2b Epidemiology of Diseases of Public Health Significance Flashcards
What is the epidemiology profile of Amoebic Dysentery?
CDC III MRC
Cause:
Parasite Entamoeba Histolytica.
Distribution:
Endemic worldwide
The highest incidence is in developing countries.
Clinical:
Most asymptomatic.
Bloody Diarrhoea.
Abdominal Pain
Fever/Chills
Identification:
Stool Sample
Incubation:
2-4 weeks
Infectivity:
Mode of transmission:
Faecal oral transmission
Reservoir:
Humans
Control:
Advice to overseas travellers on food hygiene and water treatment.
Food Hygiene Measures - Keep cooked food above 60ºC, rapidly cool cooked foo, store foods in cold temperatures, reheat foods food properly
What is the epidemiology profile of Anthrax?
CDC III MRC
Cause:
Bacteria Bacillus anthracis
Distribution:
Rare in the UK
Highest risk is occupational exposure when handling imported infected animal products.
Endemic in much of the world.
Clinical:
Cutaneous anthrax (>95% cases). Infected cut turns into a lesion that becomes papular, then vesicular and develops into a depressed black eschar (takes 2-6 days).
>20% fatality rate
Identification:
Lab culture of the infected area
Incubation:
Cutaneous anthrax - 1-12 days
Infectivity:
Spores can remain viable and infective in soil for decades.
Mode of transmission:
Direct contact with skin, ingestion or inhalation of spores from infected animals/animal products.
No person-to-person spread via the inhalational route.
Reservoir:
Infected animals
Soil
Control:
Treat with antibiotics
UK immunisation for workers dealing with infected animals (vets) or working with infected material (lab staff)
What is the epidemiology profile of Bacillus cereus?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
CDC III MRC
Cause:
Bacillus cereus bacterium.
Distribution:
Occurs worldwide.
Commonly linked with rice but other food may cause it.
Clinical:
Causes either vomiting or diarrhoeal illness depending on which toxin the bacteria produces.
Nausea, abdominal pain and vomiting, colic and diarrhoea
Illness lasts between 12-24 hours.
Identification:
Incubation:
Vomiting illness: 2-3 hours
Diarrhoeal illness: 8-12 hours
Infectivity:
No person to person spread.
Mode of transmission:
Ingestion of contaminated food.
Reservoir:
Found at low levels in many raw, dried or processed foods.
Control:
Treat supportively
Food Hygiene Measures - Keep cooked food above 60ºC, rapidly cool cooked food, store foods in cold temperatures, reheat foods food properly
What is the epidemiology profile of Campylobacter enteritis?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
CDC III MRC
Cause:
Campylobacter bacteria
Most common type is Campylobacter jejuni.
Distribution:
The most common cause of bacterial infectious intestinal disease in England and Wales, with approximately 50,000 cases reported each year (also many cases are unreported)
Occurs more frequently during the early spring and summer.
A common cause of traveller’s diarrhoea
Hyper-endemic in developing countries.
Clinical:
Most infections are self-limiting
Bloody diarrhoea
Abdominal pain
Vomiting
General infective symptoms
Typically lasts 1 week in healthy persons.
Identification:
Incubation:
Infectivity:
Mode of transmission:
Reservoir:
Control:
Causal Agent
Common Clinical Features
Geographical Distribution
Reservoir
Mode of Transmission:
Ingestion of infected undercooked meats.
Ingestion of contaminated milk, ice or water.
Person to person spread can occurs
In the UK 5% of cases come from infected pets.
Incubation Period
Commonly 2-5 days (range 1-10 days).
Period of Communicability
Throughout period of infection, usually several days to weeks.
Prevention and Control
Notifiable disease
Food hygiene as per the WHO five key steps to safer food.
Treatment
Erythromycin is not routinely used, but can reduce the time that individuals shed the bacteria in their faeces.
What are the WHO five key steps to safer food.
Wash hands and sanitize all equipment, surfaces and utensils used for food preparation.
Separate raw and cooked food, and use separate equipment and utensils for handling raw food.
Cook food thoroughly (until centre of food reaches at least 70oC), especially poultry, meat, eggs and seafood.
Reheat cooked food thoroughly, and store cooked and raw food at a safe temperature.
Use safe water and raw materials, e.g. pasteurized milk and water.
What is the epidemiology profile of Chickenpox/Shingles?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Viral infection caused by the human varicella-zoster virus (VZV).
Shingles is caused by reactivation of latent varicella infection whose genomes persist in sensory root ganglia of the brain stem and spinal cord.
Common clinical features
Generally a mild disease in children lasting 4-7 days, sometimes characterized by a short prodromal period (low-grade fever, malaise) and followed by a vesicular rash (usually on the trunk) lasting 3-4 days which become granular scabs. There are successive crops of vesicles over several days.
The most common complications from varicella infection are bacterial infections of the skin and soft tissues in children and pneumonia in adults.
Severe complications include, septicaemia, toxic shock syndrome, necrotizing fiscilitis, osteomyelitis, bacterial pneumonia and septic arthritis.
Congenital varicella syndrome occurs following infection during pregnancy (first 5 months), although most risk appears to be in weeks 13-202.
Herpes zoster (shingles) is more prevalent among older age groups.
Epidemiology
Endemic worldwide, occurring mainly in children. The incidence in older children and adults is rising in the UK and other Western countries2.
In temperate climates, 90% of individuals have been infected by age 15 and 95% by young adulthood. In tropical climates a higher proportion of cases occur in adults.
Reservoir
Humans.
Mode of transmission
Direct person to person contact, by droplet or airborne spread of vesicular fluid or respiratory secretions. Also by contact with articles recently contaminated by discharges from vesicles and mucous membranes from an infected person.
Highly contagious infecting up to 90% of those exposed.
Incubation period
2-3 weeks, commonly 14-16 days. Longer following passive immunization or in the immunodeficient.
Period of Communicability
Commonly 1-2 days following onset of rash and until all lesions are crusted (usually 5 days).
Prevention and control
Exclude children with chickenpox from school until 5 days from the onset of rash. Infected healthcare workers should be excluded from work for the same period.
What is the epidemiology profile of Chlamydia trachomatis
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Chlamydia trachomatis.
Common clinical features
In women symptoms may present as cervicitis and urethritis, which may be complicated by pelvic inflammatory disease, tubal damage, infertility and ectopic pregnancy.
Up to 70% of infections in women are asymptomatic2. Endocervical chlamydial infection has been associated with increased risk of acquiring HIV infection2.
In men symptoms may present as urethritis, which may be complicated by epididymitis1.
Asymptomatic infection may be found in up to 50% of sexually active men.
Can also infect the eye and cause trachoma: a common cause of blindness in the developing world.
Epidemiology
Occurs worldwide.
Genital Chlamydia infection is the most commonly sexually transmitted infection (STI) diagnosed in genitourinary medicine (GUM) clinics in the UK (Health Protection Agency).
The number of uncomplicated Chlamydia diagnoses in GUM clinics has risen steadily since the mid 1990s. In 2005 there were 109,832 newly diagnosed cases of uncomplicated genital Chlamydia infections reported in the UK.
In the UK the highest rates of Chlamydia are seen among females aged 16-19 years and among males aged 20-24 years (HPA).
Genital chlamydial infection is an important reproductive health problem. An estimated 10-30% of infected women develop pelvic inflammatory disease (PID).
Reservoir
Humans.
Mode of transmission
Direct sexual contact.
Incubation period
Probably 7-14 days.
Period of Communicability
Until treated.
Limited short-term immunity occurs.
Treatment
Treatment is with 7 days of doxycycline or erythromycin or a single dose of azithromycin1.
