Part of the book: Recent Advances in Infective Endocarditis
Brucellosis is considered a zoonotic disease which is still an important health problem in endemic areas such as the Middle East, the Mediterranean, and Asia. Brucellosis is a systemic infection that might affect any organ or system in the body. Ocular involvement has been reported in 21% of brucellosis patients. The most common ocular manifestations of brucellosis were considered as anterior uveitis and choroiditis. The patients with anterior uveitis were reported to be usually in the acute stage and the patients with choroiditis, papilledema, and posterior uveitis were reported to be usually in the chronic stage of the disease. Ocular manifestations of brucellosis might also involve dacryoadenitis, conjunctivitis, episcleritis, scleritis, nummular keratitis, cataract, glaucoma, exudative retinal detachment, maculopathy, and neuro-ophthalmic defects including papilledema, papillitis, and cranial nerve paresis. Optic nerve involvement in brucellosis is considered secondary to meningeal inflammation, and it usually involves both optic nerves. Premacular hemorrhage related to Brucella endocarditis was reported as a rare ocular manifestation. Since ocular brucellosis has a wide spectrum of clinical manifestations, the diagnosis is considered to be mainly dependent on positive bacteriological and serological tests. Agglutinations and/or culture has been widely used for diagnosis of brucellosis. Brucella agglutination test over 1/160 titer and positive blood culture are considered as diagnostic factors for brucellosis. Early diagnosis and prompt treatment are considered to be effective for preventing blindness from severe ocular damage. Systemic antibiotics including streptomycine, rifampicin, doxycycline along with topical or systemic corticosteroid treatment have been recommended for at least 2 months. The purpose of this chapter is to describe the ocular manifestations of brucellosis, early diagnostic procedures, and treatment with reviewing the literature.
Part of the book: Updates on Brucellosis
The renin-angiotensin system (RAS) plays an important role in the pathogenesis of inflammation and autoimmune dysfunction. Uveitis is a sight-threatening intraocular inflammatory disorder caused by infectious agents, autoimmune mechanisms, exposure to toxins and many other unknown factors. Most components of RAS have been identified in every organ including the eye. The tissue-specific RAS is believed to exert diverse physiological effects locally independent of circulating angiotensin II (AT II) which functions as the effector arm of RAS causing potent proinflammatory responses via Angiotensin type 1 receptor (AT1R). AT II mediated stimulation of tissue factor (TF), the principal initiator of the clotting cascade and a major regulator of haemostasis and thrombosis rapidly inducible by inflammatory agents in several cell lines including monocytes. Activation of NFκB, a key redox-sensitive transcription factor encoding for the TF gene, plays a key role in that mechanism amplified by locally synthesized angiotensin I. (AT I) The second arm of RAS establishes systemic and local protective axis against inflammation and autoimmune dysfunction via angiotensin-converting enzyme 2 (ACE2) which is a zinc-metallopeptidase able to cleave AT II to form angiotensin-(1–7) [AT-(1–7)]. AT-(1–7), a biologically active peptide, binds to a G-protein coupled receptor Mas, and activates signaling pathways that counteract the effects of AT II by negatively effecting inflammatory responses and negatively modulating leukocyte migration, cytokine expression and release, and fibrogenic pathways. The purpose of this chapter is to analyze both pro-inflammatory and protective role of RAS in ocular inflammation and uveitis both in humans and experimental models.
Part of the book: Renin-Angiotensin System