Splenomegaly is a condition of the spleen causing it to be enlarged. The splenic condition involving Felty syndrome is more specifically noted as "inflammatory" splenomegaly. The spleen is an important lymphatic organ that is involved in filtration of the blood by discarding old and damaged red blood cells as well as maintaining platelet levels. The spleen is a lymphatic organ, which means it is largely involved in the immune system and immune responses. When the spleen becomes enlarged, it is a strong sign of infection somewhere in the body, and can be caused by inflammatory conditions such as rheumatoid arthritis. The increased need for production assistance of white blood cells to affected areas causes hyperfunction of the spleen. This increase in defense activities ultimately causes hypertrophy of the spleen, leading to splenomegaly. The spleen is found in the left upper quadrant (LUQ) of the peritoneal cavity and due to its enlargement, can cause stress on neighboring organs.

There is no real treatment for Felty's syndrome, rather the best method in management of the disease is to control the underlying rheumatoid arthritis. Immunosuppressive therapy for RA often improves granulocytopenia and splenomegaly; this finding reflects the fact that Felty's syndrome is an immune-mediated disease. A major challenge in treating FS is recurring infection caused by neutropenia. Therefore, in order to decide upon and begin treatment, the cause and relationship of neutropenia with the overall condition must be well understood. Most of the traditional medications used to treat RA have been used in the treatment of Felty's syndrome. No well-conducted, randomized, controlled trials support the use of any single agent. Most reports on treatment regimens involve small numbers of patients.

Splenectomy may improve neutropenia in severe disease.

Use of rituximab and leflunomide have been proposed.

Use of gold therapy has also been described.

Prognosis is dependent on the severity of symptoms and the patient's overall health.

SFTS virus (SFTSV) is a Phlebovirus in the family of "Bunyaviridae". The transmission route of SFTSV is unknown, but person-to-person transmission either plays no role or at least is not an important route of transmission of SFTSV.

The life cycle of the SFTSV most likely involves arthropod vectors and animal hosts. Humans appear to be accidental hosts and play no role in the life cycle of the SFTSV. SFTSV has been detected in "Haemaphysalis longicornis" ticks.

Due to the difficulty of exploring host and amebic factors involved in the pathogenesis of amebic liver abscess in humans, most studies have been conducted with animal models (e.g., mice, gerbils, and hamsters). Histopathological findings revealed that the chronic phase of amebic liver abscess in humans corresponds to lytic or liquefactive necrosis, whereas in rodent models there is granulomatous inflammation. However, the use of animal models has provided important information on molecules and mechanisms of the host/parasite interaction in amebic liver abscess.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease recently discovered in northeast and central China. SFTS has fatality rates ranging from 12% to as high as 30% in some areas. The major clinical symptoms of SFTS are fever, vomiting, diarrhea, multiple organ failure, thrombocytopenia (low platelet count), leucopenia (low white blood cell count), and elevated liver enzyme levels.

Treatment must also include a lumenal amoebicide to prevent reinvasion of tissues by amoebae still in the intestines (see Amoebiasis). After completion of treatment with tissue amebicides, administer luminal amebicides for eradication of the asymptomatic colonization state. Failure to use luminal agents can lead to relapse of infection in approximately 10% of patients.

To date, the precise causative factor has not been verified, and the disease has been attributed by various sources to viruses, parasites, bacteria, use of antibiotics and sulfonamides, and heavy metal poisoning. Other possible causes include peracute salmonellosis, clostridial enterocolitis, and endotoxemia. "Clostridium difficile" toxins isolated in the horse have a genotype like the current human "epidemic strain", which is associated with human "C. difficile"-associated disease of greater than historical severity. "C. difficile" can cause pseudomembranous colitis in humans, and in hospitalized patients who develop it, fulminant "C. difficile" colitis is a significant and increasing cause of death.

Horses under stress appear to be more susceptible to developing colitis X. Disease onset is often closely associated with surgery or transport. Excess protein and lack of cellulose content in the diet (a diet heavy on grain and lacking adequate hay or similar roughage) is thought to be the trigger for the multiplication of clostridial organisms. A similar condition may be seen after administration of tetracycline or lincomycin to horses. These factors may be one reason the condition often develops in race horses, having been responsible for the deaths of the Thoroughbred filly Landaluce,

the Quarter Horse stallion Lightning Bar,

and is one theory for the sudden death of Kentucky Derby winner Swale.

The link to stress suggests the condition may be brought on by changes in the microflora of the cecum and colon that lower the number of anaerobic bacteria, increase the number of Gram-negative enteric bacteria, and decrease anaerobic fermentation of soluble carbohydrates, resulting in damage to the cecal and colonic mucosa and allowing increased absorption of endotoxins from the lumen of the gut.

The causative agent may be "Clostridium perfringens", type A, but the bacteria are recoverable only in the preliminary stages of the disease.

The suspect toxin could also be a form of "Clostridium difficile". In a 2009 study at the University of Arizona, "C. difficile" toxins A and B were detected, large numbers of "C. difficile" were isolated, and genetic characterization revealed them to be North American pulsed-field gel electrophoresis type 1, polymerase chain reaction ribotype 027, and toxinotype III. Genes for the binary toxin were present, and toxin negative-regulator tcdC contained an 18-bp deletion. The individual animal studied in this case was diagnosed as having peracute typhlocolitis, with lesions and history typical of those attributed to colitis X.

