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.

Some fish species serve as vectors for the disease and have subsequently spread the pathogen to other parts of the world. An example is the fathead minnow ("Pimephales promelas") which is responsible for the spread of redmouth disease to trout in Europe. Other vectors include the goldfish ("Carassius auratus"), Atlantic and Pacific salmon ("Salmo salar"), the emerald shiner ("Notropis atherinoides"), and farmed whitefish ("Coregonus" spp.). Infections have also occurred in farmed turbot ("Scophthalmus maximus"), seabass ("Dicentrarchus labrax"), and seabream ("Sparus auratus"). It can now be found in North and South America, Africa, Asia, and Australia, as well as Europe.

Enteric redmouth disease, or simply redmouth disease is a bacterial infection of freshwater and marine fish caused by the pathogen "Yersinia ruckeri". It is primarily found in rainbow trout ("Oncorhynchus mykiss") and other cultured salmonids. The disease is characterized by subcutaneous hemorrhaging of the mouth, fins, and eyes. It is most commonly seen in fish farms with poor water quality. Redmouth disease was first discovered in Idaho rainbow trout in the 1950s. The disease does not infect humans.

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 .

Humans contract "Blastocystis" infection by drinking water or eating food contaminated with feces from an infected human or animal. "Blastocystis" infection can be spread from animals to humans, from humans to other humans, from humans to animals, and from animals to animals. Risk factors for infection have been reported as following:

- International travel: Travel to less developed countries has been cited in development of symptomatic Blastocystis infection. A 1986 study in the United States found that all individuals symptomatically infected with "Blastocystis" reported recent travel history to less developed countries. In the same study, all hospital employees working in New York who were screened for "Blastocystis" were found to have asymptomatic infections.

- Military service: Several studies have identified high rates of infection in military personnel. An early account described infection of British troops in Egypt in 1916 who recovered following treatment with emetine. A 1990 study published in "Military Medicine" from Lackland AFB in Texas concluded symptomatic infection was more common in foreign nationals, children, and immunocompromised individuals. A 2002 study published in "Military Medicine" of army personnel in Thailand identified a 44% infection rate. Infection rates were highest in privates who had served the longest at the army base. A follow-up study found a significant correlation between infection and symptoms, and identified the most likely cause as contaminated water. A 2007 newspaper article suggested the infection rate of US military personnel returning from the Gulf War was 50%, quoting the head of Oregon State University's Biomedicine department.

- Consumption of Untreated Water (well water): Many studies have linked "Blastocystis" infection with contaminated drinking water. A 1993 study of children infected symptomatically with "Blastocystis" in Pittsburgh indicated that 75% of them had a history of drinking well water or travel in less developed countries. Two studies in Thailand linked "Blastocystis" infection in military personnel and families to drinking of unboiled and untreated water. A book published in 2006 noted that in an Oregon community, infections are more common in winter months during heavy rains. A research study published in 1980 reported bacterial contamination of well water in the same community during heavy rainfall. A 2007 study from China specifically linked infection with "Blastocystis sp. subtype 3" with drinking untreated water. Recreational contact with untreated water, for example though boating, has also been identified as a risk factor. Studies have shown that "Blastocystis" survives sewage treatment plants in both the United Kingdom and Malaysia. "Blastocystis" cysts have been shown to be resistant to chlorination as a treatment method and are among the most resistant cysts to ozone treatment.

- Contaminated Food: Contamination of leafy vegetables has been implicated as a potential source for transmission of "Blastocystis" infection, as well as other gastrointestinal protozoa. A Chinese study identified infection with "Blastocystis sp. subtype 1" as specifically associated with eating foods grown in untreated water.

- Daycare facilities: A Canadian study identified an outbreak of "Blastocystis" associated with daycare attendance. Prior studies have identified outbreaks of similar protozoal infections in daycares.

- Geography: Infection rates vary geographically, and variants which produce symptoms may be less common in industrialized countries. For example, a low incidence of "Blastocystis" infection has been reported in Japan. A study of individuals infected with "Blastocystis" in Japan found that many (43%, 23/54) carried "Blastocystis sp. subtype 2", which was found to produce no symptoms in 93% (21/23) of patients studied, in contrast to other variants which were less common but produced symptoms in 50% of Japanese individuals. Studies in urban areas of industrialized countries have found "Blastocystis" infection associated with a low incidence of symptoms. In contrast, studies in developing countries generally show "Blastocystis" to be associated with symptoms. In the United States, a higher incidence of "Blastocystis" infection has been reported in California and West Coast states.

- Prevalence over Time: A 1989 study of the prevalence of "Blastocystis" in the United States found an infection rate of 2.6% in samples submitted from all 48 states. The study was part of the CDC's MMWR Report. A more recent study, in 2006, found an infection rate of 23% in samples submitted from all 48 states. However, the more recent study was performed by a private laboratory located in the Western US, and emphasized samples from Western states, which have previously been reported to have a higher infection rate.

