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.

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.

Contact with farm animals can lead to disease in farmers or others that come into contact with infected animals. Glanders primarily affects those who work closely with horses and donkeys. Close contact with cattle can lead to cutaneous anthrax infection, whereas inhalation anthrax infection is more common for workers in slaughterhouses, tanneries and wool mills. Close contact with sheep who have recently given birth can lead to clamydiosis, or enzootic abortion, in pregnant women, as well as an increased risk of Q fever, toxoplasmosis, and listeriosis in pregnant or the otherwise immunocompromised. Echinococcosis is caused by a tapeworm which can be spread from infected sheep by food or water contaminated with feces or wool. Bird flu is common in chickens. While rare in humans, the main public health worry is that a strain of bird flu will recombine with a human flu virus and cause a pandemic like the 1918 Spanish flu. In 2017, free range chickens in the UK were temporarily ordered to remain inside due to the threat of bird flu. Cattle are an important reservoir of cryptosporidiosis and mainly affects the immunocompromised.

The most significant zoonotic pathogens causing foodborne diseases are , "Campylobacter", "Caliciviridae", and "Salmonella".

In 2006, a conference held in Berlin was focusing on the issue of zoonotic pathogen effects on food safety, urging governments to intervene, and the public to be vigilant towards the risks of catching food-borne diseases from farm-to-dining table.

Many food outbreaks can be linked to zoonotic pathogens. Many different types of food can be contaminated that have an animal origin. Some common foods linked to zoonotic contaminations include eggs, seafood, meat, dairy, and even some vegetables. Food outbreaks should be handled in preparedness plans to prevent widespread outbreaks and to efficiently and effectively contain outbreaks.

The common routes of transmission for the disease-causing bacteria are fecal-oral, person-to-person sexual contact, ingestion of contaminated food (generally unpasteurized (raw) milk and undercooked or poorly handled poultry), and waterborne (i.e., through contaminated drinking water). Contact with contaminated poultry, livestock, or household pets, especially puppies, can also cause disease.

Animals farmed for meat are the main source of campylobacteriosis. A study published in PLoS Genetics (September 26, 2008) by researchers from Lancashire, England, and Chicago, Illinois, found that 97 percent of campylobacteriosis cases sampled in Lancashire were caused by bacteria typically found in chicken and livestock. In 57 percent of cases, the bacteria could be traced to chicken, and in 35 percent to cattle. Wild animal and environmental sources were accountable for just three percent of disease.

The infectious dose is 1000–10,000 bacteria (although ten to five hundred bacteria can be enough to infect humans). "Campylobacter" species are sensitive to hydrochloric acid in the stomach, and acid reduction treatment can reduce the amount of needed to cause disease.

Exposure to bacteria is often more common during travelling, and therefore campylobacteriosis is a common form of travelers' diarrhea.

In the western world, GBS (in the absence of effective prevention measures) is the main cause of bacterial infections in newborns, such as septicemia, pneumonia, and meningitis, which can lead to death or long-term after effects.

GBS infections in newborns are separated into two clinical types, early-onset disease (GBS-EOD) and late-onset disease (GBS-LOD). GBS-EOD manifests from 0 to 7 living days in the newborn, most of the cases of EOD being apparent within 24 h from birth. GBS-LOD starts between 7 and 90 days after birth.

The most common clinical syndromes of GBS-EOD are septicemia without apparent location, pneumonia, and less frequently meningitis. Bacteremia without a focus occurs in 80-85%, pneumonia in 10-15%, and meningitis in 5-10% of cases. The initial clinical findings are respiratory signs in more than 80% of cases. Neonates with meningitis often have an initial clinical presentation identical to presentation in those without meningeal affectation. An exam of the cerebrospinal fluid is often necessary to rule out meningitis.

Colonization with GBS during labour is the primary risk factor for the development of GBS-EOD. GBS-EOD is acquired vertically (vertical transmission), through exposure of the fetus or the baby to GBS from the vagina of a colonized woman, either "in utero" (because of ascending infection) or during birth, after rupture of membranes. Infants can also be infected during passage through the birth canal, nevertheless, newborns who acquire GBS through this route can only become colonized, and these colonized infants usually do not develop GBS-EOD.

Roughly 50% of newborns of GBS colonized mothers are also GBS colonized and (without prevention measures) 1-2% of these newborns will develop GBS-EOD.

In the past, the incidence of GBS-EOD ranged from 0.7 to 3.7 per thousand live births in the US, and from 0.2 to 3.25 per thousand in Europe.

