BACKGROUND: The increasing global burden of tuberculosis (TB) is linked to human immunodeficiency virus (HIV) infection. METHODS: We reviewed data from notifications of TB cases, cohort treatment outcomes, surveys of Mycobacterium tuberculosis infection, and HIV prevalence in patients with TB and other subgroups. Information was collated from published literature and databases held by the World Health Organization (WHO), the Joint United Nations Programme on HIV/Acquired Immunodeficiency Syndrome (UNAIDS), the US Census Bureau, and the US Centers for Disease Control and Prevention. RESULTS: There were an estimated 8.3 million (5th-95th centiles, 7.3-9.2 million) new TB cases in 2000 (137/100,000 population; range, 121/100,000-151/100,000). Tuberculosis incidence rates were highest in the WHO African Region (290/100,000 per year; range, 265/100,000-331/100,000), as was the annual rate of increase in the number of cases (6%). Nine percent (7%-12%) of all new TB cases in adults (aged 15-49 years) were attributable to HIV infection, but the proportion was much greater in the WHO African Region (31%) and some industrialized countries, notably the United States (26%). There were an estimated 1.8 million (5th-95th centiles, 1.6-2.2 million) deaths from TB, of which 12% (226 000) were attributable to HIV. Tuberculosis was the cause of 11% of all adult AIDS deaths. The prevalence of M tuberculosis-HIV coinfection in adults was 0.36% (11 million people). Coinfection prevalence rates equaled or exceeded 5% in 8 African countries. In South Africa alone there were 2 million coinfected adults. CONCLUSIONS: The HIV pandemic presents a massive challenge to global TB control. The prevention of HIV and TB, the extension of WHO DOTS programs, and a focused effort to control HIV-related TB in areas of high HIV prevalence are matters of great urgency.

https://jamanetwork.com/journals/jamainternalmedicine/articlepdf/215525/ira20017.pdf

The growing burden of tuberculosis: global trends and interactions with the HIV epidemic.

Epstein-Barr virus.

Amphotericin B, the first commercially significant antifungal drug, has been available for more than 30 years. This polyene macrolide antifungal agent continues to play a major role in the treatment of systemic fungal infections, despite the introduction of newer agents such as the azoles. Given the proved efficacy of amphotericin B--and the increasing number of indications for antifungal agents--an extensive review of this drug is warranted. This paper discusses the clinical uses of amphotericin B, including its application in AIDS-related fungal infections, in neutropenic cancer patients who are persistently febrile, and in infections of the central nervous system, lung, peritoneum, genitourinary system, eye, and skin. The paper also reviews the drug's adverse reactions, with a discussion of administration techniques that may reduce these reactions, and its spectrum of activity, pharmacokinetics, and dosage and administration.

Amphotericin B: 30 Years of Clinical Experience

Background. Bacillary angiomatosis is an infectious disease causing proliferation of small blood vessels in the skin and visceral organs of patients with human immunodeficiency virus infection and other immunocompromised hosts. The agent is often visualized in tissue sections of lesions with Warthin—Starry staining, but the bacillus has not been successfully cultured or identified. This bacillus may also cause cat scratch disease. Methods. In attempting to identify this organism, we used the polymerase chain reaction. We used oligonucleotide primers complementary to the 16S ribosomal RNA genes of eubacteria to amplify 16S ribosomal gene fragments directly from tissue samples of bacillary angiomatosis. The DNA sequence of these fragments was determined and analyzed for phylogenetic relatedness to other known organisms. Normal tissues were studied in parallel. Results. Tissue from three unrelated patients with bacillary angiomatosis yielded a unique 16S gene sequence. A sequence obtained from a fou...

