discuss about VPD in pediatric patients

1. VACCINE PREVENTABLE
INFECTIONS IN CHILDREN
Dr. Andualem B (MD) November 2022

2. Outline
 Measles
 Pertussis
 Tetanus
 Poliomyelitis

3. MEASLES
 Outline
 Definition
 Etiology
 Epidemiology
 Transmission
 Pathogenesis
 Clinical manifestation
 Diagnosis
 Complication
 Management
 prevention

4. MEASLES
 Definition: Is an acute highly contagious viral disease
characterized by a final stage of maculopapular rash.
 Etiology:measle virus
Is an RNA , single-stranded virus.
family _ Paramyxoviridae
Genus _ Morbillivirus
Humans are the only host of measles virus.
 Has 6 major structural proteins of these the 2 most
important in terms of induction of immunity are the
hemagglutinin (H) protein and the fusion (F) protein.

5. EPIDEMIOLOGY
The measles vaccine has changed
the epidemiology of measles
dramatically.
 Endemic transmission of measles
has been interrupted in many
countries where there is widespread
vaccine coverage.
 The current rate in US is <1 case per
1,000,000 population.

6. TRANSMISSION
 The portal of entry is through the respiratory
tract or conjunctivae following Contact with
large droplets or small-droplet aerosols in which
the virus is suspended.
 Is highly contiguous.
 Approximately 90% of exposed susceptible
individuals experience measles.
 Patients are infectious 3 days before and 4-6
days after the rash.
 Highest incidence between 9 months and 2
years of age.
 M:F is equal.

7. PATHOGENESIS
 Inhalation of the virus with invasion and
multiplication in the respiratory tract.
 primary viremia with spread of the virus to
regional lymphoid tissue & the Reticulo-
Endothelial System (RES).
 In RES and lymphoid tissue Infected cells coalese
in to multinucleated cells and further multiply
and released in the circulation (Secondary
viremia).
 Dissemination of the virus to different organ
system (lung ,skin ,CNS, GIT etc) will occur.

8. PATHOLOGY
 Causes necrosis of the respiratory tract epithelium
and an accompanying lymphocytic infiltrate.
 a small vessel vasculitis on the skin and on the oral
mucous membranes.
 In lymphoreticular tissue, lymphoid hyperplasia is
prominent.
 Fusion of infected cells results in multinucleated
giant cells, the Warthin-Finkeldey giant cells that
are pathognomonic for measles, with up to 100 nuclei
and intracytoplasmic and intranuclear inclusions.

9. CLINICAL MANIFESTATIONS
 Consists of 4 phases:
 Incubation period ranges from 8-12 days.
 prodromal illness lasts 3-5 days and is characterized by;
Fever, cough, coryza, conjunctivitis,
Koplik spots, pathognomonic sign of measles,
appearing 1 to 4 days prior to the onset of the rash,
discrete red lesions with bluish white spots in the center
on the inner aspects of the cheeks at the level of the
premolars.
 exanthematous phase, patients are very sick, fever is
highly elevated as rash appears.
 The rash begins on the forehead (around the hairline),
behind the ears, and on the upper neck as a red
maculopapular eruption.

10. C/F CONTINUED. . .
 It then spreads downward to the extremities,
reaching the palms and soles in up to 50% of cases.
 With the onset of the rash, symptoms begin to
subside.
 The rash fades over about 7 days in the same
progression as it evolved, often leaving a fine
desquamation.
 Post cervical lymphadenopathy,abdominal
pain,diarrhea,pneumonia and OM, are common in
infants.
o Recovery phase

11. CHILD WITH MEASLES

12. LABORATORY FINDINGS AND DIAGNOSIS
o A reduction in the total WBC count, with lymphocytes
decreased more than neutrophils.
o ESR and CRP are normal unless there is bacterial super
infection.
 The diagnosis is almost always based on clinical and
epidemiologic findings.
 Serologic confirmation is made by
Identification of IgM antibody in the serum.
A fourfold rise in IgG antibodies in acute and
convalescent specimens collected 2-4 wk apart.
 Viral isolation from blood, urine, or respiratory
secretions can be accomplished by culture or Molecular
detection by PCR.

