Yellow discoloration of the skin, especially on the palms and the soles, but not of the sclera or inside the mouth is due to carotenemia—a harmless condition.

Jaundice, also known as icterus, is a yellowish or greenish pigmentation of the skin and whites of the eyes due to high bilirubin levels. It is commonly associated with itchiness. The feces may be pale and the urine dark. Jaundice in babies occurs in over half in the first week following birth and in most is not a problem. If bilirubin levels in babies are very high for too long, a type of brain damage, known as kernicterus, may occur.

Causes of jaundice vary from non-serious to potentially fatal. Levels of bilirubin in blood are normally below 1.0 mg/dL (17 µmol/L) and levels over 2–3 mg/dL (34-51 µmol/L) typically results in jaundice. High bilirubin is divided into two types: unconjugated (indirect) and conjugated (direct). Conjugated bilirubin can be confirmed by finding bilirubin in the urine. Other conditions that can cause yellowish skin but are not jaundice include carotenemia from eating large amounts of certain foods and medications like rifampin.

High unconjugated bilirubin may be due to excess red blood cell breakdown, large bruises, genetic conditions such as Gilbert's syndrome, not eating for a prolonged period of time, newborn jaundice, or thyroid problems. High conjugated bilirubin may be due to liver diseases such as cirrhosis or hepatitis, infections, medications, or blockage of the bile duct. In the developed world, the cause is more often blockage of the bile duct or medications while in the developing world, it is more often infections such as viral hepatitis, leptospirosis, schistosomiasis, or malaria. Blockage of the bile duct may occur due to gallstones, cancer, or pancreatitis. Medical imaging such as ultrasound is useful for detecting bile duct blockage.

Treatment of jaundice is typically determined by the underlying cause. If a bile duct blockage is present, surgery is typically required; otherwise, management is medical. Medical management may involve treating infectious causes and stopping medication that could be contributing. Among newborns, depending on age and prematurity, a bilirubin greater than 4–21 mg/dL (68-360 µmol/L) may be treated with phototherapy or exchanged transfusion. The itchiness may be helped by draining the gallbladder or ursodeoxycholic acid. The word "jaundice" is from the French "", meaning "yellow disease".

Key prevention strategies for cirrhosis are population-wide interventions to reduce alcohol intake (through pricing strategies, public health campaigns, and personal counseling), programs to reduce the transmission of viral hepatitis, and screening of relatives of people with hereditary liver diseases.

Little is known about factors affecting cirrhosis risk and progression. Research has suggested that coffee consumption appears to help protect against cirrhosis.

Regardless of the underlying cause of cirrhosis, consumption of alcohol and paracetamol, as well as other potentially damaging substances, are discouraged. Vaccination of susceptible patients should be considered for Hepatitis A and Hepatitis B.

There is currently no specific therapy. Intravenous fluids and treatment of the hepatic encephalopathy may help. Increasing dietary levels of branched chain amino acids and feeding low protein diets can help signs of hepatic encephalopathy, which is often accomplished by feeding small amounts of grain and/or beet pulp, and removing high-protein feedstuffs such as alfalfa hay. Grazing on non-legume grass may be acceptable if it is late summer or fall, although the horse should only be permitted to eat in the evening so as to avoid photosensitization. Due to the risk of gastric impaction, stomach size should be monitored.

Sedation is minimized and used only to control behavior that could lead to injury of the animal and to allow therapeutic procedures, and should preferably involve a sedative other than a benzodiazepine. Stressing the animal should be avoided if at all possible. Plasma transfusions may be needed if spontaneous bleeding occurs, to replace clotting factors. Antibiotics are sometimes prescribed to prevent bacterial translocation from the intestines. Antioxidants such as vitamin E, B-complex vitamins, and acetylcysteine may be given. High blood ammonia is often treated with oral neomycin, often in conjunction with lactulose, metronidazole and probiotics, to decrease production and absorption of ammonia from the gastrointestinal tract.

Typically no treatment is needed. If jaundice is significant phenobarbital may be used.

