The infection is treated with antibiotics. Tetracyclines and chloramphenicol are the drugs of choice for treating patients with psittacosis. Most persons respond to oral therapy doxycycline, tetracycline hydrochloride, or chloramphenicol palmitate. For initial treatment of severely ill patients, doxycycline hyclate may be administered intravenously. Remission of symptoms usually is evident within 48–72 hours. However, relapse can occur, and treatment must continue for at least 10–14 days after fever abates.

There is currently no specific treatment for the virus. A vaccine is available, but only experimentally. It has not been released to the public due to the risk it poses to already exposed birds.

Therapeutic intervention is limited to treating secondary infections. The individual bird can sometimes recover, but this is rare. If only the feathers are affected and the bird suffers no other symptoms, it can usually experience an acceptable quality of life. But if the bird's beak or nails are affected, veterinarians will recommend euthanasia.

The management of the disease lies thus mostly in prevention. Every new bird that enters a pen with other birds should be quarantined first and be tested for BFDV. Birds which are known carriers should not be introduced into new pens, especially not if those contain young birds.

They are treated with antiprotozoal agents. Recent papers have also proposed the use of viruses to treat infections caused by protozoa.

The most common medications used to treat coccidian infections are in the sulfonamide antibiotic family.

Depending on the pathogen and the condition of the animal, untreated coccidiosis may clear of its own accord, or become severe and damaging, and sometimes cause death.

Puppies are frequently infected with coccidia from the feces of their mother, and are more likely to develop coccidiosis due to their undeveloped immune systems. Stress can trigger symptoms in susceptible animals.

Symptoms in young dogs include diarrhea with mucus and blood, poor appetite, vomiting, and dehydration. Untreated the disease can be fatal.

Treatment is routine and effective. Diagnosis is made by low-powered microscopic examination of the feces, which is generally replete with oocysts. Readily available drugs eliminate the protozoa or reduce them enough that the animal's immune system can clear the infection. Permanent damage to the gastrointestinal system is rare, and a dog will usually suffer no long-lasting negative effects.

Psittacosis—also known as parrot fever, and ornithosis—is a zoonotic infectious disease caused by a bacterium called "Chlamydia psittaci" and contracted from infected parrots, such as macaws, cockatiels and budgerigars, and pigeons, sparrows, ducks, hens, gulls and many other species of bird. The incidence of infection in canaries and finches is believed to be lower than in psittacine birds.

In certain contexts, the word is used when the disease is carried by any species of bird belonging to the family Psittacidae, whereas "ornithosis" is used when other birds carry the disease.

Vaccination is the only known method to prevent the development of tumors when chickens are infected with the virus. However, administration of vaccines does not prevent transmission of the virus, i.e., the vaccine is not sterilizing. However, it does reduce the amount of virus shed in the dander, hence reduces horizontal spread of the disease. Marek's disease does not spread vertically. The vaccine was introduced in 1970 and the scientist credited with its development is Dr. Ben Roy Burmester and Dr. Frank J Siccardi. Before that, Marek's disease caused substantial revenue loss in the poultry industries of the United States and the United Kingdom. The vaccine can be administered to one-day-old chicks through subcutaneous inoculation or by "in ovo" vaccination when the eggs are transferred from the incubator to the hatcher. "In ovo" vaccination is the preferred method, as it does not require handling of the chicks and can be done rapidly by automated methods. Immunity develops within two weeks.

The vaccine originally contained the antigenically similar turkey herpesvirus, which is serotype 3 of MDV. However, because vaccination does not prevent infection with the virus, the Marek's disease virus has evolved increased virulence and resistance to this vaccine. As a result, current vaccines use a combination of vaccines consisting of HVT and gallid herpesvirus type 3 or an attenuated MDV strain, CVI988-Rispens (ATCvet code: ).

Protozoan infections are parasitic diseases caused by organisms formerly classified in the Kingdom Protozoa. They include organisms classified in Amoebozoa, Excavata, and Chromalveolata.

Examples include "Entamoeba histolytica", "Plasmodium" (some of which cause malaria), and "Giardia lamblia". "Trypanosoma brucei", transmitted by the tsetse fly and the cause of African sleeping sickness, is another example.

