seminoma
Cryptorchidism
Varicocele (14% in one study)
Trauma
Hydrocele
Mumps
Malaria
Defects in USP26 enzyme in some casesMast cells releasing inflammatory mediators appear to directly suppress sperm motility in a potentially reversible manner, and may be a common pathophysiological mechanism for several of the above-mentioned factors. Post-testicular causes
Post-testicular factors decrease male fertility due to conditions that affect the male genital system after testicular sperm production and include defects of the genital tract as well as problems in ejaculation:

Vas deferens obstruction
Lack of Vas deferens, often related to genetic markers for cystic fibrosis
Infection, e.g. prostatitis
Ejaculatory duct obstruction

Idiopathic oligospermia (oligoasthenoteratozoospermia)
In about 30% of infertile men no causative factor is found for their decrease in sperm concentration or quality by common clinical, instrumental, or laboratory means, and the condition is termed "idiopathic" (unexplained). A number of factors may be involved in the genesis of this condition, including age, infectious agents ( such as Chlamydia trachomatis), Y chromosome microdeletions, mitochondrial changes, environmental pollutants, and "subtle" hormonal changes.A review in 2013 came to the result that oligospermia and azoospermia are significantly associated with being overweight (odds ratio 1.1), obese (odds ratio 1.3) and morbidly obese (odds ratio 2.0), but the cause of this is unknown. It found no significant relation between oligospermia and being underweight. DNA damage
The human breast cancer susceptibility gene 2 (BRCA2) is employed in homologous recombinational repair of DNA damages during meiosis.
Centronuclear myopathies (CNM) are a group of congenital myopathies where cell nuclei are abnormally located in the center of muscle cells instead of their normal location at the periphery. Symptoms of CNM include severe hypotonia, hypoxia-requiring breathing assistance, and scaphocephaly. Among centronuclear myopathies, the X-linked myotubular myopathy form typically presents at birth, and is thus considered a congenital myopathy. However, some centronuclear myopathies may present later in life. Presentation
As with other myopathies, the clinical manifestations of MTM/CNM are most notably muscle weakness and associated disabilities. Congenital forms often present with neonatal low muscle tone, severe weakness, delayed developmental milestones (particularly gross motor milestones such as head control, crawling, and walking) and pulmonary complications (presumably due to weakness of the muscles responsible for respiration). Involvement of the facial muscles may cause ophthalmoplegia or ptosis. A mutation in the RYR1 gene causing CNM may also cause susceptibility to malignant hyperthermia, a potentially life-threatening reaction to anesthesia. While some patients with centronuclear myopathies remain ambulatory throughout their adult life, others may never crawl or walk and may require wheelchair use for mobility. There is substantial variability in the degree of functional impairment among the various centronuclear myopathies. Although this condition only affects the voluntary muscles, several children have had cardiac arrest, possibly due to the additional stress placed on the heart.Other observed features have been high arched palate, long digits, bell shaped chest and long face.