This condition most commonly occurs after the administration of a horse origin biological agent such as equine-derived antiserum, and usually occurs 4–10 weeks after the event. Diseases that have been vaccinated against using equine-origin antiserum, resulting in subsequent Theiler's disease, include: African horse sickness, Eastern and Western Equine Encephalitis, "Bacillus anthracis", tetanus antitoxin, "Clostridium perfringens", "Clostridium botulinum", "Streptococcus equi" subspecies "equi", Equine influenza, Equine herpesvirus type 1, pregnant mare's serum, and plasma. Although it occurs sporadically, It appears to be spreadable within a premises, and there have been outbreaks occurring on farms involving multiple horses over several months. In the Northern hemisphere it is most common between August to November. It is seen almost exclusively in adult horses, and lactating broodmares given tetanus antitoxin post foaling may be more susceptible.

Gilbert's syndrome (GS) is a mild liver disorder in which the liver does not properly process bilirubin. Many people never have symptoms. Occasionally a slight yellowish color of the skin or whites of the eyes may occur. Other possible symptoms include feeling tired, weakness, and abdominal pain.

Gilbert's syndrome is due to a mutation in the UGT1A1 gene which results in decreased activity of the bilirubin uridine diphosphate glucuronosyltransferase enzyme. It is typically inherited in an autosomal recessive pattern and occasionally in an autosomal dominant pattern depending on the type of mutation. Episodes of jaundice may be triggered by stress such as exercise, menstruation, or not eating. Diagnosis is based on higher levels of unconjugated bilirubin in the blood without either signs of other liver problems or red blood cell breakdown.

Typically no treatment is needed. If jaundice is significant phenobarbital may be used. Gilbert's syndrome affects about 5% of people in the United States. Males are more often diagnosed than females. It is often not noticed until late childhood to early adulthood. The condition was first described in 1901 by Augustin Nicolas Gilbert.

Prognosis is good, and treatment of this syndrome is usually unnecessary. Most patients are asymptomatic and have normal lifespans. Some neonates present with cholestasis. Hormonal contraceptives and pregnancy may lead to overt jaundice and icterus (yellowing of the eyes and skin).

Dubin–Johnson syndrome (DJS) is a rare, autosomal recessive, benign disorder that causes an isolated increase of conjugated bilirubin in the serum. Classically, the condition causes a black liver due to the deposition of a pigment similar to melanin. This condition is associated with a defect in the ability of hepatocytes to secrete conjugated bilirubin into the bile, and is similar to Rotor syndrome. It is usually asymptomatic, but may be diagnosed in early infancy based on laboratory tests. No treatment is usually needed.

AIP often completely resolves with steroid treatment. The failure to differentiate AIP from malignancy may lead to unnecessary pancreatic resection, and the characteristic lymphoplasmacytic infiltrate of AIP has been found in up to 23% of patients undergoing pancreatic resection for suspected malignancy who are ultimately found to have benign disease. In this subset of patients, a trial of steroid therapy may have prevented a Whipple procedure or complete pancreatectomy for a benign disease which responds well to medical therapy. "This benign disease resembles pancreatic carcinoma both clinically and radiographically. The diagnosis of autoimmune pancreatitis is challenging to make. However, accurate and timely diagnosis may preempt the misdiagnosis of cancer and decrease the number of unnecessary pancreatic resections." Autoimmune pancreatitis responds dramatically to corticosteroid treatment.

If relapse occurs after corticosteroid treatment or corticosteroid treatment is not tolerated, immunomodulators may be used. Immunomodulators such as azathioprine, and 6-mercaptopurine have been shown to extend remission of autoimmune pancreatitis after corticosteroid treatment. If corticosteroid and immunomodulator treatments are not sufficient, rituximab may also be used. Rituximab has been shown to induce and maintain remission.

