Childhood Immunization Essay Sample

Childhood Immunization Pages
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The work group for the development of these guidelines comprised paediatricians and a pharmacist from various Ministry of Health facilities. These guidelines are based on the findings of health technology assessment on the same topic, as well as a systematic review of current medical literature, taking into consideration local medical practice and local microbiology patterns and trends of antimicrobial resistance. The ranking of evidence is based on a modified version of that suggested by the Catalonia Agency for Health Technology Assessment and Research (CAHTAR) Spain, while the grading of recommendations in these guidelines emulates those used by the Scottish Intercollegiate Guidelines Network (SIGN).

The draft guidelines were posted on both the Ministry of Health Malaysia and Academy of Medicine, Malaysia websites for comment and feedback. The ranking of evidence is based on a modified version of that suggested by the Catalonia Agency for Health Technology Assessment and Research (CAHTAR) Spain, while the grading of recommendations in these guidelines emulates those used by the Scottish Intercollegiate Guidelines Network (SIGN). These guidelines have also been presented to the Technical Advisory Committee for Clinical Practice Guidelines and Health Technology Assessment and Clinical Practice Guidelines Council, Ministry of Health Malaysia for review and approval

Objective
The aim of this guideline is to aid health care providers doctors in general practice and pediatricians, in clinical decision making by providing well-balanced evidence based information on The main aim of these guidelines is to assist health care providers in clinical decision making by providing well-balanced information on childhood immunisation. It also hoped to decrease the incidence of complications.

Target Population
Thisis guideline is developed to apply to all children.

Target Group
Thiese guidelines isare meant for all health care providers. LEVEL OF EVIDENCE SCALE

| | | | |Level |Strength of evidence |Study design | | |Good |Meta-analysis of RCT, Systematic review | | |Good |Large sample RCT | | |Good to Fair |Small sample RCT | | | |Non-randomised controlled prospective trial | | |Fair |Non-randomised controlled prospective trial with historical control | | |Fair |Cohort studies | | |Poor |Case-control studies | | |Poor |Non-controlled clinical series, descriptive studies multi-centre | | |Poor |Expert committees, consensus, case reports, anecdotes |

(Adapted from Catalonian Agency for Health Technology Assessment & Research, [CAHTAR] Spain) Source Adapted From Catalonian Agency for Health Technology Assessment (CAHTA), Spain

GRADE OF RECOMMENDATIONS

| |At least one meta analysis, systematic review, or RCT, or evidence rated as good and directly applicable to the target | |A |population | | |Evidence from well conducted clinical trials, directly applicable to the target population, and demonstrating overall | |B |consistency of results; or evidence extrapolated from meta analysis, systematic review, or RCT | | |Evidence from expert committee reports, or opinions and /or clinical experiences of respected authorities; indicates | |C |absence of directly applicable clinical studies of good quality |

(Adapted from Scottish Intercollegiate Guidelines Network [SIGN])Sources: adapted from Scottish Intercollegiate Guidelines Network [SIGN]

GUIDELINES COMMITTEE
Dr Tan Kah Kee
Head & Consultant Paediatrician
Department of Paediatrics
Seremban Hospital

Dr Wong Swee Lan
Consultant Paediatrician
Department of Paediatrics
Seremban Hospital

Dr Kuan Geok Lan
Head & Consultant Paediatrician
Department of Paediatrics
Malacca Hospital

Dr Zainah Shaik Hedra
Consultant Paediatrician
Department of Paediatrics
Malacca Hospital

Dato’ Dr Jimmy Lee Kok Foo
Head & Consultant Paediatrician
Department of Paediatrics
Kuala Terengganu Hospital

Dr Hung Liang Choo
Consultant Paediatrician
Institute of Paediatrics
Kuala Lumpur Hospital

Dr Noor Khatijah Nurani
Consultant Paediatrician
Department of Paediatrics
Ipoh Hospital

Dr Lim Chiam Boon
Consultant Paediatrician
Department of Paediatrics
Seremban Hospital

Dr Nazatul Shima
Family Health Development Division
Ministry of Health Malaysia

Guidelines Coordinator
Ms Sin Lian Thye
Nursing Sister
Health Technology Assessment Unit
Ministry of Health Malaysia

Reviewed and edited by
Dr S Sivalal
Head, of Health Technology Assessment Unit, &

Deputy Director,
Medical Development Division
Ministry of Health Malaysia

CHILHOOD IMMUNISATION

Immunisation is an attempt to replace the anticipated natural primary contact between the human body and a hostile organism, with a safer artificial contact, so that any subsequent natural contact takes place in a state of heightened immunity. While advances in public health and medicine have reduced the morbidity and mortality rates accompanying certain infectious diseases, immunisation represents the single -most mass approach to prevention (Zimmerman, 1987)

The World Health Organisation (WHO) Expanded Programme on Immunisation (EPI) recommends that all countries immunise against poliomyelitis, diphtheria, pertussis, tetanus, measles, and tuberculosis (TB) infection in countries with a high incidence. In addition, Hepatitis B vaccine was expected to be integrated into the national immunisation programmes in all countries by 1997 (Ministry of Health Malaysia, 2002, level 1level 1)

Table 1: shows the EPI schedule

|Age |Vaccine |Hepatitis B Vaccine** | | | |Scheme A |Scheme B | |Birth |BCG, OPV 0 |HB1 |
| |6 weeks |DPT 1 OPV 1 |HB 2 |HB 1 | |10 weeks |DPT 2, OPV 2 | |HB 2 | |14 weeks |DPT 3, OPV 3 |HB 3 |HB 3 | |9 months |Measles, Yellow fever* | | |

* In countries where yellow fever poses a risk
** Scheme A is recommended forin countries where perinatal transmission of hepatitis B virus is frequent (e.g. South Asia), while scheme B is formay be used in thosecountries with less frequent here perinatal transmission is less frequent (e.g. Sub- Saharan Africa)

It has generally been accepted that no immunisation schedule is ideal, and thus the EPI recommends that each country determine its own schedule that best suits its needs. TheA strategic guiding principle of any immunisation programme is that protection must be achieved before infants are at high risk of a disease. In most developing countries, diseases included within the EPI strike early in life, and thus it is important to protect children through immunisation as early as possible. Apart from this, any immunisation schedule represents some degree of compromise. In addition, while acknowledging that seroconversion is age-dependent, the emphasis should be on obtaining protection in the infant at as young an age as possible (Ministry of Health Malaysia, 2002, level 1level 1).

The immunisation programme in Malaysia commenced about 40 years ago with the DPT vaccine. This was followed by the BCG vaccine in 1961 and the OPV vaccine in 1972. Measles immunisation was added to the programme in 1984, with immunisation against rubella being introduced in 1988 and against hepatitis B in 1989 (Pathmanathan, 1990). The immunisation coverage for Malaysia for 2000 was 99.97% for BCG, 95.3% for DPT (third dose), 95.4% for OPV (third dose), 88.4% for measles and 93.5% for hepatitis B (third dose) in 2000 (Ministry of Health Malaysia, 2002, level 1level 1). The new recommended immunisation schedule is as illustrated in Table 2 below:

Table 2: shows the Nnew immunization immunisation schedule.

|Immunisation |Age (months) |Age (years) | | |0 |1 |2 | |BCG |No |No (Yes) |Yes | |Hep B |Yes |Yes |Yes | |DPT |Yes |Yes |Yes | |OPV |No |Yes [IPV (killed vaccine)] |Yes (IPV) | |Hib |Yes (3 + Booster dose) |Yes (3 + Booster dose) |Yes (3 + Booster dose) | |Measles |No |Yes (Asymptomatic) |Yes | |MMR |No |Yes (Asymptomatic) |Yes |

BCG VACCINE
1.INTRODUCTION

The bacillus Mycobacterium tuberculosis causes tuberculosis. In Malaysia, the incidence of tuberculosis was 63.6 per 100,000 population in 1997, and has increasingbeen increasing steadily since 1995. The most important source of human infection is an already infected person who spreads the highly infectious bacilli throughvia respiratory droplets. Primary infections occur at any age, most often in children, and may be asymptomatic, and resolve spontaneously. However, it may also spread and cause disease in various organs including lungs, meninges, bones and bloodstream (Ministry of Health Malaysia, 2002, Level 1Level 1).

The Bacille Calmette-Guerin (BCG) vaccine is a live attenuated strain of Mycobacterium bovis, containing no adjuvant or preservative except monosodium glutamate or albumin as the stabilizer. The diluent is either saline solution or distilled water. WHO It is recommends that it be ed by WHO for administeredration at birth, and it is currently used in more than 100 countries (WHO, 2000, level 1).

2.ADVERSE EFFECTS

Following intra-dermal injection, local reaction is normal, and a papule will be forminged within 2-3 weeks, with ulceration at 6-8 weeks, followed by a scar at the end of 3 months. The adverse events are predominantly related to infection by the live attenuated bacteria, as well as being due to errors in achieving intra-dermal inoculation. They can be classified as mild and severe events and are elaborated on below.

2.1Mild Adverse Events
The most common adverse effect of subcutaneous injection is a local abscess. While the more extensive and prolonged local reactions can occur, secondary infections at the site of injections are unlikely. Sometimes, axillary or cervical lymphadenitis may develop. However, in most cases it heals spontaneously, and no treatment is required. In extreme cases, systemic treatment with erythromycin for up to one month may be helpful. In cases with adherent or fistulated lymphadenitis, drainage may be carried out and anti-tuberculous drugs instilled locally, although systemic anti-tuberculous drugs are ineffective.