Infected individuals should abstain from sexual intercourse until they and their sexual partners have completed treatment to avoid re-infection.
Prevention and control
The use of condoms reduces the risk of infection.
In the UK screening for genital Chlamydia is offered to all sexually active women
What is the epidemiology profile of Cholera?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal Agent
Vibrio cholerae bacteria, serogroups 01 and 0139
Common Clinical Features
Symptoms range from mild to moderate diarrhoea (80-90% of cases) to the severe sudden onset of profuse watery diarrhoea (rice water stool) accompanied by nausea and vomiting.
In severe cases rapid dehydration, leading to circulatory shock and possible death. In such cases immediate fluid and electrolyte replacement is required.
Severe untreated cases have a 50% mortality, but <1% fatality with the correct treatment.
Geographical Distribution
Prevalent in developing countries where sanitation and food and water hygiene are inadequate or lacking, particularly in areas effected by natural disaster, war and migration of refugees.
Worldwide there have been 7 major pandemics in the last 200 years. The current seventh pandemic (due to V. cholerae 01, biotype El Tor) began in 1961. Since which time it has spread through Asia, Africa and Latin America.
Since 1992 V. cholerae 0139, a previously unidentified serogroup has been identified as the cause of outbreaks in India and Bangladesh and reported in 11 countries of South East Asia1.
In 2002 WHO reported 142,311 cases and 4564 deaths from cholera worldwide.
Cholera is rare in industrialised countries. Between 1990 and 2000 only 80 cases of imported cholera were notified in the UK2. The risk to international travellers is low.
Reservoir
The main reservoir is humans.
Mode of Transmission
Faecal-oral route.
The ingestion of food or water contaminated by faeces or vomitus of an infected person.
Raw or undercooked contaminated seafood.
Incubation Period
<1 to 5 days, commonly 2-3 days.
Period of Communicability
Individuals remain infectious during period of diarrhoea and for up to 7 days after.
The carrier state may persist in a few cases for up to a few months.
Prevention and Control
Advice to overseas travellers on food and water hygiene.
What is the epidemiology profile of Creutzfeldt-Jakob Disease?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Transmissible spongiform encephalopathies (TSEs) are a family of rare diseases of humans and animals that are characterised by spongy degeneration of the brain and severe and fatal neurological signs and symptoms. They include Creutzfeldt-Jakobdisease (CJD), variant Creutzfeldt-Jakob disease (vCJD) and Kuru.
Creutzfeldt - Jakob disease (CJD)
CJD in it classic form is the commonest of the human TSEs. The majority (85%) of cases of CJD occur sporadically. An estimated 5-15% of cases are due to inherited mutations of the prion protein gene. A smaller percentage of cases, <5% areiatrogenic (resulting from the accidental transmission of the causative agent via contaminated surgical equipment or as a result of corneal or dura mater transplants).
Variant Creutzfeldt - Jakob disease (vCJD)
A new variant of Creutzfeldt-Jakob (vCJD) disease was first recognized in 1996 in the UK. The age distribution for vCJD is younger than for classic CJD. The median age of deaths is around 29 years (range14-74 years) of age compared with 65 years for classic CJD.
Kuru
Kuru is a disease of certain tribes in Papua New Guinea who traditionally practice cannibalism.
Causal agent
PrP, a prion protein.
Common clinical features
The onset of vCJD is with variable psychiatric symptoms followed by abnormal sensation at 2 months, ataxia at 5 months, myoclonus at 8 months, akinetic mutism at 11 months and death within 12-24 months2.
Epidemiology
Classic CJD occurs worldwide but is rare. The annual worldwide incidence is approximately 1 case per million population per year. The risk of CJD increases with age with annual incidence of approximately 2.4 cases per million per year among those aged over 50 years.
In the UK there are approximately 35 cases per year of CJD, with an average age of onset of 55-75 years2.
It is estimated that between 3,800 and 11,000 people are currently incubating vCJD in the UK2.
Reservoir
Believed to be cattle infected with Bovine spongiform encephalopathy (BSE)1.
Mode of transmission
Unknown - probable consumption of infected bovine neural tissue.
Incubation period
The incubation period for vCJD is unknown but is probably years2.
Treatment
No specific treatment is available. Treatment is supportive only.
Prevention and control
The national surveillance programme for CJD in the UK was initiated in May 1990. All reported cases of CJD and vCJD are investigated in detail.
What is the epidemiology profile of Dengue?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Dengue fever and dengue haemorrhagic (DHF) fever are caused by a flavivirus with 4 distinct serogroups (DEN- 1, DEN-2, DEN-3 and DEN-4).
Infection with 1 serogroup confers life long immunity, but provides only partial and transient protection against infection by the other 3 serogroups. Sequential infection increases the risk of more serious disease resulting in DHF.
Common clinical features
Dengue fever is characterised by the sudden onset of fever, severe frontal headache, joint and muscle pain, myalgia, anorexia, nausea, vomiting and rash (appearing 3-5 days after onset of fever).
Infants and children may have a non-specific febrile illness with rash.
DHF - is a potentially life threatening complication that is characterised by high fever, haemorrhagic phenomena - often with enlargement of the liver and in severe cases, circulatory failure1.
DHF occurs principally in children but also occurs in adults.
Epidemiology
Endemic in most countries in the tropics.
Global prevalence has increased dramatically in the last 25 years and the WHO estimates that there may be 50 million cases of dengue infection worldwide each year2.
The reasons for this increase are complex and not well understood. However, several important factors have been identified including: uncontrolled urbanization and population growth especially in South east Asia where substandard water and waste management provide a perfect environment for the Aedes mosquito to breed. Other factors include the failure of public health infrastructure to provide effective or sustained vector control programmes.
According the WHO dengue is now endemic in > 100 countries in Africa, the Americas, The Eastern Mediterranean, South East Asia and the Western Pacific. An estimated 2.5 billion people live in areas where dengue viruses are transmitted.
The highest burden of disease occurs in South East Asia and the Western Pacific but it is increasingly becoming an important public health problem in South America and the Caribbean2.
Epidemics caused by all four virus serotypes have become more frequent and larger in the last 25 years, with major epidemics occurring in many countries every 3-5 years.
In the Americas the first major epidemic started in 1981. The peak in 1982 resulted from an explosive outbreak that started in Cuba resulting in over 300,000 cases of dengue fever, 10,000 cases of DHF and 158 deaths. Subsequent epidemics have been reported in 1998 and 2002.
Almost half the dengue imported into Europe comes from Asia.
Reservoir
Aedes mosquito.
The Aedes mosquitoes commonly breed in water filled receptacles (discarded tyres, buckets, cans and cisterns) close to human habitation.
Mode of transmission
Through the bite of an infected female Aedes mosquito.
The Aedes aegypti, a domestic day biting mosquito is the principal vector for dengue transmission.
However, geographical variation in vectors occurs and in recent years, Aedes albopictus, a secondary dengue vector in Asia has become established in the United States, several Latin American and Caribbean countries.
The Aedes mosquito are most active during daylight hours, with two peak periods of biting activity (in the morning for several hours after daybreak and for several hours before dark).
Primates may also act as a reservoir for the virus in the forests of South East Asia and western Africa1.
Incubation period
3-14 days, commonly 4-7 days.
Period of Communicability
No direct person to person spread.
Patients are infective for mosquitoes from shortly before and during the febrile period.
The mosquito becomes infective 8-12 days following the blood-meals and remains infective for life (2-3 months)1.
Prevention and control
No vaccine, chemoprophylaxis or specific treatment is currently available for dengue and DHF.
Appropriate clinical management of cases significantly reduces mortality of infected persons.
Effective vector control in endemic areas.
