The high familial prevalence rate is most notable in male individuals. There are many hypotheses about the exact genetic disorder that could cause higher incidence of AAA among male members of the affected families. Some presumed that the influence of alpha 1-antitrypsin deficiency could be crucial, while other experimental works favored the hypothesis of X-linked mutation, which would explain the lower incidence in heterozygous females. Other hypotheses of genetic causes have also been formulated. Connective tissue disorders, such as Marfan syndrome and Ehlers-Danlos syndrome, have also been strongly associated with AAA. Both relapsing polychondritis and pseudoxanthoma elasticum may cause abdominal aortic aneurysm. Atherosclerosis: The AAA was long considered to be caused by atherosclerosis, because the walls of the AAA frequently carry an atherosclerotic burden. However, this hypothesis cannot be used to explain the initial defect and the development of occlusion, which is observed in the process. Other causes of the development of AAA include: infection, trauma, arteritis, and cystic medial necrosis. Pathophysiology
The most striking histopathological changes of the aneurysmatic aorta are seen in the tunica media and intima layers. These changes include the accumulation of lipids in foam cells, extracellular free cholesterol crystals, calcifications, thrombosis, and ulcerations and ruptures of the layers. Adventitial inflammatory infiltrate is present. However, the degradation of the tunica media by means of a proteolytic process seems to be the basic pathophysiologic mechanism of AAA development. Some researchers report increased expression and activity of matrix metalloproteinases in individuals with AAA.
Pseudocowpox is a disease caused by the Paravaccinia virus or Pseudocowpox virus, a virus of the family Poxviridae and the genus Parapoxvirus. : 393  Humans can contract the virus from contact with livestock infected with Bovine papular stomatitis and the disease is common among ranchers, milkers, and veterinarians. Infection in humans will present with fever, fatigue, and lesion on the skin. Signs and symptoms
Paravaccinia virus presents itself with blisters, nodules, or lesions about 4 mm in diameter, typically in the area that has made contact with livestock that is infected with bovine papular stomatitis. Lesions may begin forming as late as three weeks after contact has been made with an infected animal. In rare cases, lesions may be seen systemic. General signs of infection are also common, such as fever and fatigue. Infected livestock may present with blisters or lesions on their udders or snout. Often, however, infected livestock show little to no symptoms. Mechanism
Paravaccinia is a member of the Parapoxvirus family. It has a cylindrical body about 140 X 310 nm in size, with convex ends covered in a criss-cross pattern of rope like structures. The virus is resistant to cold, dehydration, and temperatures up to 56 °C. Upon injecting a cell with its genome, the virus begins transcription in the cytoplasm using viral RNA polymerase. As the virus progresses through the cell, the host begins to replicate the viral genome between 140 minutes and 48 hours. Diagnosis
Diagnosis of paravaccinia virus will often come from Polymerase chain reaction screening ordered by their physician.