• Viral meningitis, also known as Aseptic meningitis, is the most common type of infectious meningitis in the United States. Neonates, infants, and adults are all at risk of contracting viral meningitis. • Viral meningitis is rarely fatal, but can be debilitating. Some people only feel the symptoms for 7-10 days while others for 3-4 months, which can lead to hospitalization and prolonged absence of school or work. • Enteroviruses, the most common type of viral meningitis, occur during the summer and fall.
• Viral meningitis is spread through the exchange of respiratory and throat secretions (kissing, coughing, sneezing, and sharing a cup, utensil, lip gloss, or cigarette). Viral meningitis is also found in one's stool, which is how infants and neonates who aren't toilet trained and adults changing diapers develop it. Herpes simplex and genital herpes can cause viral meningitis in infants and neonates and chicken pox, rabies and HIV can develop it in all ages. • The incubation period is 3-7 days from the time of infection until the development of symptoms, therefore, the virus can be spread 3 days after infection until 10 days after the development of symptoms. Risk factors for development are exposure to someone with a recent viral infection or children in a day care facility or having a suppressed immune system.
• Symptoms: • • • • • • Irritability Fever (low grade) Headache Nausea/vomiting Stiff neck Sensitive to light Common symptoms such as fevers, headaches, and stiff necks can be tough to detect or might not even occur in neonates and infants.
• Is an Enterovirus as it is found in the intestine and excreted in the faeces.
The picornaviruses are a family of small viruses with a diameter of about 20-30nm and containing single stranded RNA.
Enteroviruses includes echo, coxsackie and polio viruses and the virus of hepatitis A Rhinoviruses are the common causes of common cold These two are the two important genera of picornaviruses.
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There are 3 types of polio viruses identified by neutralization tests. They have an affinity for nervous tissue. Only man and some primates are susceptible.
1. 2. 3.
Type 1 strain, the Brunhilde and Mahoney strain. Type 2 strain includes the rodent-adapted strains. The Leon and Saukett strains are the type 3 strains.
• PV, enter by the mouth, often from hand contamination from faeces, towels etc.
• PV multiplies in the throat first then in the gut. It is resistant to stomach acid and passes through the gut lining to multiply, enters the blood stream and passes thence to various internal organs.
• Symptoms are as for any flu - fever, malaise, headache, nausea, sore throat, tummy upset, muscle aches.
• From the blood it may pass to the nerves of the brain stem and spinal cord, causing muscle weakness, paralysis, heart and breathing failure.
• The incubation period is 3-5 days for minor illness and 1-2 weeks for paralysis symptoms. Onset from ingestion of virus can be 3 - 35 days. So a large number of people may have had a minor dose of polio without really being aware of it unless it got to the paralysis stage. The more severe the original flu-like illness, the more chance there is of deterioration occurring later in life (fatigue & weakness).
TRANSMISSION AND EPIDEMIOLOGY Faecal –oral route. Replicates in the oropharynx and intestinal tract Humans are the natural hosts. Poliomyelitis caused by naturally occurring wild type virus has been eradicated from the United States and from the entire western hemisphere, due to the success of the vaccine. • The rare cases in the United States occur mainly in unimmunized people exposed to wild type poliovirus while traveling abroad. • • • •
PATHOGENESIS AND IMMUNITY • Replicates in the oropharynx and small intestine especially in the lymphoid tissue.
• Spreads to the CNS through blood stream
• In the CNS, polio virus replicates in the motor neurons located in the anterior horn of the spinal cord. • Death of these cells results in paralysis of the muscles innervated by those neurons. • The virus also affects the brain stem leading to bulbar poliomyelitis with respiratory paralysis.
CLINICAL FINDINGS • 1. 2. The range of responses to poliovirus infection includes: Inapparent asymptomatic infection – quite common. Abortive poliomyelitis – mild febrile illness characterized by headache, sore throat, nausea and vomiting. Most patients recover spontaneously.
Nonparalytic poliomyelitis manifests as aseptic meningitis with fever, headache and stiff neck. Those also resolves spontaneously.
In paralytic poliomyelitis, flaccid paralysis is the predominant finding, but brain stem involvement can lead to life threatening respiratory paralysis.
• In paralytic polio, both the meninges and the brain parenchyma are often involved.
• This is termed as meningoenchephalitis.
• If the spinal cord is also involved meningomyeloencephalitis is often used. • No permanent carrier state occurs following infection by poliovirus. • Virus excretion in the faeces can occur for several months.
• Virus is produced and released into the gut (and throat initially) and can be isolated from the throat or stools for some weeks following the incubation period. • No true long term carrier status occurs. • The host's antibody response begins soon after the viraemia. • Good solid life long immunity results to the specific strain of poliovirus • Subsequent infection with other strains may still occur.
Demonstration of the virus
• • Virus may be recovered from faeces (also throat swabs), CSF Inoculation of cell cultures (monkey kidney cells, HEp-2 cells, HeLa cells, Human amnion) and recognition of cytopathic effects. Confirmation by neutralization of infectivity with specific antisera. Vaccine strains may be recovered and need to be differentiated from wild strains by molecular nucleic acid techniques (PCR). Multiple specimens over several days improves chances of recovery of the virus.
Live attenuated virus (SABIN)(1963)
• Strains of poliovirus 1, 2 and 3 which have been attenuated by passage in unnatural conditions to lose neurovirulence.
• Live strains mixed, given as oral drops (easy administration).
• Live vaccination mimics natural infection with good immunity including IgA in the gut.
• This vaccine is used in USA and most other countries.
Killed whole virus (SALK)(1957)
• • • • • • • Polio 1, 2 and 3 grown in cell cultures, mixed, killed with formalin. Deep cutaneous or intramuscular injections at 3 to 6 months of age; later boosters. Produce long lasting immunity to all three types. Does not induce IgA antibodies in the gut. Can be administered to immunocompromised individuals. Much antigen is required which makes the vaccine expensive. Effective when coverage is good (nearly 100% immunity in people regularly vaccinated). Still used in some countries (Netherlands, Scandinavia) in 1990's. OPV- 1st dose at 1 ½ months along with DPT 2nd, 3rd doses of these vaccines are given at the ages of 2 ½ , 3 ½.
• Rabies is an infectious disease of animals caused by a bullet-shaped, enveloped RNA virus, 180 x 75 nm. • Man is occasionally infected, and once infection is established in the CNS, the outcome is almost invariably fatal.
Structure of rabies virus
• Is acquired from virus in saliva entering a bite wound caused by an infected animal, usually a rabid dog.
• The severity of the bite determines the risk of infection.
• The disease does not usually spread from man to man.
• In the United States, transmission is usually from the bite of wild animals like skunks, raccoons, and bats. • Human rabies has also occurred in the United States in people who have not been bitten, so called nonbite exposures. • The important example of this type of transmission is exposure to aerosols of bat secretions containing rabies virus. • A rare example is transmission in transplants of corneas taken from patients who died of undiagnosed rabies.
Incubation: • After inoculation, the virus enters small nerve endings at the site of the bite. • The virus slowly travels up the nerve to reach the CNS where it replicates • Then travels down peripheral nerves to the salivary glands where there is further replication. • From the salivary glands it enters the saliva to be transmitted by the bite. • There is no viremic stage.
• Within the CNS , encephalitis develops, with the death of neurons and demyelination. • Infected neurons contain an eosinophilic cytoplsmic inclusion called a Negri body, which is important in lab diagnosis of rabies. CLINICAL FINDINGS • Incubation period varies according to the location of the bite from as short as 2 weeks to 16 weeks or longer. • It is shorter when bites are sustained on the head rather than on the leg, because the virus has a shorter distance to travel to reach the CNS.
SYMPTOMS • Fever, anorexia and changes in sensation at the bite site. • Within a few days, signs such as confusion, lethargy and increased salivation develop. • Most notable is the painful spasm of the throat muscles on swallowing. This results in hydrophobia.
• Within several days, the disease progresses to seizures, paralysis and coma
• Death occurs but with life support systems a few people have survived.
• Very similar picture to human rabies.
• In the stage of excitement the animal may bite vigorously and viciously at anything: sticks, stones, grass, other animals and humans, without provocation.
• Wild animals may be abnormally tame or appear sick - beware of approaching or picking up such an animal ("dumb rabies").
By assessment of:
• 1.Bite Geographical area, type of animal, severity and site of bite.
2.Animal Live - observe in cage: If survives > 8 days, then NOT rabies. Dead - brain sent to Laboratory for autopsy • Negri bodies • IFA • virus isolation
Man • Live - difficult diagnosis • skin biopsy, corneal impression • Dead - brain sent to Laboratory • "Negri bodies" in cytoplasm of brain cells; • Immunoflourescence using rabies antibody to rabies virus • Virus isolation
1. Wash wound (soap, detergent and water) 2. Anti-rabies serum (human). Passive immunisation. 3. Vaccine (intensive course). Active immunisation. • RABIES VACCINE:
A good but expensive killed virus vaccine (Human Diploid Cell Vaccine, HDCV) grown in human fibroblasts is available for safe use in man.
The unusually long incubation period of the virus permits the effective use of active immunisation with vaccine postexposure..)
2 approaches to prevent rabies in humans: Preexposure given to individuals belonging to the high risk groups such as veterinarians, zookeepers, travelers to areas of hyperendemic areas. Consists of 3 doses given on days 0, 7 and 21 or 28. Booster doses are given as needed to maintain an antibody titer of 1:5 Postexposure given to individuals who have been exposed to the virus via animal bite. The long incubation period of the disease allows the virus in the vaccine sufficient time to induce protective immunity.
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Human diploid cell vaccine Rabies vaccine absorbed (RVA) Neural tissue vaccine - 5-50% efficacy
Duck embryo vaccine
Live attenuated viruses- animals Vaccinia virus vaccine carrying surface glyco protein geneanimals
Rabies immune globulin –human (HRIG)
Antirabies serum –equine = Used in countries where HRIG not available
OTHER RABIES CAUSING VIRUSES