Infestations can be classified as either external or internal with regards to the parasites' location in relation to the host.

External or ectoparasitic infestation is a condition in which organisms live primarily on the surface of the host (though porocephaliasis can penetrate viscerally) and includes those involving mites, ticks, head lice and bed bugs.

An internal (or endoparasitic) infestation is a condition in which organisms live within the host and includes those involving worms (though swimmer's itch stays near the surface).

Medically, the term "infestation" is often reserved only for external ectoparasitic infestations while the term "infection" refers to internal endoparasitic conditions.

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.

Cattle infested with bovine pediculosis are generally treated chemically, by drugs like ivermectin and cypermethrin.

Due to the high number of hosts, eradication of tungiasis is not feasible, at least not easily so. Public health and prevention strategies should then be done with elimination as the target. Better household hygiene, including having a cemented rather than a sand floor, and washing it often, would lower the rates of tungiasis significantly.

Though vaccines would be useful, due to the ectoparasitic nature of chigoe flea, they are neither a feasible nor an effective tool against tungiasis. Nevertheless, due to the high incidence of secondary infection, those at risk of tungiasis should get vaccinated against tetanus. A better approach is to use repellents that specifically target the chigoe flea. One very successful repellent is called Zanzarin, a derivative of coconut oil, jojoba oil, and aloe vera. In a recent study involving two cohorts, the infestation rates dropped 92% on average for the first one and 90% for the other. Likewise, the intensity of the cohorts dropped by 86% and 87% respectively. The non-toxic nature of Zanzarin, combined with its "remarkable regression of the clinical pathology" make this a tenable public health tool against tungiasis.

The use of pesticide, like DDT, has also led to elimination of the "Tunga penetrans", but this control/prevention strategy should be utilized very carefully, if at all, because of the possible side effects such pesticides can have on the greater biosphere. In the 1950s, there was a worldwide effort to eradicate malaria. As part of that effort, Mexico launched the Campaña Nacional para la Erradicación de Paludismo, or the National Campaign for the Eradication of Malaria. By spraying DDT in homes, the Anopheles a genus of mosquitoes known to carry the deadly Plasmodium falciparum was mostly eliminated. As a consequence of this national campaign, other arthropods were either eliminated or significantly reduced in number, including the reduviid bug responsible for Chagas disease (American Trypanosomiasis) and "T. penetrans". Controlled, in-home spraying of DDT is effective as it gives the home immunity against arthropods while not contaminating the local water supplies and doing as much ecological damage as was once the case when DDT was first introduced.

While other species gradually gained resistance to DDT and other insecticides that were used, "T. penetrans did" not; as a result, the incidence of tungiasis in Mexico is very low when compared to the rest of Latin America, especially Brazil, where rates in poor areas have been known to be as high or higher than 50%. There was a 40-year period with no tungiasis cases in Mexico. It was not until August 1989 that three Mexican patients presented with the disease. Though there were other cases of tungiasis reported thereafter, all were acquired in Africa.

In the 15th century, topical mercury treatment was used to treat pediculosis.

As the disease is self-limiting, at least when exposure to the parasite is limited, management is mostly confined to treatment. Due to the secondary infection that can cause serious medical issues, the recommended course of action upon diagnosis is a surgical extraction of the fleas followed by the application of a topical antibiotic. Care should be taken to avoid tearing the flea during the extraction procedures as severe inflammation will result. The same will occur if part of the flea is left behind. Sterile equipment should always be used, as contaminated instruments could act as mechanical vectors for pathogens to enter the body.

There is no drug that has proven to be effective against embedded fleas. Oral niridazole was once considered a therapeutic drug, but well-designed studies are lacking and, given the severe adverse effects, this is one drug that is likely to cause more harm than good. However, it has some anecdotal evidence of lysing the fleas altogether. Oral ivermectin is considered by some in endemic areas to be a panacea against the fleas but studies using high doses have failed to validate this hypothesis. Other drugs such as topical ivermectin and metrifonate have been somewhat successful, but not enough to be significant. [2,5] For superinfections, trimethoprim, sulfamethoxazole, metronidazole, amoxicillin, (with/without clavulanate) have been used successfully, though these treat only secondary infections.

Successful topical treatments also include cryotherapy and electrodesiccation of the lesion. If formaldehyde, chloroform, or DDT are used topically, care should be taken when dealing with the resulting morbidity. The "T. penetrans" flea can also be suffocated using occlusive petrolatum, while Vaseline will kill the organism as well, most likely due to suffocation as the stigmatas would be covered. The gum of the mammee apple ("Mammea americana"), a fruit that also goes by the name Saint Domingo apricot, has also been used to kill the chigoe flea, though this has not been reported in the main "T. penetrans" literature.

Even without treatment, the burrowed fleas will die within five weeks and are naturally sloughed off as the skin sheds.