13. COMPLICATION(CXN)
 Respiratory CXN;
 Pneumonia ; is the most common cause of death.
 Caused by the virus itself(giant cell pneumonia) or bacterial
super infection(Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus
aureus).
 Croup, tracheitis, and bronchiolitis are common
complications in infants and toddlers.
 Acute otitis media is the most common complication of
measles .
 Sinusitis, mastoiditis ,Retropharyngeal abscess.
 There may be a higher rate of activation of pulmonary
tuberculoses ( due suppression of the immune system).
 Gastrointestinal cxn; Diarrhea and vomiting with
Dehydration and Appendicitis may occur from obstruction of
the appendiceal lumen by lymphoid hyperplasia.

14. COMPLICATION CONTINUED
 Central nervous system CXN
 Febrile seizures occur in <3% of children with measles.
 Encephalitis; it occurs in 1-3/1000 cases.
 More common in adolescents and adults than in
preschool or school-aged children.
 Is a post infectious, immunologically mediated
process and is not due to a direct effect by the virus.
C/F :seizures (56%), lethargy (46%), coma (28%), and
irritability (26%).
 CSF finding: lymphocytic pleocytosis in 85% of cases
and elevated protein concentration.
15% of patients die, and 20-40% suffer long-term
sequelae.

15. COMPLICATION CONTINUED
 Subacute measles encephalitis;
 Manifests 1-10 months after measles in
immunocompromised patients.
 Results from direct damage to the brain by
the virus.
 Signs and symptoms include
seizures,myoclonus,stupor, and coma.
 Progressive disease and death almost always
occur.

16. COMPLICATION CONTINUED…
 Subacute Sclerosing Panencephalitis(SSPE)
 Is chronic complication with an outcome that is
nearly fatal. Is a rare complication.
 It appears to result from a persistent infection with
an altered measles virus.
 After 7-10 yr the virus apparently regains virulence
and attacks the cells.
 Age of onset,<1 yr to <30 yr, the illness is primarily
one of children and adolescents.
 Measles at an early age favors the development of
SSPE.

17. COMPLICATION CONTINUED
Miscellaneous CXN:
 Malnutrition.
 Myocarditis.
 Hemorrhagic measles or “black measles.
 Corneal ulceration (due to border
line vit A deficiency and direct viral
kerato conjunctivitis can occur).
 Miscellaneous bacterial infections.

18. TREATMENT
 Management of measles is supportive.
 Maintenance of hydration, oxygenation, and
comfort are goals of therapy.
 Antipyretics for comfort and fever control are
useful.
 Respiratory failure due to croup or pneumonia may
require ventilatory support.
 Vitamin A supplementation
 Anti viral are not effective.
 Prophylactic antimicrobial therapy to prevent
bacterial infection is not indicated

19. PROGNOSIS AND PREVENTION
 Prognosis:
With improvements in health care and
antimicrobial therapy, better nutrition, and
decreased crowding, the death-to-case ratio fell
to 1/1,000 cases in developed nation like USA.
 Prevention; Patients shed measles virus from 7
days after exposure to 4-6 days after the onset
of rash.
exposure of susceptible individuals to patients
with measles should be avoided during this
period.
 Vaccination is the mainstay of prevention

20. Pertussis (whooping cough)
 Pertussis is an acute respiratory tract infection .
 Etiology
 Bordetella pertussisis : is the sole cause of epidemic
pertussis and the usual cause of sporadic pertussis.
 Bordetella parapertussis: is an occasional cause of
sporadic pertussis.
 B. pertussis and B. parapertussis are exclusive pathogens
of humans and some primates.
 Bordetella organisms are tiny, fastidious, gram-negative
coccobacilli that colonize only ciliated epithelium.

21. Epidemiology
 There are 60 million cases of pertussis each year
worldwide, resulting in >500,000 deaths
 Widespread use of pertussis vaccine led to a >99%
decline in cases in developed nation like USA.
 There is a high incidence of pertussis in developing
country.
 Neither natural disease nor vaccination provides
complete or lifelong immunity against pertussis re-
infection or disease.
 Protection against typical disease begins to wane 3-5 yr
after vaccination.

