Kava and Kratom and Kava

 

Kava is described in the ethnopharmacology literature as “the most important psychoactive agent in Oceania” (1).  The plant Piper methysticum is cultivated on most of the islands of Polynesia.  It is used both culturally and for medicinal purposes.  It grows as a low evergreen shrub and is grown on plantations. Roots are harvested, peeled, and chopped and then extracted with alcohol or other solvents.  In the ethnopharmacology literature the active compounds are referred to as kavapyrones and in the chemistry literature kavalactones.  Structures of the main kavalactones are illustrated in the above graphic.

Kava has been cultivated and consumed in this area since prehistoric times when it was brought to the Hawaiian Islands. The effect of consumption described over time has been that of an intoxicant - euphorigenic and increased socialization. Consumption is decreased as varying widely (p 446 of Ref 1) – from 0.5-1 liter per day to 1-2 liters at ceremonies to 4 liters per day.  There are some very high consumptions of up to 13 liters per day.  High doses produce signs of toxicity including rash, hair loss, yellow coloration of the skin, reddened eyes and decreased appetite. Where it has been studied up to 4 liters per day does not product this toxicity. The standard prepared beverages contain about 70 mg of kavalactones per 100 ml, so 4 liters at this concentration is roughly 308 mg of kavalactones.  That is slightly above the upper limit that many countries who regulate kava suggest. 

From a psychiatric perspective, the pattern of use suggests that kava can be a problematic substance for many.  Although the specific epidemiology of consumption is not detailed if most people consume 1 liter a day, toxicity occurs at greater than 4 liters a day, signs of toxicity occur at higher doses, and some people are consuming up to 13 liters per day that suggests uncontrolled use and a potential substance use problem.  

From an ethnopharmacology standpoint there have also been descriptions of hallucinations occurring from kava ingestion.  The most famous one was a vision by a chief that led to the Polynesians colonizing the Easter Islands in the 3^rd or 4^th century.  More recent descriptions suggest that additional intoxicants are needed to produce these effects and kava by itself is not a psychedelic.   

 I remember the 2002 FDA warnings about kava toxicity (2,3).  The second reference is particularly useful because it reviews what I consider to be extensive evidence that kava extracts are toxic in many ways including as a direct hepatotoxin (hepatitis, cirrhosis, liver failure), a carcinogen, at the level of effects on the cytochrome system and drug-kava interactions, and as intoxicant.  The conclusion is that there was no rationale for using it as a food additive.   Several countries banned the sale of kava based on this toxicology information.  Despite these reports of multiple incidents of hepatotoxicity more recent comments suggest that these were isolated incidents and not a reason to avoid kava.  It is not clear to me what happened in the interim because although these studies were not controlled, they met Naranjo scale probability of being the causative factor in kava induced hepatotoxicity. 

Despite the above information, kava remains generally available as a food or nutritional substance in most states.  It can be easily ordered online where it is sold as a remedy for anxiety and insomnia.  That stands in contrast to kratom that is illegal in 6 states, regulated in 30, and unregulated in 20 states. In contrast to the reviews that show clear hepatotoxic and carcinogenic potential there are current papers that question that research and reference papers with those results.  They suggest that the incidence of kava induced hepatotoxicity is “rare”, but the true epidemiology is unknown specifically the total population exposed.

That brings me to the recent paper from the Mortality and Morbidity Weekly Report (MMWR) on the combination of kava and kratom.   The paper uses the same methodology of a recent post just about kratom.  It analyzes data from the National Poison Data System (NPDS) on exposures to kava alone (single substance exposure N= 1,754) or kava and other substances (multiple substance exposures N=1,347) and the outcomes over a 15-year period to 2025. 

