Coccidiosis is a parasitic disease of the intestinal tract of animals caused by coccidian protozoa. The disease spreads from one animal to another by contact with infected feces or ingestion of infected tissue. Diarrhea, which may become bloody in severe cases, is the primary symptom. Most animals infected with coccidia are asymptomatic, but young or immunocompromised animals may suffer severe symptoms and death.

While coccidia can infect a wide variety of animals, including humans, birds, and livestock, they are usually species-specific. One well-known exception is toxoplasmosis caused by "Toxoplasma gondii".

Humans may first encounter coccidia when they acquire a puppy or kitten that is infected. Other than "T. gondii", the infectious organisms are canine and feline-specific and are not contagious to humans, unlike the zoonotic diseases.

In humans, after an incubation period of 5–19 days, the symptoms of the disease range from inapparent illness to systemic illness with severe pneumonia. It presents chiefly as an atypical pneumonia. In the first week of psittacosis the symptoms mimic typhoid fever: prostrating high fevers, joint pains, diarrhea, conjunctivitis, nose bleeds and low level of white blood cells in the blood. Rose spots can appear and these are called Horder's spots. Spleen enlargement is common towards the end of the first week. It may become a serious lung infection. Diagnosis can be suspected in case of respiratory infection associated with splenomegaly and/or epistaxis. Headache can be so severe that it suggests meningitis and some nuchal rigidity is not unusual. Towards the end of the first week stupor or even coma can result in severe cases.

The second week is more akin to acute bacteremic pneumococcal pneumonia with continuous high fevers, headaches, cough, and dyspnea. X-rays show patchy infiltrates or a diffuse whiteout of lung fields.

Complications in the form of endocarditis, liver inflammation, inflammation of the heart's muscle, joint inflammation, keratoconjunctivitis (occasionally extranodal marginal zone lymphoma of the lacrimal gland/orbit), and neurologic complications (brain inflammation) may occasionally occur. Severe pneumonia requiring intensive-care support may also occur. Fatal cases have been reported (less than 1% of cases).

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.

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.

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.

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).

The acute form of the disease is manifested by lethargy, loss of appetite, vomiting and diarrhea. Due to the severe immune system suppression, multiple secondary infections develop, causing death within two to four weeks. Typical confirmation of the acute form of the disease is by necropsy, because it progresses too quickly for the normal signs such as feather loss and beak deformity to appear.

The chronic form occurs if the bird's immune system manages to mount a reaction to the virus and any secondary infections. The characteristic feather symptoms need time to develop, as they only appear during the first moult after infection. In those species having powder down, signs may be visible immediately, as powder down feathers are continually replenished.

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.

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

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.

Six syndromes are known to occur after infection with Marek's disease. These syndromes may overlap.

- Classical Marek's disease or neurolymphomatosis causes asymmetric paralysis of one or more limbs. With vagus nerve involvement, difficulty breathing or dilation of the crop may occur. Besides lesions in the peripheral nerves, there are frequently lymphomatous infiltration/tumours in the skin, skeletal muscle, visceral organs. Organs that are commonly affected include the ovary, spleen, liver, kidneys, lungs, heart, proventriculus and adrenals.

- Acute Marek's disease is an epidemic in a previously uninfected or unvaccinated flock, causing depression, paralysis, and death in a large number of birds (up to 80%). The age of onset is much earlier than the classic form; birds are four to eight weeks old when affected. Infiltration into multiple organs/tissue is observed.

- Ocular lymphomatosis causes lymphocyte infiltration of the iris (making the iris turn grey), unequal size of the pupils, and blindness.

- Cutaneous Marek's disease causes round, firm lesions at the feather follicles.

- Atherosclerosis is induced in experimentally infected chickens.

- Immunosuppression – Impairment of the T-lymphocytes prevents competent immunological response against pathogenic challenge and the affected birds become more susceptible to disease conditions such as coccidiosis and "Escherichia coli" infection . Furthermore, without stimulation by cell-mediated immunity, the humoral immunity conferred by the B-cell lines from the Bursa of Fabricius also shuts down, thus resulting in birds that are totally immunocompromised.

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.

Borna disease is an infectious neurological syndrome of warm-blooded animals, caused by Borna disease viruses 1 and 2 (BoDV-1/2), both of which are members of the species "Mammalian 1 bornavirus". BoDV-1 an 2 cause abnormal behaviour and fatality. Borna disease viruses 1 and 2 are neurotropic viruses and members of the "Bornaviridae" family within the "Mononegavirales" order.

Although Borna disease viruses 1 and 2 are mainly seen as the causative agent of Borna disease in horses and other animals, they are also controversially discussed as human infectious agents and therefore as potential zoonotic agents. The role of BoDV-1 and -2 in human illness is controversial and it is yet to be established whether BoDV-1 or -2 cause any overt disease in humans. However, correlative evidence exists linking BoDV-1/2 infection with neuropsychiatric disorders such as bipolar disorder.

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.

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 failure of the metanephros to develop in cases of BRA and some cases involving unilateral renal agenesis (URA) is due primarily to the failure of the mesonephric duct to produce a ureteric bud capable of inducing the metanephric mesenchyme. The failed induction will thereby cause the subsequent degeneration of the metanephros by apoptosis and other mechanisms. The mesonephric duct(s) of the agenic kidney(s) will also degenerate and fail to connect with the bladder. Therefore, the means by which the fetus produces urine and transports it to the bladder for excretion into the amniotic sac has been severely compromised (in the cases of URA), or completely eliminated (in the cases of BRA). The decreased volume of amniotic fluid causes the growing fetus to become compressed by the mother's uterus. This compression can cause many physical deformities of the fetus, most common of which is Potter facies. Lower extremity anomalies are frequent in these cases, which often presents with clubbed feet and/or bowing of the legs. Sirenomelia, or "Mermaid syndrome" (which occurs approximately in 1:45,000 births) can also present. In fact, nearly all reported cases of sirenomelia also be present with BRA.

