Orf is a farmyard pox, a type of zoonosis. It causes small pustules in the skin of primarily sheep and goats, but can also occur on the hands of humans. A pale halo forms around a red centre. It may persist for several weeks before crusting and then either resolves or leaves a hard lump. There is usually only one lesion, but there may be many, and they are not painful. Sometimes there are swollen lymph glands.It is caused by a Parapoxvirus. It can occur in humans who handle infected animals or contaminated objects. One third of cases may develop erythema multiforme. Once resolved, a person can still be infected again.Generally, treatment options are limited. Injecting the lesion with cidofovir or applying imiquimod has been tried. It is sometimes necessary to cut them out. The vaccine used in sheep to prevent orf is live and has been known to cause disease in humans.The disease is endemic in livestock herds worldwide. A recent outbreak emerged in southwest Ethiopia between October 2019 and May 2020. Humans
Orf is a zoonotic disease, meaning humans can contract this disorder through direct contact with infected sheep and goats or with fomites carrying the orf virus. It causes a purulent-appearing papule locally and generally no systemic symptoms. Infected locations can include the finger, hand, arm, face and even the penis (caused by infection either from contact with the hand during urination or from bestiality). Consequently, it is important to observe good personal hygiene and to wear gloves when treating infected animals.
Comorbidities in this study included malignant hypertension (30%), TMA with a history of transplant (23%), TMA associated with pregnancy (21%), glomerulopathy (17%), systemic disease such as systemic lupus erythematosus (SLE) or progressive systemic sclerosis (PSS) (6%), and malignancy (1%). The presence of mutations in complement regulatory proteins, or of disease-associated variations in the genes encoding these proteins (i.e., in most patients with comorbid conditions as well as in patients with aHUS as a single disease), suggests that deviations from the normal genetic coding of these factors could result in a genetic predisposition to TMA. Individuals so predisposed could have aHUS episodes precipitated by one of the known disease triggers (e.g., infection, pregnancy, surgery, trauma) as well as by other systemic diseases (e.g., malignant hypertension, SLE, cancer). Mechanisms
In healthy individuals, complement is used to attack foreign substances, and the complement system is highly regulated to prevent it from damaging healthy tissues and organs. However, in most patients with aHUS, it has been demonstrated that chronic, uncontrolled, and excessive activation of complement can result from production of anti-factor H autoantibodies or from genetic mutations in any of several complement regulatory proteins (e.g., factor H, factor HR1 or HR3, membrane cofactor protein, factor I, factor B, complement C3, and thrombomodulin). This results in platelet activation, damage to endothelial cells (cells that line the blood vessels), and white blood cell activation, leading to systemic TMA, which manifests as decreased platelet count, hemolysis (breakdown of red blood cells), damage to multiple organs, and often, death.