Difference between revisions of "Komodo Dragon Mouth Niche"
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Edited by Andrew Chu & Minh Nguyen
Edited by Andrew Chu & Minh Nguyen
Revision as of 18:52, 29 August 2008
Komodo dragon – What is it?
(From the Smithsonian American Museum of Natural History)
Komodo dragon Mouth Niche
Location and Physical Conditions
Diet and Environment
The niche inside the mouth of the Komodo dragon is surprisingly no more extraordinary than the niche inside any other reptilian mouth. 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. On top of that, these dragons are born with clean and sterile mouths and are responsible for developing their own bacterial flora (1).
The truth is rather quite un-extraordinary. 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. Their diet is composed mainly on the putrefying corpses of animals, rich in protein and a plethora of thriving bacterial colonies. The rotting flesh of their prey typically gets stuck in between its 60 small, serrated teeth(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 (3). 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 (F). The conditions inside the dragon mouth niche, for the most part, are rather constant.
The bacteria 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 .
Cell to Cell communication
Communication is crucial, especially in establishing biofilms. This communication is conducted through coaggregation and coadhesion, quorum sensing, and signals via metabolic products, gene expression, and many others. Coaggregation is the active communication between bacteria in suspension that will congregate to establish a biofilm; this congregation is dictated by antagonistic and synergistic interactions, as the myriad of bacteria that inhabit the Komodo dragon’s mouth have their own needs and preconditions for growth. Coadhesion is the adhesion of bacteria to an already established biofilm, which is detected via quorum sensing (metabolic products, available 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 suitable for growth and survival .
General microbial metabolism
The 50 to 80 bacteria that cohabit 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, among many others; of these bacterial species, the ones with rather simple, minimal nutritional needs and versatile metabolisms grow the fastest, particularly two opportunistic pathogens: Pseudomonas aeruginosa and Pasteurella multocida.
Microbial metabolism – P. multocida
P. multocida grows ideally at 37 degrees Celsius in anaerobic environments. When grown in laboratory conditions, this bacteria leaves behind a musky ‘mousy’ scent as a result of anaerobic byproducts it creates (Lafeber 2006). Though it prefers anaerobic conditions, this resilient and capable bacteria can also survive in aerobic conditions making this bacteria a facultative anaerobe, where it can create ATP in the presence of oxygen if need be.
Microbial metabolism – P. Aeruginosa
Pseudomonas Aeruginosa, like P. multocida, has an optimal temperature of 37ºC, though can survive in temperatures upward to 42 ºC. It has minimal nutritional requirements, as it is able to grow on distilled water, and enjoys a very versatile metabolism—it is an aerobic microbe that is never fermentative but can grow in anaerobic conditions in the presence of nitrate—an alternative respiratory electron acceptor. It does not require growth factors and can use more than 75 organic compounds for biosynthesis.
Interestingly, routine bleeding is seen in the gums of Komodo dragons, because they bite through their gums during feeding. Why is it then that they are unaffected by the bacteria 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.
The Komodo dragon and the rich pathogenic flora in its mouth enjoy a symbiotic mutualism—both benefit from the presence of the other. The Komodo dragon’s teeth provide a suitable surface for biofilm formation and nourishment for the bacteria; the bacteria, in turn, exploit any break in the host’s immune system and are most responsible for the dragons’ success in hunting. Upon biting its prey, it is quite common for the dragon’s teeth to break off and remain embedded inside its victim. The deadly cocktail of bacteria from its teeth and toxin from its saliva renders the prey dead in merely a few days. With the prey’s death guaranteed, these giant lizards stalk leisurely, able to detect the dead animal by smell up to 5 miles (2).
Second niche – inside the Prey
The many bacteria find their second niche—within the giant lizard’s prey—much more conducive to growth. Not only do they lack the Komodo dragon’s unique antibodies and immunologic components, but they are severely immunocompromised by the lizard’s toxin, massive bodily injury incurred by the attack, and subsequent blood loss. But not all bacteria are created equal, and two bacterial species—Pseudomonas aeruginosa and Pasteurella multocida—enjoy unrivaled success in growth due to their impressive characteristics. They are the main players in the preys’ inevitable death.
(From the American Society for Microbiology)
The Komodo dragon (Varanus komodoensis)’s infamy and mythos come from its deadly bite that is guaranteed death if not treated immediately. It takes just one strong bite and the bacterium in its mouth would start wreaking havoc and compromising the prey’s immune system which ultimately leads to the prey’s death. Amongst the 57 identified bacteria found in the mouth of the Komodo dragon, Pasteurella Multocida was determined to be amongst, if not the main culprit in bringing down any prey .