The remarkable trend in multiple substance exposures was a shift from using alcohol and benzodiazepines with kava to kratom.  This coincides with an increase in kava use following an initial fall in use with the 2002 FDA warning on hepatotoxicity.  In addition, even though kava is not regulated in the US there are regulation limits in other countries (such as 250 mg of kavalactones per serving) that are not applicable in the US.  Some products have multiple 250 mg servings per container.  The lack of US specifications implies that the hepatotoxicity of kava is considered idiosyncratic rather than a population wide risk despite the lack of any organized pharmacovigilance and a recent decline in the quality of regulatory agencies. 

Since kava affects the GABA_A  receptor and kratom is a mu opioid receptor agonist there is also the pharmacodynamic risk of combining those substances. In my previous most about kratom’s mu opioid receptor affinity, it seemed that a lot of the risk from that compound was attenuated by using preparations with lower concentrations of the active drug (leaves rather than concentrated liquid).  In the case of kava, it is a GABA_A receptor allosteric modulator that binds to sites other than the benzodiazepine receptor (the effect is not reversed by flumazenil) (10).  Since kavalactones are active at multiple sites rather than a single receptor K_is are not available (see definitions in Supplementary below).  Comparing the EC50 of kavalactones (1.3-150 μM) to benzodiazepines (25-72 nM) shows a difference of 1,000 fold in potency.  The lower potency is reflected in the need for greater amounts of kavalactones to achieve similar effects of sleep and anxiety as well as lower abuse and overdose potential. 

Despite the decreased potency, the MMWR shows that there are more hospitalization and serious medical outcomes and they are more likely with the kava-kratom combination (click to enlarge). 

 

A comparison with acetaminophen is useful.  Acetaminophen is widely used and effective analgesic.  52 million people in the US take it on a weekly basis.  It has a unique pattern of hepatotoxicity that accounts for the warnings on the bottle about dose limitations and use with alcohol.  There are 500 deaths, 38,000 hospitalizations, and 100-150 liver transplantations per year from acetaminophen toxicity.  General risk benefit considerations include the need for a better pain medication, reducing the number of combination medications to reduce the exposure, and the current number of people who safely take the medication (11).  An analysis by MMWR of acetaminophen using the same technique they used for both kratom and kava would be useful.  The highest level of kava consumption I could find in US estimate was 21M kava drinkers.  It is likely they are not drinking it on a weekly basis but that is unknown.  It is also unregulated in the US so the dose of kavalactones and warnings about synergism with alcohol, benzodiazepines, opioids, and other sedative hypnotics is not available.  

The combination of kava and kratom is giving a clear early signal that it can potentially lead to serious medical outcomes.  Despite the reputation of being a benign herbal medication kava is associated with deaths and rare but very serious hepatic complications.  Like most of these situations unless there is a different regulatory environment or people decide to stop experimenting it is likely that these complications will increase.  There is no reason to use either kava or kratom.            

  

George Dawson, MD DFAPA

 

References:

1:  Food and Drug Administration. Consumer advisory: kava containing dietary supplements may be associated with severe liver injury. Silver Spring, MD: US Department of Health and Human Services, Food and Drug Administration; 2002. https://wayback.archive-it.org/7993/20170722144010/https:/www.fda.gov/Food/RecallsOutbreaksEmergencies/SafetyAlertsAdvisories/ucm085482.htm.

2. Food and Drug Administration. Scientific memorandum: kava (review of the published literature pertaining to the safety of kava for use in conventional foods). Silver Spring, MD: US Department of Health and Human Services, Food and Drug Administration; 2020. https://www.fda.gov/media/169556/download

3:  LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. Adverse Drug Reaction Probability Scale (Naranjo) in Drug Induced Liver Injury. [Updated 2019 May 4].

Bookshelf URL: https://www.ncbi.nlm.nih.gov/books/

4:  Teschke R, Wolff A. Regulatory causality evaluation methods applied in kava hepatotoxicity: are they appropriate? Regul Toxicol Pharmacol. 2011 Feb;59(1):1-7. doi: 10.1016/j.yrtph.2010.09.006. Epub 2010 Sep 18. PMID: 20854865.

5:  Stickel F, Shouval D. Hepatotoxicity of herbal and dietary supplements: an update. Archives of toxicology. 2015 Jun;89(6):851-65.

