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Tuberculosis (TB) is a major global health problem, and musculoskeletal TB occurs in approximately 10% of extrapulmonary cases. In this article we describe 2 cases of ankle joint tuberculous arthritis. Both of the patients were immunocompromised and presented with chronic pain and swelling. Both patients described a history of antecedent ankle trauma. The clinical presentations were consistent with chronic septic arthritis and were nonspecific as to a particular etiology. The pathology and microbiology results revealed infection with Mycobacterium tuberculosis . Tuberculous infection of bone and joint must be considered when predisposing epidemiological factors are present to avoid delay in therapy. Further exploration into the relationship of trauma to tuberculosis recrudescence is warranted. Level of Clinical Evidence: 4

A 66 year old Liberian woman presented with a one week history of weakness, polydipsia, polyuria and poor appetite along with a right breast swelling without fever or chills. She denied diarrhea, trauma or recent illness. She had a history of breast cancer and underwent a lumpectomy; subsequently she had bilateral breast implants with silicone over twenty years ago. Examination revealed: temperature 39.3 C and a right breast that was fluctuant and red with purulent nipple discharge without axillary lymphadenopathy. Laboratory results revealed: WBC 17x10/L and glucose 557 mg/dl. An incision and drainage of the right breast abscess and implant removal were done. Abscess fluid grew Salmonella enteritidis. Blood, stool and urine cultures were negative. She was treated with two weeks of levofloxacin.

Carrion's disease is typically biphasic with acute febrile illness characterized by bacteremia and severe hemolytic anemia (Oroya fever), followed by benign, chronic cutaneous lesions (verruga peruana). The causative agent, Bartonella bacilliformis , is endemic in specific regions of Peru and Ecuador. We describe atypical infection in an expatriate patient who presented with acute splenomegaly and anemia 3 years after visiting Ecuador. Initial serology and PCR of the patient's blood and serum were negative for Bartonella henselae , Bartonella quintana , and B. bacilliformis . Histology of splenic biopsy was suggestive of bacillary angiomatosis, but immunohistochemistry ruled out B. henselae and B. quintana . Bacilli (isolate EC-01) were subsequently cultured from the patient's blood and analyzed using multilocus sequence typing, protein gel electrophoresis with Western blotting, and an immunofluorescence assay (IFA) against a panel of sera from patients with Oroya fever in Peru. The EC-01 nucleotide sequences ( gltA and internal transcribed spacer) and protein band banding pattern were most similar to a subset of B. bacilliformis isolates from the region of Caraz, Ancash, in Peru, where B. bacilliformis is endemic. By IFA, the patient's serum reacted strongly to two out of the three Peruvian B. bacilliformis isolates tested, and EC-01 antigen reacted with 13/20 Oroya fever sera. Bacilliary angiomatosis-like lesions were also detected in the spleen of the patient, who was inapparently infected with B. bacilliformis and who presumably acquired infection in a region of Ecuador where B. bacilliformis was not thought to be endemic. This study suggests that the range of B. bacilliformis may be expanding from areas of endemicity in Ecuador and that infection may present as atypical clinical disease.

To the Editor: Herpes simplex virus (HSV) is the most common cause of sporadic fatal encephalitis across the globe and for all ages. HSV is the etiologic agent of 10%–20% of the 20,000 cases of encephalitis per year in the United States (1); >50% of untreated cases are fatal. Of the 2 types of HSV, HSV-1 and HSV-2, HSV-1 most commonly affects persons 20–40 years of age, whereas HSV-2 commonly affects neonates. This rapidly progressive disease is a common cause of fatal encephalitis in the United States. Signs and symptoms include fever and headache for a few days, followed by confusion, focal deficits, seizures or hemiparesis, hallucinations, and altered levels of consciousness (2). One third of all HSV encephalitis cases afflict children and adolescents. Lumbar puncture typically shows lymphocytic pleocytosis, increased erythrocytes, and elevated protein (2); glucose level is typically within normal limits. Serologic assays often show prior infection. Brain imaging frequently indicates unilateral frontal or temporal lobe abnormalities with edema or hematoma (3,4). The involvement of the nondominant brain hemisphere is associated with atypical signs and symptoms (5). Diagnosis is usually made by using PCR to examine viral DNA in cerebrospinal fluid (CSF) (6). This method of finding DNA in CSF is highly sensitive (98%) and specific (94%–100%). Without therapy, 70% of patients die; with therapy, 20%–30% die (6). Illness includes behavioral sequelae. A 43-year-old female immigrant from China was admitted to Flushing Hospital Medical Center in Flushing, New York, with complaints of headache, fever, and vomiting, which she had experienced for ≈1 week. She had no photophobia, confusion, or rash; neurologic examination found no abnormalities. CSF contained 81 leukocytes with 82% lymphocytes, 3 erythrocytes, protein at 194 mg/dL, and glucose at 67 mg/dL. CSF was positive for HSV-1 viral DNA by PCR. A computed tomography (CT) scan of the head showed unilateral temporal lobe edema. Intravenous acyclovir 10 mg/kg every 8 hours was administered. HIV test was negative. On day 5, a repeat CT scan showed worsening edema and hemorrhage, despite clinical improvement (Figure). CSF contained 490 leukocytes with 99% lymphocytes and protein at 336 mg/dL. After continued treatment with parenteral acyclovir, the patient’s symptoms resolved. On day 12, the patient was discharged after a final CT scan showed resolution of hemorrhage and edema and CSF contained decreased leukocytes and protein. Figure Computed tomography scan showing hemorrhage in edematous part of brain of patient with herpes simplex virus encephalitis, day 5 of hospitalization. Although this patient had classic signs of meningitis without encephalitis, the CT scan of the head showed cerebral involvement. These factors can be explained by the location of cerebral inflammation in the nondominant lobe of the brain, thereby masking signs of encephalitis. The classic teaching that viral meningitis may not need treatment may miss the occasional viral encephalitis if brain imaging and CSF PCR are not performed. Failure to perform these tests may lead to illness and death from HSV encephalitis if this disease is not considered as a possible diagnosis.

The purpose of this study is to evaluate the presence of extrapyramidal symptoms, especially cogwheel rigidity, in patients receiving lithium alone or in combination with other medications (i.e., antipsychotic or dopamine-depleting agents). Cogwheel rigidity is commonly found in Parkinson’s disease and in drug-induced parkinsonism secondary to antipsychotic or dopamine-depleting agents (1). Its prevalence among lithium-tneated patients varies, but the occurrence of these symptoms suggests that lithium may cause extrapyramidal symptoms. Previous studies of cogwheel rigidity associated with lithium treatment (2-4) have lacked controls in three areas: 1) concomitant use of antipsychotic or dopamine-depleting drugs (which may induce extrapyramidal symptoms), 2) blindness of the evaluator to the patients’ drug status, and 3) laterality of cogwheel rigidity.