This response varies from species to species.In T. tubifex, the release of triactinomyxon spores from the intestinal wall damages the worms mucosa; this may happen thousands of times in a single worm, and is believed to impair nutrient absorption. Spores are released from the worm almost exclusively when the temperature is between 10 °C and 15 °C, so fish in warmer or cooler waters are less likely to be infected, and infection rates vary seasonally. Susceptibility
Fish size, age, concentration of triactinomyxon spores, and water temperature all affect infection rates in fish, as does the species of the fish in question. The disease has the most impact on fish less than five months old because their skeletons have not ossified. This makes young fish more susceptible to deformities and provides M. cerebralis more cartilage on which to feed. In one study of seven species of many strains, brook trout and rainbow trout (except one strain) were far more heavily affected by M. cerebralis after two hours of exposure than other species were, while bull trout, Chinook salmon, brown trout, and Arctic grayling were least severely affected. While brown trout may harbor the parasite, they typically do not show any symptoms, and this species may have been M. cerebralis original host. This lack of symptoms in brown trout meant that the parasite was only discovered after nonnative rainbow trouts were introduced in Europe.
If any of these lab values are markedly elevated, investigation for other, more serious conditions is warranted.Imaging studies cannot diagnose Rotor syndrome but can help rule out other diseases that cause hyperbilirubinemia. For example, ultrasound of the liver and the biliary tree can help investigate the causes of extra-hepatic biliary obstruction. The gallbladder is visualized on oral cholecystography in Rotor syndrome while it is not visualized in Dubin Johnson syndrome. Ultimately, the best method of diagnosing the disease is the analysis of urine coproporphyrin excretion. The total urine coproporphyrin excretion in Rotor syndrome has a 2- to 5-fold elevation, with 65% constituting coproporphyrin I. Treatment
Rotor syndrome is a benign disease requiring no treatment. Jaundice is a lifelong finding, but the disease is not associated with morbidity or mortality, and life expectancy is not affected. Most individuals with Rotor syndrome are born to consanguineous couples and its diagnosis may coincidently identify consanguinity. Distinguishing Rotor syndrome from other more serious disorders is important to avoid unnecessary workup and interventions. It is also critical to reassure and calm patients or family members of patients with Rotors syndrome that the condition is benign. History
Rotor syndrome is named after the Filipino internist Arturo Belleza Rotor (1907–1988). See also
Jaundice
Bilirubin metabolism
Gilberts syndrome
Crigler–Najjar syndrome

References
External links
Hyperbilirubinemia, Conjugated at eMedicine
Rotor syndrome at NIHs Office of Rare Diseases
Mentioned in MedlinePlus Encyclopedia: Jaundice – yellow skin