Over 100 cases of liver damage attributed to kava – many resulting in death or liver transplantation as of 2015.  Mechanism unknown.  Durg induced liver disease typically reverses by stopping kava.

6:  Teschke R, Frenzel C, Schulze J, Eickhoff A. Herbal hepatotoxicity: challenges and pitfalls of causality assessment methods. World J Gastroenterol. 2013 May 21;19(19):2864-82. doi: 10.3748/wjg.v19.i19.2864. PMID: 23704820; PMCID: PMC3660812.

7:  Pantano F, Tittarelli R, Mannocchi G, Zaami S, Ricci S, Giorgetti R, Terranova D, Busardò FP, Marinelli E. Hepatotoxicity Induced by "the 3Ks": Kava, Kratom and Khat. Int J Mol Sci. 2016 Apr 16;17(4):580. doi: 10.3390/ijms17040580. PMID: 27092496; PMCID: PMC4849036.

“On the one hand, growing controversial data have been reported about the hepatotoxicity of kratom, while, on the other hand, even though kava and khat hepatotoxicity has been investigated, the hepatotoxic effects are still not clear. Chronic recreational use of kratom has been associated with rare instances of acute liver injury.”

8: Bleifuss W, Boley S, Bardwell J, Goebel C, Wilkinson J. Severe kava withdrawal managed with phenobarbital. Am J Emerg Med. 2025 Oct;96:298.e5-298.e7. doi: 10.1016/j.ajem.2025.06.016. Epub 2025 Jun 16. PMID: 40541460.

9:  Towers EB, Williams IL, Holstege CP, Farah R. Increase in Poison Center Reports Linked to Kratom-Containing Kava Products - National Poison Data System, United States, 2000-2025. MMWR Morb Mortal Wkly Rep. 2026 Apr 2;75(12):157-163. doi: 10.15585/mmwr.mm7512a1. PMID: 41926333; PMCID: PMC13046178.

10:  Chua HC, Christensen ET, Hoestgaard-Jensen K, Hartiadi LY, Ramzan I, Jensen AA, Absalom NL, Chebib M. Kavain, the Major Constituent of the Anxiolytic Kava Extract, Potentiates GABAA Receptors: Functional Characteristics and Molecular Mechanism. PLoS One. 2016 Jun 22;11(6):e0157700. doi: 10.1371/journal.pone.0157700. PMID: 27332705; PMCID: PMC4917254.

11: Lee WM. Acetaminophen (APAP) hepatotoxicity-Isn't it time for APAP to go away? J Hepatol. 2017 Dec;67(6):1324-1331. doi: 10.1016/j.jhep.2017.07.005. Epub 2017 Jul 20. PMID: 28734939; PMCID: PMC5696016.

 

Supplementary 1: Some definitions of receptor kinetics:

Ki (inhibition constant) is the equilibrium dissociation constant for an inhibitor binding to its target, representing the concentration at which 50% of the target is bound by the inhibitor at equilibrium in the absence of competing substrate.  A fundamental constant independent of experimental conditions.

EC50 (half-maximal effective concentration) is the concentration of a compound that produces 50% of its maximal response in a functional assay.

IC50 (half-maximal inhibitory concentration) is the concentration that produces 50% inhibition of a measured activity.

Both EC50 and IC50 can vary with experimental conditions.

Graphic Credits:

The kavalactone graphic was done my me according to this method.

The MMWR graphic is directly from reference 9 and is in the public domain as a US government publication. 

Is The Next Zoonosis Lurking In Your Back Yard?

 

I just had a recent adventure with rabbits.  Like the experience of many suburbanites, rabbits like to eat all our ornamental vegetation. My wife oversees that department, and she does not like to see that vegetation depleted. She has tried all the repellants and the rabbits keep coming.  She has talked about shooting them like her father used to, but I convinced her that was not a good idea.  She settled on the idea of live trapping the animals and releasing them in an area far away from the house – like a park or wildlife reserve.

