Abstract
Metritis and other reproductive diseases are very common in birds kept as domestic pets, whether they are parrots or backyard poultry. Undiagnosed, this condition is invariably fatal. This paper reviews avian reproductive anatomy and physiology, discusses the causes and clinical signs of metritis, outlines a diagnostic approach and therapeutic options.
Anatomy
The avian ovary is located beside the cranial division of the left kidney, adjacent to the adrenal gland. The ovarian blood supply enters the ovarian hilus where it is close contact with the dorsal coelomic wall. The arterial supply come from the ovario-oviductal branch of the left cranial renal artery, while venous drainage is via two ovarian veins directly into the caudal vena cava.
The oviduct can be divided into five regions: the infundibulum, the magnum, the isthmus, the uterus (shell gland) and the vagina.
The infundibulum resembles a funnel with a thin wall. It is reasonably motile, moving to envelop the developing follicle and capturing it as ovulation occurs. Fertilisation occurs in the infundibulum before the thick albumen immediately around the yolk, and the chalaza at each end of the yolk are laid down. The egg passes through infundibulum in 15 minutes.
From the infundibulum the developing egg passes into the magnum, the longest and most coiled part of the oviduct. Here there are numerous tubular glands which secrete the thin albumen. Passage through the magnum takes 3 hours.
The egg then moves into the short and thinner isthmus. Passage through the isthmus is relatively slow, taking 75 minutes during which protein is added to the albumen, and then the shell membranes (inner and outer) are added.
There is no distinct separation between the isthmus and the uterus (shell gland). This part is relatively short, although the egg stays in the uterus for 20 hours: plumping (the addition of watery solutions) occurs in the first 8 hours, and then the egg shell is formed and calcified over another 15 hours.
The vagina, S-shaped due to smooth muscle and connective tissue, is separated from the uterus by a sphincter. Passage through the vagina into the cloaca is rapid.
The oviduct is suspended from the dorsal wall of the coelom by the dorsal mesosalpinx. A ventral mesosalpinx extends ventrally from the oviduct, but has a free margin.
Reproductive Physiology
Most birds are seasonal breeders, with substantial variation between species in their reproductive strategies. This variation is based on the environmental cues (photoperiod, rainfall, food availability) used to trigger reproduction, the developmental stage of the chick at hatch, and the extent of parental care.
In seasonal laying birds e.g., psittacines, three phases of avian growth can be recognised.
Prenuptial acceleration: At the beginning of the breeding season the ovary and oviduct begin to enlarge;
Culmination phase: Ovulation and egg laying commences; and
Refractory phase: With egg laying completed, the ovary and oviduct reduce in size.
Hormonal control of reproduction is similar to that in mammals.
Environmental and social cues stimulate the release of Gonadotrophin Releasing Hormone (GnRH), which in turn stimulates the pituitary to release Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH).
FSH supports ovarian and oviductal growth, gametogenesis, and steroidogenesis.
LH also supports steroidogenesis. This steroidogenesis sees the release of oestrogen, which has effects on follicular and oviductal growth, calcium metabolism and vitellogenesis. Some female secondary behaviours are also influenced by oestrogen, such as courtship and nesting behaviours.
Progesterone is produced by granulosa cells in the large follicles as they develop, under the influence of LH. This in turn causes a surge in LH production from the pituitary just before ovulation. This surge of LH stimulates the production of prostaglandin PGF2a from ovarian follicles, causing the follicular stigma to rupture, allowing ovulation. Progesterone inhibits further ovulation and induces behavioural and physical changes associated with incubation and brood care.
Prostaglandins PGF2a and PGE (1 and 2) are released by the F1 and post-ovulatory follicles. PGE2 and PGF2a bind at specific sites in the shell gland and vagina; PGF2a binds preferentially at the shell gland, allowing PGE2 to potentiate its effects and to allow relaxation of the vagina during oviposition. Therefore PGE (1 and 2) allows relaxation of the uterovaginal sphincter, while PGF2a stimulates shell gland contractions. Uterine contractility stimulates arginine vasotocin (AVT) release from the pituitary which stimulates further contractility and release of uterine prostaglandins.
Eggs are successively laid until a clutch is formed: indeterminate layers continue to lay if eggs are removed, while determinate layers will only lay a set number of eggs. Plasma prolactin levels are elevated during incubation, which then has an inhibitory feedback on GnRH release.
