Thoroughly cleaning boats, trailers, nets and other equipment when traveling between different lakes and streams also

helps. The only EPA-approved disinfectant proven effective against VHS is Virkon AQUATIC (made by Dupont). Chlorine bleach kills the VHS virus, but in concentrations that are much too caustic for ordinary use. Disinfecting stations can be found at various inland lake boat launches in the Great Lakes region.

Fish that become infected experience hemorrhaging of their internal organs, skin, and muscle. Some fish show no external symptoms, but others show signs of infection that include bulging eyes, bloated abdomens, bruised-looking reddish tints to the eyes, skin, gills and fins. Some infected fish have open sores that may look like the lesions from other diseases or from lamprey attacks.

There may also be a nervous form of the disease where fish are constantly flashing and showing abnormal behaviour.

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.

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.

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.

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.

Persons with component deficiencies in the final common complement pathway (C3,C5-C9) are more susceptible to "N. meningitidis" infection than complement-satisfactory persons, and it was estimated that the risk of infection is 7000 times higher in such individuals. In addition, complement component-deficient populations frequently experience frequent meningococcal disease since their immune response to natural infection may be less complete than that of complement non-deficient persons.

Inherited properdin deficiency also is related, with an increased risk of contracting meningococcal disease. Persons with functional or anatomic asplenia may not efficiently clear encapsulated "Neisseria meningitidis" from the bloodstream Persons with other conditions associated with immunosuppression also may be at increased risk of developing meningococcal disease.

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

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

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.

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.

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.

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.

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: ).

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.

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.

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

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.

Feline spongiform encephalopathy (FSE) is a prion disease thought to be related or identical to Bovine spongiform encephalopathy (BSE).This disease is known to affect domestic and captive feline species. Lezmi S. et al. (2003), suggested that this infectious agent might be spread by both haematogenous and nervous pathways. Like BSE, this disease can take several years to develop. It is probable, but not proven, that the affected animals contract the disease by eating contaminated bovine meat.

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.

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:

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.

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.

Cold agglutinins develop in more than 60% of patients with infectious mononucleosis, but hemolytic anemia is rare.

Classic chronic cold agglutinin disease is idiopathic, associated with symptoms and signs in relation to cold exposure.

Causes of the monoclonal secondary disease include the following:

- B-cell neoplasms - Waldenström macroglobulinemia, lymphoma, chronic lymphoid leukemia, myeloma

- Non hematologic neoplasms

Causes of polyclonal secondary cold agglutinin disease include the following:

- Mycoplasma infections.

- Viral infections: Infectious mononucleosis due to Epstein-Barr virus (EBV) or CMV, Mumps, varicella, rubella, adenovirus, HIV, influenza, hepatitis C.

- Bacterial infections: Legionnaire disease, syphilis, listeriosis and "Escherichia coli."

- Parasitic infections: Malaria and trypanosomiasis.

- Trisomy and translocation: Cytogenetic studies in patients with cold agglutinin disease have revealed the presence of trisomy 3 and trisomy 12. Translocation (8;22) has also been reported in association with cold agglutinin disease.

- Transplantation: Cold agglutinin–mediated hemolytic anemia has been described in patients after living-donor liver transplantation treated with tacrolimus and after bone marrow transplantation with cyclosporine treatments. It is postulated that such calcineurin inhibitors, which selectively affect T-cell function and spare B-lymphocytes, may interfere with the deletion of autoreactive T-cell clones, resulting in autoimmune disease.

- Systemic sclerosis: Cold agglutinin disease has been described in patients with sclerodermic features, with the degree of anemia being associated with increasing disease activity of the patient’s systemic sclerosis. This may suggest a close association between systemic rheumatic disease and autoimmune hematologic abnormalities.

- Hyperreactive malarial splenomegaly: Hyperreactive malarial splenomegaly (HMS) is an immunopathologic complication of recurrent malarial infection. Patients with HMS develop splenomegaly, acquired clinical immunity to malaria, high serum concentrations of anti-"Plasmodium" antibodies, and high titers of IgM, with a complement-fixing IgM that acts as a cold agglutinin.

- DPT vaccination: Diphtheria-pertussis-tetanus (DPT) vaccination has been implicated in the development of autoimmune hemolytic anemia caused by IgM autoantibody with a high thermal range. A total of 6 cases have been reported; 2 followed the initial vaccination and 4 followed the second or third vaccinations.

- Other: Equestrian perniosis is a rare cause of persistent elevated titers of cold agglutinins. Also rarely, the first manifestations of cold agglutinin disease can develop when a patient is subjected to hypothermia for cardiopulmonary bypass surgery.