Classical Dengue Fever
Classical dengue fever or”break-bone fever” is an acute viral infection, caused by at least 4 serotypes(1,2,3 and 4) of dengue virus. Dengue fever can occur epidemically or endemically. Epidemics may be explosive and often start during the rainy season when the breeding of the vector mosquitoes (e.g., Aedes aegypti) is generally abundant. Temperature also plays an important role in the transmission of dengue virus by mosquitoes. Mosquitoes kept at 26 C fail to transmit DEN-2 virus. Hence, the low incidence of DHF in certain seasons could be explained by this observation.
The reservoir of infection is both man and mosquito.
Transmission:
The transmission cycle is “Man-mosquito-Man”. Aedes aegypti is the main vector. The Aedes mosquito becomes infective by feeding on a patient from the day before onset to the 5th day of illness. After an extrinsic incubation period of 8 to 10 days, the mosquito becomes infective, and is able to transmit the infection. Once the mosquito becomes infective, it remains so for life.Transovarian transmission of dengue virus has been demonstrated in laboratory.All ages and both sexes are susceptible to dengue fever. Children usually have a milder disease than adults.
Incubation period:
The illness is characterised by an incubation period of 3 to 10 days(commonly 5-6 days).
Signs and symptoms:
the onset is sudden with chills and high fever, intense headache, muscle and joint pains which prevent all movement. Within 24 hours retro-orbital pain, particularly on eye movements or eye pressure and photophobia develops. Other common symptoms include extreme weakness, anorexia, constipation, altered taste sensation, colicky pain and abdominal tenderness, dragging pain in inguinal region, sore throat and general depression. Fever is usually between 39 C and 40 C. The skin eruptions appears in 80% of cases during the remission or during second febrile phase, which lasts for 1-2 days. The rash is accompanied by similar but milder symptoms. The rash may be diffuse flushing phase, mottling or fleeting pin-point eruptions on the face, neck and chest during during the first half of the febrile period and a conspicuous rash. It starts on the chest and trunk and may spread to the extremities and rarely to the face. It may be accompanied by itching and hyperaesthesia. The rash lasts for 2 hours to several days. Fever lasts for about 5 days, rarely more than 7 days after which recovery is usually complete although convalescence may be protracted. The case fatality is exceedingly low.
Treatment:
The management of dengue fever is symptomatic and supportive. Bed rest is advisable during the acute febrile phase. Antipyretics or sponging are required to keep the body temperature below 40 C.Oral fluid and electrolyte therapy is recommended for patients with excessive sweating, vomiting or diarrhoea.Aspirin should be avoided, particularly in areas where DHF is endemic, since it may cause gastritis, bleeding and acidosis.
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TRACHOMA
Trachoma is a chronic infectious disease of the conjunctiva and cornea, caused by Chlamydia trachoma ti's, but other pathogenic microorganisms often contribute to the disease Trachoma inflammation may undergo spontaneous resolution or may progress to conjunctival scarring which can cause inward deviation of eyelashes (trichiasis) or of the lid margin (entropion). The abrasion of the cornea by eyelashes frequently result in corneal ulceration, followed by scarring and visual loss. From the public health point of view, trachoma is classified as blinding and non-blinding. A community with blinding trachoma can be recognised by the presence of persons with lesions such as entropion, trichiasis and corneal ulcers. It is the blinding trachoma often becomes blinding trachoma when other ocular pathogens interact synergistically and enhance the risk of damage of eye sight.
Diagnosis:
In epidemiology studies, more stress is now put on the upper tarsal conjunctiva as a convenient index of trachomatous inflammation in the eye as a whole. For the purpose of diagnosis in the field, cases must have at least 2 of the following diagnostic criteria:
• follicles on the upper tarsal conjunctiva
• limbal follicles or their sequelae, Herbert’s pits
• typical conjunctival scarring(trichiasis, entropion)
• vascular pannus, most marked at the superior limbus
Problem statement:
Trachoma is a major preventable cause of blindness in developing countries. The incidence and prevalence of trachoma has shown a significant decrease in many endemic countries of SEAR during the past few decades. This decrease has been mainly due to improved sanitation, water and housing, and implementation of control measures. However, trachoma, particularly its active form, still remains a public health concern in some parts of Myanmar, in the westren region of Nepal and in a few rural areas in India.
