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.

Symptoms of the most common (and most serious) form of Canavan disease typically appear in early infancy usually between the first three to six months of age. Canavan disease then progresses rapidly from that stage, with typical cases involving intellectual disability, loss of previously acquired motor skills, feeding difficulties, abnormal muscle tone (i.e., floppiness or stiffness; hypotonia), poor head control, and megalocephaly (abnormally enlarged head). Paralysis, blindness, or seizures may also occur.

There exists a less common variant of Canavan disease which is generally much less serious, and involves later onset of symptoms, which are often mild and nonspecific enough to go unrecognized as manifestations of Canavan's disease. This variant does not seem to have any effect on lifespan, and is typically limited to minor cases of speech and motor skill development delay.

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

Symptoms of endemic typhus include headache, fever, muscle pain, joint pain, nausea and vomiting. 40–50% of patients will develop a discrete rash six days after the onset of signs. Up to 45% will develop neurological signs such as confusion, stupor, seizures or imbalance.

Symptoms may resemble those of measles, rubella, or possibly Rocky Mountain spotted fever. These symptoms are likely caused by a vasculitis caused by the rickettsia.

Symptoms are different for every person depending on the type of rat-bite fever with which the person is infected. Both spirillary and streptobacillary rat-bite fever have a few individual symptoms, although most symptoms are shared. Streptobacillosis is most commonly found in the United States and spirillary rat-bite fever is generally diagnosed in patients in Africa. Rat-bite symptoms are visually seen in most cases and include inflammation around the open sore. A rash can also spread around the area and appear red or purple. Other symptoms associated with streptobacillary rat-bite fever include chills, fever, vomiting, headaches, and muscle aches. Joints can also become painfully swollen and pain can be experienced in the back. Skin irritations such as ulcers or inflammation can develop on the hands and feet. Wounds heal slowly, so symptoms possibly come and go over the course of a few months.

Symptoms associated with spirillary rat-bite fever include issues with the lymph nodes, which often swell or become inflamed as a reaction to the infection. The most common locations of lymph node swelling are in the neck, groin, and underarm. Symptoms generally appear within 2 to 10 days of exposure to the infected animal. It begins with the fever and progresses to the rash on the hands and feet within 2 to 4 days. Rash appears all over the body with this form, but rarely causes joint pain.

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.

The initial scratch or wound caused by a bite from a carrier rodent results in mild inflammatory reactions and ulcerations. The wounds may heal initially, but reappear with the onset of symptoms. The symptoms include recurring fever, with body temperature 101–104°F (38–40°C). The fever lasts for 2–4 days, but recurs generally at 4–8 weeks. This cycle may continue for months or years. The other symptoms include regional lymphadenitis, malaise, and headache. The complications include myocarditis, endocarditis, hepatitis, splenomegaly, and meningitis.

Canavan disease, also called Canavan–van Bogaert–Bertrand disease, is an autosomal recessive degenerative disorder that causes progressive damage to nerve cells in the brain, and is one of the most common degenerative cerebral diseases of infancy. It is caused by a deficiency of the enzyme aminoacylase 2, and is one of a group of genetic diseases referred to as leukodystrophies. It is characterized by degeneration of myelin in the phospholipid layer insulating the axon of a neuron and is associated with a gene located on human chromosome 17.

Infection first presents with severe abdominal pain, nausea, vomiting, and weakness, which gradually lessens and progresses to fever, and then to CNS symptoms and severe headache and stiffness of the neck.

CNS symptoms begin with mild cognitive impairment and slowed reactions, and in a very severe form often progress to unconsciousness. Patients may present with neuropathic pain early in the infection. Eventually severe infection will lead to ascending weakness, quadriparesis, areflexia, respiratory failure, and muscle atrophy, and will lead to death if not treated. Occasionally patients present with cranial nerve palsies, usually in nerves 7 and 8, and rarely larvae will enter ocular structures. Even with treatment, damage to the CNS may be permanent and result in a variety of negative outcomes depending on the location of the infection, and the patient may suffer chronic pain as a result of infection.