Advice to travellers from the UK to countries where dengue is endemic or areas with outbreaks is avoidance of mosquito bites
What is the epidemiology profile of Diphtheria?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Corynebacterium diphtheriae of which there are two main forms, respiratory and cutaneous (affecting the skin).
C. diphtheriae has 3 biotypes - gravis, intermedius, and mitis. The most serious disease is associated with gravis but any strain may produce toxin.
Common clinical features
Symptoms range from a moderately sore throat to toxic life-threatening diphtheria of the larynx or of the lower and upper respiratory tracts.
Disease can involve almost any mucous membrane. For clinical purposes, it is convenient to classify diphtheria into a number of manifestations, depending on the site of disease1;
Anterior nasal diphtheria
Pharyngeal and tonsillar diphtheria
Laryngeal diphtheria
Cutaneous (skin) diphtheria.
Cutaneous diphtheria is usually mild, typically consisting of sores or shallow ulcers and only rarely involving toxic complications.
Epidemiology
Endemic worldwide.
A resurgence of diphtheria in the former Soviet Union occurred in the 1980s followed by a large epidemic from 1990. The epidemic spread throughout all the newly independent states, and peaked in 1994-5. Between 1990 and 1998, more than 157,000 cases and 5000 deaths were reported in the region4.
Before the introduction of mass immunization in 1942 diphtheria was common in the UK with around 60,000 cases and 4,000 deaths reported each year2.
In 2005 9 cases were notified in England and Wales.
The overall case fatality rate is 5-10% with higher death rates (up to 20%) among children under 5 years old and adults aged over 40 year.
Reservoir
Humans
Mode of transmission
Airborne droplets or direct contact with infected respiratory discharges or skin ulcers.
Incubation period
2-5 days.
Period of Communicability
Untreated cases remain infectious for up to 4 weeks, after 3 days of antibiotic treatment cases are no longer infectious.
Rare chronic carriers may shed organism for 6 months or more.
Prevention and control
Immunisation with diphtheria toxoid.
What is the epidemiology profile of Ebola?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Ebolavirus (Filoviridae family).
Ebola haemorrhagic fever (EHF) is a febrile haemorrhagic illness of which there are four distinct subtypes: Zaire, Sudan, Cote d’Ivoire and Reston. Zaire, Sudan and Cote d’Ivoire cause illness in humans.
Common clinical features
Sudden onset of fever, malaise, myalgia, diarrhoea, hypotension and shock, vomiting, rash, impaired kidney and liver function and in some cases internal and external bleeding.
Case fatality rates are between 50-90%.
Epidemiology
Ebola was first identified in 1976 in Sudan and the Democratic Republic of Congo following large outbreaks.
Confirmed cases have been reported in the Democratic Republic of Congo (formerly Zaire), Gabon, Sudan, The Ivory Coast and Uganda, Cote d’ Ivoire and South Africa. Most cases have occurred in DRC, Sudan and Uganda.
Approximately 1,850 cases with over 1,200 deaths have been documented since the Ebola virus was discovered.
Reservoir
Unknown - possibly primate.
Appears to possibly originate from the rain forests in West and Central Africa and in the Western Pacific.
Mode of transmission
Person to person via contact with bodily secretions, organs and blood of infected individuals.
The handling of infected (dead and alive) chimpanzees, gorillas and forest antelopes has been documented.
Direct contact with the body of a deceased person infected with the virus.
Nosocomial transmission occurs frequently during outbreaks.
Incubation period
2-21 days.
Period of Communicability
During acute illness and may be excreted in semen for 2-3 months.
There is no carrier state.
Treatment
No effective treatment is available. Severe cases require intensive supportive care.
Prevention and Control
There is no vaccine against ebola haemorrhagic fever.
Strict isolation of cases and strict barrier nursing techniques implemented.
What is the epidemiology profile of E.coli?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Six major categories of Escherichia coli strains cause diarrhoea.
enterohaemorrhagic
enterotoxigenic
enteroinvasive
enteropathogenic
enteroaggregative
diffuse-adherent
E. coli serotype O157:H7. -Gram-negative rod-shaped bacterium producing Shiga toxin(s)
The most serious illness in humans is caused by verocytotoxic E. coli (VTEC) (also known as enterohaemorrhagic E. coli), The most common VTEC strain in Europe and North America is
E. coli O157:H7. However, other serotypes have frequently been involved in sporadic cases and outbreaks.
Common clinical features
VTEC O157 can cause a range of symptoms from asymptomatic carriage to mild diarrhoea or bloody diarrhoea (haemorrhagic colitis) and haemolytic uraemic syndrome (HUS).
HUS is characterised by acute renal failure, haemolytic anaemia and thrombocytopaenia (lowered platelets). It usually occurs in young children and is the major cause of acute renal failure in children in Britain and several other countries. HUS develops in up to 10% of patients infected with VTEC O157 (HPA)1.
Children <5 years old and the elderly are more likely to develop serious complications.
Fatality rates ranging from 1 to 5% have been reported in the UK (HPA).
Epidemiology
Important cause of bloody diarrhoea in Europe.
In 2005 there were 946 laboratory confirmed cases of VTEC 0157 in England and Wales (HPA).
The highest incidence rates in the UK are seen in children < 5 years.
The highest rates have been observed in rural areas particularly in Scotland.
Reservoir
The gastointestinal tract of animals - cattle are the most important reservoir.
Mode of transmission
Primarily through the consumption of contaminated, undercooked or raw foods, (particularly ground beef) and unpasteurised milk.
Other foods implicated in outbreaks of E.coli O157:H7 include undercooked hamburgers, dried cured salami, lettuce, yogurt, cheese and milk and radish sprouts.
Cross contamination during food preparation.
Person to person via the faeco-oral route is common.
Direct contact with animals, e.g. school visits to farms.
Waterborne transmission occurs through swimming in or consuming contaminated water.
The infectious dose of VTEC O157 appears to be very low, probably less than 100 organisms.
Incubation period
2-10 days, median 3-4 days.
Period of Communicability
While excreting pathogen, up to a week in adults and up to three weeks in children.
An asymptomatic carrier state has been reported.
Prevention and control
Developing farm and slaughterhouse-based methods to decrease contamination of meat; encouraging use of irradiation to increase the safety of ground beef; identifying ways to prevent contamination of foods eaten raw (e.g., produce).
Follow correct food hygiene practices for food preparation and cooking in domestic and commercial kitchens as described by the WHO Five keys to safer food.
These include;
* Prevent cross contamination of raw and cooked food by washing hands before, during and after food preparation. Wash and sanitize all equipment, surfaces and utensils used for food preparation.
* Separate raw and cooked food, and use separate equipment and utensils for handling raw food.
* Cook food thoroughly (until centre of food reaches at least 70oC), especially poultry, meat, eggs and seafood.
* Reheat cooked food thoroughly, and store cooked and raw food at a safe temperature.
* Use safe water and raw materials, e.g. pasteurized milk and water.
* Wash fruit and vegetables.
What is the epidemiology profile of Giardia Lamblia?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Giardia lamblia (G. intestinalis, G. duodenalis), a flagellate protozoan1.
Common clinical features
Varies from asymptomatic (approximately 25% of acute infections) to severe diarrhoea with malaise, flatulence, foul smelling greasy stools, abdominal cramps, bloating, nausea and anorexia.
Epidemiology
Giardia lamblia is the most frequently isolated intestinal protozoa in the world. It occurs in the aquatic environment throughout the world and is resistant to disinfectants used in drinking water treatment.
Prevalence is higher in areas of poor sanitation particularly in developing countries.
There were 3,169 laboratory confirmed cases of Giardia in England and Wales in 2004.
