Cross-Neutralisation of In Vitro Neurotoxicity of Asian and Australian Snake Neurotoxins and Venoms by Different Antivenoms

doi:10.3390/toxins8100302

. 2016 Oct 18;8(10):302.

doi: 10.3390/toxins8100302.

Cross-Neutralisation of In Vitro Neurotoxicity of Asian and Australian Snake Neurotoxins and Venoms by Different Antivenoms

Anjana Silva^{1

2}, Wayne C Hodgson³, Geoffrey K Isbister^{4

5}

Affiliations

¹ Monash Venom Group, Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. anjana.silva@monash.edu.
² Faculty of Medicine and Allied Sciences, Rajarata University of Sri Lanka, Saliyapura 50008, Sri Lanka. anjana.silva@monash.edu.
³ Monash Venom Group, Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. wayne.hodgson@monash.edu.
⁴ Monash Venom Group, Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. geoff.isbister@gmail.com.
⁵ Clinical Toxicology Research Group, University of Newcastle, Newcastle, NSW 2298, Australia. geoff.isbister@gmail.com.

PMID: 27763543
PMCID: PMC5086662
DOI: 10.3390/toxins8100302

Cross-Neutralisation of In Vitro Neurotoxicity of Asian and Australian Snake Neurotoxins and Venoms by Different Antivenoms

Anjana Silva et al. Toxins (Basel). 2016.

. 2016 Oct 18;8(10):302.

doi: 10.3390/toxins8100302.

Authors

Anjana Silva^{1

2}, Wayne C Hodgson³, Geoffrey K Isbister^{4

5}

Affiliations

¹ Monash Venom Group, Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. anjana.silva@monash.edu.
² Faculty of Medicine and Allied Sciences, Rajarata University of Sri Lanka, Saliyapura 50008, Sri Lanka. anjana.silva@monash.edu.
³ Monash Venom Group, Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. wayne.hodgson@monash.edu.
⁴ Monash Venom Group, Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, VIC 3800, Australia. geoff.isbister@gmail.com.
⁵ Clinical Toxicology Research Group, University of Newcastle, Newcastle, NSW 2298, Australia. geoff.isbister@gmail.com.

PMID: 27763543
PMCID: PMC5086662
DOI: 10.3390/toxins8100302

Abstract

There is limited information on the cross-neutralisation of neurotoxic venoms with antivenoms. Cross-neutralisation of the in vitro neurotoxicity of four Asian and four Australian snake venoms, four post-synaptic neurotoxins (α-bungarotoxin, α-elapitoxin-Nk2a, α-elapitoxin-Ppr1 and α-scutoxin; 100 nM) and one pre-synaptic neurotoxin (taipoxin; 100 nM) was studied with five antivenoms: Thai cobra antivenom (TCAV), death adder antivenom (DAAV), Thai neuro polyvalent antivenom (TNPAV), Indian Polyvalent antivenom (IPAV) and Australian polyvalent antivenom (APAV). The chick biventer cervicis nerve-muscle preparation was used for this study. Antivenom was added to the organ bath 20 min prior to venom. Pre- and post-synaptic neurotoxicity of Bungarus caeruleus and Bungarus fasciatus venoms was neutralised by all antivenoms except TCAV, which did not neutralise pre-synaptic activity. Post-synaptic neurotoxicity of Ophiophagus hannah was neutralised by all antivenoms, and Naja kaouthia by all antivenoms except IPAV. Pre- and post-synaptic neurotoxicity of Notechis scutatus was neutralised by all antivenoms, except TCAV, which only partially neutralised pre-synaptic activity. Pre- and post-synaptic neurotoxicity of Oxyuranus scutellatus was neutralised by TNPAV and APAV, but TCAV and IPAV only neutralised post-synaptic neurotoxicity. Post-synaptic neurotoxicity of Acanthophis antarcticus was neutralised by all antivenoms except IPAV. Pseudonaja textillis post-synaptic neurotoxicity was only neutralised by APAV. The α-neurotoxins were neutralised by TNPAV and APAV, and taipoxin by all antivenoms except IPAV. Antivenoms raised against venoms with post-synaptic neurotoxic activity (TCAV) cross-neutralised the post-synaptic activity of multiple snake venoms. Antivenoms raised against pre- and post-synaptic neurotoxic venoms (TNPAV, IPAV, APAV) cross-neutralised both activities of Asian and Australian venoms. While acknowledging the limitations of adding antivenom prior to venom in an in vitro preparation, cross-neutralization of neurotoxicity means that antivenoms from one region may be effective in other regions which do not have effective antivenoms. TCAV only neutralized post-synaptic neurotoxicity and is potentially useful in distinguishing pre-synaptic and post-synaptic effects in the chick biventer cervicis preparation.

