Helminths are extremely successful parasites capable of establishing long-lasting infections within a host. During this time, helminths compete with the host organism's cells for nutrient resources and thus possess the potential to cause harm. However, the number of organisms hosted by individuals undergoing helminthic therapy is very small and any side effects are typically only encountered in the first three months of infection. In the long term, the vast majority of clinically infected individuals are asymptomatic, with no significant nutrient loss. In fact, nutrient uptake can be enhanced in some subjects who are hosting a small number of helminths. If the side effects from helminthic therapy were to become unmanageable, they can be alleviated by the use of anthelminthic medications.[1][7][8] The most common clinical symptoms which may be encountered while undergoing helminthic therapy can include:

- Fatigue

- Gastrointestinal discomfort

- Anemia

- Fever

- Abdominal pain

- Weight loss

- Anorexia

- Diarrhea

- General malaise

Anecdotal data gathered from helminth self-treaters and their physicians and presented in socio-medical studies suggest that a much larger number of diseases may be amenable to helminthic therapy than are currently being investigated by formal clinical trials.

Urban plague is an infectious disease among rodent species that live in close association with humans in urban areas. It is caused by the bacterium Yersinia pestis which is the same bacterium that causes bubonic and pneumonic plague in humans. Plague was first introduced into the United States in 1900 by rat–infested steamships that had sailed from affected areas, mostly from Asia. Urban plague spread from urban rats to rural rodent species, especially among prairie dogs in the western United States.

Incidence can vary greatly from type-to-type, and from country-to-country.

In Germany, one study reported an incidence of 1.28 per 100,000.

A study in Italy reported an incidence of 0.56 per 100,000.

A study in Norway reported an incidence of 3.9 per 100,000 using the years from 1978 to 1999, with a lower rate in earlier decades.

The more common and serious version of Canavan disease typically result in death or development of life-threatening conditions by the age of ten, though life expectancy is variable, and is highly dependent on specific circumstances. On the other hand, the milder variants of the disorder seem not to have any effect on lifespan.

Common vectors for urban plague are house mice, black rats, and Norway rats.

There are many public health strategies that can drastically limit the transmission of "A. cantonensis" by limiting contact with infected vectors. Vector control may be possible, but has not been very successful in the past. Education to prevent the introduction of rats or snail vectors outside endemic areas is important to limit the spread of the disease. There are no vaccines in development for angiostrongyliasis.

"A. cantonensis" and its vectors are endemic to Southeast Asia and the Pacific Basin. The infection is becoming increasingly important as globalization allows it to spread to more and more locations, and as more travelers encounter the parasites. The parasites probably travel effectively through rats traveling as stowaways on ships, and through the introduction of snail vectors outside endemic areas.

Although mostly found in Asia and the Pacific where asymptomatic infection can be as high as 88%, human cases have been reported in the Caribbean, where as much as 25% of the population may be infected. In the United States, cases have been reported in Hawaii, which is in the endemic area [5]. The infection is now endemic in wildlife and a few human cases have also been reported in areas where the parasite was not originally endemic, such as New Orleans and Egypt.

The disease has also arrived in Brazil, where there were 34 confirmed cases from 2006 to 2014, including one death. The giant African land snail, which can be a vector of the parasite, has been introduced to Brazil as an invasive species and is spreading the disease. There may be more undiagnosed cases, as Brazilian physicians are not familiar with the eosinophilic meningitis associated to angiostrongyliasis and misdiagnose it as bacterial or viral.

Canavan disease is inherited in an autosomal recessive fashion. When both parents are carriers, there is a 25% chance of having an affected child. Genetic counseling and genetic testing is recommended for families with two parental carriers.

Canavan disease is caused by a defective "ASPA" gene which is responsible for the production of the enzyme aspartoacylase. Decreased aspartoacylase activity prevents the normal breakdown of "N"-acetyl aspartate, wherein the accumulation of N-acetylaspartate, or lack of its further metabolism interferes with growth of the myelin sheath of the nerve fibers of the brain. The myelin sheath is the fatty covering that surrounds nerve cells and acts as an insulator, allowing for efficient transmission of nerve impulses.