2.2Severe Adverse Events
Systemic infection by BCG is a recognized but rare consequence of vaccination, and only seen in children with severe immune deficiencies such as Severe Combined Immune Deficiency, Chronic Granulomatous disease or Di George syndrome. Other rare adverse events include BCG osteitis and osteomyelitis (WHO, 1993; 1999; 2000, Level 1level 1).

3.VACCINE EFFICACY

A meta-analysis found that BCG vaccine has high protective efficacy (approximately 80%) against meningeal and miliary tuberculosis in children. However, the protective efficacy against pulmonary disease is variable, ranging from 0% to 80%, with a lower degree of protection in tropical than in temperate regions (American Academy of Pediatrics, 2000; WHO, 1999, level 1).

4.STORAGE AND ADMINISTRATION

BCG vaccine should be stored and transported at 2oC to 8oC. The diluents should not be frozen but kept cool. The vaccine must be kept refrigerated, and once the diluent has been added, used within 4 hours, once the diluent has been added, and kept away from light (Academy of Medicine of Malaysia, 2001). Administration of BCG vaccine is through intra-dermal injection with a 25 or 26 gauge needle at the deltoid region of the upper arm, which will minimize post vaccination lymphadenopathy. Other less satisfactory techniques are percutaneous injections and use of jet injectors or bifurcated needles. [Grade C]

5.IMMUNISATION SCHEDULE

BCG is currently recommended at birth, or at first contact with health services. There is little scientific evidence on the efficacy of booster doses for BCG (WHO, 1993; 1999, level 1level 1) [Grade A].

6.SPECIAL SITUATIONS

6.1Premature and Low Birth Weight Babies
Infants less than 33 weeks are less likely to develop BCG scar and a reactive PPD tuberculin test after BCG vaccination. , and thus Ppremature babies thus need not be given BCG vaccine until discharge, when they are at least 34 weeks, and with body weight more than 1800 g to 2000 g (Sedaghatian et al, 1998, level 8) [Grade C].

6.2Babies born to HIV positive mothers
BCG should not be administeredgiven to children with symptomatic HIV infection (i.e. AIDS). However, for babies born to HIV positive mothers, since the HIV status of these babies cannot be determined at birth, as none are likely to have symptoms of HIV infection, WHO recommends that they babies born to HIV positive mothers should be administered given BCG vaccine, especially in areas where the risk of tuberculosis is high. (WHO, 1993; 1999, level 1level 1) [Grade A] DIPHTHERIA, TETANUS AND PERTUSSIS

1.INTRODUCTION

1.1Diphtheria
Diphtheria is an acute infectious disease affecting the upper respiratory tract and occasionally the skin, vagina and conjunctiva. The clinical manifestations result from the action of an exotoxin produced by Corynebacterium diphtheria (Ministry of Health Malaysia, 2002 Level 1). Diphtheria is acquired through personal contact, the incubation period being generally 2 to 5 days (Ministry of Health Malaysia, 2002). ItDiphtheria is a notifiable disease in Malaysia. There is a diminishing trend in incidence from 0.11 per 10 000 population in 1988 to 0.02 in 1998 (Ministry of Health Malaysia, 2002, level 1level 1).

Diphtheria toxoid is produced by growing C. diphtheria in a liquid medium, incubating the filtrate with formaldehyde to convert the toxin to toxoid, which is further purified and concentrated to achieve the necessary dosage. It is usually absorbed on to an adjuvant, either aluminium phosphate or aluminum hydroxide to increase the immunogenicity (Ministry of Health Malaysia, 2002, level 1level 1; Academy of Medicine of Malaysia, 2001, level 8).

1.2Tetanus
Tetanus is an acute disease caused by a highly potent neurotoxin (Tetanospasmin) produced by Clostridium tetani, which acts at the myoneural junction of skeletal muscle, and on neuronal membranes in the spinal cord, blocking inhibitory impulses to motor neurons. The disease is characterised by muscular rigidity with superimposed agonising contractions. The bacillus grows anaerobically at the site of wounds. Tetanus spores are present in the soil and may be introduced into the body during injury through puncture wounds, burns or trivial wounds. It is not spread from person to person, and the incubation period may vary from 2 days to 2 months, averaging about 10 days, although most cases occur within 14 days. Shorter incubation periods are said be associated with more heavily contaminated wounds, more severe disease and a worse prognosis. Death results from respiratory failure, hypotension, or cardiac arrhythmias (Ministry of Health Malaysia, 2002, level 1level 1; American Academy of Pediatrics, 2000, level 1level 1; Department of Health, United Kingdom, 1996, level 1level 1; National Health & Medical Research Council, Australia, 1997, level 1level 1).

Tetanus is a notifiable disease in Malaysia, with the reported incidence showing a general diminishing trend from 0.08 per 100 000 population in 1988 to 0.06 in 1998 (Ministry of Health Malaysia, 1999).

Tetanus vaccine is a toxoid extracted from the toxin through culture of C tetani. The cell free product is detoxified after treatment with formaldehyde, and usually adsorbed on to an adjuvant (either aluminium phosphate or aluminium hydroxide) to increase its immunogenicity (Ministry of Health Malaysia, 2002, Level 1level 1; Academy of Medicine of Malaysia, 2001, level 8).

1.3Pertussis
Pertussis or ‘whooping cough’ is a highly contagious disease caused by Bordetella pertussis, an aerobic, gram-negative coccobacillus that invades the epithelium of the naso-pharynx, bronchi and bronchioles. Human transmission is through aerosol droplets. The asymptomatic incubation period is 7 to 10 days (ranging from 6 to 20 days), followed by the catarrhal stage of 2 to 7 days, and finally the paroxysmal cough stage lasting 1 to 8 weeks. A definitive diagnosis based on culture of the organism is difficult to establish. A mild whooping cough syndrome can also be caused by other organisms, like Bordetella parapertussis and bronchiseptica, Mycoplasma pneumoniae, Chlamydia trachomatis and pneumoniae, and adenoviruses (Ministry of Health Malaysia, 2002 level 1; American Academy of Pediatrics, 2000, Level 1level 1).

Pertussis causes significant morbidity especially in those aged 3 months to 6 years old. Mortality may be due to secondary bacterial pneumonia, hypoxia, encephalopathy or cerebral haemorrhage. Accurate figures on prevalence of pertussis in Malaysia are not available since it However, the number of pertussis cases in Malaysia may be under-reported (Ministry of Health Malaysia, 2002, Level 1level 1).

For many years, the incidence of pertussis was controlled using combination vaccines containing whole-cell pertussis. However, concern about possible central nervous system adverse effects from this vaccine resulted in a drop in vaccination uptake and subsequent resurgence of the disease in many countries in the 1980’s and 1990’s. Consequently, many developed countries are currently using the acellular pertussis vaccine in their immunisation programme.

1.4DTP Vaccine
CThere are two types of combination vaccines of available with diphtheria, tetanus, and pertussis toxoids are of two types – whole cell (DTP) and cellular vaccine (DTaP). DTP is the most widely used vaccine against pertussis. It consists of a suspension of whole-inactivated Bordetella pertussis bacteria combined with diphtheria and tetanus toxoids adsorbed on to an aluminium salt (Ministry of Health Malaysia, 2002, Level 1). DTaP contains one or more antigens derived from Bordetella pertussis with and contains minimal or no endotoxin. The antigens include detoxified pertussis toxoid, filamentous hemagglutinin, agglutinogens and pertactin (Ministry of Health Malaysia HTA, 2002, Level 1level 1).

2. ADVERSE EFFECTS OF VACCINES

There has been much public concern on the adverse reactions to whole cell pertussis DTP vaccines, primarily focused on the whole cell pertussis component of the vaccine. The side effects includes local, systemic, and anaphylaxis reactions. The frequent local reactions were are erythema and induration with or without tenderness (Cody, 1981, level 4). A nodule may occasionally be present at the injection site for several weeks, while sterile abscesses have been reported to occur 6 to 10 times per one million doses of DTP (MMWR, 1991, Level 1level 1).

2.1Systemic Reactions
Mild systemic reactions like fever, drowsiness, fretfulness, anorexia occurs frequently (Cody 1981 level 4). Fever usually occurs 24 hours or later after vaccination. H; however, if the fever persists for more than 24 hours, it should not be assumed to be due to DTP vaccination (MMWR, 1991, Level 1level 1; MMWR, 1996; Level 1level 1).

Moderate–to-severe systemic events occur infrequently and appear to be without sequelae. These include high fever (i.e. temperature greater than 40.5 (C), within 48 hours, unexplained by another cause; persistent, inconsolable crying lasting for 3 hours or more, within 48 hours of immunisation; collapse or shock-like episodes (hypotonic-hyporesponsive episode) within 48 hours – occurring in 1 case to 1,750 doses administered (Cody, 1981, level 4). or short-lived convulsions (usually febrile) occurring within 3 days (Ministry of Health Malaysia, 2002, Level 1level 1; American Academy of Pediatrics, 2000, Level 1level 1 ).

