Nervous System and Special Senses 31500311

Community Medicine lecture

Epidemiology and prevention of Poliomyelitis and Meningitis

By

Hatim Jaber

MD MPH JBCM PhD

6 -03- 2019 1

LECTURE OBJECTIVES

• Describe the public health importance of polio and meningitis as a serious infectious diseases.

• Describe Epidemiological pattern of polio and meningitis disease; Globally and locally.

• Identify and understand the rote of transmission and risk factors of Polio and meningitis.

• Understand the importance and different types of polio and meningitis prevention.

2

Introduction

• A viral infection most often recognized by acute onset of flaccid paralysis.

• Flaccid paralysis is an illness characterized by

weakness or paralysis and reduced muscle tone without other obvious cause (e.g., trauma).

3

Introduction

• Infection with poliovirus results in a spectrum of clinical manifestations from inapparent infection to non-specific febrile illness, aseptic meningitis, paralytic disease, and death.

• Poliomyelitis is a highly infectious disease caused

by three serotypes of poliovirus.

4

Poliomyelitis

• First described by Michael Underwood in 1789

• Global eradication in near future

• In Jordan no cases - 2002

5

• Two phases of acute poliomyelitis can be distinguished:

a non-specific febrile illness (minor illness) followed, in a small proportion of patients, by

aseptic meningitis and/or paralytic disease (major illness).

• The ratio of cases of inapparent infection to paralytic disease ranges from 100:1 to 1000:1.

6

Outcomes of poliovirus infection

7

Key facts

• Polio (poliomyelitis) mainly affects children under 5 years of age.

• 1 in 200 infections leads to irreversible paralysis.

• Among those paralyzed, 5% to 10% die when their breathing muscles become immobilized.

• Cases due to wild poliovirus have decreased by over 99% since 1988, from an estimated 350 000 cases then, to 29 reported cases in 2018.

• As long as a single child remains infected, children in all countries are at risk of contracting polio.

• Failure to eradicate polio from these last remaining strongholds could result in as many as 200 000 new cases every year, within 10 years, all over the world.

• In most countries, the global effort has expanded capacities to tackle other infectious diseases by building effective surveillance and immunization systems.

8

Epidemiological pattern

• The epidemiological pattern of polio depends upon the degree of the socioeconomic development and health care services of a country.

• The pattern of the disease has been considerably modified by widespread immunization.

9

According to the WHO;

Three epidemiological patterns have now been delineated: 1. Countries with no immunization: the virus infects all

children, and by age 5 years almost all children develop antibodies to at least one of the 3 types of polio virus. In that pattern paralytic polio cases are frequent in infants.

2. Countries with partial immunization: In these countries, wild polio virus is largely replaced by vaccine virus in the environment.

3. Countries with almost total immunization coverage: in these countries polio is becoming rare, however, sporadic cases do occur rarely.

10

Causative organism • Poliovirus: belongs to “Picorna” viruses which are small RNA-

containing viruses. • Polioviruses have three antigenically distinct types, giving no

cross immunity: – Type I: “Leon”; the commonest in epidemics – Type II: “Berlinhide”; the prevailing type in endemic areas. – Type III: “Lansing”; occasionally causes epidemics.

• Polioviruses are relatively resistant and survive for a long time under suitable environmental conditions, but are readily destroyed by heat (e.g. pasteurization of milk, and chlorination of water).

11

Reservoir of infection

• Man is the only reservoir of infection of poliomyelitis.

Man: cases and carriers • Cases: all clinical forms of disease • Carriers: all types of carriers (e.g. incubatory,

convalescent, contact and healthy) except chronic type.

In endemic areas, healthy carriers are the most

frequent type encountered. 12

Foci of infection

• Pharynx: the virus is found in the oropharyngeal secretions.

• Small intestine: the virus finds exit in stools.

13

Modes of transmission

Since foci of infection are the throat and small intestines, poliomyelitis spreads by two routes:

1. Oral-oral infection: direct droplet infection

2. Faeco-oral infection: – Food-borne (ingestion) infection through the ingestion of contaminated

foods. Vehicles include milk, water, or any others that may be contaminated by handling, flies, dust….

– Hand to mouth infection. (polio virus has the ability to survive in cold environments.

Overcrowding and poor sanitation provide opportunities for exposure to infection.)

14

15

Period of infectivity

• Contact and healthy carriers: about 2 weeks

• Cases: the cases are most infectious 7 to 10 days before and after the onset of symptoms.

In the feaces, the virus is excreted commonly for 2 to 3 weeks, sometimes as long as 3 to 4 months.

