Many wild rats carry a number of diseases and parasites, but which diseases, and what percentage of the rat population is infected, vary with the population under study. Some parasites may have interesting effects on rat behavior which benefit the parasite.
Wild rats carry mycoplasma, though the percentage of the population that is infected may vary from place to place.
Wild rats do not carry the plague. When rats catch the plague, they die from it. Other wild rodents who are resistant to the plague carry it in their bloodstream, and the plague is transmitted from animal to animal by fleas. Plague epidemics were caused by the plague jumping (by flea) from these wild rodents to rats, and from rats (before or as they died) to humans. Today, the plague is treatable with antibiotics and cases are rare.
Wild rats almost never carry rabies, and there has never been a case of human rabies caused by rat bite in the United States, though such cases have been found very rarely in other countries.
Do wild rats
carry
diseases and parasites?
Yes, some of them do. Which diseases and parasites they carry, and what percentage of the rats are infected, depends on the population of rats under study.
Parasite and disease load of wild rats on farms in England
Webster and MacDonald (1995) studied the parasite and disease load of wild rats on farms in England:
red text = transmissible to humans
Stojcevic et al. (2004) examined 255 wild Norway rats captured in rural Croatia for parasites. Overall, they found that 72.6% of the rats were infected with some form of parasite. Nearly a third of the rats (32.2%) were infected with external parasites, and nearly two thirds (65.1%) with internal parasites.
Examples of single disease studies on wild rats
Many studies examine a single disease in rats in a particular location. For example:
These are just a few examples of such studies. Finding all the parasites and diseases carried by Norway rats from different populations around the world would be an enormous task and is far beyond the scope of this website.
Diseases and injuries of wild rats in a semi-natural enclosure
Calhoun (1963) conducted a two-year study in which he kept wild rats in a 1/4 acre enclosure that was almost entirely predator-proof. He provisioned the rats with regular food and water. He started with ten wild rats and allowed the individuals to breed and die naturally. The population gradually grew to nearly 200 rats over two years. Calhoun trapped 284 rats repeatedly and examined them for parasites, diseases, and injuries.
Injuries
Young rats of less than 40 days of age were nursing or near their mother and were never bitten. After the rats were weaned they started receiving a very few bites from other rats. Constant, low levels of aggression and biting continued until the rats reached social maturity at around 6 months for males and 8.1 months for females. At this age the rats received about 1.75 bites per female and 1.81 bites per male. After this age wounding increased over several months to stabilize at about 7 bites per female at age 368 days (12.3 months) and 9.5 bites per male at 266 days (8.9 months). The level of aggression in this population is probably higher than that of free-living wild rats, because this population was confined and social strife was common.
The wounds were usually small and were inflicted on the rump. If the wounds didn't become infected they typically healed within 2 weeks. However, some wounds became infected, and developed into extensive shallow festering wounds that took weeks or months to heal.
External Parasites
Diseases
Microorganisms and internal parasites
The experiment was terminated after two years. At this time, 77 females and 54 males were autopsied.
Microorganisms
Helminth parasites (worms)
Parasite infection can affect the behavior of wild rats. Webster et al. 1994 and Webster 1994 found that rats who carried Toxoplasma gondii were more active and more likely to approach novel stimuli than uninfected rats. Infected rats were also more likely to be trapped than uninfected rats. The differences in behavior may come from pathological changes caused by Toxoplasma: cysts in the brains of infected rats.
These behavioral changes in the rats may be advantageous to the parasite because these changes render the rat more likely to be eaten by a domestic cat -- the preferred host of Toxoplasma. Toxoplasma only influences behaviors that benefit itself, such as exploratory behavior, rather than causing a general alteration of the rat's behavior (Berdoy et al 1995).
For a review of the impact of Toxoplasma gondii on rat, mouse and human behavior, see Webster 2001. For more on the fascinating subject of parasites and behavior, see Moore 2002.
This is an interesting question to rat owners, because the vast majority of the pet rat population is infected with Mycoplasma pulmonis, which may cause progressively serious respiratory problems in the host. Mycoplasma is incurable, though the symptoms may be treated with antibiotics.
Do wild rats suffer from mycoplasma too?
There is evidence that wild rats do, indeed, carry mycoplasma. Owen (1976) trapped 80 wild Norway rats from three populations and examined them for parasites and diseases. Two of the populations had 95% and 100% M. pulmonis infection rates, while the third population had a 0% infection rate. The author speculated that the uninfected population could represent an isolated pocket of Mycoplasma-free rats. Overall, 75% of the rats were infected with M. pulmonis and 1.25% were infected with M. arthriditis.
Giebel et al (1990) trapped six wild Norway rats and found a species of Mycoplasma, M. moatsii, in the intestinal cells and feces of all six rats.
