This is where the sulfamethoxazole comes in; its role is in depleting the excess DHF by preventing it from being synthesised in the first place.Co-trimoxazole was claimed to be more effective than either of its components individually in treating bacterial infections, although this was later disputed. Because it has a higher incidence of adverse effects, including allergic responses, its use has been restricted in many countries to very specific circumstances where its improved efficacy has been demonstrated. It may be effective in a variety of upper and lower respiratory tract infections, kidney and urinary tract infections, gastrointestinal tract infections, skin and wound infections, sepsis, and other infections caused by sensitive organisms. Co-trimoxazole decreases the risk of recurrence of retinochoroiditis. The global problem of advancing antimicrobial resistance has led to a renewed interest in the use of co-trimoxazole more recently. Society and culture
Legal status
Trade names
Trimethoprim/sulfamethoxazole may be abbreviated as SXT, SMZ-TMP, TMP-SMX, TMP-SMZ, or TMP-sulfa.Co-trimoxazole (British Approved Name (BAN)) is manufactured and sold by many different companies. The following list of brand names is incomplete:

Economics
Trimethoprim/sulfamethoxazole is relatively inexpensive as of 2019. References
External links
"Sulfamethoxazole mixture with trimethoprim". Drug Information Portal. U.S. National Library of Medicine.
The GM1 gangliosidoses, usually shortened to GM1, are gangliosidoses caused by mutation in the GLB1 gene resulting in a deficiency of beta-galactosidase. The deficiency causes abnormal storage of acidic lipid materials in cells of the central and peripheral nervous systems, but particularly in the nerve cells, resulting in progressive neurodegeneration. GM1 is a rare lysosomal storage disorder with a prevalence of 1 to every 100,000 to 200,000 live births worldwide, although rates are higher in some regions. Cause
GM1 Gangliosidoses disorders are caused by mutations in the GLB1 gene, which codes for lysosomal hydrolase, acid beta-galactosidase (β-gal). Low levels of β-gal cause an accumulation of GM1 gangliosides. They are inherited, autosomal recessive sphingolipidoses, a class of lipid storage disorders. Diagnosis
Diagnosis of GM1 can be obtained by genetic and enzymatic testing. Types
GM1 has three forms classified by age of onset. Type 1: early infantile
Type 2: late infantile/juvenile
Type 3: adult

Early infantile GM1
Symptoms of early infantile GM1 (the most severe subtype, with onset shortly after birth) may include neurodegeneration, seizures, liver enlargement (hepatomegaly), spleen enlargement (splenomegaly), coarsening of facial features, skeletal irregularities, joint stiffness, distended abdomen, muscle weakness, exaggerated startle response to sound, and problems with gait.About half of affected patients develop cherry-red spots in the eye. Children may be deaf and blind by age 1 and often die by age 3 from cardiac complications or pneumonia.