There are no diagnostic tests for tungiasis. This is most likely because the parasite is ectoparasitic with visible symptoms. Identification of the parasite through removal, and a patient’s traveling history, should suffice for diagnosis, though the latter is clearly more useful than the former. Localization of the lesion may be a useful diagnostic method for the clinician. A biopsy may be done, though again, it is not required for diagnosis.

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.

The number of diagnosed cases of human louse infestations (or pediculosis) has increased worldwide since the mid-1960s, reaching hundreds of millions annually. There is no product or method which assures 100% destruction of the eggs and hatched lice after a single treatment. However, there are a number of treatment methods that can be employed with varying degrees of success. These methods include chemical treatments, natural products, combs, shaving, hot air, silicone-based lotions, and ethanol (ethyl alcohol).

The pharmacological treatment of pediculosis include the use of crotamiton applied twice at 24 hour interval and washed off day after that. Benzyl benzoate also can be used when combined with lindane, it is applied once and then washed off after 24 hours.

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

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.

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.

Medical doctors and dermatologists can still misdiagnose this rash as many are unfamiliar with parasitism, not trained in it, or if they do consider it, cannot see the mites.

Different methods for detection are recognized for different acariasis infections. Human acariasis with mites can occur in the gastrointestinal tract, lungs, urinary tracts and other organs which not have been well-studied. For intestinal acariasis with symptoms such as abdominal pain, diarrhea, and phohemefecia (is this hemafecia?), human acariasis is diagnosed by detection of mites in stools. For pulmonary acariasis, the presence of mites in sputum is determined by identifying the presence and number of mites in the sputum of patients with respiratory symptoms. Both physical and chemical methods for liquefaction of sputum have been developed.

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.

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.

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.

It is done through isolation of a bacteria from chickens suspected to have history of coryza and clinical finds from infected chickens also is used in the disease diagnosis. Polymerase chain reaction is a reliable means of diagnosis of the disease

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 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.

The first approach, which is the best approach at an effective management practice would be to eradicate or severely damage the Mountain and Cherry Leafhopper population because the leafhoppers are the number one vectors for this pathogen. To do this, pesticides (i.e. acephate, bifenthrin, cyfluthrin) could be applied or biological control (predators of the leafhopper) could be used. There should be a pre-season application of control measures as well as a post-season application. This is to maximize the effort at controlling both types of leafhoppers (Cherry and Mountain), thus cutting down the starting inoculum at both stages in the life cycle.

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.

Common clinical signs and symptoms of Whipple's disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms. Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of non-destructive seronegative arthritis, often of large joints.

Diagnosis is made by biopsy, usually by duodenal endoscopy, which reveals PAS-positive macrophages in the lamina propria containing non-acid-fast gram-positive bacilli. Immunohistochemical staining for antibodies against "T. whipplei" has been used to detect the organism in a variety of tissues, and a PCR-based assay is also available. PCR can be confirmatory if performed on blood, vitreous fluid, synovial fluid, heart valves, or cerebrospinal fluid. PCR of saliva, gastric or intestinal fluid, and stool specimens is highly sensitive, but not specific enough, indicating that healthy individuals can also harbor the causative bacterium without the manifestation of Whipple's disease, but that a negative PCR is most likely indicative of a healthy individual.

Endoscopy of the duodenum and jejunum can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipple's disease, and small bowel X-rays may show some thickened folds. Other pathological findings may include enlarged mesenteric lymph nodes, hypercellularity of lamina propria with "foamy macrophages", and a concurrent decreased number of lymphocytes and plasma cells, per high power field view of the biopsy.

A D-Xylose test can be performed, which is where the patient will consume 4.5g of D-xylose, a sugar, by mouth. The urine excretion of D-Xylose is then measured after 5 hours. The majority of D-Xylose is absorbed normally, and should be found in the urine. If the D-Xylose is found to be low in the urine, this suggests an intestinal malabsorption problem such as bacterial overgrowth of the proximal small intestine, Whipple's Disease, or an autoimmune with diseases such as Celiac's Disease (allergy to gluten) or Crohn's Disease (autoimmune disease affecting the small intestine). With empiric antibiotic treatment after an initial positive D-Xylose test, and if a follow-up D-Xylose test is positive (decreased urine excretion) after antibiotic therapy, then this would signify it is not bacterial overgrowth of the proximal small intestine. Since Whipple's disease is so rare, a follow-up positive D-Xylose test more likely indicates a non-infectious etiology and more likely an autoimmune etiology. Clinical correlation is recommended to rule out Whipple's disease.

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.

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.