22. Transmission
 Pertussis is extremely contagious, with attack rates
as high as 100% in susceptible individuals exposed
to aerosol droplets at close range.
 Coughing adolescents and adults (usually not
recognized as having pertussis) are the major
reservoir for B. pertussis and are the usual sources
of infection for infants and children.
 mothers provide little if any passive protection to
young infants.

23. Pathogenesis
 The exact mechanism of disease symptomatology
remains unknown.
 Only B.pertussis expresses pertussis toxin (PT), the
major virulence protein.
 PT is thought to be responsible for systemic
manifestations of disease.
 Following infection local epithelial damage will
occur and produces respiratory symptoms .

24. Clinical Manifestations
 Classically, pertussis is a prolonged disease, divided
into catarrhal, paroxysmal, and convalescent stages.
 The catarrhal stage(1-2 wk): congestion ,rhinorrhea
low-grade fever, sneezing, lacrimation.
 paroxysmal stage (2-6 wk): cough begins as a dry,
intermittent, irritative hack and evolves into the
inexorable paroxysms that are the hallmark of
pertussis.
 uninterrupted cough on a single exhalation with
Post-tussive emesis and exhaustion is characteristic.

25. Clinical Manifestations continued
 convalescent stage (≥2 wk) paroxysmal stage fades
and the number, severity, and duration of episodes of
the paroxysmal attack diminish.
 Infants <3 mo of age do not display the classic stages.
 The catarrhal phase lasts only a few days or is unnoticed,
Cough may not be prominent, Whoop infrequently occurs
,apnea and cyanosis can follow a coughing paroxysm, or
apnea can occur without a cough.
 Adolescents and previously immunized children have
foreshortening of all stages of pertussis.

26. Diagnosis
 Pertussis should be suspected in any individual who has pure or
predominant complaint of cough in the absence of fever,
myalgia, exanthem , sore throat, hoarseness, tachypnea,
wheezes, and rales.
 Leukocytosis (15,000-100,000 cells/mm3
) due to absolute
lymphocytosis is characteristic in the catarrhal stage.
 Chest radiographic findings are only mildly abnormal showing
perihilar infiltrate or edema (sometimes with a butterfly
appearance) and variable atelectasis.
 Isolation of B. pertussis in culture remains the gold standard for
diagnosis.
 The specimen is obtained with deep nasopharyngeal aspiration
or with the use of a flexible swab.

27. Treatment
 Goals of therapy are to limit the number of paroxysms, to observe the
severity of the cough, to provide assistance when necessary, and to
maximize nutrition, rest, and recovery without sequela.
 Infants <3 mo of age with suspected pertussis are always admitted to
hospital, as are those between 3 and 6 mo of age unless witnessed
paroxysms are not severe.
 An antimicrobial agent is always given when pertussis is suspected ,
primarily to limit the spread of infection(Macrolides such as
erythromycin or azithromycin).
 Isolation of the patient to prevent spread of infection from time of DX
until 5 days after initiation of macrolide therapy.
 A macrolide agent should be given promptly to all household contacts
and other close contacts.

28. Complications
 Infants <6 mo of age have excessive mortality and morbidity.
 infants <2 mo of age have the highest reported rates of
pertussis-associated hospitalization (82%), pneumonia (25%),
seizures (4%), encephalopathy (1%), and death (1%).
 The principal complications of pertussis are apnea, secondary
infections (such as otitis media and pneumonia), and physical
sequelae of forceful coughing such as rectal prolapse,
subcutaneous emphysema, hernias.
 CNS abnormalities as result of hypoxemia or hemorrhage
associated with coughing or apnea in young infants.

29. Prevention
 Universal immunization of children with pertussis
vaccine, beginning in infancy with periodic
reinforcing doses through adolescence and
adulthood, is central to the control of pertussis .

30. Tetanus
Outline
Definition
Etiology
Epidemiology
Transmission
Pathogenesis
Clinical manifestation
Diagnosis
Complication
Management
Prevention

31. Tetanus (Clostridium tetani)
 Tetanus is an acute, spastic paralytic illness Caused by the neurotoxin
produced by Clostridium tetani.
 Historically it is called lockjaw.
 Etiology
 C.tetani is a motile, gram-positive, spore-forming obligate anaerobe
whose natural habitat is soil, dust, and the alimentary tracts of
various animals.
 Tetanus spores can survive boiling but not autoclaving, whereas the
vegetative cells are killed by antibiotics, heat, and standard
disinfectants.
 C. tetani is not a tissue-invasive organism and causes illness through
the effects of a toxin, tetanospasmin, more commonly referred to
as tetanus toxin.

