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Laboratory Diagnostic Tests in the Evaluation of Fever
Published in Benedict Isaac, Serge Kernbaum, Michael Burke, Unexplained Fever, 2019
Some pulmonary pathogens are rarely identified in expectorated sputa, and require bronchoscopy or biopsy for recovery. Specimens obtained by fiberoptic bronchoscopy are appropriate for identification of Pneumocystis carinii and Legionella. Lung biopsy may be necessary in instances of invasive aspergillosis or phycomycosis. In contrast, such organisms as Cryptococcsus neoformans and Nocardia asteroides are often found in sputum. The laboratory should be advised if fungal or mycobacterial culture is required.
Potassium Iodide
Published in Sarah H. Wakelin, Howard I. Maibach, Clive B. Archer, Handbook of Systemic Drug Treatment in Dermatology, 2015
KI is a thyroid-blocking agent and is licensed for the treatment of thyrotoxicosis. It is used to protect the thyroid during therapy with radioactive iodine and may also be given pre-operatively before partial thyroidectomy. It is also used as emergency protection of the thyroid following accidental exposure to radiation. Solutions of KI are used as expectorants to reduce the stickiness of mucous in chest complaints. It is not licensed for use in any dermatological disease. Although benefit has been reported in several dermatoses, the level of evidence for these is limited to small open studies or case reports. These indications include: Fungal infections, specifically cutaneous and lymphocutaneous sporotrichosis and cutaneous cryptococcosis. These probably account for the main use of KI worldwide, given its low cost compared with systemic antifungal medication. Benefit has also been reported in other subcutaneous mycoses such as phycomycosis, human pythiosis, Nocardia brasiliensis, cutaneous cryptococcosis and rhinoentomophthoromycosis (rhinophycomycosis).Panniculitis: erythema nodosum, erythema induratum (nodular vasculitis).Neutrophilic dermatoses: Sweet’s syndrome, pyoderma gangrenosum.Miscellaneous: erythema multiforme, Behçet’s syndrome, disseminated granuloma annulare, Wegener’s granulomatosis.
Aspergillosis and Mucormycosis
Published in Rebecca A. Cox, Immunology of the Fungal Diseases, 2020
Alayn R. Waldorf, Richard D. Diamond
The aspergilli and the Zygomycetes are among the most ubiquitous saprophytic fungi in the environment. Phialoconidia (conidia) and sporangiospores (spores) from these organisms are easily isolated from decaying vegetation, soil, and air world wide.1 The term aspergillosis encompasses a broad range of disease states whose etiologic agents are members of the genus Aspergillus. Although there are about 600 known species of Aspergillus, most cases of human disease are caused by A. fumigatus, A. flavus, and A. niger.2 The agents of mucormycosis (rhinocerebral mucormycosis, phycomycosis, or zygomycosis) are classified in the order Mucorales, containing at least 12 pathogenic species,3 of which Rhizopus oryzae, Rhizomucor pusillus, and Absidia corymbifera are the most common. Aspergillosis and mucormycosis typically are characterized by tissue invasion and a predilection of the organism for blood vessel invasion with hemorrhage, necrosis, and infarction.3,4 There are several unique features of aspergillosis and mucormycosis, unlike the traditional pathogenic dimorphic fungi, that make their study particularly interesting. The etiologic agents of aspergillosis and mucormycosis are opportunistic organisms and usually only infect patients predisposed by some underlying disease or treatment. Because the hosts are predisposed, oftentimes distinct defense mechanisms are defective and it is possible to utilize this to determine which aspects of the hostߣs defense are of importance in controlling the infection. Secondly, these organisms are not dimorphic, like the true pathogenic dimorphic fungi, since they grow both in the environment and within the host as hyphal forms. However, the host must contend with several forms of the organism to successfully eliminate them. A resting, nonmetabolically active spore or conidium enters the host, it swells and germinates (in the susceptible host), and invades tissue as a hyphal organism. Each form displays different antigenic and surface features and elicits different host responses. Finally, if germination of the spore or conidium occurs, the host must compete with a rapidly growing organism that is too large to be ingested by a single cell and so must be handled by extracellular defense mechanisms.
Mucormycosis medications: a patent review
Published in Expert Opinion on Therapeutic Patents, 2021
Mohd. Imran, Alshrari A.S., Mohammad Tauseef, Shah Alam Khan, Shuaibu Abdullahi Hudu
Mucormycosis (phycomycosis or zygomycosis) is a noninfectious fungal disease caused by different genera of zygomycetes. The mucormycosis term is widely used because members of the Mucoraceae family cause most of these infections [1]. The Mucoraceae family members are present worldwide and are known to start the decay of organic materials [2]. Rhizopus arrhizus is the most common cause of mucormycosis in humans. Other fungi reported causing mucormycosis to include Mucor sp., Saksenaea sp., Absidia sp., Entomophthora sp., Basidiobolus sp., Conidiobolus sp., Apophysomyces elegans, Cunninghamella bertholletiae, and Rhizomucor pusillus [1,3]. This uncommon infection occurs when a healthy individual’s mouth, nose, eyes, cracked skin and wound come in direct contact with contaminated soil or water. After the illness, the fungi rapidly multiply at the blood vessel walls and stop the tissue/organ’s blood supply. This results in tissue destruction, and if not treated on time, leads to infection of the different parts of the body, followed by death [1–4]. This illness is also termed as ‘Black Death’ and ‘Zombie disease’ in layman’s language. However, these terms are not be used by a responsible individual to avoid misunderstanding between the patient and the public [5].