In the UK children < 5 years and adults aged 25-39 are most commonly affected. Groups with high rates of infection also include residents of institutions, travellers, gay men and the immunocompromised2.
Giardia is a common cause of traveller’s diarrhoea.
Reservoir
Humans, possibly beaver and other wild and domestic animals.
Mode of transmission
Person to person via the faecal oral route.
Ingestion of cysts in faecally contaminated drinking and recreational water.
Incubation period
Commonly 3-25 days or longer, median 7-10 days.
Period of Communicability
During period of infection.
Laboratory Diagnosis
Diagnosis is by identification of cysts or trophozoites in faeces. Repeated samplings may be required.
Treatment
Commonly used antibiotics include metronidazole and tinidazole.
Prevention and control
There is no vaccine or chemoprophylaxis for Giardia.
Follow correct food hygiene practices for food preparation and cooking in domestic and commercial kitchens.
Treatment of water supplies.
Advice to travellers abroad on safe food and water.
Hand washing.
What is the epidemiology profile of Haemophilus influenzae type B
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Haemophilus influenzae serotype b (Hib) is a bacterial infection of young children, which causes meningitis and other bacteraemic diseases including pneumonia, epiglottitis, facial cellulitis and bone and joint infections.
The most common presentation of invasive Hib disease is meningitis, frequently accompanied by bacteraemia and accounts for an estimated 60% of all cases.
Common clinical features
Hib meningitis - Symptoms may include progressive headache, stiff neck, drowsiness, intermittent fever and vomiting.
The cases fatality is 3-6%. Hearing impairment or other neurologic sequelae occur in 15-30% of surviving cases.
Epiglottis - an infection and swelling of epiglottis that may cause life-threatening airway obstruction.
Septic arthritis, cellulitis and pneumonia are common manifestations of invasive disease.
Osteomyelitis and pericarditis are less common forms of invasive disease.
Epidemiology
Worldwide, most prevalent in children aged 2 months to 3 years. Uncommon in persons aged over 5 years.
Prior to routine immunisation in the UK, HiB was the second most common cause of bacterial meningitis1.
In 2004 138 cases of Hib were reported in England and Wales (HPA).
Reservoir
Humans
Mode of transmission
Person to person, transmitted by droplet aerosol or secretions from the nasopharynx of colonized persons.
Incubation period
Unknown, probably 2-4 days.
Period of Communicability
As long as organisms are present.
Patients are no longer infectious within 24-48 hours of starting appropriate antibiotic treatment.
Prevention and control
Routine vaccination of infants.
What is the epidemiology profile of Hepatitis A?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal Agent
Hepatitis A is caused by infection with the hepatitis A virus (HAV), a positive stranded RNA virus, first identified in 1973.
Common clinical features
Infection with HAV may range from asymptomatic to symptoms of fever, malaise, abdominal pain, loss of appetite, nausea, vomiting and diarrhoea followed by dark urine and jaundice.
In young children infection with HAV is usually asymptomatic whereas symptomatic disease occurs more commonly among adults.
Approximately 15% of infected individuals will have prolonged illness or relapsing symptoms over 6-9 months.
Case fatality is low, around 0.6% increasing with age to 1.8% in adults over 50 and 10% in adults aged over 701.
Protective antibodies develop in response to infection and confer lifelong immunity.
No chronic infection is known to occur.
Geographical distribution
Endemic worldwide, prevalence is higher in countries with poor sanitation and hygiene.
In developing countries with high endemicity the peak age of infection occurs largely in early childhood, among whom HAV infection is mostly asymptomatic.
In countries where Hepatitis A is highly endemic, exposure to HAV is almost universal before the age of 10 years.
In countries with low endemicity the peak age of infection occurs mainly among adults.
The incidence of HAV has been decreasing in developed countries over the last 50 years.
Notifications of HAV in England and Wales declined from 7,316 in 1992 to 784 in 20042.
Reservoir
Humans
Mode of transmission
Person to person, primarily through the faecal-oral route.
Contaminated food and water.
Contaminated raw shellfish harvested from sewage contaminated water.
Blood exposure (rare).
Incubation period
15-50 days, average 28-30 days.
Period of Communicability
From 2 weeks before the onset of symptoms until 1 week after. Maximum infectivity occurs during latter half of the incubation period and for a few days after onset of jaundice.
Diagnosis
Demonstration of IgM antibodies to HAV (IgM anti HAV) in serum.
Prevention and control
Personal hygiene, especially among children in child day care and in schools.
Vaccination advised for travellers (aged 5 and above) to countries outside Western Europe, North America and Australasia.
What is the epidemiology profile of Hepatitis B?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Hepatitis B virus (HBV), a hepadnavirus.
Common clinical features
Many infections with HBV are asymptomatic or range from mild symptoms to fulminant hepatitis with fatigue, abdominal pain, loss of appetite, intermittent nausea, vomiting and jaundice.
The development of chronic HBV infection is age dependant, with young children more likely to develop chronic infection.
Chronic infection occurs in approximately 90% of infants infected at birth, between 30% - 50% of children infected at age 1-5 years and among 10% of adults1.
The risk of death from HBV related liver cancer or cirrhosis is approximately 25% for persons who become chronically infected during childhood.
Epidemiology
Hepatitis B virus (HBV) is a major global public health problem accounting for up to 1 million deaths per year.
The WHO estimates that approximately 2 billion people have been infected worldwide of which over 350 million are chronic carriers.
Hepatitis B is endemic in many developing countries particularly in Asia, Sub-Saharan Africa and the Pacific.
In Europe and North America HBV infection is relatively rare. In areas of low endemicity, most HBV infections are acquired by horizontal transmission in early adult life, particularly through sexual contact and intravenous drug use.
Reservoir
Humans
Mode of transmission
Through direct contact with the bodily fluids of an infected person; blood, saliva, semen, vaginal secretions and to a lesser extent in breast milk, tears and urine.
The concentration of HBV is highest in blood.
In areas of high endemicity, the most common route of transmission is perinatal or is acquired in early childhood.
Common modes of transmission:
Perinatal transmission
Sexual transmission
Close household contact
Intravenous drug use
Child to child transmission
Contaminated needles or syringes
Skin penetrating procedures including acupuncture, body piercing and tattooing.
Needle stick injuries.
The HBV virus is 50-100 times more infectious than HIV.
Incubation period
45-180 days, average 60-90 days
Period of Communicability
All persons who are HBsAg-positive are potentially infectious. The infectivity of chronically infected individuals ranges from high to modest.
Prevention and control
Provide advice and immunization to overseas travellers.
HBV prophylaxis for reported exposure incidents3.
What is the epidemiology profile of Hepatitis C?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Hepatitis C virus. There are 6 HCV genotypes and > 100 subtypes.
Common clinical features
Up to 90% of acute infections are asymptomatic.
Symptoms may include, fatigue, abdominal pain, anorexia, nausea, vomiting and jaundice (rare).
Up to 20% of individuals infected with HCV will clear the virus in 2-6 months. Of those chronically infected 75% will have some degree of active liver disease and of these 25% will progress to cirrhosis over the ensuing 20 years of whom 1-4%will develop liver cancer each year2.
Epidemiology
Endemic worldwide.
HCV is a major cause of liver disease worldwide.
The World Health Organisation estimate that 180 million people are infected with HCV worldwide, 130 million of whom are chronic HCV carriers at risk of developing liver cirrhosis and/or cancer.
In England and Wales there were 8,240 laboratory confirmed cases of HCV in 2004.
In England the prevalence of HCV is estimated to be 0.5% (approximately 200,000 individuals are chronically infected). Amongst diagnosed infections, injecting drug use is the single biggest risk factor, accounting for more than 90% of infections3, 4.
