notifiable

Hepatitis B

Common Name: 
Hep B or HBV
Parents & Caregivers
Introduction: 

Hepatitis is a viral disease that attacks the liver. There are several types of viral hepatitis, labeled A, B, C, D, and E. Hepatitis B virus or HBV is very infectious and is spread from person to person through bodily fluids including blood, semen, and vaginal fluids. People who are infected with hepatitis B can either develop an acute illness in which they become sick soon after infection or a chronic illness in which the illness does not begin to affect them for a longer period of time with more serious complications. People with chronic hepatitis B infection are likely to suffer from liver disease or liver cancer which can be life threatening. Infected infants and young children are at higher risk for developing chronic disease. Hepatitis B cannot be cured but can be prevented with a vaccine.

A brief history: 

Hepatitis was first described by Hippocrates over 2000 years ago with signs of jaundice or yellowing of the skin and eyes. Several outbreaks in the 19th and 20th Centuries are documented with global spread mainly a result of warfare. In recent history, cases in New Zealand peaked near 1984 but began declining with the introduction of the vaccine, first intended for infected mothers in 1985 and later for all children in 1988. For the last 10 years, New Zealand has maintained fewer than 100 new cases per year.

The current New Zealand situation: 

While estimates show that less than 1% of the New Zealand population are carriers of HBV, there are pockets of areas around the country with higher rates than others.

Symptoms: 

Symptoms of acute hepatitis B include nausea and vomiting, jaundice (yellow skin or eyes), dark urine (pee, mimi), pale faeces (poo, tutae), feeling unwell, lack of energy, loss of appetite, upset stomach or stomach pains, fever, and general aches and pains.

Chronic hepatitis B may be harder to detect as some infected people may not show signs or symptoms.

How do you get it?: 

Hepatitis B infection can be spread through open cuts or wounds, sexual contact, sharing drug needles, blood transfusion, and passed from infected mother to baby. Newborn babies of infected mothers can receive their first dose of hepatitis B vaccine within 24 hours of birth to prevent spread.

What are the risks?: 

Hepatitis B can be a life-long illness causing liver disease and liver cancer. Blood remains infective in those with a chronic hepatitis B infection and can infect others.

The Hepatitis Foundation of New Zealand provides a free Hepatitis B Follow-up Programme that provides information, support and regular blood tests that are vital in managing hepatitis B infection. We recommend a visit to their website (www.hepfoundation.org.nz) or you can phone them for free on 0800 332 010.

Who is most at risk?: 
  • People aged 25 years or over who are of Māori, Pacific Island or Asian ethnicity*
  • People born in Asia or the Pacific Islands*
  • Injection drug users
  • Heterosexuals with multiple partners
  • Men who have sex with men
  • Household contacts of infected persons
  • Health care and public safety workers who have exposure to blood in the workplace
  • Haemodialysis patients and blood transfusion patients

*Source: The Hepatitis B Foundation of New Zealand.

Treating the symptoms: 

There is no specific treatment for hepatitis B. Chronic hepatitis B infection can be treated with drugs like interferon and anti-viral medication. Patients with liver disease may be recommended for liver transplant. Liver cancer is almost always fatal.

The Hepatitis Foundation of New Zealand provides a free Hepatitis B Follow-up Programme that provides information, support and regular blood tests that are vital in managing hepatitis B infection. We recommend a visit to their website (www.hepfoundation.org.nz) or you can phone them for free on 0800 332 010.

Preventing Disease Spread: 
  • There is an effective vaccine available to prevent hepatitis B.
  • Contacts and family members of infected persons should practice strict hygiene measures.
  • Avoid injection drug use.
  • Engage in safe sex practices including use of condoms.
Health Professionals
Introduction (HP): 

The hepatitis B virus (HBV) attacks the liver and can result in both acute and chronic disease. It is spread via blood and bodily fluids. The most common routes of infection are through sexual contact, injection drug use, and occupational hazards for health professionals. The age at which someone is infected is a good predictor of disease outcome and severity. Roughly 2 billion people worldwide have been infected with the majority of cases in developing countries. Hepatitis B is vaccine preventable and the vaccine is included in the New Zealand National Immunisation Schedule.

Causative organism: 

The hepatitis B virus is is a DNA-containing hepadnavirus. Hepatitis B is extremely virulent and is 50-100 times more infectious than the human immunodeficiency virus (HIV).

Clinical signs, symptoms and complications: 

Adults with acute hepatitis B infection may not display symptoms. The disease may only be detectable by liver function tests.

  • Acute hepatitis B can cause symptoms that include anorexia, abdominal discomfort, malaise and fatigue, nausea and vomiting, and jaundice.
  • Acute hepatitis B infection may cause an acute hepatic necrosis, requiring an emergency liver transplantation or causing death.
  • About 10% of adults with acute hepatitis B infection will develop chronic hepatitis B infection.
  • Chronic hepatitis B infection occurs in 90% of infected infants and 30-50% of infected children between 1-4 years of age.
  • Chronic hepatitis B infection may result in cirrhosis of the liver, which increases the risk of hepatocellular carcinoma.
Method of transmission: 
  • Sexual contact.
  • Injection drug use.
  • Perinatal transmission.
  • Occupational exposure for health care or public safety workers.
  • Exposure to blood transfusion or haemodialysis patients.
Public health significance: 
  • More than 2 billion people are infected worldwide.
  • There is a 70-90% vertical transmission rate from infected mother to newborn.
  • Roughly 90% of infected infants will become chronic hepatitis B infection carriers.
  • Hepatitis B related cirrhosis and liver cancer are almost always fatal.
New Zealand epidemiology: 

Some regions in New Zealand show a significantly higher rate of hepatitis carriage. In recent history, cases in New Zealand peaked near 1984 but began declining with the introduction of the vaccine, first intended for infected mothers in 1985 and later for all children in 1988. For the last 10 years, New Zealand has maintained fewer than 100 new cases per year.

Prevention: 
  • Strict hygiene measures.
  • Prophylactic immunisation for newborns to carrier mothers.
  • Safe sex practices.
  • Avoiding injection drug use or use of clean disposable needles.

An effective vaccine has been available in New Zealand to all children from 1988. The current hepatitis B vaccine is given with the primary series at 6 weeks, 3 months, and 5 months of age.

Treatment: 

There is no specific treatment for hepatitis B infection. Chronic disease may be treated with interferon or anti-virals but management revolves mostly around comfort and nutrition.

Health professionals are encouraged to refer patients who are hepatitis B positive to The Hepatitis Foundation of New Zealand (www.hepfoundation.org.nz) for enrolment in the Hepatitis B Programme. An online referral form is available or phone 0800 332 010 for more information.

Disease Effects vs Vaccine Side Effects (Table)
Disease Description: 

Hepatitis B is one type of hepatitis virus that infects the liver and can cause ling term liver damage.

Effects of disease: 
Blood is infective whilst the person is acutely unwell and can infect others.
Approximately 2 in 10 adults with acute hepatitis B infection will not have symptoms.
Liver inflammation can cause abdominal discomfort, jaundice, anorexia, nausea and vomiting, malaise and fatigue: approximately 8 in 10.
Acute liver failure: 1 in 100, of who almost half will die or require an emergency liver transplantation.
People who become infected at birth or in early childhood usually develop a chronic hepatitis B infection. Which may lead to:
Cirrhosis of the liver, and an
Increased the risk of developing liver cancer.
Blood remains infective for life in those with a chronic hepatitis B infection and can infect others.
Common side effects of vaccine: 
Soreness/pain, redness and/or swelling around the injection site.
Fever over 38°C.
Decreased appetite, vomiting and/or diarrhoea.
Irritability, restlessness.
Unusual crying.
Fatigue.
Uncommon side effects of vaccine: 
Fever over 39°C.
Rare/very rare side effects of vaccine: 
Convulsion within 2 days of immunisation, less than 1 in 1.4 million doses.
Encephalopathy (brain inflammation), less than 1 in 1 million doses.
Anaphylaxis (severe allergic reaction), less than 1 in 1 million doses.
Urticaria (allergic skin reaction).
Hypotonic, hyporesponsive episode (HHE, a temporary period of decreased muscle tone and responsiveness) within 24 hours of immunisation, up to 47 times in 100,000 doses.
Persistent (> 3 hours) inconsolable screaming, up to 44 times in 100,000 doses.
Extensive swelling of vaccinated limb or one or both lower limbs.

Diphtheria

Parents & Caregivers
Introduction: 

Diphtheria is a rare but serious infectious disease. The bacteria usually causes infection of the throat and nose but can also cause skin infections. While some cases may be mild, the bacteria can produce dangerous toxins that cause severe complications which can be life-threatening. Such complications include heart trouble, paralysis, and kidney failure. Cases of diphtheria in New Zealand have declined significantly over the last century with very few cases reported in the last 50 years.

A brief history: 

Diphtheria used to be common in New Zealand, with a total of 794 deaths in the five years from 1917 to 1921. Fortunately, in part because of vaccination, diphtheria has disappeared from New Zealand. However, it is common in other parts of the world and is, therefore, only a plane ride away.

The current New Zealand situation: 

Since 1979, there have only been 4 confirmed diphtheria cases in New Zealand. These isolated cases occurred in 1987, 1998, 2002 and 2009.

It is believed that diphtheria vaccine protection wanes over time which is why the vaccine has been introduced into adult schedules in New Zealand.  Diphtheria vaccine is included in the childhood immunisation schedule in New Zealand and remains an essential component of child vaccine programmes worldwide.

Symptoms: 
  • Inflammation of the upper respiratory tract including the nose and throat. This may include sore throat, breathing problems, bloody or watery drainage from the nose, hoarseness, a bark-like cough, and painful swallowing.
  • Some cases will experience infection of the skin.  This may include skin lesions.
  • However,some cases may not experience any symptoms.
How do you get it?: 

Diphtheria is spread through close personal contact with someone who is infected or is a carrier of the bacteria who shows no symptoms. Spread commonly occurs through way of respiratory droplets (originating from a cough or a sneeze). The bacteria can also spread through contaminated objects or food.

What are the risks?: 

The effects of diphtheria can range from mild to severe.
•For those infected, there is the potential for the diphtheria bacteria to release harmful toxins which can spread through the blood stream and affect major organs.
•Diphtheria toxin can cause significant damage to the heart, nerves, and kidneys.
•Diphtheria can be fatal. 5-10% of those infected die, even with treatment.

Who is most at risk?: 
  • Those who are not immunised are at the greatest risk.
  • Crowded environments and poor hygiene are known to increase risk for diphtheria.
  • The majority of cases are reported in children under 10 years of age.
Treating the symptoms: 

People suspected of having diphtheria will be given an antitoxin in a jab to the muscle or into the vein. Infection is then treated with antibiotics, such as erythromycin or benzathine penicillin. Additional treatment may include intravenous fluids, oxygen, bed rest, heart monitoring, use of a breathing tube, and correction of any blocked airways.

