Electron microscopy can reveal the bullet-shaped rhabdovirus, but is not

adequate for definitive diagnosis.

The Manual or Diagnostic for Aquatic Animals, 2006, is the standard

reference for definitive tests. In most cases, cell culturization

is recommended for surveillance, with antibody tests and reverse transcription

polymerase chain reaction (RT-PCR) and genetic sequencing and comparison

for definitive confirmation and genotype classification.

Virus neutralisation is another important method of diagnosis, especially for carrier fish.

Preliminary diagnosis involves histopathological examination,

observing tissues through a microscope. Most tissue changes can be observed

as minor to major necrosis (cell death) in the liver, kidneys, spleen, and

skeletal muscle. The hematopoietic (blood-forming) areas of the kidney and

spleen are the initial area of infection, and should show necrosis.

The gill may have thickened lamellae, and the liver may have pyknotic nuclei.

Skeletal muscle accumulates blood but does not suffer much damage.

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

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.

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.

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 .

Because the risk of meningococcal disease is increased among USA's military recruits, all military recruits routinely receive primary immunization against the disease.

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.

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.

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

Meningitis A,C,Y and W-135 vaccines can be used for large-scale vaccination programs when an outbreak of meningococcal disease occurs in Africa and other regions of the world. Whenever sporadic or cluster cases or outbreaks of meningococcal disease occur in the US, chemoprophylaxis is the principal means of preventing secondary cases in household and other close contacts of individuals with invasive disease. Meningitis A,C,Y and W-135 vaccines rarely may be used as an adjunct to chemoprophylaxis,1 but only in situations where there is an ongoing risk of exposure (e.g., when cluster cases or outbreaks occur) and when a serogroup contained in the vaccine is involved.

It is important that clinicians promptly report all cases of suspected or confirmed meningococcal disease to local public health authorities and that the serogroup of the meningococcal strain involved be identified. The effectiveness of mass vaccination programs depends on early and accurate recognition of outbreaks. When a suspected outbreak of meningococcal disease occurs, public health authorities will then determine whether mass vaccinations (with or without mass chemoprophylaxis) is indicated and delineate the target population to be vaccinated based on risk assessment.

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.

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.

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: ).

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.

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.

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.

This is a terminal condition and there is currently no specific treatment for the disease.

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.

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.

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.

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.

Ataxia was observed to last for about 8 weeks in the affected animals. The ultimate result is death of the infected animals.

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.