An acute disease of young pigs that is usually associated with weaning. It is characterized clinically by paresis and subcutaneous edema.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
A toxin produced by certain pathogenic strains of ESCHERICHIA COLI such as ESCHERICHIA COLI O157. It shares 50-60% homology with SHIGA TOXIN and SHIGA TOXIN 1.
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.
Diseases of domestic swine and of the wild boar of the genus Sus.
Infections with bacteria of the species ESCHERICHIA COLI.
Glycosphingolipids containing N-acetylglucosamine (paragloboside) or N-acetylgalactosamine (globoside). Globoside is the P antigen on erythrocytes and paragloboside is an intermediate in the biosynthesis of erythrocyte blood group ABH and P 1 glycosphingolipid antigens. The accumulation of globoside in tissue, due to a defect in hexosaminidases A and B, is the cause of Sandhoff disease.
A toxin produced by certain pathogenic strains of ESCHERICHIA COLI such as ESCHERICHIA COLI O157. It is closely related to SHIGA TOXIN produced by SHIGELLA DYSENTERIAE.
Toxic substances formed in or elaborated by bacteria; they are usually proteins with high molecular weight and antigenicity; some are used as antibiotics and some to skin test for the presence of or susceptibility to certain diseases.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
Excessive accumulation of extravascular fluid in the lung, an indication of a serious underlying disease or disorder. Pulmonary edema prevents efficient PULMONARY GAS EXCHANGE in the PULMONARY ALVEOLI, and can be life-threatening.
Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)
Sulfuric acid diammonium salt. It is used in CHEMICAL FRACTIONATION of proteins.
The separation of particles from a suspension by passage through a filter with very fine pores. In ultrafiltration the separation is accomplished by convective transport; in DIALYSIS separation relies instead upon differential diffusion. Ultrafiltration occurs naturally and is a laboratory procedure. Artificial ultrafiltration of the blood is referred to as HEMOFILTRATION or HEMODIAFILTRATION (if combined with HEMODIALYSIS).
An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.
A bile acid formed by bacterial action from cholate. It is usually conjugated with glycine or taurine. Deoxycholic acid acts as a detergent to solubilize fats for intestinal absorption, is reabsorbed itself, and is used as a choleretic and detergent.
Suspensions of attenuated or killed bacteria administered for the prevention or treatment of infectious bacterial disease.

Shiga toxin-producing Escherichia coli infection: temporal and quantitative relationships among colonization, toxin production, and systemic disease. (1/33)

Edema disease, a naturally occurring disease of swine caused by Shiga toxin-producing Escherichia coli (STEC), was used as a model for the sequence of events that occur in the pathogenesis of STEC infection. The mean time from production of levels of Shiga toxin 2e (Stx2e) detectable in the feces (day 1) to the onset of clinical disease (neurologic disturbances or death) was 5 days (range, 3-9). Bacterial colonization and titers of Stx2e in the ileum peaked at 4 days after inoculation in pigs without signs of clinical disease and at 6 days after inoculation in clinically affected pigs. Animals with the greatest risk of progressing to clinical disease tended to have the highest fecal toxin titers (>/=1:4096). Stx2e was detected in the red cell fraction from blood of some pigs showing clinical signs of edema disease but was not detected in the serum or cerebrospinal fluid.  (+info)

Prevention of edema disease in pigs by passive immunization. (2/33)

