Bacterial soft rots are caused by several types of bacteria, but most commonly by species of gram-negative bacteria, "Erwinia", "Pectobacterium", and "Pseudomonas". It is a destructive disease of fruits, vegetables, and ornamentals found worldwide, and effects genera from nearly all the plant families. The bacteria mainly attack the fleshy storage organs of their hosts (tubers, corms, bulbs, and rhizomes), but they also affect succulent buds, stems, and petiole tissues. With the aid of special enzymes, the plant is turned into a liquidy mush in order for the bacteria to consume the plant cell's nutrients. Disease spread can be caused by simple physical interaction between infected and healthy tissues during storage or transit. The disease can also be spread by insects. Control of the disease is not always very effective, but sanitary practices in production, storing, and processing are something that can be done in order to slow the spread of the disease and protect yields.

Bacterial wilt of turfgrass is the only known bacterial disease of turf. The causal agent is the Gram negative bacterium Xanthomonas campestris pv. graminis. The first case of bacterial wilt of turf was reported in a cultivar of creeping bentgrass known as Toronto or C-15, which is found throughout the midwestern United States. Until the causal agent was identified in 1984, the disease was referred to simply as C-15 decline. This disease is almost exclusively found on putting greens at golf courses where extensive mowing creates wounds in the grass which the pathogen uses in order to enter the host and cause disease.

Vancomycin-resistant "Enterococcus", or vancomycin-resistant enterococci (VRE), are bacterial strains of the genus "Enterococcus" that are resistant to the antibiotic vancomycin.

Creeping bentgrass ("Agrostis stolonifera") and annual bluegrasses ("Poa annua") are the makeup of most putting greens, as well as the preferred hosts of this pathogen. Specifically, Toronto (C-15), Seaside, and Nemisilla are the cultivars of creeping bentgrass most commonly affected. The bacteria enter the plant host and interfere with water and nutrient flow, causing the plant to look drought stressed and to take on a blueish-purple color. Additionally, symptoms of bacterial wilt of turf grass include yellow leaf spots, tan or brown spots, water soaked lesions, elongated yellow leaves and shriveling of aforementioned blue or dark green leaves.Since putting greens are not a pure stand of turf, some grass blades may be resistant to the bacterium and thus remain unharmed while the surrounding turf dies, rendering the putting surface inconsistent and unsightly, especially at high-end golf courses.

There are a variety of hosts including but not limited to; banana, beans, cabbage, carrot, cassava, coffee, corn, cotton, onion, other crucifers, pepper, potato, sweet potato and tomato. For each host there are different symptoms displayed. Most symptoms are along the lines of watery and soft decay of the tissue. Cabbage and crucifers' symptoms start where the tissue makes contact with the soil. Often there is a change in color and in the case of a carrot, the whole taproot can be decayed leaving just the epidermis. Sweet potatoes show clear lesions that grow rapidly leaving a recognizable watery and soft, oozy tissue where only the peel remains intact.

Potatoes experience a cream to tan colored tuber that becomes very soft and watery. A characteristic black border separates the diseased area and the healthy tissue. Only when the secondary organism invades the infected tissue does that decay become slimy with a foul odor. Like the carrot, the whole tuber can be consumed leaving just the epidermis in the soil. The foliage becomes weak and chlorotic with upward turned leaves and lesions on the stem. The stem also rots and becomes mushy with its colorless or brown lesions.

Once the individual has VRE, it is important to ascertain which "strain".

The foamy bark canker is a disease affecting oak trees in California caused by the fungus "Geosmithia pallida" and spread by the Western oak bark beetle ("Pseudopityopthorus pubipennis"). This disease is only seen through the symbiosis of the bark beetles and the fungal pathogen. The bark beetles target oak trees and bore holes through the peridermal tissues, making tunnels within the phloem. The fungal spores are brought into these tunnels by the beetles and begin to colonize the damaged cells inside the tunnels. Symptoms of the developing fungus include wet discoloration seeping from the beetle entry holes as the fungus begins to consume phloem and likely other tissues. If bark is removed, necrosis of the phloem can be observed surrounding the entry hole(s). As the disease progresses, a reddish sap and foamy liquid oozes from entry holes, thus giving the disease the name Foamy bark canker. Eventually after the disease has progressed, the tree dies. This disease is important because of its detrimental effects on oak trees and its ability to spread to several new Californian counties in just a couple years.

Hosts associated with "Geosmithia pallida" include a number of tree species, including oak and other hardwoods, pine and spruce trees, depending on the beetle vector. In this case, the western oak bark beetles target live oak trees of western United States. Beetles tend to attack stressed trees that are already weakened from drought or injury. Symptoms causing branch dieback and tree death also include a cinnamon-colored gum seeping from multiple beetle entry holes on the bole, followed by a prolific, cream-colored foamy liquid. These symptoms, as well as signs (entry holes, larvae, beetles) of bark beetles, are key factors in diagnosis. Necrosis of xylem and phloem tissues underneath bark can be observed.

