(flesh fly or sarcophagids)Flesh flies, or sarcophagids, members of the family Sarcophagidae, can cause intestinal myiasis in humans if the females lay their eggs on meat or fruit. Accidental myiasis
Also called pseudomyiasis. Caused by flies that have no preference or need to develop in a host but that will do so on rare occasions. Transmission occurs through accidental deposit of eggs on oral or genitourinary openings, or by swallowing eggs or larvae that are on food. The cheese fly (Piophila casei) sometimes causes myiasis through intentional consumption of its maggots (which are contained in the traditional Sardinian delicacy casu marzu). Other flies that can accidentally cause myiasis are:
Musca domestica (housefly)
Fannia spp. (latrine flies)
Eristalis tenax (rat-tailed maggots)
Muscina spp.The adult flies are not parasitic, but when they lay their eggs in open wounds and these hatch into their larval stage (also known as maggots or grubs), the larvae feed on live or necrotic tissue, causing myiasis to develop. They may also be ingested or enter through other body apertures. Diagnosis
Myiasis is often misdiagnosed in the United States because it is rare and its symptoms are not specific. Intestinal myiasis and urinary myiasis are especially difficult to diagnose.Clues that myiasis may be present include recent travel to an endemic area, one or more non-healing lesions on the skin, itchiness, movement under the skin or pain, discharge from a central punctum (tiny hole), or a small, white structure protruding from the lesion. Serologic testing has also been used to diagnose the presence of botfly larvae in human ophthalmomyiasis.
Glu275 and Lys268 have also been shown to contribute to the active site, indicating there are four active sites, each of which is formed from regions of three subunits. ADSL deficiency in different people is often caused by different mutations to the enzyme, more than 50 different mutations in the ADSL gene have been discovered

Diagnosis
In terms of the diagnosis of adenylosuccinate lyase deficiency one should look for (or exam/method):
MRI
Demonstration of succinylpurines in extracellular fluids like plasma, cerebrospinal fluid and/or urine using high-pressure liquid chromatography, with or without mass spectroscopy
Genetic testing - genomic cDNA sequencing of the ADSL gene and characterization of mutant proteins. Treatment
Treatment of adenylosuccinate lyase deficiency can be done via epilepsy management with anticonvulsive drugs. Additionally the following options include:

D-ribose and uridine administration
Ketogenic diet
S-adenosyl-l-methionine

Prognosis
The prognosis of this condition in childhood usually has a stable outcome, whereas in neonatal is almost always fatal, according to Jurecka, et al. See also
Adenylosuccinate
Adenylosuccinate lyase
List of genetic disorders

References
Further reading
Saudubray, Jean-Marie; Berghe, Georges van den; Walter, John H. (2011-11-16). Inborn Metabolic Diseases: Diagnosis and Treatment. Springer Science & Business Media. ISBN 9783642157202. Blau, Nenad; Hoffmann, Georg F.; Leonard, J. V.; Clarke, Joe T. R. (2006-01-16). Physicians Guide to the Treatment and Follow-Up of Metabolic Diseases. Springer Science & Business Media. ISBN 9783540289623. == External links ==