Do Komodo Dragons Spit Acid

Komodo Dragon – What is it?

The Komodo dragon takes the cake as the largest living species of lizard, and though information technology doesn't breathe fire, it can grow to an boilerplate of 2 to 3 meters, by and large weighing lxx kg. In terms the average American layman can empathize, they can grow up to 6.5 to x feet and weigh about 154 lb [i]. These giant lizards inhabit the Indonesian islands of Komodo, Rinca, Flores, Gili Motang, and Gili Dasami, where they enjoy beingness at the top of the food concatenation with no recognized predators; likewise, with no predators, their size is attributed to island gigantism, as there are no constraints to its growth [3]. Only their notoriety worldwide stems not from their incredible size, but rather, it stems from their deadly bite. The Komodo dragon'south oral cavity is a disease manufactory, with more its off-white share of pathogenic bacteria. A single bite removes not only a skillful amount of mankind, simply transmits these lovely microbes into the prey, which dies of bacteremia, septicemia, and scattering of other infections [3][half-dozen]. Surely, the innate properties and conditions inside the Komodo dragon's mouth create an ideal paradise for these bacteria, right? Not then fast.

The Komodo Dragon (From the Smithsonian American Museum of Natural History)[3

Komodo Dragon Oral cavity Niche

Location and Physical Conditions

The niche inside the oral cavity of the Komodo dragon is surprisingly no more extraordinary than the niche within any other reptilian oral fissure. There are no pathogens unique to the Komodo dragon; its mouth has no unique pH (near neutral), temperature, or dentition to facilitate the growth of uncommon microbes. As an ectotherm (cold-blooded), it cannot even regulate its internal body temperature, including its mouth, though it enjoys a rather unusually stable core temperature [3]. On top of that, these dragons are born with clean and sterile mouths and are responsible for developing their own bacterial flora [i].

The truth is rather quite un-boggling. The dragon's mouth is a breeding ground for 50 to 80 kinds of bacterial species—most of which are pathogenic—due to its diet and environment. This is because Komodo dragons are primarily carrion eaters [7]. Their diet is equanimous mainly on the putrefying corpses of animals, rich in poly peptide and a plethora of thriving bacterial colonies. The rotting flesh of their prey typically gets stuck in betwixt its threescore small, serrated teeth [3][2]; the many bacterial species form biofilms via their pili for fimbrial adherence on to the lizard's teeth and thrive, as they are routinely treated to carrion and fresh meat [three]. Additionally, the teeth provide a hard, stable surface for colonization and an optimal growing temperature (37ºC). Komodo dragons are exposed to additional bacteria in the water, soil, and feces—which they roll in to avoid predation from larger Komodo dragons [14]. The conditions inside the dragon rima oris niche, for the most part, are rather abiding, though information technology changes during feeding (food, salivation, oxygen levels, etc.).

Microbial Interaction

Biofilm formation

The leaner in the Komodo dragon's mouth form multi-specie colonies on the surface of its teeth via fimbrial adherence (pili) as a means of maintaining homeostasis and resisting phagocytic and antimicrobial elements, pH changes, and fluctuations in temperature. Their resilience to external pressures and conditions is due to an exopolysaccharide coat, which is synthesized by glycosyltransferase enzymes on the bacterial cell's exterior. This coat is porous and has appropriate channels for nutrient uptake [eleven][12].

Jail cell to Cell advice

Communication is crucial, specially in establishing biofilms. This communication is conducted through coaggregation and coadhesion, quorum sensing, and signals via metabolic products, factor expression, and many others. Coaggregation is the active communication betwixt bacteria in suspension that volition besiege to establish a biofilm; this congregation is dictated past antagonistic and synergistic interactions, equally the myriad of bacteria that inhabit the Komodo dragon's mouth have their own needs and preconditions for growth. Coadhesion is the adhesion of leaner to an already established biofilm, which is detected via quorum sensing (metabolic products, bachelor nutrients, signals, etc.) and aforementioned means of communication. The bacteria in the Komodo dragon mouth actively communicate and work together to create a biofilm more than suitable for growth and survival [12].

General microbial metabolism

The 50 to eighty bacteria that conjugate the dragon's mouth vary in type (Gram positive or Gram negative), metabolic processes (anaerobic, aerobic, microaerophilic, or facultative), physiology, growth rates, and pathogenic properties, amid many others; of these bacterial species, the ones with rather unproblematic, minimal nutritional needs and versatile metabolisms grow the fastest, particularly two opportunistic pathogens: Pseudomonas aeruginosa and Pasteurella multocida [two][3].