Common Symptoms:

- Wet discoloration on bark

- Phloem necrosis

- Beetle entry holes

- Reddish sap oozing from entry holes

- Foamy liquid from entry holes

Yellow-band disease (similar to Yellow Blotch disease) is a coral disease that attacks colonies of coral at a time when coral is already under stress from pollution, overfishing, and climate change. It is characterized by large blotches or patches of bleached, yellowed tissue on Caribbean scleractinian corals.

Yellow-band disease is a bacterial infection that spreads over coral, causing the discolored bands of pale-yellow or white lesions along the surface of an infected coral colony. The lesions are the locations where the bacteria have killed the coral’s symbiotic photosynthetic algae, called zooxanthellae which are a major energy source for the coral. This cellular damage and the loss of its major energy source cause the coral to starve, and usually cause coral death. There is evidence that climate change could be worsening the disease.

Cytauxzoon felis is a protozoal organism transmitted to domestic cats by tick bites, and whose natural reservoir host is the bobcat. "C. felis" has been found in other wild felid species such as Florida bobcat, eastern bobcat, Texas cougar, and a white tiger in captivity. "C. felis" infection is limited to the family felidae which means that "C. felis" poses no zoonotic (transmission to humans) risk or agricultural (transmission to farm animals) risk. Until recently it was believed that after infection with "C. felis", pet cats almost always died. As awareness of "C. felis" has increased it has been found that treatment is not always futile. More cats have been shown to survive the infection than was previously thought. New treatments offer as much as 60% survival rate.

Free-living amoebae (or "FLA") in the Amoebozoa group are important causes of disease in humans and animals.

"Naegleria fowleri" is sometimes included in the group "free-living amoebae", and it causes a condition traditionally called primary amoebic meningoencephalitis. However, Naegleria is now considered part of the Excavata, not the Amoebozoa, and is considered to be much more closely related to "Leishmania" and "Trypanosoma".

Most infected cats have been healthy before a very sudden onset of severe disease. The course of clinical disease is often swift with clinical signs of lethargy and inappetence within 5 to 20 days after the tick bite. Cats develop a high fever, but the temperature may become low before death. Other clinical findings can be: dehydration, icterus (jaundice), enlarged liver and spleen, lymphadenopathy, pale mucus membranes, respiratory distress, tachycardia or bradycardia, and tick infestation (although ticks are not often found on infected cats since cats typically groom ticks off their fur). Signs of disease seen on blood work include hemolytic anemia, thrombocytopenia, increased or decreased white blood cell numbers, icterus, and elevated liver enzymes. Death usually follows the onset of clinical signs within a few days. However, more recent studies show not all cats develop clinical signs after infection, and some cats survive the infection.

Onset of symptoms begins one to nine days following exposure (with an average of five). Initial symptoms include changes in taste and smell, headache, fever, nausea, vomiting, back pain, and a stiff neck. Secondary symptoms are also meningitis-like including confusion, hallucinations, lack of attention, ataxia, cramp and seizures. After the start of symptoms, the disease progresses rapidly over three to seven days, with death usually occurring anywhere from seven to fourteen days later, although it can take longer. In 2013, a man in Taiwan died twenty-five days after being infected by "Naegleria fowleri".

It affects healthy children or young adults who have recently been exposed to bodies of fresh water. Some people have presented with a clinical triad of edematous brain lesions, immune suppression, and fever.

"Acanthamoeba spp." causes mostly subacute or chronic granulomatous amoebic encephalitis (GAE), with a clinical picture of headaches, altered mental status, and focal neurologic deficit, which progresses over several weeks to death. In addition, "Acanthamoeba spp." can cause granulomatous skin lesions and, more seriously, keratitis and corneal ulcers following corneal trauma or in association with contact lenses.

Naegleriasis (also known as primary amoebic meningoencephalitis) is an infection of the brain by the free-living unicellular "Naegleria fowleri".

"N. fowleri" is typically found in warm bodies of fresh water, such as ponds, lakes, rivers, and hot springs. It is also found in soil, poorly maintained municipal water supplies, water heaters, near warm-water discharges of industrial plants, and in poorly chlorinated or unchlorinated swimming pools, in an amoeboid or temporary flagellate stage. There is no evidence of it living in salt water. As the disease is rare, it is often not considered. Symptoms are similar to those of meningitis.

Although infection occurs rarely, it nearly always results in death, with a case fatality rate greater than 95%.

Bacteremia (also bacteraemia) is the presence of bacteria in the blood. Blood is normally a sterile environment, so the detection of bacteria in the blood (most commonly accomplished by blood cultures) is always abnormal. It is distinct from sepsis, which is the host response to the bacteria.

Bacteria can enter the bloodstream as a severe complication of infections (like pneumonia or meningitis), during surgery (especially when involving mucous membranes such as the gastrointestinal tract), or due to catheters and other foreign bodies entering the arteries or veins (including during intravenous drug abuse). Transient bacteremia can result after dental procedures or brushing of teeth.

Bacteremia can have several important health consequences. The immune response to the bacteria can cause sepsis and septic shock, which has a high mortality rate. Bacteria can also spread via the blood to other parts of the body (which is called hematogenous spread), causing infections away from the original site of infection, such as endocarditis or osteomyelitis. Treatment for bacteremia is with antibiotics, and prevention with antibiotic prophylaxis can be given in high risk situations.

"Rabbits, Hares & Lagomorphs"

Usually there do not appear to be any clinical signs. Subcutaneous cysts, warbles, may present upon larval deposition out of the body at maturation.

"Felines & Canines"

There are three forms in which Cuterebriasis may present:

- Myasis

- Cerebrospinal

- Respiratory

Myasis involves subcutaneous cyst formation due to 3rd larval instar maturation, occurring ~30 days post-entry into the body. Cysts are often found on the face, neck and trunk, but location varies with larval migration within the host. Serous discharge may be observed from these cysts, which are typically 3-5mm in diameter and include a central pore through which the larvae respire. This pore also serves as a means of exit for the larvae, which occurs anywhere between 3 and 8 weeks post-entry.

Cerebrospinal cuterebriasis results from larval migration to the brain. This is seen in cats, and is the proposed cause for feline ischemic encephalopathy and a suggestive causative agent of feline idiopathic vestibular disease. Symptoms of this type of presentation include lethargy, seizures, blindness, abnormal vocalization or gait, circling, and abnormal or no reflex responses. When affecting the central nervous system, cats are known to exhibit violent sneezing attacks that can onset weeks prior to manifestation of other clinical signs.

Respiratory disease results when larval migration occurs through the trachea, pharynx, diaphragm, or lungs. Cuterebriasis has been increasingly noted as a cause for dyspnea in felines.

Cuterebriasis is a parasitic disease affecting rodents, lagomorphs (hares, rabbits, pikas), felines and canines. The etiologic agent is the larval development of bot flies within the "Cuterebra" or "Trypoderma" genera, which occurs obligatorily in rodents and lagomorphs, respectively. Felines and canines serve as accidental hosts, but research suggests only by "Trypoderma" spp. Entrance into the body by first instar larva occurs via mucous membranes of natural orifices or open wounds as opposed to direct dermic penetration.

Coral has a symbiotic relationship with zooxanthellae that provide the coral glucose, glycerol, and amino acids. Under certain water conditions, like fluctuating temperatures and increased nitrogenous waste, corals will appear stressed. Also, these conditions allow for bacteria to grow inside the coral and compete with zooxanthellae. The bacteria produces the characteristic pale yellow lesions and eventually kills the zooxanthellae by impairing its mitosis and its ability to carry out photosynthesis. Yellow-band disease is found on coral reefs in the Caribbean.

Host tropism is the infection specificity of certain pathogens to particular hosts and host tissues. This type of tropism explains why most pathogens are only capable of infecting a limited range of host organisms.

Researchers can classify pathogenic organisms by the range of species and cell types that they exhibit host tropism for. For instance, pathogens that are able to infect a wide range of hosts and tissues are said to be amphotropic. Ecotropic pathogens, on the other hand, are only capable of infecting a narrow range of hosts and host tissue. Knowledge of a pathogen's host specificity allows professionals in the research and medical industries to model pathogenesis and develop vaccines, medication, and preventative measures to fight against infection. Methods such as cell engineering, direct engineering and assisted evolution of host-adapted pathogens, and genome-wide genetic screens are currently being used by researchers to better understand the host range of a variety of different pathogenic organisms.

Bacteremia is the presence of bacteria in the bloodstream that are alive and capable of reproducing. It is a type of bloodstream infection. Bacteremia is defined as either a primary or secondary process. In primary bacteremia, bacteria have been directly introduced into the bloodstream. Injection drug use may lead to primary bacteremia. In the hospital setting, use of blood vessel catheters contaminated with bacteria may also lead to primary bacteremia. Secondary bacteremia occurs when bacteria have entered the body at another site, such as the cuts in the skin, or the mucous membranes of the lungs (respiratory tract), mouth or intestines (gastrointestinal tract), bladder (urinary tract), or genitals. Bacteria that have infected the body at these sites may then spread into the lymphatic system and gain access to the bloodstream, where further spread can occur.