Koshimizu et al (1993) trapped 35 wild rats from 7 different species. They did not find Mycoplasma in the few R. norvegicus they captured, but they did find it in R. rattus. However, the number of R. norvegicus captured was very small, so we cannot conclude from this study that there is no Mycoplasma in that rat population.
Therefore, wild rats carry Mycoplasma, but the percentage of rats affected may vary from one population to the next.
The plague bacterium is maintained at low, steady levels (called enzootic infection) in just a few species of rodent hosts, such as Microtus spp. (voles), and Peromyscus spp. (deer mice, white-footed mice, Texas mice, cotton mice etc.). Some populations of these species are resistant to the plague and therefore form a reservoir from which outbreaks can occur in other species. Other non-rodent species have been found serologically positive to the plague as well (e.g. bears, bobcats, badgers, fox, ringtails, skunks, mountain lion, deer, African elephant, African buffalo).
The plague bacterium, Yersinia pestis, is transmitted from one animal to another by the flea. An outbreak occurs when infected fleas change host species and unload large numbers of plague bacteria onto a new, less resistant host species. In the United States, these new hosts serve as amplifying (epizootic) hosts, and they include rock squirrels, California ground squirrels, antelope ground squirrels, prairie dogs, chipmunks, woodrats, and less resistant populations of Microtus and Peromyscus. In urban areas, these hosts include the ship rat (Rattus rattus) and the Norway rat. Different species of flea may become involved in an outbreak, including the rat flea (Xenopsylla cheopis), the squirrel flea (Oropsylla montana), and the human flea (Pulex irritans). The plague is therefore carried by many different rodent species. However the rat, because it lives in close proximity to humans, has been most frequently associated with plague outbreaks in people.
Rats are not resistant to the plague, so an outbreak of the plague in rats is associated with large rat die-offs. Infected rats usually die within a few days of a high-grade bacteremia. The infected fleas do not die, however, and the rat's death forces the infected fleas to find other hosts: other rats, or humans.
Humans are therefore at risk of contracting the plague if they live near or handle plague-infected rats or their recently dead bodies. Simond (1898), one of the early observers of plague transmission, observed that handling a rat which has been dead for more than 24 hours did not lead to infection, because the infected fleas had already left the body.
The most famous outbreak of the plague was the Black Death of 1330-1352. This epidemic was spread by the ship rat and its flea, which spread the plague to humans throughout Asia and Europe. The last plague outbreak in the United States was in 1924-1925 in Los Angeles. Since then, human plague has been found as scattered cases in rural areas in the western United States (10-15 cases per year) (Levy 1999). Currently, plague-infected rodents are found in many parts of the world (CDC), but transmission to humans is relatively rare (1,000-3,000 cases per year worldwide). Today, the plague is 100% treatable with antibiotics.
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Was the Black Death really caused by Y. pestis? Over the past twenty years there have been several challenges to the theory that the Black Death was caused by Y. pestis (Twigg 1985, Scott and Duncan 2001, Cohn 2003). These authors suggest that the Black Death might have been caused by a disease other than plague, such as anthrax (Twigg 1985), an Ebola-like illness (Scott and Duncan 2001), or an unknown disease which has gone extinct (Cohn 2003). They argue that the surviving descriptions we have of the medieval Black Death differ on a number of points from a recent, well-documented Y. pestis plague epidemic in the 19th and 20th century in Southeast Asia and India called the Third Pandemic. However, a team of French paleomicrobiologists recently discovered the DNA of the plague bacillus Y. pestis in the tooth pulp of plague victims from the Black Death (Raoult et al.2000). Gilbert et al. (2004) were unable to find Y. pestis DNA in the teeth of Black Death victims, but the technique they used to examine the tooth pulp was a different and less sensitive technique than that used by the original team (Drancourt and Raoult 2004), and therefore not an exact replicate study. Most recently, Haensch et al. (2010) isolated DNA and protein
signatures specific for in human skeletons from mass graves associated
with the Black Death in northern, central and southern Europe.
They confirmed that Y. pestis
caused the Black Death and later epidemics on the entire European
continent over the course of four centuries. |
Further reading on the plague:
Are wild rats ever found to carry rabies?
Very few rats infected with rabies have ever been found in the United States. Winkler (1973) reviewed the literature on rodent rabies in the United States. He found that during the 18-year period of 1953 and 1970, a small number of rabid rats (39 rats) were found in the United States. The numbers were extremely small: only 11 rabid rats were found in the U.S. during the three year period of 1953-1955. The number of rabid rats declined during the period of time covered by the review, and by the three year period of 1968-1970 only 2 rats were found to be rabid. This decline in the number of rabid rats is probably due to an improvement in diagnostic techniques which led to fewer false positives. In Thailand, 4.7% of Norway rats (9 rats out of 192) were found to be carrying rabies (Smith et al. 1968).