There is consistent evidence of correlation a possible causal relation between DTP vaccine and acute encephalopathy, although it has been insufficient to establish causality (Baraff, 1988, level 8; Miller, 1993, level 8; Cowan, 1993, level 8). Similarly, as well as a causal relationship between DTP vaccine and permanent neurological damage has not been established (Cowan, 1993, Level 1level 1).

Immediate anaphylactic reactions such as breathlessness, hypotension and shock have been were rarely reported after DTP vaccine, and there has been no death reported since the inception of vaccine-adverse-event reporting to CDC infrom 1978 (MMWR, 1991, Level 1level 1). Severe reactions to vaccines containing diphtheria or tetanus antigens (DT) are extremely rare. An immediate anaphylactic reaction to tetanus and diphtheria toxoid containing vaccine (ie DtaP, DT or DT) is a contraindication to further doses unless the patient can be desensitised to these toxoids, due to uncertainty as to which vaccine component (diphtheria, pertussis or tetanus) mayight be responsible and the importance of tetanus immunisation. Persons who experience anaphylactic reactions may be referred to an allergist for evaluation and possible desensitization (Ministry of Health Malaysia, 2002, Level 1level 1; American Academy of Pediatrics, 2000, Level 1level 1).

Overuse of tetanus toxoid can result in polyneuropathy with an estimated incidence of 0.4 per million doses of tetanus toxoid (Ministry of Health Malaysia, 2002, Level 1level 1).

Despite some case reports, no increased risk of Guillain Barre Syndrome has been observed with the use of tetanus toxoid in whole cell or acellular pertussis vaccines (National Health & Medical Research Council, Australia, 1997, Level 1level 1). Hence, no special precautions are needed when immunising children with a history of Guillain Barre Syndrome (Ministry of Health Malaysia, 2002 Level 1level 1).

3. VACCINE EFFICACY

3.1Diphtheria Vaccine
The most important factor of an age host response to immunity with diphtheria toxoid is the modifying effect of passively acquired maternal antibodies in young infants. This passive diphtheria antibodies seem to show a transient antibody response suppression to the second injection (not first dose) of DPT vaccine, although, there has been is no response to the third injection of DPT vaccine (Ministry of Health Malaysia, 2002, Level 1level 1).

Primary immunisation with 3 doses of DTP vaccine stimulates the production of diphtheria antibody level in considerable excess of the minimum protective level (0.01 IU/ml). However, while natural immunity is life long, the duration of immunity after a primary immunisation series is variable. Studies on this issue have showed differing results, with duration of immunity ranging from 3-10 years (Ministry of Health, 2002, Level 1). This could be due to differences in vaccines, vaccination schedules and levels of community exposure to Corynebacterium diphtheria (presence of natural boosting). In contrast, a booster dose at 2 years or at school entry (4-6 years) stimulatesd abundant production of diphtheria antitoxin with mean levels above 0.1 IU/ml (Ministry of Health, 2002, Level 1). There is no defined level of antitoxin but it iswas believed that 0.01 IU/ml dose of Diphtheria is enough for clinical immunity against the disease, while for protection, a dose of 0.1 IU/ml may be needed for protection (Ministry of Health Malaysia, 2002, Level 1level 1).

The effectiveness of 3 or more doses ranged from 97 to 99.9% (Bisgard et al., 2000, level 9; Chen et al., 2000, level 9). Schoolchildren who received booster doses experienced protection against respiratory diphtheria (Bisgard et al., 2000, level 9). In Russia, it was also found that the booster doses given at 6-8 years providedshowed improved protection (Vitek et al., 1999, level 7). Thus, it iswas recommended that Diphtheria to be given as 3 primary doses with and a booster given a year after the primary doses, as well as another at 6-8 years of age.

3.2Tetanus Toxoids Vaccine
Tetanus toxoid has an efficacy of more than 95% (Ministry of Health Malaysia, 2002, Level 1) . Effective protection is provided by active immunisation, with complete primary immunisation (3 doses) conferring protection for at least 5 years. Immunity will last for at least 10 years after the 4th dose, and 20 years after the 5th dose (Ministry of Health Malaysia, 2002, Level 1level 1).

A tetanus antitoxin level of 0.01 IU/ml serum is considered as the minimum protective level (Chen, 1976, Level 1level 1). Case reports have showned that for patients with antitoxin level more than 0.01 IU/ml, the severity of tetanus was inversely proportional to the antitoxin level.

3.3Pertussis Vaccine
The effectiveness of a 3-dose whole-cell pertussis vaccination was between 71 to 90% depending on the case definition used. (De Serres, 1996, level 8; Gures, 1997, level 8). AThree or more component acellular DTP with more than three component pertussis vaccines was found to be less efficacious than those with 2 or 3 whole-cell vaccines pertussis vaccines. (Tinnion, 2000, Level 1level 1) Most studies measure pertussis antitoxin (FHA antibodies) and levels above 0.01 IU/ml are considered to be a response to the vaccine, affording a minimum protective level. (Ministry of Health Malaysia, 2002, Level 1level 1).

4. STORAGE , DOSAGE AND ADMINISTRATION

4.1Diphtheria Vaccine
Diphtheria vaccines should be stored at 2 (C to 8 (C. If the vaccine had been frozen, it should not be used (Ministry of Health Malaysia, 2002 Level 1level 1, Academy of Medicine of Malaysia, 2001, level 9). The recommended dose is 0.5 ml given intramuscularly (Ministry of Malaysia, 2002, Level 1level 1) [Grade A]

4.2Tetanus Toxoid
Tetanus toxoid is stable and able to withstand room temperature for months (WHO, 1995 Level 1level 1). However, tetanus vaccine if part of DPT should be stored at 2-8 (C, and should not be frozen or exposed to light (Ministry of Health Malaysia, 2002, Level 1level 1; National Health & Medical Research Council, Australia, 1997, Level 1level 1; Department of Health, United Kingdom, 1996, Level 1level 1). The dose is 0.5 ml given intramuscularly. For primary immunisation, tetanus vaccines should not be given as a monocomponent vaccine, but combined with diphtheria (DT) and or pertussis (DPT) (Ministry of Health Malaysia, 2002, Level 1level 1; National Health & Medical Research Council, Australia, 1997, Level 1level 1) [Grade A]

4.3Pertussis Vaccine
Pertussis vaccines should be stored at 2-8 (C and should not be frozen (Ministry of Health Malaysia, 2002, Level 1level 1; National Health & Medical Research Council, Australia, 1997, Level 1level 1; Department of Health, United Kingdom, 1996, Level 1level 1). The dose is 0.5 ml given intramuscularly at a 90˚angle to the skin (ACIP, 2002). The recommended sites of injection isare the anterolateral aspect of the thigh for infants, while for and for toddlers up to 4 years of age, the deltoid muscle is the recommended site (ACIP, 2002) ) [Grade A]

5ACCELERATED DTP IMMUNISATION SCHEDULE

The first dose of DTP at 3 months of age has been said to be too late to protect infants against pertussis (National Health & Medical Research Council, Australia, 1997, Level 1level 1; Bart, 1990, Level 1level 1). It has been shown that the first dose of DTP can be lowered to 6 weeks of age without compromising imunogenicity, for both the whole cell and acellular pertussis DTP vaccines (WHO, 1995, Level 1level 1; Bart, 1990, Level 1level 1; Ramsay, 1993, level 9; Edwards, 1995, Level 1level 1; Gustafsson, 1996, Level 1level 1). Booster doses of DTP at 12-24 months and at 4-6 years are recommended to maintain immunity against pertussis and diphtheria, where the national incidence has been successfully reduced (WHO, 1995 level 1level 1; Bart, 1990, level 1level 1; Frenkel, 1990, level 9; MMWR, 1991, Level 1level 1) ) [Grade A] POLIOVIRUS VACCINE

1. INTRODUCTION

Poliomyelitis is an acute viral infection ranging in severity from a non-specific illness to paralysis with permanent disability. A, with about 90-95% of poliovirus infection isbeing asymptomatic, whileand non- specific illness with low grade fever and sore throat occurroccurssing in 4-8% of infections. Aseptic meningitis with parasthesia occurs in 1-5% of patients a few days after the minor illness has resolved. Rapid onset of asymmetric acute flaccid paralysis with areflexia involving limbs occurs in 0.1% – 2% of infections, and residual paralytic disease involving the motor neurons (paralytic poliomyelitis) occurs in approximately 1 in 250 infections. Cranial nerve involvement and paralysis of respiratory muscles may also occur. Findings of mild pleocytosis and lymphocytic predominance in the cerebrospinal fluid (CSF) are characteristic of viral meningitis.

Adults who contracted paralytic poliomyelitis in childhood may develop the post-polio syndrome 30-40 years later, characterised by muscle pain, exacerbation of weakness, and/or new paralysis or weakness. This secondary illness resembling motor neuron disease, after an apparent silent period, is sometimes known as late post poliomyelitis muscular atrophy. Risk factors that may affect the potential for infection with poliovirus or the severity of clinical poliomyelitis include immune deficiency, injections, malnutrition, physical activity, pregnancy and tonsillectomy.

Four types of poliovirus vaccines are currently available – inactivated polio vaccine (IPV) of Salk, oral polio vaccine (OPV) of Sabin, enhanced-potency inactivated vaccine of Van Wezel (elPV) and combinations with other vaccines like DTP-IPV. The vaccines are trivalent containing a mixture of the 3 strains of poliovirus.

