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 dog, cat or bird 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. Coccidia in dogs
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 diarrhoea 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 animals 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. SYMPTOM A VOMITING OF DOGS IS YELLOW AND BLACKISH.
Signs and symptoms
Signs and symptoms of Angelman syndrome and their relative frequency in affected individuals are:

Consistent (100%)
Developmental delay, functionally severe
Speech impairment, no or minimal use of words; receptive and non-verbal communication skills higher than verbal ones
Movement or balance disorder, usually ataxia of gait and/or tremulous movement of limbs
Behavioral characteristics of the following types: any combination of atypical frequent laughter/smiling; atypically happy demeanor; easily excitable personality, often with hand flapping movements; hypermotoric behavior; short attention span

Frequent (more than 80%)
Delayed, disproportionate growth in head circumference, usually resulting in microcephaly (absolute or relative) by age 2
Seizures, onset usually less than 3 years of age
Abnormal EEG, characteristic pattern with large amplitude slow-spike waves

Associated (20–80%)
Cause
Angelman syndrome is caused by the lack of expression of a gene known as UBE3A during development. This gene is located within a region of chromosome 15 known as 15q11-q13 and is part of the ubiquitin pathway. In fact, UBE3A codes for a very selective E6-AP ubiquitin ligase for which MAPK1, PRMT5, CDK1, CDK4, β-catenin, and UBXD8 have been identified as ubiquitination targetsTypically, a fetus inherits a maternal copy of UBE3A and a paternal copy of UBE3A. In certain areas of the developing brain, the paternal copy of UBE3A is inactivated through a process known as imprinting and the fetus relies on the functioning maternal copy of UBE3A in order to develop normally. In an individual with AS, however, the maternal UBE3A gene is absent or not functioning normally.