Preventing Disease Spread: 
  • The person with diphtheria is excluded from school until they have recovered and had two negative throat swabs.
  • Contacts of the person with diphtheria are given antibiotics and may also need to have a booster vaccination with a diphtheria-toxoid containing vaccine
  • Contacts who are children are excluded from early childhood education, daycare, school and community activities until throat swabs shown they do not have the disease.
  • Adults who work with food or children are excluded from their work until throat swabs shown they do not have the disease.
Health Professionals
Causative organism: 

Diphtheria is caused by the bacteria Corynebacterium diphtheriae. The toxin produced by some diphtheria bacteria can cause serious and life-threatening infections.

Clinical signs, symptoms and complications: 

  • Membranous inflammation of the upper respiratory tract and nasopharynx, which may cause hoarseness, loss of voice or stridor (greyish membrane with a characteristic mousy smell). This may be accompanied by mildly painful tonsillitis or pharyngitis (90%).
  • Lymphadenopathy may lead to a “bull neck” appearance and the angle of the jaw may be obliterated. Unilateral or bilateral paralysis of the palatal muscles may lead to dysphagia
  • Skin and mucous membrane (mouth, vagina) lesions may occur in less serious disease. Pain, tenderness, and erythema at the site of infection progresses to ulceration with sharply defined borders and formation of a brownish grey membrane.
  • Infection by toxigenic strains may lead to toxin release, which can cause myocarditis, peripheral neuropathy with flaccid paralysis, renal failure secondary to tubular necrosis, stupor, coma and death.
  • 10% of patients die of mechanical airway obstruction or circulatory collapse.
Method of transmission: 

Humans are the only known reservoir of diphtheria. The discharge from an infected person’s nose, throat, eye and skin lesions contains the bacteria and is contagious.

  • Transmission mostly happens from intimate contact with an infected person although fomites and food-borne sources can serve as vehicles of transmission.
Public health significance: 

Diphtheria is rare in industrialised countries where immunisation programmes have run for decades. However, it's still common in some countries.

  • Since 1990, epidemic diphtheria has re-occurred through the Newly Independent States (NIS) of the former Soviet Union, including Russia, the Ukraine and the central Asian republics. In the 6 years from 1990 through 1995, the NIS accounted for more than 90% of all diphtheria cases reported to the World Health Organization from the entire world.
  • Illness is most common in low socio-economic groups living in crowded conditions. Infection can occur in immunised and partially immunised people, but disease is most severe in people who are not immunised.
  • Antibiotic treatment usually renders patients non-infectious within 24 hours.
  • An estimated 20% of those under 20 and 75% of those over 65 worldwide are thought to have insufficient immunity to diphtheria due to inadequate immunisation coverage and waning immunity.
  • While immunisation leads to the disappearance of toxigenic strains, non-toxigenic strains may become toxigenic through phage transmission. This makes the possibility of a resurgent diphtheria epidemic a real threat wherever there is insufficient community (herd) immunity.
New Zealand epidemiology: 

Between 1917 and 1921 there were 794 reported deaths in non-Māori from diphtheria. Regular epidemics of infection occurred in New Zealand until 1950, and further outbreaks occurred in Milton and the Waikato in the 1960s.

In 1998 the first case of diphtheria was reported in New Zealand since 1979, and this was the first toxigenic isolate since 1987. In 2002 a four-year-old child was reported after a toxigenic strain was isolated from a hip aspirate. The child had no toxin related symptoms and had been fully vaccinated for age; this would not be regarded as a vaccine failure. In 2009 two cases of toxigenic diphtheria were isolted, the index case had acquired a tattoo in Samoa and the second case was a a household member ot the index case. There is no current data on the proportion of New Zealand adults susceptible to diphtheria.

The 1985 National Serum Survey found that 73 percent of five year olds, 65 percent of 10 year olds and 53 percent of 15 year olds had protective levels of diphtheria antibody. The decline apparent with age suggests that there is likely to be a large and increasing pool of adults susceptible to diphtheria in New Zealand. This was the reason for the introduction of adult tetanus diphtheria (Td) vaccination in 1994 and for the addition of adult tetanus/diphtheria boosters at 45 and 65 years in 2002.

Prevention: 
  • People with diphtheria should be excluded from school until recovery and had two negative throat swabs.
  • Local health officials should be notified when cases of diphtheria occur. Public health measures include isolation of the contagious person and contact tracing to identify additional people who may be infected or at risk of infection.
  • Pharyngeal culture and prophylactic erythromycin or benzathine penicillin for close contacts.
  • Child contacts of the contagious person should be excluded from school, early childhood services and community gatherings until they are known to be culture negative.
  • Adult contacts who are food handlers or who work with children should be excluded from work until known to be culture negative.

Immunisation remains the only well-established mode of disease prevention. Diphtheria vaccination has been widely offered since World War II, leading to virtual disappearance of the disease in many countries.

  • Active immunisation against diphtheria is recommended during convalescence because having the disease does not necessarily convey immunity.
  • Fully immunised children aged up to and including six years, who are contacts of the contagious person, and who have only received three doses of diphtheria toxoid-containing vaccine within the last five years: give one injection of DTaP-IPV.
  • Fully immunised contacts aged seven years and older who have not received a booster dose of a diphtheria toxoid-containing vaccine within the last five years: if aged 7–15 years, give one injection of Tdap; if aged over 15 years, give one injection of Td or Tdap, the latter is not funded.
Treatment: 

Diphtheria antitoxin is injected daily for 14 days for respiratory diphtheria. Sensitivity testing (skin or eye testing) should be conducted as only diphtheria antitoxin of equine origin is available.

Benzathine penicillin or erythromycin is used to eliminate the bacteria, reduce toxin production and decrease infectivity. Intravenous antibiotics are used until the person is able to swallow oral antibiotics comfortably. The use of antibiotics is in addition to daily antitoxin injections.

Additional treatment may include intravenous fluids, oxygen, bed rest, heart monitoring, use of a breathing tube, and correction of any blocked airways.

Disease Effects vs Vaccine Side Effects (Table)
Disease Description: 

Diphtheria is a rare but serious bacterial illness that usually causes infection of the throat and nose but can also cause skin infections.

Effects of disease: 
Throat swelling and difficulty breathing.
Sinusitis, otitis media (ear infection),pneumonia.
Heart muscle inflammation and failure.
Kidney damage and failure.
15-20% of cases develop delayed nerve complications e.g. peripheral neuritis.
5-10% of those infected die, even with treatment.
Common side effects of vaccine: 
Soreness/pain, redness and/or swelling around the injection site.
Fever over 38°C.
Decreased appetite, vomiting and/or diarrhoea.
Irritability, restlessness.
Unusual crying.
Fatigue.
Uncommon side effects of vaccine: 
Fever over 39°C.
Muscle or joint stiffness or pain.
Redness and/or swelling more than 6 cm in size around the injection site. In a small percentage of vaccine recipients the reactions will be severe enough to limit movement of the arm and may last for about a week.
Swelling involving the entire thigh or upper arm occurs in 2–3 percent of children after administration of the fourth and fifth doses of acellular pertussis vaccine. It resolves spontaneously without long term consequences.
Rare/very rare side effects of vaccine: 
Anaphylaxis.
Urticaria.
Idiopathic thrombocytopenic purpura.
Persistent (> 3 hours) inconsolable screaming.
Hypotonic, hyporesponsive episode (HHE) with 24 hours of immunisation.
Convulsion within 2 days of immunisation.
High fever over 40°C.
Extensive swelling or weakness of the vaccinated limb.
Inflammation of the nerve in the arm causing muscle weakness and pain (brachial neuritis) occurs within four weeks of immunisation, 1- 2 times per 200,000 doses.
Encephalopathy less than once in one million doses.

Hepatitis A

Common Name: 
Hep A
Parents & Caregivers
Introduction: 

Hepatitis is a viral disease that attacks the liver. There are several types of viral hepatitis, labelled A, B, C, D, and E. Hepatitis A is transferred through the faecal-oral route either by contact with contaminated food and water with an infected person. The illness is self-limiting and does not cause a chronic infection.

A brief history: 

The earliest outbreaks of hepatitis A infection were likely in the 17th and 18th centuries however it was not until 1908 that McDonald suggested the disease may be caused by a virus. The first scientific evidence of the hepatitis A virus was from studies done during World War II.

The current New Zealand situation: 

Cases of hepatitis A are reported in New Zealand across all age groups. The majority, but not all, cases report overseas travel during the disease incubation period.

Symptoms: 

Young children may not have any symptoms of infection. Those with symptoms may have fever, tiredness, nausea, loss of appetite and/or stomach pains. The urine/mimi/wee may become dark and faeces/tuutae/poo become pale coloured. They rarely have jaundice (yellow colour of the skin and eyes).

Older children and adults usually have symptoms of fever, tiredness, nausea, loss of appetite and/or stomach pains. The urine/mimi/wee may become dark coloured and  faeces/tuutae/poo become pale coloured. They are likely to develop jaundice.

How do you get it?: 

The hepatitis A virus is transmitted through the faecal (tuutae)/oral route by:

  • Poor hygiene
  • Close contact with an infected person
  • Contaminated food, water or milk
What are the risks?: 

Symptoms usually last for several weeks but less than two months. For 1–2 people in 10 the symptoms will last or come and go for up to six months.

It is rare for very severe liver problems to develop.

The risk of dying from complications related to a hepatitis A infection increases with advancing age and in those with pre-existing liver disease.

The hepatitis A virus does not cause a chronic infection.

Who is most at risk?: 
  • Children attending early childhood centres or play groups and members of their household.
  • People with developmental disabilities who attend residential and non-residential facilities and their carers.
  • Inmates of correctional facilities.
  • Men who have sex with men.
  • Injecting drug users.
  • People with chronic liver disease or who are at risk of developing chronic liver disease, e.g. people who are hepatitis B or hepatitis C positive, people who misuse alcohol.

Occupational groups exposed to faeces/tuutae, for example:

  • Employees of early childhood services
  • Health care workers, including cleaners, exposed to faeces
  • Sex industry workers
  • People who work with sewerage
  • Members of the armed forces
Treating the symptoms: 

There is no specific treatment for hepatitis A infection.

Contact your doctor for advice before using medication to relieve pain and/or fever.

Preventing Disease Spread: 
  • Thorough hand-washing using soap and water:
    • After using the toilet or changing nappies
    • Before and after preparing food
    • Before eating
  • Immunisation against hepatitis A.
Health Professionals
Causative organism: 

Hepatitis A is a single-stranded RNA virus in the Picornaviridae family.