The species traditionally collectively termed "protozoa" are not closely related to each other, and have only superficial similarities (eukaryotic, unicellular, motile, though with exceptions). The terms "protozoa" (and protist) are usually discouraged in the modern biosciences. However, this terminology is still encountered in medicine. This is partially because of the conservative character of medical classification, and partially due to the necessity of making identifications of organisms based upon appearances and not upon DNA.

Protozoan infections in animals may be caused by organisms in the sub-class Coccidia (disease: Coccidiosis) and species in the genus "Besnoitia" (disease: Besnoitiosis).

Several pathogenic protozoans appear to be capable of sexual processes involving meiosis (or at least a modified form of meiosis). Included among these protozoans are "Plasmodium falciparum" (malaria), "Toxoplasma gondii" (toxoplasmosis), "Leishmania" species (leishmaniases), "Trypanosoma brucei" (African sleeping sickness), "Trypanosoma cruzi" (Chagas disease) and "Giardia intestinalis" (giardiasis).

Psittacine beak and feather disease (PBFD) is a viral disease affecting all Old World and New World parrots. The causative virus–beak and feather disease virus (BFDV)—belongs to the taxonomic genus Circovirus, family Circoviridae. It attacks the feather follicles and the beak and claw matrices of the bird, causing progressive feather, claw and beak malformation and necrosis. In later stages of the disease, feather shaft constriction occurs, hampering development until eventually all feather growth stops. It occurs in an acutely fatal form and a chronic form.

Cracking and peeling of the outer layers of the claws and beak make tissues vulnerable to . Because the virus also affects the thymus and Bursa of Fabricius, slowing lymphocyte production, immunosuppression occurs and the bird becomes more vulnerable to secondary infections. Beak fractures and necrosis of the hard palate can prevent the bird from eating.

Pacheco's disease is an acute and often lethal infectious disease in psittacine birds. The disease is caused by a group of herpesviruses, "Psittacid herpesvirus 1" (PsHV-1), which consists of four genotypes. Birds which do not succumb to Pacheco's disease after infection with the virus become asymptomatic carriers that act as reservoirs of the infection. These persistently infected birds, often Macaws, Amazon parrots and some species of conures, shed the virus in feces and in respiratory and oral secretions. Outbreaks can occur when stress causes healthy birds who carry the virus to shed it. Birds generally become infected after ingesting the virus in contaminated material, and show signs of the disease within several weeks.

The main sign of Pacheco's disease is sudden death, sometimes preceded by a short, severe illness. If a bird survives Pacheco's disease following infection with PsHV-1 genotypes 1, 2 or 3, it may later develop internal papilloma disease in the gastrointestinal tract.

Susceptible parrot species include the African gray parrot, and cockatoo. Native Australian birds, such as the eclectus parrot, Bourke's parrot, and budgerigar are susceptible to Pacheco's disease, although the disease itself has not been found in Australia.

Pacheco's disease is an eponymously named disease; it is named after the Brazilian veterinarian, Genesio Pacheco, who first came across the disease in 1929, in an outbreak affecting the turquoise-fronted amazon parrot, "Amazona aestiva". Initially, Pacheco's disease was thought to be a manifestation of avian psittacosis. The causative agent of the disease, a herpesvirus, was not identified until 1975.

There is some evidence that there may be a relationship between BoDV-1 infection and psychiatric disease.

In 1990, Janice E. Clements and colleagues reported in the journal "Science" that antibodies to a protein encoded by the BoDV-1 genome are found in the blood of patients with behavioral disorders. In the early 1990s, researchers in Germany, America, and Japan conducted an investigation of 5000 patients with psychiatric disorders and 1000 controls, in which a significantly higher percentage of patients than controls were positive for BoDV-1 antibodies. Subsequent studies have also presented evidence for an association between BoDV-1 and human psychiatric disorders. However, not all researchers consider the link between BoDV-1 and human psychiatric disease to be conclusively proven. A recent study found no BoDV-1 antibodies in 62 patients with the deficit form of schizophrenia.

Additional evidence for a role of BoDV-1 in psychiatric disorders comes from reports that the drug amantadine, which is used to treat influenza infections, has had some success in treating depression and clearing BoDV-1 infection. Counter-claims state that Borna virus infections are not cleared by amantadine. The issue is further complicated by the fact that amantadine is also used in the treatment of Parkinson's disease and may have direct effects on the nervous system.

