Cats and dogs can acquire the disease from the bite of a tick or flea that has fed on an infected host, such as a rabbit or rodent. For treatment of infected cats, antibiotics are the preferred treatment, including tetracycline, chloramphenicol or streptomycin. Long treatment courses may be necessary as relapses are common.

The following steps and precautions should be used to avoid infection of the septicemic plague:

- Caregivers of infected patients should wear masks, gloves, goggles and gowns

- Take antibiotics if close contact with infected patient has occurred

- Use insecticides throughout house

- Avoid contact with dead rodents or sick cats

- Set traps if mice or rats are present around the house

- Do not allow family pets to roam in areas where plague is common

- Flea control and treatment for animals (especially rodents)

There are no safe, available, approved vaccines against tularemia. However, vaccination research and development continues, with live attenuated vaccines being the most thoroughly researched and most likely candidate for approval. Sub-unit vaccine candidates, such as killed-whole cell vaccines, are also under investigation, however research has not reached a state of public use.

Optimal preventative practices include limiting direct exposure when handling potentially infected animals, such as wearing gloves and face masks while handling potentially infected animals (importantly when skinning deceased animals).

If diagnosed in time, the various forms of plague are usually highly responsive to antibiotic therapy. The antibiotics often used are streptomycin, chloramphenicol and tetracycline. Amongst the newer generation of antibiotics, gentamicin and doxycycline have proven effective in monotherapeutic treatment of plague.

The plague bacterium could develop drug-resistance and again become a major health threat. One case of a drug-resistant form of the bacterium was found in Madagascar in 1995. Further outbreaks in Madagascar were reported in November 2014 and October 2017.

Since human plague is rare in most parts of the world, routine vaccination is not needed other than for those at particularly high risk of exposure, nor for people living in areas with enzootic plague, meaning it occurs at regular, predictable rates in populations and specific areas, such as the western United States. It is not even indicated for most travellers to countries with known recent reported cases, particularly if their travel is limited to urban areas with modern hotels. The CDC thus only recommends vaccination for: (1) all laboratory and field personnel who are working with "Y. pestis" organisms resistant to antimicrobials; (2) people engaged in aerosol experiments with "Y. pestis"; and (3) people engaged in field operations in areas with enzootic plague where preventing exposure is not possible (such as some disaster areas).

A systematic review by the Cochrane Collaboration found no studies of sufficient quality to make any statement on the efficacy of the vaccine.

Starting antibiotics early is a first step in treating septicemic plague in humans. One of the following antibiotics may be used:

- Streptomycin

- Gentamicin

- Tetracycline or doxycycline

- Chloramphenicol

- Ciprofloxacin

Lymph nodes may require draining and the patient will need close monitoring.

In animals, antibiotics such as tetracyline or doxycycline can be used. Intravenous drip may be used to assist in dehydration scenarios. Flea treatment can also be used. In some cases euthanasia may be the best option for treatment and to prevent further spreading.

Several classes of antibiotics are effective in treating bubonic plague. These include aminoglycosides such as streptomycin and gentamicin, tetracyclines (especially doxycycline), and the fluoroquinolone ciprofloxacin. Mortality associated with treated cases of bubonic plague is about 1–15%, compared to a mortality of 40–60% in untreated cases.

People potentially infected with the plague need immediate treatment and should be given antibiotics within 24 hours of the first symptoms to prevent death. Other treatments include oxygen, intravenous fluids, and respiratory support. People who have had contact with anyone infected by pneumonic plague are given prophylactic antibiotics. Using the broad-based antibiotic streptomycin has proven to be dramatically successful against the bubonic plague within 12 hours of infection.

Pneumonic plague is a very aggressive infection requiring early treatment. Antibiotics must be given within 24 hours of first symptoms to reduce the risk of death. Streptomycin, gentamicin, tetracyclines and chloramphenicol are all effective against pneumonic plague.

Antibiotic treatment for seven days will protect people who have had direct, close contact with infected patients. Wearing a close-fitting surgical mask also protects against infection.

The mortality rate from untreated pneumonic plague approaches 100%.

Sylvatic plague is most commonly found in prairie dog colonies; the flea that feeds on prairie dogs (and other mammals) serves as the vector for transmission to the new host.

Sylvatic plague is primarily transmitted among wildlife through flea bites and contact with contaminated fluids or tissue, through predation or scavenging. Humans can contract plague from wildlife through flea bites and handling animal carcasses.

The first recorded epidemic affected the Eastern Roman Empire (Byzantine Empire) and was named the Plague of Justinian after emperor Justinian I, who was infected but survived through extensive treatment.

In 1977, a disease of scleractinian corals appeared on reefs off the Florida Keys in the United States and was termed white plague. It caused white lesions and was shown to be an infectious disease, being particularly prevalent in "Mycetophyllia ferox". This disease caused little mortality and occurred sporadically, but was still present in the area in 1984. It is now known as white plague type 1.