Keywords: antivenom; cross-neutralisation; neurotoxicity; snake; venom.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

**Figure 1**
Cross-neutralisation of the neurotoxicity of *Bungarus caeruleus* venom (5 µg/mL, V, black) by Thai cobra antivenom (TCAV; red), death adder antivenom (DAAV; orange), Thai neuro polyvalent antivenom (TNPAV; green), Indian polyvalent antivenom (IPAV; blue), and Australian polyvalent antivenom (APAV; purple) in the chick biventer nerve-muscle preparation compared to control (white): (a) Prevention of the inhibition of indirect twitches caused by venom (V). Note: all antivenoms except TCAV prevented neurotoxicity (* significantly different from control at 44 min, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of venom on response to exogenous agonists (ACh, CCh and KCl) in the absence of antivenom and the presence of antivenoms compared to control. Note: all antivenoms prevented the abolition of agonist responses by the venom (* significantly different from the venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 2**
Traces showing indirect twitch and agonist contractile responses of the chick-biventer nerve-muscle preparation for *B. caeruleus* venom (5 µg/mL) in the absence and the presence of Thai cobra antivenom (TCAV), Thai neuro polyvalent antivenom (TNPAV) and Indian polyvalent antivenom (IPAV). Note: the venom (red trace) inhibits indirect twitches and abolishes ACh and CCh responses indicating post-synaptic neurotoxicity. In the presence of TCAV (blue trace), the venom inhibits indirect twitches but does not abolish ACh and CCh responses indicating that the pre-synaptic neurotoxicity is not neutralised. In the presence of TNPAV (green trace) and IPAV (purple trace), venom fails to inhibit indirect twitches and fails to abolish ACh and CCh responses indicating neutralisation of both pre- and post-synaptic neurotoxicity of the venom.

