Chapter 12: Nervous System III: Senses Hole's Human Anatomy and Physiology
Nervous System and Special Senses 31500311€¦ · Nervous System and Special Senses 31500311...
Transcript of Nervous System and Special Senses 31500311€¦ · Nervous System and Special Senses 31500311...
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