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How long can C. Tetani survive in soil?

How long can C. Tetani survive in soil?


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Clostridium tetani (C. tetani) is a bacterium commonly found in soil and is excreted in the faeces of many animals (both mammals and birds) and serves, by means of the exotoxin, tetanospasmin, causes the life-threatening condition tetanus.


Soon after asking this question I found a reliable source, the National Institutes of Health. It can survive for over 40 years.


Clostridia form endospores and can survive for years as a dormant spore. You can check this article about viability of clostridial endospores but it doesn't really talk about how long it can survive.


Clostridium tetani Antigens

Clostridium tetani is a bacterium that belongs to the bacteria family Clostridiaceae, genus Clostridium. It is a Gram-positive, obligate anaerobe, rod-shaped species of pathogenic bacteria. The appearance of Clostridium tetani on a gram stain resembles drumsticks or tennis rackets, and some established strains may stain Gram negative. Clostridium tetani is commonly found in soil, saliva, dust, and manure. This bacterium cannot survive in the presence of oxygen, it is also heat-sensitive and exhibits flagellar motility. Clostridium tetani develops a terminal spore when it is mature, which gives the bacterium organism its characteristic appearance. The spore is very hard and resistant to heat and most antiseptics. Spores of Clostridium tetani can be distributed widely in manure-treated soils and on human skin.

Fig. 1 Clostridium tetani particles

Clostridium tetani causes tetanus (also known as lockjaw), an infection a disease characterized by painful muscular spasms. Tetanus can lead to respiratory failure and have a fatality rate of 10%. It has four clinical types. In the most common type, spasms begin in the jaw and then spread to the rest of the body. These spasms usually last only a few minutes each time but occur frequently for three or four weeks. Other symptoms may include fever, high blood pressure, headache, sweating, fractures due to the spasms, trouble swallowing, and a fast heart rate. High risk groups are people exposed to soil or animal feces.

Clostridium tetani usually enters host through wounds to the skin and then replicates. It produces two exotoxins, tetanolysin and tetanospasmin. Tetanus toxin is a potent neurotoxin. Tetanospasmin is known to be one of the most potent toxins, it causes the clinical manifestations of tetanus. It is encoded on a plasmid and is generated in living bacteria, then released when the bacteria lyse.

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Genome Structure

According to a study published by Yale University in 2003 entitled "The Genome Sequence of Clostridium tetani, the Causative Agent of Tetanus Disease", the genome of Clostridium tetani consists of a 2,799,250-bp chromosome encoding 2,372 open reading frames, or ORFs. An ORF is a portion of an organisms genome that potentially codes for the structure of a protein. It was found that a plasmid of Clostridium tetani, named pE88 in sequencing, harbors the genes for the tetanus toxin (tetX) and its direct transcriptional regulator TetR. The tetanus toxin and a collagenase are encoded on this 74,082-bp plasmid that contains 61 ORFs. The results of the study showed 28 of the 61 ORFs code for proteins that show similarities to those with known structures and functions including collagenase. Collegenase is an exotoxin that aids in the pathogenesis and spread of tetanus by targeting muscle and connective tissues the sequence of which was identified alongside that of the tetanus toxin. [2]

According to the Yale University 2003 study, the origin of the bacterial plasmid pE88, coding for the tetanus toxin, remains unclear. The study concluded over 50% of all ORFs on pE88 are unique to C. tetani. However, homologous ORFs were found when compared with the genomes of both Clostridium perfringens, and Clostridium acetobutylicum, coding for proteins involved in lipid degradation and amino acid decomposition. Many of these comprise the Clostridial "backbone" of ORFs.


Cell structure and metabolism

C. tetani is a bacillus (rod-shaped) gram positive bacterium, which means it possess a thick cell wall made up of multiple layers of peptidoglycan and one inner membrane. C. tetani are motile bacteria and move by the means of rotary flagellum in the peritrichous orientation. C. tetani in the presence of oxygen changes into its endospore (drum stick shaped) conformation.