The Agent of Bacillary Angiomatosis

Background Bacillary angiomatosis is an infectious disease causing proliferation of small blood vessels in the skin and visceral organs of patients with human immunodeficiency virus infection and other immunocompromised hosts. The agent is often visualized in tissue sections of lesions with Warthin-Starry staining, but the bacillus has not been successfully cultured or identified. This bacillus may also cause cat scratch disease. Methods In attempting to identify this organism, we used the polymerase chain reaction. We used oligonucleotide primers complementary to the 16S ribosomal RNA genes of eubacteria to amplify 16S ribosomal gene fragments directly from tissue samples of bacillary angiomatosis. The DNA sequence of these fragments was determined and analyzed for phylogenetic relatedness to other known organisms. Normal tissues were studied in parallel. Results Tissue from three unrelated patients with bacillary angiomatosis yielded a unique 16S gene sequence. A sequence obtained from a fourth patient with bacillary angiomatosis differed from the sequence found in the other three patients at only 4 of 241 base positions. No related 16S gene fragment was detected in the normal tissues. These 16S sequences associated with bacillary angiomatosis belong to a previously uncharacterized microorganism, most closely related to Rochalimaea quintana. Conclusions The cause of bacillary angiomatosis is a previously uncharacterized rickettsia-like organism, closely related to R. quintana. This method for the identification of an uncultured pathogen may be applicable to other infectious diseases of unknown cause.

The agent of bacillary angiomatosis. An approach to the identification of uncultured pathogens.

Microsporidia are obligate intracellular protozoal parasites that infect a variety of cell types in a broad range of invertebrates and vertebrates. They have recently come to medical attention due to the increased frequency with which members of two microsporidian genera, Enterocytozoon and Encephalitozoon, are being diagnosed in patients with the acquired immunodeficiency syndrome (AIDS). The majority of published reports of human microsporidiosis describe Enterocytozoon infection of small intestinal enterocytes. In addition, a growing number of AIDS patients have been identified with infection due to the two species of Encephalitozoon-Encephalitozoon cuniculi and Encephalitozoon hellem, observed in conjunctival, corneal, and, recently, sinonasal tissues. However, there are scant data regarding the systemic pathology and epidemiology of these infections. This article describes a patient with AIDS who died with systemic Encephalitozoon infection. The etiologic microsporidian was found to be E hellem by using antemortem biochemical and antigenic analyses. A complete autopsy, the first to be reported in a patient with this infection, revealed organisms in the eyes, urinary tract, and respiratory tract. A surprising observation was the occurrence of numerous organisms within the lining epithelium of almost the entire length of the tracheobronchial tree, suggestive of respiratory acquisition. Detailed light and electron microscopic findings and the biological and diagnostic features of microsporidiosis are discussed.

Disseminated microsporidiosis (Encephalitozoon hellem) and acquired immunodeficiency syndrome. Autopsy evidence for respiratory acquisition.

• Background and Design.— The hemophagocytic syndrome (HPS) is characterized by fever, wasting, generalized lymphadenopathy, hepatosplenomegaly, and pancytopenia, often with associated coagulopathy. The most common cutaneous manifestations are panniculitis and purpura. Cytophagic histiocytic panniculitis fits within the spectrum of HPS, and the most consistent histopathologic feature in HPS is a proliferation of mature histiocytes that exhibit prominent erythrophagocytosis and cytophagocytosis. The clinical spectrum, the underlying causes, and the histopathologic features found in HPS are broad. The characteristic phagocytic histiocytes seen in HPS have been confused with malignant histiocytes in the past, but are now known to be reactive. The clinical findings, histologic, and immunohistochemical features of 10 cases of HPS with cutaneous lesions were reviewed. Immunohistochemical markers included KP-1, βF-1, UCHL-1, L-26, MAC-387, factor XIIIa, and S100 protein. Results.— The HPS was associated with T-cell lymphoma and/or viral infection. Most biopsy specimens showed edema and hemorrhage with a lymphohistiocytic infiltrate and prominent histiocytic cells showing erythrophagocytosis and, in some cases, cytophagocytosis. The histiocytic cells showed positive reactions for KP-1 and negative reactions for the lymphoid markers. In all cases the lymphoid cells showed a mixed pattern with most cells positive for βF-1 and UCHL-1, and a small percentage positive for L-26. Conclusion.— In HPS, the prominent phagocytic histiocytes are reactive and are stimulated by T-cell lymphocytes, either neoplastic or in response to viral infection. Many of the findings in the HPS may also be due directly or indirectly to cytokines produced by proliferating T-cell lymphocytes and/or reactive phagocytic histiocytes. ( Arch Dermatol. 1992;128:193-200)