2.ADVERSE EFFECTS

There have been many reports of Vaccine Associated Paralytic Poliomyelitis (VAPP) due to OPV, with an epidemiological study estimating the risk to be 1.3 cases per million vaccines. IPV does not cause VAPP and is currently recommended to prevent VAPP in a sequential regime. However, other studies have reported the adverse events due to IPV like local reaction at injection site (43%), neurological disorders (12%), hypertension (10%) and allergic reactions (10%). Other rare but serious side effects like persistent crying, febrile seizures, apyretic seizures, uneasiness and shock have been reported (Ministry of Health Malaysia, 2002, Level 1level 1).

3. VACCINE EFFICACY

There is good evidence that OPV is efficacious. Children with diarrhoea receiving OPV should be re-immunised once the disease has resolved since it has been found that diarrhoea is a major factor in vaccine failure. The seroconversion rate for all types of poliovirus was found to be higher if an extra dose was given at birth in countries where poliomyelitis is still a problem. OPV is also found effective when given to preterm babies at 34-35 weeks of gestation (Ministry of Health Malaysia, 2002, Level 1level 1).

IPV was found to be as efficacious as OPV. It was also found that seroresponses to IPV were excellent and unaffected when combined with other vaccines in the same syringe. However, one study found that the immune response to pertussis was affected by combining DTP and IPV (Ministry of Health Malaysia, 2002, Level 1level 1).

Vaccines combining IPV with DTP are available. In addition, IPV or OPV can be given concurrently with many other vaccines like DTP, Hepatitis B, Hib, measles or MMR, and Varicella.

4. STORAGE, DOSAGE AND ROUTE OF ADMINISTRATION

The cold chain of polio vaccine should be maintained, and both OPV and IPV vaccines should be stored in the refrigerator at 4-10(C. OPV should be stored below< 0(C. After thawing, it may be stored between 2-8 ˚(C. IPV should be stored at 2-8( C.

The route of administration of OPV is by oral drops, while IPV is intramuscular, on the anterolateral aspect of the thigh or arm, or subcutaneously. Tetracoq (DPT-IPV) is administered intramuscularly as DTP vaccine is an adjuvant. ) [Grade A]

5.IMMUNISATION SCHEDULE

WHO recommendsed that 4 doses of OPV be given by 14 weeks of age, with a dose at birth in countries where poliomyelitis is still a problem.? A It is emphasized that 2- months interval is desirable between the first 2 doses to avoid interference with replication, ; the minimum interval in most circumstances beingis 6 weeks. The 3rd dose is recommended when the child is 6 – 18 months to complete the primary series, and a supplementary dose given before entering school i.e. at 4 – 6 years of age. For children not immunised in the first year of life, 2 doses of OPV should be given approximately 6 -8 weeks apart, followed by a third dose 2 -12 months later. ) [Grade A]

For children immunised with IPV only, the primary series consists of 3 doses. The first 2 doses should be given at 1-2 month (4-8 weeks) intervals beginning at 2 months of age (minimum age 6 weeks) and a 3rd dose is recommended 6-12 months after the second dose. A supplemental dose of IPV should be given before the child enters school i.e. 4 – 6 years of age. ) [Grade A].

6.SPECIAL SITUATIONS

IPV is recommended infor special cases like immuno-compromised patients such as HIV-infected and their household contacts, since OPV is contraindicated (Ministry of Health Malaysia, 2002, Level 1level 1) [Grade A] HEPATITIS B VACCINE

1.Introduction

Hepatitis B (HB) is a major chronic viral illness worldwide with long-term complications of cirrhosis and hepatocellular carcinoma resulting in high mortality and morbidity. As the treatment is far from satisfactory, the best strategy is prevention. These include active immunizationimmunisation with HB vaccine, avoidance of at-risk behaviour and possible sources of transmission, and strict adherence to universal precautions and good infection control procedures (Ministry of Health Malaysia, 2002 Level 1level 1).

Infants who become infected by perinatal transmission have a 90% risk of chronic infection and a 25% risk of dying of liver cancer. Furthermore, children younger than 5 years of age living with a person with hepatitis B infection can become infected via horizontal transmission and also have a higher likelihood of chronic infection and subsequent cirrhosis or cancer in early adulthood. In Malaysia, the incidence of HB has declined from 9.38 per 100 000 population in 1988 to 2.97 per 100 000 population in 1996. However, there are still about 1 million hepatitis B carriers in this country or about 5% of the population (Ministry of Health Malaysia, 2002, Level 1level 1).

HB immunizationimmunisation provides adequate protection in the majority of recipients and prevents both vertical and horizontal transmission. The hepatitis B vaccine contains inactivated hepatitis B virus surface antigen (HbsAg) adsorbed onto aluminium hydroxide adjuvant. Several highly effective and safe hepatitis B vaccines produced by recombinant DNA technology are available. The original plasma-derived vaccine is no longer recommended (Ministry of Health Malaysia, 2002, Level 1level 1).

ADVERSE EFFECTS

Hepatitis B vaccine is generally safe and well tolerated. The most common adverse reactions are transient soreness and redness at injection site, low grade temperature, nausea, dizziness, malaise, rash, an influenza-like syndrome, arthritis, arthralgia and myalgia, that occur less frequently in infants and children than in adults. These symptoms resolve within 24-48 hours of vaccine administration, and the frequency of these reactions decrease with subsequent doses of the vaccine. Allergic reactions have been reported infrequently and anaphylaxis is very rare (Ministry of Health Malaysia, 2002, Level 1level 1).

Cases of Guillain-Barre syndrome, rheumatoid arthritis, demyelinating diseases of the central nervous system, and lichenoid reaction have been reported after hepatitis B immunizationimmunisation. However, there is no evidence of an association between vaccination and sudden infant death syndrome, multiple sclerosis, autoimmune disease or chronic fatigue syndrome (DeBiasa et al., 2002; American Academy of Pediatrics, 2000, Level 1level 1).

Thimerosal is a derivative of ethyl mercury and has been used as a preservative in vaccines since the 1930s for its efficacy in preventing bacterial containmination in opened, multi-dose containers. There is no convincing evidence of toxicity from doses of thimerosal used in vaccines (McPhillips & Marcuse, 2001, level 2).

VACCINE EFFICACY

High seroconversion rates and protective concentrations of anti-HbBs ((10mIU/ml) are achieved when hepatitis B vaccine is administered in any of the various 3-dose schedules, including those begun soon after birth in term infants. The use of a 3-dose regimen has been shown to be highly efficacious. The vaccine is effective in preventing HB infection in individuals who produce specific anti-Hbs (Ministry of Health Malaysia, 2002, Level 1level 1). The immune response using 1 or 2 doses of a vaccine produced by one manufacturer followed by 1 or 2 more subsequent doses from a different manufacturer had been demonstrated to be comparable to a full course of immunizationimmunisation with a single product. For children with normal immune status, routine booster doses of vaccine are not recommended (American Academy of Pediatrics, 2000, Level 1level 1).

4.STORAGE, DOSAGE AND ADMINISTRATION

The vaccine should be stored at 2 to 8 (C. Freezing will destroy its potency. The vaccine is a white, slightly opalescent liquid. Any visible change in the product, such as precipitates, may indicate incorrect storage conditions and consequent reduction in immunogenicity. Such vacinesvaccines should be discarded. The dose of vaccine is 0.5 ml, and administered intramuscularly in the antero-lateral thigh for neonates and infants, and the deltoid area for children. Administration intradermally or in the buttocks has resulted in poor immune response, and is thus not recommended. Simultaneous administration with other vaccines at different sites is safe and efficacious (Ministry of Health Malaysia, 2002, Level 1level 1; DeBiasa et al., 2002, Level 1level 1). In patients with a bleeding diathesis, the risk of bleeding after intramuscular vaccine infection can be minimized by administration immediately after the patient receives replacement factor, use of a 23-gauge needle or smaller, and application of direct pressure to the immunizationimmunisation site for at least 2 minutes (American Academy of Pediatrics, 2000, Level 1level 1) ) [Grade A]

5.SPECIAL SITUATIONS

5.1.Infants Born to HbsAg-Positive Mothers

Infants born to HbsAg-positive mothers should be cleansed of blood in the delivery room. Both hepatitis B vaccine and HBIG (0.5ml intramuscularly) should be given simultaneously at different sites as soon as possible, preferably within 12 hours after birth. Subsequent doses of hepatitis B vaccine should be given as recommended.

5.2Preterm Infants
For preterm infants who weigh less than 2 kg at birth, the initial vaccine dose should not be counted in the required 3-dose schedule. Thus, a total of 4 doses are recommended in this circumstance. These infants should be tested serologically for anti-HBs and HbsAg 1 to 3 months after completion of the immunisation series. Infants with anti-HBs concentrations of less than 10mIU/ml and who are HbsAg-negative should receive 3 additional doses of vaccine at 0, 1 and 6 months followed by testing for antiHBs 1 month after the third dose (DeBiasa et al., 2002, American Academy of Pediatrics, 2000, Level 1level 1). ) [Grade A]

5.3.Serologic Testing

Susceptibility testing before immunizationimmunisation is not indicated routinely for children or adolescents. Routine post-immunisation testing for anti-HBs is also not necessary. However, testing is advised 1 to 2 months after the third vaccine dose for patients on hemodialysis patients, persons with HIV infection, those at occupational risk of exposure from sharps injuries, immunocompromised patients at risk of exposure to HBV, regular sexual contacts of HbsAg-positive persons, and infants born to HbsAg-positive mothers (American Academy of Pediatrics, 2000, Level 1level 1) ). [Grade A]

HAEMOPHILUS INFLUENZAE VACCINE

1.INTRODUCTION

Haemophilus influenzae is a respiratory pathogen of humans causing infections ranging from asymptomatic colonization of the upper respiratory tract to serious invasive disease. It is an important pathogen infor children causing considerable morbidity, mortality and health care expense, both worldwide and locally (Ministry of Health Malaysia, 2002, Level 1level 1).

