Pneumococcus FCM Final

8/3/2019 Pneumococcus FCM Final

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PNEUMOCOCCUS

A Major Etiology of Public Health

Disease


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Definition

Pneumococcal disease is an infection causedby a type of bacteria called Streptococcuspneumoniae

Serious disease most commonly in youngchildren or elderly adults and the

immunosuppresed persons

Often preceded by respiratory viral infection


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Morphology

Nonmotile, facultatively anaerobic , gram-positive,oval to lancet shaped coccus (0.5-1.2um)

Encapsulated coccus growing in pairs (dipcocci) orshort chains

Normal flora to the nasopharynxof healthy people (carriage)


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EPIDEMIOLOGY


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Pneumococcal Types

Pneumococcal types are 6A, 6B, 14, 19F, 19A and 23 F

which causes 50%-60% of infection in infancy and earlychildhood

Types 3, 4, 6B, 9V, 14 and 23F have been the most frequentcauses of bacteremic infections among adults, accountingfor 53% of such illnesses.

Susceptibility to infection may be influenced by geneticconstitution

Types 45 and 46 have been frequent among black goldminers in South America but rare in white persons in thesame area. Also common Melanesian Populations.


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Pneumococcal Infection

Two Types:

1. Due to direct extension- Conjunctivitis, otitis media, sinusitis, acute exacerbations of chronicbronchitis (AECB), pneumonia

2. Invasive Disease

- Meningitis, bacteremia, joint and bone infections, soft tissue infections,peritonitis, cardiac infections


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Pneumococcus remains the most common causeof community acquired pneumonia

Until 2000, 100,000-135,000 patients werehospitalized for pneumonia proven to be caused by S

pneumoniae infection in the United States annually.

Incidence in developed countries is estimated to be 1

and 5/1000 persons per year. Worldwide, the most common cause of death due to

pneumococcal disease is pneumonia.


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The pneumococcus is the most common cause

of otitis media

Afflicting of children at least once in their first 6

years of life

S. pneumoniae infection is estimated to cause

over 6-7 million cases of otitis media annually.These numbers have likely decreased somewhat

with the advent of universal vaccinations


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Non Invasive Disease

S pneumoniae infection is an important cause of bacterial co-

infection in patients with influenza and can increase the

morbidity and mortality in these patients.

In post mortem studies of lung specimens from patients who

died of H1N1 influenza A, twenty-nine percent of the

specimens showed evidence of bacterial co-infection, with

almost half of being S pneumoniae.


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Invasive Disease

Statistics for 2008 estimated 43,000 (14.3 per

100,000 population) cases of invasive disease

nationally, with 4,400 (1.5 cases per 100,000

population) deaths.

Children younger than 5 years and adults

older than 65 years are two identified age

groups in whom rates of disease and death

are increased


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Invasive Disease

More than half of deaths due to invasive

pneumococcal disease occur in adults with

specific risk factors (age, immunosuppression)

for severe disease.

Such risk factors are an indication for

vaccination.


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Invasive Disease

Pneumococcal meningitis

A sequela of bacteremia or an extension of

infection from the paranasal sinuses or mastoid to

the cranial cavity

Incidence rate of approx. 1.6/100,000 persons per

year

Remains one of the three commonest forms of

bacterial meningitis


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Mortality and Morbidity

WHO estimates that, worldwide, 1.6 million

deaths were caused by pneumococcal disease

in 2005

With 700,000 to 1 million of these occurring in

children younger than 5 years.


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Meningitis

Bacteremia

Pneumonia

Otitis media

Clinicalseve

rity

Incidence

1.6 million people die of pneumococcal disease every

year

0.7 1million are children < 5 years

(most from developing countries)

World Health Organization, 2007


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Conditions interfering with normal clearanceof bacteria predisposes host to pneumococcalinfections

Chronic pulmonary disease Alcoholism

Congestive heart failure

Diabetes mellitus

Chronic kidney disease

Splenic dysfunction or splenectomy

Immunosuppresed persons


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Countries with highest pneumococcal incidence rate in children

under five years

of age, 2000

0 1000 2000 3000 4000 5000 6000 7000

Sudan

Chad

Malawi

Namibia

Kenya

Botswana

Zambia

Swaziland

Zimbabwe

Central African Republic

Lesotho

incidence rate per 100000

Data Source: WHO/IVB, July 2009


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Streptococcus pneumoniae incidence rate

per 100,000 children under five years of age, 2000

Date of slide: 03 August 2009


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Mortality rate* per 100,000 children under five years of age due to