(From the Journey of Wildlife Diseases, Vol. 38, Issue 3)
Named after famed Louis Pasteur who found these bacteria originally in birds, P. Multocida is a small, Gram-negative, non-spore forming, non-motile, penicillin-sensitve rod-shaped bacteria. It is typically found in the respiratory tracts of livestock, poultry, and domesticated pet species . in a symbiotic relationship, when not found in the mouth of a Komodo dragon. Though seemingly innocuous in these animals, the same mutual beneficiary effects are absent when this bacterium is in humans. General infections in humans are caused by bites, scratches, or even licks inflicted by infected animals; however, there have been cases of infections when no animal contact was observed. Though incidences of Komodo dragon preying on human subjects have 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. As such, any documentation on P. Multocida effects on mammalian subjects have been conducted in labs with lab rats.
Severity of the infection depends upon the concentration of the bacteria and to what extent the bacteria have traveled into its new host. If the infection is restricted to the area of infection on top of the epidermis typically from a bite, rapid progression of cellulitis or rash formation, swelling, redness, tenderness, and pain in the area, followed by fevers, chills, and headaches are observed. Though typically not fatal, P. Multocida can have more detrimental effects if infecting elsewhere. Usually after a crime occurs, most criminals leave behind a trail, and P. Multocida is no different. Most infections typically leave behind a high leukocyte and neutrophil count which cause the aforementioned inflammation of the epidermis . P. Multocida can also cause respiratory problems where the upper respiratory tract can become inflamed, making breathing difficult and painful. In more serious locations, cardiovascular problems can arise where the infected host suffers from inflammation of the heart tissue and disturbance in normal heart rhythm—both of which can be lethal. To make matters worse, if the bacteria are able to enter the central nervous system and cross the blood-brain barrier, they can trigger meningitis, or inflammation of the protective tissue of the brain . This inflammation would cause many of the prey’s vital organ systems to shut down after a certain length of time.
Saliva samples were collected from 26 wild-caught and 13 captive komodo dragons from the Montgomery research team. These samples were preserved except the team did not attempt to preserve anaerobic bacteria inherent in the saliva. They found 28 Gram-negative bacteria and 29 Gram-positive bacteria from all 39 dragons. When scientists were testing this bacteria’s lethality from diluted Komodo dragon saliva, blood samples extracted from dead mice revealed that P. multicoda had a 100% mortality rate in test mice within 76 hours. The dilution went as low as almost 10% of the original concentration, but the mortality rate remained at 100% .
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 bacteria to enter the host’s cells . Even if the prey escapes from the Komodo dragon and does not initially die, if the prey has been bitten, it will succumb within a few days due to infection. Once it has entered the body and entered the circulatory system, this bacterium starts having fun with the body’s vital organ systems.
Currently and tentatively, P. Multocida is the front runner in causing animal mortality. Some researchers now believe there might be an additional unknown neurotoxin that helps these bacteria kill its prey; not that these bacteria need help in the first place, as we see that the presence of this bacterial specie, along with over fifty others in high concentrations found in the giant lizard’s mouth, makes the Komodo dragon deadly enough. Past researchers determine that wound inflictions by the Komodo dragon cause sepsis and bacteremia—the high concentration of these particular bacteria in the blood puts the prey 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 prey’s immune system and attacking vital body systems, this leaves behind a large meal and further fuel to propagate more of its existing bacteria in the Komodo dragon’s mouth’s deadly arsenal.
(A photomicrograph of Pseudomonas aeruginosa. From the Center for Disease Control)
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 50 plus others. Whether it resides in the dragon’s mouth or inside its prey, P. aeruginosa is made to survive and thrive. This simple Gram negative, aerobic rod shaped bacterium, measuring 0.5 to 0.8 micrometers to 1.5 to 3.0 micrometers, has rather simple nutritional requirements—it can grow even if the medium is distilled water. Moreover, its metabolism is extremely versatile, as it does not necessarily need growth factors and can use more than 75 organic compounds for biosynthesis.
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—it is resistant to most common antibiotics due to its permeability barrier, a blessing afforded by an extra outer membrane in Gram negative species. It has a tendency to form biofilms with other cells—with its own species or others—rendering it impervious to therapeutic concentration antibiotics and phagocytes. They accomplish this by secreting a mucoid exopolysaccharide called alginate, composed of repeating mannuronic and glucuronic acid polymers. 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, it has developed resistance to a variety of antibiotics in that manner as well. On top 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.
