rabies Rabies is an acute infectious disease caused by the rabies virus. Clinically, it is mostly characterized by specific symptoms such as hydrophobia, aerophobia, spasms of the throat muscles, and progressive paralysis. Its typical symptom is hydrophobia, where the patient experiences spasms of the swallowing muscles and is unable to swallow water, even when extremely thirsty, upon drinking water or even hearing its sound. Therefore, it is also known as hydrophobia.

A acute infectious disease caused by the rabies virus

The virus is transmitted to humans by animals infected with rabies virus after biting

Once symptoms of rabies appear, the mortality rate is nearly 100%

Vaccination against rabies after being bitten saves many lives

Rabies is an acute infectious disease caused by the rabies virus, clinically manifested mainly by specific symptoms such as hydrophobia, aerophobia, pharyngeal muscle spasms, and progressive paralysis. Its typical symptom is hydrophobia, that is, when drinking water, or even hearing the sound of water, the patient will experience spasms of the swallowing muscles and cannot swallow water. Even if the patient is extremely thirsty, they dare not drink water, hence the name hydrophobia.

Humans usually contract rabies from animals (such as dogs, cats, etc.) that have been infected with the rabies virus, with 99% of diagnosed rabies cases transmitted from infected dogs to humans. About 50% of the animals that attack humans are domestic, and the vast majority of domestic animals have not been vaccinated against rabies. Stray animals account for about 25% of the total number of animals that attack humans.

When the rabies virus enters the human body, the glycoprotein it contains can bind to the acetylcholine receptors in the human body, determining its neurotropic nature. The replication of the virus is almost limited to neurons.

When the virus first enters the body through a wound, it does not enter the bloodstream (the rabies virus is usually not detected in the blood), but replicates in the muscle tissue that was bitten, and then invades the peripheral nervous system through the motor neuron terminals and axons. Animal experiments have found that the spread of the rabies virus from the spinal cord to the brain is extremely rapid, and once it invades the brain, it rapidly proliferates. The brainstem is the first to be affected and is the most heavily infected area.

Incubation period symptoms

The period from infection to the onset of symptoms is usually asymptomatic, mostly 1-3 months, rarely within a week or more than a year. There are no reliable diagnostic methods for the incubation period of rabies.

Prodromal symptoms

The onset of rabies patients usually begins with atypical symptoms such as discomfort, anorexia, fatigue, headache, and fever. 50%-80% of patients may experience specific neurogenic pain or sensory abnormalities (such as itching, numbness, and tingling) at the original exposure site, possibly due to viral replication in the dorsal root ganglia or causing ganglion neuritis. At this stage, groundless fears, anxiety, excitement, irritability, nervousness, insomnia, or depression may also occur. The prodromal period lasts 2-10 days (usually 2-4 days).

Acute neurologic phase symptoms

Patients exhibit typical clinical symptoms of rabies, generally lasting 1-3 days. There are two manifestations, namely, furious and paralytic.

Furious patients

They have fever accompanied by significant signs of the nervous system, including hyperactivity, disorientation, hallucinations, spasms, bizarre behavior, and neck stiffness. The predominant feature is extreme fear, hydrophobia, aerophobia, episodic pharyngeal spasms, difficulty breathing, difficulty urinating and defecating, excessive sweating, and drooling.

Hydrophobia and aerophobia are special typical symptoms of this disease. Typical patients can experience severe pharyngeal spasms when they see water, hear running water, drink water, or even mention drinking water. Despite extreme thirst, they dare not drink, and even if they do, they cannot swallow, often accompanied by hoarseness and dehydration.

Bright light, noise, touch, or airflow may also trigger spasms, and severe attacks can lead to generalized painful convulsions. Due to frequent respiratory muscle spasms, it can cause difficulty breathing and cyanosis.

