Venom Ophthalmia and Ocular Complications Caused by Snake Venom

Abstract

Little is known about the detailed clinical description, pathophysiology, and efficacy of treatments for ocular envenoming (venom ophthalmia) caused by venom of the spitting elapid and other snakes, as well as ocular complications caused by snake venom injection. In this paper, we review clinical information of case reports regarding venom ophthalmia and snake venom injection with associated ocular injuries in Asia, Africa, and the United States. We also review the literature of snake venom such as their compositions, properties, and toxic effects. Based on the available clinical information and animal studies, we further discuss possible mechanisms of venom ophthalmia derived from two different routes (Duvernoy’s gland in the mouth and nuchal gland in the dorsal neck) and the pathophysiology of snake venom injection induced ocular complications, including corneal edema, corneal erosion, cataract, ocular inflammation, retinal hemorrhage, acute angle closure glaucoma, as well as ptosis, diplopia, and photophobia. Finally, we discuss the appropriate first aid and novel strategies for treating venom ophthalmia and snake envenoming.

A Neurotoxic Snake Venom without Phospholipase A2: Proteomics and Cross-Neutralization of the Venom from Senegalese Cobra, Naja senegalensis (Subgenus: Uraeus)

“…Cobras typically employ alpha-neurotoxins to paralyze prey (primary hunting strategy); hence, the abundantly expressed CTXs are likely needed for digestive and defensive (algesic) purposes [ 26 , 27 ]. In clinical envenomation, CTX is implicated in local tissue necrosis and venom ophthalmia [ 28 , 29 ], but it is unlikely the direct lethal factor of the venom since its lethal effect is much weaker compared to alpha-neurotoxins (intravenous median lethal dose, LD 50 of CTX > 1.0 µg/g, c.f. LD 50 of alpha-NTX < 0.2 µg/g, tested in mice) [ 30 , 31 ].…”

Elucidating the Venom Diversity in Sri Lankan Spectacled Cobra (Naja naja) through De Novo Venom Gland Transcriptomics, Venom Proteomics and Toxicity Neutralization

“…The high abundance of CTX (56.92% of total venom proteins) is consistent with the development of severe tissue necrosis in envenomation caused by N. naja [ 13 , 20 ]. With a median lethal dose (LD 50 ) of 1–2 ug/g in mice, cobra venom CTX usually do not cause a direct lethal activity [ 54 , 55 ] but are implicated in the local tissue damage and venom ophthalmia [ 56 , 57 ]. Cationic CTX are able to bind to the anionic phospholipid bilayer of cell membrane, thereby disrupting the membrane integrity, forming pore and initiating cell death [ 48 , 58 , 59 ].…”

“…NN-PLA04 belongs to the snake venom PLA 2 of Group IA family, and its calculated pI (5.22) indicated that it is an acidic PLA 2 . The PLA 2 sequence contains conserved amino acid residues H 53 , Y 57 and D 104 as with other svPLA 2 , and in addition, D 49 (Figure 5; positions in alignment figure: 53, 57, 104, 54, respectively) which is critical for its enzymatic activity [80,81]. In the venom proteomics, the protein abundance of PLA 2 expressed was relatively higher (~14% of total venom proteins) than the transcription level in the venom gland (~2.1% of toxin FPKM).…”

Effects of Sodium Silicate Complex against Hemorrhagic Activities Induced by Protobothrops mucrosquamatus Venom

“…Hemotoxic venom is composed of proteolytic enzymes and mixed compounds. Among the mixtures, snake venom metalloproteinases (SVMP), phospholipases A 2 (PLA 2 s), and serine proteases mainly account for systemic and local toxicities, such as hemorrhage, allergy, edema, necrosis, and even shock via circulatory system disturbance [ 6 , 7 , 8 , 9 ]. To alleviate local toxicity caused by venom, some experimental studies [ 4 , 10 , 11 ] reported a novel therapy for the early stage of envenomation using chelators to neutralize metals such as Ca 2+ , Mg 2+ , Zn 2+ , which are known co-factors in the active site of hemotoxic enzymes found in snake venom [ 12 , 13 , 14 ].…”

“…There are several issues related to antivenom therapy that compromise their effectiveness, including delayed administration of antivenoms in rural settings where public health services and health personnel are scarce [ 27 ] and limited effectiveness of antivenom against venom-induced hemorrhage, necrosis and severe soft tissue swelling developing into airway compromise [ 28 ]. In addition, subretinal hemorrhage may occur after snake envenoming, even administered with high doses of antivenom [ 9 ]. These evidences show that antivenom therapy may be only partially effective in the control of local tissue damage.…”