POLIOMYELITIS

 Poliovirus consist of 3 serotypes, types 1,2 & 3

 As of 2019, serotypes 2 & 3 have been eliminated & wildtype serotype 1 is endemic in
Pakistan & Afghanistan only
 Poliovirus is transmitted by feco-oral route
 Human are the only reservoir
 SENSORY DISTURBANCES ARE NOT A FEATURE OF POLIO
PATHOGENESIS

 Poliovirus gain host entry via gastrointestinal tract & replicate in M-cells of small intestine
 Virus spread to many sites, including reticuloendothelial system & skeletal system
 Poliovirus enters CNS along peripheral nerves or along neural pathways
 Poliovirus infects motor neuron cells of anterior horn cells and cranial nerve nuclei in
medulla oblongata
 Limb weakness occurs when >50% motor neurons are destroyed
IMMUNITY

 Transplacental immunity is acquired from mothers for 1st 4-6 moths of life
 IgG antibodies form after replication of virus in M—cells & protect against CNS invasion
 Secretory IgA prevents subsequent reinfection of gastrointestinal tract
CLINICAL FEATURES
A) INAPPARENT INFECTION:
 90-95% cases
 No disease & no sequelae

B) ABORTIVE POLIO:
 5% cases
 Flu-like syndrome with fever, malaise & headache for 2-3 days
 Physical examination may be normal or show non-specific pharyngitis or muscular
tenderness
 No sequelae develop

C) NON- PARALYTIC POLIO:

 1% cases
 Polio enters NS but does not destroy neurons
i) 1ST PHASE (MINOR ILLNESS)
o Signs of abortive polio with more intense headache, nausea & vomiting
o Soreness & stiffness of posterior muscles of neck, trunk & limbs
o Transient bladder paralysis & constipation occur frequently
o 2/3rd patients have symptoms free period between 1st & 2nd phase

i) 2ND PHASE (CNS DISEASE)

o Nuchal & spinal rigidity are basis of diagnosis of 2nd phase
o Hyperreflexia or hyporeflexia may precede weakness by 12-24 hours
o Spinal, gluteal & superficial reflexes diminish 1st
o Changes in deep tendon reflexes occur 8-12 hours after depression
superficial reflexes & indicate impeding weakness of extremities
D) PARALYTIC POLIO
 Occur in 0.1% polio
 Paralysis appears 3-8 days after initial symptoms

i) SPINAL PARALYTIC POLIO (79%)

 1st PHASE
o Presents as abortive polio & resolves after 2-3 days
o Patient remains well for 2-5 days before 2nd phase begins

 2ND PHASE
o Fever, severe headache & exacerbation of systemic symptoms
o Severe muscle pain with parasthesia, fasciculations & spasms develop
o Asymmetric flaccid paralysis occurs within 1-2 days, involving single muscles,
multiple muscles or a group of muscles
o Proximal muscles are involved to a greater extent than distal muscles
o Involvement of 1 leg is most common, followed by involvement of 1 arm
o Paralysis of legs is often accompanied by transient incontinence of bladder to
paralysis of bowel & bladder, with constipation & urinary retention
o Extent of involvement is obvious in 2-3 days & rarely progress after that
o Progression of paralysis stops when fever settles
o Recovery from paralysis, if any, is evident within 6 months & may continue to
improve for 18 months after acute disease
o Lack of improvement after several months indicates permanent paralysis
o Atrophy of limb, failure to grow & deformity are common in growing child

ii) BULBAR POLIO (19%)

o Dysfunction of cranial nerves & medullary centers
o Paralysis of cranial nerves is usually transient
o PALATAL & PHARYNGEAL PARALYSIS: (CN IX, X, XII)
 Nasal twang
 Swallowing difficulty
 Accumulated pharyngeal secretions
 Nasal regurgitation of saliva & fluids
 Deviation of palate, uvula or tongue
 Ineffective cough

o PARALYSIS OF VOCAL CORDS (CN X)