32. Epidemiology
 Tetanus occurs worldwide, incidence dropped
dramatically in developed world but remains endemic in
developing countries.
 The most common form, neonatal (or umbilical) tetanus
occur in infants of unimmunized mother, kills approximately
300,000 infants each year, with about 80% of deaths in
just 12 tropical Asian and African countries.
 Maternal tetanus results from postpartum, postabortal, or
postsurgical wound infection with C. tetani.
 An estimated 15,000-30,000 unimmunized women
worldwide die of maternal tetanus.

33. Pathogenesis
 Most non-neonatal cases of tetanus are associated
with a penetrating injury with a dirty object such as;
 A nail, fragment of glass, or unsterile injection.
 The disease may also occur in association with:
 use of contaminated suture material.
 Animal bites, abscesses ,ear and other body piercing,
chronic skin ulceration, burns, compound fractures,
frostbite, gangrene, infected insect bites, and female
circumcision.
 Rare cases have no history of trauma.

34. Pathogenesis continued……
 The introduced spores germinate, multiply, and produce tetanus toxin
in the low oxidation of an infected injury site.
 Toxin is released after vegetative bacterial cell death and lysis.
 Tetanus toxin binds at the neuromuscular junction and enters the
motor nerve by endocytosis.
 Toxin undergoes retrograde axonal transport to the cytoplasm of
the -motoneuron then it exits the motoneuron in the spinal cord and
α
next enters adjacent spinal inhibitory interneurons where it
 prevents release of the neurotransmitters glycine and -aminobutyric
γ
acid (GABA) and hence blocks the normal inhibition of antagonistic
muscles on which voluntary coordinated movement depends.
 Affected muscles sustain maximal contraction and cannot relax.

35. Pathogenesis
Adrenal
Medulla
muscle
Corticospinal N
Descending SN
NMJ
Inhibitory Interneuron
Alpha motoneuron

36. Clinical Manifestations
 Incubation period typically is 2-14 days but may be as long as months
after the injury or as early as 24hours.
 Tetanus is most often generalized but may also be localized.
Generalized tetanus:most common and sever
 Headache, restlessness, and irritability are early symptoms, often followed
by stiffness, difficulty of chewing, dysphagia, and neck muscle spasm.
 Half of cases presents with trismus (masseter muscle spasm), or lockjaw.
 Sardonic smile of tetanus (risus sardonicus) results from intractable
spasms of facial and buccal muscles.
 Opisthotonos, When the paralysis extends to abdominal, lumbar, hip, and
thigh muscles.
 Laryngeal and respiratory muscle spasm can lead to airway obstruction
and asphyxiation.

37. Clinical Manifestations continued
 Tetanus toxin does not affect sensory nerves or cortical function so, the patient is
conscious, in extreme pain, and in fearful anticipation of the next tetanic seizure.
 The seizures are characterized by sudden, severe tonic contractions of the muscles,
with fist clenching, flexion, and adduction of the arms and hyperextension of the
legs.
 The smallest disturbance by sight, sound, or touch may trigger a tetanic spasm.
 urinary retention result from bladder sphincter spasm and forced defecation may
occur.
 Fever as high as 40 ºC is common because of the substantial metabolic energy
consumed by spastic muscles.
 Autonomic effects include tachycardia, dysrhythmias, labile hypertension,
diaphoresis and vasoconstriction.
 The tetanic paralysis usually becomes more severe in the 1st wk ,stabilizes in the
2nd wk, and ameliorates gradually over the ensuing 1-4 wk.

38. Clinical Manifestations continued
 Neonatal tetanus, is a generalized tetanus, typically
manifests within 3-12 days of birth as progressive
difficulty in sucking and swallowing associated hunger, and
crying, diminished movement, stiffness and rigidity to the
touch, and spasms, with or without opisthotonos.
 The umbilical stump may hold remnants of dirt, dung,
clotted blood, or serum, or it may appear relatively
benign.
 Localized tetanus results in painful spasms of the muscles
adjacent to the wound site and may precede to
generalized tetanus but not always.