Bacteremia may also be defined by the timing of bacteria presence in the bloodstream: transient, intermittent, or persistent. In transient bacteremia, bacteria are present in the bloodstream for minutes to a few hours before being cleared from the body, and the result is typically harmless in healthy people. This can occur after manipulation of parts of the body normally colonized by bacteria, such as the mucosal surfaces of the mouth during teeth brushing, flossing, or dental procedures, or instrumentation of the bladder or colon. Intermittent bacteremia is characterized by periodic seeding of the same bacteria into the bloodstream by an existing infection elsewhere in the body, such as an abscess, pneumonia, or bone infection, followed by clearing of that bacteria from the bloodstream. This cycle will often repeat until the existing infection is successfully treated. Persistent bacteremia is characterized by the continuous presence of bacteria in the bloodstream. It is usually the result of an infected heart valve, a central line-associated bloodstream infection (CLABSI), an infected blood clot (suppurative thrombophlebitis), or an infected blood vessel graft. Persistent bacteremia can also occur as part of the infection process of typhoid fever, brucellosis, and bacterial meningitis. Left untreated, conditions causing persistent bacteremia can be potentially fatal.

Bacteremia is clinically distinct from sepsis, which is a condition where the blood stream infection is associated with an inflammatory response from the body, often causing abnormalities in body temperature, heart rate, breathing rate, blood pressure, and white blood cell count.

Human granulocytic anaplasmosis (HGA) is a tick-borne, infectious disease caused by "Anaplasma phagocytophilum", an obligate intracellular bacterium that is typically transmitted to humans by ticks of the "Ixodes ricinus" species complex, including "Ixodes scapularis" and "Ixodes pacificus" in North America. These ticks also transmit Lyme disease and other tick borne diseases.

The bacteria infect white blood cells called neutrophils, causing changes in gene expression that prolong the life of these otherwise short-lived cells.

Filariasis is a parasitic disease caused by an infection with roundworms of the Filarioidea type. These are spread by blood-feeding black flies and mosquitoes. This disease belongs to the group of diseases called helminthiases.

Eight known filarial nematodes use humans as their definitive hosts. These are divided into three groups according to the niche they occupy in the body:

- Lymphatic filariasis is caused by the worms "Wuchereria bancrofti", "Brugia malayi", and "Brugia timori". These worms occupy the lymphatic system, including the lymph nodes; in chronic cases, these worms lead to the syndrome of "elephantiasis".

- Subcutaneous filariasis is caused by "Loa loa" (the eye worm), "Mansonella streptocerca", and "Onchocerca volvulus". These worms occupy the subcutaneous layer of the skin, in the fat layer. "L. loa" causes "Loa loa" filariasis, while "O. volvulus" causes river blindness.

- Serous cavity filariasis is caused by the worms "Mansonella perstans" and "Mansonella ozzardi", which occupy the serous cavity of the abdomen. "Dirofilaria immitis", or the dog heartworm rarely infects humans.

The adult worms, which usually stay in one tissue, release early larval forms known as microfilariae into the host's bloodstream. These circulating microfilariae can be taken up with a blood meal by the arthropod vector; in the vector, they develop into infective larvae that can be transmitted to a new host.

Individuals infected by filarial worms may be described as either "microfilaraemic" or "amicrofilaraemic", depending on whether microfilariae can be found in their peripheral blood. Filariasis is diagnosed in microfilaraemic cases primarily through direct observation of microfilariae in the peripheral blood. Occult filariasis is diagnosed in amicrofilaraemic cases based on clinical observations and, in some cases, by finding a circulating antigen in the blood.

Covering sickness, or dourine (French, from the Arabic "darina", meaning mangy (said of a female camel), feminine of "darin", meaning dirty), is a disease of horses and other members of the family Equidae. The disease is caused by "Trypanosoma equiperdum", which belongs to an important genus of parasitic protozoa, and is the only member of the genus that is spread through sexual intercourse. The occurrence of dourine is notifiable in the European Union under legislation from the OIE. There currently is no vaccine and although clinical signs can be treated, there is no cure.

The olfactory system is the system related to the sense of smell (olfaction). Many fish activities are dependent on olfaction, such as: mating, discriminating kin, avoiding predators, locating food, contaminant avoidance, imprinting and homing. These activities are referred to as “olfactory-mediated.” Impairment of the olfactory system threatens survival and has been used as an ecologically relevant sub-lethal toxicological endpoint for fish within studies. Olfactory information is received by sensory neurons, like the olfactory nerve, that are in a covered cavity separated from the aquatic environment by mucus. Since they are in almost direct contact with the surrounding environment, these neurons are vulnerable to environmental changes. Fish can detect natural chemical cues in aquatic environments at concentrations as low as parts per billion (ppb) or parts per trillion (ppt).

Studies have shown that exposures to metals, pesticides, or surfactants can disrupt fish olfaction, which can impact their survival and reproductive success. Many studies have indicated copper as a source of olfactory toxicity in fishes, among other common substances. Olfactory toxicity can occur by multiple, complex Modes of Toxic Action.