Clinical signs, symptoms and complications: 
  • Incubation ranges from 15-50 days but averages 28-30 days.
  • Young children may not have any symptoms of infection. Those who do may have fever, tiredness, nausea, abdominal discomfort or pain, loss of appetite, dark coloured urine and pale coloured faeces or diarrhoea, runny nose, cough and joint pain. They rarely have jaundice.
  • Older children and adults usually have symptoms of fever, tiredness, nausea and loss of appetite, dark coloured urine and pale coloured faeces. They are likely to develop jaundice.
  • Elevated serum aminotransferase. Liver enzymes usually return to normal within six months of the illness
  • Although rare hepatitis A infection can cause fulminant hepatitis.
  • The risk of dying from complications related to a hepatitis A infection increases with advancing age and in those with pre-existing liver disease.
  • The hepatitis A virus does not cause a chronic infection.
Method of transmission: 

The hepatitis A virus is transmitted through the faecal-oral route by:

  • Poor hygiene
  • Close contact with an infected person, including sexual contact, sharing personal things like toothbrushes, face cloths and towels
  • Contaminated food, water or milk
Public health significance: 

Hepatitis A is notifiable on suspicion of the disease. Confirmation of disease is by a positive serum hepatitis A-specific IgM in the absence of recent vaccination.
Comprehensive information for identification and management of a suspected hepatitis A case and their contacts is provided in the Ministry of Health Communicable Disease Control Manual, 2012.
Administration of the hepatitis A vaccine to known contacts of hepatitis A cases has been shown to be effective in controlling outbreaks.

Normal human immunoglobulin (NHIG) may be considered for close contacts less than one year of age, where vaccination is contraindicated, the recipient is likely to have a reduced response to the vaccine or when the contact has high risk factors for severe disease.

When hepatitis A occurs at an early childhood centre all previously unimmunised staff and children at the service and those joining the centre during the six weeks after the last identified case, including identified cases in the households of attendees, may be advised to have vaccination and/or immunoglobulin if appropriate.

Prophylaxis may also be indicated when hepatitis A outbreaks occur in schools, residential care facilities and hospitals.

New Zealand epidemiology: 

Hepatitis A cases are reported in New Zealand. The majority, but not all, of cases report a history of overseas travel during the incubation period.

The number of cases reported each year between 2011 and mid-2013 has varied between 0.6 cases per 100,000 population in 2011, 1.6 cases/100,000 in 2012 and 1.0/100,000 population to mid-2013. The age range has been from toddler to older adult.

Prevention: 
  • Thorough hand-washing using soap and water:
    • After using the toilet or changing nappies
    • Before and after preparing food
    • Before eating
  • Cases are excluded from early childhood centres, school or work for one week after the start of symptoms or jaundice.
  • Vaccines are available to protect against hepatitis A.
    • Some vaccines only protect against hepatitis A, e.g. Avaxim® and Havrix® (adult and child vaccines).
    • Other vaccines combine hepatitis A protection with protection against hepatitis B, i.e. Twinrix®, or typhoid, i.e. Hepatyrix® and Vivaxim®.
    • All of the hepatitis A vaccines are available for purchase through general practice. The vaccine cost is based on whether the vaccine is for a child or adults or whether it protects against hepatitis A only or hepatitis A and another disease.  Extra practice fees for giving the vaccine may also apply.
Treatment: 

There is no specific treatment for hepatitis A infection.

Supportive care for symptom management can be provided.

Care should be taken when prescribing medicines that are metabolised by the liver for pain and/or fever.

Disease Effects vs Vaccine Side Effects (Table)
Disease Description: 

Hepatitis A is a viral infection that affects the liver. The virus does not cause chronic infection.

Effects of disease: 
Liver inflammation that can result in dark coloured urine/mimi/wee and pale coloured faeces/tuutae/poos.
Fever.
Nausea.
Loss of appetite.
Although rare hepatitis A infection can cause severe hepatitis.
The risk of dying from complications related to a hepatitis A infection increases with advancing age and in those with pre-existing liver disease.
Common side effects of vaccine: 
Discomfort/pain and/or redness at the injection site.
Fatigue.
Irritability.
Nausea, vomiting, loss of appetite.
Headache.
Fever.
Uncommon side effects of vaccine: 
Rash.
Rare/very rare side effects of vaccine: 
Pruritis (itching).
Urticaria (hives).
Anaphylaxis (severe allergic reaction).
Vaccines: 

Meningococcal disease

Parents & Caregivers
Introduction: 

Meningococcal disease is caused by the bacterium Neisseria meningitidis. At least 13 groups have been identified and of these groups A, B, C, Y and W-135 are the most likely to cause disease in humans.

Patterns of infection differ throughout the world. In New Zealand groups B and C are most likely to cause disease.

Humans are the only host of these bacteria.

A brief history: 

Although the first known epidemic of meningococcal disease was reported in 1661 the actual bacterium causing the disease was not identified until 1887 and the first publication about meningococcal meningitis not until 1905.

Although group A is the most common cause of meningococcal disease worldwide in New Zealand groups B and C are more likely to cause disease.

Vaccines that protect against meningococcal disease have been around since the 1970s but none protect against all groups that cause disease. Typically they protect against disease by groups A, C, W135 and Y because the group B meningococcus is the most effective at evading the human immune response to eliminate it.

New Zealand, Norway and Cuba have used specially manufactured vaccines against a single specific strain of meningococcal group B to slow and eventually stop epidemic levels of disease.

There are no vaccines currently available in New Zealand that protect against meningococcal group B. However, new vaccines are in the process of being licensed overseas.

The current New Zealand situation: 

In New Zealand most cases of meningococcal disease are caused by groups B and C. Disease caused by groups A, Y and W135 is infrequent.

The rate of meningococcal disease in 2011 was similar to the disease rates in the previous four years. Children less than five years who are Māori or Pacific people are over-represented in those who get meningococcal disease in New Zealand.

There have been isolated outbreaks of meningococcal groups A and C in New Zealand. The last group A outbreak was in 1985/86 in Auckland.

A New Zealand only strain of meningococcal group B bacterium caused an epidemic between 1991-2007. The epidemic mainly affected infants less than one year of age who were Māori or Pacific peoples and children aged one to four years who were of other ethnicity.

The most recent group C outbreak was in Northland during 2011.

Symptoms: 

Initial symptoms are difficult to distinguish between other viral, e.g. influenza, or bacterial infections. They usually start and progress quickly, often within 24 hours. However, infants tend to have a more gradual onset than adults.

Infants may:
Infants may have a fever, cry, appear unsettled, feed poorly, vomit, be sleepy or hard to wake, dislike bright light or have a rash or spots. They may have a bulging fontanelle.

Older children and adults may:
Have a fever, malaise, nausea, vomiting, muscle aches and pains, drowsiness, headache, dislike of bright light, neck stiffness or have a rash or spots.

Almost 80% of cases will develop a rash that does not blanch (become pale/go white) when pressed on. This type of rash is often a late sign of infection.

How do you get it?: 

Meningococcal bacteria are commonly carried in the nose and throat, and do not usually cause disease. The bacteria can be transferred from person to person through contact with saliva, e.g. intimate kissing. Saliva on shared drink bottles or pacifiers (dummies) may also have a limited role in passing the bacteria from one person to another. The bacteria may also be shared through droplets of saliva in the air from people coughing, sneezing or laughing.

What are the risks?: 

If meningococcal bacteria pass into the blood, disease usually progresses very quickly. A person with meningococcal disease may develop:

  • Meningitis (inflammation of the membranes around the brain).
  • Septicaemia (blood infection).
  • Pneumonia (lung inflammation).
  • One to two people out of every 10 who survive meningococcal disease have long term complications, e.g. extensive skin scarring, limb amputation, hearing loss, seizures or brain injury.
  • Even when the disease is identified and treated early, about one person out of every 10 will die.
Who is most at risk?: 

Infants, children less than five years of age and adolescents have an increased risk of meningococcal disease. Infants less than one year of age and children less than five years who are Māori or Pacific Peoples have the highest risk.

Being exposed to tobacco smoke, living in a crowded household or having another respiratory infection, e.g. influenza, can increase a person’s chances of carrying the bacteria.

Some groups are also at increased risk of infection: household and other close contacts of someone with the disease, e.g. those who have been intimate or shared food and beverages, infants and children attending day care or an early childhood education centre, and adolescents and young people at boarding school or living in hostels.

Some people with medical conditions that affect their immune system have an increased risk of infection, e.g. their spleen has been removed or doesn’t work properly, and those who are immune compromised from a disease or treatment of a disease.

It is not clear why some people are vulnerable to the bacteria passing into their blood leading to disease.

Treating the symptoms: 

Prompt diagnosis and early administration of injected antibiotic to patients suspected of having meningococcal infection and arranging for prompt admission to the hospital may help decrease mortality and morbidity.

Antibiotic treatment for 5–7 days is adequate therapy for most meningococcal illnesses.

Preventing Disease Spread: 

The risk of infection for household contacts of a person with the disease is highest during the first seven days and may persist for many weeks. Preventive antibiotics should be administered to close contacts as soon as possible, preferably within 24 hours of identification of the person with meningococcal disease.

During an outbreak a meningococcal immunisation programme may be commenced for those in the highest risk groups if a vaccine is available. High numbers of people immunised with a type of meningococcal vaccine called a conjugate vaccine can protect individuals and also reduce the spread of disease. This is because the conjugate vaccine reduces the number of people carrying N. meningitidis contributing to ‘herd immunity’ whilst protecting the individual from invasive disease.

Health Professionals
Causative organism: 

Neisseria meningitides is a gram-negative encapsulated, aerobic diplococcus bacterium. At least 13 serogroups have been identified and of these groups A, B, C, W135 and Y usually cause disease in humans. Different countries experience different rates of infection with each of the serogroups. In New Zealand groups B and C are most likely to cause disease.

Meningococci are further classified into types and subtypes, determined by the immunological reactivity to the PorA and PorB outer membrane proteins (OMPs) and the VR epitopes within the PorA and PorB proteins. For example the New Zealand specific meningococcal B strain that caused an epidemic between 1991-2007 was classified as (B:4:P1.7b,4).

N. meningitidis has a rapid ‘doubling time’ i.e. rapidly reproduces itself, and releases toxins, harmful porin proteins and DNA. These factors contribute to the severity of disease and rapid progression to cutaneous haemorrhage and skin necrosis, disseminated intravascular coagulation and shock.

Humans are the only host of these bacteria. The bacteria commonly colonise the nasopharynx and in most people carriage leads to immunity. However, in some people the bacteria invade the mucous membrane of the nasopharynx and cause non-invasive or invasive disease.

Clinical signs, symptoms and complications: 

he initial symptoms are difficult to distinguish from other infectious illnesses, e.g. influenza. Symptoms usually start and progress quickly, often within 24 hours. However, infants tend to have a more gradual onset than adults.

Infants

May have a fever, cry, appear unsettled, feed poorly, vomit, be sleepy or hard to wake, dislike bright light or have a rash or spots. They may have a bulging fontanelle.

Older children and adults

May have a fever, malaise, nausea, vomiting, muscle aches and pains, drowsiness, headache, dislike of bright light, neck stiffness or have a rash or spots.

Rash

Almost 80% of cases will develop a rash. The rash may begin as a blanching macula or maculopapular rash and progress to a haemorrhagic purpuric or petechial rash that does not blanch (become pale/go white) when pressed on.