An estimated 5 out of 6 people in the UK with chronic hepatitis C infection are unaware of their infection4.
Most people diagnosed with hepatitis C infection are men aged between 25 and 45 years, reflecting the fact that men are more likely to be injecting drug users3.
The prevalence of hepatitis C in injecting drug users in contact with health services is estimated at 38%3.
Reservoir
Humans
Mode of transmission
Contact with infected blood or bodily fluids. The primary mode of transmission is through contaminated blood 2, 3.
Other less efficient modes of transmission include; mother to child transmission (vertical transmission), sexual transmission, exposure to contaminated medical and dental procedures abroad, tattooing or skin piercing with blood contaminated equipment and patient to health care worker and vice versa2.
The highest risk groups are current and past injecting drug users, those who received blood products before 1986 and recipients of blood transfusions before 1991.
Incubation period
Range 2-6 weeks, commonly 6-9 weeks.
Period of Communicability
From 1 week or more before onset of first symptoms. May persist indefinitely1.
Laboratory Confirmation
Anti-HCV IgG antibody tests are normally positive within 3 months of infection2.
Prevention and control
No vaccine is available for HCV.
In 2004 the National Institute for Clinical Excellence (NICE) recommended a combination therapy with peginterferon alfa and ribavirin for people aged 18 years and over with moderate to severe chronic hepatitis C5.
What is the epidemiology profile of Herpes Simplex?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Two serotypes of herpes simplex virus have been identified. Herpes simplex virus type 1 (HSV-1) and Herpes simplex virus type 2 (HSV-2).
Common clinical features
Infection with HSV is characterized by a localised primary infection, latency and recurrence1.
Herpes simplex virus type 1 (HSV-1) is typically associated with gingivostomatitis1.
Herpes simplex virus type 2 (HSV-2) is sexually transmitted. Symptoms include genital ulcers or sores. The virus may also lead to meningoencephalitis or cause infection of the eye.
Both HSV-1 and HSV-2 can affect the genital tract and HSV-2 can cause primary infection of the mouth1.
Complications include eczema herpeticum, Bell’s Palsy, encephalitis, meningitis, ocular herpes and erythema multiforme1.
Epidemiology
Worldwide 50-90% of adults possess circulating antibodies against HSV-1 and initial infection usually occurs before age 5. There is also a secondary peak among young adults1,2.
HSV-2 infection usually begins with sexual activity and is rare before adolescence2.
Genital herpes simplex virus infection is the most common ulcerative sexually transmitted disease in the UK (Health Protection Agency).
In 2004, 18,991 new cases were diagnosed in the UK with the highest rates observed among young adults aged 20-24 years (Health Protection Agency).
Reservoir
Humans.
Mode of transmission
Direct contact with oral secretions.
Unprotected vaginal or anal sex, genital contact or through oral sex.
Incubation period
1-6 days. The virus may be shed in the saliva for 1-8 weeks after primary infection and for about 3 days in recurrent infections2.
Period of Communicability
HSV can be isolated for 2 weeks and up to 7 weeks after primary infection. HSV may be shed intermittently for years and possible lifelong in the presence or absence of clinical manifestations2.
Treatment
Oral antivirals for primary infection and reactivation.
Topical antivirals may be used for reactivation1.
Prevention and control
Sunscreen and oral antiviral may be considered to prevent reactivation1.
Personal hygiene to limit spread.
What is the epidemiology profile of HIV/Aids?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Epidemiology of Infectious Diseases: HIV/Aids
Causal agent
Human immunodeficiency virus (HIV), a retrovirus is the causative agent for Acquired Immunodeficiency syndrome (AIDS).
Two serologically and geographically distinct types, HIV-1 and HIV-2 have been identified.
Both HIV-1 and HIV-2 have the same modes of transmission and are associated with similar opportunistic infections and AIDS.
HIV-1, which is responsible for the majority of AIDS cases worldwide, is divided into three groups - the ‘major’ group M, the rarer ‘outlier’ group O and ‘new’ group N. Within the M group (which accounts for up to 90% of HIV infections worldwide), at least 9 strains (clades) of HIV-1 have been identified.
HIV-2 infections are less common and are predominantly found in West Africa. HIV-2 infection has a longer latent period before the appearance of AIDS, a less aggressive course of AIDS and a lower viral load with higher CD4 lymphocyte counts thanHIV-1 infection until late in the course of the disease when clinical AIDS is apparent.
Common clinical features
The clinical manifestations of HIV infection range from the initial acute retroviral syndrome to full blown AIDS1.
Acute retroviral syndrome (ARS) is the first stage of infection with the human immunodeficiency virus (commonly occurring between 1-6 weeks following infection) and is characterized by an acute self-limited mononucleosis-like illness lasting for a week or two2. However, primary infection may go unnoticed in up to 50% of cases.
Following exposure there is a period of viraemia during which the individual is highly infectious. Generally, within 3 weeks to 3 months following infection the immune response is accompanied by a simultaneous decline in HIV viraemia.
The stage of clinical AIDS is reached years following infection and is marked by the appearance of one or more of the typical opportunistic infections or neoplasms diagnostic of AIDS by definitional criteria1.
Untreated, half of those with HIV infection will develop AIDS within 7-10 years and of these 80-90% will die within 3-5 years2.
Epidemiology
Data from the UNAIDS 2006 Report of the Global Aids Epidemic report that in 20053.
An estimated 38.6 million people worldwide were living with HIV.
An estimated 4.1 million people became newly infected with HIV.
An estimated 2.8 million people lost their lives to AIDS.
The HIV incidence rate is believed to have peaked worldwide in the late 1990s, and to have stabilised (with the exception of increasing incidence in a number of countries).
United Kingdom
By the end of 2004 there were an estimated 58,300 people living with HIV in the UK, of whom 34% were unaware of their infection4.
The number of newly diagnosed HIV infections in the UK increased from 3,851 in 2000 to 7,275 in 2004. Of these an estimated 30% were in men who have sex with men (MSM). An estimated 60% acquired their infection heterosexually (75% of which are thought to have been acquired in Africa) and 2% through injecting drug use4.
While the number of HIV diagnoses in heterosexuals may have exceeded the number of diagnoses among MSM in recent years, many more MSM acquire HIV within the UK itself. An estimated 75% of all new HIV infections acquired in the UK in 2004 are thought to have been acquired through MSM4.
By the end of 2004 a total of 1,650 children <15 years had been diagnosed with HIV in the UK.
The level of anti-retroviral therapy (ARV) was recorded for 41,478 patients seen for care in the UK in 2004. Of these 64% were receiving 3 or more anti-retroviral drugs, 1.4% were receiving mono or dual therapy and 34% were not on HIV therapy (of which most were at too early a stage of HIV infection for ARV or were recently diagnosed with HIV infection4.
Reservoir
Humans, HIV is thought to have evolved from chimpanzee viruses2.
Mode of transmission
Person to person transmission through exposure to infected blood and tissues.
Unprotected sexual intercourse (anal or vaginal) with an infected partner.
The presence of a concurrent sexually transmitted infection (STI), especially an ulcerative one increases the risk of HIV transmission.
Transmission is especially efficient between male homosexuals in whom receptive anal intercourse and multiple sexual partners are particular risk factors1.
Sharing of contaminated needles or syringes (intravenous drug users).
Transfusion of infected blood or blood products.
Mother to child transmission (MTCT) - An estimated 15-35% of infants born to HIV positive mothers are infected through placental processes at birth2.
MTCT through breast milk.
Transmission via needle stick injury.
The transmission of HIV-2 is similar to that for HIV-1, though perinatal transmission is much less frequent.
