How does rabies manifest in rats? - briefly
Infected rats develop neurological signs including heightened aggression, excessive salivation, ataxia and progressive paralysis, culminating in death. Clinical signs typically emerge after a incubation period of several weeks.
How does rabies manifest in rats? - in detail
Rabies infection in rats typically follows an incubation period of 10‑21 days after exposure, though the duration can vary with virus strain and inoculation route. Early signs involve subtle behavioral alterations: reduced activity, loss of normal grooming, and occasional aggression or excessive tameness. These changes precede overt neurological disturbances.
Progressive symptoms include:
- Hyperexcitability or tremors, especially in the facial muscles.
- Excessive salivation, often accompanied by foaming at the mouth.
- Dysphagia and difficulty swallowing, leading to drooling.
- Paralysis of hind limbs, advancing to generalized flaccid paralysis.
- Seizure activity and erratic locomotion, reflecting central nervous system involvement.
Pathological examination reveals nonsuppurative encephalitis, neuronal degeneration, and perivascular cuffing in the brainstem and hippocampus. Viral antigen concentrates in the hippocampus, cerebellum, and spinal cord, detectable by fluorescent antibody testing or reverse‑transcriptase PCR.
Rats display relatively low natural susceptibility; most documented cases arise from experimental inoculation. In laboratory settings, high‑dose intramuscular or intracerebral administration is required to produce consistent clinical disease. Consequently, spontaneous rabies outbreaks in wild rat populations are exceedingly rare.
Diagnostic confirmation relies on post‑mortem brain tissue analysis. Direct fluorescent antibody (DFA) testing remains the standard, supplemented by quantitative PCR for viral RNA quantification. Immunohistochemistry can localize viral antigens within neuronal tissue.
Mortality is universal once clinical signs appear, with death occurring within 2‑5 days due to respiratory failure secondary to neuronal dysfunction. No specific antiviral therapy exists; supportive care does not alter the fatal outcome.