Haemorrhagic rash is often a late sign of infection.

Method of transmission: 
  • Meningococcal bacteria are commonly carried in the nose and throat, and do not usually cause disease. The bacteria can be transferred from person to person through contact with saliva, e.g. intimate kissing.
  • The bacteria may also be shared through droplets of saliva in the air from people coughing, sneezing or laughing.
  • Saliva on shared drink bottles or pacifiers (dummies) may also have a limited role in passing the bacteria from one person to another.

 

Public health significance: 

Meningococcal disease is notifiable on suspicion of disease.

  • Infants, children less than five years of age and adolescents have an increased risk of meningococcal disease. Infants less than one year of age and children less than five years who are Māori or Pacific Peoples have the highest risk.
  • Being exposed to tobacco smoke, living in a crowded household or having another respiratory infection, e.g. influenza, can increase a person’s chances of carrying the bacteria.
  • Some groups are also at increased risk of infection: household and other close contacts of someone with the disease, e.g. those who have been intimate or shared food and beverages, infants and children attending day care or an early childhood education centre, and adolescents and young people at boarding school or living in hostels.
  • Some people with medical conditions that affect their immune system have an increased risk of infection, e.g. their spleen has been removed or doesn’t work properly, and those who are immune compromised from a disease or treatment of a disease.
  • It is not clear why some people are vulnerable to the bacteria passing into their blood leading to disease.
  • Health professionals in close contact with oropharyngeal secretions of patients with meningococcal disease, e.g. those performing mouth-to-mouth resuscitation or managing an endotracheal tube (placement and/or suctioning) prior to and during the first 24 hours of antibiotic treatment of the index case and microbiology laboratory workers are considered to be at increased risk of meningococcal disease.
Prevention: 

The risk of infection for household contacts of a person with the disease is highest during the first seven days and may persist for many weeks.

Preventive antibiotics should be administered to close contacts as soon as possible, preferably within 24 hours of identification of the person with meningococcal disease but can be commenced up to 14 days after the contact.

  • The recommended antibiotics for close contacts of the index case are rifampicin, ceftriaxone and ciprofloxacin. These antibiotics have been shown to eradicate nasopharyngeal N. meningitidis colonisation.
  • Antibiotic prophylaxis is not routinely recommended for health professionals.

Close contacts are also advised to be immunised with a meningococcal conjugate vaccine. A quadrivalent meningococcal A,C,Y,W-135 conjugate vaccine is now available in New Zealand.

During an outbreak a meningococcal immunisation programme may be commenced for those in the highest risk groups if a vaccine is available. High numbers of people immunised with a meningococcal conjugate vaccine can protect individuals and also reduce the spread of disease. This is because the conjugate vaccine reduces the number of people carrying N. meningitidis contributing to ‘herd immunity’ whilst protecting the individual from invasive disease.

Treatment: 

A Cochrane review in 2008 found that the evidence from case control studies suggested that early diagnosis, early admission to hospital (within three hours) and early instigation of supportive measures, including fluid therapy, are as important as the early commencement of antibiotics.

Prompt diagnosis and early administration of injected antibiotic to patients suspected of having meningococcal infection and arranging for prompt admission to the hospital may help decrease mortality and morbidity.

  • Penicillin or a broader spectrum antibiotic e.g. cefotaxime or ceftriaxone should be administered intravenously or intramuscularly on suspicion of meningococcal disease before the person is transferred to hospital.
    • General practitioners need not be concerned that empiric penicillin will obscure the diagnosis for hospital clinicians.
  • Antibiotic treatment for 5–7 days is adequate therapy for most systemic meningococcal illnesses.
Disease Effects vs Vaccine Side Effects (Table)
Disease Description: 

Meningococcal disease is caused by the bacterium Neisseria meningitidis and can cause meningitis, septicaemia, long term complications or death.

Effects of disease: 
Meningitis (inflammation of the membranes around the brain).
Septicaemia (blood infection).
Pneumonia (lung inflammation).
Long term complications e.g. extensive skin scarring, limb amputation, hearing loss, seizures or brain injury.
Even when the disease is identified and treated quickly, about one person out of every 10 will die.
Common side effects of vaccine: 
Soreness/pain, redness, and/or swelling around the injection site.
Mild fever.
Decreased appetite, nausea, vomiting or diarrhoea.
Irritability.
Headache.
Fatigue, malaise, drowsiness.
Uncommon side effects of vaccine: 
Dizziness.
Rare/very rare side effects of vaccine: 
Anaphylaxis.
Urticaria.

Poliomyelitis

Common Name: 
Polio
Parents & Caregivers
Introduction: 

Poliomyelitis is a highly contagious viral disease caused by three types of poliovirus (types 1, 2 and 3).  Prior to the development of polio vaccines nearly every person became infected, with the highest disease rate being in infants and young children. Infection can result in irreversible paralysis, usually of the leg muscles but for 5-10% of acute flaccid paralysis cases the breathing muscles are paralysed and the person may die.

The World Health Organization is a partner in the Global Polio Eradication Initiative with Rotary International, the United States Centers for Disease Control and Prevention and UNICEF.  The goal of the Initiative is to reach every last child with polio vaccine and ensure a polio-free world for future generations. Since 1988 polio case numbers have reduced by 99%.

There are just four countries in the world that have (endemic) polio Afghanistan, India, Nigeria and Pakistan. Polio can travel from these four countries to any other “polio free” country in the world and infect people who have not had the disease or been immunised. In 2009-2010, 23 previously polio-free countries were re-infected due to imports of the virus.

Humans are the only host for polioviruses. Polio can be eradicated through immunisation. If every person is immune the polioviruses have no one to infect and will die out. Type 2 wild poliovirus was eradicated in 1999.

A brief history: 

Poliomyelitis was recorded on an Egyptian stele as far back as 1580-1350BC, in the image of a man with flaccid paralysis of a leg. It was described later by Michael Underwood in 1789. Epidemics and major outbreaks occurred over the 19th century.

A weakened (attenuated) live oral polio vaccine is used by the World Health Organization’s Expanded Programme on Immunization. There is a small risk that the weakened poliovirus in the vaccine can cause vaccine associated paralytic poliomyelitis (VAPP) in someone who is not immune to polio and is exposed to the vaccine virus.

An inactivated poliomyelitis vaccine, licensed for use in the US in the mid-90s, it is primarily used in countries that have eradicated polio. There is no risk of VAPP from the inactivated polio vaccine.
New Zealand started immunising against polio in 1961 using the oral polio vaccine. The inactivated polio vaccine was introduced in 2002 to reduce the risk of VAPP.

The current New Zealand situation: 

Until polio is eradicated worldwide there remains a risk of polio returning to “polio free countries”, including New Zealand.

Since 1962 there have been seven cases of polio reported in New Zealand, the most recent was in 1998. Four cases were laboratory confirmed as vaccine associated and two were classified as probably vaccine related, before New Zealand changed from the oral polio vaccine to the inactviated polio vaccine in 2002. One case was wild polio (not vaccine related), acquired in Tonga and imported into New Zealand.

Symptoms: 

The majority of cases (approximately 95 in 100) have no symptoms.

  • Between 4-8 in 100 cases have symptoms of a minor non-specific illness including a low grade fever, fatigue, headache, vomiting, neck stiffness, sore throat and/or muscle pain.
  • In about 1-5 in 100 cases the person develops aseptic meningitis a few days after they have recovered from their non-specific illness. They usually recover fully.
  • Up to 2 in 100 cases have a rapid onset of acute flaccid paralysis without normal reflexes in the affected areas.
How do you get it?: 

Humans are the only host for polioviruses. People infected with a poliovirus excrete the virus in their saliva and faeces whether they have symptoms of the disease or not. Poor hygiene then spreads the virus to others.

Polioviruses are passed from person-to-person through the oral-faecal or oral-oral route. Occasionally the viruses may be passed on through contaminated water, milk or food.

The incubation period is usually 3-6 days in a person with no symptoms or for a person to develop non-specific symptoms.  The incubation period between exposure and development of paralytic disease is usually 7-21 days but could be as short as 3 days or as long as 35 days.

What are the risks?: 

Most people fully recover from polio.

The complications from polio depend on what part or parts of the body have been affected by the poliovirus.
People may experience permanent muscle weakness or paralysis, difficulty passing urine and urinary tract infections, uneven limb growth (the affected leg does not grow and the unaffected leg continues to grow normally), bone deformities, heart problems, breathing problems, cranial nerve damage, brain damage and death.

People who have had polio may experience significant muscle pain and weakness 15-40 years after recovering from polio. This is called post-polio syndrome. It is thought to be related to the aging of muscles and nerves that are compensating for the original damage. The person does not have the disease again.

Who is most at risk?: 

In countries where polio remains endemic infection is more common in children less than 5 years of age. When most children have acquired protection against all three types of polio by 5 years of age and therefore are protected as they grow into adulthood the risk of acute flaccid paralysis is highest in children less than 3 years of age.

In countries that are polio free people who have not had polio or been immunised against polio are at risk of getting polio when it is imported/introduced into the country b y a traveller. In this situation adults are more likely to develop acute flaccid paralysis than children. In 1993 the Netherlands experienced a polio outbreak in a community who had chosen not to immunise against polio.

Treating the symptoms: 

Polio is incurable.

During the acute illness only supportive care can be provided to reduce complications associated with paralysis.

After the person has recovered rehabilitation can prevent or reduce post-polio deformities and increase independence.

Preventing Disease Spread: 

Polio can only be prevented through immunisation.

Household contacts of a person with polio are usually infected before the polio has been diagnosed in the first case so isolation of the person with polio in the home environment after diagnosis is not useful.

Health Professionals
Causative organism: 

Polioviruses are enteroviruses and belong to the family Picornaviridae. There are three antigenic types (serotypes 1, 2 and 3).

Type 1 appears to be the most neurovirulent of the three serotypes. Most cases are caused by type 1. Type 2 was eradicted in 1999.

The viruses are resistant to inactivation by many common detergents and disinfectants, including soaps, non-ionic detergents and lipid solvents such as ethanol, ether, and chloroform. They are rapidly inactivated by 0.3% formaldehyde or 0.5 ppm free residual chlorine, by desiccation, low humidity or by exposure to ultraviolet light.

Clinical signs, symptoms and complications: 

The incubation period is usually 3-6 days in a person with no symptoms or for a person to develop non-specific symptoms. The incubation period between exposure and development of paralytic disease is usually 7-21 days but could be as short as 3 days or as long as 35 days.

After infection the poliovirus initially incubates in the gastrointestinal tract. Polio has four possible presentations:

1. The majority of poliovirus infections (about 95%) are subclinical, inapparent infection without symptoms.

2. About 4-8% of cases only develop a minor non-specific illness. Symptoms may include low grade fever, fatigue, malaise, drowsiness, headache, vomiting, constipation, neck stiffness, sore throat and/or muscle pain.

