We present a Prototheca wickerhamii wound infection case that failed treatment with ketoconazole but was cured with amphotericin-B plus tetracycline. The patient was immunocompetent but had had local steroid injections. We reviewed another 159 cases from the literature. Prototheca has infected many areas of the human body, but most often skin, olecranon bursa, or wounds. Prior treatment with steroids and immune deficiencies are contributing factors. Itraconazole and fluconazole are reasonable initial treatments for patients with mild infections. For serious infections, or for infections that have failed azole treatment, amphotericin-B is the treatment of choice.

In 2014, ISHAM formed a new working group: "Medical Phycology: Protothecosis and Chlorellosis." The purpose of this working group is to help facilitate collaboration and communication among people interested in the pathogenic algae, to share ideas and work together. Here we present reports on recent work we have done in five areas. 1. The history of medical phycology as a branch of science. 2. Aspects of the genetics of Prototheca. 3. Aspects of the proteins of Prototheca. 4. Human infections caused by Prototheca. 5. Dairy cow mastitis caused by Prototheca.

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It has been said that 'Necessity is the mother of invention'. Certainly, that old saying applies to the terms phaeohyphomycosis and hyalohyphomycosis. In 1974 [4] and 1982 [2], these were proposed as umbrella terms to cover a growing number of new mycoses caused by moulds whose basic septate mycelial tissue forms were either phaeoid (Gr. 'phaios') or hyaline (Gr. 'hyaleos'), respectively.Primarily, they were intended to stem and counter the growing flood of new generic based disease names derived from the aetiological agents of the emerging opportunistic mycoses. Interestingly, these new mycoses were being encountered in increasing frequency during a period when medical and public health professionals were optimistically predicting that infectious diseases were well on the road to eradication [48]. After all, the incidence and prevalence of the world's killer microbial diseases, such as tuberculosis, polio and malaria, were waning. Was not smallpox on the verge of being obliterated? This hubris was based on the belief that tremendous strides had been made, especially in the Western nations, in reducing the morbidity and mortality caused by infectious diseases. This feat had been accomplished in little more than a century by raising hygiene standards, conducting massive immunization programmes and through the discovery, production and widespread use of antibiotics.It is pertinent to note here that comparable advances, with two exceptions, had not been achieved among the mycoses. One of these exceptional developments occurred in the realm of the cutaneous mycoses that were caused by several anthropophilic dermatophytes. In Europe, the appalling prevalence and incidence of favus among children, as well as adults, infected by Trichophyton schoenleinii and the epidemic of Microsporum audouinii engendered tinea capitis during World War Two, which had erupted and spread rapidly throughout the Western nations, were, to all intents and purposes, eliminated along with the endemic European infections caused by Triehophyton megninii and the post-World War Two epidemic of Trichophyton violaceum infections in Bosnia-Herzegovina [36]. The demise of human ringworm infections in epidemic form became possible when X-ray induced epilation was introduced in 1904 [78, 79] and when the epochal orally administered antifungal agent griseofulvin made its appearance in the late 1950s [8,98]. The second exception was the veterinary triumph of eradicating histoplasmosis farciminosii among equines from the UK and Western Europe by a rigidly enforced quarantine and slaughter policy [14].Ironically, the advances in the control of bacterial, parasitic and viral diseases, as well as in the treatment of non-infectious diseases, such as cancer, made it possible for some of the well known systemic mycoses to proliferate, and for new fungal diseases to emerge in unprecedented varieties and numbers. The therapeutic measures used to cure

A linear ubiquitin chain, which consists of ubiquitin molecules linked via their N- and C-termini, is formed by a linear ubiquitin chain assembly complex (LUBAC) composed of HOIP, HOIL-1L, and SHARPIN, and conjugation of a linear ubiquitin chain on the NF-κB essential modulator (NEMO) is deeply involved in NF-κB activation induced by various signals. Since abnormal activation of NF-κB is associated with inflammatory disease and malignancy, we searched for an inhibitor of LUBAC by high-throughput screening (HTS) with a Tb(3+)-fluorescein FRET system. As a result, we found that the fungal metabolite gliotoxin inhibits LUBAC selectively by binding to the RING-IBR-RING domain of HOIP, the catalytic center of LUBAC. Gliotoxin has been well-known as an inhibitor of NF-κB activation, though its action mechanism has remained elusive. Here, we show that gliotoxin inhibits signal-induced NF-κB activation by selectively inhibiting LUBAC-mediated linear ubiquitin chain formation.