In 1995, a new coral disease was described as an epizootic disease in the same reefs in the Florida Keys. Many species of coral found in the area were affected and the mortality rate of these was up to 38%. The pathogen involved was found to be a previously unknown species of bacterium in the order Rhizobiales, which was placed in the newly created genus "Aurantimonas" and given the name "Aurantimonas coralicida", and the disease was described as white plague type 2. The pathogen was isolated from a diseased colony of "Dichocoenia stokesi" and cultured in the laboratory, subsequently being used to inoculate two healthy colonies which then developed the disease. In the next few months, it had spread over of reef and was killing seventeen species of coral. Over the next four years, it spread further, but interestingly, was most severe in different regions each year.

However, white plague is an enigmatic disease. Further research cast into doubt the role of "A. coralicida" as a causative agent by finding that bacterium on healthy parts of colonies of "Orbicella annularis" affected by white plague disease but absent from diseased parts. In these diseased colonies, an α-proteobacterium similar to one which causes a disease in juvenile oysters has been implicated, being found on the diseased parts of the coral but not on the sound tissues. These anomalous findings may be caused by the fact that there are two or more diseases with similar symptoms, both known as white plague.

In 1999, a third and still more virulent variant appeared in the northern Florida Keys. White plague type III mostly affected "Colpophyllia natans" and "Orbicella annularis".

A white-plague like disease reported from the Red Sea in 2005 has been shown to be caused by a different bacterial pathogen, "Thalassomonas loyana". Further research has shown that viruses may be involved in white plague infections, the coral small circular ssDNA viruses (SCSDVs) being present in association with diseased tissue. This group of viruses is known to cause disease in plants and animals.

Common vectors for urban plague are house mice, black rats, and Norway rats.

White plague is a suite of coral diseases of which three types have been identified, initially in the Florida Keys. They are infectious diseases but it has proved difficult to identify the pathogens involved. White plague type II may be caused by the gram negative bacterium "Aurantimonas coralicida" in the order Rhizobiales but other bacteria have also been associated with diseased corals and viruses may also be implicated.

Crayfish plague first arrived in Europe in Italy in 1859, either with imported crayfish from North America, or in ballast water. After its original introduction in Italy in 1860, it spread quickly through Europe and was discovered in Sweden in 1907, in Spain in 1972, in Norway in 1971, in Great Britain in 1981, in Turkey in 1984 and in Ireland in 1987.

In 1959, to bolster dwindling stocks of native crayfish, the signal crayfish was introduced to Sweden. The signal crayfish was known to be resistant, and it was not recognised at that time that it was a carrier of the disease. After 150 years of contact, no resistance has been discovered in native European crayfish.

This species was studied and named by the German Mycologist, Friedrich Schikora (1859–1932), from a type specimen in Germany in 1906.

Contagious bovine pleuropneumonia (CBPP - also known as lung plague), is a contagious bacterial disease that afflicts the lungs of cattle, buffalo, zebu, and yaks.

It is caused by the bacterium "Mycoplasma mycoides", and the symptoms are pneumonia and inflammation of the lung membranes. The incubation period is 20 to 123 days. It was particularly widespread in the United States in 1879, affecting herds from several states. The outbreak was so severe that it resulted in a trade embargo by the British government, blocking U.S. cattle exports to Britain and Canada. This prompted the United States to establish the Bureau of Animal Industry, set up in 1884 to eradicate the disease, which it succeeded in doing by 1892.

Louis Willems, a Belgian doctor, began pioneering work in the 1850s on animal inoculation against the disease.

The bacteria are widespread in Africa, the Middle East, Southern Europe, as well as parts of Asia. It is an airborne species, and can travel up to several kilometres in the right conditions.

Urban plague is an infectious disease among rodent species that live in close association with humans in urban areas. It is caused by the bacterium Yersinia pestis which is the same bacterium that causes bubonic and pneumonic plague in humans. Plague was first introduced into the United States in 1900 by rat–infested steamships that had sailed from affected areas, mostly from Asia. Urban plague spread from urban rats to rural rodent species, especially among prairie dogs in the western United States.

Since 2002, the World Health Organization (WHO) has reported seven plague outbreaks, though some may go unreported because they often happen in remote areas. Between 1998 and 2009, nearly 24,000 cases have been reported, including about 2,000 deaths, in Africa, Asia, the Americas, and Eastern Europe. Ninety-eight percent of the world's cases occur in Africa.

The infection is treated with antibiotics. Intravenous fluids and oxygen may be needed to stabilize the patient. There is a significant disparity between the untreated mortality and treated mortality rates: 10-60% untreated versus close to 0% treated with antibiotics within 8 days of initial infection. Tetracycline, Chloramphenicol, and doxycycline are commonly used. Infection can also be prevented by vaccination.

Some of the simplest methods of prevention and treatment focus on preventing infestation of body lice. Complete change of clothing, washing the infested clothing in hot water, and in some cases also treating recently used bedsheets all help to prevent typhus by removing potentially infected lice. Clothes also left unworn and unwashed for 7 days also cause both lice and their eggs to die, as they have no access to their human host. Another form of lice prevention requires dusting infested clothing with a powder consisting of 10% DDT, 1% malathion, or 1% permethrin, which kill lice and their eggs.