• In polio cases, infectivity in the pharyngeal foci is around one week, and in the intestinal foci 6-8 weeks.

• Incubation Period: 7-14 days 16

Susceptibility

• Age: more than 95% reported in infancy and childhood with over 50% of them in infancy.

• Sex: no sex ratio differences, but in some countries, males are infected more frequently than females in a ratio 3:1.

• Risk factors: (provocative factors of paralytic polio in individuals infected with polio virus): fatigue, trauma, intramuscular injections, operative procedures, pregnancy, excessive muscular exercise…

• Immunity: The maternal antibodies gradually disappear during the first 6 months of life. Immunity following infection is fairly solid, although infection with other types of polio virus can still occur.

17

Sequelae of polio infection

Polio infection

Inapparent infection Clinical poliomyelitis

Abortive polio

(minor illness)

Involvement of CNS

(major illness)

Paralytic

polio

Non-paralytic

polio

Spinal polio

Bulbar polio

Bulbospinal polio

18

Complications and case fatality

• Respiratory complications: pneumonia, pulmonary edema

• Cardiovascular complications: myocarditis, cor pulmonale.

• Late complications: soft tissue and bone deformities, osteoporosis, and chronic distension of the colon.

• Case fatality: varies from 1% to 10% according to the form of disease (higher in bulbar), complications and age ( fatality increases with age).

19

Prevention General prevention: • Health promotion through environmental sanitation.

• Health education (modes of spread, protective value of vaccination).

Active immunization:

– Salk vaccine (intramuscular polio trivalent killed vaccine).

– Sabin vaccine (oral polio trivalent live attenuated vaccine).

20

Prevention

• Seroprophylaxis by immunoglobulins:

Not a practical way of giving protection because it must be given either or before or very shortly after exposure to infection.

(0.3 ml/kg of body weight).

21

Inactivated Polio Vaccine Oral Polio Vaccine

• Contains 3 serotypes of vaccine virus • Grown on monkey kidney (Vero) cells

• Inactivated with formaldehyde

• Contains 2-phenoxyethanol, neomycin, streptomycin, polymyxin B

Highly effective in producing immunity to poliovirus

• 50% immune after 1 dose

• >90% immune after 2 doses

• >99% immune after 3 doses

• Duration of immunity not known with certainty

22

Polio Vaccination Schedule

Vaccine

IPV

IPV

IPV

IPV

Age

2 months

4 months

6-18 months

4-6 years*

Minimum Interval

---

4 wks

4 wks

4 wks

*the fourth dose of IPV may be given as

early

as 18 weeks of age 23

Polio Vaccination of Previously Vaccinated Adults

• Previously complete series – administer one dose of IPV

• Incomplete series – administer remaining doses in series

– no need to restart series

24

Control of patient, contacts and the immediate environment:

1) Report to local health authority: Obligatory case report of

paralytic cases as a Disease under surveillance by WHO, Class 1.

2) Isolation: Enteric precautions in the hospital for wild virus

disease; of little value under home conditions because many household contacts are infected before poliomyelitis has been diagnosed.

3) Concurrent disinfection: Throat discharges, feces and articles

soiled therewith. Terminal cleaning. 4) Quarantine: Of no community value.

25

5) Protection of contacts: Immunization of familial and other close contacts is recommended but may not contribute to immediate control; the virus has often infected susceptible close contacts by the time the initial case is recognized. 6) Investigation of contacts and source of infection: Occurrence of a single case of poliomyelitis due to wild poliovirus must be recognized as a public health emergency prompting immediate investigation and planning for a large-scale response. A thorough search for additional cases of AFP in the area around the case assures early detection, facilitates control and permits appropriate treatment of unrecognized and unreported cases. 7) Specific treatment: None; however, Physical therapy is used to

attain maximum function after paralytic poliomyelitis.

26

Polio Eradication

• Last case in United States in 1979 and in Jordan in 2002

• Western Hemisphere certified polio free in 1994

• Last isolate of type 2 poliovirus in India in October 1999

• Global eradication goal>>>>>>>> 2020

27

Wild Poliovirus 1988

28

CNS infections

• Meningitis Infection of the subarachnoid space with meningeal

involvement • Encephalitis Inflammation of brain • Meningoencephalitis Inflammation of brain with meningeal involvement • Brain Abscess Pathogens may be bacterial, TB, viral, fungal, or parasitic

29

What is Meningitis ?

• Meningitis is an inflammation of the meninges, the thin lining that surrounds the brain and the spinal cord.