In 2008, after widespread use of antenatal screening and intrapartum antibiotic prophylaxis, the Centers for Disease Control and Prevention of United States reported an incidence of 0.28 cases of GBS-EOD per thousand live births in the US.

Though maternal GBS colonization is the key determinant for GBS-EOD, other factors also increase the risk. These factors are:

- Onset of labour before 37 weeks of gestation (premature birth)

- Prolonged rupture of membranes (longer duration of membrane rupture) (≥18 h before delivery)

- Intrapartum (during childbirth) fever (>38 °C, >100.4 °F)

- Amniotic infections (chorioamnionitis)

- Young maternal age

Nevertheless, most babies who develop GBS-EOD are born to colonized mothers without any of these risk factors. Heavy GBS vaginal colonization is also associated with a higher risk for GBS-EOD. Women who had one of these risk factors but who are not GBS colonized at labour are at low risk for GBS-EOD compared to women who were colonized prenatally, but had none of the aforementioned risk factors.

Presence of low levels of anticapsular antibodies against GBS in the mother are also of great importance for the development of GBS-EOD.

Because of that, a previous sibling with GBS-EOD is also an important risk factor for the development of the infection in subsequent deliveries, probably reflecting the lack of protective antibodies in the mother.

Overall, the case fatality rates from GBS-EOD have declined, from 50% observed in studies from the 1970s to between 2 and 10% in recent years, mainly as a consequence of improvements in therapy and management. Fatal neonatal infections by GBS are more frequent among premature infants.

GBS-LOD affects infants from 7 days to 3 months of age and has a lower case fatality rate (1%-6%) than GBS-EOD. Clinical syndromes of GBS-EOD are bacteremia without a focus (65%), meningitis (25%), cellulitis, osteoarthritis, and pneumonia.

Prematurity has been reported to be the main risk factor. Each week of decreasing gestation increases the risk by a factor of 1.34 for developing GBS-LOD.

GBS-LOD is not acquired through vertical transmission during delivery; it can be acquired later from the mother from breast milk or from environmental and community sources.

GBS-LOD commonly shows nonspecific signs, and diagnosis should be made obtaining blood cultures in febrile newborns. Hearing loss and mental impairment can be a long-term consequence of GBS meningitis.

The World Health Organization recommends the following:

- Food should be properly cooked and hot when served.

- Consume only pasteurized or boiled milk and milk products, never raw milk products.

- Make sure that ice is from safe water.

- If you are not sure of the safety of drinking water, boil it, or disinfect it with chemical disinfectant.

- Wash hands thoroughly and frequently with soap, especially after using the toilet and after contact with pets and farm animals.

- Wash fruits and vegetables thoroughly, especially if they are to be eaten raw. Peel fruits and vegetables whenever possible.

- Food handlers, professionals and at home, should observe hygienic rules during food preparation.

- Professional food handlers should immediately report to their employer any fever, diarrhea, vomiting or visible infected skin lesions.

GBS is also an important infectious agent able to cause invasive infections in adults. Serious life-threatening invasive GBS infections are increasingly recognized in the elderly and in individuals compromised by underlying diseases such as diabetes, cirrhosis and cancer. GBS infections in adults include urinary tract infection, skin and soft-tissue infection (skin and skin structure infection) bacteremia without focus, osteomyelitis, meningitis and endocarditis.

GBS infection in adults can be serious, and mortality is higher among adults than among neonates.

In general, penicillin is the antibiotic of choice for treatment of GBS infections. Erythromycin or clindamycin should not be used for treatment in penicillin-allergic patients unless susceptibility of the infecting GBS isolate to these agents is documented. Gentamicin plus penicillin (for antibiotic synergy) in patients with life-threatening GBS infections may be used.

"B. suis" is a Gram-negative, facultative, intracellular coccobacillus, capable of growing and reproducing inside of host cells, specifically phagocytic cells. They are also not spore-forming, capsulated, or motile. Flagellar genes, however, are present in the "B. suis" genome, but are thought to be cryptic remnants because some were truncated and others were missing crucial components of the flagellar apparatus. Interestingly, in mouse models, the flagellum is essential for a normal infectious cycle, where the inability to assemble a complete flagellum leads to severe attenuation of the bacteria.

"B. suis" is differentiated into five biovars (strains), where biovars 1-3 infect wild boar and domestic pigs, and biovars 1 and 3 may cause severe diseases in humans.

