Many viruses can be responsible for systemic vasculitis, the most frequent being hepatitis B virus-related polyarteritis nodosa (HBV-PAN), even though its incidence has decreased over the past few decades. Mixed cryoglobulinemia has been shown to be associated with hepatitis C virus (HCV) infection in more than 80% of the patients, but it remains asymptomatic in most of them with only a minority developing vasculitis. Human immunodeficiency virus (HIV), erythrovirus B19, cytomegalovirus, varicella-zoster virus and human T-cell lymphotropic virus (HTLV)-1 have also been reported to be associated with or implicated in the development of vasculitides. On the other hand, some bacteria, fungi or parasites can also cause vasculitis, mainly by direct invasion of blood vessels or septic embolization, leading, e.g., to the well-known feature of 'mycotic aneurysm'. Syphilitic aortitis and/or cerebrovascular disease and rickettsial diseases are other, more specific, bacteria-induced vasculitides. Recognizing an infectious origin of vasculitides is of great importance because treatment strategies differ from those applied to non-infectious forms. Effective antimicrobial drugs are mandatory to treat bacterial, parasitic or fungal infections, while the combination of antiviral agents and plasma exchanges has been proven to be effective against HBV-PAN. This latter strategy might also be effective against HIV-associated vasculitis and, unlike cytotoxic agents, does not jeopardize the outcome of HIV-infected patients. In the context of HCV-related cryoglobulinemic vasculitis, antiviral drugs are necessary to achieve recovery, in combination with low-dose corticosteroids and/or rituximab. In the near future, newer antiviral agents will probably also have their place in the therapeutic armamentarium for these patients.