Use of antibiotics may also be associated with some forms of colitis-X. In humans, "C. difficile" is the most serious cause of antibiotic-associated diarrhea, often a result of eradication of the normal gut flora by antibiotics. In one equine study, colitis was induced after pretreatment with clindamycin and lincomycin, followed by intestinal content from horses which had died from naturally occurring idiopathic colitis. (A classic adverse effect of clindamycin in humans is "C. difficile"-associated diarrhea.) In the experiment, the treated horses died. After necropsy, "Clostridium cadaveris" was present, and is proposed as another possible causative agent in some cases of fatal colitis.

This depends on the age of the animal affected and the efficiency of its immune system.

Colostral protection lasts up to 5 months of age, after which it decreases to an all-time low to increase yet again at about 12 months of age.

- Prenatal infection: virus travels from infected mother to fetus via the placenta. In this case, the time of gestation determines the result of the infection.

- If the fetus is infected in the first 30 days of fetal life, death and absorption of all, or some of the fetuses may occur. In this case, some immunotolerant healthy piglets may be born.

- If the infection happens at 40 days, death and mummification may occur. Also in this case, some or all the fetuses are involved, i.e. some of the fetuses can be born healthy and immunotolerant, or else carriers of the disease.

- If the viruses crosses the placenta in the last trimester, neonatal death may occur, or the birth of healthy piglets with a protective pre-colostral immunity.

- Postnatal infection (pigs up to 1 year of age): Infection occurs oro-nasally, followed by a viremic period associated with transitory leucopenia.

- Infection in adults (over 1 year of age): These subject would have an active, protective immune system which protects them from future exposures (e.g. mating with an infected male).

Therefore, it is important to note that the virus is particularly dangerous for the sow in her first gestation, which would be at 7–8 months of age, as she would have a particularly low antibody count at this age and could easily contract the virus via copulation.

Colitis X, equine colitis X or peracute toxemic colitis is a catchall term for various fatal forms of acute or peracute colitis found in horses, but particularly a fulminant colitis where clinical signs include sudden onset of severe diarrhea, abdominal pain, shock, and dehydration. Death is common, with 90% to 100% mortality, usually in less than 24 hours. The causative factor may be "Clostridium difficile", but it also may be caused by other intestinal pathogens. Horses under stress appear to be more susceptible to developing colitis X, and like the condition pseudomembranous colitis in humans, there also is an association with prior antibiotic use. Immediate and aggressive treatment can sometimes save the horse, but even in such cases, 75% mortality is considered a best-case scenario.

SMEDI (an acronym of stillbirth, mummification, embryonic death, and infertility) is a reproductive disease of swine caused by "Porcine parvovirus" ("PPV") and "Porcine enterovirus". The term SMEDI usually indicates "Porcine enterovirus", but it also can indicate "Porcine parvovirus", which is a more important cause of the syndrome. SMEDI also causes abortion, neonatal death, and decreased male fertility.

From an economic standpoint SMEDI is an important disease because of the loss of productivity from fetal death in affected herds. Initial infection of a herd causes the greatest effect, but losses slow over time. The disease is spread most commonly by ingestion of food and water contaminated with infected feces and occasionally through sexual contact and contact with aborted tissue. A vaccine is available (ATCvet code: ).

The disease develops from March to September, with the highest infections occurring in June. The disease is found almost exclusively in the western United States and Canada, mostly in high mountain areas such as Colorado and Idaho. The CTFV was first isolated from human blood in 1944.

No specific treatment for CTF is yet available. The first action is make sure the tick is fully removed from the skin, then acetaminophen and analgesics can be used to help relieve the fever and pain. Aspirin is not recommended for children, as it has been linked to Reye’s syndrome in some viral illnesses. Salicylates should not be used because of thrombocytopenia, and the rare occurrence of bleeding disorders. People who suspect they have been bitten by a tick or are starting to show signs of CTF should contact their physicians immediately.

Brucellosis in humans is usually associated with the consumption of unpasteurized milk and soft cheeses made from the milk of infected animals, primarily goats, infected with "Brucella melitensis" and with occupational exposure of laboratory workers, veterinarians, and slaughterhouse workers. Some vaccines used in livestock, most notably "B. abortus" strain 19, also cause disease in humans if accidentally injected. Brucellosis induces inconstant fevers, miscarriage, sweating, weakness, anaemia, headaches, depression, and muscular and bodily pain. The other strains, "B. suis" and "B. canis", cause infection in pigs and dogs, respectively.

The mortality of the disease in 1909, as recorded in the British Army and Navy stationed in Malta, was 2%. The most frequent cause of death was endocarditis. Recent advances in antibiotics and surgery have been successful in preventing death due to endocarditis. Prevention of human brucellosis can be achieved by eradication of the disease in animals by vaccination and other veterinary control methods such as testing herds/flocks and slaughtering animals when infection is present. Currently, no effective vaccine is available for humans. Boiling milk before consumption, or before using it to produce other dairy products, is protective against transmission via ingestion. Changing traditional food habits of eating raw meat, liver, or bone marrow is necessary, but difficult to implement. Patients who have had brucellosis should probably be excluded indefinitely from donating blood or organs. Exposure of diagnostic laboratory personnel to "Brucella" organisms remains a problem in both endemic settings and when brucellosis is unknowingly imported by a patient. After appropriate risk assessment, staff with significant exposure should be offered postexposure prophylaxis and followed up serologically for six months. Recently published experience confirms that prolonged and frequent serological follow-up consumes significant resources without yielding much information, and is burdensome for the affected staff, who often fail to comply. The side effects of the usual recommended regimen of rifampicin and doxycycline for three weeks also reduce treatment adherence. As no evidence shows treatment with two drugs is superior to monotherapy, British guidelines now recommend doxycycline alone for three weeks and a less onerous follow-up protocol.