Control of the beetle vector is the most effective management technique for disease prevention. Conventional methods of tree thinning and the use of insecticides have been used to combat the western bark beetles, but are only effective before the beetles have colonized and before the fungus has invaded the tree. Other cultural techniques of sanitation and overall health of the oak trees by keeping up with watering, fertilizer or mulch needs, and pruning may help. It is very important to diagnose foamy bark canker disease correctly and promptly in order to manage the disease properly because if a tree is already infected, the removal of the tree is the most effective way to prevent the disease from spreading.

Shot hole disease (also called Coryneum blight) is a serious fungal disease that creates BB-sized holes in leaves, rough areas on fruit, and concentric lesions on branches. The pathogen that causes shot hole disease is "Wilsonomyces carpophilus".

The foamy bark canker is a disease affecting oak trees in California caused by the fungus "Geosmithia pallida" and spread by the Western oak bark beetle ("Pseudopityopthorus pubipennis"). This disease is only seen through the symbiosis of the bark beetles and the fungal pathogen. The bark beetles target oak trees and bore holes through the peridermal tissues, making tunnels within the phloem. The fungal spores are brought into these tunnels by the beetles and begin to colonize the damaged cells inside the tunnels. Symptoms of the developing fungus include wet discoloration seeping from the beetle entry holes as the fungus begins to consume phloem and likely other tissues. If bark is removed, necrosis of the phloem can be observed surrounding the entry hole(s). As the disease progresses, a reddish sap and foamy liquid oozes from entry holes, thus giving the disease the name Foamy bark canker. Eventually after the disease has progressed, the tree dies. This disease is important because of its detrimental effects on oak trees and its ability to spread to several new Californian counties in just a couple years.

"W. carpophilus" can remain viable for several months and spores are often airborne. Since the fungi thrive in wet conditions, overhead watering should be avoided. Remove and dispose of any infected buds, leaves, fruit and twigs. In fall, fixed copper or Bordeaux mixture can be applied.

German entomologist Fritz Zumpt describes myiasis as "the infestation of live human and vertebrate animals with dipterous larvae, which at least for a period, feed on the host's dead or living tissue, liquid body substances, or ingested food". For modern purposes however, this is too vague. For example, feeding on dead or necrotic tissue is not generally a problem except when larvae such as those of flies in the family Piophilidae attack stored food such as cheese or preserved meats; such activity suggests saprophagy rather than parasitism; it even may be medically beneficial in maggot debridement therapy (MDT).

Currently myiasis commonly is classified according to aspects relevant to the case in question:

- The classical description of myiasis is according to the part of the host that is infected. This is the classification used by ICD-10. For example:

- dermal

- sub-dermal

- cutaneous (B87.0)

- creeping, where larvae burrow through or under the skin

- furuncular, where a larva remains in one spot, causing a boil-like lesion

- nasopharyngeal, in the nose, sinuses or pharynx (B87.3)

- ophthalmic or ocular, in or about the eye (B87.2)

- auricular, in or about the ear

- gastric, rectal, or intestinal/enteric for the appropriate part of the digestive system (B87.8)

- urogenital (B87.8)

- Another aspect is the relationship between the host and the parasite and provides insight into the biology of the fly species causing the myiasis and its likely effect. Thus the myiasis is described as either:

- obligatory, where the parasite cannot complete its life cycle without its parasitic phase, which may be specific, semispecific, or opportunistic

- facultative, incidental, or accidental, where it is not essential to the life cycle of the parasite; perhaps a normally free-living larva accidentally gained entrance to the host

Accidental myiasis commonly is enteric, resulting from swallowing eggs or larvae with one's food. The effect is called "pseudomyiasis". One traditional cause of pseudomyiasis was the eating of maggots of cheese flies in cheeses such as Stilton. Depending on the species present in the gut, pseudomyiasis may cause significant medical symptoms, but it is likely that most cases pass unnoticed.

"Hole in the head can be reversed by removing all activated carbon and conducting large percentage water changes. Greater than 90% water changes may need to be done to reduce the effects of activated carbon. More commonly, cures are made by moving the fish to a new aquarium that has never had fish develop HLLE in it.

The first control method is preventive and aims to eradicate the adult flies before they can cause any damage and is called vector control. The second control method is the treatment once the infestation is present, and concerns the infected animals (including humans).

