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.

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

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.

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.

There are several diseases that are caused by avian reovirus, which includes, avian arthritis/tenosynovitis, runting-stunting syndrome, and blue wing disease in chickens. Blue wing disease affects young broiler chickens and has an average mortality rate of 10%. It causes intramuscular and subcutaneous hemorrhages and atrophy of the spleen, bursa of Fabricius, and thymus. When young chickens are experimentally infected with avian reovirus, it is spread rapidly throughout all tissues. This virus is spread most frequently in the skin and muscles, which is also the most obvious site for lesions. Avian arthritis causes significant lameness in joints, specifically the hock joints. In the most severe cases, viral arthritis has caused the tendon to rupture. Chickens that have contracted runting-stunting syndrome cause a number of individuals in a flock to appear noticeably small due to its delayed growth. Diseased chicks are typically pale, dirty, wet, and may have a distending abdomen. Some individuals may display “helicopter-like” feathers in their wings and other feather abnormalities. The virus has also been shown to cause osteoporosis.

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.

Coccidiosis is a significant disease for chickens, especially affecting the young chicks. It can be fatal or leave the bird with compromised digestion. There are chick feed mixes that contain a coccidiostat to manage exposure levels and control disease. In an outbreak, coccidiocidal medications are given. Examples are toltrazuril (Baycox) or amprolium. After multiple infections, surviving chickens become resistant to the coccidia.

Although infection of avian reovirus is spread worldwide, it is rarely the sole cause of a disease. For chickens, the most common manifestation of the disease is joint/limb lameness. Confirming infection of avian reovirus can be detected through an ELISA test by using and observing the expression of σC and σB proteins. However, isolating and identifying reoviruses from tissue samples is very time consuming. Isolation is most successfully attained through inoculation of material into chick embryo cultures or fertile chicken eggs. Inoculation of embryonic eggs through the yolk sac has shown that the virus usually kills the embryos within 5 or 6 days post inoculation. Analyzing the samples, the embryos appeared hemorrhagic and necrotic lesions on the liver were present. (Jones, Onunkwo, 1978). There have also been approaches to identify avian reoviruses molecularly by observing infected tissues with dot-blot hybridization, PCR, and a combination of PCR and RFLP. This combination allows for the reovirus strain to be typed.

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.

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.

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.

Swine vesicular disease is most commonly brought into a herd by the introduction of a subclinically infected pig.

The disease can be transmitted in feed containing infected meat scraps, or by direct contact with infected feces (such as in an improperly cleaned truck).

The most common medications used to treat coccidian infections are in the sulfonamide antibiotic family.

Depending on the pathogen and the condition of the animal, untreated coccidiosis may clear of its own accord, or become severe and damaging, and sometimes cause death.

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.

Morbidity and mortality range from both extremes as the significance correlate with the underlying systemic 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.

Mortality is indirect and caused by complications. After cholangitis occurs, patients typically die within 5–10 years.

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.

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

The majority of people survive measles, though in some cases, complications may occur. Possible consequences of measles virus infection include bronchitis, sensorineural hearing loss, and—in about 1 in 10,000 to 1 in 300,000 cases—panencephalitis, which is usually fatal. Acute measles encephalitis is another serious risk of measles virus infection. It typically occurs two days to one week after the breakout of the measles rash and begins with very high fever, severe headache, convulsions and altered mentation. A person with measles encephalitis may become comatose, and death or brain injury may occur.

There seems to be beneficial responses to clindamycin therapy as the lesions regress. This leads to the hypothesis that microorganisms may be playing a role in the initial stages of Kyrle disease.

A family with Kyrle disease were examined which their skin lesions were benign. However, when three of the young adult members were closely examined, they had posterior subcapsular cataracts and two of those three developed multiple tiny yellow-brown anterior stromal corneal opacities. In order to determine if there is any correlation between Kyrle disease and the ocular observations, more cases of Kyrle disease are to be analyzed.

All in all, since Kyrle disease is relatively rare, more cases need to be studied and analyzed in order to understand the underlying pathogenesis and to improve the management of the disease.

Pressure ulcers can trigger other ailments, cause considerable suffering, and can be expensive to treat. Some complications include autonomic dysreflexia, bladder distension, bone infection, pyarthroses, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation (Marjolin's ulcer - secondary carcinomas in chronic wounds). Sores may recur if those with pressure ulcers do not follow recommended treatment or may instead develop seromas, hematomas, infections, or wound dehiscence. Paralyzed individuals are the most likely to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from kidney failure and amyloidosis.

Pressure ulcers are also painful, with individuals of all ages and all stages of pressure ulcers reporting pain.

Extramammary Paget's disease is usually seen in isolation and is associated with an underlying invasive malignancy about 12% of the time. It is associated with an underlying adnexal malignancy about 24% of the time. Paget's disease of the breast is almost always associated with an underlying invasive malignancy, i.e. breast cancer (e.g. mammary ductal carcinoma).

As of November 2013, no identifiable cause for the disease had been found. Pathogenic bacteria did not seem to be present, and though the plague might be caused by a viral or fungal pathogen, no causal agent had been found. Each episode of plague might have a different cause.

Other possible causes of the condition that have been suggested include high sea temperatures, oxygen depletion and low salinity due to freshwater runoff. Research suggests that high water temperatures are indeed linked to the disease, increasing its incidence and virulence. The disease also seems more prevalent in sheltered waters than in open seas with much wave movement. One result of global warming is higher sea temperatures. There is a wave of unusually warm water along the west coast of the United States, which is where all of the sea stars are dying off. These may impact both on starfish and on echinoderm populations in general, and a ciliate protozoan parasite ("Orchitophrya stellarum") of starfish, which eats sperm and effectively emasculates male starfish, thrives at higher temperatures.

Research in 2014 showed that the cause of the disease is transmissible from one starfish to another and that the disease-causing agent is a microorganism in the virus-size range. The most likely candidate causal agent was found to be the sea star-associated densovirus (SSaDV), which was found to be in greater abundance in diseased starfish than in healthy ones.