3. About 1-5% of cases are nonparalytic poliomyelitis. Initial symptoms are non-specific (fever, malaise, vomiting, sore throat). One to two days later symptoms of meningeal irritation from aseptic meningitis develop. Recovery is usually complete however nonparalytic poliomyelitis can progress to the paralytic form of the disease.

4. Between 0.1-2% of cases are paralytic poliomyelitis. The paralytic form of the disease occurs when the poliovirus spreads to the motor neurons of the anterior horn cells in the spinal cord (spinal poliomyelitis) and/or brain stem (bulbar paralysis). The cranial nerves may also be affected by polioviruses. The area paralysed depends on the anatomic location of the motor neuron damage. Although the motor neurons do not recover and are not replaced it is possible for other muscles to compensate for the paralysis, resulting in partial or complete recovery from paralytic poliomyelitis for some people.

In polio-free countries with pockets of non-immune/unimmunised communities adults are more likely to present with paralytic poliomyelitis. In countries with endemic polio children less than 3 years are more likely to develop paralytic polio.

The person initially experiences symptoms of a minor non-specific illness, becomes symptom free, then one to three day later develops fever with a rapid onset of descending acute flaccid paralysis. Adolescents and adults may not experience the minor illness symptoms but develop more severe pain in the affected extremities. The progression of paralysis usually stops once the fever abates. Paralysis is usually asymmetrical with reduced or absent deep tendon reflexes. The sensory nerves are not affected.
The diagnosis of paralytic poliomyelitis is based on the clinical course, isolation of poliovirus in two stool samples and the presence of a neurologic deficit 60 days after symptom onset. Neurologic deficit may be complete or partial flaccid paralysis or weakness.
The two stool samples must be taken at least 24 hours apart in the first 14 days after the onset of paralysis are required to diagnose paralytic poliomyelitis. The laboratory must be notified before sending the specimen. Isolation of the virus in stool samples is important to determine if the virus is wild-type or vaccine related.

The differential diagnoses for acute flaccid paralysis include infection by other enteroviruses, other viruses (e.g., Epstein-Barr virus, human immunodeficiency virus, mumps virus), campylobacter jejuni, hypokalaemia, antibiotic reaction (aminoglycosides, tetracyclines, polymixin B), chemical poisoning, cephalic tetanus, fungal-mycotoxins, wasp venom, Guillain-Barre Syndrome, Bell’s Palsy, transverse myelitis.

The complications from polio depend on the anatomic location of the motor neuron damage. People may experience permanent muscle weakness or paralysis, difficulty passing urine and urinary tract infections, uneven limb growth (the affected leg does not grow and the unaffected leg continues to grow normally), bone deformities, heart problems, breathing problems, cranial nerve damage, brain damage and death.

The fatality rate from poliomyelitis varies depending on the presentation. For paralytic spinal poliomyelitis 2-5% of child cases and 15-30% of adult cases may result in death. Up to 75% of cases with bulbar poliomyelitis will die.
People who are immunocompromised are more likely to experience complications and a fatal outcome from poliomyelitis.

Post-polio syndrome occurs 15-40 years after a person has recovered from paralytic poliomyelitis. It is characterised by exacerbation of existing weakness, development of new weakness or paralysis and/or increased muscle pain. Increasing length of time since the acute infection, presence of residual impairment form the acute illness and being female are risk factors for post-polio syndrome. The pathogenesis of post-polio syndrome does not involve ongoing or recurrent poliovirus infection. It is thought to be related to the aging of muscles and nerves that are compensating for the original damage.

Method of transmission: 

Humans are the only host for polioviruses.

Polioviruses are transmitted person to person via the oral-faecal or oral-oral route. They have occasionally been transmitted through contaminated water, milk or food.
All infected people shed the virus in their stool, including those with subclinical/inapparent infection.
The person is most infectious immediately before to 1-2 weeks after the onset of symptoms. However the virus is excreted in saliva for approximately two weeks and in faeces for three to six weeks and sometimes longer.

People who are immunocompromised may excrete the virus for years (chronic excretor).

Public health significance: 

All cases of acute flaccid paralysis in New Zealand must be investigated as suspected poliomyelitis and notified to the Medical Officer of Health immediately.

Acute flaccid paralysis in persons aged less than 15 years should also be reported to the New Zealand Paediatric Surveillance Unit (NZPSU) based at the University of Otago. The NZPSU will send case investigation and follow up forms to clinicians, continue to monitor that New Zealand has eradicated polio and provide information to the World Health Organization.

Any confirmed case of poliomyelitis in New Zealand constitutes a Public Health Emergency of International Concern (PHEIC). The Director of Public Health at the Ministry of Health should be contacted urgently. The New Zealand National Poliomyelitis Response Plan outlines the actual response and is published on the Ministry of Health website. (http://www.health.govt.nz).

The infection rate of non-immune household or institutional contacts is as high as 90-100%.
Both a live oral polio vaccine (OPV) and an inactive polio vaccine (IPV) are effective at preventing disease from polioviruses because inhibition of poliovirus replication in and dissemination from the gastrointestinal tract (OPV) and/or inhibiting viraemia (IPV) following infection prevents disease.

As humans are the only host polioviruses can be eradicated through immunisation. In developed countries with high sanitation and hygiene standards immunisation coverage of 66-80% can prevent outbreaks of polio. In developing countries with lower sanitation and hygiene standards immunisation coverage needs to be much higher with 94-97% of the population having completed a primary course of three doses of polio vaccine.

Until polio is eradicated worldwide there remains a risk of polio returning to “polio free countries”, including New Zealand.

New Zealand epidemiology: 

Polio became a notifiable disease in New Zealand in 1908. Since then epidemics (about 1000 cases) were recorded in 1916, 1925, 1937, 1948/49, 1952/53 and 1955/56. Use of the Salk inactivated polio vaccine began in 1956 for older children and extended to all those aged 6 months to 29 years in 1956. The use of this vaccine delayed the next polio epidemic to 1961.

The Sabin oral vaccine was introduced to New Zealand in 1961 for children less than 12 months of age. Its use was extended to school aged children, and all adolescents and adults in 1962. There have not been any cases of locally acquired wild-type polio in New Zealand since 1962.

Since 1962 there have been seven cases of polio reported in New Zealand, the most recent was in 1998. Four cases were laboratory confirmed as vaccine associated (two vaccine recipients and two unimmunised contacts of vaccine recipients). Two were classified as probably vaccine related. In 1976 an infant was diagnosed with wild-type polio acquired in Tonga and imported into New Zealand.

New Zealand changed from using the live oral polio vaccine to the inactivated injectable polio vaccines in 2002.

Until polio is eradicated worldwide there remains a risk of polio returning to “polio free countries”, including New Zealand.

Prevention: 

High standards of public sanitation and hygiene will contribute to reducing the spread of poliovirus.

Immunisation is the only way to prevent the disease.

The inactivated polio vaccine (IPV) is used in New Zealand to provide individual protection and herd immunity against polio without the risk of vaccine associated paralytic poliomyelitis (VAPP) that is associated with use of the live oral polio vaccine. IPV can also be safely administered to people who are immunocompromised and close contacts of people who are immunocompromised.

A combination of oral and inactive injected polio vaccines are acceptable to provide a primary course and booster dose of polio vaccines.

Occupational vaccination and travel:
There is no evidence that routine IPV boosters are required however they are currently recommended to reduce any possible risk form waning immunity when there is an increased risk of exposure to poliovirus.

If more than 10 years has elapsed since completing a primary course of three polio containing vaccines or polio containing booster vaccine a booster dose of IPV is recommended (but not funded) for:

  • Travellers to countries where poliomyelitis remains endemic.
  • Individuals at particular risk of exposure (e.g., sewerage workers, laboratory workers routinely handling faecal specimens which may contain wild or vaccine-derived polioviruses).
  • Healthcare workers in direct contact with a case of poliomyelitis.
Treatment: 

Polio is incurable.

During the acute illness only supportive care can be provided to reduce complications associated with paralysis.

After the person has recovered physical rehabilitation can prevent or reduce post-polio deformities and increase independence.

 

Disease Effects vs Vaccine Side Effects (Table)
Disease Description: 

Poliomyelitis is a highly contagious viral disease caused by three types of poliovirus (types 1, 2 and 3).

 

 

 

Effects of disease: 
The majority of cases (approximately 95 in 100) have no symptoms.
Between 4-8 in 100 cases have symptoms of a minor non-specific illness including a low grade fever, fatigue, headache, vomiting, neck stiffness, sore throat and/or muscle pain.
In about 1-5 in 100 cases the person develops aseptic meningitis a few days after they have recovered from their non-specific illness.
The majority of people fully recover from polio.
Up to 2 in 100 cases have a rapid onset of acute flaccid paralysis without normal reflexes in the affected areas.
The complications from polio depend on what part or parts of the body have been affected by the poliovirus.
People may experience permanent muscle weakness or paralysis, difficulty passing urine and urinary tract infections, uneven limb growth (the affected leg does not grow and the unaffected leg continues to grow normally), bone deformities, heart problems, breathing problems, cranial nerve damage, brain damage and death.
People who have had polio may experience significant muscle pain and weakness 15-40 years after recovering from polio. This is called post-polio syndrome.
Common side effects of vaccine: 
Soreness/pain, redness and/or swelling around the injection site.
Fever over 38°C.
Decreased appetite, vomiting and/or diarrhoea.
Irritability, restlessness.
Unusual crying.
Fatigue.
Uncommon side effects of vaccine: 
Fever over 39.5°C.
Induration (area of hard inflammation).
Swelling involving the entire thigh or upper arm occurs in 2–3 percent of children after administration of the fourth and fifth doses of acellular pertussis vaccine. It resolves spontaneously without long term consequences.
Rare/very rare side effects of vaccine: 
Anaphylaxis.
Urticaria.
Idiopathic thrombocytopenic purpura.
Persistent (> 3 hours) inconsolable screaming.
Hypotonic, hyporesponsive episode (HHE) with 24 hours of immunisation.
Convulsion within 2 days of immunisation.
Inflammation of the nerve in the arm causing muscle weakness and pain (brachial neuritis) occurs within four weeks of immunisation, 1- 2 times per 200,000 doses
Encephalopathy less than once in one million doses.

Mumps

Parents & Caregivers
Introduction: 

Mumps is a viral illness. It is often recognised by swelling and tenderness of one or more parotid (salivary) glands although some people with mumps have no symptoms and others may only have symptoms in other organs e.g., meningitis or one or both testicles inflamed.

A brief history: 

Mumps was first recognised in the fifth century BC by Hippocrates. Mumps was described as an illness accompanied by swelling of the ear and painful enlargement of the testes, either unilaterally or bilaterally. It was not recognised as an infectious disease until the 19th century. The first safe and immunogenic attenuated mumps virus vaccine became available in 1967. The origin of the word mumps is obscure but may be related to the old English verb, which means ‘grimace, grin, or mumble.’

In the years before the introduction of mumps vaccine the disease was most commonly reported among young school-age children.