 Hoarseness or aphonia
 Asphyxia
 Rope sign – Weakness of hyoid muscle leading to acute angulation
between chin & larynx

o INVOLVEMENT OF VITAL CENTERS OF BRAIN

 Irregular breathing
 Blood pressure changes (especially hypertension)
 Flushing & mottling of skin
 Cardiac arrhythmias
 Rapid body temperature changes
 o LANDRY TYPE ASCENDING PARALYSIS: Uncommon
iii) POLIOENCEPHALITIS (2%)
o Involves higher centres of the brain
o Irritability, disorientation, drowsiness, coarse tremors present
o Seizures, spastic paralysis, hyperreflexia & coma observed
o Respiratory insufficiency leads to hypercarbia & hypoxia

PARALYTIC POLIO WITH RESPIRATORY INSUFFICIENCY

 Occurs in certain patterns of paralytic polio, without involvement of vital centres

i) PURE SPINAL POLIO
o Involvement of cervical & thoracic segment of spinal cord leads to paralysis of
diaphragm & intercostal muscles

ii) PURE BULBAR POLIO

o Involvement of cranial nerves IX, X & XII results in paralysis of pharynx, larynx &
tongue & consequent airway obstruction

iii) BULBOSPINAL POLIO

o Paralysis of respiratory muscles & cranial nerves leading to respiratory
insufficiency

 FEATURES OF RESPIRATORY INSUFFICIENCY

o Breathlessness
o Anxious expression
o Tachypnea
o Use of alae nasi & accessory muscles of respiration
o Poor cough
o Paradoxical abdominal movements due to diaphragm paralysis
o Relative immobility of intercostal muscles
o Deltoid paralysis indicates impeding respiratory failure

INVESTIGATION

 Polio should be considered in any unimmunized or incompletely immunized child with

paralytic disease
 Vaccine associated paralytic polio (VAPP) should be considered in any child with
paralytic disease occurring 7-14 days after receiving OPV

INVESTIGATION NOTES

STOOL SPECIMENS o 2 stool specimens, 8-10g weight, collected 24-28 hours

apart, as soon as possible after onset of paralysis
o Stool sample should be collected within 14 days of onset of
paralysis
o Poliovirus concentration highest in 1st week after onset of
paralysis
CSF R/E o Before 2nd week: WBC: 20-300 cells/mm3, Proteins: Normal
o By 2nd week: WBC: normal, Proteins, 50-100 mg/dl

PCR To differentiate wild-type & vaccine-type strain

 SEROLOGY o Seroconversion
o ≥ 4x increase in antibody titres from acute illness phase to
3-6 weeks alter
TREATMENT DIFFERENTIAL DIAGNOSIS
A) ABORTIVE POLIO  Guillain Barre syndrome
 Analgesics, sedatives  Transverse myelitis
 Attractive diet  Spinal cord trauma,
 Bed rest until fever has resolve for several days abscess or tumour
 Avoid exertion of 2 weeks after onset of  Myasthenia gravis
disease  Tick bite paralysis
 Neurological & musculoskeletal assessment
after 2 months to detect any minor involvement

B) NON-PARALYTIC POLIO
 Analgesics & hot packs for 15-20 minutes, every 2-4 hours to reduce muscle pain &
spasm
 Place plywood beneath mattress to provide firm bed to patient
 Foot board t keep feet at 90° to legs
 Gentle physiotherapy
 Neurological & musculoskeletal assessment after 2 months to detect any minor
involvement

C) SPINAL PARALYTIC POLIO

 Hospital admission with complete physical rest for 1st 2-3 weeks
 Appealing diet with high fluid intake
 Maintain neutral position with feet at 90° to legs, knees slightly flexed & hip & spine
straight
 Change position every 3-6 hours to bed sores
 Hot packs & analgesics to reduce pain
 Allow active & passive movements when pain is relieved
 Avoid constipation (Constipation  acute gastric dilation  ↓ respiratory efficiency)
 In case of bladder paralysis:
o Bethanecol
o Manual compression with running water, if bethanecol fails
o Catheterization
o Bladder paralysis is usually transient
 Orthopedic & psychiatrist consultation