Providing infected pregnant women with antiretrovirals significantly reduces the risk of MTCT.
Incubation period
Following exposure HIV nucleic acid sequences may be detected in the blood within 1-4 weeks following infection and HIV antibodies can be detected within 4-12 weeks1.
The time from HIV infection to diagnosis of AIDS has an observed range of less than 1 year to 15 years or longer. The increasing availability of anti-HIV treatment has reduced the development of clinical AIDS in most industrialized countries2.
For perinatally acquired HIV infection, the time to development of clinical AIDS may be shorter than in adults. Signs associated with HIV infection appear in over 80% of seropostive infants by the age of 5 months. Approximately 50% of children with perinatally acquired HIV infection are alive at 9 years.
Period of Communicability
From shortly after the onset of the HIV infection extending throughout life.
Infectivity during the first months is considered to be high; it increases with viral load, with worsening clinical status and with the presence of other STIs2.
Prevention and control
Public health education to reduce high risk behaviours associated with the transmission of HIV.
No vaccine is currently available.
Highly active antiretroviral therapy (HAART) reduces disease progression.
What is the epidemiology profile of influenza?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Influenza is an acute viral disease of the respiratory tract, caused by 3 types of influenza virus: A, B and C.
Influenza A and B are responsible for most clinical illness.
Influenza A is commonly associated with widespread epidemics, type B is infrequently associated with regional or widespread epidemics and type C is commonly associated with sporadic cases1,2.
Common clinical features
Symptoms range from asymptomatic infection (20% of infections) to the sudden onset of fever, chills, headache, myalgia, anorexia, muscle aches, sore throat and cough. Up to 30% of infected individuals have upper respiratory symptoms but no fever and up to 25% of children may also have nausea, vomiting or diarrhoea if infected by influenza B or A (H1N1)2,3.
In healthy individuals influenza is usually a self-limiting illness lasting up to 7 days.
Severe illness and death occur primarily among the elderly and those with underlying chronic cardiac, pulmonary, renal or metabolic disease anaemia or immunosuppresion1. In these groups, the infection may lead to severe complications including bacterial pneumonia and death.
Epidemiology
In the northern hemisphere influenza occurs during the winter months (December - March).
Major genetic changes in the influenza A virus (antigenic shift) occurs at irregular intervals, resulting in the emergence of new sub-types, that may lead to widespread epidemics or a pandemic in populations who have little or no immunity2.
Pandemics have occurred 3 times in the last century. In 1918-19 ‘Spanish Flu’ which affected large parts of the worlds population is estimated to have caused 20-40 million deaths (a large proportion of which were among healthy young adults). More recently, two other influenza A pandemics occurred in 1957 (Asian Influenza) and 1968 (Hong Kong Influenza) which caused significant morbidity and mortality worldwide.
Due to frequent minor genetic changes (antigenic drift) in influenza viruses, vaccines are adjusted annually to include the most recent circulating influenza A(H3N2), A(H1N1) and influenza B viruses.
The composition of influenza virus vaccines for use each year are determined by the WHO Influenza Surveillance Network. The network, a partnership of 4 WHO Collaborating Centres and 112 National Influenza Centres in 83 countries, is responsible for monitoring the influenza viruses circulating in humans and rapidly identifying new strains.
Based on information collected by the network the WHO recommends each year a vaccine to target the 3 most virulent strains in circulation.
In the UK influenza activity is monitored through weekly reports of new consultations for ‘influenza-like illness’ from sentinel GP practices (Royal College of General Practitioners), together with virological surveillance2.
In the UK between 3,000 and 30,000 excess winter deaths per year are attributed to influenza3.
Reservoir
Humans are the primary reservoir for human infection.
Birds and mammals such as swine are likely sources of new human subtypes.
Mode of transmission
Airborne via droplet infection from coughing and sneezing.
Transmission may also occur through fine aerosols and by hand to mucous membrane contact2.
Incubation period
Commonly 1-3 days.
Period of Communicability
From 1 day before and 3-5 days from the onset of symptoms and from 3 days prior and up to 9 days after the onset of symptoms in young children.
Prevention and control
Basic general hygiene (handwashing) to reduce risk of transmission.
Routine immunisation of at-risk individuals is currently recommended in the UK.
The current UK (2005) recommendations are:
All those aged 65 and over.
All those aged six months and over in the following risk groups;
Chronic respiratory disease, including asthma.
Chronic heart disease.
Chronic renal failure.
Chronic liver disease.
Diabetes.
Immunosuppression.
Health and social care staff directly involved in patient care.
Those living in long-stay residential care homes or other long stay care facilities.
Those who are the main carer for an elderly or disabled persons.
What is the epidemiology profile of Japanese Encephalitis?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
A mosquito-borne viral encephalitis caused by a flavivirus1.
(Culex tritaeniorhynchus group)
Common clinical features
The majority of cases of JE infections are mild (fever and headache) or are asymptomatic.
Children and the elderly suffer most clinical disease.
However, approximately 1 in 200 infections result in severe disease characterized by rapid onset of high fever, headache, neck stiffness, disorientation, coma, seizures, spastic paralysis and death4.
Cases-fatality is up to 60% of cases with symptoms of severe disease.
30% of persons who survive suffer from lasting damage to the central nervous system.
Epidemiology
JE is endemic in tropical parts of South East Asia and the Far East including; Australia (islands of Torres Strait), Bangladesh, Bhutan, Brunei, Myanmar, Cambodia, China, India, Indonesia, Japan, Korea, Laos, Malaysia, Nepal, Pakistan, Papua New Guinea, Philippines, Russia, Singapore, Sri Lanka, Thailand, Vietnam and the Pacific Islands.
JE occurs primarily in rural agricultural areas where flooding irrigation is practiced, especially where rice growing and pig farming coexist. However, in many areas of Asia these ecological conditions may occur near or occasionally within urban area3,4.
Transmission is seasonal and occurs in the summer and autumn in temperate regions of China, Japan, Korea and eastern Russia. Elsewhere, seasonal patterns of transmission vary within the rainy season and by irrigation practices3.
JE is the leading cause of childhood viral encephalitis in Asia with 30,000-50,000 clinical cases reported each year4.
The risk of infection with JE in travellers is extremely low.
Reservoir
Ardeid birds (herons and egrets), pigs.
Mode of transmission
Transmitted by the bite of infected mosquitoes from the Culex tritaeniorhynchus and Culex vishnui groups.
No person to person transmission.
Incubation period
5-15 days.
Period of Communicability
Virus not usually demonstrable in human blood after the onset of disease.
Mosquitoes remain infective for life.
Prevention and control
Travellers should undergo careful risk assessment that takes into consideration their itinerary, season of travel, duration of stay and planned activities. This risk of JE should be balanced against the risk of potential adverse affects of vaccination.
Immunisation recommended for those going to reside in areas where JE is endemic or epidemic.
Travellers to South East Asia and the Far East should be immunised if staying for a month or longer in endemic areas during the transmission season, especially if travelling in rural areas
What is the epidemiology profile of Legionnaires Disease?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Infection caused by the bacterium Legionella pneumophilia, of which two distinct forms exist; Legionnaires disease (LD)
Pontiac fever (PF)1
Common clinical features
Both characterized initially by anorexia, malaise, myalgia, headache and fever.
Legionnaires disease is the more severe form of legionellosis and is characterized by pneumonia, commencing 2-10 days after exposure.
Pontiac fever is characterized by the acute onset of flu-like, non-pneumonic illness. Patients recover within 2-5 days without treatment.
Epidemiology
Approximately 300 cases are reported in the UK each year.
Approximately 50% of cases are contracted abroad.
LD has been reported to be responsible for between 0.5% and 15% of community acquired pneumonias2.