Paralytic patients

There are no typical excited phase and hydrophobia, but rather begin with high fever, headache, vomiting, pain at the bite site, followed by limb weakness, abdominal distension, ataxia, muscle paralysis, incontinence, presenting with a transverse myelitis or ascending spinal cord paralysis, and other Guillain-Barre syndrome (GBS) manifestations. The lesions are limited to the spinal cord and medulla oblongata, without involving the brainstem or higher central nervous system.

Paralytic period symptoms

Patients gradually enter a quiet state in the late stage, with spasms ceasing, and they become gradually quiet, exhibiting flaccid paralysis, especially common in the bitten limb. The eye muscles, facial muscles, and masticatory muscles may also be affected, manifesting as strabismus, ocular motor dysfunction, drooping jaw, inability to close the mouth, and lack of facial expressions.

Subsequently, the patient's breathing gradually weakens or becomes irregular, and may exhibit Cheyne-Stokes respiration; the pulse becomes rapid and weak, blood pressure drops, reflexes disappear, and pupils dilate. Patients usually enter a coma state before death, and respiratory arrest occurs shortly after coma. The entire natural course of rabies after onset generally lasts 7-10 days. The cause of death is usually due to pharyngeal spasms leading to suffocation or respiratory and circulatory failure.

The diagnosis of rabies requires a comprehensive assessment based on the patient's epidemiological history, clinical manifestations, and laboratory test results. Laboratory evidence is necessary for confirming a diagnosis.

Clinical diagnosis can be made in cases that meet any of the following criteria:

1. Typical clinical manifestations of furious rabies

2. Clear history of animal exposure + typical paralytic rabies clinical manifestations

Confirmation of a clinical diagnosis can be made if the case meets the clinical diagnosis criteria and any of the following:

1. Positive rabies virus isolation (mouse or cell culture isolation): suitable for samples with high virus content such as brain tissue and saliva.

2. Positive rabies virus antigen detection (fluorescent antibody test, direct rapid immunohistochemistry, enzyme-linked immunosorbent assay): suitable for brain tissue, skin hair follicle samples from the nape of the neck.

3. Positive rabies virus nucleic acid detection (RT-PCR, Real-time PCR): suitable for samples such as saliva and brain tissue.

4. For individuals who have not been vaccinated against rabies, positive rabies virus neutralizing antibody detection (mouse brain neutralization test, rapid fluorescent focus inhibition test): suitable for serum and cerebrospinal fluid samples.

In suspected rabies cases, performing magnetic resonance imaging (MRI) with appropriate preventive measures may aid in diagnosis. Regardless of the clinical presentation, the presence of vague, faint abnormal high signals in the T2 imaging of the brainstem, hippocampus, hypothalamus, deep and subcortical white matter, and deep and cortical gray matter on MRI suggests a potential case of rabies. In the late stages of the disease, when the patient enters a coma, enhanced MRI can clearly show these changes, which can be used to differentiate rabies from other viral encephalitis. CT imaging of the brain has almost no diagnostic value.

Differential diagnosis should be made with diseases such as tetanus, viral encephalitis, poliomyelitis, and Guillain-Barré syndrome (GBS).

Rabies patients should be isolated and provided with quiet bed rest, high-nutrient therapy through central venous catheterization, and strict disinfection of the patient's secretions, excretions, and contaminated items.

When it comes to treatment, there is no effective clinical treatment for an active rabies infection. Treatment primarily focuses on post-exposure measures, including wound care and vaccine administration. For category III exposure, the correct and timely administration of passive immunizing agents (rabies immune globulin, rabies immunoglobulin for human use, etc.) is crucial. Additionally, it is important to prevent tetanus infection in cases of deep wounds.

If a patient is diagnosed with rabies, strict isolation and care measures should be implemented, including maintaining quiet bed rest, preventing all forms of stimuli such as sound, light, and drafts, and providing high-nutrient therapy through central venous catheterization. Healthcare personnel should wear masks, gloves, and isolation gowns, and all secretions, excretions, and contaminated items must be strictly disinfected.