Different origins:

– Mechanical: eg. tumours

– Infectious: Cerebrospinal fluid (CSF) found

infected

• Viruses

• Fungi

• Parasites

• BACTERIA 30

Meningitis???

Meningitis is an inflammation (swelling) of the protective membranes covering the brain and spinal cord.

A bacterial or viral infection of the fluid surrounding the brain and spinal cord usually causes the swelling.

However, injuries, cancer, certain drugs, and other types of infections also can cause meningitis.

It is important to know the specific cause of meningitis because the treatment differs depending on the cause.

Causes of Meningitis

• Bacterial

1. - Haemophilus influenzae

2. - Listeria

3. - Meningococcus

4. - Mumps

5. - Pneumococcus

6. - Group A Streptococcus

7. - Group B Streptococcus

• Viral

1. - Arboviral (mosquito-borne) diseases

2. - Influenza

3. - LaCrosse Encephalitis virus

4. - West Nile Virus

5. - Also enteroviral

32

Types

• Acute either pyogenic or viral.

• Chronic due to tuberculosis or fungal.

33

:

ETIOLOGICAL AGENT

"Normal" Adults (6-21 yrs)

Neisseria meningitidis

Streptococcus pneumoniae

Children (3 months - 6 years)

Haemophilus influenzae

Neisseria meningitidis

Streptococcus pneumoniae

Staphylococcus aureus

Mycobacterium tuberculosis

Infants (½ - 3 months)

Streptococcus, Group B

Listeria monocytogenes

Escherichia coli

Pyogenic meningitis.

Neonates

Escherichia coli

Streptococcus, Group B

Staphylococcus aureus

Listeria monocytogenes

Streptococcus, Group A

Diabetics, alcoholics, elderly,

debilitated, diseased

(untreated)

Listeria monocytogenes

Streptococcus pneumoniae

Treponema pallidum 34

NAMES OF DISEASE:

Fungal meningitis

Cryptococcosis

Torulosis

Tubercular meningitis

Amoebic meningitis

Syphilitic meningitis

CHRONIC MENINGITIS

35

Symptoms can be the same for Viral and Bacterial

1. Fever and chills

2. Mental status changes

3. Nausea and vomiting

4. Sensitivity to light (photophobia)

5. Severe headache

6.Stiff neck

36

37

Initial symptoms and signs

Symptoms or Sign Relative frequency%

Headache >90

Fever >90

Meningismus >85

Altered sensorium >80

Kernig’s or Brudzinski’s signs

>50

Focal findings 10-20

Papilledema <1

38

For Public Health Response Meningitis can be:

Viral

OR

Bacterial

Both can create Public Health Problems but not all Meningitis is created equal

39

Viral Meningitis

Clinical description: A syndrome characterized by acute onset of meningeal symptoms- fever, and cerebrospinal fluid pleocytosis (white cells in the spinal fluid) with bacteriologically sterile cultures.

Confirmed: a clinically compatible illness diagnosed as aseptic meningitis,

with no laboratory evidence of bacterial or fungal meningitis

40

Mumps virus

Polio virus

Coxsackie B virus

Echovirus

Arboviruses

Human Herpesvirus 1 (Herpes simplex 1 virus)

Lymphocytic choriomeningitis viruses-Arenavirus

Encephalomyocarditis viruses

Louping ill virus

Pseudolymphocytic meningitis virus

Hepatitis viruses

Adenovirus

Rhinovirus

Coxsackie A virus

ETIOLOGICAL AGENTS:

Viral meningitis

41

Bacterial causes of Meningitis

Many bacteria but some are of specific importance in public health:

1. Streptococcus pneumoniae

2. Haemophilus influenza Serotype b (Hib)

3. Neisseria meningitidis (Nm) (also called meningococcal meningitis)

42

Meningococcal meningitis

Meningococcal meningitis is a bacterial form of meningitis, a serious infection of the thin lining that surrounds the brain and spinal cord.

Meningococcal meningitis is associated with high fatality (up to 50% when untreated) and high frequency (more than 10%) of severe sequelae. Early antibiotic treatment is the most important measure to save lives and reduce complications.

Meningococcal meningitis

Meningococcal meningitis is observed worldwide but the highest burden of the disease is in the meningitis belt of sub-Saharan Africa, stretching from Senegal in the west to Ethiopia in the east. Around 30 000 cases are still reported each year from that area.

Serogroup specific vaccines are used for prevention (routine immunization) and in response to outbreaks (prompt reactive vaccination).