D) BULBAR PARALYTIC POLIO

 Hospital admission with complete physical rest for 1st 2-3 weeks
 Maintain airway & monitor vitals (Pulse, BP, temperature, respiratory rate)
 IV fluid given until NG feed or oral feed is tolerated
 Avoid risk of inhalation of saliva, food & vomitus by elevating foot end of bed 20-25°
& keeping patient face to one side
 Regular suction of pharynx & oral cavity
 Tracheostomy may be needed in patients with vocal cord paralysis or constriction of
hypopharynx
 Mechanical ventilators may be needed in case of respiratory insufficiency
COMPLICATIONS

 ACUTE GASTRIC DILATION

o Leads to respiratory insufficiency
o Immediate gastric aspiration & external application of ice bags are indicated

 MELENA
o Due to intestinal erosion
o May be severe enough to require blood transfusion

 COMPLICATIONS OF IMMOBILITY
o Immobility  skeletal decalcification  hypercalcemia + hypercalciuria 
nephrocalcinosis + urinary calculi
o High fluid intake is advised

 CONVULSIONS
o Hypertension, headache & dimness of vision predict seizures
o Mild hypertension is common in acute stage

 ACUTE PULMONARY EDEMA

o Occurs particularly in patients with arterial hypertension

 Muscle paralysis  limb deformities

 Leg length discrepancy
 Scoliosis
 Urinary tract infections
 Hypertension
 Kidney stones
 Myocarditis
 Paralytic ileus
POST-POLIO SYNDROME

 Occurs in 30-40% of patients who experienced paralytic polio in childhood

 Patients experience muscle pain, exacerbation of existing weakness or development of
new weakness or paralysis
 Risk factors include female sex, increasing length of time since acute poliovirus infection
& presence of permanent residual impairment
 No treatment available
PROGNOSIS

 Inapparent polio, abortive polio & non-paralytic polio have good prognosis with no long
term sequelae
 Mortality rate is 60% in severe bulbar polio
 Mortality rate is 5-10% in less severe bulbar polio & spinal polio
 Tonsillectomy increase risk of bulbar polio
 Increased physical activity, exercise & fatigue during early phase of illness lead to higher
risk of paralytic disease
 IM injections increase risk of localized disease
ACUTE FLACCID PARALYSIS SURVEILLANCE

 DEFINITION OF AFP:
o Sudden onset of floppy weakness in a child aged less than 15 years due to any
cause or paralytic disease
POLIO ERADICATION STRATEGIES

 ROUTINE IMMUNIZATION
o Ensuring routine immunization in general population to reduce number of
susceptible children

 NATIONAL IMMUNIZATION DAYS

o 3 monthly NID’s provide a temporary barrier to circulation of wild-type virus

 AFP SURVEILLANCE
o Any case of AFP is notified & investigated for polio

 MOP-UP
o Door-to-door campaigns in high risk areas identified by AFP surveillance

POLIO VACCINES EFFICACY

 After 3 doses of OPV, 70% children develop immunity against Polio virus 1 & 3
 Even after 7-8 doses of OPV, 4-5% remain susceptible to developing polio
 Poor efficacy of OPV may be due to malnutrition, gastroenteritis & infection with other
enteroviruses, which compete with vaccine virus for receptors on enterocytes
 IPV provided 99& immunity after 3 doses
OPV VS IPV VACCINE

OPV IPV

Live, attenuated virus Killed virus

Oral route Subcutaneous route
Inexpensive More expensive
Easy to administer Required trained health workers
Provides humoral & gut immunity Provides humoral immunity
Risk of VAPP (1:750,000) No risk of VAPP
Produces IgA antibodies in oropharynx & Produces IgG antibodies that prevent
GIT bulbar polio & PPS

CASES OF POLIO IN PAKISTAN

YEAR CASES YEAR CASES

2005 28 2015 54
2011 198 2016 20
2012 58 2017 08
2013 98 2018 12
 2014 306
ENTERIC FEVER
 Caused by S. typhi & S. paratyphi, in ratio of 10:1
 Infecting dose: 105 – 109 organisms
 Transmitted by feco-oral route via flies, food & fomites
 Clinical syndrome of fever & systemic symptoms is caused by release of
pro-inflammatory cytokines from infected cells
 Children <5 years’ age have highest incidence & highest rate of complications.
 Increased risk of infection in HIV patients & individuals with H. pylori