Microbial metabolism – P. multocida

P. multocida grows ideally at 37 degrees Celsius in anaerobic environments. When grown in laboratory weather condition, this leaner leaves behind a musky 'mousy' scent as a upshot of anaerobic byproducts it creates. Though information technology prefers anaerobic weather, this resilient and capable bacteria can also survive in aerobic conditions making this bacteria a facultative anaerobe, where information technology can create ATP in the presence of oxygen if demand exist [9].

Microbial metabolism – P. Aeruginosa

Pseudomonas aeruginosa, like P. multocida, has an optimal temperature of 37ºC, though tin survive in temperatures upward to 42 ºC. Information technology has minimal nutritional requirements, as it is able to abound on distilled water, and enjoys a very versatile metabolism—it is an aerobic microbe that is never fermentative simply can abound in anaerobic conditions in the presence of nitrate—an alternative respiratory electron acceptor. It does non crave growth factors and can utilize more than 75 organic compounds for biosynthesis [v].

Symbiotic Relationship

Host Immunity

Interestingly, routine bleeding is seen in the gums of Komodo dragons, because they seize with teeth through their gums during feeding. Why is it then that they are unaffected past the leaner in their mouths? Research suggests that the Komodo dragons' exposure to these pathogens for generations have enabled them to evolve innate antibodies and immunologic components to render the bacteria harmless [1][2].

Symbiosis

The Komodo dragon and the rich pathogenic flora in its mouth savor a symbiotic mutualism—both benefit from the presence of the other. The Komodo dragon'due south teeth provide a suitable surface for biofilm formation and nourishment for the bacteria; the leaner, in turn, exploit whatever break in the host's immune system and are nearly responsible for the dragons' success in hunting. Upon biting its casualty, it is quite common for the dragon's teeth to intermission off and remain embedded inside its victim. The deadly cocktail of bacteria from its teeth and toxin from its saliva renders the prey expressionless in just a few days. With the casualty's expiry guaranteed, these behemothic lizards stem leisurely, able to discover the dead fauna by smell upwards to v miles [2].

Second niche – within the Prey

The many bacteria discover their 2nd niche—within the giant lizard's prey—much more conducive to growth. Not only do they lack the Komodo dragon'south unique antibodies and immunologic components, merely they are severely immunocompromised by the lizard'due south toxin, massive bodily injury incurred by the assault, and subsequent claret loss. But non all bacteria are created equal, and two bacterial species—Pseudomonas aeruginosa and Pasteurella multocida [5][10]—relish unrivaled success in growth due to their impressive characteristics. They are the main players in the preys' inevitable death.

Pasteurella Multocida

Pasteurella Multocida (From the American Gild for Microbiology)[6

The Komodo dragon's (Varanus komodoensis) infamy and mythos come from its deadly bite that is guaranteed death if non treated immediately. It takes just one strong bite and the bacterium in its oral fissure would kickoff wreaking havoc and compromising the casualty's immune system which ultimately leads to the prey'due south decease. Amongst the 57 identified bacteria found in the mouth of the Komodo dragon, Pasteurella Multocida was adamant to exist amongst, if not the primary culprit in bringing downwards any prey [10].

Named afterward famed Louis Pasteur who institute these leaner originally in birds, P. Multocida is a small, Gram-negative, not-spore forming, non-motile, penicillin-sensitve rod-shaped bacteria. It is typically establish in the respiratory tracts of livestock, poultry, and domesticated pet species [9] in a symbiotic relationship, when non found in the mouth of a Komodo dragon. Though seemingly innocuous in these animals, the same mutual beneficiary furnishings are absent when this bacterium is in humans. General infections in humans are caused past bites, scratches, or fifty-fifty licks inflicted past infected animals; all the same, there have been cases of infections when no animal contact was observed. Though incidences of Komodo dragon preying on human subjects accept occurred, no physical evidence of their effects on humans has been documented due to the fact that Komodo dragons have never left traces of their human encounters. Equally such, whatever documentation on P. Multocida effects on mammalian subjects have been conducted in labs with lab rats [10].