The principal control method of adult populations of myiasis inducing flies involves insecticide applications in the environment where the target livestock is kept. Organophosphorus or organochlorine compounds may be used, usually in a spraying formulation. One alternative prevention method is the sterile insect technique (SIT) where a significant number of artificially reared sterilized (usually through irradiation) male flies are introduced. The male flies compete with wild breed males for females in order to copulate and thus cause females to lay batches of unfertilized eggs which cannot develop into the larval stage.

One prevention method involves removing the environment most favourable to the flies, such as by removal of the tail. Another example is the crutching of sheep, which involves the removal of wool from around the tail and between the rear legs, which is a favourable environment for the larvae. Another, more permanent, practice which is used in some countries is mulesing, where skin is removed from young animals to tighten remaining skin – leaving it less prone to fly attack.

To prevent myiasis in humans, there is a need for general improvement of sanitation, personal hygiene, and extermination of the flies by insecticides. Clothes should be washed thoroughly, preferably in hot water, dried away from flies, and ironed thoroughly. The heat of the iron kills the eggs of myiasis-causing flies.

Diagnosis is clinical. Sensation is tested using graded monofilament.

The bacteria invade the lacrimal glands of the eye, causing keratitis, uveitis, and corneal ulceration. Cattle show signs of pain, increased lacrimation, excessive blinking, and conjunctivitis. More severe cases may show systemic signs such as anorexia and weight loss. Chronic untreated cases can become blind. Diagnosis is usually based on the clinical signs, but the bacteria can be cultured from lacrimal swabs, or visualised on smears of lacrimal secretions.

Shade, insect repellent-impregnated ear tags, and lower stocking rates may help prevent IBK. Early identification of the disease also helps prevent spread throughout the herd. Treatment is with early systemic use of a long-acting antibiotic such as tetracycline or florfenicol. Subconjunctival injections with procaine penicillin or other antibiotics are also effective, providing a "bubble" of antibiotic which releases into the eye slowly over several days.

Anti-inflammatory therapy can help shorten recovery times, but topical corticosteroids should be used with care if corneal ulcers are present.

"M. bovis" uses several different serotyped fimbriae as virulence factors, consequently pharmaceutical companies have exploited this to create vaccines. However, currently available vaccines are not reliable.

The diagnosis is aided by obtaining a history of the circumstances surrounding the bite. The time the bite was experienced, the location of the bite, and examination of the bite is noted. The person may have drainage from the site of the bite. They may also be febrile. Swelling may also occur. Because the wound from the bite may have healed over the punctures, the wound it may be opened and explored. The site is anesthetized prior to exploration of the wound for is examined for damage. Neurovascular status is assessed. Immune status may determine treatment as does

the presence of transplanted tissue or organs, rheumatic disease, diabetes, HIV/AIDS and sickle cell disease.

Swollen glands (lymph nodes) and red streaks radiating upward may be evident.

The diagnosis of a cat with rabies is evident by observing the cat. Cats with rabies may also appear restless, pant, and attack other animals, people, or objects. Animals with rabies typically die within a few days of appearing sick. Vaccination of the cat can prevent rabies being transmitted by the cat through a bite. If the cat is suspected of being infected with rabies, the person begins treatment with rabies vaccine.

Cat bites can often be prevented by:

- instructing children not to tease cats or other pets.

- being cautious with unfamiliar cats.

- approaching cats with care, even if they appear to be friendly.

- avoiding rough play with cats and kittens.

Rough play causes is perceived as aggressive. This will lead to the cat being defensive when approached by people. Preventing cat bites includes not provoking the cat.

Possible complications include the horse becoming a chronic carrier of the disease, asphyxia due to enlarged lymph nodes compressing the larynx or windpipe, bastard strangles (spreading to other areas of the body), pneumonia, guttural pouch filled with pus, abscesses, purpura haemorrhagica, and heart disease. The average length for the course of this disease is 23 days.

The most accepted cause that has the most evidence is the use of activated carbon in closed aquarium ecosystems.

A similar study also points to carbon as a cause of HLLE

Many other causes have been suggested, but have not been substantiated by any peer-reviewed studies.

As with many streptococcal infections, penicillin or penicillin-derivative antibiotics are the most effective treatments. However, some authorities are of the opinion that use of antibiotics is contra-indicated once abscesses have begun to form, as they pre-dispose to lymphatic spread of the infection (so-called bastard strangles) which has a much higher mortality rate.

