Treatment
EPI is often treated with pancreatic enzyme replacement products (PERPs) such as pancrelipase, that are used to break down fats (via a lipase), proteins (via a protease), and carbohydrates (via amylase) into units that can be digested. Pancrelipase is typically porcine derived and requires large doses. Other animals
Causes and pathogenesis
Chronic pancreatitis is the most common cause of EPI in cats. In dogs, where the condition has been deemed common, the usual cause is by pancreatic acinar atrophy, arising as a result of genetic conditions, a blocked pancreatic duct, or prior infection.In dogs, EPI is most common in young German Shepherds, and in Finland Rough Collies, and is inherited. In German Shepherds, the method of inheritance is through an autosomal recessive gene. In these two breeds, at least, the cause appears to be immune-mediated as a sequela to lymphocytic pancreatitis. The German Shepherd makes up about two-thirds of cases seen with EPI. Other breeds reported to be predisposed to EPI include terrier breeds, Cavalier King Charles Spaniels, Chow Chows, and Picardy Shepherds. Symptoms
In animals, signs of EPI are not present until 85 to 90 percent of the pancreas is unable to secrete its enzymes. In dogs, symptoms include weight loss, poor hair coat, flatulence, increased appetite, coprophagia, and diarrhea. Feces are often yellow-gray in color with an oily texture. There are many concurrent diseases that mimic EPI, and severe pancreatitis is one that if allowed to continue unabated can lead to EPI.
Exit from host cell
The cytosol of the host cell contains nutrients, adenosine triphosphate, amino acids, and nucleotides which are used by the bacteria for growth. For this reason, as well as to avoid phagolysosomal fusion and death, rickettsiae must escape from the phagosome. To escape from the phagosome, the bacteria secrete phospholipase D and hemolysin C. This causes disruption of the phagosomal membrane and allows the bacteria to escape. Following generation time in the cytoplasm of the host cells, the bacteria utilizes actin based motility to move through the cytosol.RickA, expressed on the rickettsial surface, activates Arp2/3 and causes actin polymerization. The rickettsiae use the actin to propel themselves throughout the cytosol to the surface of the host cell. This causes the host cell membrane to protrude outward and invaginate the membrane of an adjacent cell. The bacteria are then taken up by the neighboring cell in a double membrane vacuole that the bacteria can subsequently lyse, enabling spread from cell to cell without exposure to the extracellular environment. Consequences of infection
Rickettsia rickettsii initially infect blood vessel endothelial cells, but eventually migrate to vital organs such as the brain, skin, and the heart via the blood stream. Bacterial replication in host cells causes endothelial cell proliferation and inflammation, resulting in mononuclear cell infiltration into blood vessels and subsequent red blood cell leakage into surrounding tissues. The characteristic rash observed in Rocky Mountain spotted fever is the direct result of this localized replication of rickettsia in blood vessel endothelial cells.