Streptococcus pneumoniae, 2000

Date of slide: 03 August 2009

10-


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Global Streptococcus pneumoniae cases in

children under five years of age

Top 10 countries, 2000Total= 14.5 million cases, 66% in 10 countries

0 0.5 1 1.5 2 2.5 3 3.5 4

Philippines

Kenya

DR Congo

Ethiopia

Indonesia

Bangladesh

Pakistan

Nigeria

China

India

Millions

Data Source: WHO/IVB, July 2009


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PATHOPHYSIOLOGY


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Colonization and Carrier State

In the first years of life, rates of pneumococcal carriageare high

In children, pneumococcal carriage can be up to 12

distinct serotypes

Pneumococcal carriage rates decline with age

Homotypic anticapsular antibody - body reaction aftercolonization of a given pneumococcal. Reduces thelikelihood of being colonized with the same homotypicstrain.


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Pathogenesis

Colonization of the human nasopharynx may

occur on the day of birth - the type acquired

usually being that of the mother

Injury to any region of the respiratory

epithelium may disturb the relationship

between host and parasite and be followed by

clinical illness


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Pathogenesis

Pathogenesis primarily due to host response

to infection

Three Classes of Virulence Factors:

A. Colonization and migration (spreading) B. Tissue destruction

C. Phagocytic survival


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Pathogenesis

Cellular components:

Complex polysaccharide capsule: Antiphagocytic

Encapsulated (smooth) strains are virulent

Nonencapsulated (rough) strains are avirulent

Type-specific anticapsular antibodies are protective

Capsular polysaccharides are soluble (a.k.a., specific solublesubstances) and free polysaccharides can bind opsonins and

further inhibit phagocytosis


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Pneumococcal colonization: adherence to host cells (nasopharynx) andreplication

Migration (spreading)

organisms may gain access to areas of the upper and/or lowerrespiratory tracts (sinuses, bronchi, eustachian tubes) by direct

extension


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Under normal conditions in a healthy host, anatomic and ciliaryclearance mechanisms prevent clinical infection. However,

clearance may be inhibited by chronic (smoking, allergies,bronchitis) or acute (viral infection, allergies) factors, which canlead to infection

Conjunctivitis, otitis media, sinusitis, Acute exacerbations ofchronic bronchitis (AECB), pneumonia

Alternatively, pneumococci may reach normally sterile areas,such as the blood, peritoneum, cerebrospinal fluid, or joint

fluid, by hematogenous spread after mucosal invasion


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inflammatory response: S pneumoniae cell wall componentsand capsule activate the alternative complement pathway;

antibodies to the cell wall polysaccharides activate the classiccomplement pathway

In the absence of previously acquired serotype-specificantibodies, clinically apparent infection is likely to occur.

Meningitis, bacteremia, joint and bone infections, soft tissueinfections, peritonitis, cardiac infections


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Immune response

Naturally acquired immunity: Type-specific

anticapsular immunity

Artificially acquired immunity: Immunization

via polyvalent vaccine prophylaxis


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CLINICAL MANIFESTATIONS


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Non-Invasive

Conjunctivitis - bilateral and purulent

Otitis Media - usually accompanied by fever and pain

Sinusitis - preceded by a viral infection followed by the

development of a purulent discharge and cough

Acute exacerbations of chronic bronchitis - shortness ofbreath, increased production and/or purulence of sputum,

increased sputum tenacity, cough

Pneumonia - may be preceded by a viral illness that is

followed by an acute onset of high fever

often withrigors, cough productive of rust-colored sputum, pleuritic

pain, exertional dyspnea, tachypnea, tachycardia, sweats,

malaise, and fatigue


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Invasive

Bacteremia- most common manifestation of invasivepneumococcal disease; most cases resolve spontaneously

Meningitis nonspecific and nuerologic signs andsymptoms

Joint and bone infections Septic arthritis (4%) ankles and knees

Osteomyelitis (20%) femur and humerus (children),vertebra (adult)

Soft tissue infections - uncommon Peritonitis - abdominal pain, anorexia, emesis, diarrhea

Cardiac infections - rare; endocarditis, pericarditis


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DIAGNOSIS


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Diagnosis

Two points to remember:

1. Treatment can be started without

determining the microbiologic agent in

uncomplicated, nonsevere, community-

acquired pneumonia

2. Efforts to identify the agent are important

when the disease are more severe and when

the dia nosis of neumonia is not clearl


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Diagnosis

Essentials of Diagnosis

Productive cough, fever, rigors, dyspnea, early

pleuritic chest pain

Consolidating lobar pneumonia on chestradiograph

Gram-positive diplococci on Gram stain of


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Diagnosis

Diagnosis requires isolation of the organism in

culture, although the Gram stain appearance

of sputum can be suggestive

Sputum and blood cultures can be used. It is

positive in 60% and 25% of cases

A good-quality sputum sample shows gram-

positive diplococci

A rapid urinary antigen test for S. pneumoniae,

can assist with early diagnosis in adults


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Diagnosis

Nonspecific findings:

Elevated PMN count >15,000/L

Leukopenia in 10% of cases a poor

prognostic sign

Elevated values in liver function tests

Anemia, low serum albumin levels,hyponatremia, and elevated serum cratinine

levels in 20-30% of patients


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Treatment

Initial antimicrobial therapy for pneumonia is

empiric

Uncomplicated pneumococcal pneumonia

caused by penicillin-susceptible strains of

pneumococcus may be treated on an

outpatient basis with amoxicillin, 750 mg

orally twice daily for 710 days


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TREATMENT


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Treatment

Initial antimicrobial therapy for pneumonia is

empiric

Uncomplicated pneumococcal pneumonia

caused by penicillin-susceptible strains of

pneumococcus may be treated on an

outpatient basis with amoxicillin, 750 mg

orally twice daily for 710 days


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Treatment

For penicillin-allergic patients, alternatives are

azithromycin, clarithromycin, doxycycline,

levofloxacin and moxifloxacin

Monitor for clinical response (eg, less cough,

defervescence within 23 days) because

pneumococci have become increasinglyresistant to penicillin and the second-line

agents.


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Treatment

For hospitalized patients:

Parenteral therapy is generally recommended

at least until there has been clinical

improvement. Aqueous penicillin G, 2 million

units intravenously every 4 hours, or

ceftriaxone, 1 g intravenously every 24 hours,

is effective for strains that are not highlypenicillin-resistant The total duration of

therapy is not well defined, but 1014 days is

standard.


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Prevention

Pneumococcal polysacharride vaccine

PPV contains 25 g of capsular polysaccharide

from 23 pneumococcal serotypes that cause

invasive disease

The vaccine is cost effective among individuals

over the age of 65 years for prevention of

bacteremia.


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Prevention

Target Groups for PPV

all immunocompetent individuals age 65 or

greater

Younger patients that put them at high risk for

invasive pneumococcal disease


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Prevention

Clinical Risk Groups

1. Asplenia or splenic dysfunction

2. Chronic respiratory disease

3. Chronic heart disease

4. Chronic kidney disease

5. Chronic liver disease6. Diabetes mellitus

7. Others - cerebrospinal fluid leaks, individuals

in long-term care facilities, alcoholism,


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Prevention

The efficacy of pneumococcal vaccine in

immunosuppressed patients is less certain

Present recommendations include vaccination

of individuals with human immunodeficiency

virus (HIV) infection, leukemia, lymphoma,

Hodgkin's disease, multiple myeloma, organtransplantation, or chronic use of

glucocorticoids


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Prevention

Pneumococcal vaccine can be given

simultaneously with other vaccines but should

be administered at a separate site

A single revaccination is appropriate for

individuals over the age of 65 who received

initial vaccination more than 5 years earlier

Revaccination is also recommended forimmunocompromised patients and individuals

with functional or anatomic asplenia.


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Prevention

Pneumococcal Conjugate Vaccine (PCV)

a 7-valent protein-conjugated polysaccharide

vaccine

Valency indicates the number of serotypes

included in the vaccine

Efficacy estimate is 93% against invasive

disease caused by serotypes in the vaccine


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Prevention

Preparations

Prevnar a 7-valent pneumococcal conjugate

Pneumovax a 23-valent polysaccharide

vaccine for persons 2 years and older

Dosages and Schedule of Administration PCV-7 is given as a 0.5-mL IM dose

A total of 4 doses - given at 6, 10, 14 weeks

and 12-15 months


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Efficacy of an 11-valent pneumococcal

conjugate vaccine against radiologically

confirmed pneumonia among children less

than 2 years of age in the Philippines: arandomized, double-blind, placebo-

controlled trial.

RESULT: 22.9% reduction of community-acquired radiologically confirmed pneumonia

in children younger than 2 years of age in the

11-valent tetanus-diphtheria toxoid-


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Prevention

Considerations

High-risk children older than 23 months shouldreceive both PCV-7 and PPV-23

When both are indicated, they should not be givensimultaneously, give 6-8 weeks apart

If splenectomy or immunosuppression can beanticipated, vaccination should be done at least 2

weeks beforehand Contraindicated to those with severe allergic reaction

after a previous dose


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Prevention

Other Prevention Strategies

Prevention of illnesses that predispose

individuals to pneumococcal infections

Influenza vaccination

Improve management and control of diabetes,

HIV infection, heart disease, and lung disease

Smoking cessation

Reduction of antibiotic misuse


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THANK YOU

Pneumococcus FCM Final

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