Virulence

Severity of the infection depends upon the concentration of the bacteria and to what extent the leaner have traveled into its new host. If the infection is restricted to the area of infection on tiptop of the epidermis typically from a bite, rapid progression of cellulitis or rash formation, swelling, redness, tenderness, and pain in the area, followed past fevers, chills, and headaches are observed. Though typically not fatal, P. Multocida can have more detrimental furnishings if infecting elsewhere. Ordinarily afterwards a crime occurs, nearly criminals leave behind a trail, and P. Multocida is no different. Most infections typically get out behind a high leukocyte and neutrophil count which cause the aforementioned inflammation of the epidermis [ix]. P. Multocida tin can also cause respiratory problems where the upper respiratory tract can become inflamed, making breathing hard and painful. In more serious locations, cardiovascular problems can arise where the infected host suffers from inflammation of the middle tissue and disturbance in normal heart rhythm—both of which tin can be lethal. To make matters worse, if the leaner are able to enter the primal nervous arrangement and cross the claret-brain barrier, they can trigger meningitis, or inflammation of the protective tissue of the brain[9]. This inflammation would cause many of the prey's vital organ systems to shut downward after a certain length of time. When scientists were testing this bacteria's lethality from diluted Komodo dragon saliva, results revealed that P. multicoda had a 100% bloodshed rate in test mice within 76 hours [10]. The dilution went as depression as almost two% of the original concentration, just the bloodshed charge per unit remained at 100% [10].

What gives these bacteria its deadliness? A bacteriophage encodes the toxin which gives P. Multocida its deadliness. This toxin activates Rho GTPases which cause actin stress fiber formation (swelling on the epidermis), which allows the leaner to enter the host's cells [ix]. Even if the prey escapes from the Komodo dragon and does not initially die, if the casualty has been bitten, it will succumb within a few days due to infection. One time it has entered the body and entered the circulatory organisation, this bacterium starts having fun with the torso's vital organ systems.

Currently and tentatively, P. Multocida is the forepart runner in causing animate being mortality. Some researchers now believe at that place might be an boosted unknown neurotoxin that helps these bacteria kill its casualty; not that these bacteria need help in the first place, as we see that the presence of this bacterial specie, forth with over l others in loftier concentrations found in the giant lizard's oral fissure, makes the Komodo dragon deadly enough. Past researchers make up one's mind that wound inflictions by the Komodo dragon cause sepsis and bacteremia—the high concentration of these particular bacteria in the blood puts the casualty into shock, totally overwhelms its immune system, and rapidly spreads in the body, debilitating the prey and ultimately leading to its death. Through compromising the casualty's immune system and attacking vital body systems, this leaves behind a large repast and further fuel to propagate more than of its existing bacteria in the Komodo dragon'due south oral cavity's deadly arsenal.

Pseudomonas Aeruginosa

A photomicrograph of Pseudomonas aeruginosa. From the Centers for Disease Command and Prevention (CDC)[2

P. multocida's insidious partner-in-crime is P. aeruginosa, both of which are usually the fastest growing, most successful bacterial species among the many fifty plus others. Whether it resides in the dragon's oral fissure or inside its prey, P. aeruginosa is made to survive and thrive. This simple Gram negative, aerobic rod shaped bacterium, measuring 0.v to 0.8 micrometers to one.5 to 3.0 micrometers, has rather simple nutritional requirements—it can abound even if the medium is distilled water. Moreover, its metabolism is extremely versatile, every bit it does non necessarily need growth factors and can utilise more than than 75 organic compounds for biosynthesis [5].

Microbial resistance

This beast of a bacteria is tolerant to fluxes in temperature—its optimum temperature is 37ºC, but it can survive in temperature as high as 42ºC—and is resistant to high concentrations of salts and dyes, and weak antiseptics. As if P. aeruginosa wasn't hard enough to kill already, its notoriety stems from its resistance to antibiotics—information technology is resistant to most common antibiotics due to its permeability barrier, a blessing afforded by an extra outer membrane in Gram negative species [v]. It has a trend to course biofilms with other cells—with its own species or others—rendering it impervious to therapeutic concentration antibiotics and phagocytes. They attain this by secreting a mucoid exopolysaccharide called alginate, equanimous of repeating mannuronic and glucuronic acrid polymers [12]. Also, as it is ubiquitous in the soil, its long-time exposure to natural antibiotics produced by its soil-dwelling bacilli, actinomycetes, and mold friends, information technology has developed resistance to a variety of antibiotics in that manner besides. On peak of that, Pseudomonas harbor plasmids that encode for antibiotic resistance (R-factors and RTFs), which they can replicate and transfer to others via transduction or conjugation [5].