However, no rats were found to be infected with rabies in surveys of wild rat populations in Sri Lanka (Patabendige and Wimalaratne 2003), Poland (Wincewicz 2002), and Bangkok, Thailand (Kantakamalakul 2003).
Have rats ever caused rabies in humans?
Rats and other small rodents have never caused a single case of human rabies in the United States (CDC).
A very few cases of humans infected with rabies by rats have been reported in countries such as Poland, Israel, Thailand and Surinam. In Poland, out of 9,998 cases of human rabies from 1990 to 1994, four were caused by rats (0.04%), while the vast majority were caused by foxes (Zmudziñski and Smreczak 1995, described in Wincewicz 2002). In Israel, one case of human rabies was caused by a bite from a small rodent -- possibly a rat or mouse (Gdalevich et al. 2000). In Thailand, out of 7,000 human rabies cases reported each year, 1% are caused by rat bites (Kamoltham et al. 2002). The majority of rabies cases in Thailand are caused by dogs (86.3%) (Pancharoen et al. 2001). An outbreak of paralytic rabies in children in Surinam was attributed to rat bites (Verlinde et al 1975).
Why is rabies so rare in rats?
The answer is unclear. Currently, it is presumed that rats are so small that they almost never survive the attack of a larger rabid animal, like a raccoon, skunk, or fox.
How fast does rabies progress in rats?
The speed of rabies progression depends on the rat's age, body weight, rabies strain, and rabies dose. The higher the dose, the faster the progression (Baer et al. 1965). The incubation period for wild type rabies (called "street rabies virus") is two to three weeks following injection to the foot in the laboratory (14-18 days: Kitselman and Mital 1967; median 16 days, range 10-25 days: Baer et al. 1968) and mortality is high (100%: Kitselman and Mital 1967; 63.6%: Baer et al. 1968).
Note, however, that a bite from a rabid predator would differ substantially from a needle injection to the foot: a predator's bite might create several wounds, all of which could be inoculated with the rabies virus. A natural bite may also be inflicted on the body of the rat instead of an extremity, and hence closer to the central nervous system. Hypothetically, such bites might be followed by a more rapid progression of the rabies virus and hence a shorter incubation time.
How does the rat's incubation period compare to that of other species?
Comparing rats with other species, raccoons (the most common wild animal carrier of rabies, Krebs et al. 1999, 2002) have an incubation period of about five weeks (estimated by Tinline et al. 2002). Vampire bats survived an average of 12 days after experimental infection (Setien et al. 1998). Ferrets incubate rabies for 22-33 days (Niezgoda et al. 1997a, b. 1998). Dogs incubate rabies from one week to several months (Fekadu 1993, Fekadu and Shaddock 1984).
Humans have a rabies incubation period of 1-3 months, but symptoms have been observed as quickly as a few days after inoculation, and as long as several years later (Rupprecht 2002, Lakhanapal and Sharma 1985).
Don't rats have a dry bite?
Pet rat owners commonly believe that if rats survive an attack by a rabid animal and then survive the disease long enough to bite a human, transmission is impossible because rats have a dry bite. The rat's bite is thought to be "dry" because of the forward position of the teeth in the mouth: this position is thought to prevent the teeth from getting wet. Rabies is transmitted by saliva from a bite, hence, rats could not transmit rabies (or any other saliva-borne disease) even if they did carry it.
This is not, in fact, the case. Rats can and do transmit saliva-borne diseases via bites, such as rat bite fever (Graves and Janda 2001, Grude 2001, Schuurman et al. 1998, Hagelskjaer et al. 1998, Hockman et al. 2000, Weber 1982), septic arthritis (Downing et al. 2001) and ratpox (Marennnikova et al 1988). And, as described above, rats have transmitted rabies to humans in a few rare cases.
Large rodent species and rabbits, which also have forward-placed teeth, have also occasionally transmitted rabies to humans.
Do all individuals with rabies shed the virus in their saliva?
No. As an example, 63% of ferrets infected with raccoon rabies had rabies in their salivary glands, and slightly less than half, 47%, shed the virus in their saliva (Niezgoda et al 1998). Other strains of rabies were shed at even lower rates in the saliva: 13% of ferrets infected with bat rabies had it in their salivary glands, and 4% shed it in their saliva. With skunk rabies, the numbers are even lower: 4% had it in their salivary glands, and none shed it in their saliva (Niezgoda et al. 1997b).
Therefore, even if an animal has the rabies virus, it may not shed the virus in its saliva.
Animal rabies vectors
In the United States, the animals that test positive for rabies most frequently are raccoons, skunks, bats, and foxes, cats, and dogs (in decreasing order of importance) (Krebs et al. 2002). About 2% of cases of animal rabies involve other wild animal species, including large rodents, rabbits and hares (Krebs et al. 1999).
