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Medical research on rabies

Definition of rabies

Rabies is a rabies virus caused by a zoonotic acute infection of the central nervous system. Because rabies patients are afraid of drinking the outstanding clinical manifestations of this disease has also been called "fear of water disease (hydrophobia)", but sick animals do not have this feature. The main clinical manifestations of manic, endemic fear, fear of the wind afraid of water, salivation and pharyngeal muscle cramps, and ultimately paralyzed and life-threatening. In 1885 the French scientist Pasteur for the first time the use of rabbit brain spinal cord prepared attenuated rabies vaccine applied to the human treatment success, this is the first time in human history to conquer rabies, so as to prevent rabies vaccine pioneer.

Rabies Complications

Major complications are increased intracranial pressure, hypothalamic involvement caused by excessive or excessive secretion of antidiuretic hormone (caused by diabetes insipidus), autonomic dysfunction caused by high blood pressure, hypotension, arrhythmia (supraventricular tachycardia, Bradycardia, or even stop) or hypothermia. Spasm common, can be systemic or focal. Respiratory dysfunction, such as hyperventilation and respiratory alkalosis in the prodromal and acute phase common. Progressive hypoxia will occur later. Complications reported include congestive heart failure, acute renal failure, superior vena cava thrombosis, secondary infection of the lung or urinary system, and gastrointestinal bleeding.

Rabies drug treatment

Rabies is the most dangerous of all infectious diseases, viral diseases, once the disease, the prognosis is poor. So far there is no specific treatment, clinical application of a variety of new drugs such as interferon α, adenosine, transfer factor and high-dose human anti-rabies globulin treatment, have failed. Therefore, in time after the bitten emphasis on preventive treatment of patients after the onset of symptomatic comprehensive treatment based.

1. Strict isolation of patients to prevent saliva and other pollution.

2. Guardianship treatment should be completed by the immunization of medical staff to dark room, dark, surrounded by no noise, water sound. Nursing staff do not wear hard-soled shoes, do not shake bed, take something to gently hold. Do not give patients to eat stimulating food. For manic, convulsive patients can be used sedatives, such as phenobarbital (phenobarbital sodium) or diazepam, to keep it quiet. Note to maintain nutrition and water, electrolyte balance, should be intravenous infusion of glucose saline, dextran 40, plasma and potassium supplementation and correct acid-base balance.

3. to take all measures to maintain the patient's cardiovascular system and respiratory function tachycardia, arrhythmia, elevated blood pressure can be used β-blockers treatment. Respiratory failure is the main cause of death in rabies, so if necessary, can be used tracheotomy, artificial respirator and other measures to maintain breathing, to correct respiratory failure.

Must be noted that once the incidence of rabies, although the mortality rate is very high, but by monitoring treatment, there is still hope of survival, it should be actively rescued.

The pathogenesis of rabies

Rabies virus on nerve tissue has a strong affinity, mainly through nerve retrograde, centripetal to the central transmission, generally not into the blood.

The course of rabies disease can be divided into the following three stages:

1 nerve outside the small amount of breeding period virus bites after the site of skin or mucosal invasion, first in the local wound of striated muscle cells in a small amount of reproduction, and neuromuscular junction of the acetylcholine receptor binding, invasion of peripheral nerve. From the local wound to invade the peripheral nerve is not shorter than 72h.

2. Peripheral nerve invasion from the central nervous system along the peripheral nerve axon of the virus spread to the heart, the speed of about 5cm / d. After reaching the dorsal root ganglion, began to multiply, and then invade the spinal cord, and then spread to the central nervous system. The main violations of the brain stem and cerebellum and other parts of the neurons. But also in the diffusion process to terminate in a certain area, the formation of special clinical manifestations.

3. From the central nervous system to the various organs of the spread of the virus from the central nervous system to the peripheral nerve centrifugal diffusion, invasion of various tissues and organs, especially salivary glands, tongue taste buds, olfactory nerve epithelium, etc. most of the virus. As the vagus nerve, swallowing the nucleus and hypoglossal nerve damage, can occur respiratory muscle and swallowing muscle spasms, clinical patients with fear of water, difficulty breathing, difficulty swallowing and other symptoms; sympathetic stimulation, so that saliva secretion and out Sweat increased; vagus ganglia, sympathetic ganglia and cardiac ganglion damage, can cause patients with cardiovascular system dysfunction, or even sudden death.

It is believed that the local presence of the virus is not the only factor that causes the difference of clinical manifestations. Humoral and cell-mediated immunity have protective effects in the early stage, but when the virus enters the nerve cells, the immune-mediated damage and pathogenesis are also related. In immunosuppressed mice, the death was delayed after inoculation with rabies virus, and after passive immunization with serum or immune cells, death was accelerated. In human rabies, the lymphocytes of rabies virus-positive cells were more manic-type, rapid death. Myelin basic protein (MBP) has its own immune response is also manic type, the disease progressed rapidly, the brain tissue can be seen by the antibody, complement and cytotoxic T cell-mediated immune damage.


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Read:  2016-12-12 17:08:46  Glory Science Life science source - ELISA Kits - Antibodies - Research Products
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