While obviously preventable by staying away from rodents, otherwise hands and face should be washed after contact and any scratches both cleaned and antiseptics applied. The effect of chemoprophylaxis following rodent bites or scratches on the disease is unknown. No vaccines are available for these diseases.

Improved conditions to minimize rodent contact with humans are the best preventive measures. Animal handlers, laboratory workers, and sanitation and sewer workers must take special precautions against exposure. Wild rodents, dead or alive, should not be touched and pets must not be allowed to ingest rodents.

Those living in the inner cities where overcrowding and poor sanitation cause rodent problems are at risk from the disease. Half of all cases reported are children under 12 living in these conditions.

Murine typhus (also called endemic typhus) is a form of typhus transmitted by fleas (Xenopsylla cheopis), usually on rats. (This is in contrast to epidemic typhus, which is usually transmitted by lice.) Murine typhus is an under-recognized entity, as it is often confused with viral illnesses. Most people who are infected do not realize that they have been bitten by fleas.

Occupations at risk include veterinarians, slaughterhouse workers, farmers, sailors on rivers, sewer maintenance workers, waste disposal facility workers, and people who work on derelict buildings. Slaughterhouse workers can contract the disease through contact with infected blood or body fluids. Rowers, kayakers and canoeists also sometimes contract the disease. It was once mostly work-related but is now often also related to adventure tourism and recreational activities.

The infections are acquired through rat bites or scratches. It can occur as nosocomial infections (i.e., acquired from hospitals), or due to exposure or close associations with animals preying on rats, mice, squirrels, etc. Sodoku is mostly seen in Asia. The incubation period is 4 to 28 days.

It is caused by the bacteria "Rickettsia typhi", and is transmitted by the fleas that infest rats. While rat fleas are the most common vectors, cat fleas and mouse fleas are less common modes of transmission. These fleas are not affected by the infection. Human infection occurs because of flea-fecal contamination of the bites on human skin. Rats, cats, opossums maintain the rickettsia colonization by providing it with a host for its entire life cycle. Rats can develop the infection, and help spread the infection to other fleas that infect them, and help multiply the number of infected fleas that can then infect humans.

Less often, endemic typhus is caused by "Rickettsia felis" and transmitted by fleas carried by cats or opossums.

In the United States of America, murine typhus is found most commonly in southern California, Texas and Hawaii. In some studies, up to 13% of children were found to have serological evidence of infection.

Doxycycline has been provided once a week as a prophylaxis to minimize infections during outbreaks in endemic regions. However, there is no evidence that chemoprophylaxis is effective in containing outbreaks of leptospirosis, and use of antibiotics increases antibiotics resistance. Pre-exposure prophylaxis may be beneficial for individuals traveling to high-risk areas for a short stay.

Effective rat control and avoidance of urine contaminated water sources are essential preventive measures. Human vaccines are available only in a few countries, such as Cuba and China. Animal vaccines only cover a few strains of the bacteria. Dog vaccines are effective for at least one year.

When proper treatment is provided for patients with rat-bite fever, the prognosis is positive. Without treatment, the infection usually resolves on its own, although it may take up to a year to do so. A particular strain of rat-bite fever in the United States can progress and cause serious complications that can be potentially fatal. Before antibiotics were used, many cases resulted in death. If left untreated, streptobacillary rat-bite fever can result in infection in the lining of the heart, covering over the spinal cord and brain, or in the lungs. Any tissue or organ throughout the body may develop an abscess.

Various pesticides such as rodenticides may cause secondary poisoning. Some pesticides require multiple feedings spanning several days; this increases the time a target organism continues to move after ingestion, raising the risk of secondary poisoning of a predator.