I researched the legality of it all.  I was surprised to find out that rabbits are considered a nuisance animal in the state of Minnesota.  As such you can kill them by various means other than poisoning without a license and at any time. There are obstacles to both relocating rabbits or how to dispose of them. I contacted both the county and city natural resource departments. They told me it was illegal to relocate rabbits onto city, county, or state lands including parks and wildlife areas.  The officials confirmed that I did not need a hunting license to kill them, but that if I did kill a rabbit, I needed to report it to the DNR.  I did not let anyone know I thought that killing a rabbit was bad karma and I had no intention of killing them.

I was advised that if I did kill a rabbit, I needed to handle it with nitrile gloves and double bag it in plastic.  Even then I must contact my garbage hauler to make sure that I could dispose of it in the trash. There were no further instructions from officials on the next step if the garbage hauler refuses to take it – but based on how the conversations were going I thought it was probably digging a deep hole in the yard.

Minnesota is populated by one true rabbit species – the Eastern Cottontail (Sylvilagus floridanus) and two hare species – the Snowshoe Hare (Lepus americanus) and the White-tailed Jack Rabbit (Lepus townsendii).  The hares are probably more common in the north.  The defining characteristics of rabbits versus hares include fewer chromosomes (44 versus 48), altricial birth state versus precocial, shorter gestation (30-31 days versus 42 days), smaller bodies and shorter ears, highly social versus solitary, and softer food preference (grass and leafy vegetables opposed to bark, twigs, and buds).  An altricial birth state means offspring are born in a state where they are unable to feed or regulate body temperature and as a result need a prolonged period of close parenting. In the past 10 years there have also been cladistic analyses based on nuclear and mitochondrial DNA.  Like all taxonomy there is some mismatch of classification.  Jackrabbits are hares and Rock hares are rabbits.     

Even before I heard those biosecurity measures from public officials, I researched the issue of rabbit to human disease transmission (1).  Domestic pet rabbits were noted to spread the expected pathogens like E. coli, Salmonella spp, Yersinia pseudotuberculosis, and Cryptosporidium.  They can also be a source of Hepatitis E.   Pasteurella multocida and Bordetella bronchiseptica can be spread as respiratory infections in humans.  Rabies was detected in one group of rabbits thought to have been infected by a wild animal.  Dermatophytes and rabbit fur mites can cause localized infections in humans.

Wild rabbits harbor Francisella tularensis the infectious bacteria causing tularemia. Tularemia is a systemic multisystem disease that can be difficult to diagnose and treat. In the worst case it can cause shock and death.  It has also been implicated as an agent that could be used for bioterrorism.   Rabbits can also have Babesia spp and Anaplasma phagocytophilum the infectious agents that cause babesiosis and human granulocytic anaplasmosis.  

Babesiosis is caused by the obligate intraerythrocytic protozoan parasite Babesia microti (2).  Severity of the illness is related to degree of parasitemia (concentration of parasites in the bloodstream) and host factors that lead to compromised immune response including age. In the extreme cases it can lead to life threatening complications that require acute care like acute renal failure, disseminated intravascular coagulation (DIC), congestive heart failure, acute respiratory distress syndrome (ARDS), and others.

Human granulocytic anaplasmosis is caused by intracellular bacteria from the Anaplasmataceae family – in this case Anaplasma phagocytophilum (3).  It is a tick-borne disease meaning that the major reservoir for the agent is small mammals who transmit it to humans via a tick vector.  Most people who are infected present with an acute flu-like illness that can progress to involved multiple systems (rash, pneumonitis, myocarditis, meningoencephalitis, secondary infections, coma).

Most of the infections identified from rabbits come from direct contact, contact with infected surfaces, and contact with blood, feces, or other bodily fluids. People raising rabbits as pets, as a food source, or hunters would appear to be at highest risk and the suggested biosecurity measures would be protective.  In talking with the local wildlife officials their concern was that rabbit relocation could be a significant source of disease spread – specifically Rabbit Hemorrhagic Fever – a viral illness that results in most rabbits dying of hepatic necrosis 48-72 hours post infection. 

