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.

Campylobacteriosis is usually self-limited without any mortality (assuming proper hydration is maintained). However, there are several possible complications.

"Salmonella" bacteria can survive for some time without a host; thus, they are frequently found in polluted water, with contamination from the excrement of carrier animals being particularly important.

The European Food Safety Authority highly recommends that when handling raw turkey meat, consumers and people involved in the food supply chain should pay attention to personal and food hygiene.

An estimated 142,000 Americans are infected each year with "Salmonella" Enteritidis from chicken eggs, and about 30 die. The shell of the egg may be contaminated with "Salmonella" by feces or environment, or its interior (yolk) may be contaminated by penetration of the bacteria through the porous shell or from a hen whose infected ovaries contaminate the egg during egg formation.

Nevertheless, such interior egg yolk contamination is theoretically unlikely. Even under natural conditions, the rate of infection was very small (0.6% in a study of naturally contaminated eggs and 3.0% among artificially and heavily infected hens).

The FDA has published guidelines to help reduce the chance of food-borne salmonellosis. Food must be cooked to 68–72 °C (145–160 °F), and liquids such as soups or gravies must be boiled. Freezing kills some "Salmonella", but it is not sufficient to reliably reduce them below infectious levels. While "Salmonella" is usually heat-sensitive, it does acquire heat resistance in high-fat environments such as peanut butter.

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

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.

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.

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.

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, .

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.

According to a ProMED article, disease in sheep has been controlled in the UK by a vaccine (ATCvet code: QI04AA01), originally developed by Scotland's Moredun Research Institute by Prof John Russell Greig. In 2009, however, a shortage of vaccine combined with an increase in the number of ticks found in sheep pasture areas cause an increased risk of this disease.

Louping-ill (also known as Ovine Encephalomyelitis, Infectious Encephalomyelitis of Sheep, Trembling-ill) is an acute viral disease primarily of sheep that is characterized by a biphasic fever, depression, ataxia, muscular incoordination, tremors, posterior paralysis, coma, and death. Louping-ill is a tick-transmitted disease whose occurrence is closely related to the distribution of the primary vector, the sheep tick "Ixodes ricinus". It also causes disease in red grouse, and can affect humans. The name 'louping-ill' is derived from an old Scottish word describing the effect of the disease in sheep whereby they 'loup' or spring into the air.

OPA has been found in most countries where sheep are farmed, with the exception of Australia and New Zealand. OPA has been eradicated in Iceland.

No breed or sex of sheep appears to be predisposed to OPA. Most affected sheep show signs at 2 to 4 years of age.

OPA is not a notifiable disease, and therefore it is difficult to assess its prevalence.

Ovine pulmonary adenocarcinoma (OPA), also known as ovine pulmonary adenomatosis, or jaagsiekte, is a chronic and contagious disease of the lungs of sheep and goats. OPA is caused by a retrovirus called jaagsiekte sheep retrovirus (JSRV).

Smoke inhalation injury, either by itself but more so in the presence of body surface burn, can result in severe lung-induced morbidity and mortality. The most common cause of death in burn centers is now respiratory failure. The September 11 attacks in 2001 and forest fires in U.S. states such as California and Nevada are examples of incidents that have caused smoke inhalation injury. Injury to the lungs and airways is not only due to deposition of fine particulate soot but also due to the gaseous components of smoke, which include phosgene, carbon monoxide, and sulfur dioxide.

Chlorine is a relatively common gas in industry with a variety of uses. It is used to disinfect water as well as being a part of the sanitation process for sewage and industrial waste. Chlorine is also used as a bleaching agent during the production of paper and cloth. Many household cleaning products, including bleach, contain chlorine. Given the volume and ease of chlorine for industrial and commercial use, exposure could occur from an accidental spill or a deliberate attack. The National Institute for Occupational Safety and Health recommends that a person wear splash proof goggles, a face shield and a respirator mask when working in the vicinity of chlorine gas. Because chlorine is a gas at room temperature, most exposure occurs via inhalation. Exposure may also occur through skin or eye contact or by ingesting chlorine-contaminated food or water. Chlorine is a strong oxidizing element causing the hydrogen to split from water in moist tissue, resulting in nascent oxygen and hydrogen chloride that cause corrosive tissue damage. Additionally oxidation of chlorine may form hypochlorous acid, which can penetrate cells and react with cytoplasmic proteins destroying cell structure. Chlorine’s odor provides early warning signs of exposure but causes olfactory fatigue or adaptations, reducing awareness of exposure at low concentrations. With increased exposure, symptoms may progress to labored respirations, severe coughing, chest tightness, wheezing, dyspnea, and broncospasm associated with a decrease in oxygen saturation level. . Severe exposure may result in changes in upper and lower airways resulting in an acute lung injury, which may not be present until several hours after exposure. A recent chlorine gas leak in Pune, India, landed 20 individuals in the hospital. Though that was an accidental exposure, chlorine gas has been used as a weapon of warfare since World War I, most recently in 2007 in Iraq.

