Introduction

Rabies is a rapidly progressive, acute, fulminant, and fatal encephalitis in humans and animals that is caused by infection with rabies virus.

-Rabies virus is usually transmitted to humans by the bite of an infected animal.

-Live virus enters the nerve tissue at the time of the bite, multiplies at the site, and then spreads centripetally along peripheral nerves toward the spinal cord or brain stem via retrograde fast axonal transport. It replicates in gray matter and then spreads  to the salivary glands, adrenal glands, and heart. 

Symptoms & Signs 

-The average incubation period is one to three months. 

-The clinical spectrum can be divided into three phases

1.Prodromal phase: 

-The first symptom is usually the paresthesia at the bite site 

-Patient later develops malaise, headache, photophobia, fever, anorexia, nausea, vomiting and sore throat 

2.Acute neurologic phase: 

–Hydrophobia (fear of water), Aerophobia (fear when feeling a breeze) 

-Sympathetic overactivity (Increased salivation, ‘foaming at the mouth’, perspiration, lacrimation, pupillary dilatation, nervousness)

-Psychotic symptoms (hallucinations, delusions, bizarre behavior)

-Two acute neurologic forms of rabies are seen in humans: 

the encephalitic (furious) form in 80% and

the paralytic form in 20%.

3.Coma: Convulsive seizures, coma and death

-The major cause of death is cardiorespiratory arrest. 

Diagnosis 

1.Rabies antigens: diagnosis by rabies specific antigens 

2.Serology: Diagnosis by rabies specific antibodies,  detected by immunofluorescence or neutralization tests. 

3.Viral isolation: Isolation of the virus in the brain neurons. 

Negri bodies: the most characteristic pathologic finding in rabies; They are eosinophilic cytoplasmic inclusions in the brain or the spinal cord. They are composed of rabies virus proteins and viral RNA 

4.Animal observation: 

‘Rabid or suspected rabid’ animals: should be killed humanely immediately after the bite and sent for laboratory examination of neural tissues 

‘Normal’ animals: should be held for observation for 10 days 

If they appear abnormal during or after 10 days: kill humanely and send tissues to laboratory 

If they appear normal during or after 10 days: individualized treatment 

Prevention

–Avoid contact with any unfamiliar domestic animals and wild animals 

–Immunize all household dogs and high risk pets 

–Vaccination: Four 1-mL doses of rabies vaccine should be given IM in the deltoid area. 

Post-Exposure Prophylaxis 

It involves wound cleaning, vaccination and passive immunity 

Wound cleaning: 

-Thoroughly clean the wound with soap and antiseptics 

-Animal bite wounds should not be sutured

Vaccination: Four doses of rabies vaccine over a 14 day period 

-Give the vaccine only in deltoid region in adults or anterolaterial thigh in children 

–Never administer the vaccine in the gluteal area because antibody responses have been lower after administration at this site 

-Pregnancy is not a contraindication for immunization.

Passive immunity: One dose of HRIG along with the first dose of the vaccine 

-HRIG is not indicated beyond the 7th day after vaccination is begun, because an antibody response is most likely occurred 

-HRIG should never be administered in the same syringe or into the same injection site as the vaccine, because the antibody and vaccine will neutralize each other.

-HRIG should not be given to those with immunoglobulin A deficiency, because small amounts of immunoglobulin A present in HRIG might cause a severe allergic reaction.

Treatment 

-There is no successful treatment for clinical rabies. 

-Symptomatic and Palliative treatment using sedatives, antipsychotics, anxiolytics, and pain killers

Poliomyelitis is a disease of the anterior horn motor neurons of the spinal cord and brainstem caused by the poliovirus. 

-Anterior horn cells control the skeletal muscle cells of the trunk and limbs 

-In up to 95% of cases, poliovirus infection is asymptomatic 

-the viral transmission is oral to oral or fecal to oral 

-Acutely, the polio virus enters the body through the GI tract, reproduces in the GI lymphoid tissue, and then spreads to the large motor nuclei of the spinal cord, the brainstem, reticular formation, hypothalamus, thalamus, cerebellum and cerebral cortex. 

Symptoms & Signs

Thankfully, not every polio infection results in paralysis. It can be divided into following types based on the severity. 

Abortive poliomyelitis: fever, headache, vomiting, diarrhea, constipation, and sore throat lasting 2–3 days.

Nonparalytic poliomyelitis: Above symptoms plus meningeal irritation and muscle spasm but no frank paralysis 

Paralytic poliomyelitis: 

Asymmetrical paralysis; Proximal limb muscles are more often involved than distal, and lower limb involvement is more common than upper. 

1.Spinal poliomyelitis: involves the muscles innervated by the spinal nerves, flaccid and weak muscles, absent tendon reflexes and fasciculations 

2. Bulbar poliomyelitis: involves the muscles innervated by the cranial nerves  IX and X; seen in up to 20 percent of polio patients with paralysis; affects swallowing, speech, facial muscles 

Post-poliomyelitis syndrome:  Fatigue, pain, respiratory problems, sleep problems, increased risk of falls 

Guillain-Barré syndrome: Always think of GBS in the differential diagnosis of polio paralysis. GBS is distinguished from polio by its symmetry, disturbances in sensation, lack of preceding aseptic meningitis, absence of a CSF pleocytosis, presence of multifocal demyelination on electrodiagnostic testing 

Diagnosis

Virus isolated and typed from throat swabs and rectal swabs; PCR amplification of poliovirus RNA from the CSF 

Treatment 

Treatment of poliomyelitis is supportive 

-Pain relief, physical therapy

-Mechanical ventilation for respiratory failure 

-Intubation or tracheostomy for secretion control 

Prevention 

the trivalent live OPV, the inactive (Salk) parenteral vaccine is currently used in the United States for all four recommended doses (at ages 2 months, 4 months, 6–18 months, and at 4–6 years).