Marek's disease is a highly contagious viral neoplastic disease in chickens. It is named after József Marek, a Hungarian veterinarian. Marek's disease is caused by an alphaherpesvirus known as 'Marek's disease virus' (MDV) or "Gallid alphaherpesvirus 2" (GaHV-2). The disease is characterized by the presence of T cell lymphoma as well as infiltration of nerves and organs by lymphocytes. Viruses "related" to MDV appear to be benign and can be used as vaccine strains to prevent Marek's disease. For example, the related Herpesvirus of Turkeys (HVT), causes no apparent disease in turkeys and continues to be used as a vaccine strain for prevention of Marek's disease (see below). Birds infected with GaHV-2 can be carriers and shedders of the virus for life. Newborn chicks are protected by maternal antibodies for a few weeks. After infection, microscopic lesions are present after one to two weeks, and gross lesions are present after three to four weeks. The virus is spread in dander from feather follicles and transmitted by inhalation.

The mode of transmission of BoDV-1/2 is unclear but probably occurs through intranasal exposure to contaminated saliva or nasal secretions. Following infection, individuals may develop Borna disease, or may remain subclinical, possibly acting as a carrier of the virus.

Dimercaprol and dimercaptosuccinic acid are chelating agents that sequester the arsenic away from blood proteins and are used in treating acute arsenic poisoning. The most important side effect is hypertension. Dimercaprol is considerably more toxic than succimer.

DMSA monoesters, e.g. MiADMSA, are promising antidotes for arsenic poisoning. Calcium sodium edetate is also used.

Supplemental potassium decreases the risk of experiencing a life-threatening heart rhythm problem from arsenic trioxide.

White band disease (Acroporid white syndrome) is a coral disease that affects acroporid corals and is distinguishable by the white band of dead coral tissue that it forms. The disease completely destroys the coral tissue of Caribbean acroporid corals, specifically elkhorn coral ("Acropora palmata") and staghorn coral ("A. cervicornis"). The disease exhibits a pronounced division between the remaining coral tissue and the exposed coral skeleton. These symptoms are similar to white plague, except that white band disease is only found on acroporid corals, and white plague has not been found on any acroporid corals. It is part of a class of similar disease known as "white syndromes", many of which may be linked to species of "Vibrio" bacteria. While the pathogen for this disease has not been identified, "Vibrio carchariae" may be one of its factors. The degradation of coral tissue usually begins at the base of the coral, working its way up to the branch tips, but it can begin in the middle of a branch.

White band disease causes the affected coral tissue to decorticate off the skeleton in a white uniform band for which the disease was given its name. The band, which can range from a few millimeters to 10 centimeters wide, typically works its way from the base of the coral colony up to the coral branch tips. The band progresses up the coral branch at an approximate rate of 5 millimeters per day, causing tissue loss as it works its way to the branch tips. After the tissue is lost, the bare skeleton of the coral may later by colonized by filamentous algae.

There are two variants of white band disease, type I and type II. In Type I of white band disease, the tissue remaining on the coral branch shows no sign of coral bleaching, although the affected colony may appear lighter in color overall. However, a variant of white band disease, known simply as white band disease Type II, which was found on Staghorn colonies near the Bahamas, does produce a margin of bleached tissue before it is lost. Type II of white band disease can be mistaken for coral bleaching. By examining the remaining living coral tissue for bleaching, one can delineate which type of the disease affects a given coral.

The outcome of Potter's Sequence is poor. A series of 23 patients in 2007 recorded 7 deaths, 4 in the neonatal period. All 16 survivors have chronic kidney disease, with half developing end stage renal failure (median age 0.3 years, range 2 days to 8.3 years). Survivors had growth impairment (44%) and cognitive and motor development delay (25%)

The first child to survive Bilateral Renal Agenesis (BRA), Abigail Rose Herrera Beutler, was born on July 2013 to US Congresswoman Jaime Herrera Beutler.

A few weeks before she was born, Dr. Jessica Bienstock, a professor of maternal-fetal medicine at Johns Hopkins Hospital, administered a series of saline solution injections into the mother's womb to help the baby's lungs to develop. After Abigail was born, the procedure was considered a success. The infant did not need artificial respiration and could breathe on her own. Her parents kept her on kidney dialysis at home until old enough for a kidney transplant. On February 8, 2016, at the age of two, Abigail received a kidney from her father at the Lucile Packard Children's Hospital Stanford in California.

