Amikacin Treatment for <i>Mycobacterium Marinum</i> Infection

Arai, Hiroko; Nakajima, Hiroshi; Naito, Shizuo; Kaminaga, Yoichiro; Nagai, Ryukichi

doi:10.1111/j.1346-8138.1986.tb02960.x

Cited by 7 publications

(2 citation statements)

References 6 publications

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“…The agent was first administered successfully in 1986, by Arai et al [60] . The authors of the present review were able to find one more case of the successful treatment of M. marinum infection using amikacin, by Aubry et al [9] .…”

Section: Aminoglycosidesmentioning

confidence: 99%

Treatment ofMycobacterium marinumcutaneous infections

Rallis

Koumantaki-Mathioudaki

2007

Expert Opinion on Pharmacotherapy

119

101

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Mycobacterium marinum is a non-tuberculous mycobacterium found in non-chlorinated water, with worldwide prevalence. It is the most common atypical Mycobacterium that causes opportunistic infection in humans. It presents as a solitary, red-to-violaceous plaque or nodule with an overlying crust or verrucous surface, or as inflammatory nodules or abscesses, usually in a sporotrichotic type of distribution. Deep infections may also occur. Although diagnosis is confirmed by isolation and identification of the organism in practice diagnosis remains largely presumptive based on clinicohistological features and the response to treatment. Polymerase chain reaction allows the routine early detection of the organism from a biopsy specimen. In the near future, it seems possible that histopathological examination might be greatly assisted by the rapidly improving possibilities with in vivo imaging. There have been many therapeutic modalities used effectively in the treatment of M. marinum infections. Spontaneous remission has also been reported in untreated infections and in immunocompetent hosts. However, there is no proven treatment of choice because M. marinum is naturally multi-drug resistant species and treatment is based primarily on the personal experience and preference of individual investigators, without the benefit of large studies. In superficial cutaneous infections minocycline, clarithromycin, doxycycline and trimethoprim-sulfamethoxazole as monotherapy are effective treatment options, but drug resistance varies and thereby combination therapy usually of two drugs may be required. Ciprofloxacin has shown considerable effectiveness. In cases of severe infections, including those with a sporotrichoid distribution pattern, a combination of rifampicin and ethambutol seems to be the recommended regimen. The use of isoniazid, streptomycin and pyrazinamide as empirical treatment options should be avoided. Surgical treatment is not usually recommended and must be cautiously applied. Cryotherapy, X-ray therapy, electrodesiccation, photodynamic therapy and local hyperthermic therapy have been reported as effective therapeutic alternatives. M. marinum infection should always be included in the differential diagnosis of all cases with poor-healing wounds in upper extremities and a history of exposure to aquariums.

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Section: Aminoglycosidesmentioning

confidence: 99%

Treatment ofMycobacterium marinumcutaneous infections

Rallis

Koumantaki-Mathioudaki

2007

Expert Opinion on Pharmacotherapy

119

101

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“…Furthermore, MSU crystals can directly activate both dormant and active macrophages via the Syk and JNK kinase signaling pathways ( 36 ), stimulating the production of cytokines such as IL-1β, Transforming Growth Factor-beta (TGF-β), and others. These cytokines induce inflammation and metabolic reprogramming through either the MyD88-dependent pathway or the Reactive Oxygen Species (ROS)-NLRP3 signaling pathway ( 37 – 39 ). Thus, macrophage NLRP3 inflammasomes play a crucial role in MSU-induced macrophage-associated inflammation.…”

Section: Ua Induces Macrophages To Produce Inflammatory Cytokinesmentioning

confidence: 99%

The dysregulation of immune cells induced by uric acid: mechanisms of inflammation associated with hyperuricemia and its complications

Li,

Yuan,

Deng

et al. 2023

Front. Immunol.

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Changes in lifestyle induce an increase in patients with hyperuricemia (HUA), leading to gout, gouty arthritis, renal damage, and cardiovascular injury. There is a strong inflammatory response in the process of HUA, while dysregulation of immune cells, including monocytes, macrophages, and T cells, plays a crucial role in the inflammatory response. Recent studies have indicated that urate has a direct impact on immune cell populations, changes in cytokine expression, modifications in chemotaxis and differentiation, and the provocation of immune cells by intrinsic cells to cause the aforementioned conditions. Here we conducted a detailed review of the relationship among uric acid, immune response, and inflammatory status in hyperuricemia and its complications, providing new therapeutic targets and strategies.

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