In general, AIHA in children has a good prognosis and is self-limiting. However, if it presents within the first two years of life or in the teenage years, the disease often follows a more chronic course, requiring long-term immunosuppression, with serious developmental consequences. The aim of therapy may sometimes be to lower the use of steroids in the control of the disease. In this case, splenectomy may be considered, as well as other immunosuppressive drugs. Infection is a serious concern in patients on long-term immunosuppressant therapy, especially in very young children (less than two years).

As the number of published cases of AIP has increased, efforts have been focused on defining AIP as a distinct clinical and pathologic entity and toward developing some generally agreed upon diagnostic criteria and nomenclature. Terms frequently encountered are autoimmune or autoimmune-related pancreatitis, lymphoplasmacytic sclerosing pancreatitis, idiopathic tumefactive chronic pancreatitis, idiopathic pancreatitis with focal irregular narrowing of the main pancreatic duct, and non-alcoholic duct destructive chronic pancreatitis. There are also a large number of case reports employing descriptive terminology such as pancreatitis associated with Sjögren’s syndrome, primary sclerosing cholangitis, or inflammatory bowel disease. Some of the earliest cases were reported as pancreatic pseudotumor or pseudolymphoma.

Much literature exists regarding the treatment of AIHA. Efficacy of treatment depends on the correct diagnosis of either warm- or cold-type AIHA.

Warm-type AIHA is usually a more insidious disease, not treatable by simply removing the underlying cause. Corticosteroids are first-line therapy. For those who fail to respond or have recurrent disease, splenectomy may be considered. Other options for recurrent or relapsed disease include immunosuppressants such as rituximab, danazol, cyclophosphamide, azathioprine, or cyclosporine.

Cold agglutinin disease is treated with avoidance of cold exposure. Patients with more severe disease (symptomatic anemia, transfusion dependence) may be treated with rituximab. Steroids and splenectomy are less efficacious in cold agglutinin disease.

Paroxysmal cold hemoglobinuria is treated by removing the underlying cause, such as infection.

Since the essential pathology is due to the inability to absorb vitamin B from the bowels, the solution is therefore injection of IV vitamin B. Timing is essential, as some of the side effects of vitamin B deficiency are reversible (such as RBC indices, peripheral RBC smear findings such as hypersegmented neutrophils, or even high levels of methylmalonyl CoA), but some side effects are irreversible as they are of a neurological source (such as tabes dorsalis, and peripheral neuropathy). High suspicion should be exercised when a neonate, or a pediatric patient presents with anemia, proteinuria, sufficient vitamin B dietary intake, and no signs of pernicious anemia.

This is a rare disease with prevalence about 1 in 200,000 to 1 in 600,000. Studies showed that mutations in "CUBN" or "AMN" clustered particularly in the Scandinavian countries and the Eastern Mediterranean regions. Founder effect, higher clinical awareness to IGS, and

frequent consanguineous marriages all play a role in the higher prevalence of IGS among these populations

Clinically affected dogs present with splenomegaly, icterus, anemia and thrombocytopenia.

Many dogs may succumb to infection without veterinary intervention.

The preventative measure of keeping cats inside in areas with high infection rates can prevent infection. Approved tick treatments for cats can be used but have been shown not to fully prevent tick bites.

The most often used treatments for cytauxzoonosis are imidocarb dipropionate and a combination of atovaquone and azithromycin. Although imidocarb has been used for years, it is not particularly effective. In a large study, only 25% of cats treated with this drug and supportive care survived. 60% of sick cats treated with supportive care and the combination of the anti-malarial drug atovaquone and the antibiotic azithromycin survived infection.

Quick referral to a veterinarian equipped to treat the disease may be beneficial. All infected cats require supportive care, including careful fluids, nutritional support, treatment for complications, and often blood transfusion.

Cats that survive the infection should be kept indoors as they can be persistent carriers after surviving infection and might indirectly infect other cats after being themselves bitten by a vector tick.

Vaccination

There is one intra-nasal FIP vaccine available: its use is controversial but in an independent study the authors concluded that vaccination can protect cats with no or low FCoV antibody titres and that in some cats vaccine failure was probably due to pre-existing infection.