Invasive disease is associated with encapsulated strains of the organism. There are six capsular serotypes, designated a-f, the majority of invasive diseases being caused by Haemophilus influenzae type B Meningitis is the most common invasive Hemophilus influenza type B (Hib) infection. Most cases of Hib meningitis in Malaysia occur in children under 12 months old,of age and it is rarely encountered in those under 3 months of age and beyond 5 years of age (Ministry of Health Malaysia, 2002, Level 1level 1).

The Hib vaccines available presently consist of polyribosylribitol phosphate (PRP) chemically linked (conjugated) to a variety of carrier proteins. This e carrier protein used in conjugating Hib vaccine ensures a good antibody response to the Hib capsular polysaccharide. Four types of vaccine are available – PRP-outer membrane protein conjugate vaccine (PRP-OMP), PRP-tetanus toxoid conjugate (PRP-T), PRP-Hib oligosaccharide conjugated vaccine (PRP-HbOC) and PRP-diphtheria toxoid conjugate vaccine (PRP-D)- of which only the first are currently available in Malaysia (Ministry of Health Malaysia, 2002, Level 1level 1).

2.ADVERSE EFFECTS

Adverse reactions to Hib conjugate vaccines are few, mostly p. Pain, redness, and swelling at infection site, occuroccurring in aboutpproximately 5-25% of recipients. These symptoms are mild and last for less than 24 hours. Systemic reactions such as fever and irritability are infrequent (Ministry of Health Malaysia, 2002, Level 1level 1).

The cCombination vaccine (DTwP +Hib) is well tolerated by infants and no significant side-effects have been reported (Ministry of Health Malaysia, 2002, level 1level 1; Hussey, 2002; Cherian, 2002; Araujo, 2000). The local reactions reported were mainly transient pain, redness, induration and some low-grade fever (Lolekha, 2001). No vaccine-related serious adverse events have occurred when (DTaP-IPV) and Hib vaccine are used, either when by mixeding in the same syringe or when given separately (Knutsson, 2001). There was Aa lower incidence of adverse events has been reported following the Hib+DTaP-based combination vaccine compared to the Hib+DTwP (Gylca, 2000, level 8).

3.VACCINE EFFICACY

The protective superiority of any one of the three vaccines – PRP-T, PRTP-OMP and HbOC – hasve not been demonstrated, and clinical efficacy studies indicate that these vaccines are suitable for prevention of Hib disease in infants and children. In randomized controlled trials, antibody response to some vaccines PRP-OMP was higher after the first dose compared to other Hib vaccines, but but the levels were not significantly different after 3 doses (Ministry of Health Malaysia, 2002, Level 1level 1).

4.COMBINATION OF VACCINES

Effective immunizationimmunisation of children against multiple disease is best tackled by giving several antigens in one injection. The preparation of the single injection could be done either during manufacture of vaccines or immediately before administration (Ministry of Health Malaysia, 2002 level 1).

DTwP mixed with PRP-T and given concurrently with OPV, PRP-T mixed with DTwP, DTPw-IPV mixed with Hib and separate HBV achieved satisfactory antibody production against PRP (Araujo, 2000; Ministry of Health Malaysia, 2002, level 1). There was no interference to any of the components when OPV, DTaP and Hib vaccine were given separately or when DTaP was mixed with Hib and given with OPV (Rennels et al, 2000, level 2).

5.STORAGE, DOSAGE AND ROUTE OF ADMINISTRATION

Conjugate vaccines should be stored at 2-8(C, and must not be frozen. Each dose of conjugate vaccine is 0.5ml and given intramuscularly. The use of fractional dose regimens showed adequate serological response and immunological memory (Ministry of Health Malaysia, 2002. level 1level 1; Fernandez, 2000). [Grade A]

6.SCHEDULE

There is good evidence that immunisation with three doses of PRP-T vaccine at 2, 3, 4 or 2, 4, 6 months is highly immunogenic (Ministry of Health Malaysia, 2002 Level 1level 1). [ Grade A] ).

The highimpressive efficacy of PRP-T given in infancy and virtual disappearance of the disease in the UK, suggest that the booster dose may not be required for a population where high vaccination coverage (>90%) is achieved (Ministry of Health Malaysia, 2002; level 1level 1; Health, 2002). [Grade A]

A single Hib vaccine dose is efficacious in preventing Hib invasive disease in children between the ages of 1-4 years. The need for cCatch-up should always be considered when introducing Hib vaccine in routine immunizationimmunisation programs (Gallo, 2002). [Grade A]

7.SPECIAL SITUATIONS

7.1Premature Babies

Although most immature infants may show an inadequate antibody response to the initial immunizationimmunisations, many pre-term infants can, however, benefit from vaccination when starting immunizationimmunisation is commenced at the same chronological age as term infants (Kristensen, 1996; American Academy of Pediatrics, 2000, Level 1level 1). ) [Grade A]

7.2Thalassaemia and Splenectomy
Hib conjugate vaccine is immunogenic in patients with Thalassemia major irrespective of whether or not a splenectomy had been performed. However, or not , although it has been suggested that there are a need to assess the need as well as thend timing of booster vaccination to maintain long-term immunity has to be assessed (Cimaz, 2001; level 9; Kristensen, 1994, level 8; Ambrosino, 1992, level 8). ) [Grade C]

7.3HIV Infection
The effectiveness of the Hib conjugated vaccine has been found to be was reduced in HIV infected infants (Read, 1998, level 8; Gibb, 1995, 1996, level 8; Rutstein, 1996, level 8; Peters, 1996, level 9, Madhi, 2002, level 8). They wereas found to have titers above below the protective level at 1 year, and thus, the need for re-immunizationimmunisation of children with HIV infection against Hib requires further evaluation (Gibb, 1996, level 8). ) [Grade C ] MEASLES, MUMPS AND RUBELLA VACCINE

1.INTRODUCTION

1.1Measles

Measles is a highly infectious viral (RNA) disease and a major health issue. It affects almost the entire population in the absence of an immunisation programme. Measles is transmitted primarily by respiratory droplets from person to person. Primary viraemia occurs 2-4 days following exposure with an intense secondary viraemia occurring 3-4 days later. CIn community studies in from developing countries have documented case fatality rates of up to 3-15% have been documented. The mMortality is highest in children under 2 years of age, those who are malnourished, and living in crowded conditions (Ministry of Health Malaysia, 2002, Level 1level 1).

Measles vaccine is a live attenuated vaccine cultured in chick embryo cells. The vaccine contains a stabiliser that makes it more heat resistant. However, after reconstitution, at 22 (C to 25 (C, it will lose 50% of its potency, while it becomes completely inactivated in 1 hour, at temperatures of over 37(C.

The efficacy of mMeasles vaccine efficacy is 95% for persons vaccinated at 12 months, and 98% for those vaccinated at 15 months of age. A local evaluation of vaccine efficacy showed seroconversion rates ranging from 93.7-98.9% for children aged 9-24 months, with rates being better for those aged 11-24 months (96.4-98.9%) than those who were 9-10 months old (93.7-95.3%) (Ministry of Health Malaysia, 2002, Level 1level 1).

The majority of vaccinated individuals appear to develop life long immunity, but waning vaccine- induced immunity does exist (secondary vaccine failure). However, tThe measles that occurs in immunised persons has been reported to be milder than in those who were not unimmunised persons. There is a minimum primary vaccine failure rate of 2-5%, which could which would be higher if the vaccine were givenis given before 12 months of age (Ministry of Health Malaysia, 2002, Level 1level 1).

1.2Mumps

Mumps is a paramyxovirus infection. It occurs primarily in children, with a peak incidence at 5-9 years of age Complications include pancreatitis, oophoritis, orchitis (unilateral orchitis has been reported in up to 20% of clinical mumps cases in post-pubertal males with clinical mumps, althoughbut sterility is rare), hepatitis, myocarditis and thyroiditis. Benign meningeal signs appear in up to 15% of cases, but permanent sequelae is rare. A serious rare complication is unilateral nerve deafness.

Mumps vaccine is a live attenuated vaccine prepared in chick embryo cell cultures. and Tthe most widely used strain at present is Jeryl Lynn B (Bakshi et al., 1990), while the other strains available are Rubini and Urabe. The Urabe strain was withdrawn in 1992 after an association with increased risk of aseptic meningitis was reported in other countries (Furesz , 1990), while the Rubini strain has been shown to be associated with primary vaccine failure (Schlegel, 1999); Goh, 1999).