Rabbit Hemorrhagic Disease Virus (RHDV) was first described in China in 1984 and has spread worldwide (4).  It is a small non-enveloped RNA virus about 40 nm in diameter.  The genome is about 8 kilodaltons is size. It is taxonomically classified in the Calciviridae family.  That family has 11 genera (Norovirus, Nebovirus, Sapovirus, Lagovirus, Vesivirus, Nacovirus, Bavovirus, Recovirus, Salovirus, Minovirus, and Valovirus) (5).  Of the major genera Norovirus and Sapovirus cause acute gastroenteritis in humans.  The etiological agent can only be distinguished by laboratory testing. The Lagovirus genus also includes European brown hare syndrome virus (EBHSV) (6).  While the original RHDV virus was species specific – there is a newer strain (RHDV2 (GI.2) that infects both rabbits and hares and is lethal to both.

All these details build a compelling story far beyond suburban landscapers wanting to protect their plants.  The recent pandemic and likely crossover of a bat coronavirus into the human population as well as past crossovers like human immunodeficiency virus and avian influenza highlight the dangers of proximity to animals with high levels of infection. There have been two recent worldwide epidemics of rabbit hemorrhagic disease virus (RHDV) initially from 1984 to the 1990s and more recently from 2010 to present.  At no point in my medical career was I made aware of this viral spread despite hearing about viral spread in other species like elk wasting disease. Evolutionary biologists have suggested the RHDV virus has been in existence for 150 years (7-10). 

The pathogenesis of the virus is known at this point. It causes apoptosis of hepatic cells and hepatic necrosis.  One of the main protective mechanisms’ antioxidant suppression of oxidative stress is overwhelmed.  Apoptosis of endothelial cells leads to procoagulant activity and disseminated intravascular coagulopathy (DIC) and resulting hemorrhage and shock. RHDV2 has enhanced virulence factors and previous infection with RHDV does not confer immunity.     

The risk of RHDV crossover to human is estimated to be low based on several factors.  First, in a large study of human exposure of 269 people exposed to infected rabbits there were no episodes of disease or antibody formation to the virus in any of those people.  Second, there is continued host specificity to lagomorphs with limited documented crossovers to other species (Alpine musk deer, Eurasian badgers).  Third, there is limited ability for viral replication in other mammalian models including mice with immune deficits (interferon 1 receptor deficits). Fourth, high specificity for histo-blood group antigens (HBGAs) (11-12) – that is the virus binds to rabbits specific HBGAs and cell receptor specificities.  Fifth, the molecular biology of the rabbit versus human HBGAs are such that there are no functional binding sites for RHDV virus.

In my efforts to understand why rabbits are considered a nuisance animal and a biohazard, I uncovered an interesting set of factors. Given the rabbit exclusive pandemics that have occurred I can understand why wildlife officials are concerned about the spread of disease from transported rabbits.  The concern about disease transfer to humans from feces, saliva, other bodily fluids, and rabbits carcasses also makes sense. One of my colleagues pointed out that there is a tularemia vaccination for dogs.  Other rabbit predators may be as susceptible as humans to many of these diseases and they are probably relatively protected from RHDV because of the aforementioned factors.  This post also highlights the need for veterinary virologists and epidemiologists to track the evolution and crossover potential of these viruses.   That used to happen in an organized way for Influenza viruses through the World Health Organization (WHO) but the current anti-science and anti-medicine administration has pulled the US out of that organization and had probably negatively impacted the viral surveillance necessary to prevent zoonoses.