**Figure 3**
Cross-neutralisation of the neurotoxicity of *Bungarus fasciatus* venom (7.5 µg/mL, V, black) by Thai cobra antivenom (TCAV; red), death adder antivenom (DAAV; orange), Thai neuro polyvalent antivenom (TNPAV; green), Indian polyvalent antivenom (IPAV; blue), and Australian polyvalent antivenom (APAV; purple) in the chick biventer nerve-muscle preparation compared to control (white): (a) Prevention of the inhibition of indirect twitches caused by venom. Note: all antivenoms prevented neurotoxicity (twitch height as a percentage of the initial at 78 min not different from the control, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of venom on response to exogenous agonists (ACh, CCh and KCl) in the absence of antivenom and the presence of antivenoms compared to control. Note: all antivenoms prevented the abolition of agonist responses by the venom (* significantly different from the venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 4**
Cross-neutralisation of the neurotoxicity of *Ophiophagus hannah* venom (5 µg/mL, V, black) by, Thai cobra antivenom (TCAV; red), death adder antivenom (DAAV; orange), Thai neuro polyvalent antivenom (TNPAV; green), Indian polyvalent antivenom (IPVA), and Australian polyvalent antivenom (APAV) in chick biventer nerve-muscle preparation compared to control (white): (a) Prevention of the inhibition of indirect twitches caused by venom (V). Note: all antivenoms prevented neurotoxicity (twitch height as a percentage of the initial at 60 min not different from the control, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of venom on the response to exogenous agonists (ACh, CCh and KCl) in the absence of antivenom and the presence of antivenoms compared to control. Note: all antivenoms prevented the abolition of agonist responses by the venom (* significantly different from venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 5**
Cross-neutralisation of the neurotoxicity of *Naja kaouthia* venom (5 µg/mL, V, black) by Thai cobra antivenom (TCAV; red), death adder antivenom (DAAV; orange), Thai neuro polyvalent antivenom (TNPAV; green), Indian polyvalent antivenom (IPVA), and Australian polyvalent antivenom (APAV) in chick biventer nerve-muscle preparation compared to control (white): (a) Prevention of the inhibition of indirect twitches caused by venom (V). Note: all antivenoms except IPAV prevented neurotoxicity (* significantly lower from the control at 44 min, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of venom on the response to exogenous agonists (ACh, CCh and KCl) in the absence of antivenom and presence of antivenoms compared to control. Note: all antivenoms except IPAV prevented the abolition of agonist responses by the venom (* significantly different from the venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 6**
Cross-neutralisation of the neurotoxicity of *Notechis scutatus* venom (5 µg/mL, V, black) by Thai cobra antivenom (TCAV; red), Thai neuro polyvalent antivenom (TNPAV; green), Indian polyvalent antiveom (IPAV; blue), death adder antivenom (DAAV; orange), and Australian polyvalent antivenom (APAV; purple) in chick biventer nerve-muscle preparation compared to control: (a) Prevention of the inhibition of indirect twitches caused by venom (V). Note: all antivenoms except TCAV prevented neurotoxicity (* significantly lower from the control at 48 min, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of *N. scutatus* venom on the response to exogenous agonists (ACh, CCh and KCl) in the absence and the presence of antivenoms compared to controls. Note: all antivenoms prevented the abolition of agonist responses by the venom (* significantly different from the venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 7**
Cross-neutralisation of the neurotoxicity of *Oxyuranus scutellatus* venom (5 µg/mL, V, black) by Thai cobra antivenom (TCAV; red), Thai neuro polyvalent antivenom (TNPAV; green), Indian polyvalent antivenom (IPAV; blue), death adder antivenom (DAAV; orange), and Australian polyvalent antivenom (APAV; purple) in the chick biventer nerve-muscle preparation compared to control: (a) Prevention of the inhibition of indirect twitches caused by venom (V). Note: TCAV and IPAV failed to prevent neurotoxicity (twitch height as a percentage of the initial at 140 min is different from the control, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of venom on the response to exogenous agonists (ACh, CCh and KCl) in the absence and the presence of antivenoms compared to controls. Note: all antivenoms prevented the inhibition of agonist responses by the venom (* significantly different from the venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 8**
