In general, the term "infestation" refers to parasitic diseases caused by animals such as arthropods (i.e. mites, ticks, and lice) and worms, but excluding conditions caused by protozoa, fungi, bacteria, and viruses, which are called infections.

Infestation is the state of being invaded or overrun by pests or parasites. It can also refer to the actual organisms living on or within a host.

Pediculosis is an infestation of lice (blood-feeding ectoparasitic insects of the order Phthiraptera). The condition can occur in almost any species of warm-blooded animal (i.e. mammals and birds), including humans. Although "pediculosis" in humans may properly refer to lice infestation of any part of the body, the term is sometimes used loosely to refer to "pediculosis capitis", the infestation of the human head with the specific head louse.

Head-lice infestation is most frequent on children aged 3–10 and their families. Approximately 3% of school children in the United States contract head lice. Females are more frequently infested than males. Those of African descent rarely suffer infestation due to differences in hair texture.

Head lice are spread through direct head-to-head contact with an infested person. From each egg or "nit" may hatch one nymph that will grow and develop to the adult louse. Lice feed on blood once or more often each day by piercing the skin with their tiny needle-like mouthparts. While feeding they excrete saliva, which irritates the skin and causes itching. Lice cannot burrow into the skin.

The symptoms of this disease include:

- Severe pruritus

- Pain

- Inflammation and swelling

- Lesions and ulcerations, with black dots in the center

Left untreated, secondary infections, such as bacteremia, tetanus, and gangrene, can occur.

In all cases, tungiasis by itself only caused morbidity, though secondary infection may lead to mortality. The life cycle section presents the Fortaleza stages from the flea’s developmental perspective. It should be noted that the discussion is specific to symptoms of human infection. The clinical presentation in humans follows the Fortaleza Classification as the stage of infection will determine the symptoms present. The following discussion will give an overview of the symptoms beginning in stage 2 because patients are not likely to present themselves at the early stages of infection, mostly because the flea’s burrowing is usually not felt. This may be due to a keratolytic enzyme secreted during stage 1.

The patient with a single flea may present as early as stage 2 when, though the erythema is barely perceptible, a boring pain and the curious sensation of pleasant itching occur. This inflammatory reaction is the initial immunological response to the infestation. Heavily infested patients may not notice a stage 2 infection due to the other fleas’ causing irritation as well. Feces may be seen, but this is more common in the 3rd stage.

Around the third day after penetration, erythema and skin tenderness are felt, accompanied by pruritus (severe itching) and a black furuncular nodule surrounded by a white halo of stretched skin caused by the expansion of the flea. Fecal coils may protrude from the center of the nodule where the flea’s anus is facing upward. They should be washed off quickly as the feces may remain in the skin unless removed. During this 3a substage, pain can be severe, especially at night or, if the nodule is on the foot, while walking. Eggs will also begin to be released and a watery secretion can be observed. The radical metamorphosis during the 3rd to 6th day after penetration, or neosomy, precedes the formation of a small caldera-like rim rampart as a result of the increased thickness of the flea’s chitin exoskeleton. During the caldera formation, the nodule shrinks a bit and it looks as if it is beginning to dry out; this takes 2 weeks and comprises substage 3b.

At the third week after penetration and substage 4a, the eggs’ release will have stopped and the lesion will become smaller and more wrinkled. As the flea is near death, fecal and water secretion will stop altogether. Pain, tenderness, and skin inflammation will still be present. Around the 25th day after penetration, the lesion looks like a black crust and the flea’s carcass is removed by host repair mechanisms and the skin begins to heal. With the flea gone, inflammation may still persist for a while.

Although patients would not present within the 5th stage of tungiasis as the flea would be dead and no longer in the body, this stage is characterized by the reorganization of the skin (1–4 weeks) and a circular residue of 5–10 mm in diameter around the site in penetration. An intraepithelial abscess, which developed due to the presence of the flea, will drain and later heal. Although these disease residues would persist for a few months, tungiasis is no longer present.

In severe cases, ulcers are common, as well as complete tissue and nail deformation. A patient may be unable to walk due to severe pain if too many of the lesions are present in the feet. Suppuration (pus formation), auto-amputation of digits (via ainhum), and chronic lymphedema may also be seen.

