ulcerative colitis
Introduction
Introduction to ulcerative enteritis Ulcerative enteritis is caused by Clostridium colonium (also known as Clostridium entericus). The strain is rod-shaped and is Gram-positive; the bacteria are 3~4m long, 1m wide, straight or slightly curved, both ends are obtuse, the spores are smaller than the bacteria, located at the proximal end of the bacteria, artificial culture, Only a few cells can form spores. The disease is characterized by sudden onset and rapid and massive death, which is distributed worldwide. Most poultry can be infected with this disease, cockroaches are the most sensitive, and laboratory artificial infections are successful, and many other poultry can naturally be infected. The disease often invades young birds, and young birds such as 4 to 19 weeks old chickens, 3 to 8 weeks old turkeys, and 4 to 12 weeks old cockroaches are more susceptible, and adult ticks can also be infected. The disease is often associated with coccidiosis, or secondary to coccidiosis, aplastic anemia, infectious bursal disease, and stress factors. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific population Mode of infection: fecal-mouth transmission Complications: lower gastrointestinal bleeding colon cancer rectal cancer nodular erythema iritis iritis ciliary body inflammation keratitis fatty liver
Cause
Cause of ulcerative enteritis
Autoimmune factors (30%):
It has been proved that non-specific anti-colon mucosal antibodies have been detected in the serum of patients, and anti-E. coli 014 antibodies in serum can cross-react with colonic epithelial antigens, indicating the presence of humoral immune disorders. In tissue culture, the colonic epithelium of patients It can be damaged by lymphocytes, and the immune cells are dysfunctional. The immune complex deposition is detected by fluorescence immunoassay in the colonic mucosa of the patient.
Neuropsychiatric factors (15%):
Trauma, emotional stress or excessive fatigue can cause cerebral cortical function disorder, subcortical central hyperactivity, intestinal movement through autonomic nerves (autonomic nerves), intestinal vascular and smooth muscle spasm, long-term tissue ischemia and hypoxia, resistance Reduced tolerance, increased capillary permeability, intestinal mucosa prone to inflammatory changes, congestion, edema, erosion, ulcers, bleeding. It can be said that the occurrence of this disease is related to genetic factors, based on autoimmune function, infection and neuropsychiatry factors are the incentives.
Infection (20%):
Because the inflammation of the colonic mucosa of this disease is similar to some infectious diarrhea, such as bacterial dysentery and amoebic dysentery, it is considered to be the triggering factor of the disease.
Genetic (10%):
The incidence of this disease varies greatly among different races, different populations, and different constitutions. The incidence of Caucasians is much higher than that of yellows and blacks.
Prevention
Ulcerative enteritis prevention
Do routine hygiene work, and disinfect the premises and utensils regularly. Feces and bedding should be cleaned up and biothermally disinfected to reduce the harm caused by the spread of pathogens. Avoid crowding, overheating, overeating and other adverse factors, effectively control the occurrence of coccidiosis, and have a positive effect on the prevention of this disease. For the contaminated field of this disease, it is necessary to isolate the bacteria and bacteria in time, and isolate the sick birds.
Complication
Ulcerative enteritis complications Complications lower gastrointestinal bleeding colon cancer rectal cancer nodular erythema iritis iridocyclitis keratitis fatty liver
Toxic megacolon
It is a serious complication, seen in acute fulminant ulcerative colitis and acute severe patients. Its incidence is about 2%. The patient developed intermittent hyperthermia and is in a state of severe poisoning. The abdomen quickly swells, has tenderness, and the bowel sounds weaken or disappear. Due to rapid colon expansion, thinning of the intestinal wall, blood circulation disorders, prone to intestinal necrosis. The mortality rate is extremely high. Up to 30% to 50%.
2. Colon perforation
Most occur on the basis of toxic megacolon expansion. Perforation leads to diffuse peritonitis or a localized abscess. Most of the perforation sites are in the sigmoid colon or the spleen of the colon. Patients with high fever and symptoms of infection. Abdominal distension, extensive muscle tension in the left abdomen, fluoroscopy or plain film examination.
Symptom
Ulcerative symptoms of enteritis Common symptoms Chronic abdominal pain, abdominal pain, diarrhea, abdominal pain, diarrhea, abdominal pain, nausea, vomiting, nausea and vomiting, nausea, lower abdominal pain, lower right abdominal pain, vomiting
It often occurs under the sputum, discharges white water and dilute the feces, and the spirit is stunned. If the course of disease is 1 week or longer, the body is abnormally thin.
Examine
Examination of ulcerative enteritis
Early lesions are characterized by small yellow lesions, marginal hemorrhage, and can be seen on both the serosal and mucosal surfaces. When the area of the ulcer is increased, it may be in the form of a lentil or a substantially circular outline, sometimes fused to form a large necrotizing pseudomembranous plaque. Ulcers may penetrate deep into the mucosa, but older lesions are often superficial and have raised edges that form crater-like ulcers. Causes peritonitis and intestinal adhesions.
Diagnosis
Diagnosis and diagnosis of ulcerative enteritis
diagnosis
Ulcerative enteritis is easier to diagnose based on post-mortem macroscopic lesions. A clinical diagnosis can be made based on typical intestinal ulcers and associated hepatic necrosis and splenomegaly hemorrhage. Confirmation of the diagnosis requires further pathogen examination.
Differential diagnosis
The disease should be differentiated from coccidiosis, trichomoniasis, necrotic enteritis and inclusion body hepatitis.