39. Clinical manifestation continued
 Cephalic tetanus ;is a rare form of localized
tetanus involving the bulbar musculature that occurs with
wounds or foreign bodies in the head, nostrils ,or face.
 It also occurs in association with chronic otitis media.
 Cephalic tetanus is characterized by retracted eyelids,
deviated gaze, trismus, risus sardonicus, and spastic
paralysis of the tongue and pharyngeal musculature.

40.  Opisthotonus – arched posture due to
involvement of abdominal, lumbar, hip and
thigh muscles (“board” like rigidity in which
the back of the head and heals touch ground)

41. Diagnosis
 Diagnosis is established clinically.
 Results of routine laboratory studies are usually
normal.
 A peripheral leukocytosis may result from a
secondary bacterial infection of the wound or may
be stress induced from the sustained tetanic spasms
 C. tetani is not always visible on Gram stain of
wound material and is isolated in only about 30%
of cases.

42. DIFFERENTIAL DIAGNOSIS
 Trismus may result from parapharyngeal,
retropharyngeal, or dental abscesses or, rarely,
from acute encephalitis involving the brainstem.
 Either rabies or tetanus may follow an animal bite,
and rabies may manifest as trismus with seizures.

43. Management principles
 Eradication of C. tetani and the wound environment
conducive to its anaerobic multiplication.
 Neutralization of all accessible tetanus toxin.
 Control of seizures and respiration.
 provision of meticulous supportive care
 Prevention of recurrences.

44. Management continued….
 Human tetanus immunoglobulin (TIG) and antibiotics should be given
before any surgical procedure.
 TIG should be given as soon as possible in order to neutralize toxin
that diffuses from the wound into the circulation before the toxin can
bind at distant muscle .
 Antitoxin (TAT) 50,000-100,000 U, with half given intramuscularly
and half intravenously can be given if TIG is not available.
 Penicillin G (100,000 U/kg/day divided every 4-6 hr IV for 10-14
days) remains the antibiotic of choice .
 Active immunization with a 3 doses of vaccine started at time of
diagnosis.
 Diazepam should be administered to provides both muscle
relaxation and seizure control.

45. Management continued…..
 Meticulous supportive care in a quiet, dark,
separated room is most desirable.
 Endotracheal intubation or tracheostomy should be
done to prevent aspiration of secretions before
laryngospasm develops.
 Cardiorespiratory monitoring, frequent suctioning,
and maintenance of the patient's substantial fluid,
electrolyte, and caloric needs are fundamental.
 Nursing attention to mouth, skin, bladder, and bowel
function is needed to avoid ulceration, and infection.

46. Complications
 Aspiration of secretions and pneumonia .
 Endotracheal intubation and mechanical ventilation with their
hazards, including pneumothorax and mediastinal emphysema.
 The seizures may result in lacerations of the mouth or tongue,
in intramuscular hematomas or rhabdomyolysis with
myoglobinuria and renal failure, or in long bone or spinal
fractures.
 Venous thrombosis, pulmonary embolism, gastric ulceration with
or without hemorrhage, paralytic ileus, and decubitus
ulceration are constant hazards.
 Iatrogenic apnea(from diazepam), Cardiac arrhythmias and
disordered autonomic nervous system.

47. Prognosis
 The most important factor that influences outcome is the
quality of supportive care.
 Mortality is highest in the very young and the very old.
 A favorable prognosis is associated with a long
incubation period, absence of fever, and localized disease.
 An unfavorable prognosis is associated with onset of
trismus <7 days after injury and with onset of generalized
tetanic spasms <3 days after onset of trismus
 Reported case fatality rates for generalized tetanus are 5-
35%, and for neonatal tetanus they extend from <10%
with intensive care treatment to >75% without it.

48. Prevention
 Tetanus is an entirely preventable disease.
 Active immunization should begin in early infancy at
2, 4, and 6 mo of age, with a booster at 4-6 yr of
age and at 10-yr intervals thereafter throughout
adult life.
 Immunization of women with tetanus toxoid prevents
neonatal tetanus.
 Tetanus prevention measures after trauma consist of
inducing active immunity to tetanus toxin and of
passively providing antitoxic antibody.