If the patient is not vaccinated, tetanus is often a complication due to secondary infection. Gangrene is another common complication of severe infestation and superinfection. Staphylococcus aureus and Wolbachia endobacteria can be transmitted by the chigoe flea, as well as nearly 150 other different pathogens. For these reasons, the chigoe flea should be removed as soon as possible.

An ectoparasitic infestation is a parasitic disease caused by organisms that live primarily on the surface of the host.

Examples:

- Scabies

- Crab louse (pubic lice)

- Pediculosis (head lice)

- "Lernaeocera branchialis" (cod worm)

There are several complications with the terminology:

Acariasis is a term for a rash, caused by mites, sometimes with a papillae (pruritic dermatitis), and usually accompanied by severe itching sensations. An example of such an infection is scabies.

The closely related term, mange, is commonly used with domestic animals (pets) and also livestock and wild mammals, whenever hair-loss is involved. "Sarcoptes" and "Demodex" species are involved in mange, but both of these genera are also involved in human skin diseases (by convention only, not called mange). "Sarcoptes" in humans is especially severe symptomatically, and causes the condition scabies noted above.

Another genus of mite which causing itching but rarely causes hair loss because it burrows only at the keratin level, is "Cheyletiella." Various species of this genus of mite also affect a wide variety of mammals, including humans.

Mite infestation sometimes implies an ectoparasitic, cutaneous condition such as dermatitis. However, it is possible for mites to invade the gastrointestinal and urinary tracts.

MeSH uses the term "Mite Infestations" as pertaining to Acariformes. However, mites not in this grouping can be associated with human disease. (See "Classification", below.)

The term Acari refers to ticks and mites together, which can cause ambiguity. (Mites are a paraphyletic grouping).

Mites can be associated with disease in at least three different ways: (1) cutaneous dermatitis, (2) production of allergin, and (3) as a vector for parasitic diseases. The language used to describe mite infestation often does not distinguish among these.

Most of the mites which cause this affliction to humans are from the order Acari, hence the name Acariasis. The entire taxonomic classification to order would be:

- Kingdom: Animalia

- Phylum: Arthropoda

- Subphylum: Chelicerata

- Class: Arachnida

- Order: Acari (At the order level, there is still substantial argument among researchers as to how to categorize Acari. Some call it a subclass, others a superorder, "Acarina".)

Specific species involved include:

- Acariformes

- Trombidiformes

- "Trombicula" species (trombiculosis or chiggers)

- "Demodex" species (Demodicosis)

- "Pyemotes tritici"

- "Cheyletiella"

- Sarcoptiformes

- "Sarcoptes scabiei" (Scabies)

- Parasitiformes

- "Dermanyssus gallinae"

- "Liponyssoides sanguineus"

- "Ornithonyssus bacoti", "Ornithonyssus bursa", "Ornithonyssus sylviarum"

- Another candidate is "Androlaelaps casalis". However, based on this mite's life style as a predator on other mite species (such as the previously-mentioned "Dermanyssus gallinae"), it is highly unlikely to be a cause of acariasis.

Some of these reflect reports existing of human infestation by mites previously believed not to prey on humans.

Tungiasis (also known as "nigua", "pio" and "bicho de pie", or "pique" or sand flea disease) is an inflammatory skin disease caused by infection with the female ectoparasitic "Tunga penetrans" (also known as chigoe flea, jigger, nigua or sand flea), found in the tropical parts of Africa, the Caribbean, Central and South America, and India. "Tunga penetrans" is the smallest known flea, measuring 1 mm across. It is also known in Latin America as the "nigua" and "bicho de pie" (Spanish) or "bicho de pé" (Portuguese), literally ""foot bug"". "Tunga penetrans" is a member of the genus "Tunga", which comprises 13 species.

Tungiasis causes skin inflammation, severe pain, itching, and a lesion at the site of infection that is characterized by a black dot at the center of a swollen red lesion, surrounded by what looks like a white halo. Desquamation of the skin is always seen, especially after the flea expands during hypertrophy.

As of 2009, tungiasis is present worldwide in 88 countries with varying degrees of incidence. This disease is of special public health concern in highly endemic areas such as Nigeria, Trinidad and Tobago, and Brazil, where its prevalence, especially in poor communities, has been known to approach 50%.

