Astheno teratozoospermia

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Asthenoteratozoospermia (Astheno-teratozoospermia)

Definition

Asthenozoospermia = reduced sperm motility (< 32% total motility or < 30% progressive motility by WHO 2010 criteria, revised from the older cutoff of ≥ 50%).
Teratozoospermia = increased proportion of morphologically abnormal sperm (< 4% normal forms by strict Kruger criteria).
Asthenoteratozoospermia (AT) = the simultaneous presence of both - reduced motility AND abnormal morphology - in the same semen sample, without necessarily having reduced sperm count. When all three parameters are affected (count + motility + morphology), it is termed oligoasthenoteratozoospermia (OAT).

WHO 2010 Reference Values (Lower 5th Centile)

ParameterWHO 2010 Lower Limit
Sperm concentration≥ 15 million/mL
Total motility≥ 40%
Progressive motility≥ 32%
Normal morphology (strict criteria)≥ 4%
Viability≥ 58%
  • Berek & Novak's Gynecology, p. 2028

Causes

Asthenozoospermia (Reduced Motility)

  • Epididymal dysfunction - the epididymis plays a key role in sperm maturation and gaining motility; "epididymal asthenozoospermia" is recognized as a discrete entity
  • Leukocytospermia - leukocytes impair motility through reactive oxygen species (oxidative stress)
  • Antisperm antibodies - interfere with sperm movement and function
  • Accessory gland infection (Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma hominis)
  • Varicocele - causes elevated testicular temperature and oxidative stress
  • Immotile cilia syndrome / Primary ciliary dyskinesia - structural axonemal defects (dynein arm abnormalities) cause complete immotility
  • Partial ejaculatory duct obstruction
  • Sperm DNA fragmentation - associated with impaired motility and elevated miscarriage risk
  • Prolonged abstinence (>10 days) - sperm overflow into the urethra, reducing progressive motility and increasing DNA fragmentation
  • Systemic disease: rheumatologic conditions (sulfasalazine therapy is a noted cause of asthenozoospermia), febrile illness
  • Idiopathic - in many cases no cause is found

Teratozoospermia (Abnormal Morphology)

  • Globozoospermia - round-headed sperm lacking acrosomes (rare, specific defect)
  • Varicocele - stress-induced morphological defects
  • Genetic/chromosomal abnormalities
  • Congenital lipodystrophy (CGL) - specifically associated with teratozoospermia
  • Fever / heat exposure
  • Chemotherapy / gonadotoxins
  • Gender-affirming hormone therapy - progressive worsening of morphology and motility with prolonged exposure
  • Idiopathic

Clinical Significance

  • Teratozoospermia using older (MacLeod) criteria was associated with IUI failure; however, using strict Kruger criteria, morphology of 2-4% has not been found predictive of IUI failure compared to >4% in two recent retrospective studies - Berek & Novak's Gynecology, p. 2388
  • Asthenozoospermia reduces fertilizing capacity - progressive motility is needed for natural conception and IUI
  • Sperm DNA fragmentation correlates with IVF impairment and elevated miscarriage risk
  • Combined AT significantly reduces natural conception probability and IUI success

Investigations

  1. Semen analysis - minimum 2 samples, 2-7 weeks apart (spermatogenesis takes 70-90 days)
  2. WHO morphology assessment - strict Kruger criteria
  3. Computer-Aided Sperm Analysis (CASA) - objective motility scoring (limited by lack of standardization)
  4. Sperm DNA fragmentation index (DFI) - SCSA, TUNEL, COMET assay
  5. Leukocyte count - peroxidase staining; >1 million/mL = leukocytospermia
  6. Antisperm antibody testing - immunobead test or mixed agglutination reaction
  7. Postcoital test - limited prognostic value but can identify cervical-sperm interaction problems
  8. Genital tract cultures - for Chlamydia, Ureaplasma, Mycoplasma
  9. Hormonal workup - FSH, LH, testosterone, prolactin
  10. Scrotal ultrasound - for subclinical varicocele
  11. Genetic testing - karyotype, Y-chromosome microdeletion if severe

Management

General Measures

  • Avoid prolonged abstinence (optimal ≤ 2 days before collection/IUI)
  • Eliminate gonadotoxins: heat exposure, tobacco, alcohol, anabolic steroids, recreational drugs
  • Treat underlying infection (appropriate antibiotics for documented bacteriospermia)

Medical Treatment

  • Antioxidants - A 2024 network meta-analysis (PMID 37495550) examined antioxidant effects on OAT sperm parameters; combinations of antioxidants (vitamin C, E, selenium, CoQ10, carnitine) show some benefit in improving motility and morphology
  • Empirical hormonal therapy - A 2025 network meta-analysis (PMID 41347881) compared antiestrogens (clomiphene, tamoxifen) vs FSH for idiopathic male infertility
  • L-carnitine / acetyl-L-carnitine - epididymal energy substrate for sperm motility
  • Varicocele repair - if varicocele is identified, surgical ligation can improve motility and morphology
  • Probiotics - A 2024 systematic review (PMID 38530761) evaluated probiotic supplementation for male infertility

Assisted Reproduction

  • Intrauterine Insemination (IUI) - first-line ART; success dependent on degree of morphology/motility impairment. Strict morphology 2-4% does not predict IUI failure vs >4%
  • IVF - if IUI fails; standard IVF requires adequate motility for fertilization
  • ICSI (Intracytoplasmic Sperm Injection) - preferred when motility and morphology are severely impaired; bypasses the need for normal sperm function; also used for antisperm antibodies
  • Surgical sperm retrieval - if no viable sperm obtained by ejaculation despite treatment

Key Points Summary

FeatureDetail
AT definitionMotility < 32% + morphology < 4% normal forms
Key mechanismMitochondrial dysfunction, oxidative stress, axonemal defects
Most common epididymal causeEpididymal asthenozoospermia
Genetic cause of complete immotilityPrimary ciliary dyskinesia (dynein arm defect)
Key investigationSemen analysis x2, DNA fragmentation index
First-line ARTIUI (mild AT); ICSI (severe AT)
Morphology cutoff for IUI irrelevance2-4% strict Kruger (not predictive of IUI failure)
Recent evidence note: A 2024 network meta-analysis (PMID 37495550) on antioxidants in OAT and a 2025 network meta-analysis (PMID 41347881) on empirical hormonal treatments are the most current systematic evidence for management. These may refine or update specific treatment recommendations from older textbook editions.
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