Cross-neutralisation of the neurotoxicity of *Acanthophis antarcticus* venom (5 µg/mL, V, black) by Thai cobra antivenom (TCAV; red), Thai neuro polyvalent antivenom (TNPAV; green), Indian polyvalent antivenom (IPAV; blue), death adder antivenom (DAAV; orange), Australian polyvalent antivenom (APAV; purple) in chick biventer nerve-muscle preparation compared to control: (a) Prevention of the inhibition of indirect twitches caused by venom (V). Note: TCAV and IPAV failed to prevent neurotoxicity (twitch height as a percentage of the initial at 48 min is different from the control, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of venom on the response to exogenous agonists (ACh, CCh and KCl) in the absence and the presence of antivenoms compared to controls. Note: all antivenoms prevented the inhibition of agonist responses by the venom (* significantly different from the venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 9**
Cross-neutralisation of the neurotoxicity of *Pseudonaja textillis* venom (5 µg/mL, V, black) by Thai cobra antivenom (TCAV; red), Thai neuro polyvalent antivenom (TNPAV; green), Indian polyvalent antivenom (IPAV; blue), death adder antivenom (DAAV; orange), and Australian polyvalent antivenom (APAV; purple) in the chick biventer nerve-muscle preparation compared to control (white): (a) Prevention of the inhibition of indirect twitches caused by venom (V). Note: only APAV prevented neurotoxicity (* twitch height as a percentage of the initial at 28 min significantly different from the control, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of *P. textillis* venom on the response to exogenous nicotinic receptor agonists (ACh, CCh and KCl) in the absence and the presence of antivenoms. Note: only APAV prevented the abolition of ACh and CCh responses by the venom (* significantly different from the venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 10**
Cross-neutralisation of the neurotoxicity of 1 µg/mL vs. 5 µg/mL *P. textillis* venom by Thai cobra antivenom (TCAV; red): (a) Inhibition of indirect twitches caused by 1 µg/mL (V1) vs. 5 µg/mL (V5) *P. textillis* venom in the presence of TCAV. Note: TCAV does not prevent the twitch abolition caused by 1 µg/mL *P. textillis* venom (* significantly lower from the control at 120 min, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of 1 µg/mL (V1) vs. 5 µg/mL (V5) *P. textillis* venom on the response to exogenous nicotinic agonists (ACh, CCh and KCl) in the absence and presence of TCAV. Note: TCAV failed to prevent the abolition of agonist responses caused by 1 µg/mL venom (no significant difference from the venom, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 11**
Cross-neutralisation of the neurotoxicity of the long-chain α-neurotoxins (α-bungarotoxin and α-elapitoxin-Nk2a; black) by Thai cobra antivenom (TCAV; red) and Australian polyvalent antivenom (APAV; purple) in the chick biventer nerve-muscle preparation compared to control (white): (a) Prevention of the inhibition of indirect twitches caused by 100 nM α-bungarotoxin (T). Note: APAV and TCAV effectively prevented neurotoxicity (no difference from the control at 22 min, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of α-bungarotoxin on response to exogenous nicotinic receptor agonists (ACh, CCh and KCl) in the absence and the presence of antivenoms. Note: APAV and TCAV prevented the abolition of agonist responses caused by the toxin (* significantly different from the venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test); (c) Prevention of the inhibition of indirect twitches caused by 100 nM α-elapitoxin-Nk2a (T). Note: APAV and TCAV prevented neurotoxicity (twitch height as a percentage of the initial at 44 min not different from the control, one-way ANOVA followed by Bonferroni’s post-hoc test); (d) The effect of 100 nM α-elapitoxin-Nk2a on response to exogenous agonists (ACh, CCh and KCl) in the presence of antivenoms. Note: APAV and TCAV prevented the abolition of agonist responses by the venom (* significantly different from the toxin, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 12**
Cross-neutralisation of the neurotoxicity of the short-chain α-neurotoxins (α-scutoxin and α-elapitoxin-Ppr-1; T, black) by Thai cobra antivenom (TCAV; red) and Australian polyvalent antivenom (APAV; purple) in chick biventer nerve-muscle preparation compared to control (white); (a) Prevention of the inhibition of indirect twitches caused by α-scutoxin (T). Note: APAV and TCAV partially prevented neurotoxicity (* significantly lower from the control and the toxin at 54 min, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of 100 nM α-scutoxin on the response to exogenous nicotinic receptor agonists (ACh, CCh and KCl) in the absence and the presence of antivenoms compared to control. Note: APAV and TCAV prevented the abolition of agonist responses caused by the toxin (* significantly different from the venom, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test); (c) Prevention of the inhibition of indirect twitches caused by 100 nM α-elapitoxin-Ppr-1 (T). Note: APAV and TCAV prevented neurotoxicity (twitch height as a percentage of the initial at 44 min not different from the control, one-way ANOVA followed by Bonferroni’s post-hoc test); (d) The effect of 100 nM α-elapitoxin-Ppr1 on the response to exogenous nicotinic receptor agonists (ACh, CCh and KCl) in the absence and the presence of antivenoms compared to control. Note: APAV and TCAV prevented the abolition of agonist responses by the venom (* significantly different from the toxin, p < 0.05, one-way ANOVA followed by Bonferroni’s post-hoc test).