Potter sequence is the atypical physical appearance of a baby due to oligohydramnios experienced when in the uterus. It includes clubbed feet, pulmonary hypoplasia and cranial anomalies related to the oligohydramnios. Oligohydramnios is the decrease in amniotic fluid volume sufficient to cause deformations in morphogenesis of the baby.

Oligohydramnios is the cause of Potter sequence but there are many things that can lead to oligohydramnios. It can be caused by renal diseases such as bilateral renal agenesis (BRA), atresia of the ureter or urethra causing obstruction of the urinary tract, polycystic or multicystic kidney diseases, renal hypoplasia, amniotic rupture, toxemia, or uteroplacental insufficiency from maternal hypertension.

The term "Potter sequence" was initially intended to only refer to cases caused by BRA; however, it is now commonly used by many clinicians and researchers to refer to any case that presents with oligohydramnios or anhydramnios regardless of the source of the loss of amniotic fluid.

Presently, treatments make it possible for quicker recovery. If the tear is not serious, physical therapy, compression, elevation and icing the knee can heal the meniscus. More serious tears may require surgical procedures. Surgery, however, does not appear to be better than non surgical care.

Initial treatment may include physical therapy, bracing, anti-inflammatory drugs, or corticosteroid injections to increase flexibility, endurance, and strength.

Exercises can strengthen the muscles around the knee, especially the quadriceps. Stronger and bigger muscles will protect the meniscus cartilage by absorbing a part of the weight. The patient may be given paracetamol or anti-inflammatory medications.

For patients with non-surgical treatment, physical therapy program is designed to reduce symptoms of pain and swelling at the affected joint. This type of rehabilitation focuses on maintenance of full range of motion and functional progression without aggravating the symptoms. Physical therapists can utilize modalities such as electric stimulation, cold therapy and ultrasonography, etc.

Recently, accelerated rehabilitation programs have been used and show to be as successful as the conservative program. The program reduces the time the patient spends using crutches and allows weight bearing activities. The less conservative approach allows the patient to apply a small amount of stress and prevent range of motion losses. It is likely that a patient with a peripheral tear may pursue the accelerated program and a patient with a larger tear will use the conservative program.

Xanthochromism (also called xanthochroism or xanthism) is an unusually yellow pigmentation in an animal. It is often associated with the lack of usual red pigmentation and its replacement with yellow. The cause is usually genetic but may also be related to the animal's diet. A Cornell University survey of unusual-looking birds visiting feeders reported that 4% of such birds were described as xanthochromistic (compared with 76% albinistic). The opposite of xanthochromism, a deficiency in or complete absence of yellow pigment, is known as "axanthism".

Birds exhibiting genetic xanthochromism, especially deliberately bred mutations of several species of parrot in aviculture, are termed "lutinos". Wild birds in which xanthochromism has been recorded include yellow wagtail, wood warbler, Cape May warbler, rose-breasted grosbeak, evening grosbeak, red-bellied woodpecker, scarlet tanager, northern cardinal, great spotted woodpecker, common tailorbird, crimson-breasted shrike, kākāriki and kea.

Treatment of the unhappy triad usually requires surgery. An ACL surgery is common and the meniscus can be treated during the surgery as well. The MCL is rehabilitated through time and immobilization. Physical therapy after the surgery and the use of a knee brace help speed up the healing process.

A typical surgery for a blown knee includes:

- Patellar tendon autograft (An autograft is a graft that comes from the patient)

- Hamstring tendon autograft

- Quadriceps tendon autograft

- Allograft (taken from a cadaver) patellar tendon, Achilles tendon, semitendinosus, gracilis, or posterior tibialis tendon

The goal of reconstruction surgery is to prevent instability and restore the function of the torn ligament, creating a stable knee. There are certain factors that the patient must consider when deciding for or against surgery.

Brachygnathism or colloquially Parrot Mouth, is the uneven alignment of the upper and lower teeth in horses. In serious cases, the upper teeth protrude beyond the lower teeth. Problem with parrot mouth occur if the molars at the back of the mouth are also uneven, resulting in large hooks forming on the upper molars and the rear of the lower back molars. Horses with parrot mouth often require dental treatment at least every six months to remove the hooks and maintain alignment.

The equivalent conditions in humans are termed retrognathism or prognathism depending on whether the lower jaw is too far back or too far forward respectively.