Research studies have suggested the following items are not risk factors for contracting "Blastocystis" infection:

- Consumption of municipal water near water plant (not a risk factor): One study showed that municipal water was free of "Blastocystis", even when drawn from a polluted source. However, samples taken far away from the treatment plant showed cysts. The researchers suggested that aging pipes may permit intrusion of contaminated water into the distribution system.

- Human-to-Human transmission among adults (not a risk factor): Some research suggests that direct human-to-human transmission is less common even in households and between married partners. One study showed different members of the same household carried different subtypes of Blastocystis.

Experimental infection in immunocompetent and immunocompromised mice has produced intestinal inflammation, altered bowel habits, lethargy and death. Chronic diarrhea has been reported in non-human higher primates.

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

Simple precautions can be taken to prevent getting shigellosis: wash hands before handling food and thoroughly cook all food before eating. The primary prevention methods are improved sanitation and personal and food hygiene, but a low-cost and efficacious vaccine would complement these methods.

Since shigellosis is spread very quickly among children, keeping infected children out of daycare for 24 hours after their symptoms have disappeared, will decrease the occurrence of shigellosis in daycares.

Bacteria with resistance to antibiotics predate medical use of antibiotics by humans. However, widespread antibiotic use has made more bacteria resistant through the process of evolutionary pressure.

Reasons for the widespread use of antibiotics in human medicine include:

- increasing global availability over time since the 1950s

- uncontrolled sale in many low or middle income countries, where they can be obtained over the counter without a prescription, potentially resulting in antibiotics being used when not indicated. This may result in emergence of resistance in any remaining bacteria.

Other causes include:

- Antibiotic use in livestock feed at low doses for growth promotion is an accepted practice in many industrialized countries and is known to lead to increased levels of resistance.

- Releasing large quantities of antibiotics into the environment during pharmaceutical manufacturing through inadequate wastewater treatment increases the risk that antibiotic-resistant strains will develop and spread.

- It is uncertain whether antibacterials in soaps and other products contribute to antibiotic resistance, but antibacterial soaps are discouraged for other reasons.

A World Health Organization (WHO) report released April 2014 stated, "this serious threat is no longer a prediction for the future, it is happening right now in every region of the world and has the potential to affect anyone, of any age, in any country. Antibiotic resistance—when bacteria change so antibiotics no longer work in people who need them to treat infections—is now a major threat to public health."

Currently, no licensed vaccine targeting "Shigella" exists. Several vaccine candidates for "Shigella" are in various stages of development including live attenuated, conjugate, ribosomal, and proteosome vaccines. "Shigella" has been a longstanding World Health Organization target for vaccine development, and sharp declines in age-specific diarrhea/dysentery attack rates for this pathogen indicate that natural immunity does develop following exposure; thus, vaccination to prevent the disease should be feasible. Shigellosis is resistant to many antibiotics used to treat the disease, so vaccination is an important part of the strategy to reduce morbidity and mortality.

The newborn`s exposure to the maternal vaginal bacterial flora which contains aerobic and anaerobic bacterial flora can lead to the development of anaerobic bacterial infection. These infections include cellulitis of the site of fetal monitoring (caused by "Bacterodes" spp.), bacteremia, aspiration pneumonia (caused by "Bacterodes" spp.), conjunctivitis (caused by clostridia,) omphalitis (caused by mixed flora), and infant botulism. Clostridial species may play a role in necrotizing enterocolitis. Management of these infection necessitates treating of the underlying condition(s) when present, and administration of proper antimicrobial therapy

Condition predisposing to anaerobic infections include: exposure of a sterile body location to a high inoculum of indigenous bacteria of mucous membrane flora origin, inadequate blood supply and tissue necrosis which lower the oxidation and reduction potential which support the growth of anaerobes. Conditions which can lower the blood supply and can predispose to anaerobic infection are: trauma, foreign body, malignancy, surgery, edema, shock, colitis and vascular disease. Other predisposing conditions include splenectomy, neutropenia, immunosuppression, hypogammaglobinemia, leukemia, collagen vascular disease and cytotoxic drugs and diabetes mellitus. A preexisting infection caused by aerobic or facultative organisms can alter the local tissue conditions and make them more favorable for the growth of anaerobes. Impairment in defense mechanisms due to anaerobic conditions can also favor anaerobic infection. These include production of leukotoxins (by "Fusobacterium" spp.), phagocytosis intracellular killing impairments (often caused by encapsulated anaerobes and by succinic acid ( produced by "Bacteroides" spp.), chemotaxis inhibition (by "Fusobacterium, Prevotella" and "Porphyromonas" spp.), and proteases degradation of serum proteins (by Bacteroides spp.) and production of leukotoxins (by "Fusobacterium" spp.).