After an abscess has burst, it is very important to keep the wound clean. A diluted povidone-iodine solution has been used with good results to disinfect the open hole, flushing the inside with a syringe tipped catheter or with a teat cannula, followed by gentle scrubbing to keep the surrounding area clean.

Symptomatic therapy is an alternative treatment, and is where warm packs are used to mature the abscesses so making it less painful and more comfortable for the horse itself; but once the abscesses have been matured they must be kept clean to prevent further infections.This treatment for "S.equi" only helps to reduce pain for the horse rather than curing the infection.

Underlying cause of neuropathy is first treated. Necrotic portions of the wound are removed and wound is kept moist at associations. Infected ulcers are administered antibiotics.

Skin grafting is one of the options. It has been shown that ultrasound may increase the acceptance of graft at trophic ulcer sites.

Subungual hematomas are treated by either releasing the pressure conservatively when tolerable or by drilling a hole through the nail into the hematoma (trephining), or by removing the entire nail. Trephining is generally accomplished by using a heated instrument to pass through the nail into the blood clot. Removal of the nail is typically done when the nail itself is disrupted, a large laceration requiring suturing is suspected, or a fracture of the tip of the finger occurs. Although general anesthesia is generally not required, a digital nerve block is recommended to be performed if the nail is to be removed.

Subungual hematomas typically heal without incident, though infection or disruption of the nail (onycholysis) may occur.

For precious animals ;

- Repeat screening, case management to abate sources

- Medical and environmental evaluation,

- veterinary evaluation, chelation, case management

- If necessary, veterinary hospitalization, immediate chelation, case management.

The mainstays of treatment are removal from the source of lead and, for precious animals who have significantly high blood lead levels or who have symptoms of poisoning, chelation therapy with a chelating agent.

Diagnosis is based on "post mortem" examination (necropsy) and testing; examination of the dead body is not definitive as many animals die early in the course of the disease and conditions found are non-specific; general signs of poor health and Aspiration pneumonia, which may be the actual cause of death, are common. On microscopic examination, lesions of CWD in the central nervous system resemble those of other TSEs. In addition, scientists use immunohistochemistry to test brain, lymph, and neuroendocrine tissues for the presence of the abnormal prion protein to diagnose CWD; positive IHC findings in the obex is considered the gold standard.

As of 2015 there were no commercially feasible diagnostic tests that could be used on live animals. It is possible to run a bioassay, taking fluids from cervids suspected of infection and incubating them in transgenic mice that express the cervid prion protein, to determine if the cervid is infected, but there are ethical issues with this and it is not scalable.

The current reference range for acceptable blood lead concentrations in healthy persons without excessive exposure to environmental sources of lead is less than 5 µg/dL for children. It was less than 25 µg/dL for adults. Previous to 2012 the value for children was 10 (µg/dl). The current biological exposure index (a level that should not be exceeded) for lead-exposed workers in the U.S. is 30 µg/dL in a random blood specimen.

In 2015, US HHS/CDC/NIOSH designated 5 µg/dL (five micrograms per deciliter) of whole blood, in a venous blood sample, as the reference blood lead level for adults. An elevated BLL is defined as a BLL ≥5 µg/dL. This case definition is used by the ABLES program, the Council of State and Territorial Epidemiologists (CSTE), and CDC’s National Notifiable Diseases Surveillance System (NNDSS). Previously (i.e. from 2009 until November 2015), the case definition for an elevated BLL was a BLL ≥10 µg/dL. The U.S. national BLL geometric mean among adults was 1.2 μg/dL in 2009–2010.

Blood lead concentrations in poisoning victims have ranged from 30->80 µg/dL in children exposed to lead paint in older houses, 77–104 µg/dL in persons working with pottery glazes, 90–137 µg/dL in individuals consuming contaminated herbal medicines, 109–139 µg/dL in indoor shooting range instructors and as high as 330 µg/dL in those drinking fruit juices from glazed earthenware containers.

Cavitations are an area of dead bone caused by a dearth of blood flow to that part of the bone. A cavitation is a hole in the blood vessel that cannot be visually detected with the naked eye. Jawbone cavitations, also called neuralgia-inducing cavitational osteonecrosis (NICO) if they are associated with pain, are extraction sites in the jaw that have not healed.

