(1) diffuse, interstitial process associated with primary, systemic amyloidosis and a median survival of 16 months after diagnosis; (2) Endobronchial amyloid causing obstruction that is usually amenable to treatment with laser therapy; and (3) isolated, pulmonary nodular amyloidosis that is not associated with systemic disease and follows a benign course. Our two cases are examples of pulmonary nodular amyloidosis. Pulmonary disease is uncovered as an incidental finding with one or more nodular opacities seen on chest imaging suggesting a malignant process. Transbronchial lung biopsy may establish the diagnosis with light microscopy showing amorphous, extracellular deposits that stain pink with hematoxylin and eosin. Under polarized light, amyloid produces apple-green birefringence. In our two cases of primary nodular amyloidosis, elevated monoclonal proteins were not found, consistent with the absence of systemic involvement in this presentation of disease. Further, follow-up chest imaging has revealed no change in the pulmonary nodular opacities, reflecting the benign course of this disease. year-old homeless male with a history of untreated Schizophrenia was brought in for evaluation of fatigue and altered mental status. On presentation, the patient was noted to be disheveled and confused with initial BP 128/61, P88, RR 17, and T99.9. Physical exam was remarkable for numerous nits on hair and clothing, and skin with innumerate number of excoriated, hemorrhagic papules. Rectal exam revealed no masses but guaiac negative brownish stool. Initial laboratories included: WBC 13.7, HGB 3.7, HCT 11.5, PLT 375, MCV 72, RDW 16, and 71% PMN. Gastric lavage was negative for occult blood. Computed tomography of head and a diagnostic lumbar puncture were normal. Serum anemia work-up was remarkable for low ferritin (11) and iron (76). Folate and vitamin B12 levels were normal. The remaining laboratories, imaging studies, and cultures were all within normal limits. He was treated for pediculosis with permethrin and received blood transfusion with an appropriate increase in blood counts. His mental status and leukocytosis significantly improved as pediculosis and anemia were treated. Blood counts has remained stable after treating pediculosis. IMPLICATIONS/DISCUSSION: The 3 most common arthropod exoparasites in humans are Pediculus capitis (head louse), Pediculus corporis (body louse), and Phthirus pubis (pubic louse). They belong to the order Anoplura, the sucking lice that feed on blood approximately 5 times per day for approximately 40 minutes each time. Hemorrhagic macules or papules develop at the sites of feeding lice, and vertical excoriations due to scratching and postinflammatory hyperpigmentation are common (aka, vagabond's disease). These lice can be transmitted directly from person to person. They are also a potential vector for transmission of diseases such as typhus, louse-borne relapsing fever, and endocarditis. Bacterial superinfection at the sites of infestation is also common. Zoonotic pediculosis (louse infestation) has been reported as a major cause of anemia in domestic animals. This possibility, however, has not been reported in humans. Our case presents a homeless male wtih severe iron-deficient anemia associated with chronic pediculosis. This case supports the hypothesis that louse infestation is an uncommon cause of anemia in humans. To our knowledge this is the first case report of its kind (Internet and Medline search from 1960 to present). year-old woman presented with chest pain and syncope after exertion. The chest tightness was associated with shortness of breath, nausea, and diaphoresis. She first experienced exertional angina at age 18 during military training. The episodes had increased in frequency since. Her vital signs were normal. The cardiac examination was normal with the exception of a a left-sided heave and a loud, persistently split S2 that widened with inspiration. An electrocardiogram demonstrated normal sinus rhythm, right axis deviation, and T-wave inversion in the inferior and anterior leads. Three troponin assays were negative. Echocardiography revealed right ventricular enlargement, dilated pulmonary arteries with pressures of 50 mm Hg, normal chamber sizes, normal valves, and no septal defects. A ventilation/perfusion scan, ANA and RF were normal. A right heart catheterization confirmed pulmonary artery hypertension with a systolic pressure of 70 mmHg and a normal wedge pressure. A bubble study looking for small septal defects was normal. Angiography confirmed the presence of dilated pulmonary arteries without evidence of thromboembolic disease. IMPLICATIONS/DISCUSSION: Primary pulmonary hypertension is a diagnosis of exclusion, with a prevalence of one to two people per million. Because of its low incidence and protean nature, the most cost effective strategy is to exclude common etiologies of pulmonary hypertension such as pulmonary embolism, valve disease, lupus, CREST and left heart failure. Right heart catheterization is the best diagnostic test. The median survival after diagnosis is 2.5 years. Intravenous epoprostenol is the drug of choice, but oral vasodilators are also used. Anticoagulation has been shown to prolong life; some patients may also respond to oral vasodilators. Anticoagulation improves mortality by decreasing thombosis and thromboembolism. This patient was started on a trial of oral bosentan and warfarin. Since primary pulmonary hypertension has no cure, an exhaustive search for secondary causes is warranted in any patient with this diagnosis. Other than these findings, her neurological examination was unremarkable. MRI of the head revealed multiple foci of hyperintensities in the white matter; bilateral enhancement of the tentorium and cranial nerves III, V, VII; and unremarkable orbits (Fig 1,2,3) . Cerebrospinal fluid (CSF) revealed a protein level of 600 mg/dl; WBC 210/uL (lymphocytes 95%) and glucose 91 mg/dl. Serum and CSF were positive for Lyme antibodies on ELISA. The result was confirmed by western blot assay on the CSF. The patient was started on intravenous ceftriaxone 2 gm every 24 hrs. On the 4th day of antibiotic therapy, she developed left sided LMN facial palsy. After 4 weeks, a repeat CSF study showed significant improvement: the protein level fell to 82 mg/dl and WBC count to 33/ul. Six weeks after ceftriaxone therapy, the diplopia, trigeminal neuralgia and facial palsy resolved completely. IMPLICATIONS/DISCUSSION: Though facial palsy is a relatively common presentation of Lyme disease, multiple cranial neuropathies may be the initial manifestation and must be borne in mind. The diagnosis can be easily missed in such cases without any antecedent history of tick bite or rash. A history of travel or residence in an endemic area is a useful clue. In addition, MRI may play an important role in the diagnosis. Our patient's MRI at admission revealed bilateral enhancement of meninges and cranial nerves III, V and VII indicating evidence of inflammation that preceded the full clinical expression. To our knowledge, multiple cranial neuropathies as the initial manifestation and evidence of gadolinium enhanced MRI lesions of the involved cranial nerves have been rarely reported. Recognizing these subtle imaging findings, combined with high clinical suspicion is the key to diagnosis and allows early treatment which can help prevent further complications.