High risk groups include, diabetics, the elderly, the immunocompromised, persons with chronic lung disease, heavy alcohol users and smokers.
Case fatality for LD is 10-15% of cases (higher during nosocomial outbreaks).
Reservoir
Environmental water.
Legionellae grow at temperatures between 25 and 450 C, and so the highest risk occurs with water systems that lead to the aerosolisation of water stored at these temperatures.
Legionella is chlorine resistant.
Mode of transmission
Inhalation of contaminated aerosols from devices including cooling towers, air conditioning cooling towers, hot water systems, humidifiers and Jacuzzis.
Incubation period
LD - 2-10 days, commonly 5-6 days.
PF - 5-66 hours, commonly 24-48 hours.
Period of Communicability
Person to person spread has not been demonstrated.
Prevention and control
Methods of prevention include.
Appropriate design, maintenance and monitoring of water systems.
Maintenance and hygiene of wet cooling systems.
Disinfection, regular cleaning and changing of water in indoor fountains and whirlpool spas.
Use of sterile water for respiratory therapy devices.
What is the epidemiology profile of Leprosy?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
A chronic bacterial disease of the skin, peripheral nerves and (in lepromatous patients) the upper airway caused by Mycobacterium leprae.
Common clinical features
Leprosy is a chronic infectious disease affecting the skin and peripheral nerves, but has a wide range of clinical manifestations. Patients are classified as having either paucibacillary or multibacillary leprosy.
Paucibacillary leprosy is a milder disease and is characterized by up to 5 hypopigmented skin macules1.
Multibacillary leprosy is associated with multiple (> 5) skin lesions, nodules, plaques, thickened dermis, and frequent involvement of the nasal mucosa1.
Untreated it can cause permanent damage to the skin, nerves, limbs and eyes.
Epidemiology
In 1981 the WHO recommended the use of multi-drug therapy as a standard treatment for leprosy and in 1991 the World Health Assembly passed a resolution declaring its commitment to eliminate leprosy as a public health problem by the end of 2000.
As a result there has been a dramatic decrease in the global burden of leprosy over the last 20 years. Worldwide cases decreased from approximately 5.2 million in 1985 to 410,000 cases at the end of 2004. This decrease has been the result of widespread use of multi-drug therapy.
Between 1985 and 2005 over 14 million leprosy cases were diagnosed and treated with multi-drug therapy.
In nine countries in Asia, Africa and Latin America (Angola, Brazil, Central African Republic, Democratic Republic of Congo, India, Madagascar, Mozambique, Nepal and the United Republic of Tanzania) leprosy is still considered a public health problem and accounts for a > 80% of the global disease burden.
Reservoir
Humans
Mode of transmission
Thought to be person to person via respiratory droplets.
Incubation period
9 months to 20 years. The average is thought to be 4 years from tuberculoid leprosy and 8 years for lepromatous leprosy2.
Period of Communicability
Infectiousness is lost in most cases following the first dose of multi-drug therapy1.
Diagnosis and Treatment
Multi-drug therapy is highly effective. The World Health Organisation recommends multi drug treatment comprising dapsone, rifampicin and clofazimine.
Prevention and control
Early detection.
Adequate treatment of cases with multiple drug therapy (MDT) which consists of dapsone, rifampicin and clofazimine.
Prevention of disabilities and rehabilitation for leprosy patients.
What is the epidemiology profile of Lyme Disease?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
A tick-borne, spirochaetal, zoonotic disease caused by the bacterium Borelia burgdorferi.
Three genomic groups of B. burgdorferi have been identified in Europe; B burgdorferi sensu stricto, B. garinni and B. afzelii1.
First recognized in 1975
Common clinical features
The first sign of infection is typically characterized by the development of a circular rash, erythema migrans (EM), which occur in approximately 70-80% of infected persons. The rash begins at the site of tick bite after 3-30 days (typically 7-10 days) following exposure.
A distinctive feature of the rash it that it gradually expands over a period of several days, reaching up to 30cm across (often with central clearing).
Multiple secondary lesions may also develop.
With or without EM, symptoms may include malaise, fatigue, fever, headache, stiff neck, myalgia, migratory arthralgia and/or lymphadenopathy, which may last up to several weeks1.
Untreated, infection may spread to other parts of the body causing symptoms including, facial palsy, severe headaches, aseptic meningitis, chorea, cerebellar ataxia, myelitis and encephalitis and cardiac abnormalites1.
Approximately 60% of patients with untreated infection will have intermittent bouts of arthritis, with sever joint pain and swelling (usually knee, elbow or ankle). In addition, up to 5% of untreated patients may develop chronic neurological complaints months to years following infection.
Epidemiology
Lyme disease occurs in the temperate regions of North America (the Northeast, mid-Atlantic and north Central regions), Europe and Asia.
Infection occurs primarily in the summer, with a peak in June and July.
In the UK an average of 300 laboratory confirmed cases are reported annually to the Health Protection Agency, of which most are acquired in the UK. Areas where infection is acquired include Exmoor, the New Forest, the South Downs, parts of Wiltshire and Berkshire, Thetford Forest, the Lake district, the Yorkshire Moors and the Scottish Highlands.
About, 20% of confirmed cases in the UK are acquired abroad2.
However, estimates suggest that between 1000 and 2000 cases of lyme disease occur each year in the UK.
Reservoir
Mice, other rodents and small mammals are the bacterial reservoirs. Birds may also be a reservoir. Deer are an important host for adult ticks2.
Mode of transmission
Transmitted through the bite of Ixodes ticks that are infected with B. burgdorferi.
Ticks become infected when they feed on birds or mammals that carry the bacterium in their blood.
Incubation period
For EM, 3-32 days (mean 7-10 days).
Period of Communicability
No evidence of person to spread.
Prevention and control
Currently no vaccine against lyme disease is available.
Avoid tick bites.
Early treatment with antibiotics helps to prevent the development of complications.
What is the epidemiology profile of Malaria?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Malaria in humans is caused by four different species of the protozoan parasite Plasmodium: Plasmodium falciparum, P. vivax, P. ovale and P. malariae.
Common clinical features
Malaria typically produces a string of recurrent attacks, each of which has 3 stages - chills, followed by fever and then sweating.
Plasmodium. falciparum is responsible for most malaria deaths worldwide. It is most prevalent in sub-Saharan Africa and in certain areas of South East Asia and the Western Pacific.
P. falciparum may present with a varied clinical picture, including one or more of the following, fever, chills, sweats, anorexia, nausea, lassitude, headache, muscle and joint pain, cough and diarrhoea1. If treated inadequately the disease may progress to severe malaria, of which the most important manifestations are; acute encephalopathy (cerebral malaria), severe anemia, icterus, renal failure, hypoglycaemia and respiratory distress1.
Plasmodium vivax, is the most geographically widespread of the species. Once found in temperate climates, P. vivax is now found mostly in the tropics, especially throughout Asia.
P. vivax produces less severe symptoms including, a slowly rising fever of several days duration followed by a shaking chill and rapidly rising temperature, commonly accompanied by headache, nausea and profuse sweating. Following a fever free period this cycle of symptoms may recur daily, every other day or every third day. An untreated primary attack may last from a week to a month. Relapses can occur at irregular intervals for up to 5 years1.
Plasmodium malariae, infections produce typical malaria symptoms and can persist in the blood for very long periods (possibly for life) without producing symptoms.
Plasmodium ovale, is less common and generally occurs in West Africa. It can cause relapses.
Pregnant women are particularly vulnerable to malaria as pregnancy reduces a woman’s immunity to malaria, making her more susceptible to malaria infection and increasing the risk of illness, severe anaemia and death. For the unborn child, maternal malaria increases the risk of spontaneous abortion, stillbirth, premature delivery and low birth weight - a leading cause of child mortality.