The streptobacillosis form of rat-bite fever is known by the alternative names Haverhill fever and epidemic arthritic erythema. It is a severe disease caused by "Streptobacillus moniliformis", transmitted either by rat bite or ingestion of contaminated products (Haverhill fever). After an incubation period of 2–10 days, Haverhill fever begins with high prostrating fevers, rigors (shivering), headache, and polyarthralgia (joint pain). Soon, an exanthem (widespread rash) appears, either maculopapular (flat red with bumps) or petechial (red or purple spots) and arthritis of large joints can be seen. The organism can be cultivated in blood or articular fluid. The disease can be fatal if untreated in 20% of cases due to malignant endocarditis, meningoencephalitis, or septic shock. Treatment is with penicillin, tetracycline, or doxycycline.

A large burden of adult worms in the intestines promotes symptoms such as nausea, heartburn, dyspepsia, and diarrhea from two to seven days after infection, while small worm burdens generally are asymptomatic. Eosinophilia presents early and increases rapidly.

The classic characterization of the group of neurodegenerative, lysosomal storage disorders called the neuronal ceroid lipofuscinoses (NCLs) is through the progressive, permanent loss of motor and psychological ability with a severe intracellular accumulation of lipofuscins, with the United States and northern European populations having slightly higher frequency with an occurrence of 1 in 10,000. There are four classic diagnoses that have received the most attention from researchers and the medical field, differentiated from one another by age of symptomatic onset, duration, early-onset manifestations such as blindness or seizures, and the forms which lipofuscin accumulation takes.

In the early infantile variant of NCL (also called INCL or Santavuori-Haltia), probands appear normal at birth, but early visual loss leading to complete retinal blindness by the age of 2 years is the first indicator of the disease; by 3 years of age a vegetative state is reached and by 4 years isoelectric encephalograms confirm brain death. Late infantile variant usually manifests between 2 and 4 years of age with seizures and deterioration of vision. The maximum age before death for late infantile variant is 10–12 years. Juvenile NCL (JNCL, Batten Disease, or Spielmeyer-Vogt), with a prevalence of 1 in 100,000, usually arises between 4 and 10 years of age; the first symptoms include considerable vision loss due to retinal dystrophy, with seizures, psychological degeneration, and eventual death in the mid- to late-20s or 30s ensuing. Adult variant NCL (ANCL or Kuf’s Disease) is less understood and generally manifests milder symptoms; however, while symptoms typically appear around 30 years of age, death usually occurs ten years later.

All the mutations that have been associated with this disease have been linked to genes involved with the neural synapses metabolism – most commonly with the reuse of vesicle proteins.

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

Leptospiral infection in humans causes a range of symptoms, and some infected persons may have no symptoms at all. Leptospirosis is a biphasic disease that begins suddenly with fever accompanied by chills, intense headache, severe myalgia (muscle ache), abdominal pain, conjunctival suffusion (red eye), and occasionally a skin rash. The symptoms appear after an incubation period of 7–12 days. The first phase (acute or septic phase) ends after 3–7 days of illness. The disappearance of symptoms coincides with the appearance of antibodies against "Leptospira" and the disappearance of all the bacteria from the bloodstream. The patient is asymptomatic for 3–4 days until the second phase begins with another episode of fever. The hallmark of the second phase is meningitis (inflammation of the membranes covering the brain).

Ninety percent of cases of the disease are mild leptospirosis. The rest experience severe disease, which develops during the second stage or occurs as a single progressive illness. The classic form of severe leptospirosis is known as Weil's disease, which is characterized by liver damage (causing jaundice), kidney failure, and bleeding. Additionally, the heart and brain can be affected, meningitis of the outer layer of the brain, encephalitis of brain tissue with same signs and symptoms; and lung affected as the most serious and life-threatening of all leptospirosis complications. The infection is often incorrectly diagnosed due to the nonspecific symptoms.

