Causes Tests Diagnosis and Treatment of Cholera
Cholera is an acute diarrheal infectious disease caused by ingestion of food or water contaminated with Vibrio cholerae. Each year, there are an estimated 3 million to 5 million cholera cases and another 100,000 to 120,000 deaths. The peak of the disease occurs in summer, which can cause diarrhea to become dehydrated or even die within a few hours.
Cholera is caused by Vibrio cholerae. The serotypes of Vibrio cholerae O1 and O139 can cause disease outbreaks.
Most disease outbreaks are caused by Vibrio cholerae O1, and the type O139 first identified in Bangladesh in 1992 is limited to Southeast Asia.
Non-O1 non-O139 Vibrio cholerae can cause mild diarrhea, but it will not cause disease epidemics. Recently, new mutant strains have been discovered in some regions of Asia and Africa.
According to observations, these strains can cause more severe cholera disease and higher mortality.
Vibrio cholerae exists in water, and the most common cause of infection is the consumption of water contaminated with the feces of patients.
Vibrio cholerae can produce cholera toxin, causing secretory diarrhea, even if you no longer eat, it will continue to diarrhea. Washing water-like feces is a feature of cholera.
Treatment department: Infectious Diseases
Common morbidity:Digestive system
Common causes:Caused by Vibrio cholerae infection
Common causes:Caused by Vibrio cholerae infection
Common symptoms:Sudden diarrhea, followed by vomiting, decreased blood pressure, weak pulse, etc.
How to prevent cholera effectively?
Cholera is an acute intestinal infectious disease caused by Vibrio cholerae.
Its morbidity is rapid and spreads quickly. It needs more attention in summer.
Table of Content
- Clinical manifestations
Cholera is caused by Vibrio cholerae. Vibrio cholerae is negative for Gram stain and is sensitive to drying, sunlight, heat, acid and general disinfectants.
The pathogenicity of Vibrio cholerae is endotoxin and exotoxin. Normal gastric acid can kill Vibrio.
When gastric acid is temporarily low or the number of invading virus bacteria increases, Vibrio not killed by gastric acid enters the small intestine, rapidly multiplies in alkaline intestinal fluid, and produces a large number of strong exotoxins. This exotoxin has ADP-ribosyltransferase activity.
After entering the cell to catalyze the intracellular NAD + ADP ribosyl group covalently bound to the subunit. This subunit will not be able to hydrolyze the GTP itself bound to GDP.
This subunit is in a continuous activation state, constantly activating adenylate cyclase, resulting in increased cAMP levels in small intestinal epithelial cells, resulting in a continuous outflow of large amounts of sodium ions and water.
The effect of this exotoxin on the intestinal mucosa causes a large amount of secretion of intestinal fluid, which is very large and exceeds the capacity of intestinal reabsorption. In the clinic, there is severe diarrhea and severe dehydration, resulting in a significant reduction in plasma volume, a lack of salt in the body, and blood Concentration, peripheral circulatory failure occurs.
Due to severe diarrhea, electrolyte loss, potassium and sodium deficiency, muscle cramps, acidosis, and even shock and acute renal failure.
What are the clinical manifestations of Cholera?
1. Emetic period
The diarrhea period usually begins with sudden diarrhea and then vomiting.
Generally, there is no obvious abdominal pain, and there is no serious feeling of urgency.
It is difficult to count stools several times a day, and the volume is large, ranging from 2000 to 4000ml per day, and more than 8000ml in severe cases.
It was yellow water sample at first, and soon turned into watery watery stools. A few patients had bloody watery or tarry watery stools.
After diarrhea, there was ejection and borderline vomiting. The stomach contents first, followed by watery, watery rice swillings.
Vomiting is usually not accompanied by nausea, spray-like, and its contents are similar to the characteristics of stool.
A small number of patients are not accompanied by vomiting during diarrhea.
Severe diarrhea caused a large loss of body fluids and electrolytes, resulting in circulatory failure, manifested by decreased blood pressure, weak pulse, hemoglobin and plasma proportion increased significantly, urine output decreased or even no urine.
The excretion of organic acids and nitrogen products in the body is hindered, and patients often have initial symptoms of acidosis and uremia.