Crayfish plague, "Aphanomyces astaci", is a water mold that infects crayfish, most notably the European "Astacus" which dies within a few weeks of being infected. When experimentally tested, species from Australia, New Guinea and Japan were also found to be susceptible to the infection.

As the infection is usually transmitted into humans through animal bites, antibiotics usually treat the infection, but medical attention should be sought if the wound is severely swelling. Pasteurellosis is usually treated with high-dose penicillin if severe. Either tetracycline or chloramphenicol provides an alternative in beta-lactam-intolerant patients. However, it is most important to treat the wound.

Rinderpest (also cattle plague or steppe murrain) was an infectious viral disease of cattle, domestic buffalo, and many other species of even-toed ungulates, including buffaloes, large antelope and deer, giraffes, wildebeests, and warthogs. The disease was characterized by fever, oral erosions, diarrhea, lymphoid necrosis, and high mortality. Death rates during outbreaks were usually extremely high, approaching 100% in immunologically naïve populations. Rinderpest was mainly transmitted by direct contact and by drinking contaminated water, although it could also be transmitted by air. After a global eradication campaign, the last confirmed case of rinderpest was diagnosed in 2011.

On 14 October 2010, the United Nations Food and Agriculture Organization (FAO) announced that field activities in the decades-long, worldwide campaign to eradicate the disease were ending, paving the way for a formal declaration in June 2011 of the global eradication of rinderpest. On 25 May 2011, the World Organisation for Animal Health announced the free status of the last eight countries not yet recognized (a total of 198 countries were now free of the disease), officially declaring the eradication of the disease. In June 2011, the United Nations FAO confirmed the disease was eradicated, making rinderpest only the second disease in history to be fully wiped out (outside laboratory stocks), following smallpox.

Rinderpest is believed to have originated in Asia, later spreading through the transport of cattle. The term "Rinderpest" is a German word meaning "cattle-plague". The rinderpest virus (RPV) was closely related to the measles and canine distemper viruses. The measles virus emerged from rinderpest as a zoonotic disease between 1000 and 1100 AD, a period that may have been preceded by limited outbreaks involving a virus not yet fully acclimated to humans.

Rinderpest virus (RPV), a member of the genus "Morbillivirus", is closely related to the measles and canine distemper viruses. Like other members of the "Paramyxoviridae" family, it produces enveloped virions, and is a negative-sense single-stranded RNA virus. The virus was particularly fragile and is quickly inactivated by heat, desiccation and sunlight.

Measles virus evolved from the then-widespread rinderpest virus most probably between the 11th and 12th centuries. The earliest likely origin is during the seventh century; some linguistic evidence exists for this earlier origin.

Currently, no vaccine against relapsing fever is available, but research continues. Developing a vaccine is very difficult because the spirochetes avoid the immune response of the infected person (or animal) through antigenic variation. Essentially, the pathogen stays one step ahead of antibodies by changing its surface proteins. These surface proteins, lipoproteins called variable major proteins, have only 30–70% of their amino acid sequences in common, which is sufficient to create a new antigenic "identity" for the organism. Antibodies in the blood that are binding to and clearing spirochetes expressing the old proteins do not recognize spirochetes expressing the new ones. Antigenic variation is common among pathogenic organisms. These include the agents of malaria, gonorrhea, and sleeping sickness. Important questions about antigenic variation are also relevant for such research areas as developing a vaccine against HIV and predicting the next influenza pandemic.

Feeding on a human who carries the bacterium infects the louse. "R. prowazekii" grows in the louse's gut and is excreted in its feces. The disease is then transmitted to an uninfected human who scratches the louse bite (which itches) and rubs the feces into the wound. The incubation period is one to two weeks. "R. prowazekii" can remain viable and virulent in the dried louse feces for many days. Typhus will eventually kill the louse, though the disease will remain viable for many weeks in the dead louse.

Epidemic typhus has historically occurred during times of war and deprivation. For example, typhus killed hundreds of thousands of prisoners in Nazi concentration camps during World War II. The deteriorating quality of hygiene in camps such as Auschwitz, Theresienstadt, and Bergen-Belsen created conditions where diseases such as typhus flourished. Situations in the twenty-first century with potential for a typhus epidemic would include refugee camps during a major famine or natural disaster. In the periods between outbreaks, when human to human transmission occurs less often, the flying squirrel serves as a zoonotic reservoir for the "Rickettsia prowazekii" bacterium.

Henrique da Rocha Lima in 1916 then proved that the bacterium "Rickettsia prowazekii" was the agent responsible for typhus; he named it after H. T. Ricketts and Stanislaus von Prowazek, two zoologists who had died from typhus while investigating epidemics. Once these crucial facts were recognized, Rudolf Weigl in 1930 was able to fashion a practical and effective vaccine production method by grinding up the insides of infected lice that had been drinking blood. It was, however, very dangerous to produce, and carried a high likelihood of infection to those who were working on it.

A safer mass-production-ready method using egg yolks was developed by Herald R. Cox in 1938. This vaccine was widely available and used extensively by 1943.