Seroconversion after a single dose of mumps vaccine was reported to rangeing from 90-100%. The duration of vaccine induced immunity is unknown (antibodies have been are shown to persist for 9.5 years after MMR administration) but epidemiological and serological data over the past 30 years indicate the persistence of antibodies and continuing protection against infection… Although there are fears that a single dose immunisation as part of the MMR may shift the occurrence of mumps infection to an older age group, epidemiological data has shown a dramatic overall reduction in cases and complications. It is anticipated that a two dose MMR policy will effectively deal with most cases of primary vaccine failure that have a risk of mumps in later life. (Ministry of Health Malaysia, 2002, Level 1level 1).

The Urabe strain was withdrawn in 1992 after an association with increased risk of aseptic meningitis was reported in other countries (Furesz , 1990), while the Rubini strain has been shown to be associated with primary vaccine failure (Schlegel, 1999; Goh, 1999).

1.3Rubella
Rubella is an RNA virus belonging to the Togaviridae group of viruses. It is transmitted through droplet spread, while and congenital infection occurs as a result of viraemia during pregnancy. The teratogenic effects are produced as a result of an inflammatory response to the virus, and depressed mitosis, resulting in hypoplasia in the developing foetus. Rubella associated defects occur in 100% of pregnancies if infection occurs in the first 11 weeks, 50% in infections at from 11-12 weeks and 35% infrom 13-16 weeks. The common permanent manifestations of congenital rubella include sensorineural deafness, mental retardation, cataracts, congenital heart defect, retinopathy, spastic diplegia, growth retardation, hepatosplenomegaly, thrombocytopenia and meningoencephalitis.

Rubella vaccine is a freeze-dried preparation that is stored at 2-8˚C, and when reconstituted with diluent fluid, is given in a dose of 0.5 mL subcutaneously. A serum antibody to rubella is induced in at least 95% of recipients following a single dose at 12 months of age or laterolder. Vaccine induced antibody has been shown to persist for at least 16 years and protection against clinical rubella appears to be long term. However primary vaccine failures do occur and antibody levels can wane (Ministry of Health, 2002, level 1).

1.4MMR Vaccine

The MMR vaccine is a freeze-dried preparation containing live attenuated measles, mumps and rubella viruses.

2.ADVERSE EFFECTS OF MMR

There are minimal adverse reactions following vaccination with MMR including local pain, local induration, malaise, fever or a rash which that usually occurs a week after immunizationimmunisation, lasting for 2-3 days. Potentially serious complications include Idiopathic Thrombocytopaenic Purpura (ITP) (3.3 per 100,000), arthropathy, febrile convulsions, urticaria (0.6 per 10 000) and parotid swelling. However, the mumps component of the MMR vaccine is known to be associated with meningitis at anthe estimated rate of 1 in 50,000 to 1 in 1 million doses, which, is far less common than with the natural illness (10-15%). (Ministry of Health Malaysia, 2002, Level 1level 1).

The current evidence only establishes a causal relation between MMR vaccination and anaphylaxis, thrombocytopenia, febrile seizures, and acute arthritis. However, nNo causal link has been established linking MMR to autism and inflammatory bowel diseases (Ministry of Health Malaysia, 2002, Level 1level 1; Madsen et al, 2002; Taylor et al, 2002); Madsen, 2002; Taylor, 2002; Davis, 2002; Kaye, 2002). The general contraindications to MMR vaccine are as for all live vaccines (Ministry of Health Malaysia, 2002, Level 1). Although no anaphylactic death associated with administration of MMRmeasles-mumps-rubella vaccine has been reported, this adverse event can be life threatening. Adrenaline should be available for immediate use at any site where vaccines are administered in case symptoms of anaphylaxis occur (ACIP, 1998; American Academy of Pediatrics, 2000, Patja, 2000).

Children with allergy to eggs can safely receive MMR vaccine since the rare, serious allergic reactions after MMR are believed to be caused not by egg antigens, but by other components of the vaccine (e.g., gelatin MMR, its component vaccines, and other vaccines contain hydrolyzed gelatin as a stabilizer) (Ministry of Health Malaysia, 2002, Level 1level 1).

3. VACCINE EFFICACY

The vaccine is highly immunogenic with seroconversion rates of 96-100% for measles, 90-100% for mumps and 99-100% for rubella. Protection conferred by a single dose given after 12 months of age is long lasting in the majority of persons. However between 5-10% of vaccinated individuals may either have primary vaccine failure or lose protection, while 99% of individuals who receive two doses (separated by at least 4 weeks) after 12 months of age have long lasting immunity to measles (Ministry of Health Malaysia, 2002. level 1).

There is conflicting evidence on the efficacy of MMR vaccination under 12 months of age. There has been a suggestion that as immunisation rates improve, maternal antibodies may wane sooner in mothers who received immunisation rather than the natural disease, hence allowing for a lowering of the minimum age for measles and other immunisation (Ministry of Health Malaysia, 2002, Level 1level 1).

4.STORAGE, DOSAGE AND ROUTE OF ADMINISTRATION

MMR vaccine should be stored at 2(C to 8(C and must be protected from ultraviolet light. Reconstituted measles vaccine is very unstable and quickly loses potency at room temperature after reconstitution, and hence should be discarded if not used within 8 hours even if stored in a refrigerator (ACIP, 1998). The dosage is 0.5 ml given by intramuscular or deep subcutaneous injection (Department of Health, United Kingdom, 1996). [Grade C].

2. SCHEDULE

A 2-dose MMR is recommended to be given at 12 months and at school entry (6 to 7 years). However, for Sabah, it is recommended that monovalent measles vaccine to be given to children at 6 months of age, followed by MMR at 12 months and at school entry (6 to 7 years) (WHO/ ACIP 1998). [Grade A]

6.SPECIAL SITUATIONS

6.1.Measles ImmunizationImmunisation in HIV Infected Children: HIV-infected children, adolescents, and young adults without evidence of severe immuno-suppression should receive MMR vaccine. The first dose should be administered at 12 months of age. The second dose may be given as soon early as 28 days after the first dose. In the event of an outbreak in the community, vaccination with mono-valent measles vaccine (or MMR) is recommended for infants as young as 6 months when exposure to natural measles is considered likely. Children vaccinated before the first birthday should be revaccinated with MMR at 12 months, and an additional dose may be given as soon as 28 days later (AAP, 1999) [Grade A]

6.2.Steroid Treatment
Patient who received steroids at a dose that is equivalent to or greater than a prednisone dose of 2 mg/kg of body weight per day, or a total of 20 mg per day, or on alternate days for an interval of 14 days or longer, should avoid vaccination with MMRmeasles-mumps-rubella; and its component vaccines for at least 1 month after cessation of steroid therapy. Similarly, tThose receiving prolonged or extensive topical, aerosol, or other local corticosteroid therapy that causes clinical or laboratory evidence of systemic immuno-suppression, should also avoid vaccination with MMRmeasles-mumps-rubella for at least 1 month after cessation of therapy. Such Ppersons who receive doses of systemic corticosteroids equivalent to a prednisone dose of 2 mg/kg or more of body weight or 20 mg or more daily or on alternate days during an interval of less than 14 days generally can generally receive MMRmeasles-mumps-rubella, or its component vaccines, immediately after cessation of treatment, although some prefer waiting until 2 weeks after completion of therapy. MMR,easles-mumps-rubella or its component vaccines, generally should not generally be administered to persons who have a disease that, suppresses the immune response, or those and who are receiving either systemic or locally administered corticosteroids (ACIP 1998). [Grade A].

Recent evidence indicates that high doses of immunoe globulins can inhibit the immune response to measles and rubella vaccine for 3 months or more, and he months. Hence, MMR immunisation should be delayed (ACIP 1998). [Grade A].

REFERENCES

1. Academy of Medicine of Malaysia 2001 Malaysian Immunisation Manual, College of Paediatrics 2. American Academy of Paediatric In: pickering Lk, ed 2000 Red Book: Report of the committee on infectious Diseases 25th ed. Elk Grove Village. 3. Bakshi SS, cooper LZ (1990) Rubella and mumps vaccine. Paed Clin N Am, 37(3), pp 651-67 4.