P. aeruginosa is hard to kill. That goes without saying; but its ability to play the part 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 barrier against bacteria—and allows the bacteria safe passage into the prey. Once tissue defenses are compromised, there’s no tissue—spare a few—P. aeruginosa can’t infect; it can cause infections in the urinary tract, respiratory system, soft tissue, bone and joints, and gastrointestinal region to name a few, and trigger bacteremia and septicemia.
Once the Komodo bites into its unfortunate victim, its teeth usually breaks off and remain embedded in the animal; the invasion begins. Once inside, P. aeruginosa can disassociate from the biofilms on the teeth and invade healthy tissues. Their incredible growth can be attributed to several factors. For one, it is one of the most vigorous, fast swimming bacteria via a single polar flagellum. Secondly, it encodes a mucoid capsule—possibly lipopolysaccharides—to avoid phagocytosis and related bacterial responses. Thirdly, the bacteria produce two 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 work synergistically to break down lipids and lecithin. Its virulence doesn’t end there. Fifthly, it releases two extracellular protein toxins—exoenzyme S and exotoxin A. Exoenzyme S functions to impair phagocytic cell activity in the bloodstream and internal organs to set the stage for invasion. Exotoxin A inhibits protein synthesis in its target cell by causing ADP ribosylation of eukaryotic elongation factor 2. This dream team of physiological prowess, metabolic versatility, and toxic muscle makes for a bacterial powerhouse.
In comparing captive versus wild-type Komodo Dragons, a drastic and dramatic difference in bacteria concentration and type is observed between the two. Wild Komodo dragons have both a higher population and variety of bacteria 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 name it) and putrefying carcasses laden and seasoned with many kinds of bacteria . 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 eat everything). 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 enjoy. Surprisingly, in a study of 13 captive dragons, there are six species of bacteria that are found exclusively in captive Komodo dragons; however, not all of them exhibited the bacteria; rather, they have a combination of the following bacteria: 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 captive dragons were kept prior to when the research was conducted. These factors include the environmental flora in their pens, the bacteria in their water, and perhaps bacteria from the complex they were in. In the end, the Komodo dragon mouth niche can be summed up in the simple aphorism: “You are what you eat.”
As aforementioned in the Montgomery research, there have been speculations on whether the Komodo dragon makes use of venom to bring down its prey. Up until recently, venom production was thought to be exclusive to only two species of lizards: the gila monster and the Mexican beaded lizard who evolved their venom ability independent of snakes. However, researchers from Australia’s University of Melbourne lead by Bryan Fry believe that all venomous snakes and lizards descended from a common ancestry about 200 million years ago. Fry’s team determined that the snake’s closest relatives are the lizards known as ‘iguanians’ which includes over 1440 species, which the Komodo dragon is a part .
One might ask – how could the possible existence of lizard venom go unnoticed? Well, as you know the Komodo dragon’s mouth is a seething septic melting pot of many bacteria which are toxic and fatal. However, this still unnamed toxin allegedly has apparent less detrimental effects on humans compared to than the dragon’s usual prey. Shortly after, a similarly related paper published by Fry’s co-authors suggested that this new evidence provides support that the original classifications of lizards and snakes need to be revised based upon new DNA analysis .
The rich diversity of pathogenic bacteria found in the Komodo dragon mouth niche is the product of the giant lizards’ environment 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 mouth and dentition provide a solid base (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 can be summed up in the simple aphorism: “You are what you eat.”
Auffenberg, W. The Behavioral Ecology of the Komodo Monitor. University Press of Florida. Gainesville, Florida. 406 pp.
Lafeber, Thomas, MD., J. Robert Cantey, MD. “Pasteurella Multocida Infections.” eMedicine. April 2006. http://www.emedicine.com/MED/topic1764.htm
Montgomery, Joel M. “Aerobic Salivary Bacteria in Wild and Captive Komodo Dragons.” Journey of Wildlife Diseases, Vol. 38, Issue 3. Wildlife Disease Assocaiation, 20002. http://www.jwildlifedis.org/cgi/reprint/38/3/545.pdf
Todar, Kenneth. “Pseudomonas Aeruginosa.” Todar’s Online Textbook of Bacteriology. University of Wisconsin-Madison. 2008. http://www.textbookofbacteriology.net/pseudomonas.html
Young, Emma. “Lizards’ Poisonous Secret is Revealed.” NewScientist. Nov. 2005. http://www.newscientist.com/article.ns?id=dn8331
Edited by Andrew Chu & Minh Nguyen, students of Rachel Larsen