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.

Currently, the only reliable way to prevent GBS-EOD is intrapartum antibiotic prophylaxis (IAP) - administration of antibiotics during delivery. Intravenous penicillin or ampicillin given at the onset of labour and then again every four hours until delivery to GBS colonized women have been proven to be very effective at preventing vertical transmission of GBS from mother to baby and GBS-EOD

(penicillin G, 5 million units IV initial dose, then 2.5–3.0 million units every 4 hours until delivery or ampicillin, 2 g IV initial dose, then 1 g IV every 4 hours until delivery).

Penicillin-allergic women without a history of anaphylaxis (angioedema, respiratory distress, or urticaria) following administration of a penicillin or a cephalosporin (low risk of anaphylaxis) could receive cefazolin (2 g IV initial dose, then 1 g IV every 8 hours until delivery) instead of penicillin or ampicillin. Clindamycin (900 mg IV every 8 hours until delivery), and vancomycin (1 g IV every 12 hours until delivery) are used to prevent GBS-EOD in infants born to penicillin-allergic mothers. Erythromycin is not recommended under any circumstances today.

Antibiotic susceptibility testing of GBS isolates is crucial for appropriate antibiotic selection for IAP in penicillin-allergic women, because resistance to clindamycin, the most common agent used (in penicillin-allergic women), is increasing among GBS isolates. Appropriate methodologies for testing are important, because resistance to clyndamicin (antimicrobial resistance) can occur in some GBS strains that appear susceptible (antibiotic sensitivity) in certain susceptibility tests.

If appropriate IAP in GBS colonized women starts at least 2 hours before the delivery, the risk of neonatal infection is also somehow reduced.

True penicillin allergy is rare with an estimated frequency of anaphylaxis of one to five episodes per 10,000 cases of penicillin therapy. Penicillin administered to a woman with no history of β-lactam allergy has a risk of anaphylaxis of 0.04 to 4 per 100,000. Maternal anaphylaxis associated with GBS IAP occurs, but any morbidity associated with anaphylaxis is offset greatly by reductions in the incidence of GBS-EOD.

Home births are becoming increasingly popular in the UK. Recommendations for preventing GBS infections in newborns are the same for home births as for hospital births. Around 25% of women having home births probably carry GBS in their vaginas at delivery without knowing, and it could be difficult to follow correctly the recommendations of IAP and to deal with the risk of a severe allergic reaction to the antibiotics outside of a hospital setting.

IAPs have been considered to be associated with the emergence of resistant bacterial strains and with an increase in the incidence of early-onset infections caused by other pathogens, mainly Gram-negative bacteria such as "Escherichia coli". Nevertheless, most studies have not found an increased rate of non-GBS early-onset sepsis related to the widespread use of IAP.

Other strategies to prevent GBS-EOD have been studied, and chlorhexidine intrapartum vaginal cleansing has been proposed to help preventing GBS-EOD, nevertheless no evidence has been shown for the effectiveness of this approach.

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.

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.

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.

Outbreaks of zoonoses have been traced to human interaction with and exposure to animals at fairs, petting zoos, and other settings. In 2005, the Centers for Disease Control and Prevention (CDC) issued an updated list of recommendations for preventing zoonosis transmission in public settings. The recommendations, developed in conjunction with the National Association of State Public Health Veterinarians, include educational responsibilities of venue operators, limiting public and animal contact, and animal care and management.

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.

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".

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.

"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.

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.

"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.

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.

Fetal infection is of most consequence as this can result in the birth of a persistently infected neonate. The effects of fetal infection with BVDV are dependent upon the stage of gestation at which the dam suffers acute infection.

BVDV infection of the dam prior to conception, and during the first 18 days of gestation, results in delayed conception and an increased calving to conception interval. Once the embryo is attached, infection from days 29–41 can result in embryonic infection and resultant embryonic death.

Infection of the dam from approximately day 30 of gestation until day 120 can result in immunotolerance and the birth of calves persistently infected with the virus.

BVDV infection between 80 and 150 days of gestation may be teratogenic, with the type of birth defect dependent upon the stage of fetal development at infection. Abortion may occur at any time during gestation. Infection after approximately day 120 can result in the birth of a normal fetus which is BVD antigen-negative and BVD antibody-positive. This occurs because the fetal immune system has developed, by this stage of gestation, and has the ability to recognise and fight off the invading virus, producing anti-BVD antibodies.