Cows and horses as well as pet animals are also susceptible to the effects of lead toxicity. Sources of lead exposure in pets can be the same as those that present health threats to humans sharing the environment, such as paint and blinds, and there is sometimes lead in toys made for pets. Lead poisoning in a pet dog may indicate that children in the same household are at increased risk for elevated lead levels.

Diagnosis includes determining the clinical signs and the medical history, with inquiry into possible routes of exposure. Clinical toxicologists, medical specialists in the area of poisoning, may be involved in diagnosis and treatment.

The main tool in diagnosing and assessing the severity of lead poisoning is laboratory analysis of the blood lead level (BLL).

Blood film examination may reveal basophilic stippling of red blood cells (dots in red blood cells visible through a microscope), as well as the changes normally associated with iron-deficiency anemia (microcytosis and hypochromasia). However, basophilic stippling is also seen in unrelated conditions, such as megaloblastic anemia caused by vitamin B12 (colbalamin) and folate deficiencies.

Exposure to lead also can be evaluated by measuring erythrocyte protoporphyrin (EP) in blood samples. EP is a part of red blood cells known to increase when the amount of lead in the blood is high, with a delay of a few weeks. Thus EP levels in conjunction with blood lead levels can suggest the time period of exposure; if blood lead levels are high but EP is still normal, this finding suggests exposure was recent. However, the EP level alone is not sensitive enough to identify elevated blood lead levels below about 35 μg/dL. Due to this higher threshold for detection and the fact that EP levels also increase in iron deficiency, use of this method for detecting lead exposure has decreased.

Blood lead levels are an indicator mainly of recent or current lead exposure, not of total body burden. Lead in bones can be measured noninvasively by X-ray fluorescence; this may be the best measure of cumulative exposure and total body burden. However this method is not widely available and is mainly used for research rather than routine diagnosis. Another radiographic sign of elevated lead levels is the presence of radiodense lines called lead lines at the metaphysis in the long bones of growing children, especially around the knees. These lead lines, caused by increased calcification due to disrupted metabolism in the growing bones, become wider as the duration of lead exposure increases. X-rays may also reveal lead-containing foreign materials such as paint chips in the gastrointestinal tract.

Fecal lead content that is measured over the course of a few days may also be an accurate way to estimate the overall amount of childhood lead intake. This form of measurement may serve as a useful way to see the extent of oral lead exposure from all the diet and environmental sources of lead.

Lead poisoning shares symptoms with other conditions and may be easily missed. Conditions that present similarly and must be ruled out in diagnosing lead poisoning include carpal tunnel syndrome, Guillain–Barré syndrome, renal colic, appendicitis, encephalitis in adults, and viral gastroenteritis in children. Other differential diagnoses in children include constipation, abdominal colic, iron deficiency, subdural hematoma, neoplasms of the central nervous system, emotional and behavior disorders, and intellectual disability.

Runner's toe is a common condition seen in runners caused by downward pressure or horizontal separation of nail plate from the nail bed. This repetitive traumatic injury leads to bleeding and pooling of blood underneath the nail plate. Clinically, it is characterized by reddish-black discoloration of the toe nail. The nail plate may also become thicker and more brittle as a result of the injury (onychochauxis). Fortunately, the deformed nail plate will gradually grow out and be replaced by new, normal-appearing nail plate in several months time. Infrequently, the toe may become painful and require surgical drainage.

Runner's toe is often associated with malfitting shoes and insufficient space for the toes. Some susceptible runners may also have Morton's toe. In this variant of human foot anatomy, the second toe extends further out than the great toe. The key to prevention of runner's toe is to purchase properly fitted shoes.

The condition also results from a traumatic injury, such as slamming a finger in a door, or from sports activities, such as climbing or hiking rugged terrain. A subungual hematoma that results from the repetitive thrusting of the longest toe into a shoe's toe box is called jogger's toe or runner's toe.

The bleeding comes from the (vascular) nail bed underlying the (avascular) nail plate. A laceration of the nail bed causes bleeding into the constricted area underneath the hard nail plate. Throbbing pain is common. The nail develops a black discoloration overlying the nail bed but under the nail plate.

The most important aspect of treatment of pyometra is quick action to provide supportive care. Female dogs are often septic and in shock (see septic shock). Intravenous fluids and antibiotics should be given immediately. Once the female dog has been stabilized, then the treatment of choice is an emergency spay. In livestock the treatment of choice for minor cases is Dinopost Tremethamine (Lutalyse). Supportive antibiotic treatment may be recommended also. Severe cases require surgery.