The chigoe flea is properly classified as a member of the order Siphonaptera as it is a flea. Although commonly referred to as chiggers, true chiggers are mites which are minute arachnids. Mites penetrate the skin and feed on skin cells that are broken down by an enzyme they secrete from their mouthparts, but they do not lay eggs in the host as "T. penetrans" does. Moreover, in mites, the adult and the larval forms both feed on other animals. This is not the case with "T. penetrans", as only the adults feed on mammals and it is only the female that stays attached to the host.

"Tunga penetrans" is also known by the following names: chigoe flea, sand flea, nigua, chigger flea, jigger flea, bicho de pé, pico, sikka, kuti, and piqui, among many others.

Tyzzer’s disease is an acute epizootic bacterial disease found in rodents, rabbits, dogs, cats, birds, pandas, deer, foals, cattle, and other mammals including gerbils. It is caused by the spore-forming bacterium "Clostridium piliforme", formerly known as "Bacillus piliformis". It is an infectious disease characterized by necrotic lesions on the liver, is usually fatal, and is present worldwide. Animals with the disease become infected through oral ingestion of the bacterial spores and usually die within a matter of days. Animals most commonly affected include young, stressed animals in laboratory environments, such as immature rodents and rabbits. Most commonly affected wild animals include muskrats "(Ondatra zibethicus)" and occasionally cottontail rabbits "(Lepus sylvaticus)". Even today, much remains unknown about Tyzzer’s disease, including how and why it occurs.

Common clinical signs of Tyzzer’s Disease include watery diarrhea, depression, emaciation, and a ruffled coat. Other observed clinical signs include melena, depression, lethargy, and decreased temperature. In muskrats, this disease is characterized by extensive hemorrhaging within the lower intestine and abdomen. Due to the fast-acting nature of this disease, infected individuals often do not live long enough to exhibit symptoms. It is not uncommon for an infected animal to die within 1-10 days of disease contraction.

During necropsy, inflammation of the ileum, cecum, and colon are commonly present. Perhaps the most distinctive trait of this disease, however, is the grayish yellow necrotic lesions found on the liver of diseased animals. The number of these spots present can range from one to countless. Occasionally, lesions are discovered in the lower intestinal tract and heart as well. Even with physical signs and symptoms present, a conclusive diagnosis is dependent upon the presence of "C. piliforme" within the liver of the infected animal.

Clinical appearance of the disease includes depression, a serous nasal discharge, and sporadically minor facial inflammation in mild form of the disease. In severe form, there is severe inflammation of one or both infraorbital sinuses with edema of the surrounding tissue. The swelling can cause closure of one eye or both of them. Intermandibular space and wattles of corks do swell as a course of the disease .

Infectious coryza is a serious bacterial disease of chickens which affects respiratory system and it is manifested by inflammation of the area below the eye, nasal discharge and sneezing...The disease is found all over the world causing high economic losses. Economic loss is due to stumping off and reduction of egg production in case of laying chickens. The disease was discovered early 1930s by considering clinical signs

After an incubation period of up to seven days, the signs associated with swine vesicular disease occur. The first sign is a transient mild fever. Other signs include:

- Vesicles in the mouth and on the snout and feet

- Lameness and an unsteady gait, shivering and jerking–type leg movements

- Ruptured vesicles can cause ulcers on limbs and feet, and foot pads may be loosened.

Young animals are more severely affected. Recovery often occurs within a week. There is no mortality.

Swine vesicular disease has the same clinical signs as foot-and-mouth disease, and can only be diagnosed by laboratory testing.

Swine vesicular disease (SVD) is an acute, contagious viral disease of swine caused by the swine vesicular disease virus, an enterovirus. It is characterized by fever and vesicles with subsequent ulcers in the mouth and on the snout, feet, and teats. The pathogen is relatively resistant to heat, and can persist for a long time in salted, dried, and smoked meat products. Swine vesicular disease does not cause economically-important disease, but is important due to its similarity to foot-and-mouth disease.

Diagnosis is based on a circular "bull's-eye" rash at the site of infection called erythema chronicum migrans, which is very similar to that seen in Lyme disease. However, the symptoms of STARI are mild, and resemble influenza, with fatigue, muscle pains, and headache. Fever is sometimes seen, but is not characteristic.

The most common symptoms are diarrhea, abdominal pain, weight loss, and joint pains. The joint pains may be due to migratory non-deforming arthritis, which may occur many years before any digestive tract symptoms develop; they tend to involve the large joints but can occur in any pattern and tend not to damage the joint surface to the point that the joint becomes deformed. Fever and chills occur in a small proportion of people.