In the 368 human cases of rabies caused by large rodent bites (95%) and rabbit (5%) bites between 1985 and 1994 in the United States, 86% were caused by woodchucks (Childs et al. 1997). In Maryland between 1981 and 1986, 1.2% of rabies cases in humans and domestic animals were caused by woodchucks or rabbits (80% of these cases were from woodchucks) (Moro et al. 1991.
The woodchuck (or groundhog, Marmota monax) occasionally carries rabies, primarily in areas where raccoons are experiencing an outbreak of rabies at the same time. Rabies infections in large rodents and rabbits therefore reflect a spillover from another 'reservoir' species, like raccoons, but such spillovers are unknown in small rodents (like rats) in the United States.
Conclusion
So, the upshot is that wild rats have never caused rabies in humans in the United States and only extremely rarely in other countries. Rats are therefore not considered a serious rabies risk. Rabies shots are not considered necessary after a rat bite (Jaffe 1983). Since 1969, the Public Health Service has advised that "bites of rabbits, squirrels, chipmunks, rats, and mice seldom, if ever, call for rabies prophylaxis" (CDC 1969).
What causes it?
Rat bite fever is a rare disease that can be caused by two different organisms: Streptobacillus moniliformis and Spirillum minus. S. moniliformis is part of the natural nasal and oral flora of rats and other rodents (e.g. mice, squirrels, weasels, gerbils, Washburn 1995, Wilkins 1988).
About 10% to 100% of domestic rats carry S. moniliformis, depending on the population. Fifty percent to 100% of wild rats carry it (Washburn 1995).
How is it transmitted?
Transmission occurs through contact with the urine, saliva, or secretions from the eye or nose of an infected animal.
The most common form of transmission is a rat bite (e.g. Bhatt and Mirza 1992, Graves and Janda 2001, Grude et al. 2001, Hagelsjaer et al. 1998, Mathiasen and Rix 1993, McHugh et al. 1985, Na Ayuthaya and Niumpradit 2005, Rordorf et al. 2000, Sens et al. 1989).
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Rat bite fever from domestic rats Laboratory rats: Rat bite fever from laboratory rats has been found in laboratory personel (e.g. Anderson et al. 1983) though recent attempts to eradicate S. moniliformis from laboratory rat populations have been largely successful (Wullenweber 1995, USF). Pet rats: A few cases of rat bite fever from pet rat
bites have been reported in pet shop employees and rat owners
(Albedwawi et al.2006, Andre et al.2005, Downing et
al. 2001, Grude et al. 2001, Legout et al. 2005,
Mignard et al.2007, Schuurman et al. 1998, Shvartsblat et
al. 2004, Pollock et al. 2005, Schaschter et al.2006,
van Nood and Peters 2005). Streptobacillus
moniliformis has been isolated in the saliva of a pet rat
(Hayashimoto et al.
2008). Rat bite fever may be transmitted from a pet rat to a
human through a bite, or by sharing oral flora via kissing or sharing
food. |
Bites of other rodents, such as mice, squirrels, and gerbils, may also cause rat bite fever (Washburn 1995).
Animals that preyed on a rodent that carried S. moniliformis may also transmit the bacteria to humans (Washburn 1995). S. moniliformis may also be transmitted by consuming food or water that was contaminated with rat feces, in which case the resulting disease is called Haverhill fever (McEvoy et al. 1987, Place and Sutton 1934).
Rat bite fever from Streptobacillus moniliformis
Rat-bite fever caused by S. moniliformis (called streptobacillary rat bite fever) is the type found most often in the United States. The person experiences fever, chills, headache, and muscle pain within 2-10 days of exposure (though symptoms may appear as early as the next day and as late as 22 days after exposure) (Pollock 2005). A few cases may not show a fever (Shehle et al. 2003). This is followed by a diffuse rash mainly on the hands and feet. Joints may become swollen, red and painful, and septic arthritis may develop (Dendle et al. 2006, Elliott 2007, Hockman et al. 2000).
If untreated, the disease may infect the heart and may cause serious complications (e.g. Rodorf et al. 2000, Pollock et al. 2005, Shvartsblat et al. 2004 ). Without treatment, mortality has been measured at 10% (Elliott, 2007) and 13% (Frans et al. 2001). The disease is treated with antibiotics, and if caught early the prognosis is excellent.
Rat bite fever from Spirillum minus
Rat-bite fever caused by Spirillum minus (called spirillary rat bite fever) is more common in Africa and Asia, where it is called sodoku. It is the less serious form of rat bite fever. In this form the person develops a rash with red or purple plaques, and the wound may re-open, but joints are rarely involved.
If untreated it subsides and returns again every 2 to 4 days. This can go on for up to a year but most cases resolve within four to eight weeks (HealthOz). Treatment with antibiotics has an excellent prognosis.
References and further reading: