Enterotoxemia
Clostridium perfringens
Edema Disease of Swine
Capripoxvirus
Toxoids
Bacterial Toxins
Comparison of four techniques for the detection of Clostridium perfringens type D epsilon toxin in intestinal contents and other body fluids of sheep and goats. (1/28)
Polyclonal capture enzyme-linked immunosorbent assay (PC-ELISA), monoclonal capture ELISA (MC-ELISA), mouse neutralization test (MNT), and counterimmunoelectrophoresis (CIEP), were compared for their ability to detect epsilon toxin in intestinal contents and body fluids of sheep and goats. When used to evaluate intestinal contents of sheep artificially spiked with epsilon prototoxin, PC-ELISA detected 0.075 mouse lethal dose (MLD)50/ml, whereas the MNT, MC-ELISA, and CIEP detected 6, 25, and 50 MLD50/ml, respectively. Amounts of epsilon toxin detected by PC-ELISA, MC-ELISA, MNT, and CIEP in sheep pericardial fluid artificially spiked with epsilon prototoxin were 0.075, 0.75, 6, and 200 MLD50/ml, respectively. For assaying epsilon toxin in aqueous humor, PC-ELISA and MC-ELISA detected 0.075 MLD50/ml, whereas CIEP detected 200 MLD50/ml (MNT was not evaluated). When 51 samples of intestinal contents of sheep and goats (32 positive and 19 negative to MNT) were analyzed by the other 3 techniques, the relative sensitivity of PC-ELISA, MC-ELISA, and CIEP was 93.75, 84.37, and 37.50%, respectively. The specificity of PC-ELISA, MC-ELISA, and CIEP was 31.57, 57.89, and 84.21%, respectively. The absolute sensitivity of PC-ELISA, MC-ELISA, CIEP, and MNT was 90.90, 69.69, 15.15, and 54.54%. The absolute specificity of the 4 techniques was 100%. These results show that there is a marked inconsistency among techniques routinely used to detect Clostridium perfringens epsilon toxin. Until more consistent results are achieved, the diagnosis of enterotoxemia should not only be based solely on epsilon toxin detection, but also on clinical and pathological data. (+info)Clostridium perfringens type A and beta2 toxin associated with enterotoxemia in a 5-week-old goat. (2/28)
Postmortem examination of a Boer buck kid that died peracutely revealed diffusely congested, edematous bowel. Clostridium perfringens Type A was isolated. Some isolates carried the gene for beta2 toxin, suggesting a role for beta2 toxin in caprine enterotoxemia, a common cause of death in growing kids. (+info)The pathology of peracute experimental Clostridium perfringens type D enterotoxemia in sheep. (3/28)
The pathological findings in sheep with peracute experimental Clostridium perfringens type D enterotoxemia are described. Of 16 animals inoculated intraduodenally with a whole culture of this microorganism and a starch solution in the abomasum, 12 developed clinical signs including increased respiratory efforts, recumbency, paddling, bleating, convulsions, blindness, and opisthotonus. Diarrhea was not observed in any of the animals. The time lapse between the beginning of intraduodenal infusion and onset of clinical signs varied between 30 minutes and 26 hours, and the clinical course varied between 1 and 9 hours. Gross postmortem changes were observed in these 12 animals and included pulmonary edema; excess pericardial, peritoneal, or pleural fluid with or without strands of fibrin; liquid small intestinal contents; leptomeningeal edema; cerebellar coning; and subcapsular petechiae on kidneys. Histological changes consisted of severe edema of pleura and interlobular septa and around blood vessels and airways and acidophilic, homogeneous, proteinaceous perivascular edema in the brain. Five of 12 animals (42%) with clinical signs consistent with enterotoxemia lacked specific histological lesions in the brain. None of the intoxicated or control animals developed nephrosis. Glucose was detected in the urine of 3 of 6 animals that were tested for this analyte. These results stress the importance of the use of histological examination of the brain, coupled with epsilon toxin detection, for a definitive diagnosis of C. perfringens type D enterotoxemia in sheep. (+info)Enterotoxemia associated with beta2 toxin-producing Clostridium perfringens type A in two Asiatic black bears (Selenarctos thibetanus). (4/28)
Beta2 (beta2) toxin-producing Clostridium perfringens type A strains were found to be associated with necrotic and hemorrhagic intestinal lesions in 2 Asiatic black bears (Selenarctos thibetanus) that died suddenly. Ten isolates were obtained from the liver, lungs, heart, and small and large intestine of the animals and were examined by multiplex polymerase chain reaction for the genes encoding the 4 lethal toxins (alpha, beta, epsilon, and iota) for classification into toxin types as well as for the genes encoding enterotoxin and the novel beta2-toxin for subclassification. In addition, the cpb2 sequence of the 10 isolates was different from the published sequence of cpb2 of pig type C isolate CWC245, whereas it was highly similar to the cpb2 sequence of the C. perfringens type A strain 13. This finding suggests the existence of 2 cpb2 subtypes. This is the first report of enterotoxemia associated with the presence of C. perfringens producing beta2-toxin in the tissues and intestinal content of Asiatic black bears. (+info)Development and application of an oral challenge mouse model for studying Clostridium perfringens type D infection. (5/28)
Clostridium perfringens type D isolates cause enterotoxemia in sheep, goats, and probably cattle. While the major disease signs and lesions of type D animal disease are usually attributed to epsilon toxin, a class B select agent, these bacteria typically produce several lethal toxins. Understanding of disease pathogenesis and development of improved vaccines are hindered by the lack of a small-animal model mimicking natural disease caused by type D isolates. Addressing this need, we developed an oral challenge mouse model of C. perfringens type D enterotoxemia. When BALB/c mice with a sealed anus were inoculated by intragastric gavage with type D isolates, 7 of 10 type D isolates were lethal, as defined by spontaneous death or severe clinical signs necessitating euthanasia. The lethalities of the seven type D isolates varied between 14 and 100%. Clinical signs in the lethally challenged mice included seizures, convulsions, hyperexcitability, and/or depression. Mild intestinal gas distention and brain edema were observed at necropsy in a few mice, while histology showed multifocal acute tubular necrosis of the kidney and edema in the lungs of most challenged mice that developed a clinical response. When the lethality of type D isolates in this model was compared with in vitro toxin production, only a limited correlation was observed. However, mice could be protected against lethality by intravenous passive immunization with an epsilon toxin antibody prior to oral challenge. This study provides an economical new model for studying the pathogenesis of C. perfringens type D infections. (+info)Clinicopathologic features of experimental Clostridium perfringens type D enterotoxemia in cattle. (6/28)
(+info)Clostridium perfringens epsilon toxin increases the small intestinal permeability in mice and rats. (7/28)
(+info)Antibody response to the epsilon toxin of Clostridium perfringens following vaccination of Lama glama crias. (8/28)
BACKGROUND: Enterotoxaemia produced by Clostridium perfringens A, C and D is an important cause of mortality in young llamas. There is no data on antibody responses following vaccination with epsilon toxin. METHODOLOGY: Twenty-six L. glama crias were divided into four groups which were vaccinated with a commercial vaccine (Mancha Gangrena Enterotoxemia, Instituto Rosembusch Sociedad Anonima, Argentina) on days 0, 21 and 42 or left as unvaccinated controls. An indirect ELISA was compared with the mouse neutralization test (MNT) for measuring titers to C. perfringens type D epsilon toxin and used to determine titers in sera taken before vaccination and 16, 28, 49, 59, and 93 days later. RESULTS: The ELISA gave comparable results to the MNT and showed animals vaccinated once failed to develop raised titers. A week following a second vaccination, mean antibody titers rose significantly (P < 0.05) and 7/12 animals developed high titers which were present in only one animal at the end of the study (day 93). A third vaccination resulted in a decrease in mean antibody titers a week later. CONCLUSIONS: Llamas develop antibodies to Clostridium perfringens type D epsilon toxin after two vaccinations at a 21-day interval. Further studies are indicated to determine if these inoculations protect against enterotoxemia and the most appropriate vaccination schedule. (+info)Enterotoxemia is a condition characterized by the presence of toxins (specifically, enterotoxins) produced by certain types of bacteria in the intestines. This condition primarily affects ruminant animals such as sheep, goats, and cattle, although it can also occur in other species including humans.
The bacteria responsible for enterotoxemia are often part of the normal gut flora but can cause disease when they overgrow and produce large amounts of toxins. The most common bacterial species associated with enterotoxemia are Clostridium perfringens types C and D, and occasionally type A. These bacteria produce potent enterotoxins that can cause damage to the intestinal lining, leading to inflammation, diarrhea, dehydration, and potentially fatal septicemia.
Enterotoxemia can occur in animals of any age but is most commonly seen in young animals that have not yet fully developed their immune system or have been recently weaned. The condition can be triggered by a variety of factors, including dietary changes, overeating, stress, and viral infections.
Prevention of enterotoxemia typically involves vaccination against the causative bacteria and good management practices to minimize stress and prevent overeating. Treatment may involve supportive care such as fluid therapy, antibiotics, and anti-toxins, but the prognosis is often guarded, especially in severe cases.
'Clostridium perfringens' is a type of Gram-positive, rod-shaped, spore-forming bacterium that is commonly found in the environment, including in soil, decaying vegetation, and the intestines of humans and animals. It is a major cause of foodborne illness worldwide, producing several toxins that can lead to symptoms such as diarrhea, abdominal cramps, nausea, and vomiting.
The bacterium can contaminate food during preparation or storage, particularly meat and poultry products. When ingested, the spores of C. perfringens can germinate and produce large numbers of toxin-producing cells in the intestines, leading to food poisoning. The most common form of C. perfringens food poisoning is characterized by symptoms that appear within 6 to 24 hours after ingestion and last for less than 24 hours.
In addition to foodborne illness, C. perfringens can also cause other types of infections, such as gas gangrene, a serious condition that can occur when the bacterium infects a wound and produces toxins that damage surrounding tissues. Gas gangrene is a medical emergency that requires prompt treatment with antibiotics and surgical debridement or amputation of affected tissue.
Prevention measures for C. perfringens food poisoning include proper cooking, handling, and storage of food, as well as rapid cooling of cooked foods to prevent the growth of the bacterium.
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.
Clostridium infections are caused by bacteria of the genus Clostridium, which are gram-positive, rod-shaped, spore-forming, and often anaerobic organisms. These bacteria can be found in various environments, including soil, water, and the human gastrointestinal tract. Some Clostridium species can cause severe and potentially life-threatening infections in humans. Here are some of the most common Clostridium infections with their medical definitions:
1. Clostridioides difficile infection (CDI): An infection caused by the bacterium Clostridioides difficile, previously known as Clostridium difficile. It typically occurs after antibiotic use disrupts the normal gut microbiota, allowing C. difficile to overgrow and produce toxins that cause diarrhea, colitis, and other gastrointestinal symptoms. Severe cases can lead to sepsis, toxic megacolon, or even death.
2. Clostridium tetani infection: Also known as tetanus, this infection is caused by the bacterium Clostridium tetani. The spores of this bacterium are commonly found in soil and animal feces. They can enter the body through wounds, cuts, or punctures, germinate, and produce a potent exotoxin called tetanospasmin. This toxin causes muscle stiffness and spasms, particularly in the neck and jaw (lockjaw), which can lead to difficulty swallowing, breathing, and potentially fatal complications.
3. Clostridium botulinum infection: This infection is caused by the bacterium Clostridium botulinum and results in botulism, a rare but severe paralytic illness. The bacteria produce neurotoxins (botulinum toxins) that affect the nervous system, causing symptoms such as double vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness. In severe cases, botulism can lead to respiratory failure and death.
4. Gas gangrene (Clostridium perfringens infection): A rapidly progressing soft tissue infection caused by Clostridium perfringens or other clostridial species. The bacteria produce potent exotoxins that cause tissue destruction, gas production, and widespread necrosis. Gas gangrene is characterized by severe pain, swelling, discoloration, and a foul-smelling discharge. If left untreated, it can lead to sepsis, multi-organ failure, and death.
5. Clostridioides difficile infection (C. difficile infection): Although not caused by a typical clostridial species, C. difficile is a gram-positive, spore-forming bacterium that can cause severe diarrhea and colitis, particularly in hospitalized patients or those who have recently taken antibiotics. The bacteria produce toxins A and B, which damage the intestinal lining and contribute to inflammation and diarrhea. C. difficile infection can range from mild to life-threatening, with complications such as sepsis, toxic megacolon, and bowel perforation.
Capripoxvirus is a genus of viruses in the family Poxviridae, subfamily Chordopoxvirinae. This genus includes three species of poxviruses that primarily infect members of the Artiodactyla order (even-toed ungulates), such as sheep, goats, and cattle. The three species are:
1. Sheeppox virus (SPPV) - causes sheeppox in sheep and goatpox in goats
2. Goatpox virus (GTPV) - causes goatpox in goats and sometimes in sheep
3. Lumpy skin disease virus (LSDV) - causes lumpy skin disease in cattle
These viruses are large, complex, enveloped double-stranded DNA viruses with a linear genome of approximately 150 kilobases. They replicate in the cytoplasm of infected cells and can cause severe diseases in their respective hosts, characterized by fever, lesions on the skin and mucous membranes, and secondary bacterial infections. Vaccination is an important control strategy for capripoxviruses.
Toxoids are inactivated bacterial toxins that have lost their toxicity but retain their antigenicity. They are often used in vaccines to stimulate an immune response and provide protection against certain diseases without causing the harmful effects associated with the active toxin. The process of converting a toxin into a toxoid is called detoxication, which is typically achieved through chemical or heat treatment.
One example of a toxoid-based vaccine is the diphtheria and tetanus toxoids (DT) or diphtheria, tetanus, and pertussis toxoids (DTaP or TdaP) vaccines. These vaccines contain inactivated forms of the diphtheria and tetanus toxins, as well as inactivated pertussis toxin in the case of DTaP or TdaP vaccines. By exposing the immune system to these toxoids, the body learns to recognize and mount a response against the actual toxins produced by the bacteria, thereby providing immunity and protection against the diseases they cause.
I'm happy to help, but I want to clarify that the term "sheep diseases" refers to a wide range of health issues that can affect sheep populations. It's not a single medical condition with a specific definition. Here are some examples of common diseases that can affect sheep:
1. Ovine Johne's Disease (OJD): A chronic, infectious disease caused by the bacterium Mycobacterium avium subspecies paratuberculosis. It affects the intestines and can cause weight loss, diarrhea, and death.
2. Footrot: A highly contagious bacterial infection that affects the feet of sheep, causing lameness, swelling, and pain. It's caused by the bacteria Dichelobacter nodosus.
3. Caseous Lymphadenitis (CL): A chronic infectious disease caused by the bacterium Corynebacterium pseudotuberculosis. It affects the lymph nodes and can cause abscesses, weight loss, and death.
4. Contagious Ecthyma (Orf): A highly contagious viral infection that affects the skin and mucous membranes of sheep, causing sores and lesions.
5. Mastitis: An inflammation of the mammary gland in sheep, usually caused by a bacterial infection. It can cause decreased milk production, fever, and loss of appetite.
6. Pneumonia: A respiratory infection that can affect sheep, causing coughing, difficulty breathing, and fever. It can be caused by various bacteria or viruses.
7. Enterotoxemia: A potentially fatal disease caused by the overproduction of toxins in the intestines of sheep, usually due to a bacterial infection with Clostridium perfringens.
8. Polioencephalomalacia (PEM): A neurological disorder that affects the brain of sheep, causing symptoms such as blindness, circling, and seizures. It's often caused by a thiamine deficiency or excessive sulfur intake.
9. Toxoplasmosis: A parasitic infection that can affect sheep, causing abortion, stillbirth, and neurological symptoms.
10. Blue tongue: A viral disease that affects sheep, causing fever, respiratory distress, and mouth ulcers. It's transmitted by insect vectors and is often associated with climate change.
I believe there may be a misunderstanding in your question. "Goat diseases" refers to illnesses that affect goats specifically. It does not mean diseases that are caused by goats or related to them in some way. Here are some examples of goat diseases:
1. Caprine Arthritis Encephalitis (CAE): A viral disease that affects goats, causing arthritis, pneumonia, and sometimes encephalitis.
2. Caseous Lymphadenitis (CL): A bacterial disease that causes abscesses in the lymph nodes of goats.
3. Contagious Caprine Pleuropneumonia (CCPP): A contagious respiratory disease caused by mycoplasma bacteria.
4. Johne's Disease: A chronic wasting disease caused by a type of bacterium called Mycobacterium avium subspecies paratuberculosis.
5. Pasteurellosis: A bacterial disease that can cause pneumonia, septicemia, and other infections in goats.
6. Salmonellosis: A bacterial disease caused by Salmonella bacteria, which can cause diarrhea, fever, and septicemia in goats.
7. Soremouth (Orf): A viral disease that causes sores and scabs around the mouth and nose of goats.
These are just a few examples of diseases that can affect goats. If you have any specific questions about goat health or diseases, I would recommend consulting with a veterinarian who specializes in small ruminants.
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.
I'm sorry for any confusion, but "goats" is not a term commonly used in medical definitions. It is a common noun referring to the domesticated animal species Capra aegagrus hircus. If you have any questions about a specific medical condition or term, please provide that and I would be happy to help.
Enterotoxemia