**Figure 13**
Cross-neutralisation of the neurotoxicity of the pre-synaptic neurotoxin from *Oxyuranus scutellatus*, taipoxin (100 nM, T, black), by Thai neuro polyvalent antivenom (TNPAV, green), Indian polyvalent antivenom (IPAV, blue) and Australian polyvalent antivenom (APAV, orange) in the chick biventer nerve-muscle preparation: (a) Prevention of the inhibition of indirect twitches caused by 100 nM taipoxin (T). Note: All antivenoms except IPAV effectively prevented the neurotoxicity (* significant difference from the control at 140 min, One-way ANOVA followed by Bonferroni’s post-hoc test); (b) The effect of taipoxin on the response to exogenous agonists (ACh, CCh and KCl) in the absence and the presence of antivenoms compared to control. Note: neither the toxin alone nor the toxin in the presence of antivenoms was able to abolish the agonist responses (no significant difference among groups, one-way ANOVA followed by Bonferroni’s post-hoc test).

See this image and copyright information in PMC

Cited by

The Effect of Australian and Asian Commercial Antivenoms in Reversing the Post-Synaptic Neurotoxicity of O. hannah, N. naja and N. kaouthia Venoms In Vitro.
Huynh TM, Hodgson WC, Isbister GK, Silva A. Huynh TM, et al. Toxins (Basel). 2022 Apr 13;14(4):277. doi: 10.3390/toxins14040277. Toxins (Basel). 2022. PMID: 35448886 Free PMC article.
Analysis of the efficacy of Taiwanese freeze-dried neurotoxic antivenom against Naja kaouthia, Naja siamensis and Ophiophagus hannah through proteomics and animal model approaches.
Liu CC, You CH, Wang PJ, Yu JS, Huang GJ, Liu CH, Hsieh WC, Lin CC. Liu CC, et al. PLoS Negl Trop Dis. 2017 Dec 15;11(12):e0006138. doi: 10.1371/journal.pntd.0006138. eCollection 2017 Dec. PLoS Negl Trop Dis. 2017. PMID: 29244815 Free PMC article.
Delayed LY333013 (Oral) and LY315920 (Intravenous) Reverse Severe Neurotoxicity and Rescue Juvenile Pigs from Lethal Doses of Micrurus fulvius (Eastern Coral Snake) Venom.
Lewin MR, Gilliam LL, Gilliam J, Samuel SP, Bulfone TC, Bickler PE, Gutiérrez JM. Lewin MR, et al. Toxins (Basel). 2018 Nov 17;10(11):479. doi: 10.3390/toxins10110479. Toxins (Basel). 2018. PMID: 30453607 Free PMC article.
Pharmacoinformatic Approach to Explore the Antidote Potential of Phytochemicals on Bungarotoxin from Indian Krait, Bungarus caeruleus.
Rajendran BK, Xavier Suresh M, Bhaskaran SP, Harshitha Y, Gaur U, Kwok HF. Rajendran BK, et al. Comput Struct Biotechnol J. 2018 Oct 31;16:450-461. doi: 10.1016/j.csbj.2018.10.005. eCollection 2018. Comput Struct Biotechnol J. 2018. PMID: 30455855 Free PMC article.
The Bold and the Beautiful: a Neurotoxicity Comparison of New World Coral Snakes in the Micruroides and Micrurus Genera and Relative Neutralization by Antivenom.
Yang DC, Dobson J, Cochran C, Dashevsky D, Arbuckle K, Benard M, Boyer L, Alagón A, Hendrikx I, Hodgson WC, Fry BG. Yang DC, et al. Neurotox Res. 2017 Oct;32(3):487-495. doi: 10.1007/s12640-017-9771-4. Epub 2017 Jul 3. Neurotox Res. 2017. PMID: 28674788

See all "Cited by" articles

References

1. Kasturiratne A., Wickremasinghe A.R., De Silva N., Gunawardena N.K., De Silva N., Pathmeswaran A., Premaratna R., Savioli L., Lalloo D.G., De Silva H.J. The global burden of snakebite: A literature analysis and modelling based on regional estimates of envenoming and deaths. PLoS Med. 2008;5:302. doi: 10.1371/journal.pmed.0050218. - DOI - PMC - PubMed
1. Harrison R.A., Hargreaves A., Wagstaff S.C., Faragher B., Lalloo D.G. Snake envenoming: A disease of poverty. PLoS Negl. Trop. Dis. 2009;3:302. doi: 10.1371/journal.pntd.0000569. - DOI - PMC - PubMed
1. Gutiérrez J.M., Williams D., Fan H.W., Warrell D.A. Snakebite envenoming from a global perspective: Towards an integrated approach. Toxicon. 2010;56:1223–1235. doi: 10.1016/j.toxicon.2009.11.020. - DOI - PubMed
1. Williams S.S., Wijesinghe C.A., Jayamanne S.F., Buckley N.A., Dawson A.H., Lalloo D.G., De Silva H.J. Delayed psychological morbidity associated with snakebite envenoming. PLoS Negl. Trop. Dis. 2011;5:302. doi: 10.1371/journal.pntd.0001255. - DOI - PMC - PubMed
1. Ranawaka U.K., Lalloo D.G., De Silva H.J. Neurotoxicity in snakebite-the limits of our knowledge. PLoS Negl. Trop. Dis. 2013;7:302. doi: 10.1371/journal.pntd.0002302. - DOI - PMC - PubMed