49. POLIOMYELITIS(POLIO)
 Outline
 Definition
 Etiology
 Epidemiology
 Transmission
 Pathogenesis
 Clinical manifestation
 Diagnosis
 Management
 Complication
 prevention

50. POLIOMYELITIS(POLIO)
 Is acute viral infection that can result in
permanent paralysis.
 Peak age is in infancy and young childhood.
 90% of the cases occur before 5 yrs of age.
 Etiology: caused by polio virus, an RNA virus.
Family- Picornaviridae
Genus- Enterovirus
It consist of 3 antigenically distinct serotypes
(types 1, 2, and 3).
The polioviruses are extremely hardy and can
retain infectivity for several days at room
temperature.

51. TRANSMISSION
Transmission is feco-oral route.
Man is the only reservoir.
Highly infectious ,100% of exposed
acquire.
Poor sanitation and crowding have
permitted the continued transmission
of poliovirus in certain poor countries
in Africa and Asia, despite massive
global efforts to eradicate polio.

52. TRANSMISSION CONTINUED
Period of communicability ;few days before and 7-
10 days after the symptoms.
Poliovirus has been isolated from feces for >2 wk
before paralysis to several weeks after the onset
of symptoms.
 Infants acquire immunity transplacentally from their
mothers. Transplacental immunity disappears at a
variable rate during the 1st
4-6 months of life
Active immunity after infection or vaccine is life
long. but protects against the infecting serotype
only.

53. PATHOGENESIS
 Ingestion of the virus, the virus will invade and
multiply in the pharynx(tonsils) or ileum .
 Spread to the regional lymph nodes.
 primary viremia occur and spread the virus to RES.
 further replication in RES with secondary viremia
and release of more viruses in the blood and
infection of CNS will occur.
 Primary target are motor neurons in the anterior horn
of the spinal cord and brain.
 Pathology; in acute case there is lymphocytic cellular
infiltration.
 Later, decrease cellular infiltration ,neuronal
necrosis, decrease in neurons, cavity and cyst
formation.

54. CLINICAL MANIFESTATIONS(C/F)
 The incubation period is 8-12 days, with a range of 5-35
days.
 Poliovirus infections follow 1 of several courses.
1. in apparent infection(90-95% of cases ); causes no
disease and no sequelae.
2. abortive poliomyelitis(5%);causes mild flu like illness
with fever, sore throat and headache. The illness is
short-lived, lasting up to 2-3 days.
3. Non paralytic Poliomyelitis(1%); signs of abortive
poliomyelitis are present, as are more intense
headache, nausea, and vomiting, as well as soreness
and stiffness of the posterior muscles of the neck,
trunk, and limbs.

55. C/F CONTINUED…..
o Fleeting paralysis of the bladder and constipation are
frequent.
o Can preset as a biphasic illness, first phase(minor illness or
signs of abortive poliomyelitis) and the second
phase(major illness or CNS disease).
4.Paralytic Poliomyelitis(0.1% ); Paralysis appears 3-8 days after
the initial symptoms.
 paralytic polio occurring in about 1/1,000 infections among
infants to about 1/100 infections among adolescents.
 Follows non paralytic poliomyelitis
 Causes 3 clinically recognizable syndromes .
 syndromes represent a continuum of infection differentiated
only by the portions of the CNS most severely affected.


56. C/F CONTINUED
 Spinal paralytic poliomyelitis; is the most
common type.
 May occur as the 2nd phase of biphasic
illness.
o Is characterized by asymmetric flaccid
paralysis that occurs within 1-2 days.
 Severe muscle pain is present, and sensory and
motor phenomena (e.g., paresthesia,
hyperesthesia, fasciculations and spasms) may
develop.
 Single muscles, multiple muscles, or groups of
muscles may be involved in any pattern.

57. C/F CONTINUED . . .
 Involvement of 1 leg is most common, followed by
involvement of 1 arm.
 nuchal stiffness or rigidity, muscle tenderness,
initially hyperactive deep tendon reflexes (for a
short period) followed by absence of reflexes.
 Paralysis of the lower limbs is often accompanied
by bowel and bladder dysfunction ranging from
transient incontinence to paralysis with
constipation and urinary retention.
 Sensation is intact; sensory disturbances, if
present, suggest a disease other than poliomyelitis

58. C/F CONTINUED. . .
 The extent of involvement is usually obvious within
2-3 days; only rarely does progression occur beyond
this interval.
 Little recovery from paralysis is noted in the 1st
days or weeks, but, if it is to occur, is usually
evident within 6 months.
 Lack of improvement from paralysis within the 1st
several weeks or months after onset is usually
evidence of permanent paralysis.
 Atrophy of the limb, failure of growth, and
deformity are common and are especially evident
in the growing child.