The effect of treatment with verotoxin 2e (VT2e) specific antiserum was evaluated in 3 Danish pig herds with edema disease (ED). The antiserum was prepared by immunizing horses with a VT2e toxoid. The study was performed as a randomized blind field trial with parallel treatment and control groups. There were approximately 50 piglets in each group in each of the 3 herds and 741 piglets were included in the study (244 from herd A, 249 from herd B, and 247 from herd C). Treatment groups received 2, 4, or 6 mL anti-VT2e serum intramuscularly the day before weaning. Control groups were treated with 6 mL normal horse serum or 6 mL RPMI 1640 medium as placebo. All pigs that died in the trial period (1 d before weaning to 44 d after weaning) were examined pathologically and microbiologically. Mortality due to ED, mortality due to other causes, and adverse effects due to treatment were recorded. As there was no mortality due to ED, herd B was excluded from statistical calculations on mortality. The content of horse antibodies specific to VT2e in serum from pigs was analyzed in an indirect ELISA. A higher dose of anti-VT2e serum was reflected in higher optical density values in the indirect ELISA. Transient adverse reactions, seen as vomiting, ataxia, and cyanosis, occurred shortly after the injection of horse serum in 1.5% of the pigs, and one pig died. There were no statistically significant differences in mortality due to other causes among the 3 treatment groups in herds A and C. Only pigs from which F18+, VT2e+, ST-, LT- hemolytic E. coli (0139 or O-rough) was isolated were diagnosed as dead due to ED. Deaths due to ED in the control groups were 8.1% and 12.0% in herds A and C, respectively, compared with 0% and 0.7% in the corresponding serum groups. The difference between treatment and control groups was statistically significant (P<0.0001). It was not possible to establish an effect of dose (2, 4, or 6 mL) of anti-VT2e serum, because only one pig died of ED in the treatment groups. It was concluded that passive immunization by intramuscular injection of a VT2e-specific antiserum can be used for protecting piglets against ED.  (+info)

Intervention with Shiga toxin (Stx) antibody after infection by Stx-producing Escherichia coli. (3/33)

Shiga toxins (Stxs) produced by Escherichia coli (STEC) cause systemic vascular damage, manifested as hemolytic uremic syndrome in humans and as edema disease in pigs. Edema disease, a naturally occurring disease of pigs, was used to determine whether Stx antibodies, administered after infection and after the onset of Stx production, could prevent the systemic vascular damage and clinical disease caused by Stxs. A total of 119 STEC-infected pigs were treated with low, medium, or high doses of Stx antibody or with placebo. After inoculation with STEC, antibodies or placebo was injected intraperitoneally at 2 days postinoculation (DPI; low dose) or 4 DPI (medium and high doses). Edema disease was prevented with the low- and high-dose Stx antibody treatments administered at 2 and 4 DPI, respectively. High-dose antibody treatment also reduced the incidence and extent of vascular lesions. The degree of protection depended on the dose of antibody and the time of administration.  (+info)

The AIDA autotransporter system is associated with F18 and stx2e in Escherichia coli isolates from pigs diagnosed with edema disease and postweaning diarrhea. (4/33)

Pathogenic Escherichia coli strains are known to cause edema disease (ED) and postweaning diarrhea (PWD) in piglets. Although the exact mechanisms of pathogenicity that lead to ED-PWD remain to be elucidated, E. coli-borne Shiga-like toxin and adhesion-mediating virulence factors such as F18 adhesin or F4 fimbriae are believed to play a central role in ED-PWD. In light of these observations we investigated whether another E. coli adhesin, the plasmid-encoded AIDA (adhesin involved in diffuse adherence) might also be present in ED-PWD-causing E. coli isolates. For rapid screening for the AIDA system in large numbers of isolates, a multiplex PCR method along with a duplex Western blot procedure was developed. When screening 104 strains obtained from pigs with or without ED-PWD, we observed a high prevalence of the AIDA operon in porcine E. coli isolates, with over 25% of all strains being AIDA positive, and we could demonstrate a significant association of the intact AIDA gene (orfB) with ED-PWD, while defects in orfB were associated with the absence of disease. Although our data hint toward a contribution of AIDA to ED-PWD, further studies will be necessary since the presence of the AIDA genes was also associated with the presence of the Shiga-like toxin and F18 adhesin genes, two reported virulence factors for ED-PWD.  (+info)

Antimicrobial susceptibility of pathogenic Escherichia coli isolated from pigs in Korea. (5/33)

The in vitro susceptibilities of 285 isolates of Escherichia coli from preweaned and postweaned pigs with diarrhea and edema disease were tested with the 15 commonly used antimicrobial drugs by an agar dilution minimal inhibitory concentration procedure according to National Committee for Clinical Laboratory Standards (NCCLS) guidelines. All E. coli isolates tested in this study belonged to enterotoxigenic E. coli, attaching and effacing E. coli, or Shiga toxin-producing E. coli. Field isolates had low MIC90 for ceftiofur (1 microg/ml). No correlation in antimicrobial resistance was found in three types of E. coli.  (+info)

Characteristics of capsules in enterotoxemic Escherichia coli O139:K12 strains causing swine edema disease. (6/33)

The characteristics of the capsule of the enterotoxemic Escherichia coli (ETEEC) O139:K12 strains that strongly adhere to Hep-2 cells were examined. Electron microscopic studies using the freeze-substitution technique revealed that ETEEC strains had a capsule of approximately 25 nm. These strains show hydrophobic surface properties and strong adherence to human polymorphonuclear leukocytes (PMNs). In contrast, ETEEC strains RK-O139 and ED-1 show weak adherence to HEp-2 cells and fail to express the capsule layer on the cell surface. These ETEEC strains possess hydrophilic surface properties and also adhere to PMNs. The lipopolysaccharide (LPS) analysis by means of sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) showed that ETEEC strains had the same LPS profile and long O-side chains of LPS. Furthermore, all strains were resistant to serum killing activity. These results suggest that the capsule of ETEEC strains does not contribute as an antiphagocytic factor, but as an adherence factor to host cells.  (+info)

Characterization of F107 fimbriae of Escherichia coli 107/86, which causes edema disease in pigs, and nucleotide sequence of the F107 major fimbrial subunit gene, fedA. (7/33)

F107 fimbriae were isolated and purified from edema disease strain 107/86 of Escherichia coli. Plasmid pIH120 was constructed, which contains the gene cluster that codes for adhesive F107 fimbriae. The major fimbrial subunit gene, fedA, was sequenced. An open reading frame that codes for a protein with 170 amino acids, including a 21-amino-acid signal peptide, was found. The protein without the signal sequence has a calculated molecular mass of 15,099 Da. Construction of a nonsense mutation in the open reading frame of fedA abolished both fimbrial expression and the capacity to adhere to isolated porcine intestinal villi. In a screening of 28 reference edema disease strains and isolates from clinically ill piglets, fedA was detected in 24 cases (85.7%). In 20 (83.3%) of these 24 strains, fedA was found in association with Shiga-like toxin II variant genes, coding for the toxin that is characteristic for edema disease strains of E. coli. The fimbrial subunit gene was not detected in enterotoxigenic E. coli strains. Because of the capacity of E. coli HB101(pIH120) transformants to adhere to isolated porcine intestinal villi, the high prevalence of fedA in edema disease strains, and the high correlation with the Shiga-like toxin II variant toxin-encoding genes, we suggest that F107 fimbriae are an important virulence factor in edema disease strains of E. coli.  (+info)

Inhibitory activities of colicins against Escherichia coli strains responsible for postweaning diarrhea and edema disease in swine. (8/33)

The efficacies of colicins E1 and N against Escherichia coli strains responsible for postweaning diarrhea and edema disease, two of the most prevalent disease problems for pigs in the United States, were determined in vitro. These proteins may provide an environmentally sound means for the prevention of these infections in swine.  (+info)

Edema disease of swine, also known as porcine edema disease, is a condition that primarily affects young pigs between 2 weeks and 5 months of age. It is characterized by the sudden onset of neurological symptoms and fluid accumulation in various tissues, particularly in the brain and skin around the neck and shoulders.

The cause of edema disease is a bacterial toxin called Shiga-like toxin IIe (Stx2e) produced by certain strains of Escherichia coli (E. coli) bacteria. These bacteria colonize the pig's small intestine and produce the toxin, which then enters the bloodstream and damages the endothelial cells that line the blood vessels. This damage leads to increased permeability of the blood vessels, allowing fluid to leak out into surrounding tissues and causing edema (swelling).

The neurological symptoms of edema disease are thought to be caused by the direct toxic effects of Stx2e on nerve cells in the brainstem. The exact mechanism is not fully understood, but it is believed that the toxin disrupts the normal functioning of these nerve cells, leading to symptoms such as muscle weakness, tremors, and difficulty breathing.

Treatment of edema disease typically involves supportive care, such as fluid therapy and antibiotics to control the E. coli infection. Prevention measures include vaccination against E. coli strains that produce Stx2e and maintaining good hygiene practices in pig farming operations.

"Swine" is a common term used to refer to even-toed ungulates of the family Suidae, including domestic pigs and wild boars. However, in a medical context, "swine" often appears in the phrase "swine flu," which is a strain of influenza virus that typically infects pigs but can also cause illness in humans. The 2009 H1N1 pandemic was caused by a new strain of swine-origin influenza A virus, which was commonly referred to as "swine flu." It's important to note that this virus is not transmitted through eating cooked pork products; it spreads from person to person, mainly through respiratory droplets produced when an infected person coughs or sneezes.

Shiga toxin 2 (Stx2) is a protein toxin produced by certain strains of the bacterium Escherichia coli (E. coli), specifically those that belong to serotype O157:H7 and some other Shiga toxin-producing E. coli (STEC) or enterohemorrhagic E. coli (EHEC).

Stx2 is named after Dr. Kiyoshi Shiga, who first discovered the related Shiga toxin in 1898. It is a powerful cytotoxin that can cause damage to cells lining the intestines and other organs. The toxin inhibits protein synthesis in the cells by removing an adenine residue from the 28S rRNA of the 60S ribosomal subunit, leading to cell death.

Exposure to Stx2 can occur through ingestion of contaminated food or water, or direct contact with infected animals or their feces. In severe cases, it can lead to hemorrhagic colitis, which is characterized by bloody diarrhea and abdominal cramps, and hemolytic uremic syndrome (HUS), a serious complication that can cause kidney failure, anemia, and neurological problems.

It's important to note that Stx2 has two major subtypes, Stx2a and Stx2b, which differ in their biological activities and clinical significance. Stx2a is considered more potent than Stx2b and is associated with a higher risk of developing HUS.

Edema is the medical term for swelling caused by excess fluid accumulation in the body tissues. It can affect any part of the body, but it's most commonly noticed in the hands, feet, ankles, and legs. Edema can be a symptom of various underlying medical conditions, such as heart failure, kidney disease, liver disease, or venous insufficiency.

The swelling occurs when the capillaries leak fluid into the surrounding tissues, causing them to become swollen and puffy. The excess fluid can also collect in the cavities of the body, leading to conditions such as pleural effusion (fluid around the lungs) or ascites (fluid in the abdominal cavity).

The severity of edema can vary from mild to severe, and it may be accompanied by other symptoms such as skin discoloration, stiffness, and pain. Treatment for edema depends on the underlying cause and may include medications, lifestyle changes, or medical procedures.

Swine diseases refer to a wide range of infectious and non-infectious conditions that affect pigs. These diseases can be caused by viruses, bacteria, fungi, parasites, or environmental factors. Some common swine diseases include:

1. Porcine Reproductive and Respiratory Syndrome (PRRS): a viral disease that causes reproductive failure in sows and respiratory problems in piglets and grower pigs.
2. Classical Swine Fever (CSF): also known as hog cholera, is a highly contagious viral disease that affects pigs of all ages.
3. Porcine Circovirus Disease (PCVD): a group of diseases caused by porcine circoviruses, including Porcine CircoVirus Associated Disease (PCVAD) and Postweaning Multisystemic Wasting Syndrome (PMWS).
4. Swine Influenza: a respiratory disease caused by type A influenza viruses that can infect pigs and humans.
5. Mycoplasma Hyopneumoniae: a bacterial disease that causes pneumonia in pigs.
6. Actinobacillus Pleuropneumoniae: a bacterial disease that causes severe pneumonia in pigs.
7. Salmonella: a group of bacteria that can cause food poisoning in humans and a variety of diseases in pigs, including septicemia, meningitis, and abortion.
8. Brachyspira Hyodysenteriae: a bacterial disease that causes dysentery in pigs.
9. Erysipelothrix Rhusiopathiae: a bacterial disease that causes erysipelas in pigs.
10. External and internal parasites, such as lice, mites, worms, and flukes, can also cause diseases in swine.

Prevention and control of swine diseases rely on good biosecurity practices, vaccination programs, proper nutrition, and management practices. Regular veterinary check-ups and monitoring are essential to detect and treat diseases early.

Escherichia coli (E. coli) infections refer to illnesses caused by the bacterium E. coli, which can cause a range of symptoms depending on the specific strain and site of infection. The majority of E. coli strains are harmless and live in the intestines of healthy humans and animals. However, some strains, particularly those that produce Shiga toxins, can cause severe illness.

E. coli infections can occur through various routes, including contaminated food or water, person-to-person contact, or direct contact with animals or their environments. Common symptoms of E. coli infections include diarrhea (often bloody), abdominal cramps, nausea, and vomiting. In severe cases, complications such as hemolytic uremic syndrome (HUS) can occur, which may lead to kidney failure and other long-term health problems.

Preventing E. coli infections involves practicing good hygiene, cooking meats thoroughly, avoiding cross-contamination of food during preparation, washing fruits and vegetables before eating, and avoiding unpasteurized dairy products and juices. Prompt medical attention is necessary if symptoms of an E. coli infection are suspected to prevent potential complications.

Globosides are a type of glycosphingolipids, which are molecules that consist of a lipid and a carbohydrate. They are found in animal tissues, especially in the nervous system. The term "globoside" refers to a specific structure of these molecules, where the carbohydrate portion consists of a complex chain of sugars, including galactose, N-acetylgalactosamine, and glucose. Globosides play important roles in cell recognition and interaction, and abnormalities in their metabolism have been associated with certain diseases, such as paroxysmal nocturnal hemoglobinuria (PNH).

Shiga toxin 1 (Stx1) is a protein toxin produced by certain strains of the bacterium Escherichia coli (E. coli), specifically those that belong to serotype O157:H7 and some other Shiga toxin-producing E. coli (STEC) or enterohemorrhagic E. coli (EHEC).

Shiga toxins are named after Kiyoshi Shiga, who discovered the first strain of E. coli that produces this toxin in 1897. These toxins inhibit protein synthesis in eukaryotic cells and cause damage to the endothelial cells lining blood vessels, which can lead to various clinical manifestations such as hemorrhagic colitis (bloody diarrhea) and hemolytic uremic syndrome (HUS), a severe complication that can result in kidney failure.

Shiga toxin 1 is composed of two subunits, A and B. The B subunit binds to specific glycolipid receptors on the surface of target cells, facilitating the uptake of the toxin into the cell. Once inside the cell, the A subunit inhibits protein synthesis by removing an adenine residue from a specific region of the 28S rRNA molecule in the ribosome, thereby preventing peptide bond formation and leading to cell death.

Shiga toxin 1 is highly toxic and can cause significant morbidity and mortality, particularly in children, the elderly, and immunocompromised individuals. Antibiotics are generally not recommended for the treatment of Shiga toxin-producing E. coli infections because they may increase the risk of developing HUS by inducing bacterial lysis and releasing more toxins into the circulation. Supportive care, hydration, and close monitoring are essential for managing these infections.

Bacterial toxins are poisonous substances produced and released by bacteria. They can cause damage to the host organism's cells and tissues, leading to illness or disease. Bacterial toxins can be classified into two main types: exotoxins and endotoxins.

Exotoxins are proteins secreted by bacterial cells that can cause harm to the host. They often target specific cellular components or pathways, leading to tissue damage and inflammation. Some examples of exotoxins include botulinum toxin produced by Clostridium botulinum, which causes botulism; diphtheria toxin produced by Corynebacterium diphtheriae, which causes diphtheria; and tetanus toxin produced by Clostridium tetani, which causes tetanus.

Endotoxins, on the other hand, are components of the bacterial cell wall that are released when the bacteria die or divide. They consist of lipopolysaccharides (LPS) and can cause a generalized inflammatory response in the host. Endotoxins can be found in gram-negative bacteria such as Escherichia coli and Pseudomonas aeruginosa.

Bacterial toxins can cause a wide range of symptoms depending on the type of toxin, the dose, and the site of infection. They can lead to serious illnesses or even death if left untreated. Vaccines and antibiotics are often used to prevent or treat bacterial infections and reduce the risk of severe complications from bacterial toxins.

'Escherichia coli' (E. coli) is a type of gram-negative, facultatively anaerobic, rod-shaped bacterium that commonly inhabits the intestinal tract of humans and warm-blooded animals. It is a member of the family Enterobacteriaceae and one of the most well-studied prokaryotic model organisms in molecular biology.

While most E. coli strains are harmless and even beneficial to their hosts, some serotypes can cause various forms of gastrointestinal and extraintestinal illnesses in humans and animals. These pathogenic strains possess virulence factors that enable them to colonize and damage host tissues, leading to diseases such as diarrhea, urinary tract infections, pneumonia, and sepsis.

E. coli is a versatile organism with remarkable genetic diversity, which allows it to adapt to various environmental niches. It can be found in water, soil, food, and various man-made environments, making it an essential indicator of fecal contamination and a common cause of foodborne illnesses. The study of E. coli has contributed significantly to our understanding of fundamental biological processes, including DNA replication, gene regulation, and protein synthesis.

Pulmonary edema is a medical condition characterized by the accumulation of fluid in the alveoli (air sacs) and interstitial spaces (the area surrounding the alveoli) within the lungs. This buildup of fluid can lead to impaired gas exchange, resulting in shortness of breath, coughing, and difficulty breathing, especially when lying down. Pulmonary edema is often a complication of heart failure, but it can also be caused by other conditions such as pneumonia, trauma, or exposure to certain toxins.

In the early stages of pulmonary edema, patients may experience mild symptoms such as shortness of breath during physical activity. However, as the condition progresses, symptoms can become more severe and include:

* Severe shortness of breath, even at rest
* Wheezing or coughing up pink, frothy sputum
* Rapid breathing and heart rate
* Anxiety or restlessness
* Bluish discoloration of the skin (cyanosis) due to lack of oxygen

Pulmonary edema can be diagnosed through a combination of physical examination, medical history, chest X-ray, and other diagnostic tests such as echocardiography or CT scan. Treatment typically involves addressing the underlying cause of the condition, as well as providing supportive care such as supplemental oxygen, diuretics to help remove excess fluid from the body, and medications to help reduce anxiety and improve breathing. In severe cases, mechanical ventilation may be necessary to support respiratory function.

Brain edema is a medical condition characterized by the abnormal accumulation of fluid in the brain, leading to an increase in intracranial pressure. This can result from various causes, such as traumatic brain injury, stroke, infection, brain tumors, or inflammation. The swelling of the brain can compress vital structures, impair blood flow, and cause neurological symptoms, which may range from mild headaches to severe cognitive impairment, seizures, coma, or even death if not treated promptly and effectively.

Ammonium sulfate is a chemical compound with the formula (NH4)2SO4. It is a white crystalline solid that is highly soluble in water and is commonly used in fertilizers due to its high nitrogen content. In a medical context, it can be used as a laxative or for lowering the pH of the gastrointestinal tract in certain medical conditions. It may also be used in the treatment of metabolic alkalosis, a condition characterized by an excessively high pH in the blood. However, its use in medical treatments is less common than its use in agricultural and industrial applications.