Other severe manifestations include extreme fatigue, hearing loss, respiratory distress, and azotemia.

The great majority of trichinosis infections have either minor or no symptoms and no complications. There are two main phases for the infection: enteral (affecting the intestines) and parenteral (outside the intestines). The symptoms vary depending on the phase, species of "Trichinella", quantity of encysted larvae ingested, age, sex, and host immunity.

Prodromal symptoms are flu-like ones, such as fever, cough, myalgia, headache, lethargy, and shortness of breath, which rapidly deteriorates into acute respiratory failure. It is characterized by the sudden onset of shortness of breath with rapidly evolving pulmonary edema; it is often fatal despite mechanical ventilation and intervention with potent diuretics. It has a fatality rate of 36%.

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.

Neuronal ceroid lipofuscinosis (NCL) is the general name for a family of at least eight genetically separate neurodegenerative disorders that result from excessive accumulation of lipopigments (lipofuscin) in the body's tissues. These lipopigments are made up of fats and proteins. Their name comes from the word stem "lipo-", which is a variation on "lipid" or "fat", and from the term "pigment", used because the substances take on a greenish-yellow color when viewed under an ultraviolet light microscope. These lipofuscin materials build up in neuronal cells and many organs, including the liver, spleen, myocardium, and kidneys.

Hantavirus pulmonary syndrome (HPS) is one of two potentially fatal syndromes of zoonotic origin caused by species of hantavirus. These include

Black Creek Canal virus (BCCV), New York virus (NYV), Sin Nombre virus (SNV), and certain other members of Hantavirus genera that are native to the United States and Canada. Specific rodents are the principal hosts of the hantaviruses including the hispid cotton rat ("Sigmodon hispidus") in southern Florida, which is the principal host of Black Creek Canal virus., the rice rat also in the south east, the deer mouse ("Peromyscus maniculatus") in Canada and the Western United States is the principal host of Sin Nombre virus. The white-footed mouse ("Peromyscus leucopus") in the eastern United States is the principal host of New York virus.

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.

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.

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.

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.

Helminthic therapy, an experimental type of immunotherapy, is the treatment of autoimmune diseases and immune disorders by means of deliberate infestation with a helminth or with the ova of a helminth. Helminths are parasitic worms such as hookworms, whipworms, and threadworms that have evolved to live within a host organism on which they rely for nutrients. These worms are members of two phyla; nematodes, which are primarily used in human helminthic therapy, and flat worms.(Trematodes)

Helminthic therapy consists of the inoculation of the patient with specific parasitic intestinal nematodes (helminths). A number of such organisms are currently being investigated for their use as treatment including: "Trichuris suis" ova, commonly known as pig whipworm eggs; "Necator americanus", commonly known as hookworms; "Trichuris trichiura" ova, commonly referred to as human whipworm eggs; and "Hymenolepis diminuta", commonly known as rat tapeworm cysticerci.

While the latter four species may be considered to be mutualists - providing benefit to their host without causing longterm harm - there are other helminth species that have demonstrated therapeutic effects but which also have a potential to cause less desirable or even harmful effects and therefore do not share the ideal characteristics for a therapeutic helminth. These include "Ascaris lumbricoides", commonly known as human giant roundworm; "Strongyloides stercoralis", commonly known as human roundworm; "Enterobius vermicularis", commonly known as pinworm or threadworm; and "Hymenolepis nana", also known as dwarf tapeworm.

Current research targets Crohn's disease, ulcerative colitis, inflammatory bowel disease, multiple sclerosis, and asthma.

Helminthic infection has emerged as one possible explanation for the low incidence of autoimmune diseases and allergies in less developed countries, together with the significant and sustained increase in autoimmune diseases in industrialized countries.