PATHOGENESIS
 After ingestion, S. typhi invades body via gut mucosa in terminal ileum & enters blood
stream via lymphatics
 Bacteria spread throughout blood & colonize organs of reticuloendothelial system, where
they replicate within macrophages
 After a period of replication, secondary bacteremia occurs leading to clinical symptoms
CLASSIFICATION OF TYPHOID FEVER BY DRUG RESISTANCE

CLASSIFICATION CASE DEFINITION

o Typhoid fever caused by S. typhi ± S. paratyphi A, B or C

strains
NON-RESISTANT o Sensitive to 1st line drugs (Chloramphenicol, ampicillin,
TYPHOID FEVER trimethoprim-sulfamethoxazole) & 3rd generation
cephalosporins
o With or without resistance to 2nd line drugs (fluoroquinolones)

o Typhoid fever caused by S. typhi ± S. paratyphi A, B or C

MULTI-DRUG strains
RESISTANT (MDR) o Resistant to 1st line drugs (Chloramphenicol, ampicillin,
TYPHOID FEVER trimethoprim-sulfamethoxazole)
o With or without resistance to 2nd line drugs (fluoroquinolones)

EXTENSIVE DRUG o Typhoid fever caused by S. typhi ± S. paratyphi A, B or C

RESISTANT (XDR) strains
TYPHOID FEVER o Resistant to 1st & 2nd line drugs & 3rd generation cephalosporins

CLINICAL FEATURES
 INCUBATION PERIOD: 4-14 days
 Most common symptoms are fever (95%), coated tongue (76%) & anorexia (70%)
 Clinical features are more severe with more toxicity & complications in disease caused
by MDR & XDR typhoid fever
 Fever pattern is stepwise, characterized by rising temperature over the course of each
day, which drops by next morning
 Peaks & troughs rise over time to give continuous, high grade fever
1ST WEEK

 GI manifestations develop: coated tongue, diffuse abdominal pain & tenderness

 Severe, right upper quadrant, colicky pain may occur
 Monocytic infiltration of Peyer’s patches  narrowing of bowel lumen  constipation
 Patient develops dry cough, dull, frontal headache, delirium & stuporous malaise
 Near end of the 1st week, fever plateaus at 103-104°F
 Salmon coloured, blanching, truncal maculopapules, 1-4 cm wide rash (Rose spots)
 Rose spots are usually <5 in number & resolve within 2-5 days
 Rose spots caused by bacterial emboli in skin
2ND WEEK

 Signs & symptoms progress

 Abdomen becomes distended
 Hepatosplenomegaly occurs at this stage
 Relative bradycardia & dicrotic pulse may be appreciated (Double beat with 2nd beat
weaker than the 1st)
3RD WEEK

 Patient becomes more toxic & anorexic with significant weigh loss
 Complications are likely to occur in this phase
 Conjunctivae are injected
 Thready pulse, tachypnea & audible crackles in lung bases
 Severe abdominal distention with diarrhea
 Typhoid state may occur (Apathy, confusion, psychosis)
 Necrotic Peyer patches may lead to peritonitis & bowel perforation
 Overwhelming toxemia, myocarditis & intestinal bleed may lead to death
4TH WEEK

 If patient survives to 4th week, fever, mental health & abdominal distention slowly improve
 Intestinal & neurologic complications may occur
 Weakness & weight loss last for months
 Some survivors become carrier of S. typhi

DIFFERENTIAL DIAGNOSIS:
 Malaria
 Urinary tract infection
 Acute vital hepatitis
 Dengue fever
COMPLICATIONS