Meningococcal meningitis • Worldwide distribution

• Sporadic, cluster or large epidemic

• 12 serogroups:

•Europe, Americas: B, C

•Asia: A

•Africa: A, C, W135, X

• Africa: 80 % of the burden

45

Case-Fatality Ratio by Serogroup and Age-Group, United States, 1997-2011

Serogroup <5 years 5-10 years 11-19 years 20 years Total

B 4% 22% 15% 23% 13%

C 13% 9% 12% 16% 13%

Y 0% 13% 13% 12% 10%

W <1% 0% 0% 10% 7%

Total 5% 12% 15% 15% 12%

ABCs cases from 1997-2011 estimated to the US population

The Meningitis Belt

21 countries and 300 million

people at risk

700 000 cases in the past 10

years

10-50 % case fatality rates

10-20 % of survivors suffer

permanent brain damage

47

Figure 1. Trends of epidemic meningitis diisease in the

African Belt, 1970-2006

0

20,000

40,000

60,000

80,000

100,000120,000

140,000

160,000

180,000

200,0001

97

0

19

73

19

76

19

79

19

82

19

85

19

88

19

91

19

94

19

97

20

00

20

03

20

06

Years

Cases

48

Transmission:

• Strictly a human disease • Direct transmission, person to person • Close and prolonged contact. • Average incubation period 4 days, ranging between 2 and

10 days. • Carried in the pharynx – can overwhelm the body’s

defenses allowing infection to spread through the bloodstream and to the meninges.

• 1-10% of asymptomatic carriers. Up to 10- 25% during epidemics.

49

Neisseria meningitidis Nasopharynx

Streptococcus

pneumoniae

Nasopharynx or direct

extension across

skull fracture

Listeria

monocytogenes

GI tract, placenta

Haemophilus

influenzae

Nasopharynx

Staphylococcus aureus Bacteremia, skin, or foreign

body

Staphylococcus

epidermidis

Skin or foreign body

Organism Site of entry

50

Neisseria meningitidis Prophylaxis

People who qualify as close contacts of a person with meningitis caused by N. meningitidis are

1. Family and household contacts

2. Child or nursery school contacts

3. Anyone exposed to patient’s oral secretions

51

Hib Prophylaxis

The entire household, regardless of age, should receive prophylaxis in these cases if-

- There is 1 household contact younger than 48 months who has not been fully immunized against Hib, or

- An immunocompromised child (a child with a weakened immune system) of any age is in the household.

52

Bacterial Meningitis- Outbreaks Local Health Departments

1. Investigate cases immediately

2. Report cases to Regional Epidemiologist and Infectious Disease Epidemiology

3. Determine who is at risk by interviewing physician, family or possibly the case

4. Organize notes and respond as though this will be an outbreak

5. Send isolates to OLS

53

Complication.

1. Cerebrovascular involvement.

2. Cerebral odema.

3. Hydrocephalus.

4. Septic shock.

5. Disseminated intravascular coagulation.

6. Acute respiratory distress syndrome.

54

Tuberculous meningitis.

• Clinical feature.

• Diagnosis.

• Treatment.

55

Fungal meningitis-predisposing factors.

1. Glucosteroid therapy 2. Malignancy (particularly of the lymphoreticular system) 3. Collagen - vascular disease. 4. Sarcoidosis - a disorder involving many organs where there is

formation of epithelioid cell 5. Diabetes mellitus 6. Pregnancy 7. Alcoholism 8. Genetic impairment of host defense mechanisms - 50%. T-cell

diseases (Di George Syndrome, Nezelof's syndrome) 9. TB

10. AIDS

56

Outcomes Can Be Severe, Even with Treatment

• Serious outcomes include meningitis (most common clinical presentation) and meningococcemia (bloodstream infection)1

• Death rate of 10%-15%, even with antibiotic therapy1

References: 1. CDC. Epidemiology and Prevention of Vaccine-Preventable

Diseases.

(The Pink Book). 2015:231-246. 2. CDC. MMWR. 2013;62(RR-2):1-28. 57

– Death rate even higher (up to 40%) for patients who develop meningococcemia1

• Up to 20% of people who survive meningococcal disease suffer lifelong disability2

– Amputation of arms or legs, hearing loss, brain damage

Courtesy of National Meningitis

Association

57

PREVENTION:

Neisseria meningitidis - each dose of the multivalent vaccine

provides A, C, Y and W-135

capsular polysaccharides. Effective in children over 3 months of age.

Streptococcus pneumoniae - each dose of the multivalent

vaccine provides 23 types of capsular polysaccharide covering the majority of

strains causing meningitis. Recommended for children over 2 years of age.

Haemophilus influenzae – each dose of the monovalent vaccine provides the capsular

polysaccride from serotype b. organisms. Recommended for children

over 18 months of age.