Cutaneous Histopathologic, Immunohistochemical, and Clinical Manifestations in Patients With Hemophagocytic Syndrome

Background: In HIV-1-positive patients there have been no prospective studies that show an increase in cutaneous neoplasms. Objective: We observed HIV-1-positive patients to determine whether or not there was an increased incidence of cutaneous malignancies. Methods: A total of 724 HIV-1-positive patients were examined during a 36-month period for the development of cutaneous malignancies. Results: The most common cutaneous neoplasm found was Kaposi's sarcoma, especially in patients with late-stage disease. Basal cell carcinomas were the next most frequent tumor. We have also seen three malignant melanomas and two squamous cell carcinomas. Five patients had malignant lymphoma. One patient had a primary lymphoma of subcutaneous soft tissue; in one patient multiple cutaneous lesions developed. Conclusion: The distribution and prevalent types of cutaneous neoplasms in HIV-1-positive patients appear to differ from those found in other immunosuppressed populations. This may be the result of the different patterns and periods of immunosuppression in these patients and/or associated cocarcinogens to which these patients frequently are exposed.

Cutaneous neoplasms in a military population of HIV-1-positive patients******

of a preexisting lesion, have static or burned-out lesions without scale or erythema and, as found in white patients, these lesions present as alabaster-white areas. Active lesions are inflammatory and have variable erythema and at times slight scale. The scale usually does not aggregate around the follicular orifices of remaining hair shafts to the extent encountered in lichen planopilaris. The pull test (tug test) in patients with active lesions is invariably positive for anagen hairs, a finding rarely encountered in other forms of alopecia except active lichen planopilaris and occasionally in discoid lupus erythematosus. In our experience with pseudopelade in adults, in addition to that previously described, two other clinical forms ofpseudopelademayalso beencountered: (1) a somewhat diffuse form usually centered over the crown, predominantly occurring in black women and (2) an acute "fulminant" form that can quickly result in extensive alopecia. We regard the histology of the active lesion as characteristic. Lymphocytes surroundand infiltrateouter sheath epithelium predominantly between the infra-infundibulum and the upper hair bulb without involvement of the bult itself. Sebaceous epithelium is usually absent or extensively involved by a lymphocyte-mediated process. In old or end-stage lesions, fibrous strands (fibrous stele) replace absent follicles and, on occasion, persistent vertically oriented naked hair shafts remain as foreign bodies. Although the collagenous adventitia ofthe follicle may be at first expanded and possibly increased, a true scar is not formed. The reticular dermis is uninvolved and remains structurally normal. The etiology of pseudopelade is unknown, but the pathogenesis in our view is a T lymphocyte-mediated inflammation ofthe outer hairsheath that ultimately results in the permanent destruction of the follicle. Although, as far as we can determine, pseudopelade has not been described in children, there is no reason why this unusual form of alopecia should be limited to adults, and we believe that the case described in this briefreport meets all the necessary criteria. We found hydroxychloroquine to be safe and effective in the management of pseudopelade in this child.

https://www.jaad.org/article/S0190-9622(08)80707-4/pdf

Peter Angritt

Papers

Disseminated microsporidiosis (Encephalitozoon hellem) and acquired immunodeficiency syndrome. Autopsy evidence for respiratory acquisition.

Cutaneous Histopathologic, Immunohistochemical, and Clinical Manifestations in Patients With Hemophagocytic Syndrome

Cutaneous neoplasms in a military population of HIV-1-positive patients******

Neutrophilic eccrine hidradenitis in HIV-infected patients

Epithelioid angiomatosis in hiv infection: neoplasm or cat-scratch disease?