The current New Zealand situation: 

The last mumps epidemic was in 1994, when there were 188 hospitalisations. However, mumps cases are still occurring in New Zealand.

Symptoms: 

Most children under two years of age have no symptoms when they get mumps. Those who get mumps as adults are more likely to experience severe disease.

When symptoms are present they usually include fever, headache, malaise, muscle aches, poor appetite, swelling, and tenderness of one or more salivary glands (just below the ear lobe).

However, some people may have no involvement of salivary glands and have symptoms from other organ involvement.

On average fever usually lasts 1-6 days, but salivary gland swelling can last for 10 days or longer.

It usually takes between 6-18 days from exposure to the first symptom but could also range from 12-25 days.

How do you get it?: 

Mumps is spread by infected droplets in the air from breathing, coughing and sneezing, and also by direct contact with infected saliva.

A person with mumps may be infectious from seven days before the salivary glands swell until nine days after. The most infectious period is between two days before illness and four days afterwards. People without symptoms are also infectious.

What are the risks?: 

Adults are more likely to experience severe mumps disease.

Viral meningitis occurs in up to 15% of mumps cases (almost always without long term consequences),
Temporary deafness to high frequency sounds is more common, occurring in 4 in 100 cases.
Orchitis (inflamed testicle), usually one sided, occurs in 20-25% of post-pubertal males. Oophoritis (inflamed ovary) occurs in 5% of post-pubertal females. Sterility occurs rarely.
Encephalitis (brain inflammation) occurs in 1 in 6,000 cases, and 1 in 100 of those with encephalitis die.
Profound and permanent deafness, usually on one side, occurs in 1 in 15,000 cases.
Overall the case fatality rate from mumps is about 1.8 per 10,000 cases.
Pancreatitis, neuritis, arthritis, mastitis, nephritis, thyroiditis and pericarditis may also occur.
Mumps in the first trimester of pregnancy may increase the rate of miscarriage, but there is no evidence that it causes fetal abnormalities.

Who is most at risk?: 

Unvaccinated adolescents and adults are most at risk.

Pregnant women who get mumps during the first 3 months of pregnancy have an increased risk of miscarriage.

Treating the symptoms: 

There is no treatment for the mumps infection. Treatment of symptoms is aimed at improving comfort.

Preventing Disease Spread: 

Immunisation given on time is the best method of preventing mumps. The measles, mumps, rubella vaccine (MMR) is given as part of the standard immunisation schedule at 15 months and 4-5 years of age. In New Zealand there is no single mumps vaccine available.

People with mumps are excluded from early childhood education, school and work until nine days after the appearance of swollen salivary glands.
Contacts of mumps cases, who are not immune to mumps e.g., those who are unimmunised, are excluded from early childhood education, school and work until 26 days after the appearance of swollen glands in the last case they were in contact with.

Health Professionals
Causative organism: 

Mumps virus is a member of the genus Rubulavirus in the family Paramyxoviridae.

Humans are the only known natural hosts.

Clinical signs, symptoms and complications: 

The diagnosis of mumps is usually made on the presence parotitis. However, infection from other viruses e.g., coxsackieviruses and Epstein–Barr virus, can infrequently cause parotitis.

Method of transmission: 

Mumps is spread by infected droplets in the air from breathing, coughing and sneezing, and also by direct contact with infected saliva. Viraemia leads to organ involvement including the kidneys, meninges, joints and particularly the parotid (salivary) glands or respiratory tract involvement.

Public health significance: 

Mumps is notifiable to the Medical Officer of Health immediately on suspicion of the disease.

New Zealand epidemiology: 

The last mumps epidemic was in 1994, when there were 188 hospitalisations. However, mumps cases are still occurring in New Zealand. In 2010 41 cases of mumps were notified and of these 16 were laboratory confirmed. Most cases occurred in children aged 15 months-3 years and those over 20 years. One person was hospitalised and no one died.

Prevention: 

Some infants may have passive immunity from transplacental transfer of maternal mumps antibodies during the later weeks of pregnancy. This passive protection dependent on maternal immunity to mumps and wanes by 6-12 months of age in most infants.

Treatment: 

There is no treatment for the mumps infection. Treatment is symptomatic and aimed at improving comfort.

Disease Effects vs Vaccine Side Effects (Table)
Disease Description: 

A highly contagious viral infection spread by droplets in the air and saliva. It is typically recognised by fever and swollen, tender salivary glands.

Effects of disease: 
Adults are more likely to experience severe mumps disease.
Fever, headache, and swelling and tenderness of one or more parotid (salivary) glands.
Viral meningitis: Up to 15 in 100, usually followed by full recovery.
Temporary deafness to high frequency sounds is more common, occurring in 4 in 100 cases.
Orchitis (inflammation of the testicle): 20-25 in 100 post pubertal males, usually only one testicle is affected. Sterility occurs rarely.
Oophoritis (inflammation of the ovaries): 5 in 100 post pubertal females.
Encephalitis: 1 in 6000, and 1 in 100 of those with encephalitis die.
Profound and permanent deafness, usually on one side, occurs in 1 in 15,000 cases.
Overall case fatality rate of 1.8 in 100,000.
Pancreatitis, neuritis, arthritis, mastitis, nephritis, thyroiditis and pericarditis may also occur.
Mumps contracted during the first trimester of pregnancy increases the risk of miscarriage. There is no evidence it causes fetal abnormalities.
Common side effects of vaccine: 
Measles component:
Fever over 39.5˚C and/or rash 6–12 days after immunisation.
Mumps component:
Parotid and/or submaxillary swelling 10–14 days after immunisation.
Rubella component:
Mild rash, fever and/or lymphadenopathy between two and four weeks after immunisation.
Joint symptoms may occur after the vaccine, the incidence of which is age related. More adult women than children get joint symptoms about two to four weeks after immunisation.
Rare/very rare side effects of vaccine: 
Anaphylaxis.
Temporary thrombocytopenia.
Encephalitis occurs once in one million doses. There may be some long-term effects from this.
Aseptic mumps meningitis.
Convulsion associated with fever.
Vaccines: 

Rubella

Common Name: 
German measles
Parents & Caregivers
Introduction: 

Rubella, also known as German measles, is caused by a virus. It is usually a mild disease, but when it occurs in pregnant women during pregnancy it can result in severe damage to the developing baby.

A brief history: 

The number of rubella cases has fallen dramatically since the vaccine became available in 1970. Prior to this, extensive outbreaks of rubella occurred every 6-9 years. The last such outbreak started in Europe in 1962/1963 and spread to the USA and other countries including New Zealand in 1964/1965 causing many cases of Congenital Rubella Syndrome.

The current New Zealand situation: 

Outbreaks of rubella continue to occur both in New Zealand and in nearby Pacific Island countries.

Symptoms: 

Rubella infection without symptoms is common. When symptoms are present they include a brief widespread rash, swollen lymph glands and painful joints, the latter mainly occurring in adults.

The rubella rash looks similar to other rashes and the only way to diagnose rubella is by a blood test.

How do you get it?: 

Rubella is spread from person to person by airborne respiratory secretions (coughing and sneezing). The incubation period varies from 14 to 23 days. Infants with Congenital Rubella Syndrome should be considered infectious until they are one year old.

What are the risks?: 

Rubella is usually a mild disease in children. Adults tend to have more complications, including temporary painful or swollen joints. Rubella may also occasionally present as a more severe illness, indistinguishable from measles.

  • About 5 in 10 cases of rubella develop a rash and painful swollen glands.
  • Nearly 5 in 10 adolescents and adults have painful joints (temporary).
  • Encephalitis (inflammation of the brain) occurs in 1 out of 6,000 cases.

Rubella is of serious concern if contracted in the early stages of pregnancy, as it is highly likely to cause severe abnormalities in the developing baby. These include cataracts, deafness, heart abnormalities, mental retardation and behavioural problems. These abnormalities are referred to as Congenital Rubella Syndrome.

Who is most at risk?: 
  • The unborn baby is most at risk.
  • Those without a prior history of rubella immunisation or confirmed rubella disease and women born in New Zealand between 1965 and 1967 are at an increased risk.
  • Immigrant women of child bearing age who have not received rubella or MMR (measles, mumps, rubella) vaccine are also at risk.
Treating the symptoms: 

There is no specific treatment for infection.

Preventing Disease Spread: 

Rubella vaccine, as part of the MMR (measles, mumps, rubella) vaccine is the best method of prevention.

Cases of rubella must be kept away from early childhood services or school for 7 days after the rash appears.

Health Professionals
Causative organism: 

The rubella virus is from the togavirus family. It is easily killed by heat and UV light.

Clinical signs, symptoms and complications: 

Symptoms may be absent or mild and in 30%-50% of cases.

Usually a mild disease in children. Adults tend to have more complications.

  • A discrete macular rash appears on the forehead about 7 days following infection and spreads down the trunk and limbs.
  • Mild conjunctivitis, cervical lymphadenopathy and arthralgia may occur.
  • Small petechial lesions (Focheimer spots) may be seen on the palate.
  • Splenomegaly may occur.

The most serious complication of rubella infection is Congenital Rubella Syndrome (CRS), which results when the rubella virus attacks a developing fetus. When infection occurs during the first trimester of pregnancy up to 85% of infants will be born with some type of birth defect, including deafness, eye defects, heart defects, mental retardation and more.

The risk of damage reduces to 10-20% by about 16 weeks gestation and has rarely been reported when infection occurred after 16 weeks gestation.

The rubella rash looks similar to other rashes. The only way to diagnose rubella is by a blood test.

Method of transmission: 

Spread is from person to person through the air (by coughing, sneezing) and is moderately contagious.
The incubation period varies from 14 to 23 days.
The disease is most contagious when the rash is erupting, but the virus can be spread from seven days before, to seven days after the rash appears.

Public health significance: 

German physicians first described rubella; hence, it is commonly known as German measles.

In 1941 an ophthalmologist reported a link between maternal rubella and congenital cataracts. A pandemic of rubella in 1964 led to recognition of an expanded congenital rubella syndrome (CRS), which includes hepatitis, splenomegaly, encephalitis, mental retardation as well as the more familiar association with deafness, cataracts and heart disease.

Rubella has a very similar pattern to measles, epidemiologically. It has respiratory spread that is greater in crowded societies, and periodically may disappear from a geographic area only to reappear in epidemic form.

The seriousness of CRS can be seen when reviewing the latest major American epidemic in 1964-65. There were 30,000 pregnancies affected out of 12.5 million rubella cases, including 2,000 cases of encephalitis. Of these pregnancies, 5000 women had surgical abortions, over 6000 women had spontaneous abortions and among the 20,000 infants who survived pregnancy, 11,600 were deaf, 3,580 were blind and 1,800 with mental retardation.

Not every country can offer free rubella immunisation and regional epidemics do occur periodically. In 2003 there were large epidemics in several Pacific Island nations.