Virulence

P. aeruginosa is difficult to kill. That goes without saying; but its ability to play the function of the opportunistic pathogen is no less impressive. P. aeruginosa rarely, if ever, infects uncompromised tissues. That's where the Komodo dragon comes in; after ripping off a nice chunk of flesh off the prey, aside from inducing massive blood loss, the Komodo compromises the skin—which serves as the pivotal external bulwark confronting bacteria—and allows the bacteria safe passage into the casualty. Once tissue defenses are compromised, there's no tissue—spare a few—P. aeruginosa tin can't infect; information technology can cause infections in the urinary tract, respiratory organization, soft tissue, os and joints, and gastrointestinal region to name a few, and trigger bacteremia and septicemia.

Once the Komodo bites into its unfortunate victim, its teeth unremarkably breaks off and remain embedded in the animal; the invasion begins. One time within, P. aeruginosa tin disassociate from the biofilms on the teeth and invade good for you tissues. Their incredible growth can be attributed to several factors. For one, it is ane of the about vigorous, fast swimming bacteria via a single polar flagellum. Secondly, it encodes a mucoid sheathing—possibly lipopolysaccharides—to avoid phagocytosis and related bacterial responses. Thirdly, the bacteria produce ii extracellular proteases in the form of elastase and alkaline protease; the elastase effectively cleaves host antibodies, collagen, and related complement and lyses fibronectin, exposing receptors for attachment on the mucosa of tissues; the alkaline protease aids elastase in lysing fibrin and disrupting the formation of fibrin. Fourthly, P. aeruginosa produces three soluble proteins in the form of a pore-forming cytotoxin and two hemolysins in the form of phospholipase and lecithinase—both piece of work synergistically to pause down lipids and lecithin. Its virulence doesn't end there. Fifthly, information technology releases two extracellular poly peptide toxins—exoenzyme S and exotoxin A. Exoenzyme Southward functions to impair phagocytic cell activity in the bloodstream and internal organs to fix the stage for invasion. Exotoxin A inhibits protein synthesis in its target cell by causing ADP ribosylation of eukaryotic elongation factor 2 [5]. This dream squad of physiological prowess, metabolic versatility, and toxic muscle makes for a bacterial powerhouse.

Current Research

Research #1

In comparing convict versus wild-blazon Komodo Dragons, researchers sought to find differences in the type and concentration of bacteria in their mouths and the underlying reasons for them—a desperate and dramatic difference in bacteria concentration and type was observed between the ii. Saliva samples were collected from 26 wild-defenseless and xiii convict komodo dragons from the Montgomery research squad. They plant 28 Gram-negative bacteria and 29 Gram-positive leaner from all 39 dragons. When scientists were testing for bacterial lethality from diluted Komodo dragon saliva, blood samples extracted from dead mice revealed that P. multicoda had a 100% mortality charge per unit in test mice within 76 hours. The dilution went equally low as almost ten% of the original concentration, but the mortality rate remained at 100% [12]

Wild Komodo dragons have both a college population and variety of leaner than their captive Komodo dragon brethren. The foremost reason for this disparity can be seen in a comparison of both of their diets. Wild dragons prefer meals of large animals (wild buffalo, boar, humans…you proper name information technology) and putrefying carcasses laden and seasoned with many kinds of bacteria [8]. In addition, many of the bacteria found exclusively in the saliva of wild dragons are found in the fecal matter of animals, which the dragon comes in incidental contact with when they eat the intestines (and they consume everything) [14]. Captive dragons, however, are fed a sterile diet—vitamin-enriched, fresh bodies which lack the lovely array of pathogenic bacteria that its wild type brethren bask. Surprisingly, in a study of 13 captive dragons, in that location are vi species of bacteria that are found exclusively in captive Komodo dragons; nevertheless, not all of them exhibited the leaner; rather, they have a combination of the post-obit leaner: Klebsiella Pneumoniae, Stenotrophomonas Maltophila, Kurthia Sp., Staphylococcus Capitis, Staphylococcus Caseolyticus, and Staphylococcus Cohnii. Why would this be the case? Environmental factors as to where these convict dragons were kept prior to when the research was conducted. These factors include the environmental flora in their pens, the bacteria in their h2o, and perchance bacteria from the complex they were in [ten].

