polio final yr.pptx

8/11/2019 polio final yr.pptx

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AFP

Acute flaccidparalysisweakness in one or more limbs,or the

respiratory or bulbar muscles, resulting from

damagedlowermotor neurones.


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Signs

thereis weakness with reduced tone

(flaccidweakness)

andreducedorabsentreflexes


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D/d

Polio

Enterovirus 71

Gullian barre syndrome

Injection neuritis

Tick bite

Botulinum toxicity

Diptheritic neuropathy

Rabies


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differences of AFP

Direct viral damage to

anterior horn cells eg

polio

Immune medicated

damage to peripheral

nevers

Paralysis onsetDuring(or straight after)

febrile illness

Several weeks after

febrile illness

Pattern of

paralysis

Asymmetrical Symmetrical

Time to reach

maximum weakness

Short(e.g.23days) Long (e.g.714days)

Sensory involvement No Often (depending onexact disease)

CSF Increased lymphocytes increased

protein(e.g.100mg/dLes

peciallylate in the

disease)

Pain Often limb muscle pain Often back pain


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polio- mobin


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historical background

First recorded case of polio is a

hieroglyph from Memphis, drawn

in approximately 1400BC, which

depicts a temple priest calledSiptah showing typical clinical

signs of paralytic poliomyelitis

was recorded in the late 1700s

with the first epidemic in the late

1800s.

The cases that were reported in

1979 where mild and self-limited

and do not result in paralysis


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modern history

1789 - British physician Michael Underwood provides thefirst clinical description of polio, referring to it as "debility of

the lower extremities."1840 - German physician Jacob von Heinepublishes a 78-page monograph in 1840 which not only describes theclinical features of the disease, but also notes that itssymptoms suggest the involvement of the spinal cord.

1908- Austrian physicians Karl Landsteiner and Erwin Poppermake the first hypothesis that polio may be caused by avirus.


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Treatment history

Polio patients whose

muscles were paralysed

faced months, perhapsyears, of arduous physical

therapy to strengthen

weakened muscles

Patients were often placedin iron lungs to help with

breathing regulation


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Bacteriological history

Poliovirus was first identified in

1909 by inoculation of specimensinto monkeys. The virus was first

grown in cell culture in 1949 whichbecame the basis for vaccines


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vaccine history

1955 Inactivated vaccine

1961 Types 1 and 2 monovalent OPV

1962 Type 3 monovalent OPV

1963 Trivalent OPV

1987 Enhanced IPV (IPV)


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EnterovirusSerotypes


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polio= gray matterMyelitis= inflammation

of the spinal cord


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PoliovirusEnterovirus (RNA)(Picornavirus)Three serotypes: 1, 2, 3

Rapidly inactivated by heat, formaldehyde,

chlorine, ultraviolet light

no cross immunization

Transmitted by oronasal route

By water and milk


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Poliomyelitis Pathogenesis

Entry into mouth

Replication in pharynx, GI tract,local lymphatics

Hematologic spread to lymphatics and central

nervous system

Viral spread along nerve fibersDestruction of motor neurons


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Outcomes of poliovirus infectionPrognosis


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Epidemiology

Reservoir Human

Transmission Fecal-oral Oral-oral

possible

Communicability 7-10 days before onset

Virus present in stool 3-6 weeks


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Epidemiology

Most affects children under the age of 5 years in

developing tropical countries.

Incubation period ranges from 6 to 20 days


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risk factors

infants and elderly

living with infected person

compromised immune system

lack of immunization

extreme stress or strenuous activity

travel to an area that has experienced polio outbreak


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incubation period

The incubation period for poliomyelitis is

commonly 6 to 20 days with a range from

3 to 35 days. The response to poliovirus

infection is highly variable and has been

categorized based on the severity of

clinical presentation.


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symptoms

Acute stage: generally lasts 7 to 10

days.May include fever, pharyngitis, headache,anorexia, nausea, and vomiting.

Illness may progress to aseptic meningitis and

menigoencephalitis in 1% to 4% of patients.

These patients develop a higher fever & sever

headache with stiffness of the neck and back


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symptoms

Paralytic disease occurs 0.1% to 1% of those whobecome infected with the polio virus.

Paralysis of the respiratory muscles or from cardiac

arrest if the neurons in the medulla oblongata are

destroyed.


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signs

In cases with paralysis superficial reflexes

usually are absent first, and deep tendon

reflexes disappear when the muscle

group isparalyzed.


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Recovery

Patientshave some or full recovery from

paralysis,most clinical recovery occurs during

the 1 month and almost complete within 6months

.

Limited recovery may occur for about 2 years.


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fate

Among children who are paralysed by polio:

30% make a full recovery

30% are left with mild paralysis

30% have medium to severe paralysis

10% die


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paralytic polio-3 types

Spinal polio- the most common, and accounted for

79% of paralytic cases from 1969-1979. It is

characterized by asymmetric paralysis that mostoften involves the legs.

Bulbar polio- accounts for 2% of cases and leads to

weakness of muscles innervated by cranial nerves.

Bulbospinal polio- it accounts for 19% of cases and

is a combination of bulbar and spinal paralysis


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diagnostic studies

Virus Culture

The laboratory diagnosis of polio is confirmed by isolation of virus by cultures,

from the stool or throat swab or cerebrospinal fluid (rare). In an infected person,

the virus is most likely to be cultured in stool cultures.

Serologic test

Acute and convalescent serum sample may be tested for rise in antibody titer

(antibodies to the poliovirus), but the report can be difficult to interpret as in

many cases, the rise in titer may occur prior to paralysis.

Cerebrospinal fluid test

Infection with polio virus may cause an increased number of white blood cells

and a mildly elevated protein level in cerebrospinal fluid


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Treatment-acute stage

Bed rest, analgesics, hot packs, and

anatomical positioning of the limbsgentle passive ROM exercises of all joints


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treatment-acute stage

close monitoring of respiratory and cardiovascularfunctioning is essential during the acute stage of

poliomyelitis along with fever control and pain relievers for

muscle spasms.

Mechanical ventilation, respiratory therapy may be

needed depending of the severity of patients.


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Convalescent stage

From 2 days after the temperature return to normal andcontinues for 2 years

Muscle power improves

Physical therapy is recommended for full recovery.

Passive stretching exercises and wedging casts can be

used for mild to moderate contractures.


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convalescent stage

Surgical release of tight fascia and muscle

aponeuroses and lengthening of tendons may benecessary for contractures persisting longer than 6

months.

Orthoses should be used until no further recovery

is anticipated.


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chronic stage

Static joint instability can be controlled byOrthoses.Dynamic joint instability result in a fixed

deformity that cannot be controlled by

Orthoses.


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chronic stage

Soft tissue surgery, such as tendon transfers, should bedone in young children before the development of any

fixed bony changes.

Bony procedures for correcting a deformity can be

delayed until skeletal growth is near completion.


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prevention

The best preventive measure for poliomyelitis is

ensuring hygiene and encouraging good sanitation

practices. But, polio prevention begins with poliovaccination. Polio vaccine has been developed

against all 3 subtypes of the poliovirus and is very

effective in producing protective antibodies that

induces immunity against the poliovirus and

provides protection from paralytic polio.


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vaccine

Two types of vaccine are available:

an inactivated (killed) polio vaccine (IPV) and

a live attenuated (weakened) oral polio vaccine (OPV


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scheduleepi


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polio final yr.pptx