Feline hepatic lipidosis shares similar symptoms to other problems, including liver disease, renal failure, feline leukemia, Feline infectious peritonitis and some cancers. Diagnosis requires tests that target the liver to make an accurate diagnosis. Jaundice is highly indicative of the disease. Blood tests and a liver biopsy will confirm the presence of the disease.

White band disease causes the affected coral tissue to decorticate off the skeleton in a white uniform band for which the disease was given its name. The band, which can range from a few millimeters to 10 centimeters wide, typically works its way from the base of the coral colony up to the coral branch tips. The band progresses up the coral branch at an approximate rate of 5 millimeters per day, causing tissue loss as it works its way to the branch tips. After the tissue is lost, the bare skeleton of the coral may later by colonized by filamentous algae.

There are two variants of white band disease, type I and type II. In Type I of white band disease, the tissue remaining on the coral branch shows no sign of coral bleaching, although the affected colony may appear lighter in color overall. However, a variant of white band disease, known simply as white band disease Type II, which was found on Staghorn colonies near the Bahamas, does produce a margin of bleached tissue before it is lost. Type II of white band disease can be mistaken for coral bleaching. By examining the remaining living coral tissue for bleaching, one can delineate which type of the disease affects a given coral.

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

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.

Untreated, the disease has a mortality rate upwards of 90%. Cats treated in the early stages can have a recovery rate of 80–90%. Left untreated, the cats usually die from severe malnutrition or complications from liver failure. Treatment usually involves aggressive feeding through one of several methods.

Cats can have a feeding tube inserted by a veterinarian so that the owner can feed the cat a liquid diet several times a day. They can also be force-fed through the mouth with a syringe. If the cat stops vomiting and regains its appetite, it can be fed in a food dish normally. The key is aggressive feeding so the body stops converting fat in the liver. The cat liver has a high regeneration rate and the disease will eventually reverse assuming that irreparable damage has not been done to the liver.

The best method to combat feline hepatic lipidosis is prevention and early detection. Obesity increases the chances of onset. In addition, if a cat stops eating for 1–2 days, it should be taken to a vet immediately. The longer the disease goes untreated, the higher the mortality rate.

Diagnosis of lymphoid tumors in poultry is complicated due to multiple etiological agents capable of causing very similar tumors. It is not uncommon that more than one avian tumor virus can be present in a chicken, thus one must consider both the diagnosis of the disease/tumors (pathological diagnosis) and of the virus (etiological diagnosis). A step-wise process has been proposed for diagnosis of Marek’s disease which includes (1) history, epidemiology, clinical observations and gross necropsy, (2) characteristics of the tumor cell, and (3) virological characteristics

The demonstration of peripheral nerve enlargement along with suggestive clinical signs in a bird that is around three to four months old (with or without visceral tumors) is highly suggestive of Marek's disease. Histological examination of nerves reveals infiltration of pleomorphic neoplastic and inflammatory lymphocytes. Peripheral neuropathy should also be considered as a principal rule-out in young chickens with paralysis and nerve enlargement without visceral tumors, especially in nerves with interneuritic edema and infiltration of plasma cells.

The presence of nodules on the internal organs may also suggest Marek's disease, but further testing is required for confirmation. This is done through histological demonstration of lymphomatous infiltration into the affected tissue. A range of leukocytes can be involved, including lymphocytic cell lines such as large lymphocyte, lymphoblast, primitive reticular cells, and occasional plasma cells, as well as macrophage and plasma cells. The T cells are involved in the malignancy, showing neoplastic changes with evidence of mitosis. The lymphomatous infiltrates need to be differentiated from other conditions that affect poultry including lymphoid leukosis and reticuloendotheliosis, as well as an inflammatory event associated with hyperplastic changes of the affected tissue.

Key clinical signs as well as gross and microscopic features that are most useful for differentiating Marek’s disease from lymphoid leukosis and reticuloendotheliosis include (1) Age: MD can affect birds at any age, including 5% in unvaccinated flocks; (4) Potential nerve enlargement; (5) Interfollicular tumors in the bursa of Fabricius; (6) CNS involvement; (7) Lymphoid proliferation in skin and feather follicles; (8) Pleomorphic lymphoid cells in nerves and tumors; and (9) T-cell lymphomas.

In addition to gross pathology and histology, other advanced procedures used for a definitive diagnosis of Marek’s disease include immunohistochemistry to identify cell type and virus-specific antigens, standard and quantitative PCR for identification of the virus, virus isolation to confirm infections, and serology to confirm/exclude infections.

The World Organisation for Animal Health (OIE) reference laboratories for Marek’s disease include the Pirbright Institute, UK and the USDA Avian Disease and Oncology Laboratory, USA.