5. Aristegui J et al., (1998) Assessment of the immunogenicity and reactogenicity of a quadrivalent diphtheria, tetanus, acellular pertussis and hepatitis B (DTPa-HBV) vaccine administrated in a single injection with H Influenza type b conjugate vaccine to infants at 2, 4 and 6 months of age. Vaccine, 16(20); pp 1976-1981. 6. Baraff LJ, Shields WD & Beckwith L (1988) Infants and children with convulsions and hypotonic hyporesponsive episodes following diphtheria-tetanus-pertussis immunisation. Pediatrics, 81, pp 789-794 7. Bart KJ, Lin KF, (1990) Vaccine preventable disease and imunisation in the developing world Pediatr Clin N Am, 37(3), pp 734-456 8. Begue P et al, (1997) Immunogenicity and reactogenicity of a booster dose of diphtheria, tetanus, accellular pertussis and inactivated poliomyelitis vaccines given concurrently with Haemophilus type b conjugate vaccine or as pentavalent vaccine. Pedaitric Infectious Disease Journal; 16(8), Aug, pp 787 -94 9. Bhaskaram P et al (1997) Systemic and muscosal immune response
to polio vaccination with additional dose in newborn period. Journal of Tropical Pediatrics, 43 (4), pp 232-4 10. Bisgard KM et al (2000) Dipththeria vaccine effectiveness: A case control study in Russia. Journal of infectious disease, 181 ( suppl 1), pp S 184-187 11. Booy R et al (1992) Immunogenecity of combined diphtheria, pertussis and tetanus vaccine given at 2, 3 4 months versus 3, 5, 9 months. Lancet , 239, pp 507-510 12. Centers for Disease Control (1991) Diptheria, tetanus, and pertusis: recommendations for vaccine use and other preventive measures: recommendation of the ImmunizationImmunisation Practice Advisory Committee (ACIP) MMWR, 40 (no. RR-10) 13. Centers for Disease Control (1996) Update Vaccine Side Effect, Adverse Reactions Contraindications and Precautions Recommendations of the Advisory Committee on ImmunizationImmunisation Practices (ACIP) MMR, 45 (RR-12, p 1-35 14. Chen RT et al (2000) Ukraine 1992: First assessment of diphtheria vaccine effectiveness during the recent resurgence of diphtheria in the former soviet union. Journal of infectious disease, 18 ( supp 1), pp S 178-183 15. Cimaz R, Mensi C, D’Angelo E, Fantola E, Milone V, Biasio LR, Carnelli V, Zanetti AR (2001) Safety and immunogenicity of a conjugate vaccine against Haemophilus influenzae type b capsular polysaccharide-tetanus vaccination is related to the number of doses administration. J Infect Dis, 183(12), Jun 15, pp 1819-21 16. Chen ST, Puthucheary SD (1976) Some epidemiological aspects of diphtheria in Malaysia Tropical & Geographical Medicine, 28(3), pp 211-5 17. Choo KE, Ariffin WA, Ahmad T, Lim WL, Gururaj Ak, (1990) Pyogenic meningitis in hospitalized children in Kelantan, Malaysia. Ann Trop Paediatr 10(1), Mar, pp 89-98 18. Clemens JD, Ferreccio C & Levin MM (1992) Impact of Hib polysaccharide- tetanus protein conjugate vaccine on response to concurrently administered DTP vaccine. JAMA 267, pp 637-8 19. Cody Cl, Baraff LJ & Cherry JD (1981) Nature and rates of adverse reactions with DTP and DT immunisation in infants and children. Pediatrics, 68, pp 650-660 20. Cowan LD, Griffin MR, Howson CP & Katz M (1993) Acute enceohalopathy and chronic neurological damage after pertusssi vaccine. Vaccine, 11 (14), Nov, pp 1371-9 21. Dagan R et al (1997) Safety and immunogenicity of a combined pentavalent diphtheria, tetanus, acellular pertussis, inactivated poliovirus and Haemophilus influenza type b tetanus conjugate vaccine in infants compared with a whole cell pertussis pentavalent vaccine. Pediatric Infectious Disease Journal
16(2), pp 1113-21 22. De Serres G,Bouliane N, Duval B et. al., (1996) Effectiveness of a whole cell pertussis vaccine child care centres and schools. Pediatri Infect Dis J, 15(6), Jun, pp 519-24 23. DeBiasa RL, Daley MF, Simoes EAF (2002) Immunisation. Current Pediatric Diagnosis And Treatment 24. Department of Health, United Kingdom (1996) Immunisation against Infectious Disease (“The Green Book’): HMSO 25. Desphande JM et al (1996) Absence of wild poliovirus circulation among healthy children in a rural area with high oral poliovirus vaccination coverage. Indian Journal of Medical Research 103; pp 289-93 26. Edwards KM, Meade BD, Decker Md, et al., (1995) Comparison of 13 acellular pertussis vaccines: overview and serologic response. Pediatrics, 96 (3 pt 2), pp 548-57 27. Frenkel LD (1990) Routine immunisation for American children in the 1990s. Ped Cli N Am, 37(3), pp 531-547 28.

29. Furesz J, Contreras G. (1990) Vaccine-related mumps meningitis–Canada. Can Dis Wkly Rep. 16(50), Dec 15, pp 253-4. 30. Galazka AM (1993) The immunological basis for immunisation series: Module 2 -Diphtheria. WHO/EPI/gen/93.13 31. Galazka AM (1993) The immunological basis for immunisation series: Module 3 -Tetanus. WHO/EPI/gen/93.13 32. Guris D, Strebel PM, Tachdjian R (1992) Effectiveness of the pertussis vaccination program as determined by use of the screening method: United States 1992-1994. J Infect Dis, 176(2), Aug, pp 456-63 33. Gutafsson L, Hallander HO, Olin p et al., (1996) A controlled trial of two acellular vaccines and one whole-cell vaccine against pertussis. N Engl J Med, 334 (6), Feb 8, pp 341-8 34. Gallo G, Ciofi Degli Atti ML, Cerquetti M, Piovesan C, Tozzi AE, Salmaso S (2002) Impact of a regional Hib vaccination programme in Italy. Vaccine, 20(7), Jan 15, pp 993-5 35. Gibb D, Spoulou V, Giacomelli A, Griffiths H, Masters J, Misbah S, Nokes L, Pagliaro A, Giaquinto C, Kroll S, et al. (1995) Antibody responses to Haemophilus influenzae type b and Streptococcus pneumoniae vaccines in children with human immunodeficiency virus infection. Pediatr Infect Dis J. 14(2), Feb, pp 129-35. 36. Gibb D, Giacomelli A, Masters J, Spoulou V, Ruga E, Griffiths H, Kroll S, Giaquinto C, Goldblatt D. (1996) Persistence of antibody responses to Haemophilus influenzae type b polysaccharide conjugate vaccine in children with vertically acquired human immunodeficiency virus infection. Pediatr Infect
Dis J. 15(12), Dec, pp 1097-101. 37. Gutafsson L, Hallander HO, Olin p et al., (1996) A controlled trial of two acellular vaccines and one whole-cell vaccine against pertussis. N Engl J Med, 334 (6), Feb 8, pp 341-8 38.

39. Kristensen K (1994) Vaccination of splenectomised children. antibody response to Haemophilus influenzae type b conjugate vaccine. Ugeskr Laeger, 156(2), Jan 10, pp 191-3 40. Lolekha S, Hiranchote A, Simasathien S (2001) Safety and immunogenicity of combined or associated administration of PRP-T vaccine with diphtheria, tetanus and pertusis vaccine in Thai children. J Trop Pediatr, 47(1), Feb, pp 24-9 41. Madhi SA, Petersen K, Khoosal M, Huebner RE, Mbelle N, Mothupi R, Saloojee H, Crewe-Brown H, Klugman KP (2002) Reduced effectiveness of Haemophilus influenzae type b conjugate vaccine in children with a high prevalence of human immunodeficiency virus type 1 infection. Pediatr Infect Dis. J. 21(4), Apr, pp 315 -21 42. Gyhrs A et al (1999) Immunogenicity and safety of a tetrravalent diphtheria-tetanus-accellular pertussis-inactivated poliovirus vaccine. Scandinavian Journal of Infectious Disease, 31(6), pp 579-85 43. Halperin SA et al (1996) Effects of inactivated poliovirus vaccine on the antibody response to Bordetella pertussis antigens when combined with DPT vaccine. Clinical Infectious Disease, 22 (1), pp 59-62 44. Ion-Nedelcu N et al., (1997) Sequential and combined use of inactivated and oral poliovirus vaccine. Journal of Infectious Disease, 175 (sup 1), pp S241-6 45. Jenkinson D (1988)_ Duration of effectiveness of pertussis vaccine: evidence from a 10 year community study. Br Med J (Clin Res Ed), 296 (6622), Feb 27, pp 612-4 46. Jonville-Bera Ap et al (1999) Adverse effects of the vaccine Tetracoq. IPAD/DTCP and DTCP. A French study of regional drug monitoring centres. Archives de Pediatrie 6(5), pp 510-5 47. Kaplan Sl, Brian A, Lauer (1994) Immunogenicity and safety of Hib vaccine alone or mixed with DTP vaccine in infants. Journal of Pediatrics, 124, pp 323-327 48. Kolasa MS et al (2000) Impact of the sequential poliovirus immunisation schedule: a demonstration project. American Journal of Preventive Medicine, 18 (20), pp 140-5 49. Kotb MM et al (1993) Epidemiological evaluation of oral polio vaccine efficacy in Cairo Journal of the Egyptian Public Health Association, 68(5-6), pp 617-25 50. Kurikka S et al ( 1996) Comparison of five different vaccination schedules with Hib-tetanus toxoid conjugated vaccine. Journal of Pediatrics
128 (40), pp 524-30 51. Langue J et al (1999) Safety and immunogenecity of Hib-tetanus toxoid conjugated, presented in a dual chamber syringe with DPT-IPV comibination vaccine. European Journal of Pediatrics . 158(9), PP 717-22 52. Lee EL, Khoo BH, Puthucheary SD, Thong ML (1997) Purulent Meningitis in Childhood. Med J Malaysia, 32, pp 114-19. 53. Long SS, Deforest A, Smith DG, Lazaro C (1990) Longtidinal study of adverse reactions following diphtheria-tetanus-pertussis vaccine in infancy. Pediatrics 85(3), Mar, pp 294-302 54. Lyn P, Pan EL, (1988) Management and outcome of childhood meningitis in East Malaysia. Med J Malaysia, 43, pp 90-6 55. Madge, Nicola, et al. The national childhood encephalopathy study: a 10-year follow-up./A report on the medical,social,behavioral and educ. outcomes after serious neurologic illness 56. McPhillips H, Marcuse EK. (2001) Vaccine Safety. Curr Probl Pediat ,31(4),Apr, pp 91-121. 57. Madsen KM, Hviid A, Vestergaard M, Schendel D, Wohlfahrt J, Thorsen P, Olsen J, Melbye M. (2002) MMR vaccination and autism–a population-based follow-up study]. Ugeskr Laeger. 164(49), Dec 2, pp5741-4. 58. McPhillips H, Marcuse EK. (2001) Vaccine Safety. Curr Probl Pedia ,31(4),Apr, pp 91-121. 59. Miller D, Madge N, Diamond J, Wadsworth J, Rose E (1993) Perutssis immunistion and serious acute neurological illnessess in children. BMJ, 307(6913), Nov 6, pp 1171-6 60. Ministry of Health (2000) Malaysian Health Facts