The hallmarks of anaerobic infection include suppuration, establishment of an abscess, thrombophlebitis and gangrenous destruction of tissue with gas generation. Anaerobic bacteria are very commonly recovered in chronic infections, and are often found following the failure of therapy with antimicrobials that are ineffective against them, such as trimethoprim–sulfamethoxazole (co-trimoxazole), aminoglycosides, and the earlier quinolones.

Some infections are more likely to be caused by anaerobic bacteria, and they should be suspected in most instances. These infections include brain abscess, oral or dental infections, human or animal bites, aspiration pneumonia and lung abscesses, amnionitis, endometritis, septic abortions, tubo-ovarian abscess, peritonitis and abdominal abscesses following viscus perforation, abscesses in and around the oral and rectal areas, pus-forming necrotizing infections of soft tissue or muscle and postsurgical infections that emerge following procedures on the oral or gastrointestinal tract or female pelvic area. Some solid malignant tumors, ( colonic, uterine and bronchogenic, and head and neck necrotic tumors, are more likely to become secondarily infected with anaerobes. The lack of oxygen within the tumor that are proximal to the endogenous adjacent mucosal flora can predispose such infections.

Vaccination

There is one intra-nasal FIP vaccine available: its use is controversial but in an independent study the authors concluded that vaccination can protect cats with no or low FCoV antibody titres and that in some cats vaccine failure was probably due to pre-existing infection.

Prevention of FCoV infection, and therefore FIP, in kittens

Kittens are protected from infection by maternally derived antibody until it wanes, usually around 5–7 weeks of age, therefore it is possible to prevent infection of kittens by removing them from sources of infection. However, FCoV is a very contagious virus and such prevention does require rigorous hygiene.

Bacillary dysentery is a type of dysentery, and is a severe form of shigellosis.

Bacillary dysentery is associated with species of bacteria from the Enterobacteriaceae family. The term is usually restricted to "Shigella" infections.

Shigellosis is caused by one of several types of "Shigella" bacteria. Three species are associated with bacillary dysentery: "Shigella sonnei, Shigella flexneri" and "Shigella dysenteriae". A study in China indicated that "Shigella flexneri" 2a was the most common serotype.

Salmonellosis caused by "Salmonella enterica" (serovar "Typhimurium") has also been described as a cause of bacillary dysentery, though this definition is less common. It is sometimes listed as an explicit differential diagnosis of bacillary dysentery, as opposed to a cause.

Bacillary dysentery should not be confused with diarrhea caused by other bacterial infections. One characteristic of bacillary dysentery is blood in stool, which is the result of invasion of the mucosa by the pathogen.

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.

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.

Transmission is fecal-oral and is remarkable for the small number of organisms that may cause disease (10 ingested organisms cause illness in 10% of volunteers, and 500 organisms cause disease in 50% of volunteers). "Shigella" bacteria invade the intestinal mucosal cells but do not usually go beyond the lamina propria. Dysentery is caused when the bacteria escape the epithelial cell phagolysosome, multiply within the cytoplasm, and destroy host cells. Shiga toxin causes hemorrhagic colitis and hemolytic-uremic syndrome by damaging endothelial cells in the microvasculature of the colon and the glomeruli, respectively. In addition, chronic arthritis secondary to "S. flexneri" infection, called reactive arthritis, may be caused by a bacterial antigen; the occurrence of this syndrome is strongly linked to HLA-B27 genotype, but the immunologic basis of this reaction is not understood.

They are usually spread by eating or drinking food or water contaminated with the feces of an infected person. They may occur when a person who prepares food is infected. Risk factors include poor sanitation as is found among poor crowded populations. Occasionally they may be transmitted by sex. Humans are the only animal infected.

Bovine malignant catarrhal fever (BMCF) is a fatal lymphoproliferative disease caused by a group of ruminant gamma herpes viruses including Alcelaphine gammaherpesvirus 1 (AlHV-1) and Ovine gammaherpesvirus 2 (OvHV-2) These viruses cause unapparent infection in their reservoir hosts (sheep with OvHV-2 and wildebeest with AlHV-1), but are usually fatal in cattle and other ungulates such as deer, antelope, and buffalo.

BMCF is an important disease where reservoir and susceptible animals mix. There is a particular problem with Bali cattle in Indonesia, bison in the US and in pastoralist herds in Eastern and Southern Africa.

Disease outbreaks in cattle are usually sporadic although infection of up to 40% of a herd has been reported. The reasons for this are unknown. Some species appear to be particularly susceptible, for example Pére Davids deer, Bali cattle and bison, with many deer dying within 48 hours of the appearance of the first symptoms and bison within three days. In contrast, post infection cattle will usually survive a week or more.