Research #2

As aforementioned in the Montgomery research, at that place take been speculations on whether the Komodo dragon makes utilise of venom to bring downwardly its casualty. Upwards until recently, venom production was thought to exist exclusive to only two species of lizards: the Gila monster and the Mexican beaded lizard that evolved their venom ability contained of snakes. Yet, researchers from Australia's University of Melbourne lead past Bryan Fry believe that all venomous snakes and lizards descended from a common beginnings almost 200 one thousand thousand years ago. Fry'due south team determined that the snake's closest relatives are the lizards known as 'iguanians' which includes over ane,440 species, which the Komodo dragon is a part [13].

One might ask: How could the possible existence of lizard venom in Komodo dragons become unnoticed? Most biologists attributed the dragon's successes to its rima oris, a playground for a myriad of pathogenic bacteria; notwithstanding, this withal unnamed toxin allegedly has apparent less detrimental effects on humans compared to the dragon'south usual prey. A similarly related paper published past Fry'southward co-authors provides new evidence, based on Dna analysis, and support for the necessary revisal of original classifications of lizards and snakes [thirteen].

Conclusion

The rich variety of pathogenic leaner found in the Komodo dragon mouth niche is the product of the giant lizards' surround and diet. Prolonged, generational exposure to these bacteria have enabled the Komodo dragons to develop innate antibodies, which allow for both to engage in a mutually beneficial symbiosis; the dragon's rima oris and dentition provide a solid base of operations (biofilms), optimal temperature, and nourishment for bacterial growth; the bacteria—most notably P. multocida and P. Aeruginosa—effectively disables and kills the lizards' prey. In the end, the Komodo dragon mouth niche tin be summed up in the unproblematic aphorism: "Yous are what you eat."

References

[1]"Explore by Fauna Faust: Into the Dragon'due south Mouth." Animal Stories. 2008. Shedd The World's Aquarium. 29 Aug 2008 <http://www.sheddaquarium.org/1526.html>.

[2]Layton, Julia. "Are Komodo dragon's mouth deadlier than a cobra's venom?." Howstuffworks. 2008. 29 Aug 2008 <http://animals.howstuffworks.com/animate being-facts/komodo-bite.htm/printable>.

[3]Lutz, Dick and J. Marie Lutz. Komodo, the Living Dragon: Living Dragon. Salem: DIMI Press, 1997.

[4]"Komodo Dragon." Honolulu Zoo. 2008. Honolulu Zoo. 29 Aug 2008 <http://www.honoluluzoo.org/komodo_dragon.htm>.

[5]"Komodo Dragon." Reptiles and Amphibians. 2008. Central Pets. 29 Aug 2008 <http://world wide web.centralpets.com/animals/reptiles/lizards/lzd5840.html>.

[6]Auffenberg, W. The Behavioral Environmental of the Komodo Monitor. Academy Press of Florida. Gainesville, Florida. 406 pp.

[7]Irvin, Randall. Attachment and Colonization of Pseudomonas aerugionsa: Role of the Surface Structures. 'Pseudomonas aeruginosa as an Opportunistic Pathogen. 1993.

[8]Centers for Disease Command and Prevention. http://www.cdc.gov/index.htm

[nine]Cohen, Jesse. Smithsonian National Zoological Park. http://www.amnh.org/exhibitions/lizards/images/komodo_smithsonian.jpg

[10]Rogers A H. (2008). Molecular Oral Microbiology. Caister Bookish Press

[11]Lafeber, Thomas, MD., J. Robert Cantey, MD. "Pasteurella Multocida Infections." eMedicine. April 2006. http://world wide web.emedicine.com/MED/topic1764.htm

[12]Montgomery, Joel M. "Aerobic Salivary Leaner in Wild and Captive Komodo Dragons." Journey of Wild fauna Diseases, Vol. 38, Issue iii. Wildlife Illness Assocaiation, 20002. http://world wide web.jwildlifedis.org/cgi/reprint/38/3/545.pdf

[13]Robinson, Richard A., Gable Moffitt, Neal Thomson, and Marissa Cohen. Brigham Young University. MicrobeLibrary.org. http://www.microbelibrary.org/microbelibrary/files/ccImages/Articleimages/Atlas_ColonyMorphology/Pasteurella-multocida_Morphology_fig14.jpg

[14]Young, Emma. "Lizards' Poisonous Secret is Revealed." NewScientist. Nov. 2005. http://www.newscientist.com/commodity.ns?id=dn8331

Edited past Chu, Andrew and Nguyen, Minh, students of Rachael Larson.