New Zealand epidemiology: 

Outbreaks of rubella continue to occur in New Zealand. Although rubella immunisation was offered from 1979 to all girls in year 7 (form 1), it was not offered to boys until 1992, allowing spread in the community. There were 100 cases 232 reported between August 1989 and February 1990, some among pregnant women, and there were three cases of CRS reported. The outbreaks of rubella in 1993 and a larger one in 1995 have mostly involved young adult males, who would not have been offered immunisation. These outbreaks emphasise the need to immunise both boys and girls to reduce the risk of exposure in pregnant women, as well as to reduce illness in men. Rubella has been a notifiable disease since 1996. In 2003 there were 26 cases of rubella notified, of which three cases were laboratory confirmed; and in 2004 there were 25 cases notified, of which three were laboratory confirmed. It is important that suspected cases are notified and are laboratory confirmed so that public health control programmes can limit spread. No cases of CRS in New Zealand newborns reported to the New Zealand Paediatric Surveillance Unit between 1998 and 2010. 

Prevention: 

Respiratory diseases are difficult to control in large populations. People who are infectious with rubella should always avoid coming into contact with pregnant women.

Post-exposure prophylaxis with immunoglobulin and vaccination in pregnant women has not been established as effective and is not recommended.

The major prevention method is by national immunisation programmes.
MMR (measles, mumps, rubella) vaccines are widely available and recommended by the World Health Organization.

Disease Effects vs Vaccine Side Effects (Table)
Disease Description: 

Rubella is a viral disease that causes a rash and swollen glands. It causes severe damage to unborn babies if acquired during pregnancy.

Effects of disease: 
About 5 in 10 cases of rubella develop a rash and painful swollen glands.
Nearly 5 in 10 adolescents and adults have painful joints (temporary).
About 1 in 6,000 develops inflammation of the brain.
For women in early pregnancy, 85% of babies infected during the first eight weeks after conception will have a major congenital abnormality such as deafness, blindness, brain damage, or a heart defect. This risk decreases to 10-20% by about 16 weeks gestation. After 16 weeks fetal abnormalities are rare.
Common side effects of vaccine: 
Measles component:
Fever over 39.5˚C and/or rash 6–12 days after immunisation.
Mumps component:
Parotid and/or submaxillary swelling 10–14 days after immunisation.
Rubella component:
Mild rash, fever and/or lymphadenopathy between two and four weeks after immunisation.
Joint symptoms may occur after the vaccine, the incidence of which is age related. More adult women than children get joint symptoms about two to four weeks after immunisation.
Rare/very rare side effects of vaccine: 
Anaphylaxis.
Temporary thrombocytopenia.
Encephalitis occurs once in one million doses. There may be some long-term effects from this.
Aseptic mumps meningitis.
Convulsion associated with fever.
Vaccines: 

Pertussis

Common Name: 
Whooping cough
Parents & Caregivers
Introduction: 

Pertussis, commonly known as whooping cough, is a highly infectious bacterial infection spread by coughing and sneezing. It causes severe bouts of coughing, which may be accompanied by vomiting and a whooping sound. Pertussis can last up to 3 months and is sometimes referred to as the ‘100 day cough.’ The symptoms are more obvious in children, because infants and adults are less likely to ‘whoop.’

The current New Zealand situation: 

New Zealand has epidemics every 3-5 years with several thousand cases (mostly young children) reported in each epidemic. Older adolescents and adult pertussis often goes unrecognised and is often under reported. Up to a third of adolescents and young adults with a persistent cough have evidence of recent pertussis infection.

Symptoms: 

Pertussis can be divided into three stages:

The initial stage, following the incubation stage, is called the catarrhal stage is the most infectious. It lasts 7-10 days and can include a runny nose, sneezing, slight fever, and a mild irritating cough.

The second stage or paroxysmal stage usually lasts 2-4 weeks, but can persist for up to 10 weeks. A paroxysm is a spasm of coughing followed by a big breath in or high pitched whoop in children. Infants and adults generally do not have the characteristic 'whoop' sound. Infants and young children often appear very ill, and may turn blue and vomit with coughing bouts.

The convalescent stage may last for months. Although the cough eventually disappears after several weeks, coughing fits may recur whenever the patient suffers any subsequent respiratory infection.

 

How do you get it?: 

Pertussis is highly contagious and is spread by coughing and sneezing. It infects around 90% of non-immune household contacts and 50 to 80% of non-immune school contacts. Many babies catch it from their older siblings or parents - often before they are old enough to be fully vaccinated.

What are the risks?: 

Around five in 10 babies who catch pertussis before the age of 12 months require hospitalisation and 1-2 in 100 of those hospitalised die from pertussis infection. Severe coughing can temporarily stop the oxygen supply to the brain (hypoxia). In around two in 1000 children pertussis leads to permanent brain damage, paralysis, deafness or blindness. Secondary infections such as pneumonia and ear infections can occur.

The disease is usually milder in adolescents and adults, consisting of a persistent cough similar to that found in other upper respiratory infections, although some adults will collapse or experience a rib fracture from violent coughing. Both hospitalisations and deaths are likely to be under-estimated in adults due to the lack of the ‘whooping’ sound.

Who is most at risk?: 

Those most at risk of serious disease are infants under 12 months of age. Infants who do not receive doses of pertussis containing vaccine at the scheduled times of 6 weeks, 3 months, and 5 months have up to a five-fold increased risk of being hospitalised with pertussis.

Preventing Disease Spread: 

On-time immunisations for infants at 6 weeks, 3 months and 5 months in addition to children receiving boosters at four years and 11 years is the best prevention.

If a pregnant woman has high levels of circulating protection against whooping cough during the last weeks of pregnancy some of this will pass through the placenta and may protect the newborn from severe whooping cough for up to six weeks after delivery. Pregnant women can safely receive a whooping cough booster immunisation from 20 weeks of pregnancy but preferably in the third trimester. The vaccine is free for women between 28-38 weeks of pregnancy through their Doctor.

Breastfeeding does not provide direct protection against whooping cough.

Antibiotics do not cure pertussis but are given to reduce the spread of infection to others.

All cases of pertussis should be excluded from early childhood services, school, or community gatherings until they are well enough to attend and have either received five days of antibiotics or three weeks have elapsed since the onset of coughing spasms.

 

Health Professionals
Causative organism: 

Pertussis is caused by a bacterium, Bordetella pertussis; a gram-negative bacillus, which colonises the upper respiratory tract. There are other organisms such as Bordetella parapertussis, Mycoplasma pneumoniae and Chlamydia pneumoniae, which can cause a pertussis-like illness.

Clinical signs, symptoms and complications: 

Pertussis disease can be divided into three stages:

Catarrhal stage

Can last 7-10 days and includes a runny nose, sneezing, low-grade fever, and a mild cough (all similar symptoms to the common cold).

 Paroxysmal stage

  • Usually lasts 1-6 weeks, but can persist for up to 10 weeks.
  • The characteristic symptom is a burst, or paroxysm, of numerous, rapid coughs.
  • At the end of the paroxysm the patient suffers from a long inhaling effort that is characterized by a high-pitched whoop.
  • Infants and young children often appear very ill and distressed, and may turn blue and vomit. Infants generally do not have the characteristic “whoop” sound.

Convalescent stage

  • May last for months.
  • Although the cough usually disappears after 2-3 weeks, paroxysms may recur whenever the patient suffers any subsequent respiratory infection.
  • Disease is more severe in infants and young children.
  • The cough may persist for up to 3 months and is often associated with vomiting.
  • Severe coughing may lead to brain hypoxia. In 1-3 per 1000 children, whooping cough leads to permanent brain damage, paralysis, deafness or blindness.

The disease is usually milder in adolescents and adults, consisting of a persistent cough similar to that found in other upper respiratory infections. However, these individuals are still able to transmit the disease to others, including unimmunised or incompletely immunised infants.

Pertussis immunity wanes over time; both following natural disease and vaccination (immunity lasts 4–10 years). Re-infection may present as a persistent cough, rather than typical pertussis.

 

Method of transmission: 

Pertussis is spread through the air by infectious droplets and is highly contagious infecting 90% of susceptible household contacts and 50 to 80% of susceptible school contacts. The incubation period is commonly 7-10 days, with an upper limit of 21 days. Many babies contract pertussis from their older siblings or parents.

Public health significance: 

Pertussis kills about 250,000 children worldwide each year. Many children are left with brain damage from pertussis infection. Pertussis is highly infectious and around 90% of non-immune household contacts will contract it.

Most countries have epidemics every three to five years.

Both hospitalisation and deaths from pertussis are likely to be underestimated as infants, particularly preterm, may either present without characteristic symptoms or be misclassified as sudden infant death syndrome.

It has been estimated that up to 20% of severe adult coughs 1-3 months untreated, could be caused by pertussis infection. These individuals are a significant reservoir of infection.

Some countries such as USA, Australia and Canada are now identifying higher rates of pertussis infection, especially in adolescents and adults. The cause of this is not yet fully explained however these countries are introducing pertussis boosters for adolescents.

Those most at risk are young babies. Around 50% of those who catch pertussis before the age of 12 months require hospitalisation. Children under 12 months who are ill enough to be admitted to hospital have a 1-2 in 100 chance of dying.

Currently available vaccines prevent disease much better than they prevent infection. They will not eradicate pertussis but in countries with very high immunisation coverage rates (>95%), the three to fiuve yearly epidemics affect fewer individuals and the resultant disease is less severe than in unvaccinated communities.

 

New Zealand epidemiology: 

The estimated pertussis case fatality rate in New Zealand for the period 1970 to 1992 was 0.4 percent. This is comparable to reported case fatality rates from the UK and the US over a similar period. There were no deaths from pertussis in New Zealand between 1988 and 1995, one death in 1996, and since 1999 there has been one death each year up to 2004. Morbidity from pertussis in New Zealand has been described primarily using hospital discharge data. National passive surveillance data has been available since 1996, when pertussis became a notifiable disease. Comparison of notification and hospitalisation data from 1996 and 1997 demonstrates that fewer than 50 percent of hospitalised cases are notified. The three to four year periodicity of pertussis epidemics in New Zealand is similar to that seen in many other countries. The decrease in the pertussis hospitalisation rate that occurred following the introduction of mass immunisation has not been sustained.

Prevention: 

There is almost no maternal protection passed to the newborn against pertussis via breastmilk.

Cases should be excluded from school or daycare until the infectious period is over (21 days from the onset of coughing or after 5 days of antibiotics). Some countries recommend health care workers and/or daycare workers with confirmed pertussis infection be placed on sick leave until fully recovered.

Pertussis vaccines were initially developed in the 1940s.

There are two types of pertussis vaccine commonly used internationally: whole cell pertussis vaccine (wP) and acellular vaccine (aP). Both vaccines have similar efficacy but acellular vaccines cause significantly fewer adverse reactions than whole cell vaccines. Where feasible and available, acellular vaccines should be used in preference to whole cell vaccines.

Acellular pertussis-containing vaccines have now replaced whole-cell vaccines in many countries, including New Zealand. There are a number of acellular pertussis vaccines, which contain three or more purified components of B. pertussis: pertussis toxin (PT), filamentous haemagglutinin (FHA), pertactin (PRN), and fimbrial antigens or agglutinogens.