Publication types

Actions

MeSH terms

Actions
Actions
Actions
Actions
Actions
Actions
Actions
Actions
Actions

Substances

Actions
Actions
Actions

LinkOut - more resources

Full Text Sources
Other Literature Sources
- scite Smart Citations

[1] Kasturiratne A., Wickremasinghe A.R., De Silva N., Gunawardena N.K., De Silva N., Pathmeswaran A., Premaratna R., Savioli L., Lalloo D.G., De Silva H.J. The global burden of snakebite: A literature analysis and modelling based on regional estimates of envenoming and deaths. PLoS Med. 2008;5:302. doi: 10.1371/journal.pmed.0050218. - DOI - PMC - PubMed

[2] Kasturiratne A., Wickremasinghe A.R., De Silva N., Gunawardena N.K., De Silva N., Pathmeswaran A., Premaratna R., Savioli L., Lalloo D.G., De Silva H.J. The global burden of snakebite: A literature analysis and modelling based on regional estimates of envenoming and deaths. PLoS Med. 2008;5:302. doi: 10.1371/journal.pmed.0050218. - DOI - PMC - PubMed

[3] Harrison R.A., Hargreaves A., Wagstaff S.C., Faragher B., Lalloo D.G. Snake envenoming: A disease of poverty. PLoS Negl. Trop. Dis. 2009;3:302. doi: 10.1371/journal.pntd.0000569. - DOI - PMC - PubMed

[4] Harrison R.A., Hargreaves A., Wagstaff S.C., Faragher B., Lalloo D.G. Snake envenoming: A disease of poverty. PLoS Negl. Trop. Dis. 2009;3:302. doi: 10.1371/journal.pntd.0000569. - DOI - PMC - PubMed

[5] Gutiérrez J.M., Williams D., Fan H.W., Warrell D.A. Snakebite envenoming from a global perspective: Towards an integrated approach. Toxicon. 2010;56:1223–1235. doi: 10.1016/j.toxicon.2009.11.020. - DOI - PubMed

[6] Gutiérrez J.M., Williams D., Fan H.W., Warrell D.A. Snakebite envenoming from a global perspective: Towards an integrated approach. Toxicon. 2010;56:1223–1235. doi: 10.1016/j.toxicon.2009.11.020. - DOI - PubMed

[7] Williams S.S., Wijesinghe C.A., Jayamanne S.F., Buckley N.A., Dawson A.H., Lalloo D.G., De Silva H.J. Delayed psychological morbidity associated with snakebite envenoming. PLoS Negl. Trop. Dis. 2011;5:302. doi: 10.1371/journal.pntd.0001255. - DOI - PMC - PubMed

[8] Williams S.S., Wijesinghe C.A., Jayamanne S.F., Buckley N.A., Dawson A.H., Lalloo D.G., De Silva H.J. Delayed psychological morbidity associated with snakebite envenoming. PLoS Negl. Trop. Dis. 2011;5:302. doi: 10.1371/journal.pntd.0001255. - DOI - PMC - PubMed

[9] Ranawaka U.K., Lalloo D.G., De Silva H.J. Neurotoxicity in snakebite-the limits of our knowledge. PLoS Negl. Trop. Dis. 2013;7:302. doi: 10.1371/journal.pntd.0002302. - DOI - PMC - PubMed

[10] Ranawaka U.K., Lalloo D.G., De Silva H.J. Neurotoxicity in snakebite-the limits of our knowledge. PLoS Negl. Trop. Dis. 2013;7:302. doi: 10.1371/journal.pntd.0002302. - DOI - PMC - PubMed

Save citation to file

Email citation

Add to Collections

Add to My Bibliography

Your saved search

Create a file for external citation management software

Your RSS Feed

Cross-Neutralisation of In Vitro Neurotoxicity of Asian and Australian Snake Neurotoxins and Venoms by Different Antivenoms

Affiliations

Cross-Neutralisation of In Vitro Neurotoxicity of Asian and Australian Snake Neurotoxins and Venoms by Different Antivenoms

Authors

Affiliations

Abstract

Conflict of interest statement

Figures

Similar articles

Cited by

References

Publication types

MeSH terms

Substances

LinkOut - more resources

Full Text Sources

Other Literature Sources

Abstract

Conflict of interest statement

Figures

Similar articles

Cited by

References

Publication types

MeSH terms

Substances

Related information

LinkOut - more resources

Full Text Sources

Other Literature Sources