In contrast, biovar 2 found in wild boars in Europe shows mild or no clinical signs and cannot infect healthy humans, but does infect pigs and hares.

Swine brucellosis is a zoonosis affecting pigs, caused by the bacterium "Brucella suis". The disease typically causes chronic inflammatory lesions in the reproductive organs of susceptible animals or orchitis, and may even affect joints and other organs. The most common symptom is abortion in pregnant susceptible sows at any stage of gestation. Other manifestations are temporary or permanent sterility, lameness, posterior paralysis, spondylitis, and abscess formation. It is transmitted mainly by ingestion of infected tissues or fluids, semen during breeding, and suckling infected animals.

Since brucellosis threatens the food supply and causes undulant fever, "Brucella suis" and other "Brucella" species ("B. melitensis, B. abortis, B. ovis, B. canis") are recognized as potential agricultural, civilian, and military bioterrorism agents.

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.

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.

Some disease-carrying arthropods use cats as a vector, or carrier. Fleas and ticks can carry pathogenic organisms that infect a person with Lyme disease, tick borne encephalitis, and Rocky mountain spotted fever

Ultraviolet (UV) radiation is implicated in cattle with no pigmentation around the eyelids and cattle with prominently placed eyes. Exudate from the sun-burnt skin around the eyes can contain bacteria and attracts flies. UV light also directly damages the corneal epithelium, leading to a breakdown in host innate immunity.

Dust, dried-up plants, tall vegetation, and oversized or incorrectly placed ear tags may cause mechanical damage to the eye and facilitate bacterial colonization.

The disease may be complicated by concurrent infection with viruses such as infectious bovine rhinotracheitis virus (bovine herpesvirus 1) or adenovirus, bacteria such as "Mycoplasma boviculi" or "Listeria monocytogenes", or infestation by "Thelazia", a nematode.

Vitamin A deficiency is also implicated.

IBK is most prevalent in summer and early autumn.

A recent Meat and Livestock Australia report "estimates that the disease costs Australian beef producers AU$23.5 million annually in lost production and treatment costs".

The mainstay of eradication is the identification and removal of persistently infected animals. Re-infection is then prevented by vaccination and high levels of biosecurity, supported by continuing surveillance. PIs act as viral reservoirs and are the principal source of viral infection but transiently infected animals and contaminated fomites also play a significant role in transmission.

Leading the way in BVD eradication, almost 20 years ago, were the Scandinavian countries. Despite different conditions at the start of the projects in terms of legal support, and regardless of initial prevalence of herds with PI animals, it took all countries approximately 10 years to reach their final stages.

Once proven that BVD eradication could be achieved in a cost efficient way, a number of regional programmes followed in Europe, some of which have developed into national schemes.

Vaccination is an essential part of both control and eradication. While BVD virus is still circulating within the national herd, breeding cattle are at risk of producing PI neonates and the economic consequences of BVD are still relevant. Once eradication has been achieved, unvaccinated animals will represent a naïve and susceptible herd. Infection from imported animals or contaminated fomites brought into the farm, or via transiently infected in-contacts will have devastating consequences.

Paravaccinia virus originates from livestock infected with bovine papular stomatitis. When a human makes physical contact with the livestock's muzzle, udders, or an infected area, the area of contact will become infected. Livestock may not show symptoms of bovine papular stomatitis and still be infected and contagious. Paravaccinia can enter the body though all pathways including: skin contact by mechanical means, through the respiratory tract, or orally. Oral or respiratory contraction may be more likely to cause systemic symptoms such as lesions across the whole body

A person who has not previously been infected with paravaccinia virus should avoid contact with infected livestock to prevent contraction of disease. There is no commercially available vaccination for cattle or humans against paravaccinia. However, following infection, immunization has been noted in humans, making re-infection difficult. Unlike other pox viruses, there is no record of contracting paravaccinia virus from another human. Further, cattle only show a short immunization after initial infection, providing opportunity to continue to infect more livestock and new human hosts.

Feline zoonosis are the viral, bacterial, fungal, protozoan, nematode and arthropod infections that can be transmitted to humans from the domesticated cat, "Felis catus". Some of these are diseases are reemerging and newly emerging infections or infestations caused by zoonotic pathogens transmitted by cats. In some instances, the cat can display symptoms of infection (these may differ from the symptoms in humans) and sometimes the cat remains asymptomatic. There can be serious illnesses and clinical manifestations in people who become infected. This is dependent on the immune status and age of the person. Those who live in close association with cats are more prone to these infections. But those that do not keep cats as pets are also able to acquire these infections because of the transmission can be from cat feces and the parasites that leave their bodies.

