Fraser syndrome is a disorder that affects the development of the child prior to birth. Infants born with Fraser syndrome often have eyes that are malformed and completely covered by skin. Also the child is born with fingers and toes that are fused together along with abnormalities within the urine tract. As this disorder relates to vaginal atresia, infants born with Fraser syndrome are also born with malformations in their genitals.

Occurring at a rate between 1 in 10,000 to 1 in 50,000 with a male-to-female ratio of 2.3-6:1, bladder exstrophy is relatively rare. For those individuals with bladder exstrophy who maintain their ability to reproduce, the risk of bladder exstrophy in their children is approximately 500-fold greater than the general population.

The prognosis for vaginal atresia is one that is complicated. There are variations in patients' anatomic findings as well as an absence in consistent surgical techniques which makes it difficult to give a prognosis for this condition. Along with other conditions that give rise to an abnormal perineum (i.e. ambiguous genitalia and other various abnormalities that range from cloaca to urogenital sinus), individuals with vaginal atresia often report reconstruction as an outcome of treatment. Due to this, it is difficult to compare outcomes between individuals with vaginal atresia.

Even with successful surgery, patients may have long-term problems with:

- incontinence, where serious usually treated with some form of continent urinary diversion such as the Mitrofanoff

- depression and psycho-social complications

- sexual dysfunction

The main treatment for isolated epispadias is a comprehensive surgical repair of the genito-urinary area usually during the first 7 years of life, including reconstruction of the urethra, closure of the penile shaft and mobilisation of the corpora. The most popular and successful technique is known as the modified Cantwell-Ransley approach. In recent decades however increasing success has been achieved with the complete penile disassembly technique despite its association with greater and more serious risk of damage.

Upon delivery, the exposed bladder is irrigated and a non-adherent film is placed to prevent as much contact with the external environment as possible. In the event the child was not born at a medical center with an appropriate exstrophy support team then transfer will likely follow. Upon transfer, or for those infants born at a medical center able to care for bladder exstrophy, imaging may take place in the first few hours of life prior to the child undergoing surgery.

Primary (immediate) closure is indicated only in those patients with a bladder of appropriate size, elasticity, and contractility as those patients are most likely to develop a bladder of adequate capacity after early surgical intervention.

Conditions that are absolute contraindications despite bladder adequacy include duplication of the penis or scrotum and significant bilateral hydronephrosis.

Cloacal exstrophy (EC) is a severe birth defect wherein much of the abdominal organs (the bladder and intestines) are exposed. It often causes the splitting of both male and female genitalia (specifically, the penis and clitoris respectively), and the anus is occasionally sealed.

Cloacal exstrophy is a rare birth defect, present in 1/200,000 pregnancies and 1/400,000 live births.

It is caused by a defect of the ventral body wall—mesodermal migration is inhibited and folding fails.

Imperforate anus has an estimated incidence of 1 in 5000 births. It affects boys and girls with similar frequency. However, imperforate anus will present as the low version 90% of the time in females and 50% of the time in males.

Imperforate anus is an occasional complication of sacrococcygeal teratoma.

With a high lesion, many children have problems controlling bowel function and most also become constipated. With a low lesion, children generally have good bowel control, but they may still become constipated.

For children who have a poor outcome for continence and constipation from the initial surgery, further surgery to better establish the angle between the anus and the rectum may improve continence and, for those with a large rectum, surgery to remove that dilated segment may significantly improve the bowel control for the patient. An antegrade enema mechanism can be established by joining the appendix to the skin (Malone stoma); however, establishing more normal anatomy is the priority.

Gastroschisis is a similar birth defect, but in gastroschisis the umbilical cord is not involved and the lesion is usually to the right of midline. Parts of organs may be free in the amniotic fluid, and not enclosed in a membranous (peritoneal) sac. Gastroschisis is less frequently associated with other defects than omphalocele.

Omphaloceles occurs more frequently with increased maternal age.

Other related syndromes are Pentalogy of Cantrell, Beckwith-Wiedemann, and OEIS complex (omphalocele, exstrophy of the cloaca, imperforate anus, spinal defects).

Caused by malrotation of the bowels while returning to the abdomen during development. Some cases of omphalocele are believed to be due to an underlying genetic disorder, such as Edward's syndrome (trisomy 18) or Patau syndrome (trisomy 13).

Beckwith–Wiedemann syndrome is also associated with omphaloceles.