SYSTEM COMPLICATIONS SYSTEM COMPLICATIONS

INTESTINAL o Hemorrhage o Pneumonia

(<1%) RESPIRATORY o Empyema
o Perforation (0.5 - (1-6%) o Bronchopleural
1.0%) fistula
o Peritonitis
CNS o Encephalopathy o Cholecystitis
(3-35%) o Cerebral edema HEPATOBILIARY o Hepatitis
o Subdural SYSTEM o Hepatic abscess
abscess (1-26%) o Splenic abscess
o Meningitis o Paralytic ileus
o Ataxia
o Seizures
o Guillain Barre
Syndrome
o Endocarditis o UTI
CVS o Myocarditis o Renal abscess
(1-5%) o Pericarditis GENITOURINARY o Pelvic infections
o Congestive (<1%) o Testicular
cardiac failure abscess
o Epididymitis
BONE & JOINTS o Osteomyelitis
(<1%) o Septic arthritis

Risk factors for Complications:

o Residence in endemic areas o Asplenia
o Cardiac abnormalities o Immunodeficiency
o Sickle cell anemia o Diabetes

INVESTIGATIONS

INVESTIGATION NOTES

CBC o WBC: Often ↓ but may be 20,000 – 25,000/mm3 in younger

children
o Platelets: ↓ platelets indicates severe illness & may
accompany DIC
o 1st week:
 Blood C/S: 40-60% positive
 Bone marrow C/S
CULTURES o 2nd week:
&  Widal test: Not sensitive or specific
ANTIBODY TESTS  Typhidot: 26.7% sensitive, 61.5% specific,
o 3rd week:
 Stool C/S
o 4th week:
 Urine C/S
LFT Increased
PCR Allows rapid diagnosis
TREATMENT

 Adequate rest, hydration. Soft diet, unless patient has abdominal distention
 Maintain fluid electrolyte balance
 Antipyretics
 Admit in case of
o Persistent vomiting
o Severe diarrhea
o Abdominal distention

SUSCEPTIBILITY ANTIBIOTIC DOSE DURATION

(mg/kg/day) (days)
UNCOMPLICATED TYPHOID FEVER

Chloramphenicol 50-75 14-21

FULLY SENSITIVE
Amoxicillin 75-100 14
Ofloxacin, ciprofloxacin 15 5-7
MDR
Cefixime 15-20 7-14
QUINOLONE Azithromycin 8-10 7
RESISTANT
Ceftriaxone 75 10-14
SEVERE TYPHOID FEVER – OPTIMAL THERAPY

FULLY SENSITIVE Ofloxacin, ciprofloxacin 15 10-14

MDR Ofloxacin, ciprofloxacin 15 10-14
QUINOLONE Ceftriaxone 60 10-14
RESISTANT
Cefotaxime 80 10-14
SEVERE TYPHOID FEVER – ALTERNATE THERAPY

FULLY SENSITIVE Chloramphenicol 100 14-21

Amoxicillin 100 14-21
MDR Ceftriaxone 60 10-14
Cefotaxime 80 10-14
QUINOLONE Azithromycin 10-20 7
RESISTANT
Ofloxacin, ciprofloxacin 20 7-14
WHO advises Azithromycin as only remaining 1st antibiotic for XDR typhoid in low
resource areas

DEXAMETHASONE

 Recommended for severely ill patient with shock, obtundation or coma

 DOSE:
 o 3mg/kg x stat,
o Then, 1 mg/kg x 6 hourly for 48 hours
 Dexamethasone may mask signs of abdominal complications & should be used carefully

PROGNOSIS

 Relapses occur in 2-4% cases

 Complications & mortality increased in MDR & XDR typhoid cases
 <2% risk of children becoming chronic carrier (Individual who excrete S. typhi for
≥3 months after infection

PREVENTION

 Adequate sanitation
 Chlorination of water
 Avoid foods from street vendors
VACCINES

 V1 CAPSULAR POLYSACCHARIDE VACCINE

o Recommended for children ≥2 years’ age
o Single intramuscular dose
o Booster every 2 years
o 70-80% protective efficacy

 LIVE ATTENUATED TY21a VACCINE

o Oral vaccine
o 67-82% efficacy for ~5 years
o Avoid vaccine in immunocompromised individuals
o Stop proguanil, mefloquine & antibiotics 3 days before until 3 days after Ty21a