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Agent factors:
a) Agent:
The classical endemic trachoma of developing countries is caused by C.trachoma-tis of immune types A, B or C. The sexually transmitted C. trachoma ti's(serotypes D,E, F, G, H , I, J or K) may also infect, causing an eye disease difficult to differentiate from endemic trachoma. Milder cases of this are usually called “inclusion conjunctivitis”. These strains rarely produce permanent visual loss but they cause respiratory infections( pneumonia) in infants and genital tract infections in adults.
b) Reservoir:
Children with active disease, chronically infected older children and adults.
c) Source of infection:
Ocular discharges of infected persons and fomites
d) Communicability:
Trachoma is a disease of low infectivity. It is infective as long as active lesions are present in the conjunctiva, but not after complete cicatrization.
Host factors:
a) Age:
In endemic areas, children may show signs of the disease at the age of only a few months. But typically, children from the age of two to five years are the most infected, and this contributes not only to the high rate of blindness but also to the rate of occurrence among children.
b) Sex:
Prevalence equal in younger age groups. In older age groups, females have been found to be affected more than males. The explanation for this may be that women remain more in contact with children who infect them. Further, females are more exposed to irritating factors such as smoke than males.
c) Predisposing Factors:
Direct sunlight, dust, smoke and irritants such as kajal or surma may predispose to infection.
Environmental factors:
a) Season:
Seasonal epidemics are associated with vastly increased number of eye-seeking flies. The higher temperature and rainfall favour the increase in fly population.
b) Quality of Life:
Trachoma is associated with poor quality of life. The disease thrives in conditions of poverty, ignorance, poor personal hygiene, squalor, illiteracy and poor housing. As living conditions improve the disease tends to regress.
c) Customs:
The custom of applying kajal or surma to the eyes is a positive risk factor.
Mode of transmission:
In communities where trachoma is endemic, eye-to-eye transmission can be considered as a rule. This may occur by direct or indirect contact with ocular discharges of infected persons or fomites, e.g., infected fingers, towels, kajal or surma. Eye-seeking flies (e.g., Musca spp., Hippelatus spp) play some role in spreading the infection by mechanical transmission. In countries where only sporadic cases of trachoma occur, genital localisation of C.trachoma-tis(urethral, cervical) may lead to venereal transmission.
It has been shown that trachoma is a familial disease. When one case is detected, others will almost certainly be found in the family group. There is a continuous feedback of infection, partly as a result of grandfather’s or sisters and brothers tending small children.
Incubation period:
5 to 12 days
Control of trachoma:
Trachoma control still requires long-term effort. It requires proper planning and organization, which should include the following elements:
1. Assessment of the problem:
The primary objective of a programme for the control of trachoma is the prevention of blindness. Control programmes should be focussed on communities with a substantial prevalence of “blinding trachoma” as indicated by the presence of corneal blindness, trachomatous trichiasis and entropion, and moderate and severe trachomatous inflammation.Such communities are likely to be found in countries with blindness rates that are above 0.5%. The first task therefore is to undertake an epidemiological survey to identify and delimit communities with blinding trachoma; assess the magnitude of the problem, local conditions and other cause of blindness and to obtain information on existing facilities. The basic principles of these surveys are set out in the WHO publication: “ Methods of Assessment of Avoidable Blindness “
2. Chemotherapy:
In trachoma control the main activity is chemotherapeutic intervention. The objective of chemotherapy is to reduce severity, lower the incidence and in the long run decrease the prevalence of trachoma. The antibiotic of choice is 1% ophthalmic ointment or oily suspension of tetracyclines. Erythromycin and rifampicin have also been used in the treatment of trachoma. Treatment may be given to the entire community- this is known as mass treatment (or blanket treatment). In some programmes, selective treatment is chosen in which case, the whole population at a risk is screened, and treatment is applied only to persons with active trachoma.
a) Mass treatment:
A prevalence of more than 5% severe and moderate trachoma in children under 10 years is an indication for mass or blanket treatment. The treatment consists of the application twice daily of tetracycline 1% ointment to all children for 5 consecutive days each month or once daily for 10 days each month for 6 consecutive months, or for 60 consecutive days. An alternative antibiotic is erythromycin.
From the practical point of view, one of the main difficulties is the need for repeated applications of the antibiotic over long periods of time. Emphasis is now being placed on the active participation of the community itself in trachoma control activities and on the utilization of village health guides(primary health care workers). This makes possible a wider coverage and a greater efficacy of the programme.
b)Selective treatment:
In communities with a low to medium prevalence, treatment should be applied to individuals by case finding rather than by community-wide coverage, the principals of treatment remaining the same. For the selective treatment to be effective, the whole population at risk must be screened for case finding.