58

Where the Burden of Disease Falls1

59 Reference: 1. CDC. MMWR. 2013;62(RR-2):1-28. 2. CDC.

www.cdc.gov/meningococcal/images/ meningococcal-graph-lg.jpg. Accessed April 4, 2018.

<1 year of

age

16 through

21 years of

age

≥65 years of

age

Getty I

mages/T

err

y V

ine

G

etty I

mages/K

idS

tock

Getty I

mages/R

ick L

ow

e

Age-Specific Fatalities from Meningococcal Disease1-16

60

Age Group (Years)

Nu

mb

er

of

Death

s

Approximately 1 in 5 deaths

overall occurred in this age

group

Sources for References 1-16: Deaths: Final data as reported in National Vital Statistics Reports for 1999 through 2014.

United States, 1999-

2014

Why Boost at 16 Years of Age?

• Antibody persistence studies indicate that protective levels of circulating antibody decline 3 to 5 years after a single MenACWY dose1

• Vaccine effectiveness case−control study suggests that many adolescents are not protected 5 years after vaccination1,2

61 References: 1. CDC. MMWR. 2013;62(RR-2):1-28. 2. Cohn AC et al.

Pediatrics 2017;139(2):e20162193.

“[A] single dose of meningococcal conjugate vaccine administered

at age 11 or 12 years is unlikely to protect most adolescents

through the period of increased risk at ages 16 through 21

years”─ACIP1

Waning Antibody Protection in Serogroup C: The Need for Boosting

62

Pe

rce

nta

ge w

ith

hSB

A t

ite

r ≥

1:8

Reference: Robertson C, et al. Vaccine 2016;34:5273–5278

hSBA = Serum bactericidal assay using human complement.

4-6 years after 1 dose

28 days after booster dose

99.6%

44.2%

Invasive Meningococcal Disease in 5-24 Year-Olds Massachusetts, 1988-2011 and MCV4 Uptake in 13-17 Year-

Olds, Massachusetts, 2006-2011

63

Menveo

(MCV4-CRM)

Meningococcal Vaccines

Conjugate vaccines Menactra (MCV4-D) Licensed 2005 Approved for use in those 9 months–55 years, IM A,C,Y,W-135 conjugated to diphtheria toxoid Does not require reconstitution

Menveo (MCV4-CRM) Licensed 2010 Approved for use in those 2 months–55 years, IM A,C,Y,W-135 conjugated to CRM197 Requires reconstitution

Polysaccharide vaccine (MSPV4) Licensed in 1978, for use in those > 2 years of age, SC Polysaccharide from A,C,Y,W-135 Requires reconstitution

64

Meningococcal Vaccine Recommendations

Routine vaccination of all persons aged 11-18 years with conjugate at the earliest opportunity

MCV4 should be used in persons 2-10 years recommended to receive meningococcal vaccine

Conjugate vaccine may be used in persons 11-55 years, polysaccharide vaccine should be used for higher–risk persons >55 years

Conjugate vaccine also recommended for higher-risk persons aged 19-55 years: college freshmen living in dorms

microbiologists routinely exposed to isolates of N. meningitidis

military recruits

travelers to or residents in countries in which N. meningitidis is hyperendemic or epidemic

those with terminal complement component deficiency or functional or anatomic asplenia (2 doses)

those with HIV infection “may elect vaccination”

ACIP 65

66

Booster Dose Schedule

Ages 11 to 18:

At age 16, if primary dose at age 11 or 12 years

At age 16 through 18, if primary dose at age 13 through 15 years

No booster needed if primary dose on or after age 16 years

At-risk, ages 2 to 55:

Persons aged 2 through 6 years: after 3 years

Persons aged 7 years or older: after 5 years

67

Transfer of care, office to hospital

• KEY POINT: Parenteral antibiotics must be started as soon as possible. – Evidence of pre-hospital antibiotics is inconclusive

68

Transfer with droplet precautions

69

Chemoprophylaxis of Close Contacts

1. Close contacts include:

1. Household members, daycare center classmates, and teachers

2. Anyone directly exposed to oral secretions

2. Treat as soon as possible

3. Secondary cases rare

Prophylaxis and control measures

Prophylaxis and control measures

71

WHO strategy: Performance and Availability of vaccines

• PS vaccines

Poorly immunogenic in children < 2y

Immunity short lived: requires multiple doses

Does not protect from carriage

Routine immunization not feasible in the Belt countries

Limited supply, affordability

bivalent AC

trivalent ACW

tetravalent ACWY

72