In its more advanced form, malabsorption (insufficient absorption of nutrients from the diet) leads to wasting and the enlargement of lymph nodes in the abdomen. Neurological symptoms (discussed below) are more common in those with the severe form of the abdominal disease. Chronic malabsorptive diarrhea leads to the poor absorption of fat, causing steatorrhea (fatty, offensive stool), flatulence, and abdominal distension. Protein-losing enteropathy may also occur, causing depletion of albumin, a blood protein, which may lead to peripheral edema caused by the lowered oncotic pressures.

Hyperpigmentation of the skin occurs in almost half; some also have skin nodules. Various eye problems, such as uveitis, may occur; this is typically associated with deteriorating vision and pain in the affected eye. Endocarditis (infection of the heart valve) has been reported in a small number of cases, sometimes in people with no other symptoms of Whipple's disease; this is typically noticed as breathlessness and leg swelling due to fluid accumulation as the heart is unable to pump fluid through the body.

Of those affected by Whipple's disease, 10–40% of people have problems related to the involvement of the brain; the symptoms relate to the part of the brain that is affected. The most common problems are dementia, memory loss, confusion, and decreased level of consciousness. Eye movement disturbances and myorhythmia (rapidly repetitive movements of the muscles) of the face, together referred to as "oculomasticatory myorhythmia", are highly characteristic for Whipple's disease. Weakness and poor coordination of part of the body, headaches, seizures, as well as a number of more uncommon neurological features, are present in some cases.

Whipple's disease is a rare, systemic infectious disease caused by the bacterium "Tropheryma whipplei". First described by George Hoyt Whipple in 1907 and commonly considered a gastrointestinal disorder, Whipple's disease primarily causes malabsorption but may affect any part of the body including the heart, brain, joints, skin, lungs and the eyes. Weight loss, diarrhea, joint pain, and arthritis are common presenting symptoms, but the presentation can be highly variable and approximately 15% of patients do not have these classic signs and symptoms.

Whipple's disease is significantly more common in men, with 87% of the patients being male. When recognized and treated, Whipple's disease can usually be cured with long-term antibiotic therapy; if the disease is left untreated, it is ultimately fatal.

Pacheco's disease is an acute and often lethal infectious disease in psittacine birds. The disease is caused by a group of herpesviruses, "Psittacid herpesvirus 1" (PsHV-1), which consists of four genotypes. Birds which do not succumb to Pacheco's disease after infection with the virus become asymptomatic carriers that act as reservoirs of the infection. These persistently infected birds, often Macaws, Amazon parrots and some species of conures, shed the virus in feces and in respiratory and oral secretions. Outbreaks can occur when stress causes healthy birds who carry the virus to shed it. Birds generally become infected after ingesting the virus in contaminated material, and show signs of the disease within several weeks.

The main sign of Pacheco's disease is sudden death, sometimes preceded by a short, severe illness. If a bird survives Pacheco's disease following infection with PsHV-1 genotypes 1, 2 or 3, it may later develop internal papilloma disease in the gastrointestinal tract.

Susceptible parrot species include the African gray parrot, and cockatoo. Native Australian birds, such as the eclectus parrot, Bourke's parrot, and budgerigar are susceptible to Pacheco's disease, although the disease itself has not been found in Australia.

No serious long-term effects are known for this disease, but preliminary evidence suggests, if such symptoms do occur, they are less severe than those associated with Lyme disease.

White band disease (Acroporid white syndrome) is a coral disease that affects acroporid corals and is distinguishable by the white band of dead coral tissue that it forms. The disease completely destroys the coral tissue of Caribbean acroporid corals, specifically elkhorn coral ("Acropora palmata") and staghorn coral ("A. cervicornis"). The disease exhibits a pronounced division between the remaining coral tissue and the exposed coral skeleton. These symptoms are similar to white plague, except that white band disease is only found on acroporid corals, and white plague has not been found on any acroporid corals. It is part of a class of similar disease known as "white syndromes", many of which may be linked to species of "Vibrio" bacteria. While the pathogen for this disease has not been identified, "Vibrio carchariae" may be one of its factors. The degradation of coral tissue usually begins at the base of the coral, working its way up to the branch tips, but it can begin in the middle of a branch.

Six syndromes are known to occur after infection with Marek's disease. These syndromes may overlap.