59. C/F CONTINUED . . .
 Bulbar poliomyelitis :may occur as a clinical entity
without apparent involvement of the spinal cord.
 Characterized by involvement of motor nuclei of the
cranial nerve.( cr.nerve 9,10,12 are commonly involved).
 clinical findings seen includes; respiratory difficulty,
inability to swallow smoothly ,accumulated pharyngeal
secretion, accumulation of saliva in the pharynx,
absence of effective coughing, nasal regurgitation of
saliva and fluids as a result of palatal paralysis.
 involvement of vital centers in the medulla, which
manifest as irregularities in rate, depth, and rhythm of
respiration.
 CVS alterations, including blood pressure changes,
cardiac arrhythmias and change in body temperature.

60. C/F CONTINUED. . .
 The course of bulbar disease is variable; some
patients die as a result of extensive, severe
involvement of the vital centers in the medulla.
 Others recover partially but require ongoing
respiratory support, and others recover completely.
 Polioencephalitis;is a rare form of the disease in
which higher centers of the brain are severely
involved.
 Seizures, coma, and spastic paralysis with
increased reflexes may be observed.
 Irritability, disorientation, drowsiness, and coarse
tremors are often present.

61. DIAGNOSIS
 Poliomyelitis should be considered in any unimmunized or
incompletely immunized child with paralytic disease.
 confirmed by isolation and identification of poliovirus in
the stool, with specific identification of wild-type and
vaccine-type strains.
 2 stool specimens should be collected 24-48 hr apart.
 Poliovirus concentrations are high in the stool in the 1st
week after the onset of paralysis.
 Polioviruses may be isolated from 80-90% of specimens
from acutely ill patients and <20% in specimen collected
3-4Wks later.
 CSF pleocytosis with 20-300 cells/mm3
with CNS
involvement, polymorphonuclear cells predominates early
followed by mononuclear cells
 CSF protein is normal initially and raises to 50-100 mg/dL
by the 2nd
wk of illness.

62. DIFFERENTIAL DIAGNOSIS
 Poliomyelitis should be considered in the
differential diagnosis of any case of
paralysis.
 DDX includes acute flaccid paralysis
caused by other viruses (West Nile virus,
Rabies ,varicella zoster virus, non polio
entero virus)
 GBS (gullian barre’ syndrome).
 Transverse myelitis.
 Other neuropathies.

63. TREATMENT
There is no specific antiviral treatment
for poliomyelitis.
 The management is supportive which
includes;
 analgesics, sedatives, an attractive diet.
 bed rest until the child's temperature is
normal.
 Avoidance of exertion for the ensuing 2 wk
is desirable.
 Maintain airway ,adequate ventilation,
control HTN ,bladder and bowel care.

64. PROGNOSIS
 The outcome of inapparent, abortive poliomyelitis and
aseptic meningitis syndromes is uniformly good, with death
being exceedingly rare and with no long-term sequelae.
 less severe bulbar involvement and/or spinal poliomyelitis,
the mortality rate varies from 5% to 10%,
 In severe bulbar poliomyelitis, the mortality rate may be as
high as 60%.
 paralysis is more likely to develop in male children but
female adults.
 Mortality and the degree of disability are greater after the
age of puberty.
 Major cause of death is respiratory failure.

65. PREVENTION
 Vaccination is the only effective method of
preventing poliomyelitis.
 Hygienic measures help limit the spread of the
infection among young children, but immunization
is necessary to control transmission among all age
groups
 polio vaccine (IPV and OPV) ;both vaccine
established efficacy in preventing poliovirus
infection and paralytic poliomyelitis.
 Both vaccines induce production of antibodies
against the 3 strains of poliovirus.
 All children should receive 3-5 doses of OPV or IPV.

66. THANK YOU