Ultrafiltration is a medical process that separates fluids and dissolved solutes based on their size and charge. It's a type of membrane filtration that uses a semipermeable membrane with pores small enough to allow the passage of water and low molecular weight solutes, while retaining larger molecules and cells.

In clinical practice, ultrafiltration is often used in patients with acute or chronic kidney failure to remove excess fluid from the bloodstream, a process known as renal replacement therapy or dialysis. During this procedure, the patient's blood is passed through a hollow fiber membrane, and pressure differences across the membrane cause water and small solutes to move through the pores, while larger molecules such as proteins and cells are retained.

Ultrafiltration can also be used in other medical contexts, such as plasma exchange or therapeutic apheresis, where specific components of the blood are removed for therapeutic purposes.

Diarrhea is a condition in which an individual experiences loose, watery stools frequently, often exceeding three times a day. It can be acute, lasting for several days, or chronic, persisting for weeks or even months. Diarrhea can result from various factors, including viral, bacterial, or parasitic infections, food intolerances, medications, and underlying medical conditions such as inflammatory bowel disease or irritable bowel syndrome. Dehydration is a potential complication of diarrhea, particularly in severe cases or in vulnerable populations like young children and the elderly.

Deoxycholic acid is a bile acid, which is a natural molecule produced in the liver and released into the intestine to aid in the digestion of fats. It is also a secondary bile acid, meaning that it is formed from the metabolism of primary bile acids by bacteria in the gut.

Deoxycholic acid has a chemical formula of C~24~H~39~NO~4~ and a molecular weight of 391.57 g/mol. It is a white crystalline powder that is soluble in water and alcohol. In the body, deoxycholic acid acts as a detergent to help break down dietary fats into smaller droplets, which can then be absorbed by the intestines.

In addition to its role in digestion, deoxycholic acid has been investigated for its potential therapeutic uses. For example, it is approved by the US Food and Drug Administration (FDA) as an injectable treatment for reducing fat in the submental area (the region below the chin), under the brand name Kybella. When injected into this area, deoxycholic acid causes the destruction of fat cells, which are then naturally eliminated from the body over time.

It's important to note that while deoxycholic acid is a natural component of the human body, its therapeutic use can have potential side effects and risks, so it should only be used under the supervision of a qualified healthcare professional.

Bacterial vaccines are types of vaccines that are created using bacteria or parts of bacteria as the immunogen, which is the substance that triggers an immune response in the body. The purpose of a bacterial vaccine is to stimulate the immune system to develop protection against specific bacterial infections.

There are several types of bacterial vaccines, including:

1. Inactivated or killed whole-cell vaccines: These vaccines contain entire bacteria that have been killed or inactivated through various methods, such as heat or chemicals. The bacteria can no longer cause disease, but they still retain the ability to stimulate an immune response.
2. Subunit, protein, or polysaccharide vaccines: These vaccines use specific components of the bacterium, such as proteins or polysaccharides, that are known to trigger an immune response. By using only these components, the vaccine can avoid using the entire bacterium, which may reduce the risk of adverse reactions.
3. Live attenuated vaccines: These vaccines contain live bacteria that have been weakened or attenuated so that they cannot cause disease but still retain the ability to stimulate an immune response. This type of vaccine can provide long-lasting immunity, but it may not be suitable for people with weakened immune systems.

Bacterial vaccines are essential tools in preventing and controlling bacterial infections, reducing the burden of diseases such as tuberculosis, pneumococcal disease, meningococcal disease, and Haemophilus influenzae type b (Hib) disease. They work by exposing the immune system to a harmless form of the bacteria or its components, which triggers the production of antibodies and memory cells that can recognize and fight off future infections with that same bacterium.

It's important to note that while vaccines are generally safe and effective, they may cause mild side effects such as pain, redness, or swelling at the injection site, fever, or fatigue. Serious side effects are rare but can occur, so it's essential to consult with a healthcare provider before receiving any vaccine.

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