- Classical Marek's disease or neurolymphomatosis causes asymmetric paralysis of one or more limbs. With vagus nerve involvement, difficulty breathing or dilation of the crop may occur. Besides lesions in the peripheral nerves, there are frequently lymphomatous infiltration/tumours in the skin, skeletal muscle, visceral organs. Organs that are commonly affected include the ovary, spleen, liver, kidneys, lungs, heart, proventriculus and adrenals.

- Acute Marek's disease is an epidemic in a previously uninfected or unvaccinated flock, causing depression, paralysis, and death in a large number of birds (up to 80%). The age of onset is much earlier than the classic form; birds are four to eight weeks old when affected. Infiltration into multiple organs/tissue is observed.

- Ocular lymphomatosis causes lymphocyte infiltration of the iris (making the iris turn grey), unequal size of the pupils, and blindness.

- Cutaneous Marek's disease causes round, firm lesions at the feather follicles.

- Atherosclerosis is induced in experimentally infected chickens.

- Immunosuppression – Impairment of the T-lymphocytes prevents competent immunological response against pathogenic challenge and the affected birds become more susceptible to disease conditions such as coccidiosis and "Escherichia coli" infection . Furthermore, without stimulation by cell-mediated immunity, the humoral immunity conferred by the B-cell lines from the Bursa of Fabricius also shuts down, thus resulting in birds that are totally immunocompromised.

Pogosta disease is a viral disease, established to be identical with other diseases, Karelian fever and Ockelbo disease. The names are derived from the words Pogosta, Karelia and Ockelbo, respectively.

The symptoms of the disease include usually rash, as well as mild fever and other flu-like symptoms; in most cases the symptoms last less than 5 days. However, in some cases, the patients develop a painful arthritis. There are no known chemical agents available to treat the disease.

It has long been suspected that the disease is caused by a Sindbis-like virus, a positive-stranded RNA virus belonging to the Alphavirus genus and family Togaviridae. In 2002 a strain of Sindbis was isolated from patients during an outbreak of the Pogosta disease in Finland, confirming the hypothesis.

This disease is mainly found in the Eastern parts of Finland; a typical Pogosta disease patient is a middle-aged person who has been infected through a mosquito bite while picking berries in the autumn. The prevalence of the disease is about 100 diagnosed cases every year, with larger outbreaks occurring in 7-year intervals.

Marek's disease is a highly contagious viral neoplastic disease in chickens. It is named after József Marek, a Hungarian veterinarian. Marek's disease is caused by an alphaherpesvirus known as 'Marek's disease virus' (MDV) or "Gallid alphaherpesvirus 2" (GaHV-2). The disease is characterized by the presence of T cell lymphoma as well as infiltration of nerves and organs by lymphocytes. Viruses "related" to MDV appear to be benign and can be used as vaccine strains to prevent Marek's disease. For example, the related Herpesvirus of Turkeys (HVT), causes no apparent disease in turkeys and continues to be used as a vaccine strain for prevention of Marek's disease (see below). Birds infected with GaHV-2 can be carriers and shedders of the virus for life. Newborn chicks are protected by maternal antibodies for a few weeks. After infection, microscopic lesions are present after one to two weeks, and gross lesions are present after three to four weeks. The virus is spread in dander from feather follicles and transmitted by inhalation.

Cherry X disease also known as Cherry Buckskin disease is caused by a plant pathogenic phytoplasma. Phytoplasma's are obligate parasites of plants and insects. They are specialized bacteria, characterized by their lack of a cell wall, often transmitted through insects, and are responsible for large losses in crops, fruit trees, and ornamentals. The phytoplasma causing Cherry X disease has a fairly limited host range mostly of stone fruit trees. Hosts of the pathogen include sweet/sour cherries, choke cherry, peaches, nectarines, almonds, clover, and dandelion. Most commonly the pathogen is introduced into economical fruit orchards from wild choke cherry and herbaceous weed hosts. The pathogen is vectored by mountain and cherry leafhoppers. The mountain leafhopper vectors the pathogen from wild hosts to cherry orchards but does not feed on the other hosts. The cherry leafhopper which feeds on the infected cherry trees then becomes the next vector that transmits from cherry orchards to peach, nectarine, and other economic crops. Control of Cherry X disease is limited to controlling the spread, vectors, and weed hosts of the pathogen. Once the pathogen has infected a tree it is fatal and removal is necessary to stop it from becoming a reservoir for vectors.