CNS MODULE. Dr Hamed Al-Zoubi Ass. Prof. of Microbiology

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1 CNS MODULE Dr Hamed Al-Zoubi Ass. Prof. of Microbiology

2 Enteroviruses Picornaviridae family 1. Enteroviruses a) Polioviruses types 1, 2 and 3 b) Coxsackieviruses A1-A24 (no A23), B1-B6 c) Echoviruses 1 34 (no 10 or 28) d) Enteroviruses Rhinovirus a) Rhinoviruses Hepatovirus a) Hepatitis A virus 4. Cardiovirus

3 Polioviruses It cause poliomyelitis Associated with man since ancient times Egyptian hieroglyph indicates presence since 1400 BC Salk vaccine 1960s - Sabin vaccine

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5 Poliovirus Enterovirus (RNA) Three serotypes: 1, 2, 3 Minimal heterotypic immunity between serotypes Rapidly inactivated by heat, formaldehyde, chlorine, ultraviolet light tolerates in stomach acidity Most poliovirus infections are asymptomatic

6 Poliovirus Epidemiology Reservoir Transmission Human Fecal-oral Oral-oral possible Communicability 7-10 days before onset Virus present in stool 3-6 weeks

7 Steps: Polioviruses / pathogenesis Entry into mouth Replication in pharynx, GI tract, local lymphatics - Hematologic spread to RES and central nervous system -Viral spread along nerve fibers (neuromuscular junction) Destruction of motor neurons commonly in the grey matter of anterior horn of spinal cord

8 Pathogenesis

9 Ancient Greek poliós, meaning "grey", myelós marrow, referring to the grey matter of the spinal cord, and the suffix -itis, which denotes inflammation. Inflammation of the spinal cord s grey matter, although a severe infection can extend into the brainstem and even higher structures

10 Polioviruses / Clinically Incubation period: days 4 possible outcomes: 1. Asymptomatic infection (~ 90%) 2. Abortive infection (Flu like symptoms) or minor disease 3. Non-paralytic poliomyelitis (aseptic meningitis) 4. Paralytic poliomyelitis 0.1-1% (major disease)

11 Outcomes of Poliovirus Infection Asymptomatic Aseptic menigitis Minor non-cns illness Paralytic Percent

12 Paralytic poliomyelitis Paralytic poliomyelitis: Secondary to permanent damage of Lower motor neurons / No sensory involvement Flaccid paralysis Asymmetrical Usually affects the proximal muscles (commonly legs) Muscle atrophy is generally observed several weeks after the beginning of symptoms. Recovery may be complete, partial, or absent.

13 Paralytic poliomyelitis Paralysis develops more frequently in: Adults, muscle trauma (injections, exercise), tonsillectomy and pregnancy (no congenital effect). N.b: brain stem involvement may lead to death? why.

14 Polioviruses / Diagnosis Virus is produced and released into the gut (and throat initially) and can be isolated from the throat or stools for nearly a week following the incubation period (longer in immunosuppressed) The host's antibody response begins soon after the viremia. Samples: Stool, throat swab or CSF 1. Culture: CPE and neutralization assays 2. RT-PCR 3. Serology: not helpful

15 Polioviruses / treatment No specific antiviral drug (Pleoconaril?) Symptomatic treatment Surgical / ventilator / physiotherapy Prevention is more significant: 1. Education 2. Surveillance 3. vaccine

16 Poliovirus vaccine Ø Live attenuated (OPV, Sabin) or Inactivated (IPV, Salk) Trivalent vaccines Immunity type post vaccination Ø Adverse effects Rare local reactions (IPV) No serious reactions to IPV have been documented Paralytic poliomyelitis (OPV) 1:2.5 million vaccines

17 Intramuscular Poliovirus Vaccine (IPV) Salk Consists of formalin inactivated virus of all 3 poliovirus serotypes 3 doses Produces serum antibodies only: does not induce local immunity and thus will not prevent local infection of the gut. It prevents paralytic poliomyelitis since viraemia is essential for the pathogenesis of the disease.

18 Oral Poliovirus Vaccine (OPV) Sabin Consists of live attenuated virus of all 3 serotypes Produced by the repeated passage of the virus through nonhuman cells at subphysiological temperatures 3 doses Produces local immunity through the induction of an IgA response as well as systemic immunity. Cheaper Post vaccine poliomyelitis 1: 2.5 million vaccines

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20 Poliovirus eradication map

21 Poliovirus eradication map

22 Rabies Rabies means madness Main properties of the virus: Belongs to Rhabodoviruses family (RNA viruses) Surrounded by a bullet shaped capsid and a lipoprotein envelop It has a broad range of hosts, all mammals basically but also birds, reptiles. More than 50% of cases occur in dogs, others include foxes, raccons, bats...

23 Rabies - pathogenesis Enters via a break in the skin or across mucosal surface, attaching to muscles and replicates in the muscles: can be stopped at this stage only. Then to peripheral neurons and migrate by retrograde flow to the cord then to the entire CNS then again via peripheral nerve to the entire body e.g saliva It replicates in the brain (brain stem, medulla and grey matter)

24 Pathology: ØNerve cell degeneration Øeosinophilic Intr-acytoplasmic inclusion bodies (Negri s bodies)

25 Transmission: Through non intact skin Rabies Bites of rabid animals (bats, cats, dogs, racoons, foxes, skunks) Abrasion or scratches on skin Also Mucous membrane exposed to saliva from licks Inhalation of bats secretions Human-to-human: Never has been confirmed, but corneal transplants has been reported in 8 cases.

26 Incubation period: Rabies 1 week 5 year (1 week 3 months on average) Risk of developing rabies after a bite: 5-80%. Depends upon. Severity of exposure : depth, bite directly on skin or through clothings Location of the bite The biting animal, Multiple bites or single **Bites on head and neck have shorter incubation time (as short as 15 days) because of rich peripheral nerve supply

27 Two clinical patterns: Rabies Paralytic (dumb) and Furious (encephalitis) Non-specific symptoms: Fever, headache, bite site pain numbness and pain Dry throat, cough, insomnia 1. Dumb 20% of cases: Brain stem and spinal cord mainly involved Symmetrical ascending paralysis May develops into encephalitis in 2-3 weeks > coma and death

28 Rabies 2. Furious 80% of cases: Hydrophobia, water exaggerated respiratory tract irritant reflex Anxiety, biting, agitation, arrhythmias, seizures Encephalitis (delirium, convulsions, coma and death) Prognosis: üonce symptoms occur: fatal in 3-21 days

29 Diagnosis: 1- Incubation period: No test is useful Assess the risk and initiate prophylactic treatment 2- Symptomatic: Skin biopsy from the nape of the neck (hair follicle) do direct fluorescent antibody staining or PCR Saliva: PCR 3- After death: brain biopsy (Negri bodies)

30 Rabies / treatment No effective antiviral exists. Postexposure Prophylaxis/PEP: 1. Wound care: immediate thorough washing with soap and water and povidine-iodine (90% risk reduction) TIG (tetanus Ig) Antibiotic to caver for anaerobic bacteria

31 Rabies 2. Passive immunity: Anti rabies immunoglobulin 20 IU/kg Half at wound area and half I.M (gluteal muscle) As soon s possible 3. Active immunisation: Killed virus I.M in deltoid muscle 5 doses at 0, 3, 7, 14 and 30 days

32 Prevention: Vaccination of animals and those who work with animals Inhibit animals smuggling

33 The End