C. tetani synthesizes ATP by the use of a sodium motive force as well as fermentation. The bacterium relies on the breakdown of amino acids (driven into the cell with the help of sodium ion pumps) by various enzymes into pyruvate. The pyruvate can then be fermented into lactate as well as converted into acetyl-CoA. The pyruvate can also donate electrons to a membrane bound electron transport system with the help of a ferredoxin oxidoreductase reaction. The electron transport system results in the secretion of sodium ions thus creating a sodium motive force, which leads to the synthesis of ATP by sodium ion driven ATP synthases. (Bruggeman et al)


7 things you may not have known about tetanus

Tetanus doesn’t grab many headlines these days. In this era of superbugs and COVID-19, a disease that can be prevented by vaccination and sensible wound management might seem almost tame.

But tetanus is anything but. Cases may not be as common as they once were, but this disease still poses a mortal threat to horses and humans alike. Clostridium tetani is an anaerobic organism, meaning it thrives in moist, low-oxygen conditions. So if the environment is right in a wound contaminated with C. tetani spores, the bacteria are activated, multiply and release powerful neurotoxins that cause painful muscle contraction and spasms. Often the muscles of the head and neck are among the most obviously affected, which is why tetanus is commonly called “lockjaw.” Horses with the disease often adopt a characteristic “sawhorse” stance, as well, as muscles in the back and torso seize. More than 50 percent of horses who contract tetanus die or must be euthanatized.

Thanks to vaccination, tetanus is rare among America’s horses, but it does occur. “I wish there were zero cases,” says Simon Peek, BVSc, MRCVS, PhD, DACVIM, of the University of Wisconsin-Madison. “It’s such a horrible disease that we𠆝 prefer to never see it again. Yet we continue to have sporadic cases, and it’s always tragic when we do.”

So you are unlikely to ever see a case of tetanus firsthand, but you’ll still want to take the threat seriously. The frontline of defense is vaccination---it’s easy, effective and inexpensive. Beyond that, it’s wise to become familiar enough with tetanus to understand when horses are most at risk and why. To help you, we’ve provided an overview (see “In Focus: Tetanus,” page 30) along with the following collection of lesser known facts about this deadly disease.

1. Horses are particularly susceptible.

Horses are at higher risk of developing tetanus than other animals. First, as a species, horses are unusually vulnerable to the C. tetani infection---a relatively small amount of the toxins produced by the pathogen can be deadly. In contrast, chickens and other birds are highly resistant---a lethal dose is up to 300,000 higher per pound of body weight than for a horse. Likewise, it takes a fairly high dose of toxin to cause dogs and cats to develop tetanus.

Second, horses are very likely to be exposed to C. tetani. The organism’s spores are widespread in the environment the soil in most regions is contaminated with them. C. tetani spores are often present in the digestive tract of animals, as well. “These soil bacteria can become part of normal flora in the horse’s intestine and are therefore present in manure,” explains Nat Messer, DVM, DABVP, professor emeritus of the University of Missouri. When deposited on the ground, the bacteria go dormant and can survive almost indefinitely.

Finally, many cuts, abrasions and other wounds occur on the very areas of the horse’s body where the risk of exposure to C. tetani is highest and where conditions are right for the organism to flourish: the lower legs. Because it is anaerobic, C. tetani cannot thrive in healthy, oxygen-rich tissues, so the horse’s lower limbs, which are not well-oxygenated to begin with, would provide a welcoming environment. In contrast, tetanus is less likely to develop from wounds to larger muscle groups elsewhere on the body that are well supplied with blood.

2. virtually any wound—not just punctures�n lead to tetanus.

In the classically imagined tetanus scenario, a horse steps on a rusty nail that pushes C. tetani spores deep into the resulting puncture wound, where the bacteria multiply and ultimately release the toxins that cause disease. In reality, though, tetanus can result from virtually any break in the skin that allows C. tetani spores to enter the body. In fact, health officials warn that superficial wounds that may be overlooked or less carefully cleaned pose an outsized tetanus risk compared to punctures or more severe injuries likely to receive prompt and thorough medical attention.

Tetanus is also a postpartum risk for mares and for their newborn foals. “Mares after foaling can develop tetanus from contamination of the uterus, and foals are at risk via umbilical infections---though these cases are less common than from puncture wounds,” says Messer.

Lastly, tetanus can occur after surgery, although modern veterinary practices have pretty much eliminated this threat. “Most veterinarians are fastidious about proper surgical technique and cleanliness,” says Peek, 𠇊nd prior to doing procedures such as castration they make sure that the horse has had appropriate tetanus vaccination.”