3. Surgical correction:
Antibiotic ointment is just one component of a trachoma control programme. Individuals with lid deformities should be actively sought out, so that necessary surgical procedures can be performed and followed-up. It has an immediate impact on preventing blindness.
4. Surveillance:
Once control of blindness trachoma has been achieved, provision must be made to maintain surveillance, which may be necessary for several years after active inflammatory trachoma has been controlled. Since trachoma is a familial disease, the whole family group should be under surveillance.
5. Health education:
In the long run, most of the antibiotic treatment must be carried out by the affected population itself. To do this, the population need to be educated. The mothers of young children should be the target for health education. Measures of personal and community hygiene should also be incorporated in programs of health education. Thus real primary prevention could only come through health education for the total elimination of transmission.
6. Evaluation:
Lastly evaluation. Trachoma control programme must be evaluated at frequent intervals. The effect of intervention can be judged by changes in the age-specific rates of active trachoma and in the prevention of trichiasis and entropion.
The 28th World Health Assembly in 1975, in a resolution requested the Director-General of WHO “to encourage Member countries to develop national programmes for the prevention of blindness especially aimed at the control of trachoma, xerophthalmia, onchocerciasis and other causes”.
HEPATITIS E
The infection caused by the hepatitis E virus(HEV) which was discovered in 1990, is essentially a waterborne disease. Formerly termed enterically transmitted hepatitis non-A, non-B. HEV is a 29nm to 32nm RNA virus. Water or food supplies contaminated by faeces in which the virus is excreted have been implicated in major outbreaks reported in all parts of the world that have a hot climate. After an incubation period of 2-10 weeks, with an average of 5 to 6 weeks, a self-limiting acute viral hepatitis appears,lasting for a period of several weeks,which is followed by recovery.No case of chronic disease has been reported.Mainly young adults,aged 15-40 years, have been affected by acute hepatitis E.The virus has at least 4 different types: genotypes 1,2,3 and 4.Genotypes 1 and 2 have been found only in humans .Genotypes 3 and 4 circulate in several animals(including pigs,wild boars, and deer) without causing any disease, and occassionally infect humans.
SIGNS AND SYMPTOMS:
- An initial phase of mild fever,anorexia,nausea and vomiting, lasting for a few days, some persons may also have abdominal pain, itchng, skin rash, or joint pain.
- Jaundice with dark urine and pale stools
- Slightly enlarged, tender liver( hepatomegaly)
DIAGNOSIS:
Diagnosis is made by the level of anti-HEV antibodies in the serum.No confirmatory assay is currently available.Anti-HEV IgM antibodiies have been determined; however,their usefulness for the diagnosis of acute hepatitis E infection remains to be confirmed.
TREATMENT:
There is no specific treatment capable of altering the course of acute hepatitis E.As the disease is usually self-limiting,hospitalization is generally not required.Most important is the avoidence of unnecessary medications. Hospitalization is required for people with fulminant hepatitis, and should also be considered for symptomatic pregnant women.Immunosuppressed people with chronic hepatitis E benefit from specific treatment using ribavirin.
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What is hepatitis d?vaccine and treatment of hepatitis d?
What is hepatitis a? vaccine schedule?hep a vaccine?
What is hepatitis b? hepatitis b vaccine schedule?hep b vaccine?
What is hepatitis c? hepatitis c vaccine schedule?hep c vaccine?
Hepatitis D
A new form or hepatitis that is considered to be a widespread treat is “delta hepatitis “ or hepatitis D. Hepatitis D virus is and unusual, single-stranded, circular RNA virus with a number of similarities to certain plant vira satellites and viroids.Hepatitis D is a liver disease in both acute and chronic forms caused by hepatitis D virus that requires HBV for its replication. Hepatitis D virus cannot occur in the absence of hepatitis B virus.HBV-HDV co-infection is considered the most severe form of chronic viral hepatitis
due to more rapid progression towards liver- related death and hepatocellular carcinoma.
Transmission:
The routes of HDV transmission are the same as for HBV
• Percutaneously
• Sexual
• In contact with infected blood or blood products.
• Vertical transmission is possible but rare
Symptoms:
•Symptoms are same as for hepatitis B
• Acute hepatitis
Risk factors:
• High prevalence in persons who inject drugs
• Sex workers
• Migrants from high HDV prevalence countries
• People who are not immune to HBV
Prevention:
•A vaccine against hepatitis B is the only method to prevent HDV infection.
• Blood safety
• Injection safety
Treatment:
• Pegylated interferon alpha for at least 48 weeks.
• Liver transplantation may be considered for cases of fulminant hepatitis and end-stage liver disease.