Persons who are partially immune or who have been taking prophylactic drugs may show an atypical clinical picture and a prolonged incubation period.
Epidemiology
Reservoir
Humans.
Mode of transmission
Transmitted by various species of infective female Anopheles mosquitoes. Most species feed and night; some important vectors have biting peaks at dusk or in the early morning.
Injection or transfusion of contaminated blood may also transmit malaria.
Congenital transmission is rare.
The mosquitoes that can transmit malaria are found not only in malaria endemic areas, but are also found in areas where malaria has been eliminated. The latter areas are thus constantly at risk of re-introduction of the disease.
Period of Communicability
Humans may infect mosquitoes as long as infective gametocytes are present in the blood.
Anopheles mosquitoes remain infective for life.
Prevention and control
As outlined by Bradley et al. the A, B, C, D of malaria prevention, is essential to prevent the risk of malaria infection among UK travellers.
Awareness -Know about the risk of malaria infection
Bites -Prevent or avoid
Compliance - With appropriate malaria chemoprophylaxis
Diagnose - Breakthrough malaria swiftly and obtain treatment promptly
What is the epidemiology profile of Marburg Heamorrhagic Fever?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Marburg virus of the Filoviridae family.
Marburg haemorrhagic fever is caused by the same family of viruses that causes Ebola haemorrhagic fever. Clinically they are almost indistinguishable.
Common clinical features
Sudden onset of fever, malaise, myalgia, diarrhoea, hypotension and shock, vomiting, rash, impaired kidney and liver function and in some cases internal and external bleeding.
Case fatality rates are between 50-90%.
Epidemiology
Marburg haemorrhagic fever was first recognised in 1967 following outbreaks in Marburg and Frankfurt, German and Belgrade among laboratory workers handling African green monkeys from Uganda1.
MHF is rare, and has only been documented in parts of Uganda, Western Kenya, Zimbabwe (possibly), Democratic Republic of Congo (formerly Zaire).
Reservoir
Unknown possibly primate.
Mode of transmission
Person to person via contact with bodily secretions, organs and blood of infected individuals.
Transmission via infected semen can occur up to seven weeks after clinical recovery.
Nosocomial transmission occurs frequently during outbreaks.
Incubation period
3-9 days.
Period of Communicability
During acute illness.
Treatment
No specific treatment is indicated.
No effective treatment is available. Severe cases require intensive supportive care.
Prevention and control
There is no vaccine against Marburg haemorrhagic fever.
Strict isolation
What is the epidemiology profile of Meningococcal Disease?
Causal agent
Common clinical features
Epidemiology
Mode of transmission
Incubation period
Period of communicabilirt
Laboratory confirmation method
Prevention and control methods
Treatment
Causal agent
Meningococcal meningitis and meningococcal septicaemia are systemic infections caused by the bacteria Neisseria meningitidis. The infection may present as meningitis, septicaemia or a combination of both1.
Meningococci are divided into at least 13 distinct serogroups. The most common are serogroups A, B, C, Y and W135. Most disease in the UK is caused by group B.
Common clinical features
The early symptoms are non-specific and are often mistaken for a viral infection1.
Meningococcal infection progresses rapidly, with the clinical picture changing hourly1.
In infants symptoms can include the sudden onset of fever, floppiness, high-pitched crying, neck retraction with arching of the back and sometimes vomiting. In infants there is progressive irritability, altered consciousness and sometimes convulsions1.
Common symptoms in children and adults can include the sudden onset of fever, malaise, increasing headache, nausea, photophobia, neck stiffness and often vomiting.
In meningococcal septicaemia, a rash may develop along with signs of advancing shock and isolated limb and/or joint pain. The rash may be non-specific early on but as the disease progresses the rash may become petechial or purpuric and may not blanch3.
Meningococcal sepsis occurs without meningitis in 5-10% of invasive meningococcal infections.
Meningococcal disease has a case fatality rate of approximately 10%, in the UK. Case fatality ratios increase with age and is higher in those with septicaemia than in those with meningitis alone3.
Of patients who recover 11-19% develop permanent sequelae, including hearing loss, brain damage, seizures and loss of limb.
Epidemiology
Endemic worldwide.
The highest burden of meningococcal disease occurs in sub-Saharan Africa (the Meningitis Belt) an area from Senegal in the West to Ethiopia in the east where high rates of sporadic infections occur in annual cycles with periodical large scale epidemics2. In 1996, Africa experienced the largest recorded outbreak of epidemic meningitis in history with over 250 000 cases and 25,000 deaths registered.
N. meningititis A, C and W135 are the main serogroups involved in the meningococcal activity in Africa.
In 2005 1,462 laboratory confirmed cases of N. meningitidis were reported in England and Wales. The majority of meningococcal infections occur in children under 5 years, with a peak incidence at 6 months of age. There is a smaller, secondary peak in incidence among young adults aged between 15-19 years of age (HPA).
Meningococcal disease shows a marked seasonal variation with the highest incidence occurring during the winter.
Most cases of meningococcal disease occur sporadically, with <5% of cases occurring in clusters. Outbreaks are more common among teenagers and young adults and outbreaks have been reported in schools and universities (HPA).
Since the introduction of Men C vaccine into the UK routine immunisation programme the number of laboratory confirmed group C cases have fallen by over 90% among all age groups immunised. Cases among other age groups have fallen by two-thirds as a result of reduced carriage rates3.
In the UK serogroup B is now responsible for >85% of laboratory confirmed cases (HPA).
Reservoir
Humans
Mode of transmission
Person to person, transmitted by droplet aerosol or secretions from the nasopharynx of colonized persons.
Transmission usually requires either frequent or prolonged close contract.
Risk factors for the development of disease is not fully understood but may include age, season, smoking, preceding influenza A infection and living in closed or semi-closed communities such as military barracks.
Incubation period
2-10 days, commonly 3-4 days.
Period of Communicability
While live meningococci are present in discharges from nose and mouth.
Meningococci usually disappears from the nasopharynx within 24 hours of appropriate antimicrobial treatment.
Up to 10% of people may be asymptomatic carriers with nasopharyngeal colonization by N. meningititis. However, less than 1% of those colonized will progress to invasive disease1.
High carriage rates of up to 25% have been observed in 15-19 year olds.
Carriage confers natural immunity.
Treatment
An immediate dose of benzyl penicillin for suspected meningococcal infection should be given.
Children aged < 1 year - 300mg
Children aged 1-9 years - 600mg
Adults and children aged >10 years - 1200mg
Prevention and control
In the UK immunisation against meningococcal group C is recommended for persons under the age of 25 years and for all first year university students.
Public health action is indicated for confirmed or suspected cases. There are 4 key actions in response to a suspected case as outlined by Hawker et al1.
Ensure rapid admission to hospital and pre-admission benzyl penicillin.
Ensure appropriate laboratory investigations are undertaken.
Arrange for chemoprophylaxis for close contact and immunisation if infection is due to a vaccine preventable strain.
Provide information about meningococcal disease to parents, GPs and educational establishments.
Chemoprophylaxis
Chemoprophylaxis should be offered to close contacts of cases, irrespective of vaccination status4.
Close Contacts
Close contact are those who have had prolonged close contact with the case in a household type setting during the seven days before the onset of illness. These include; those living and/or sleeping in the same household (including extended household), pupils in the same dormitory, boy/girlfriends, or university students sharing a kitchen in a hall of residence4.
Those who have had transient close contact with a case only if they have been directly exposed to large particle droplets/secretions from the respiratory tract of a case around the time of admission to hospital4.
