Colistin-induced nephrotoxicity is particularly likely in patients with hypoalbuminemia.The main toxicity described with aerosolised treatment is bronchospasm,  which can be treated or prevented with the use of β2-adrenergic receptor agonists such as salbutamol or following a desensitisation protocol. Mechanism of action
Colistin is a polycationic peptide and has both hydrophilic and lipophilic moieties. These cationic regions interact with the bacterial outer membrane by displacing magnesium and calcium bacterial counter ions in the lipopolysaccharide. The hydrophobic and hydrophilic regions interact with the cytoplasmic membrane just like a detergent, solubilizing the membrane in an aqueous environment. This effect is bactericidal even in an isosmolar environment.Colistin binds to lipopolysaccharides and phospholipids in the outer cell membrane of Gram-negative bacteria. It competitively displaces divalent cations (Ca2+ and Mg2+) from the phosphate groups of membrane lipids, which leads to disruption of the outer cell membrane, leakage of intracellular contents and bacterial death. Pharmacokinetics
No clinically useful absorption of colistin occurs in the gastrointestinal tract. For systemic infection, colistin must therefore be given by injection. Colistimethate is eliminated by the kidneys, but colistin is eliminated by non-renal mechanism(s) that are as of yet not characterised. History
Colistin was first isolated in Japan in 1949 by Y. Koyama, from a flask of fermenting Bacillus polymyxa var. colistinus, and became available for clinical use in 1959.Colistimethate sodium, a less toxic prodrug, became available for injection in 1959. In the 1980s, polymyxin use was widely discontinued because of nephro- and neurotoxicity.
This in turn affects the human immune systems ability to fight infection, in total there are 9 possible types of this condition. Diagnosis
Chronic mucocutaneous candidiasis can be diagnosed in an affected individual via the following methods/tests:

Types
Treatment
Management for an individual with chronic mucocutaneous candidiasis consists of the following (relapse occurs once treatment is ceased, in many cases):
Systemic anti-fungal therapy (e.g., Fluconazole)
Transfer factor
Combination therapy
Screening (annually)

See also
Candidiasis
List of cutaneous conditions

Notes
^  Indicates 9 references to specific, numbered pages in the Online Mendelian Inheritance in Man database. References
Further reading
Kauffman, Carol A.; Pappas, Peter G.; Sobel, Jack D.; Dismukes, William E. (2011). Essentials of Clinical Mycology. Springer Science & Business Media. ISBN 9781441966407. Retrieved 9 June 2017. Ostler, H. Bruce (2004). Diseases of the Eye and Skin: A Color Atlas. Lippincott Williams & Wilkins. ISBN 9780781749992. Retrieved 9 June 2017. == External links ==