cultures returned negative; multiple sputum samples revealed heavy group C streptococci growth. Discussion: Lemierre’s Syndrome, or jugular vein sup- purative thrombophlebitis, is a condition characterized by infectious involvement of the carotid sheath vessels. Clinical manifestations are the triad of antecedent pharyngitis, septic emboli, and persistent fever. Subsequent thrombophlebitis typically develops within one week of pharyngitis. Clinical warning signs include jugular vein/sternocleidomastoid muscle tenderness and swellingwith presence of pulmonary septic emboli on chest radiograph. Ultrasound represents a rapid way to evaluate for jugular venous thrombosis, and CT scan should be utilized to assess for pulmonary abscesses and cavitations. Causative organisms include normal oropharyngeal flora, namely Fusobacterium necropho- rum, Eikenella corrodens and Streptococci pyogenes/bacteroides . Empiric antibiotic therapy should include a beta-lactamase
84 J La State Med Soc VOL 166 March/April 2014
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