Other anomalies of the classic Potter sequence infant include a parrot beak nose, redundant skin, and the most common characteristic of infants with BRA which is a skin fold of tissue extending from the medial canthus across the cheek. The ears are slightly low and pressed against the head making them appear large. The adrenal glands often appear as small oval discs pressed against the posterior abdomen due to the absence of upward renal pressure. The bladder is often small, nondistensible and may be filled with a minute amount of fluid. In males the vas deferens and seminal vesicles may be absent, while in females the uterus and upper vagina may be absent. Other abnormalities include anal atresia, absence of the rectum and sigmoid colon, esophageal and duodenal atresia, and a single umbilical artery. Presence of a diaphragmatic hernia is also common in these fetuses/infants. Additionally, the alveolar sacs of the lungs fail to properly develop as a result of the reduced volume of amniotic fluid. Labor is often induced between 22 and 36 weeks of gestation (however, some of these pregnancies may go to term) and unaborted infants typically survive for only a few minutes to a few hours. These infants will eventually die as either a result of pulmonary hypoplasia or renal failure.

Symptoms of arsenic poisoning begin with headaches, confusion, severe diarrhea, and drowsiness. As the poisoning develops, convulsions and changes in fingernail pigmentation called leukonychia striata (Mees's lines, or Aldrich-Mees's lines) may occur. When the poisoning becomes acute, symptoms may include diarrhea, vomiting, vomiting blood, blood in the urine, cramping muscles, hair loss, stomach pain, and more convulsions. The organs of the body that are usually affected by arsenic poisoning are the lungs, skin, kidneys, and liver. The final result of arsenic poisoning is coma and death.

Arsenic is related to heart disease (hypertension-related cardiovascular disease), cancer, stroke (cerebrovascular diseases), chronic lower respiratory diseases, and diabetes.

Chronic exposure to arsenic is related to vitamin A deficiency, which is related to heart disease and night blindness.

Inorganic arsenites (arsenic(III)) in drinking water have a much higher acute toxicity than organic arsenates (arsenic(V)). The acute minimal lethal dose of arsenic in adults is estimated to be 70 to 200 mg or 1 mg/kg/day.

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.

Arsenic poisoning is a medical condition that occurs due to elevated levels of arsenic in the body. If exposure occurs over a brief period of time symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhea that contains blood. Long-term exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhea, heart disease, numbness, and cancer.

The most common reason for long-term exposure is contaminated drinking water. Groundwater most often becomes contaminated naturally; however, contamination may also occur from mining or agriculture. Recommended levels in water are less than 10–50 µg/l (10–50 parts per billion). Other routes of exposure include toxic waste sites and traditional medicines. Most cases of poisoning are accidental. Arsenic acts by changing the functioning of around 200 enzymes. Diagnosis is by testing the urine, blood, or hair.

Prevention is by using water that does not contain high levels of arsenic. This may be achieved by the use of special filters or using rainwater. There is not good evidence to support specific treatments for long-term poisoning. For acute poisonings treating dehydration is important. Dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) may be used while dimercaprol (BAL) is not recommended. Hemodialysis may also be used.

Through drinking water, more than 200 million people globally are exposed to higher than safe levels of arsenic. The areas most affected are Bangladesh and West Bengal. Acute poisoning is uncommon. The toxicity of arsenic has been described as far back as 1500 BC in the Ebers papyrus.

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.

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.

Cryptomnesia occurs when a forgotten memory returns without it being recognized as such by the subject, who believes it is something new and original. It is a memory bias whereby a person may falsely recall generating a thought, an idea, a tune, or a joke, not deliberately engaging in plagiarism but rather experiencing a memory as if it were a new inspiration.

An unhappy triad (or terrible triad, "horrible triangle", O'Donoghue's triad or a "blown knee") is an injury to the anterior cruciate ligament, medial collateral ligament, and medial meniscus. Analysis during the 1990s indicated that this 'classic' O'Donoghue triad is actually an unusual clinical entity among athletes with knee injuries. Some authors mistakenly believe that in this type of injury, acute tears of the medial meniscus always present with a concomitant lateral meniscus injury. However, the 1990 analysis showed that lateral meniscus tears are more common than medial meniscus tears in conjunction with sprains of the ACL.

A tear of a meniscus is a rupturing of one or more of the fibrocartilage strips in the knee called menisci. When doctors and patients refer to "torn cartilage" in the knee, they actually may be referring to an injury to a meniscus at the top of one of the tibiae. Menisci can be torn during innocuous activities such as walking or squatting. They can also be torn by traumatic force encountered in sports or other forms of physical exertion. The traumatic action is most often a twisting movement at the knee while the leg is bent. In older adults, the meniscus can be damaged following prolonged 'wear and tear' called a degenerative tear.

Tears can lead to pain and/or swelling of the knee joint. Especially acute injuries (typically in younger, more active patients) can lead to displaced tears which can cause mechanical symptoms such as clicking, catching, or locking during motion of the knee joint. The joint will be in pain when in use, but when there is no load, the pain goes away.

A tear of the medial meniscus can occur as part of the unhappy triad, together with a tear of the anterior cruciate ligament and medial collateral ligament.