Prevention of FCoV infection, and therefore FIP, in kittens

Kittens are protected from infection by maternally derived antibody until it wanes, usually around 5–7 weeks of age, therefore it is possible to prevent infection of kittens by removing them from sources of infection. However, FCoV is a very contagious virus and such prevention does require rigorous hygiene.

The go-to immunosuppressive drug in FIP is prednisolone.

An experimental polyprenyl immunostimulant (PI) is manufactured by Sass and Sass and tested by Dr. Al Legendre, who described survival over 1 year in three cats diagnosed with FIP and treated with the medicine. In a subsequent field study of 60 cats with non-effusive FIP treated with PI, 52 cats (87%) died before 200 days, but eight cats survived over 200 days from the start of PI treatment for and four of those survived beyond 300 days. There are anecdotal reports on the internet of cats surviving even longer.

Rangeliosis is a disease of dogs and other species, caused by the hemoprotozoan parasite "Rangelia vitalii".

Several drugs are effective for fascioliasis, both in humans and in domestic animals. The drug of choice in the treatment of fasciolosis is triclabendazole, a member of the benzimidazole family of anthelmintics. The drug works by preventing the polymerization of the molecule tubulin into the cytoskeletal structures, microtubules. Resistance of "F. hepatica" to triclabendazole has been recorded in Australia in 1995 and Ireland in 1998.

Praziquantel treatment is ineffective.

There are case reports of nitazoxanide being successfully used in human fasciolosis treatment in Mexico. There are also reports of bithionol being used successfully.

More recently, Mirazid, an Egyptian drug made from myrrh, has been investigated as an oral treatment of trematode-caused ailments including fascioliasis.

Nitazoxanide has been found effective in trials, but is currently not recommended. The life cycle includes freshwater snails as an intermediate host of the parasite.

Treatment of asymptomatic carriers should be considered if parasites are still detected after 3 months. In mild-to-moderate babesiosis, the treatment of choice is a combination of atovaquone and azithromycin. This regimen is preferred to clindamycin and quinine because side effects are fewer. The standard course is 7 to 10 days, but this is extended to at least 6 weeks in people with relapsing disease. Even mild cases are recommended to be treated to decrease the chance of inadvertently transmitting the infection by donating blood. In life-threatening cases, exchange transfusion is performed. In this procedure, the infected red blood cells are removed and replaced with uninfected ones.

Imizol is a drug used for treatment of babesiosis in dogs.

Extracts of the poisonous, bulbous plant "Boophone disticha" are used in the folk medicine of South Africa to treat equine babesiosis. "B. disticha" is a member of the daffodil family Amaryllidaceae and has also been used in preparations employed as arrow poisons, hallucinogens, and in embalming. The plant is rich in alkaloids, some of which display an action similar to that of scopolamine.

Fasciolosis is caused by two digenetic trematodes "F. hepatica" and "F. gigantica". Adult flukes of both species are localized in the bile ducts of the liver or gallbladder. "F. hepatica" measures 2 to 3 cm and has a cosmopolitan distribution. "F. gigantica" measures 4 to 10 cm in length and the distribution of the species is limited to the tropics and has been recorded in Africa, the Middle East, Eastern Europe and south and eastern Asia. In domestic livestock in Japan, diploid (2n = 20), triploid (3n = 30) and chimeric flukes (2n/3n) have been described, many of which reproduce parthenogenetically. As a result of this unclear classification, flukes in Japan are normally referred to as "Fasciola" spp. Recent reports based on mitochondrial genes analysis has shown that Japanese "Fasciola" spp. is more closely related to "F. gigantica" than to "F. hepatica". In India, a species called "F. jacksoni" was described in elephants.

"Cytauxzoon felis" belongs to the order Piroplasmida and the family Theileriidae. "C. felis" is related to "Theileria spp". of African ungulates. It is not a bacterium, not a virus, and not a fungus but is instead a protozoan that infects the blood cells of cats.