Providing basic sanitation and safe drinking water and food is the key for controlling the disease. In developed countries, enteric fever rates decreased in the past when treatment of municipal water was introduced, human feces were excluded from food production, and pasteurization of dairy products began. In addition, children and adults should be carefully educated about personal hygiene. This would include careful handwashing after defecation and sexual contact, before preparing or eating food, and especially the sanitary disposal of feces. Food handlers should be educated in personal hygiene prior to handling food or utensils and equipment. Infected individuals should be advised to avoid food preparation. Sexually active people should be educated about the risks of sexual practices that permit fecal-oral contact.

Those who travel to countries with poor sanitation should receive a live attenuated typhoid vaccine—Ty21a (Vivotif), which, in addition to the protection against typhoid fever, and may provide some protection against paratyphoid fever caused by the "S. enterica" serotypes A and B. In particular, a reanalysis of data from a trial conducted in Chile showed the Ty21a vaccine was 49% effective (95% CI: 8–73%) in preventing paratyphoid fever caused by the serotype B. Evidence from a study of international travelers in Israel also indicates the vaccine may prevent a fraction of infections by the serotype A, although no trial confirms this. This cross-protection by a typhoid vaccine is most likely due to O antigens shared between different "S. enterica" serotypes.

Exclusion from work and social activities should be considered for symptomatic, and asymptomatic, people who are food handlers, healthcare/daycare staff who are involved in patient care and/or child care, children attending unsanitary daycare centers, and older children who are unable to implement good standards of personal hygiene. The exclusion applies until two consecutive stool specimens are taken from the infected patient and are reported negative.

FCoV is common in places where large groups of cats are housed together indoors (e.g. breeding catteries, animal shelters, etc.). The virus is shed in feces and cats become infected by ingesting or inhaling the virus, usually by sharing cat litter trays, or by the use of contaminated litter scoops or brushes transmitting infected microscopic cat litter particles to uninfected kittens and cats. Direct, cat-to-cat, virus transmission does not commonly occur.

Wound myiasis occurs when fly larvae infest open wounds. It has been a serious complication of war wounds in tropical areas, and is sometimes seen in neglected wounds in most parts of the world. Predisposing factors include poor socioeconomic conditions, extremes of age, neglect, mental disability, psychiatric illness, alcoholism, diabetes, and vascular occlusive disease.

The term "bovine malignant catarrhal fever" has been applied to three different patterns of disease:

- In Africa, wildebeests carry a lifelong infection of AlHV-1 but are not affected by the disease. The virus is passed from mother to offspring and shed mostly in the nasal secretions of wildebeest calves under one year old. Wildebeest associated MCF is transmitted from wildebeest to cattle normally following the wildebeest calving period. Cattle of all ages are susceptible to the disease, with a higher infection rate in adults, particularly in peripartuent females. Cattle are infected by contact with the secretions, but do not spread the disease to other cattle. Because no commercial treatment or vaccine is available for this disease, livestock management is the only method of control. This involves keeping cattle away from wildebeest during the critical calving period. This results in Massai pastoralists in Tanzania and Kenya being excluded from prime pasture grazing land during the wet season leading to a loss in productivity. In Eastern and Southern Africa MCF is classed as one of the five most important problems affecting pastoralists along with East coast fever, contagious bovine pleuropneumonia, foot and mouth disease and anthrax.Hartebeests and topi also may carry the disease. However, hartebeests and other antelopes are infected by a variant, Alcelaphine herpesvirus 2.

- Throughout the rest of the world, cattle and deer contract BMCF by close contact with sheep or goats during lambing. The natural host reservoir for Ovine herpesvirus 2 is the subfamily Caprinae (sheep and goats) whilst MCF affected animals are from the families Bovidae, Cervidae and suidae. Susceptibility to OHV-2 varies by species, with domestic cattle and zebus somewhat resistant, water buffalo and most deer somewhat susceptible, and bison, Bali cattle, and Pere David's deer very susceptible. OHV-2 viral DNA has been detected in the alimentary, respiratory and urino-genital tracts of sheep all of which could be possible transmission routes. Antibody from sheep and from cattle with BMCF is cross reactive with AlHV-1.

- AHV-1/OHV-2 can also cause problems in zoological collections, where inapparently infected hosts (wildebeest and sheep) and susceptible hosts are often kept in close proximity.

- Feedlot bison in North America not in contact with sheep have also been diagnosed with a form of BMCF. OHV-2 has been recently documented to infect herds of up to 5 km away from the nearest lambs, with the levels of infected animals proportional to the distance away from the closest herds of sheep.

The incubation period of BMCF is not known, however intranasal challenge with AHV-1 induced MCF in one hundred percent of challenged cattle between 2.5 and 6 weeks.

Shedding of the virus is greater from 6–9 month old lambs than from adults. After experimental infection of sheep, there is limited viral replication in nasal cavity in the first 24 hours after infection, followed by later viral replication in other tissues.