At the practical level, if you are a suburbanite interested in protecting your hastes from rabbits, barriers like wire cages are recommended by the public officials I talked with.  Be sure to check with them about live trapping and relocation or other means of controlling rabbits. The literature I reviewed on live trapping recommended always using gloves when handling the trap to avoid contaminants and prevent the transfer of human scent to the trap.  Rabbit waste and carcasses should also be avoided by homeowners and pets.  Some of the pathogens in the table are transmitted by ticks – so the same precautions to prevent Lyme Disease apply.   In terms of surveillance, your state department of natural resources is probably the best resource.   They directed me to the problem of RHDV that is not listed in the human literature but is an ongoing global problem for rabbits at the epizootic level.

The lesson from rabbits so far is that non-humans also have epidemics or epizootics. The only epizootics that humans seem to pay attention to affect domesticated animals or potential high risk crossover situations like avian influenza. Those contacts of humans and animals in suburbia bear watching both for the immediate threats and implications for handling biological materials – but also the potential long term consequences. (13-16).    

 

George Dawson, MD, DFAPA

Supplementary 1:  I thought this was an excellent graphic but could not figure out where to put it in the above essay. It is an estimate of worldwide mortality due to infectious diseases. Zoonotic origins are on the left of the diagram and non-zoonotic on the right.  The authors point out that boundary is not as clear cut as it seems since common causes of crossover like bats, rats, and mice occupy the same biosphere.  In the case of rabbits I would say the backyard is the same biosphere.  

60% of human diseases have animal origins.  Based on the lab origins rhetoric of the past few years Mother Nature is by far the most significant bioterrorist.  It also speaks to why any reasonable approach to prevent these outbreaks requires infectious disease and epidemiology expertise in both human and veterinary medicine.

The graph also contains the implicit information on the non-zoonotic side.  The increasing candida auris infections are thought to be due to man-made climate change.  Warm blooded animals were thought to have natural resistance to fungal infections based on higher body temperature where fungi could not survive. That evolutionary advantage is vanishing due to increasing ambient temperatures and fungal adaptation.  There are also 5 vaccine preventable diseases. There is an active anti-vaccination campaign that has reduced access to some of these vaccinations.         

Graphic is reproduced here via Copyright: © 2022 Weiss RA et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, CC BY 4.0 which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.  Original work is cited as reference 14.

Supplementary 2:  Map of outbreak of RHDV2 a variant that was first detected in France in 2015.  Top map is from the USDA and the bottom map is from reference 17 per Creative Commons Attribution 4.0 (CC BY 4.0) International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format.

Photo Credit:  Photo of an Eastern Cottontail rabbit that I took in my back yard.  I was 5 feet away and the rabbit did not move it just continued to stare at me.  This is highly unusual behavior for wild rabbits who are generally programmed to run explosively in circles to avoid predators.  Similar behavioral changes are often signs of illness in wild animals but this rabbit eventually started moving and hopped away.  

References:

1:  Cotton CN.  Zoonoses: Animals other than dogs and cats.  UpToDate.  Accessed March 31, 2026.  https://www.uptodate.com/contents/zoonoses-animals-other-than-dogs-and-cats

2:  Krause PJ.  Babesiosis: Clinical manifestations and diagnosis.  UpToDate.  Accessed March 31, 2026.  https://www.uptodate.com/contents/babesiosis-clinical-manifestations-and-diagnosis

 3:  Dumler JS.  Biology of Anaplasmataceae.  UpToDate.  Accessed March 31, 2026.  https://www.uptodate.com/contents/biology-of-anaplasmataceae

4:  Abrantes J, van der Loo W, Le Pendu J, Esteves PJ. Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review. Vet Res. 2012 Feb 10;43(1):12. doi: 10.1186/1297-9716-43-12. PMID: 22325049; PMCID: PMC3331820.

5:  Smertina E, Hall RN, Urakova N, Strive T, Frese M. Calicivirus Non-structural Proteins: Potential Functions in Replication and Host Cell Manipulation. Front Microbiol. 2021 Jul 14;12:712710. doi: 10.3389/fmicb.2021.712710. PMID: 34335548; PMCID: PMC8318036.

