1. Chicken pox  Etiology : VZV  Epidemiology :  Mild illness  More serous among infants, adults, & immune compromised  Contagious from 23 – 48 hr before the rash & until vesicles are crusted, 3-7 d. after onset of rash.  Vzv is transmitted by airborne spread or direct contact.

2.  Clinical manifestations:  a cute febrile rash illness.  prodromal symptoms.  moderate elevated of temp.  rash ; intensely pruritic ery the matous macules ; papular stage to form clear fluid filled vesicles.  clouding & umbilication begin in 24-48hr.  presence of lesions in various stages of evolution is c.r. of varicella.  distribution of rash is predominatly central.

3.  Congenital varicella syndrome :  microphthalrmia  cataracts.  optic atrophy.  microcephaly, hydrocephaly  moto & sensory deficits.  dignosis :  leukopenia ; followed by a relative & absolute lymphocytosis.  LFT.

4.  Treatment :  indications of antiviral D. : 1- individuals 13y. of age or older. 2- Children 12m. of age of older. With chronic cutaneous or pulmonary disorders, receiving short term, intermittent corticosteroids ; receiving long – term salicglate therapy.  A cyclovir 20 mg/kg/dose, 4 doses / d., for 5 days.  Prevention : Vacc.  live v. vacc. To children at 12-18m.  12 m. to 12y. receive a single vacc. Dose.  A dolescents & adults require 2 vacc. doses.  VZIG is recommended for immunocompromised children, pregnant women & new borns exposed to maternal varicella.

5.  Transmission :  Humans are the only reservoir for the polio v.  Polio v. spread by fecal – oral route.  Active immunity after natural inf. is probably lifelong. (against the infecting serotype only)  Clinical mani festations :  in a pparent inf. 90-95%  abortive polio. 5%  non paralytic polio. 1%  paralytic polio. 0.1% Poliomyelitis

6.  non paralytic polio:  headache, nausea, stiffness of the post. m. of the neck, trunk, & limbs.  In early stages the reflexes are normally active ; change in reflexes,  or  pecede weakness by 12-24 hr.  Superficial reflexes are usu. The first to diminish.  Changes in deep tendon reflexes 8-24 hr. after the super ficial reflexes are depressed & indicate impending paresis of the extremities.  Tenden reflexes are absent with paralysis.  Sensary defects do not occur in poliomye litis.  Paralytic polio : 1- spinal paralytic polio. 2- bulbar polio. 3- polioence phalitis

7.  diagnosis :  suspected cases  2 stool specimens  c. s. f.  Treatment :  supportive.  I. M. injections & surgical procedures are C. I. during the acute phase.  Paralytic polio. : Hospitalize tion, complete physical rest, suitable body a lignment, moist hot packs, high fluid intake, Tr. of constipation & urinary retention.  Prognosis : Increased physical activity, exercise, & fatigue during the early phase of illness ; considered as factors leading to increase risk for paralytic dis.  Prevention : Vaccine

8.  Clinical manifestations :  weakness begins in the lower extremities, progressively involve trunk, upper limbes & finally the bulbar M.  Proximal & distal M. involved symmetrically ; asymmetry found in 9%.  Tenderness on palpation & pain in the muscles is common in initial stages.  Weakness may progress to inability to walk & later to flaccid tetraplegia.  Bulbar involvement in half of cases.  Dusphagina & facial weakness.  Urinary incontinence or retention of urine is usually transient.  Tendon reflexes are lost.  Autonomic n. system may be involved Guillain – Barre syndrome

9.  Prognosis : Prognosis is generally good ; 3 clinical features ass. With poor prognosis: 1- cranial n. involvement. 2- intubation. 4- maximum disability at the time of presentation.  diagnosis :  C. S. F. : protein is elevated l glucose is normal, there is no pleocytosis.  Motor n. conduction velocities are reduced.  Sensory n. conduction time is slow.  Serologic test for campylobacter inf.  Treatment  Admission to hospital.  I.V. I G. for 2, 3 or 5 days.  Plasmapgeresis, steroids, & or immunosuppressive Drugs.  Supportive care.