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)

In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.

Currently, antibiotic drugs such as penicillin or tetracycline are the only effective methods for disease treatment. Within wild populations, disease control consists of reducing the amount of bacterial spores present in the environment. This can be done by removing contaminated carcasses and scat.

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.

Prevention is through use of Stock coryza-free birds. In other areas culling of the whole flock is a good means of the disease control. Bacterin also is used at a dose of two to reduce brutality of the disease. Precise exposure has also has been used but it should be done with care. Vaccination of the chicks is done in areas with high disease occurrence. Treatment is done by using antibiotics such as erythromycin, Dihydrostreptomycin, Streptomycin sulphonamides, tylosin and Flouroquinolones .

There is no vaccine for SVD. Prevention measures are similar to those for foot-and-mouth disease: controlling animals imported from infected areas, and sanitary disposal of garbage from international aircraft and ships, and thorough cooking of garbage. Infected animals should be placed in strict quarantine. Eradication measures for the disease include quarantining infected areas, depopulation and disposal of infected and contact pigs, and cleaning and disinfecting

contaminated premises.

The reservoirs of the disease are carrier chickens which could be health but harboring the disease or chronically sick chickens. The disease affects all ages of chickens. The disease can persist in the flock for 2-3 weeks and signs of the disease are seen between 1–3 days post infection. Transmission of the disease is through direct interaction, airborne droplets and drinking contaminated water. Chicken having infection and those carriers contribute highly to the disease transmission

Treatment is with penicillin, ampicillin, tetracycline, or co-trimoxazole for one to two years. Any treatment lasting less than a year has an approximate relapse rate of 40%. Recent expert opinion is that Whipple's disease should be treated with doxycycline with hydroxychloroquine for 12 to 18 months. Sulfonamides (sulfadiazine or sulfamethoxazole) may be added for treatment of neurological symptoms.

The disease is regarded as extremely rare, with an incidence (new number of cases per year) of one case per million people. The patients are predominantly male (86% in a survey of American patients), although in some countries the rate of women receiving a diagnosis of Whipple's disease has increased in recent years. It occurs predominantly in those of Caucasian ethnicity, suggesting a genetic predisposition in that population.

"T. whipplei" appears to be an environmental organism that is commonly present in the gasterointestinal tract but remains asymptomatic. Several lines of evidence suggest that some defect—inherited or acquired—in immunity is required for it to become pathogenic. The possible immunological defect may be specific for "T. whipplei", since the disease is not associated with a substantially increased risk of other infections.

The disease is usually diagnosed in middle age (median 49 years). Studies from Germany have shown that age at diagnosis has been rising since the 1960s.

Infections are treated with antibiotics, particularly doxycycline, and the acute symptoms appear to respond to these drugs.

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.

Vaccination is the only known method to prevent the development of tumors when chickens are infected with the virus. However, administration of vaccines does not prevent transmission of the virus, i.e., the vaccine is not sterilizing. However, it does reduce the amount of virus shed in the dander, hence reduces horizontal spread of the disease. Marek's disease does not spread vertically. The vaccine was introduced in 1970 and the scientist credited with its development is Dr. Ben Roy Burmester and Dr. Frank J Siccardi. Before that, Marek's disease caused substantial revenue loss in the poultry industries of the United States and the United Kingdom. The vaccine can be administered to one-day-old chicks through subcutaneous inoculation or by "in ovo" vaccination when the eggs are transferred from the incubator to the hatcher. "In ovo" vaccination is the preferred method, as it does not require handling of the chicks and can be done rapidly by automated methods. Immunity develops within two weeks.

The vaccine originally contained the antigenically similar turkey herpesvirus, which is serotype 3 of MDV. However, because vaccination does not prevent infection with the virus, the Marek's disease virus has evolved increased virulence and resistance to this vaccine. As a result, current vaccines use a combination of vaccines consisting of HVT and gallid herpesvirus type 3 or an attenuated MDV strain, CVI988-Rispens (ATCvet code: ).

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.

Some herbaceous hosts naturally have the Cherry X Disease. Once the spreads to the cherry hosts, with the help of the mountain leafhoppers, the cherry leafhoppers can spread the disease around to other woody hosts. Here are some approaches at management with each host type:

There are numerous steps one has to take to try to manage the disease as best as possible. The aim is at prevention because once the pathogen reaches the cherry trees, disease will surely ensue and there is no cure or remedy to prevent the loss of fruit production as well as the ultimate death of the tree.

Pacheco's disease is an eponymously named disease; it is named after the Brazilian veterinarian, Genesio Pacheco, who first came across the disease in 1929, in an outbreak affecting the turquoise-fronted amazon parrot, "Amazona aestiva". Initially, Pacheco's disease was thought to be a manifestation of avian psittacosis. The causative agent of the disease, a herpesvirus, was not identified until 1975.

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.

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.