6:  Fitzner A, Niedbalski W, Kęsy A, Rataj B, Flis M. European Brown Hare Syndrome in Poland: Current Epidemiological Situation. Viruses. 2022 Oct 31;14(11):2423. doi: 10.3390/v14112423. PMID: 36366520; PMCID: PMC9698305.

EBHSV can infect Sylvilagus spp but not European rabbits Oryctolagus cuniculus. 

7:  Fitzner A, Niedbalski W, Hukowska-Szematowicz B. Simultaneous Occurrence of Field Epidemics of Rabbit Hemorrhagic Disease (RHD) in Poland Due to the Co-8:  8: 

8:  Presence of Lagovirus europaeus GI.1 (RHDV)/GI.1a (RHDVa) and GI.2 (RHDV2) Genotypes. Viruses. 2025 Sep 26;17(10):1305. doi: 10.3390/v17101305. PMID: 41157577; PMCID: PMC12568209.

9:  Abrantes J, van der Loo W, Le Pendu J, Esteves PJ. Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review. Vet Res. 2012 Feb 10;43(1):12. doi: 10.1186/1297-9716-43-12. PMID: 22325049; PMCID: PMC3331820.

10:  Kerr PJ, Kitchen A, Holmes EC. Origin and phylodynamics of rabbit hemorrhagic disease virus. J Virol. 2009 Dec;83(23):12129-38. doi: 10.1128/JVI.01523-09. Epub 2009 Sep 16. PMID: 19759153; PMCID: PMC2786765.

11:  Stowell CP, Stowell SR. Biologic roles of the ABH and Lewis histo-blood group antigens Part I: infection and immunity. Vox Sang. 2019 Jul;114(5):426-442. doi: 10.1111/vox.12787. Epub 2019 May 9. PMID: 31070258.

12:  Stowell SR, Stowell CP. Biologic roles of the ABH and Lewis histo-blood group antigens part II: thrombosis, cardiovascular disease and metabolism. Vox Sang. 2019 Aug;114(6):535-552. doi: 10.1111/vox.12786. Epub 2019 May 14. PMID: 31090093.

13:  Carman JA, Garner MG, Catton MG, Thomas S, Westbury HA, Cannon RM, Collins BJ, Tribe IG. Viral haemorrhagic disease of rabbits and human health. Epidemiol Infect. 1998 Oct;121(2):409-18. doi: 10.1017/s0950268898001356. PMID: 9825794; PMCID: PMC2809540.

14:  Weiss RA, Sankaran N. Emergence of epidemic diseases: zoonoses and other origins. Fac Rev. 2022 Jan 18;11:2. doi: 10.12703/r/11-2. PMID: 35156099; PMCID: PMC8808746. (open access)

15:  Galindo-González J. Avoiding novel, unwanted interactions among species to decrease risk of zoonoses. Conserv Biol. 2024 Jun;38(3):e14232. doi: 10.1111/cobi.14232. Epub 2024 Jan 3. PMID: 38111356.

16:  Bengis RG, Leighton FA, Fischer JR, Artois M, Mörner T, Tate CM. The role of wildlife in emerging and re-emerging zoonoses. Rev Sci Tech. 2004 Aug;23(2):497-511. PMID: 15702716.

17:  Sun Z, An Q, Li Y, Gao X, Wang H. Epidemiological characterization and risk assessment of rabbit haemorrhagic disease virus 2 (RHDV2/b/GI.2) in the world. Vet Res. 2024 Mar 26;55(1):38. doi: 10.1186/s13567-024-01286-x. PMID: 38532494; PMCID: PMC10967181.

18:  Sharma R, Patil RD, Singh B, Chakraborty S, Chandran D, Dhama K, Gopinath D, Jairath G, Rialch A, Mal G, Singh P, Chaicumpa W, Saikumar G. Tularemia - a re-emerging disease with growing concern. Vet Q. 2023 Dec;43(1):1-16. doi: 10.1080/01652176.2023.2277753. Epub 2023 Nov 18. PMID: 37916743; PMCID: PMC10732219.