Treatment: 

Antibiotics have no role in treating pertussis. However they are given to reduce transmission of the organism and may be given to all household and other close contacts of the patient.

Identification of pertussis infection and prescription of antibiotics for women in the third trimester of pregnancy minimises the spread to non-immune infants in the first month of life.

Disease Effects vs Vaccine Side Effects (Table)
Disease Description: 

Pertussis is a highly infectious bacterial disease of the respiratory system. Symptoms inlcude a severe cough which can last for many weeks. Pertussis is very serious in young infants.

Effects of disease: 
Secondary infections such as pneumonia and ear infections can occur.
Around 5 in 10 infants who catch pertussis before the age of six months require hospitalisation.
Severe coughing can temporarily stop the oxygen supply to the brain (hypoxia).
Around 1-2 in 100 hospitalised infants younger than 12 months die.
Around 2 in 1000 children with paroxysmal cough develop permanent brain damage, paralysis, deafness or blindness.
Urinary incontinence in adults
Some adults will collapse or experience a rib fracture from violent coughing.
Common side effects of vaccine: 
Soreness/pain, redness and/or swelling around the injection site.
Fever over 38°C.
Decreased appetite, vomiting and/or diarrhoea.
Irritability, restlessness.
Unusual crying.
Fatigue.
Redness and/or swelling more than 6 cm in size around the injection site. In a small percentage of vaccine recipients the reactions will be severe enough to limit movement of the arm and may last for about a week.
Swelling involving the entire thigh or upper arm occurs in 2–3 percent of children after administration of the fourth and fifth doses of acellular pertussis vaccine. It resolves spontaneously without long term consequences.
Uncommon side effects of vaccine: 
Fever over 39°C.
Muscle or joint stiffness or pain.
Rare/very rare side effects of vaccine: 
High fever over 40°C.
Persistent (> 3 hours) inconsolable screaming.
Hypotonic, hyporesponsive episode (HHE) with 24 hours of immunisation.
Inflammation of the nerve in the arm causing muscle weakness and pain (brachial neuritis) occurs within four weeks of immunisation, 1- 2 times per 200,000 doses.
Urticaria.
Anaphylaxis.
Convulsion within 2 days of immunisation.

Measles

Parents & Caregivers
Introduction: 

Measles is one of the most infectious diseases in humans. It is also known by the names English measles, morbilli and rubeola. Measles is now the third most common vaccine-preventable cause of death among children throughout the world.

A brief history: 

Before a measles vaccine was developed most people had measles by the age of 20. Universal vaccination was introduced in 1969 into New Zealand although the coverage of the vaccine has been poor until recent years. The last two major measles epidemics in NZ  occurred in the 1990s with thousands of cases, hundreds of hospitalisations and seven deaths. Smaller outbreaks continue to occur, mainly in communities where vaccine uptake has been low. Outbreaks tend to start when someone brings the disease back from an overseas trip.  As measles is extremely infectious it can spread very quickly.

The current New Zealand situation: 

New Zealand continues to have outbreaks of measles, although at lower rates than previously. Due to higher immunisation rates in children by the age of two years outbreaks particularly affect unvaccinated older children, teenagers and adults.

Symptoms: 

The illness begins with fever, cough, runny nose and conjunctivitis (inflammation in the eyes), which lasts for 2-4 days. It may be possible to see small white spots (Koplik spots) inside the mouth. A rash appears 2-4 days after the first symptoms, beginning at the hairline and gradually spreading down the body to the arms and legs. The rash lasts for up to one week. It usually takes 10-12 days from exposure to the first symptom.

How do you get it?: 

Measles is spread through the air by infectious droplets or direct contact with secretions from the nose or throat of infected persons, for example by touching items or surfaces contaminated with secretions. The person with measles is most infectious during the first 2-4 days of symptoms and stays infectious until 3-4 days after the rash appears.

What are the risks?: 

Complications from measles are common. The measles virus suppresses the immune system, lowering the body’s ability to fight other infections.

Common complications include ear infections, diarrhoea, and pneumonia. In New Zealand more thatn 15 per 100 cases are hospitaised. Pneumonia accounts for nearly two thirds of measles deaths.

Approximately 1 per 1000 cases develop encephalitis (inflammation of the brain), of these 15% die and approximately one third are left with permanent brain damage.

One in 100,000 cases will,  years later, develop subacute sclerosing panencephalitis (SSPE, a degenerative brain disease). This condition is always fatal.

Other complications include immune thrombocytopenic purpura (ITP, affecting the blood clotting) and inflammation of the small airways in the lungs, heart, kidneys or liver.

The risk of complications and death are higher in children under 5 years and adults over 20 years of age.

Measles during pregnancy increases the risk of miscarriage and premature labour.

Anyone who has a weakness of their immune system is at greater risk of very serious disease. These people are often unable to be immunised and rely on protection from those around them being immunised.

Death occurs in approximately 1 per 1,000 reported cases of measles overall in western countries.

Who is most at risk?: 

Anyone who has not received at least one dose of a measles containing vaccine e.g., the combined measles, mumps, rubella (MMR) vaccine or who has not already had the disease.

Treating the symptoms: 

There is no cure for measles infection.

Acute cases are treated with Vitamin A.

Preventing Disease Spread: 

Immunisation given on time is the best way to prevent measles. Two doses of the MMR (measles, mumps, rubella) vaccine is 99% effective in preventing measles. MMR vaccine, if given within 72 hours of exposure to measles virus, may provide protection to the unimmunised and thus limit the spread of measles.
In the event of a measles outbreak unimmunised children (with no history of prior measles infection) who have contact with infected cases are advised NOT to attend school or early childhood services until notified.

Health Professionals
Causative organism: 

Measles is a paramyxovirus, genus Morbillus. It is an RNA virus. Measles virus can survive for up to 2 hours in air, but is sensitive to heat, light and acidic pH.

Clinical signs, symptoms and complications: 

Early symptoms include fever, runny nose, cough, loss of appetite, and conjunctivitis or "pink eye." Characteristic white Koplik’s spots may occur in the oral mucosa.

After 3 to 5 days the rash appears at the hairline, moves to the face and upper neck, then proceeds down the body and usually lasts 4-6 days.

Measles is often a serious disease, with up to 30% of reported cases experiencing one or more complications.

Complications include:

  • Diarrhoea (8%), ear infections (7-9%) and pneumonia (1-6%), which accounts for nearly two thirds of measles-related deaths.
  • Acute encephalitis may develop in 1 in 1000 cases, of whom 15% die and a further 25% - 35% are left with permanent neurological damage.
  • Approximately 1 in 100,000 cases will develop subacute sclerosing panencephalitis (SSPE). This serious complication can lead to permanent brain damage.

Measles during pregnancy increases the risk of premature labour, miscarriage, and low-birth-weight infants, although birth defects have not been linked to measles exposure.

Measles can be especially severe in persons with compromised immune systems. Immunisation for household contacts is important to protect those who are immunocpmpromised.

The measles, mumps and rubella vaccine viruses are considered non-transmissable meaning they are not passed from the vaccine recipient to their contacts.

Method of transmission: 

Measles is one of the most contagious viral diseases and can be transmitted from four days before until four days after the appearance of the rash.

  • It is spread through the air by infectious droplets and is highly contagious.
  • It takes an average of 10-12 days from exposure to the first symptom, which is usually fever.
  • The measles rash doesn't usually appear until approximately 14 days after exposure, 3-5 days after the fever begins.
Public health significance: 

Measles is endemic globally, although a few countries with developed economies and high immunisation coverage have virtually eliminated wild measles virus.

  • Regular epidemics still persist in many countries.
  • Developing countries have a higher burden on morbidity and mortality from measles.
  • Measles has been earmarked as a candidate for elimination through the implementation of global mass immunisation programmes.
New Zealand epidemiology: 

Large scale measles epidemics occur when the number in the susceptible population increases and the immunisation coverage is low. It has been estimated that to prevent recurrent outbreaks of measles, 95 percent of the population must be immune. Since measles vaccine efficacy is 90–95 percent and not all children receive the first scheduled dose, the only way to achieve this level of immunity is by implementing a two dose immunisation strategy, as is now recommended. In 2000 a mathematical model was developed to estimate the future timing of measles epidemics in New Zealand. The results suggested that if no changes were made to the MMR schedule of 15 months and 11 years, the next measles epidemic would be between 2002 and 2004. Therefore from January 2001 the National Immunisation Schedule was changed to give the first dose of MMR at 15 months and the second dose at four years of age, prior to school entry. In 2005 the measles mathematical model was updated to calculate the effect of the measles catch-up in 2001 and to estimate the effect of changing the National Immunisation Schedule to give MMR at age 15 months and at age four years before school entry. As the incidence of measles decreases in New Zealand, it is important to continue high MMR immunisation coverage to lower the risk of imported measles causing outbreaks. Every suspected case of measles will need laboratory confirmation and characterisation to inform the local medical officer of health, so that public health control measures can be put in place.

Prevention: 

Measles is so highly infectious that immunisation is the only effective prevention.

Exclusion of cases from daycare, school and work, as well as exclusion of unimmunised individuals during an outbreak may reduce but not eliminate transmission.

If a child is exposed and has not been vaccinated, measles vaccine may prevent disease if given within 72 hours of exposure.

Immune globulin (0.6 mL/kg IM, to a maximum dose of 15 mL) may prevent or lessen the severity of measles if given within six days of exposure.

Measles vaccine is produced from a live attenuated (weakened) strain (Edmonston or Schwarz strains) of measles virus prepared in chick fibroblasts (embryo cell culture).

The attenuated measles vaccine virus undergoes the infectious cycle in the host, triggering an immune response and the development immunity.

Disease Effects vs Vaccine Side Effects (Table)
Disease Description: 

Measles is a highly infectious viral disease that can often have serious complications.

Effects of disease: 
Otitis media (ear infection): approximately 7-9 in 100.
Diarrhoea: approximately 8 in 100.
Pneumonia: approximately 6 per 100
Acute encephalitis (brain inflammation): approximately 1 per 1000
Subacute sclerosing panencephalitis (SSPE, a degenerative brain disease that is always fatal): 1 in 100,000.
The risk of complications and death are higher in children under 5 years and adults over 20 years of age and chronically ill.
Maternal measles increases risk for miscarriage and premature labour.
Overall death rate approximately 1 per 1000.
Common side effects of vaccine: 
Approximately 6 per 100 have a mild to moderate fever
Approximately 2 per 100 have a rash or runny eyes
Uncommon side effects of vaccine: 
Fever over 39.5 degrees Celsius less that 2 per 100.
Rare/very rare side effects of vaccine: 
Anaphylaxis.
Temporary thrombocytopenia, approximately 1 per 30,000
Encephalitis may occur once in one million doses
Aseptic mumps meningitis in approximately 1 per 100,000
Vaccines: 
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