Chapter 173 Avian Reproductive Tract Disorders
Avian reproductive disorders are a result of complex combinations of hormonal, physiologic, and behavioral actions reacting to photoperiods, food availability, and availability of nest sites. Environmental influences unique to captivity may induce reproductive and hormonal activity in several ways. For instance, artificial lighting may interfere with the normal photoperiod and annual light cycles, resulting in inappropriate cycling. Food is typically available ad libitum in captivity, and it often is high-fat, calorically dense seed or foods high in simple carbohydrates, such as corn and fruit. These foods may actually stimulate reproduction. A lack of an appropriate mate may also cause reproductive problems. Most pet birds are not intended for breeding and do not have mates. As a result, some of these birds select an abnormal mate such as their human cohabitants or cage furniture. Along with all of these common environmental influences, there may be genetic factors that contribute to a lack of normal reproductive hormonal balance.
Reproductively driven birds may display instinctual territorial and mate-related behaviors. These behaviors may include but are not limited to aggression, biting, and excessive vocalization. These “undesirable” behaviors may jeopardize their value as pets, diminishing the pet-human relationship, and even result in these birds losing their homes.
Reproduction often is not desired in pet birds. Egg production and hormonal cycling may lead to diseases of the reproductive system or systemic, endocrine, and metabolic disorders. Therefore, avian practitioners have sought medical and surgical methods to limit reproductive drive and hormone production.
Medical therapy for chronic egg laying focuses on stopping egg production while removing predisposing stimuli and correcting any secondary diseases that may be present. Pharmacologic, behavioral, nutritional, environmental, and surgical options are used alone or in combination, depending on the needs of the individual patient. Pharmacologic options have included medroxyprogesterone acetate, levonorgestrel, human chorionic gonadotropin, testosterone, and leuprolide acetate.
|Leuprolide acetate||150–800 mg/kg IM||Administered every 14 days; three doses are usually adequate|
|Human chorionic gonadotropin||250–500 IU/kg IM on days 1, 3, and 7||Stable in refrigerator 60 days|
|500–1000 IU/kg IM||If a second egg is laid, repeat dose on day 3; if a third egg is laid, repeat dose on day 7|
|Arginine vasotocin||0.01–1.0 mg/kg IM||Stable in standard freezer|
|Prostaglandin E (Prepidil Gel)||0.1 ml/100 g||May freeze into aliquots and thaw|
|0.002–0.1 mg/kg||Applied topically prior to administration; relaxes uterovaginal sphincter while inducing uterine contractions|
|Prostaglandin F-2-alpha (Lutalyse)||0.02–0.1 mg/kg IM||May not relax uterovaginal sphincter when inducing uterine contractions|
|Topically applied to prolapsed uterine tissue to stop hemorrhage and shrink tissues|
Salpingohysterectomy may be elected or necessary if medical therapy is not successful and if there is no intent to breed the affected hen. Laparoscopic salpingohysterectomy may be performed as a preemptive measure on juvenile birds to prevent egg production and its associated diseases.
Diagnosis of egg binding or dystocia in a severely compromised patient may be made based on history and physical examination alone, and the patient may not be stable enough to survive other diagnostic procedures. Rapid diagnosis and therapy are crucial for a successful outcome.
PGF2a, oxytocin, and AVT do not cause relaxation of the uterovaginal sphincter while inducing powerful oviductal contractions. This may result in reverse peristalsis, severe pain, and/or rupture of the uterus. Therefore, prior to their use determine if the uterovaginal sphincter is open.