Salpingitis and Metritis
Salpingitis (inflammation of the oviduct and mesosalpinx) and metritis (inflammation of the shell gland) are relatively common conditions in domestic psittacines and backyard poultry. Predisposing causes include malnutrition, excessive abdominal fat, excessive egg laying, egg-binding and other reproductive disorders. Primary infectious metritis (e.g., Newcastle Disease virus, Infectious Bronchitis virus), while recorded in large poultry flocks, is uncommon in the domestic situation. Secondary infections (e.g., E. coli, Klebsiella spp, Pseudomonas spp), either haematogenous or ascending infections, can be complicating factors in some cases.
Affected birds usually have a history of often extremely good egg production. They are often on a predominantly seed diet with inadequate vitamin and mineral supplementation. There may be a history of infertility, or embryonic or neonatal mortality. Previous medical records, if available, may reveal a history of reproductive disorders such as egg-binding.
Affected birds often display an 'unwell' appearance: weight loss, ruffled plumage, anorexia, and lethargy. If they are still laying eggs, these eggs may be malformed (soft-shelled, stress lines, abnormal shape) or have streaking of blood on the shell. On closer physical examination there may be a distended abdomen and a cloacal discharge. This abdominal distension may be attributable to fluid accumulation (yolk-related peritonitis) or retained eggs or caseous material in the oviduct. Backyard hens often have a pale comb, reflecting chronic illness.
Diagnosis of suspected metritis can be confirmed by:
The presence of a leucocytosis which can be either heterophilic or monocytic, depending on the chronicity of the problem;
Clinical biochemistries may show a hypercalcaemia (if the bird is still reproductively active) and a hyperamylasaemia (if there is concurrent pancreatic disease associated with a yolk peritonitis;
Radiology may reveal retained eggs, an enlarged oviduct, or the presence of abdominal fluid;
Ultrasound can distinguish between fluid enlargement and organ enlargement, and may reveal retained eggs or fluid in the oviduct;
Endoscopy (if there is not free fluid in the abdomen) can demonstrate a swollen and inflamed oviduct;
If abdominal fluid is present, abdominocentesis can help to differentiate the inciting causes.
Treatment for metritis can be conservative or surgical, although it is the author's experience that conservative treatments are usually unsuccessful.
Conservative therapy revolves around 'reproductive rest' through environmental and hormonal manipulation and the use of anti-inflammatory drugs (e.g., meloxicam 0.2-0.5mg/kg BID) and antibiotics. If there is material in the oviduct (e.g., caseous pus, eggs, or fluid) the use of prostaglandins may be indicated. Using PGE2 to relax the uterovaginal sphincter and stimulate oviductal contractility may assist in this regard. The author has used PGF2a in two ostriches to successfully treat metritis, but cannot recommend this for domestic birds without prior treatment with PGE2.
As mentioned above, this conservative therapy is often unsuccessful. In valuable breeding birds an attempt to combine this therapy with a laparotomy and retrograde flushing of the oviduct can be made. However, in many cases the definitive therapy is a salpingohysterectomy.
As with any avian surgery, pre-surgical evaluation and conditioning are important. Yolk peritonitis and underlying liver, lung and kidney disease all carry a higher risk of surgical complications, while an enlarged oviduct that fills the abdomen can make anaesthesia and surgery difficult. Therefore, if time permits, the clinician should make every effort to improve the nutritional status of the patient and 'turn off' the reproductive cycle.
Using standard avian anaesthesia and analgesic protocols, the patient is positioned in either dorsal or right lateral recumbency. The choice is up to the surgeon, but the left lateral approach usually gives the best exposure. No attempt is made to perform an ovariectomy (the blood supply is tightly adherent to major blood vessels, making removal extremely risky), although large or necrotic follicles can be ligated and removed.
The large blood vessel running between infundibulum and ovary must be identified and ligated, and then the dorsal suspensory ligament blood vessels (cranial, middle & caudal oviductal arteries) are ligated or cauterised as the ligament is broken down. The ventral mesosalpinx is also broken down. This allows the oviduct to be gently exteriorised. At this stage, inserting a Q-Tip into cloaca helps to delineate this structure and identify the vagina. This should be ligated, and the oviduct removed. Abdominal closure and post-operative care are routine.
Long-term follow-up is important, as continued yolk release with subsequent yolk-related peritonitis has been reported in several species following routine salpingohysterectomy.