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Executive Summary

Erratum available for this chapter. Actinomycosis results from pathogen introduction following a breakdown in mucocutaneous protective barriers. Spread within the host is by direct invasion of adjacent tissues, typically forming sinus tracts that cross tissue planes. The most common species causing human disease is Actinomyces israelii.

Curriculum

There are 3 common anatomic sites of infection. Infection may contribute to chronic tonsillar airway obstruction. Thoracic disease most commonly is secondary to aspiration of oropharyngeal secretions but may be an extension of cervicofacial infection. It occurs rarely after esophageal disruption secondary to surgery or nonpenetrating trauma.

Thoracic presentation includes pneumonia , which can be complicated by abscesses, empyema, and rarely, pleurodermal sinuses. Focal or multifocal mediastinal and pulmonary masses may be mistaken for tumors. Abdominal actinomycosis usually is attributable to penetrating trauma or intestinal perforation. The appendix and cecum are the most common sites; symptoms are similar to appendicitis. Slowly developing masses may simulate abdominal or retroperitoneal neoplasms. Intra-abdominal abscesses and peritoneal-dermal draining sinuses occur eventually.

Chronic localized disease often forms draining sinus tracts with purulent discharge. As the arthroconidia, which become lodged in the distal bronchioles, become spherules, and inflammation results. To disseminate, the spherules may enter the pulmonary vascular system or the lymphatic system after being phagocytosed by macrophages. Although a humoral response is seen, it appears to have little effect on pathogenicity of the organism.

Cryptococcus neoformans var. Capsule: the attached capsule has been shown to act as an antiphagocytic barrier, deplete complement, produce antibody unresponsiveness, interfere with antigen presentation, alter cytokine secretion, and enhance HIV replication. A T h 1 cellular immune response is required for adequate control of the disease: as CD4 cell count decreases to less than , a sparse inflammatory response occurs at the site of infection. Humoral immunity is important to reduce yeast burden and improve survival; it enhances phagocytosis, natural killer cell function, and clearing of capsular polysaccharide.

Once transitioned, the yeast, within macrophages, enters the lymphatics to the reticuloendothelial system where they grow. Macrophages from HIV infected patients engulf less yeast and inhibit yeast growth less well than those from patients without HIV. Paracoccidioides brasiliensis causes disease primarily through environmental exposure to the organism in endemic regions, although microniche has not been established. IgA, IgE, and IgG are significantly increased in the juvenile form and may have accompanying eosinophilia. Sporothrix schenckii causes disease primarily through direct inoculation from minor trauma associated with soil, plants, and plant products.

Penicillium marneffeii causes disease primarily through environmental exposure to the organism in the endemic region. It is thought that inhalation of the conidia into the lungs is the initial site of infection. The lesions tend to progressively increase in size with crusting and associated seropurulent exudate.

Cutaneous manifestations can resemble many other diseases; a high index of suspicion is required for diagnosis. The oral manifestations, along with cutaneous disease, should be helpful in raising histoplasmosis as a possible diagnosis in the right clinical setting. The prominent mucosal involvement, accompanied by pulmonary and cutaneous findings in a patient from an endemic region, should raise the possibility of this diagnosis.

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Extensive cutaneous involvement with osteoarticular disease in a patient with the appropriate exposure should raise the possibility of this diagnosis. The pathology specimen will often appear consistent with a fungal infection, but the organism is not seen even with special stains; a high index of suspicion is necessary to continue to consider sporotrichosis. Disseminated fungal infection in an HIV-positive patient from or who visited the endemic region should strongly suggest this diagnosis.


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Serum complement fixation, immunodiffusion, and ELISA assays are available but, because of low sensitivity and specificity, should only be used to stimulate further evaluation in a patient suspected of having blastomycosis, not for definitive diagnosis. PCR may be used on sputum or other tissue samples for identification but is not commonly available. Serum galactomannan testing for Aspergillus was positive in two-thirds of patients with penicilliosis in one study. Primary prophylaxis is not recommended for those with a CD4 greater than , regardless of region of residence.

Antifungal prophylaxis is not recommended in the United States or Europe. Ameen, M, Robles, WS. Treatment of skin disease comprehensive therapeutic strategies. This book evaluates the evidence for treatments for many different diseases of the skin. It grades them as A, double-blind studies; B, clinical trial with greater than or equal to 20 subjects; C, clinical trial with less than 20 subjects; D, case series of more than 4 subjects; and E, anecdotal case reports.

Tropical Diseases Bulletin

Andrews' diseases of the skin. This is an excellent review of the salient features of mucocutaneous candidiasis. Robles, WS, Ameen, M. Proc Am Thorac Soc. This is a review of epidemiology, clinical manifestations, pathology, and treatment of numerous fungal infections that involve the skin. The most recent edition of this standard textbook contains excellent reviews on all pathogens mentioned here, see section O. Mycoses, chapters to All rights reserved.

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Changes in Clinical Diagnostics and Tracking Infectious Diseases

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Behavioural change models for infectious disease transmission: a systematic review (2010–2015)

Registration is free. Register for free and gain unlimited access to:. Powered By Decision Support in Medicine. Key symptoms of the disease Key cutaneous findings of the disease How did the patient develop a disseminated fungal infection? What was the primary source from which the infection spread? Which individuals are of greater risk of developing a disseminated fungal infection?

Beware: there are other diseases that can mimic a disseminated fungal infection: What laboratory studies should you order and what should you expect to find? What imaging studies will be helpful in making or excluding the diagnosis of a disseminated fungal infection?

Scientific Advisory Group

The principles of this rating system were developed by the Infectious Disease Society of America and the U. This rating system allows assessments of recommendations to which adherence is critical. Increasingly, HSCT has been used to treat neoplastic diseases, hematologic disorders, immunodeficiency syndromes, congenital enzyme deficiencies, and autoimmune disorders e. Moreover, HSCT has become standard treatment for selected conditions 7,11, HSCTs are classified as either allogeneic or autologous on the basis of the source of the transplanted hematopoietic progenitor cells.

Cells used in allogeneic HSCTs are harvested from a donor other than the transplant recipient.


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Such transplants are the most effective treatment for persons with severe aplastic anemia 13 and offer the only curative therapy for persons with chronic myelogenous leukemia Allogeneic donors might be a blood relative or an unrelated donor. Allogeneic transplants are usually most successful when the donor is a human lymphocyte antigen HLA -identical twin or matched sibling.

However, for allogeneic candidates who lack such a donor, registry organizations e.