61. Ministry of Health Malaysia (1999) Annual Report
62. Ministry of Health Malaysia (2002) Childhood Immunisation. Health Technology Assessment 63. MMWR Use of Diphtheria Toxoid-Tetanus Toxoid-Acellular Pertussis Vaccine as a Five-Dose Series. November17, 2000 / 49(RR13); 1-8. 64. Morbidity & Mortality Weekly Report. (1996) Progress toward poliomyelitis eradication People ‘s Republic of China, 1990-1996, 49(49), pp 1076-9 65. Morbidity & Mortality Weekly Report. (1997) Progress toward poliomyelitis eradication Africa, 46 (15), pp 321-5 66. Morbidity & Mortality Weekly Report. (1998) impact of sequential IPV/OPV schedule on vaccination coverage levels- United State, 47 (47) pp 1017-9 67. Myauz JA (1996) effect of diarrhoea on the humoral response to oral polio vaccination . Pediatric Infectious Disease Journal, 15(3), pp 204-9 68. National Health and Medical Research Council, Australia. (1997) Australian Immunisation hand book. 6th edition 69. Peters VB Sood SK (1996) Immunity to Haemophilus
influenzae type b polysaccharide capsule after vaccination with the complete series of oligosaccharide CRM197 conjugate vaccine in infants with human immunodeficiency virus infection.. J Pediatr. 128(3), Mar, pp 363-5. 70. Olin P et al (1998) Potential exposure to SV 40 in polio vaccines used in Sweden during 1957, no impact on cancer incidence rates 1960-1993. Development in Biological Standardization,94, pp 227-33 71. Osei-Kwasi M et al (1999) Randomised controlled trial of trivalent oral polio vaccine (Sabin) starting at birth in Ghana. Bulletin of World Health Organisation, 73(1), pp 41-6 72. Pasn X (1999) Investigation on the effect and strategy of polio eradication in Hainan province. Chung-Hua Liu Hsing Ping Hsueh Tsa Chih Chinese. Journal of Epidemiology, 20(2), pp 78-80 73. Pathmanathan I (1990) Strategies to Achieve EPI Targets. National Symposium on Practical Immunisation. Ministry of Health Malaysia 74. Patricia E, Vermer-deBondt,Jerry Labdie, hans C Rumke (1998) Rate of recurrent collapse after vaccination with whole cell pertussis vaccine. BMJ, 316(7135), Mar 21, pp 902-03 75. Plotkin SA (1997) The effectiveness of whole-cell pertussis vaccine. Dev Biol Stand, 89, pp 171-4 76. Posey et al ( 1997) The effects of diarrhoea on oral polio vaccine failure in Brazil. Journal of Infectious Disease, 175(supp1), pp S 258-63 77. Puthhucheary SD, Thong ML (1984) The spectrum of clinical conditions associated with 40 cases of haemophilus bacteremia. Singapore Medical J 25(3), pp 152-6 78. Ramsay MEB, Rao N. Begg NT et al.,(1993) Antibody response to accelerated immunistion with dipththeria, tetanus, pertussis vaccine. Lancet, 342 pp 203-5 79. Read JS, Frasch CE, Rich K, Fitzgerald GA, Clemens JD, Pitt J, Pelton SI, Hanson IC, Handelsman E, Diaz C, Fowler MG. (1998) The immunogenicity of Haemophilus influenzae type b conjugate vaccines in children born to human immunodeficiency virus-infected women. Women and Infants Transmission Study Group. Pediatr Infect Dis J,17(5), May, pp 391-7 80. Rennels MB, Englund JA, Bernstein DI, Losonsky GA, Anderson EL, Pichichero ME, Munoz FM, Wolff MC. (2000) Diminution of the anti-polyribosylribitol phosphate response to a combined diphtheria-tetanus-acellular pertussis/Haemophilus influenzae type b vaccine by concurrent inactivated poliovirus vaccination. Pediatr Infect Dis J. 19(5), May, pp 417-23. 81. Rutstein RM, Rudy BJ, Cnaan A. (1996) Response of human immunodeficiency virus-exposed and -infected infants to Haemophilus influenzae type b conjugate vaccine. Arch Pediatr Adolesc Med.
150(8), Aug, pp 838-41. 82. Ridway D (2000) The logic of causation and the risk of paralytic poliomyelitis for an American child. Epidemiol. Inf, 12491, pp 113-20 83. Rohani MY, Raudzah A, Norazah A, Zaidatul AAR, Ng AJ, Ng PP, Murtaza M, Asma IM, Yasim MY, Cheong YM (1997) Epidemiology of Haemophilus Influenzae infections in Malaysia Hospitals. Int Med Research J, 1(2), pp 111-15 84. Rothstein EP et al (1993) Simultaneous administration of diphtheria and tetanus toxoids and accellular pertussis vaccine with MMR and oral polio vaccine.American Journal of Diseases of Children, 147(8), Aug , pp 121-38 85. Sedaghatian MR, et al,(1998) Bacille Calmette Guerin vaccination in pre-term infants; Int J Tuberc Lung Dis,2 (8), Aug, pp 679-82 86. Taylor B, Miller E, Lingam R, Andrews N, Simmons A, Stowe J. (2002) Measles, mumps, and rubella vaccination and bowel problems or developmental regression in children with autism: population study. BMJ. 324 (7334), Feb, pp 393-6. 87. Thayyil-Sudhan S et al (1998) Is zero dose oral polio vaccine effective in a preterm baby . Annal of Tropical Paediatrics. 18(4),Dec, pp 321-4 88. The Australian Collage of Paediatrics Policy Statement. (1994) Contraindications to immunisation against pertussis. J Paediatr Child Health, 30(4), Aug, pp 310-1 89. Thom ML et al (1997) Parental knowledge and choice regarding live and inactivated poliovirus vaccines. Archives of Pediatrics & Adolescent Medicine. 151(8), pp 809-12 90. Tinnion ON & Hanlon M (2000) Cochrane Database Systematic Review (2): CD 001478 91. Vitek CR et al (1999) Risk of diphtheria among schoolchildren in the Russian Federation in relation to time since last vaccination. The Lancet, 353, Jan 30, pp 355-358 92. Ward NA et al (1997) Measles, mumps, rubella and varicella combination vaccine: safety and immunogenicity alone and in combination with other caccines given to children. Clinical Infectious Desease. 24(5), pp925-31 93. Watember N, Dagan R & Arbell Y. (1991) Safety and Immunogenicity of Hib mixed in the same syringe with DTP vaccine in young infants. Paediatr Infect Dis J,10, pp 758-63 94. WHO (1995) Factors affecting the immunogenicity of oral polio vaccine: a prospective evaluation in Brazil and Gambia. World Health Organisation Collaboration Study Group on Oral Poliovirus vaccine. Journal of Infectious Disease 171(5), pp 1097-106 95. WHO (1997) Combined immunizationimmunisation of infants with oral inactivated poliovirus vaccines: results of a randomised trial in the Gambia, Oman and Thailand. WHO Collaboration Study Group on Oral and
Inactivated Poliovirus Vaccines. Journal of Infectious Disease. 175 (supp1), pp S 215-27 96. WHO (1998) Geneva. Global eradication of poliomyelitis by the year 2000 World Health Assembly Resolution WHA 41.28) 97. WHO .Expanded Program on Immunisation. Immunisation Policy . WHO/EPI/GEN/86/7 98. WHO .Expanded Program on Immunisation. Immunisation Policy . WHO/EPI/GEN/95.03 99. WHO Immunisation policy (1995)- Global programme for vaccines and immunisation WHO/EPI/Gen/95.3 100. Zimmerman B, Gold R, Lavi S (1987) Immunisation. Profraduate Medicine, 82,(5): 112-7 Read JS, Frasch CE, Rich K, Fitzgerald GA, Clemens JD, Pitt J, Pelton SI, Hanson IC, Handelsman E, Diaz C, Fowler MG. (1998) The immunogenicity of Haemophilus influenzae type b conjugate vaccines in children born to human immunodeficiency virus-infected women. Women and Infants Transmission Study Group. Pediatr Infect Dis J,17(5), May, pp 391-7 101.

102. Zimmerman RK et al (1999) Poliovirus vaccine options. American Family Physician. 59(1), pp 113-8; 125-6 103.

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