In sheep, intrauterine growth restriction can be caused by heat stress in early to mid pregnancy. The effect is attributed to reduced placental development causing reduced fetal growth. Hormonal effects appear implicated in the reduced placental development. Although early reduction of placental development is not accompanied by concurrent reduction of fetal growth; it tends to limit fetal growth later in gestation. Normally, ovine placental mass increases until about day 70 of gestation, but high demand on the placenta for fetal growth occurs later. (For example, research results suggest that a normal average singleton Suffolk x Targhee sheep fetus has a mass of about 0.15 kg at day 70, and growth rates of about 31 g/day at day 80, 129 g/day at day 120 and 199 g/day at day 140 of gestation, reaching a mass of about 6.21 kg at day 140, a few days before parturition.)

In adolescent ewes (i.e. ewe hoggets), overfeeding during pregnancy can also cause intrauterine growth restriction, by altering nutrient partitioning between dam and conceptus. Fetal growth restriction in adolescent ewes overnourished during early to mid pregnancy is not avoided by switching to lower nutrient intake after day 90 of gestation; whereas such switching at day 50 does result in greater placental growth and enhanced pregnancy outcome. Practical implications include the importance of estimating a threshold for "overnutrition" in management of pregnant ewe hoggets. In a study of Romney and Coopworth ewe hoggets bred to Perendale rams, feeding to approximate a conceptus-free live mass gain of 0.15 kg/day (i.e. in addition to conceptus mass), commencing 13 days after the midpoint of a synchronized breeding period, yielded no reduction in lamb birth mass, where compared with feeding treatments yielding conceptus-free live mass gains of about 0 and 0.075 kg/day.

In both of the above models of IUGR in sheep, the absolute magnitude of uterine blood flow is reduced. Evidence of substantial reduction of placental glucose transport capacity has been observed in pregnant ewes that had been heat-stressed during placental development.

In dairy cattle, ketosis is a common ailment that usually occurs during the first weeks after giving birth to a calf. Ketosis is in these cases sometimes referred to as "acetonemia". A study from 2011 revealed that whether ketosis is developed or not depends on the lipids a cow uses to create butterfat. Animals prone to ketosis mobilize fatty acids from adipose tissue, while robust animals create fatty acids from blood phosphatidylcholine (lecithin). Healthy animals can be recognized by high levels of milk glycerophosphocholine and low levels of milk phosphocholine. Point of care diagnostic tests are available and are reasonably useful.

In sheep, ketosis, evidenced by hyperketonemia with beta-hydroxybutyrate in blood over 0.7 mmol/L, occurs in pregnancy toxemia. This may develop in late pregnancy in ewes bearing multiple fetuses, and is associated with the considerable glucose demands of the conceptuses. In ruminants, because most glucose in the digestive tract is metabolized by rumen organisms, glucose must be supplied by gluconeogenesis, for which propionate (produced by rumen bacteria and absorbed across the rumen wall) is normally the principal substrate in sheep, with other gluconeogenic substrates increasing in importance when glucose demand is high or propionate is limited. Pregnancy toxemia is most likely to occur in late pregnancy because most fetal growth (and hence most glucose demand) occurs in the final weeks of gestation; it may be triggered by insufficient feed energy intake (anorexia due to weather conditions, stress or other causes), necessitating reliance on hydrolysis of stored triglyceride, with the glycerol moiety being used in gluconeogenesis and the fatty acid moieties being subject to oxidation, producing ketone bodies. Among ewes with pregnancy toxemia, beta-hydroxybutyrate in blood tends to be higher in those that die than in survivors. Prompt recovery may occur with natural parturition, Caesarean section or induced abortion. Prevention (through appropriate feeding and other management) is more effective than treatment of advanced stages of ovine ketosis.

IUGR affects 3-10% of pregnancies. 20% of stillborn infants have IUGR. Perinatal mortality rates are 4-8 times higher for infants with IUGR, and morbidity is present in 50% of surviving infants.

According to the theory of thrifty phenotype, intrauterine growth restriction triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment rich in food it may be more prone to metabolic disorders, such as obesity and type II diabetes.

Spider lamb syndrome, also known as spider syndrome and more formally as ovine hereditary chondrodysplasia, is a homozygous recessive disorder affecting the growth of cartilage and bone in sheep. It is a semilethal trait, which is thought to have been first observed in the 1970s, and is most common in sheep of the Suffolk and Hampshire breeds. The mutation which causes spider lamb syndrome is found on ovine chromosome 6, and involves the inactivation of fibroblast growth factor receptor 3.

Afflicted animals may be visibly deformed at birth and unable to stand, or seemingly normal for the first 4 to 6 weeks of their lives.

The name derives from the limbs of afflicted animals being thin, elongated, and "spider-like".

Ketosis is deliberately induced by use of a ketogenic diet as a medical intervention in cases of intractable epilepsy. Other uses of low-carbohydrate diets remain controversial. Carbohydrate deprivation to the point of ketosis has been argued to have both negative and positive effects on health.