3. One tell-tale sign can signal the onset of tetanus.

A stiff gait and/or hyperreactivity are often the earliest indicators of tetanus but they also are associated with a variety of other conditions, which can make the initial diagnosis difficult. “If a horse overreacts to visual or sound stimuli, and he travels with a choppy stride, you might think he is tying up or has laminitis or neck pain,” says Amy Johnson, DVM, DACVIM, of the University of Pennsylvania. “There are several things that might be suspected, rather than an early case of tetanus.”

Another common tetanus sign is spasm of the muscles on the head and face. “The horse develops a classic facial expression with ears erect and pointed backward,” says Johnson. “He looks like he’s grimacing, because the muscles of the lips are pulled back, showing the teeth.” (The term for this in human medicine is risus sardonicus, or “sardonic laughter,” which denotes an involuntary smile due to contraction of the muscles around the lips.)

“In milder cases a horse might not show all of these signs,” says Johnson. There is one indicator, however, that points pretty clearly toward tetanus: the visibility of the third eyelid. “If you wave your hand toward the eye, you’ll see the third eyelid flash up,” she says. “This is not something you would see in a healthy horse. And along with other clues, it will suggest a tetanus diagnosis.”

4. The disease’sincubation period can last several weeks.

The speed of tetanus onset is influenced by several factors, including the location of the wound, its severity and its level of contamination. If tetanus spores become lodged in well-oxygenated tissues, they may remain dormant after healing for long periods, until a bruise or another injury at the same site creates conditions that activate the organism and enable it to multiply.

𠇊 lot depends on the level of contamination of the wound and the amount of toxin being produced, and the location---and how long it has been going on,” says Messer. More foreign material in a wound is likely to mean more C. tetani spores and faster proliferation. On the other hand, the quick discovery, cleaning and treatment of a wound will reduce the threat of tetanus.


REFERENCES:

Johnson, E. A., Summanen, P., & Finegold, S. M. (2007). Clostridium. In P. R. Murray (Ed.), Manual of Clinical Microbiology (9 th ed., pp. 889-910). Washington, D.C.: ASM Press.

Ryan, J. R. (2004). Clostridium, Peptostreptococcus, Bacteroids, and other Anaerobes. In K. J. Ryan, & C. G. Ray (Eds.), Sherris Medical Microbiology: An Introduction to Infectious Diseases (4th ed., pp. 309-326). USA: McGraw-Hill.

Gibson, K., Bonaventure Uwineza, J., Kiviri, W., & Parlow, J. (2009). Tetanus in developing countries: a case series and review. Canadian Journal of Anaesthesia, 56(4), 307-315.

Sexton, D. J. Tetanus. www.uptodate.com

Public Health Agency of Canada. (2007). Vaccine preventable diseases: Tetanus. Retrieved April, 9, 2010, from http://www.phac-aspc.gc.ca/im/vpd-mev/tetanus-eng.php

Songer, J. G. (2010). Clostridia as agents of zoonotic disease. Veterinary Microbiology, 140(3-4), 399-404.

Campbell, J. I., Lam, T. M., Huynh, T. L., To, S. D., Tran, T. T., Nguyen, V. M., Le, T. S., Nguyen, V. C., Parry, C., Farrar, J. J., Tran, T. H., & Baker, S. (2009). Microbiologic characterization and antimicrobial susceptibility of Clostridium tetani isolated from wounds of patients with clinically diagnosed tetanus. American Journal of Tropical Medicine & Hygiene, 80(5), 827-831.

Rutala, W. A. (1996). APIC guideline for selection and use of disinfectants. American Journal of Infection Control, 24(4), 313-342.

Russel, A. D. (2001). Chemical Sporicidal and Sporostatic Agents. In S. S. Block (Ed.), Disinfectaion, Sterilization and Preservation (5th ed., pp. 529-541). Philadelphia PA: Lippincott Williams and Wilkins.

Pflug, I. J., Holcomb, R. G., & Gomez, M. M. (2001). Principles of the thermal destruction of microorganisms. In S. S. Block (Ed.), Disinfection, Sterilization, and Preservation (5th ed., pp. 79-129). Philadelphia, PA: Lipincott Williams and Wilkins.