Histomoniasis (or histomonosis), also known as blackhead disease, is a commercially important disease of poultry, particularly of chickens and turkeys, due to parasitic infection of a protozoan, "Histomonas meleagridis". The protozoan is transmitted to the bird by the nematode parasite "Heterakis gallinarum". "H. meleagridis" resides within the eggs of "H. gallinarum", so birds ingest the parasites along with contaminated soil or food. Earthworms can also act as a paratenic host.

"Histomonas meleagridis" specifically infects the cecum and liver. Symptoms of the infection include depression, reduced appetite, poor growth, increased thirst, sulphur-yellow diarrhoea, listlessness, and dry, ruffled feathers. The head may become cyanotic (bluish in colour), hence the common name of the disease, blackhead disease; thus the name 'blackhead' is in all possibility a misnomer for discoloration. The disease carries a high mortality rate, and is particularly highly fatal in poultry, and less in other birds. Currently, no prescription drug is available to treat this disease.

Poultry (especially free-ranging) and wild birds commonly harbor a number of parasitic worms with only mild health problems from them. Turkeys are much more susceptible to getting blackhead than are chickens. Thus, chickens can be infected carriers for a long time because they are not removed or medicated by their owners, and they do not die or stop eating/defecating. "H. gallinarum" eggs can remain infective in soil for four years, a high risk of transmitting blackhead to turkeys remains if they graze areas with chicken feces in this time frame.

Histomoniasis is characterized by blackhead in birds. "H. meleagridis" is released in the cecum where the eggs of the nematode undergo larval development. The parasite migrates to the mucosa and submucosa where they cause extensive and severe necrosis of the tissue. Necrosis is initiated by inflammation and gradual ulceration, causing thickening of the cecal wall. The lesions are sometimes exacerbated by other pathogens such as "Escherichia coli" and coccidia. Histomonads then gain entry into small veins of the blood stream from the cecal lesions and migrate to the liver, causing focal necrosis. Turkeys are noted to be most susceptible to the symptoms in terms of mortality, sometimes approaching 100% of a flock. Diagnosis can be easily performed by necropsy of the fresh or preserved carcass. Unusual lesions have been observed in other organs of turkey such as the bursa of Fabricius, lungs, and kidneys.

Symptoms appear within 7–12 days after infection and include depression, reduced appetite, poor growth, increased thirst, sulphur-yellow diarrhoea, listlessness, drooping wings, and unkempt feathers. Young birds have a more acute disease and die within a few days after signs appear. Older birds may be sick for some time and become emaciated before death. The symptoms are highly fatal to turkeys, but effect less damage in chickens. However, outbreaks in chickens may result in high morbidity, moderate mortality, and extensive culling, leading to overall poor flock performance. Concurrence of "Salmonella typhmurium" and "E. coli" was found to cause high mortality in broiler chickens.

There are several diseases that are caused by avian reovirus, which includes, avian arthritis/tenosynovitis, runting-stunting syndrome, and blue wing disease in chickens. Blue wing disease affects young broiler chickens and has an average mortality rate of 10%. It causes intramuscular and subcutaneous hemorrhages and atrophy of the spleen, bursa of Fabricius, and thymus. When young chickens are experimentally infected with avian reovirus, it is spread rapidly throughout all tissues. This virus is spread most frequently in the skin and muscles, which is also the most obvious site for lesions. Avian arthritis causes significant lameness in joints, specifically the hock joints. In the most severe cases, viral arthritis has caused the tendon to rupture. Chickens that have contracted runting-stunting syndrome cause a number of individuals in a flock to appear noticeably small due to its delayed growth. Diseased chicks are typically pale, dirty, wet, and may have a distending abdomen. Some individuals may display “helicopter-like” feathers in their wings and other feather abnormalities. The virus has also been shown to cause osteoporosis.

Although infection of avian reovirus is spread worldwide, it is rarely the sole cause of a disease. For chickens, the most common manifestation of the disease is joint/limb lameness. Confirming infection of avian reovirus can be detected through an ELISA test by using and observing the expression of σC and σB proteins. However, isolating and identifying reoviruses from tissue samples is very time consuming. Isolation is most successfully attained through inoculation of material into chick embryo cultures or fertile chicken eggs. Inoculation of embryonic eggs through the yolk sac has shown that the virus usually kills the embryos within 5 or 6 days post inoculation. Analyzing the samples, the embryos appeared hemorrhagic and necrotic lesions on the liver were present. (Jones, Onunkwo, 1978). There have also been approaches to identify avian reoviruses molecularly by observing infected tissues with dot-blot hybridization, PCR, and a combination of PCR and RFLP. This combination allows for the reovirus strain to be typed.