Metritis is inflammation of the wall of the uterus, whereas endometritis is inflammation of the functional lining of the uterus, called the endometrium The term pelvic inflammatory disease (PID) is often used for metritis.

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.

These terms can apply to any species of mammal. Amongst domestic animals, metritis and endometritis are most common in cattle after parturition, and the diseases are often called postpartum metritis or postpartum endometritis. These diseases in cattle are caused by bacteria and occasionally viruses. The most common bacteria that cause postpartum metritis and endometritis in cattle are "Escherichia coli", "Trueperella" (previously "Arcanobacterium") "pyogenes" and anaerobic bacteria such as "Prevotella" species and "Fusobacterium necrophorum". The virus most consistently associated with postpartum uterine disease in cattle is Bovine Herpesvirus 4 (BoHV-4). In addition, "Several specific diseases are associated with metritis or endometritis. These include brucellosis, leptospirosis, campylobacteriosis, and trichomoniasis"

In cattle, bacterial infection of the uterus affects almost all animals after parturition. Of course this doesn't mean they will get disease. In fact beef cattle rarely have disease unless they have a predisposing factor such as retained placenta or difficult parturition. However, uterine disease is common in dairy cattle - particularly high-milk-yield cows such as Holstein-Friesian cows.

Contagious equine metritis is a sexually transmitted infection in horses, recognized since 1977.

In 2014 a study reported about the first successful vaccination trials in cattle. The infection rate declined significantly.Vinícius Silva Machado, Marcela Luccas de Souza Bicalho u. a.: "Subcutaneous Immunization with Inactivated Bacterial Components and Purified Protein of Escherichia coli, Fusobacterium necrophorum and Trueperella pyogenes Prevents Puerperal Metritis in Holstein Dairy Cows." In: "PLoS ONE." 9, 2014, S. e91734, .

Stress often serves as the final precursor to BRD. The diseases that make up BRD can persist in a cattle herd for a long period of time before becoming symptomatic, but immune systems weakened by stress can stop controlling the disease. Major sources of stress come from the shipping process

and from the co-mingling of cattle.

Weather may be another possible factor. Cases are more common in the fall (although this is the traditional time to sell cattle), and while the relationship between weather and BRD is poorly understood, it is often suggested to avoid transporting cattle during extreme weather.

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.

Vaccines against anaplasmosis are available. Carrier animals should be eliminated from flocks. Tick control may also be useful although it can be difficult to implement.

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 the absence of vaccination (often because calves are bought unvaccinated), antibiotics can help to stop the bacterial factors of the disease. The Virginia Cooperative Extension recommends Micotil, Nuflor, and Baytril 100 as newer antibiotics that do not need daily dosing, but also notes that Naxcel, Excenel, and Adspec are effective as well.

In addition to disease caused by direct bacterial infection, some foodborne illnesses are caused by enterotoxins (exotoxins targeting the intestines). Enterotoxins can produce illness even when the microbes that produced them have been killed. Symptom appearance varies with the toxin but may be rapid in onset, as in the case of enterotoxins of "Staphylococcus aureus" in which symptoms appear in one to six hours. This causes intense vomiting including or not including diarrhea (resulting in staphylococcal enteritis), and staphylococcal enterotoxins (most commonly staphylococcal enterotoxin A but also including staphylococcal enterotoxin B) are the most commonly reported enterotoxins although cases of poisoning are likely underestimated. It occurs mainly in cooked and processed foods due to competition with other biota in raw foods, and humans are the main cause of contamination as a substantial percentage of humans are persistent carriers of "S. aureus". The CDC has estimated about 240,000 cases per year in the United States.

- "Clostridium botulinum"

- "Clostridium perfringens"

- "Bacillus cereus"

The rare but potentially deadly disease botulism occurs when the anaerobic bacterium "Clostridium botulinum" grows in improperly canned low-acid foods and produces botulin, a powerful paralytic toxin.

"Pseudoalteromonas tetraodonis", certain species of Pseudomonas and Vibrio, and some other bacteria, produce the lethal tetrodotoxin, which is present in the tissues of some living animal species rather than being a product of decomposition.

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

Globally, infants are a population that are especially vulnerable to foodborne disease. The World Health Organization has issued recommendations for the preparation, use and storage of prepared formulas. Breastfeeding remains the best preventative measure for protection of foodborne infections in infants.