Galanis, E., King, A. S., Varughese, P., & Halperin, S. A. (2006). Changing epidemiology and emerging risk groups for pertussis. Canadian Medical Association Journal, 174(4), 451-452.

Greenberg, D. P., Doemland, M., Bettinger, J. A., Scheifele, D. W., Halperin, S. A., Waters, V., & Kandola, K. (2009). Epidemiology of pertussis and haemophilus influenzae type b disease in Canada with exclusive use of a diphtheria-tetanus-acellular pertussis- inactivated poliovirus-haemophilus influenzae type b pediatric combination vaccine and an adolescent-adult tetanus-diphtheria-acellular pertussis vaccine: Implications for disease prevention in the United States. Pediatric Infectious Disease Journal, 28(6), 521-528.

Frampton, J. E., & Keating, G. M. (2006). Reduced-antigen, combined diphtheria, tetanus, and acellular pertussis vaccine (Boostrix): a review of its use as a single-dose booster immunization. Biodrugs, 20(6), 371-389.

Collins, C. H., & Kennedy, D. A. (1999). Laboratory acquired infections. Laboratory acquired infections: History, incidence, causes and prevention (4th ed., pp. 1-37). Woburn, MA: BH.

Agent Summary Statements:Bacterial Agents. (1999). In J. Y. Richmond, & R. W. Mckinney (Eds.), Biosafety in Microbiological and Biomedical Laboratories (BMBL) (4th ed., pp. 88-117). Washington, D.C.: Centres for Disease Control and Prevention.

Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009. (2009).

Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.


Clostridium Perfringens

Clostridium perfringens (Figure 4) is an anerobic gram positive spore forming rod shaped bacterium. Clostridium perfringens is found in soil and is a member of the normal gut flora. This strand of Clostridium produces harmful toxins that cause Gas Gangrene (Clostridium myonecrosis - which is caused by Clostridium perfringens’ alpha toxin) and Clostridium food poisoning (enterotoxin).

Gas gangrene (Figure 5) occurs due to wound infection of limbs (open fractures and extensive soft tissue injuries). Clostridium perfringens grow rapidly in ischemic tissues and anerobic conditions. These toxins cause tissue necrosis and produce gas gangrene. The gases form bubbles in the muscles (crepitus) and cause a characteristic foul smell due to the decomposing tissues. These toxins can enter the blood stream, causing damage to the organs and even death. This is a rapidly spreading infection that may require amputation. Gas gangrene is treated with surgery, antibiotics—intravenous penicillin and clindamycin. Hyperbaric oxygen could be useful.


The Real Deal: What the Evidence Shows

What Causes Tetanus?

Clostridium tetani in active and spore forms. Source: Wikipedia.

The infectious agent is bacterium Clostridium tetani, which comes in two forms. In its active (vegetative) state, it is an obligate anaerobe, which means it is poisoned and dies in an oxygenated environment, such as when oxygen-carrying blood is around. But in its dormant state, it is a spore wrapped in a very resistant coating. In this spore form, it can withstand oxygen, chemical agents, and even boiling water.

While proper wound cleansing is always good practice, it will not prevent tetanus. The spores can easily survive washing with water or hydrogen peroxide. They will easily survive in a person’s bloodstream as well. They will not get flushed out completely if the wound bleeds.

Where Is Clostridium tetani Found?

C. tetani can live in this dormant spore form for as long as 40 years in animal intestines and in soil/feces in the environment.

These spores are plentiful almost everywhere. If your skin is punctured by any non-sterile object, you may become infected by this bacterium. This includes nails as wells as rose thorns, sewing needles, splinters, insect bites, and burns. Only one or two spores is needed to start an infection.

Continuing the Clostridium tetani Life Cycle

Once the wound closes, your body puts things back in place and your blood returns to your capillaries. The bacterium is now safe from oxygen and the spore germinates, reverting back to its active state. Then it multiplies freely.

What is Tetanus, Exactly?

Tetanus patient in a convulsion, 1847 (Wellcome)

In three to twenty-one days after germination, tetanus (also known as lockjaw) disease symptoms begin. These are typically fatigue, soreness, and irritability.

C. tetani excretes two neurotoxins called tetanolysin and tetanospasmin that damage tissue and interfere with nerves and muscle contractions. This unregulated muscle contraction leads to severe muscle spasms that can result in bone fractures.