People can acquire cat-associated infections through bites, scratches or other direct contact of the skin or mucous membranes with the cat. This includes 'kissing' or letting the animal lick the mouth or nose. Mucous membranes are easily infected when the pathogen is in the mouth of the cat. Pathogens can also infect people when there is contact with animal saliva, urine and other body fluids or secretions, When fecal material is unintentionally ingested, infection can occur. Feline zooinosis can be acquired by a person by inhalation of aerosols or droplets coughed up by the cat.

In the United States, forty percent of homes have at least one cat. Some contagious infections such as campylobacteriosis and salmonellosis cause visible symptoms of the disease in cats. Other infections, such as cat scratch disease and toxoplasmosis, have no visible symptoms and are carried by apparently healthy cats.

Babesiosis is a vector-borne illness usually transmitted by "Ixodes scapularis" ticks. "B. microti" uses the same tick vector as Lyme disease, and may occur in conjunction with Lyme. The organism can also be transmitted by blood transfusion. Ticks of domestic animals, especially "Rhipicephalus (Boophilus) microplus" and "R. (B.) decoloratus" transmit several species of "Babesia" to livestock, causing considerable economic losses to farmers in tropical and subtropical regions.

In the United States, the majority of babesiosis cases are caused by "B. microti", and occur in the Northeast and northern Midwest from May through October. Areas with especially high rates include eastern Long Island, Fire Island, Nantucket Island, and Martha's Vineyard.

In Europe, "B. divergens" is the primary cause of infectious babesiosis and is transmitted by "I. ricinus".

Babesiosis has emerged in Lower Hudson Valley, New York, since 2001.

In Australia, babesiosis of types "B. duncani" and "B. microti" has recently been found in symptomatic patients along the eastern coastline of the continent. A similar disease in cattle, commonly known as tick fever, is spread by "Babesia bovis" and "B. bigemina" in the introduced cattle tick "Rhipicephalus microplus". This disease is found in eastern and northern Australia.

The PI cattle that do survive ill-thrift are susceptible to mucosal disease. Mucosal disease only develops in PI animals and is invariably fatal. Disease results when a PI animal is superinfected with a cytopathic biotype arising from mutation of the non-cytopathic strain of BVDV already circulating in that animal. The cp BVDV spreads to the gastro-intestinal epithelium, and necrosis of keratinocytes results in erosion and ulceration. Fluid leaks from the epithelial surface of the gastro-intestinal tract causing diarrhoea and dehydration. In addition, bacterial infection of the damaged epithelium results in secondary septicaemia. Death occurs in the ensuing days or weeks.

"Moraxella bovis" is a Gram-negative rod-shaped aerobe. This bacterium is an obligate intracellular parasite of the mucous membranes, and can usually be isolated from the respiratory tract, vagina, and conjunctiva of healthy animals. Transmission of IBK is through direct contact with mucous membranes and their secretions and indirect contact where flies act as a mechanical vector. Asymptomatic carrier animals can also be source of infection.

A table of isolated cases of babesiosis, which may be underestimated given how widely distributed the tick vectors are in temperate latitudes.

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.

Paravaccinia is a member of the Parapoxvirus family. It has a cylindrical body about 140 X 310 nm in size, with convex ends covered in a criss-cross pattern of rope like structures. The virus is resistant to cold, dehydration, and temperatures up to 56 °C. Upon injecting a cell with its genome, the virus begins transcription in the cytoplasm using viral RNA polymerase. As the virus progresses through the cell, the host begins to replicate the viral genome between 140 minutes and 48 hours.

Several species of rickettsia bacteria cause anaplasmosis in ruminants:

- Cattle:

- "Anaplasma marginale" - found worldwide.

- "Anaplasma centrale" - found mainly in South America, Africa and the Middle East.

- Sheep and goats:

- "Anaplasma ovis" - found worldwide.

In an endemic herd, only a minority of the animals develops clinical signs; most animals either eliminate the infection or become asymptomatic carriers. The mortality rate is about 1%, but up to 50% of the animals in the herd can be asymptomatically infected, resulting in losses in production. Once the symptoms appear, paratuberculosis is progressive and affected animals eventually die. The percentage of asymptomatic carriers that develop overt disease is unknown.