Haverhill fever (or epidemic arthritic erythema) is a form of "rat-bite fever" caused by the bacterium "Streptobacillus moniliformis", an organism common in rats and mice. Symptoms begin to appear two to ten days after a rat bite injury. The illness resembles a severe influenza, with a moderate fever (38-40 °C, or 101-104 °F), chills, joint pain, and a diffuse red rash, located mostly on the hands and feet. The causative organism can be isolated by blood culture, and penicillin is the most common treatment. Treatment is usually quite successful, although the body can clear the infection by itself in most cases. Complications are rare, but can include endocarditis and meningitis.

Despite its name, it can present without being bitten by a rat.

The disease was recognized from an outbreak which occurred in Haverhill, Massachusetts in January, 1926. The organism "S. moniliformis" was isolated from the patients. Epidemiology implicated infection via consumption of milk from one particular dairy.

Laws and rules for food producers may improve food safety for consumers, such as the rules established by the European Commission for inspections, rodent control, and improved hygiene. A similar protocol exists in the United States, in the USDA guidelines for farms and slaughterhouse responsibilities in inspecting pork.

A robovirus is a zoonotic virus that is transmitted by a rodent vector (i.e., "ro"dent "bo"rne).

Roboviruses mainly belong to the Arenaviridae and Hantaviridae family of viruses. Like arbovirus ("ar"thropod "bo"rne) and tibovirus ("ti"ck "bo"rne) the name refers to its method of transmission, known as its vector. This is distinguished from a clade, which groups around a common ancestor. Some scientists now refer to arbovirus and robovirus together with the term ArboRobo-virus.

Public education about the dangers of consuming raw and undercooked meat, especially pork, may reduce infection rates. Hunters are also an at-risk population due to their contact and consumption of wild game, including bear. As such, many states, such as New York, require the completion of a course in such matters before a hunting license can be obtained.

Laboratory animal allergy (LAA) is an occupational disease of laboratory animal technicians and scientists. It manifests as an allergic response to animal urine, specifically the major urinary proteins (Mups) of rodents, and can lead to the development of asthma. A study of 5641 workers in Japan who were exposed to laboratory animals found 23.1% had one or more allergic symptoms; globally the prevalence among at risk workers is estimated between 11 and 30% According to the National Institutes of Health, prevention of animal allergy depends on the control of allergens in the work environment. This involves a combination of measures to eliminate or control allergen exposure, including engineering controls, administrative controls, and personal protective equipment.

The protein product of the mouse "Mup17" gene, known as "Mus m 1", "Ag1" or "MA1", accounts for much of the allergenic properties of mouse urine. Similarly, the product of the rat "Mup13" gene, "Rat n 1", is also a potent human allergen. One study found that two thirds of laboratory workers who had developed asthmatic reactions to animals had antibodies to Rat n 1.

Based on studies conducted in the United States, the prognosis for individuals with ALECT2 amyloidosis is guarded, particularly because they are elderly and their kidney disease is usually well-advanced at the time of presentation. End-stage renal disease develops in 1 out of 3 patients and has a median renal survival of 62 months. A suggested prognostic tool is to track creatinine levels in ALect2 patients. The attached Figure gives survival plotss for individuals with LECT2 renal amyloidosis and serum creatinine levels less than 2 mg/100 ml versus 2 mg/100 ml or greater than 2 mg/100 ml. The results show that afflicted individuals with lower creatinine levels have a ~four-fold higher survival rate.

Secondary poisoning is poisoning that can result when one organism comes into contact with or ingests another organism that has poison in its system. It typically occurs when a predator eats an animal, such as a mouse, rat, or insect, that has previously been poisoned by a commercial pesticide. If the level of toxicity in the prey animal is sufficiently high, it will harm the predator.

Mammals susceptible to secondary poisoning include humans, with infants and small children being the most susceptible. Pets such as cats and dogs, as well as wild birds, also face significant risk of secondary poisoning.

Currently, there is no proven, safe treatment for monkeypox. The people who have been infected can be vaccinated up to 14 days after exposure.