Tetanus Infographic (click for a larger version)

There is no cure. Recovery can take an agonizing several months in an intensive care setting. Treatment may include sedatives, muscle relaxers, weeks in a dark, silent room to give your nervous system time to recuperate, medically-induced temporary paralysis, and perhaps surgery. Tetanus may have permanent, life-long complications such as neurological damage.

Without treatment, 1 out of 4 infected people die due to respiratory or heart failure (higher rate for newborns). Even with treatment, 1 in 10 die.

If you do survive tetanus, you still are not immune to a subsequent tetanus infection. The is no such thing as “natural immunity” to tetanus. Tetanus is not spread from person to person, so there is also zero protection from herd immunity.

Keep in mind that most doctors today have never seen a tetanus case, which can lead to a fatal delay in diagnosis should symptoms begin.

How Do I Prevent Tetanus?

Tetanus Incidence per 100,000 in the United States, 1947-2000

Getting the tetanus vaccine, along with regular boosters, is the only sure way to prepare your immune system to fight the bacterium before it can infect you. The vaccine contains an inactivated toxin called a toxoid, which stimulates your immune system to create antibodies and memory B cells against the tetanus toxin.

If your boosters have lapsed, you can still receive a tetanus shot and an antitoxin injection post-puncture. The Tetanus Immunoglobulin (TIG) antitoxin (also known as a toxoid) can attack and neutralize C. tetani toxins circulating in your bloodstream.

So it is vital to get TIG and tetanus shots immediately after getting injured.


Cephalic tetanus presenting with bilateral facial palsy

We discuss the case and differential diagnoses of an elderly man who presented with bilateral facial palsy. He had injured his forehead in the garden during a fall on his face and the open wound was contaminated by soil. He then presented to the emergency department with facial weakness causing difficulty speaking. The penny dropped when he started developing muscle spasms affecting his lower jaw a day after admission. It also became clear that he could not open his mouth wide (lock jaw). The combination of muscle spasms and lock jaw (trismus) made tetanus the most likely possibility, and this was proven when he had samples taken from his wound and analysed under the microscope, which showed Clostridium tetani bacilli. C. tetani spores are widespread in the environment, including in the soil, and can survive hostile conditions for long periods of time. Transmission occurs when spores are introduced into the body, often through contaminated wounds. Tetanus in the United Kingdom is rare, but can prove fatal if there is a delay in recognition and treatment.

Keywords: Cephalic tetanus facial nerve palsy trismus.


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Transmission

Regardless of the reservoir, transmission must occur for an infection to spread. First, transmission from the reservoir to the individual must occur. Then, the individual must transmit the infectious agent to other susceptible individuals, either directly or indirectly. Pathogenic microorganisms employ diverse transmission mechanisms.

Contact Transmission

Contact transmission includes direct contact or indirect contact. Person-to-person transmission is a form of direct contact transmission. Here the agent is transmitted by physical contact between two individuals (Figure 1) through actions such as touching, kissing, sexual intercourse, or droplet sprays. Direct contact can be categorized as vertical, horizontal, or droplet transmission. Vertical direct contact transmission occurs when pathogens are transmitted from mother to child during pregnancy, birth, or breastfeeding. Other kinds of direct contact transmission are called horizontal direct contact transmission. Often, contact between mucous membranes is required for entry of the pathogen into the new host, although skin-to-skin contact can lead to mucous membrane contact if the new host subsequently touches a mucous membrane. Contact transmission may also be site-specific for example, some diseases can be transmitted by sexual contact but not by other forms of contact.

Figure 1. Direct contact transmission of pathogens can occur through physical contact. Many pathogens require contact with a mucous membrane to enter the body, but the host may transfer the pathogen from another point of contact (e.g., hand) to a mucous membrane (e.g., mouth or eye). (credit left: modification of work by Lisa Doehnert)

When an individual coughs or sneezes, small droplets of mucus that may contain pathogens are ejected. This leads to direct droplet transmission, which refers to droplet transmission of a pathogen to a new host over distances of one meter or less. A wide variety of diseases are transmitted by droplets, including influenza and many forms of pneumonia. Transmission over distances greater than one meter is called airborne transmission.

Indirect contact transmission involves inanimate objects called fomites that become contaminated by pathogens from an infected individual or reservoir (Figure 2). For example, an individual with the common cold may sneeze, causing droplets to land on a fomite such as a tablecloth or carpet, or the individual may wipe her nose and then transfer mucus to a fomite such as a doorknob or towel. Transmission occurs indirectly when a new susceptible host later touches the fomite and transfers the contaminated material to a susceptible portal of entry. Fomites can also include objects used in clinical settings that are not properly sterilized, such as syringes, needles, catheters, and surgical equipment. Pathogens transmitted indirectly via such fomites are a major cause of healthcare-associated infections

Figure 2. Fomites are nonliving objects that facilitate the indirect transmission of pathogens. Contaminated doorknobs, towels, and syringes are all common examples of fomites. (credit left: modification of work by Kate Ter Haar credit middle: modification of work by Vernon Swanepoel credit right: modification of work by “Zaldylmg”/Flickr)

Vehicle Transmission

The term vehicle transmission refers to the transmission of pathogens through vehicles such as water, food, and air. Water contamination through poor sanitation methods leads to waterborne transmission of disease. Waterborne disease remains a serious problem in many regions throughout the world. The World Health Organization (WHO) estimates that contaminated drinking water is responsible for more than 500,000 deaths each year. [3] Similarly, food contaminated through poor handling or storage can lead to foodborne transmission of disease (Figure 3).

Figure 3. Food is an important vehicle of transmission for pathogens, especially of the gastrointestinal and upper respiratory systems. Notice the glass shield above the food trays, designed to prevent pathogens ejected in coughs and sneezes from entering the food. (credit: Fort George G. Meade Public Affairs Office)

Dust and fine particles known as aerosols, which can float in the air, can carry pathogens and facilitate the airborne transmission of disease. For example, dust particles are the main mode of transmission of hantavirus to humans. Hantavirus is found in mouse feces, urine, and saliva, but when these substances dry, they can disintegrate into fine particles that can become airborne when disturbed inhalation of these particles can lead to a serious and sometimes fatal respiratory infection.

Although droplet transmission over short distances is considered contact transmission as discussed above, longer distance transmission of droplets through the air is considered vehicle transmission. Unlike larger particles that drop quickly out of the air column, fine mucus droplets produced by coughs or sneezes can remain suspended for long periods of time, traveling considerable distances. In certain conditions, droplets desiccate quickly to produce a droplet nucleus that is capable of transmitting pathogens air temperature and humidity can have an impact on effectiveness of airborne transmission.

Vector Transmission

Diseases can also be transmitted by a mechanical or biological vector, an animal (typically an arthropod) that carries the disease from one host to another. Mechanical transmission is facilitated by a mechanical vector, an animal that carries a pathogen from one host to another without being infected itself. For example, a fly may land on fecal matter and later transmit bacteria from the feces to food that it lands on a human eating the food may then become infected by the bacteria, resulting in a case of diarrhea or dysentery (Figure 4).

Figure 4. (a) A mechanical vector carries a pathogen on its body from one host to another, not as an infection. (b) A biological vector carries a pathogen from one host to another after becoming infected itself.

Biological transmission occurs when the pathogen reproduces within a biological vector that transmits the pathogen from one host to another (Figure 4). Arthropods are the main vectors responsible for biological transmission (Table 1). Most arthropod vectors transmit the pathogen by biting the host, creating a wound that serves as a portal of entry. The pathogen may go through part of its reproductive cycle in the gut or salivary glands of the arthropod to facilitate its transmission through the bite. For example, hemipterans (called “kissing bugs”) transmit Chagas disease to humans by defecating when they bite, after which the human scratches or rubs the infected feces into a mucous membrane or break in the skin.

Biological vectors include mosquitoes, which transmit malaria and other diseases, and lice, which transmit typhus. Other arthropod vectors can include arachnids, primarily ticks, which transmit Lyme disease and other diseases, and mites, which transmit scrub typhus and rickettsial pox. Biological transmission, because it involves survival and reproduction within a parasitized vector, complicates the biology of the pathogen and its transmission. There are also important non-arthropod vectors of disease, including mammals and birds. Various species of mammals can transmit rabies to humans, usually by means of a bite that transmits the rabies virus. Chickens and other domestic poultry can transmit avian influenza to humans through direct or indirect contact with avian influenza virus A shed in the birds’ saliva, mucous, and feces.



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