A large amount of electrolytes such as sodium and potassium were lost in the blood, and the patient developed systemic electrolyte disorders. Sodium deficiency can cause muscle spasms, especially the gastrocnemius and rectus abdominis.
Potassium deficiency can cause hypokalemia syndrome, such as hypotonic muscle tension, disappearance of tendon reflex, tympanic bowel, tachycardia, arrhythmia, etc. Due to the massive loss of bicarbonate ions, metabolic acidosis may occur, in severe cases, the unconsciousness and blood pressure drop.
2. Dehydration collapse period
The appearance of patients with dehydration and prostration is very obvious.
In severe cases, the eyes are deep. The voice is hoarse. The skin is dry and shrunken. Elasticity disappears. The abdomen is sunken. The lips are dry, thirsty and the thirst is drunk. There are muscle cramps or convulsions.
3. Recovery period
A small number of patients (more common in children) may have a febrile reaction at this time, and the body temperature rises to 38 ℃ – 39 ℃. This usually subsides after 1 to 3 days, so this period is also called the reaction period.
The average course of disease is 3 to 7 days.
What are the tests for Cholera?
1. Blood test
Red blood cell count and hemoglobin increased, white blood cell count increased, neutrophil and large monocyte count increased. Serum potassium, sodium, chloride, and carbonate decreased, blood pH decreased, and urea nitrogen increased.
Before treatment, due to intracellular potassium ion migration, serum potassium can be within the normal range.
When acidosis is corrected, potassium ion moves into the cell and hypokalemia occurs.
2. Urine examination
A small number of patients may have protein, red, white blood cells and cast in the urine.
3. Pathogen inspection
(1) Routine microscopic examination revealed mucus and a little red and white blood cells.
(2) Smear staining Take a stool or early culture smear for Gram stain microscopic examination, and Gram-negative Vibrio is slightly curved.
(3) Hanging drop inspection Fresh stools were examined by hanging drop or dark field microscopy. Vibrio bacteria with active movements and shuttles were visible.
(4) Braking test: Take watery stools or alkaline peptone water-enriched bacteria from the patients in the acute phase for 6 hours to grow superficial growths, and then conduct a dark field microscopy to observe the power.
If there is a shuttle-like animal, add a drop of O1 group of multivalent serum.
In case, it is O1 group of Vibrio cholerae, due to the action of antigen and antibody, it will agglomerate and the movement of Vibrio will stop.
If after adding O1 group serum, can not stop exercise, should use O139 serum to repeat the test.
(5) Enrichment culture: All stools of suspected cholera patients should be enriched culture except for microscopic examination.
Feces should be collected before using antibacterial drugs, and should be sent to the laboratory for cultivation as soon as possible.
The enrichment medium generally uses alkaline peptone water with a pH of 8.4, and the surface can form a bacterial membrane after incubation at 36 ° C to 37 ° C for 6 to 8 hours. At this time, further separation and cultivation should be carried out, and power observation and braking test should be carried out.
(6) Gentamicin agar plates or alkaline agar plates are commonly used for separation and culture. The former is a strong selective medium. The Vibrio cholerae can grow into small colonies after being cultured at 36 ℃ to 37 ℃ for 8 to 10 hours.
The latter requires 10 to 20 hours of cultivation. Select suspicious or typical colonies, apply antiserum of Vibrio cholerae “O” antigen for slide agglutination test, and report if positive.
In recent years, DNA probes of cholera toxin genes have also been used abroad for colony hybridization, which can quickly identify the toxin-producing O1 group of Vibrio cholerae.
(7) PCR detection Recently, PCR technology has been applied abroad to quickly diagnose cholera. Among them, the cholera strain is distinguished from non-V.
Cholerae by identifying the C. toxin gene subunit CtxA and the toxin synergic fimbriae gene (TcpA) in the PCR product, and then distinguishing the classical biotype from the El Hold biotype Vibrio cholerae.
Results can be obtained within 4 hours.
(8) Identification test Identification of classical biotype, Elto biotype and O139 type Vibrio cholerae.
4. Serological examination
Can be used for serum agglutination test. Take 1 sera each on the 1st to 3rd and 10th to 15th days of onset.
If the antibody titer of the 2nd sera increases 4 times or more than the 1st sera, it has diagnostic value.
