A 31-year-old Jamaican man with disseminated nonmeningeal coccidioidomycosis that involved the spine, ribs, pelvis, liver, and spleen did not clinically respond to a prolonged course of both amphotericin B deoxycholate and liposomal amphotericin B therapy. After institution of voriconazole monotherapy, the patient had a favorable (albeit slow) radiological and clinical response without adjunctive surgical intervention.Less than 1% of patients infected with Coccidioides immitis develop chronic pulmonary or disseminated coccidioidomycosis [1,2]. For patients unfortunate enough to develop disseminated coccidioidomycosis, successful management often requires a combined medical and surgical approach [3][4][5]. We report the case of an HIV-negative Jamaican man with severe disseminated nonmeningeal coccidioidomycosis who did not respond to amphotericin B therapy but appeared to clinically respond to voriconazole monotherapy without surgical intervention.Case report.On 19 March 2003, a previously healthy 31-yearold black Jamaican man incarcerated in Taft, California, was admitted to a local hospital with a nonproductive cough, shortness of breath, fever, chills, back pain, and a 9-kg weight loss over the preceding 2 months. A chest radiograph revealed diffuse pulmonary infiltrates. Coccidioidomycosis was diagnosed by histopathological examination of specimens obtained by transbronchial biopsy. The findings of an examination of a CSF sample were unremarkable. On 29 March 2003, after 5 days of antifungal therapy, a once-daily, 40-mg regimen of amphotericin B (∼1 mg/kg) was substituted for fluconazole.On day 24 of therapy, the patient was transferred to the Federal Medical Center and Saint Mary's Hospital in Rochester, Minnesota, for further management. He complained of fever, chills, night sweats, and neck pain. Physical examination revealed a small, cachectic-appearing man (weight, 44 kg) with tachycardia, bilateral basilar rales, tenderness to palpation along the cervical spine, and normal neurological findings.The findings of CT and MRI scans and microbiological studies confirmed disseminated coccidioidomycosis (figures 1-3). Multiple lesions were present in the lungs, liver, spleen, ribs, pelvis, left femur, and paraspinous and pelvic musculature. MRI of the head and spine revealed a right cerebellar infarct; an inflammatory mass encasing the right vertebral artery; extensive vertebral osteomyelitis with paravertebral abscesses at C4, C5, T2, and T4; epidural abscesses at T2, T8, and T9, causing spinal cord displacement; and paraspinous muscle abscesses at T7, T8, L5, S2, and S3.A second examination of CSF samples revealed a WBC count of !1 cell/mL, a glucose level of 61 mg/dL, and a total protein level of 30 mg/dL. Complement-fixation antibody titer to Coccidioides species was 1:2 in the CSF sample and 1:1024 in the serum sample. The patient's leukocyte count was 21,200 cells/ mL, with an erythrocyte sedimentation rate (ESR) of 102 mm/ h, an alkaline phosphatase level of 663 U/L, an alanine aminotransferase level of ...
The purpose of this paper is to present the genetic distribution at the HLA-A, B, C, and DR loci in the Hopi and the Navajo. A sample of 100 out-patients from each tribe was selected at the Public Health Service Indian Hospital in Keam's Canyon, Arizona, and was typed for the antigens at the four loci. The distributions of the alleles and the haplotypes are similar in each tribe. A distance measure, f, confirms the genetic similarity of the two populations. It is concluded that the great cultural diversity of the Hopi and the Navajo is the result of a cultural evolution and diversification that has greatly outstripped the genetic evolution at the major histocompatibility loci over the past 20,000 years.
In a cross-sectional study of Hopi and Navajo Indians with non-insulin-dependent diabetes mellitus, we found vascular complications to be strongly related to the duration of diabetes. In patients with diabetes of at least 10 yr duration, retinopathy was found in 57%, nephropathy in 40%, peripheral neuropathy in 21%, and peripheral vascular disease in 28%. For the Hopi and Navajo, the duration-specific prevalence rates of microvascular disease were very similar to prevalence rates found in many other populations. Thus we question the concept, based on reports in the late 1960s, that the Hopi and Navajo Indians have hyperglycemia as an isolated chemical abnormality unaccompanied by other manifestations of diabetes mellitus.
"Navajo arthritis" was described in 1971 as an acute, self-limited, asymmetric polyarthritis of unknown etiology seen in Navajo Indian patients. This description was before published accounts relating HLA-B27 to certain seronegative arthropathies. Review of 92 cases of arthritis seen between 1977 through 1979 in adult Navajo Indians revealed 16 cases of complete Reiter's syndrome, 6 cases of incomplete Reiter's syndrome, and 7 cases of ankylosing spondylitis. The phenotype frequency of HLA-B27 in this Navajo population is 36% and, of the Reiter's syndrome and ankylosing spondylitis patients tested, 85% were found to be HLA-B27 positive. We suggest that "Navajo arthritis" may not be a unique form of arthritis affecting only the Navajo, but a variant of either Reiter's syndrome or ankylosing spondylitis.In 1971, Muggia, Bennahum, and Williams described 21 cases of an acute, self-limited, asymmetric polyarthritis of unknown etiology in Navajo patients (I). The entity was termed "Navajo arthritis" and felt to be a distinct syndrome. Our recent clinical experience
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