What is the diagnosis for Cholera?
1. Diagnostic criteria
i. Anyone who has symptoms of diarrhea and vomiting, and stool-cultured Vibrio cholerae positive.
ii. Cholera epidemic period has typical symptoms of cholera in epidemic areas and stool culture is negative for no other reason can be checked.
If conditions can do double serum lectin test A titer of 4 times or more can be diagnosed.
iii. If diarrhea symptoms are found within 5 days before the stool culture is positive during the outbreak detection, it can be diagnosed as mild cholera.
2. Suspected standards
i. In cases of non-epidemic areas with typical symptoms of diarrhea, before the diagnosis of etiological examination is not confirmed
ii. Cholera epidemic period, who have been exposed to cholera patients, who have diarrhea symptoms and no other reasons can be investigated.
Serological examination is suitable for retrospective diagnosis after illness, and is not helpful for early diagnosis. Diagnosis must identify the following diarrheal diseases:
ii. Bacterial food poisoning caused by Salmonella, Staphylococcus, Proteus, etc.
iii. Diarrhea caused by Vibrio parahaemolyticus
iv. Enterotoxigenic coliform diarrhea
v. Viral (Especially rotavirus) gastroenteritis
vi. Parasitic diarrhea
vii, Diarrhea caused by certain poisons (such as organophosphorus pesticides, arsenic trioxide, etc.).
The diagnosis and identification of mild atypical cholera cases are difficult.
Generally only mild diarrhea, without vomiting, normal blood pressure and pulse, clear mind, short course of disease, healed spontaneously within three or two days. Outbreaks of cholera or dry cholera are relatively rare.
No vomiting, diarrhea, or dehydration are seen after the onset, but they quickly transition to shock and severe toxic circulatory failure. The mortality rate is extremely high.
What is the treatment for Cholera?
The treatment principle of this disease is strict isolation, rapid replenishment of water and electrolytes, correction of acidosis, supplemented by antibacterial treatment and symptomatic treatment.
1. General treatment and nursing
(1) Close isolation according to infectious diseases of the digestive tract until 6 days after the symptoms disappear, and the vibrio feces will be negative for 3 consecutive times before the isolation can be lifted.
Patient materials and excrement must be strictly disinfected. System to prevent cross infection.
(2) Rest patients with severe disease must rest in bed until their symptoms improve.
(3) Suspension of severe vomiting and diarrhea. When the vomiting is stopped, diarrhea can be relieved, and a liquid diet can be given.
When the patient can tolerate the diet, slowly increase the diet.
(4) The supplement of water is the basic treatment of cholera. Light patients can take oral rehydration, and heavy patients need intravenous rehydration. After the symptoms improve, they should be replaced by oral rehydration.
(5) Specimen collection The vomit feces specimens are collected immediately after the patient is admitted to the hospital and sent for routine examination and bacterial culture.
Note that the specimens should be sent for inspection immediately after collection.
(6) Observe the changes of the condition closely and measure the vital signs every 4 hours, accurately record the amount of entry and exit, and indicate the frequency, volume and traits of the stool.
2. Treatment and nursing of infusion
Principles of infusion therapy: early, rapid and appropriate amount, salt first, sugar first, then fast first, slow acid, calcium correction, see urine potassium supplement.
3. Symptomatic treatment and nursing
(1) Frequent vomiting can be given to atropine.
(2) For severe diarrhea, adrenal cortex hormones can be used as appropriate.
(3) Muscle spasm can be intravenously infused with 10% calcium gluconate, hot compress, massage.
(4) After a large number of fluids to correct acidosis in peripheral circulatory failure, blood pressure still does not rise, you can use alamin or dopamine drugs.
(5) People with uremia should strictly control the body intake, prohibit protein diet, strengthen oral and skin care, and use dialysis therapy if necessary.
4. Cause treatment and nursing
Tetracycline can shorten the course of treatment to reduce diarrhea and shorten the time of fecal detoxification and reduce the phenomenon of bacteria. It can be intravenously infused until the condition improves.
It can also be treated with doxycycline, co-trimoxazole, pipemidic acid and other drugs.
5. Matters needing attention
Common complications of this disease include acidosis, uremia, heart failure, pulmonary edema, and hypokalemia syndrome.