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HEPATITIS C
Until a few years ago, the only types of viral hepatitis that could be confirmed were type A and type B. All other were described as infection could be confirmed in blood tests of patients. Since the hepatitis C virus was identified in the year 1989, it has been shown to be the major cause of parenterally transmitted non-A, non-B hepatitis
Description:
 |
| hepatitis c |
Hepatitis C virus is an enveloped single-stranded RNA virus which appears to be distantly related(possibly in its evolution) to flavi viruses, although hepatitis C is not transmitted by arthropod vectors. It is most common blood-borne pathogen.
World problem:
The hepatitis C virus reaches across the globe with highest prevalence in north Africa ana south Asia. A major challenge is buying treatments and vaccines to the various viral genotypes which affect treatment response.
Hepatitis C virus infects nearly 2% of the general population, but 90% of long-term injection drug users.
Egypt has the highest prevalence of hepatitis C with more than 14% of people infected. Upto 85% of patients with acute HCV infection leads to chronic infection defined by persistently detectable HCV RNA for greater than or equals to 6 months.Approximately 20% of patients with chronic Hepatitis C will develop cirrhosis and half of those patients will progress to decompensated cirrhosis or hepatocellular carcinoma.
Transmission:
• Through IV drug use
• Through sexual contact
• Hemodialysis
• Household, occupational or perinatal exposure
Symptoms:
• Patients with acute HCV are often asymptomatic and undiagnosed
• Fatigue
• Anorexia
• Weakness
• Jaundice
• Abdominal pain
• Dark urine
Diagnostic tests:
• Hepatitis C antibody test
Reactive
Non-reactive
• PCR(polymerase chain reaction)
Qualitative HCV RNA
Quantitative HCV RNA
• HCV genotype
• Tests for liver damage
Magnetic resonance elastography(MRE)
Transient elastogrpahy
Liver biopsy
Prevention:
Major prevention problems persists in the developing countries. Many of them cannot afford the anti-HCV blood test kits, where the use of contaminated equipment for injection and other medical and dental procedures is widespread. Health education programs are also needed to inform the general public and health care workers about the risk of transmitting infection with the use of unsterile equipment. Surveillance on a globe scale needs to be strengthened in order to improve medical knowledge of transmission of the virus.
Treatment:
1- Treatment with Pegylated interferon+ ribavirin
2- Sodobovir + other antiviral medicines
3- HARVONI(ledipasvir/sofobovir 90/400mg tablets)
Treatment goals:
• Eradicate HCV infection
• Prevent the development of chronic HCV infection and sequelae
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Hepatitis B
Hepatitis B(formerly known as “serum” hepatitis) is an acute systemic infection with major pathology in the liver, caused by hepatitis B virus and transmitted usually by the parenteral route. It is clinically characterized by a tendency to a long incubation period and a protracted illness with a variety of outcomes. Usually it is an acute self-limiting infection, which may be either sub-clinical or symptomatic.
Problem statement :
Hepatitis B is endemic throughout the world, especially in tropical and developing countries and also in some regions of Europe. Its prevalence varies from country to country and depends upon a complex mix of behavioral, environmental and host factors. In general, it is lowest in countries or areas with high standards of living.
The HBV infection is a global problem, with 66% of all the world’s population living in areas where there are high levels of infection.
More than 2 billion people world wide have evidence of past or current HBV infection and 350 million are chronic carries of the virus, which is harboured in the liver, the virus causes 60-80% of all primary liver cancer, which is one of the three top causes of cancer death in East and SEAR(South- East Asia Region), the Pacific Basin and Sub-Saharan Africa.
Agent Factors:
a) Agent:
Hepatitis B virus was discovered by Blumberg in 1963. Efforts to grow this virus have been so far unsuccessful. HBV is a complex, 42-nm, double standard DNA virus, originally known as the “Dane particle”. It replicates in the liver cells.
b)Reservoir of infection:
Man is the only reservoir of infection which can be spread either from carriers or from cases. The continued survival of infection is due to the large number of individuals who are carriers of the virus, estimated to number over 350 million world-wide.
c)Infective material:
Contaminated blood is the main source of infection, although the virus has been found in body secretions such as saliva, vaginal secretions and semen of infected persons.
d) Resistance:
The virus is quite stable and capable of surviving for days on environmental surfaces. It can be readily destroyed by sodium hypoclorite, as is by heat sterilization in an autoclave for 30 to 60 minutes.
e) Periods of communicability:
The virus is present in the blood during the incubation period(for a month before jaundice) and acute phase of the disease. Period of communicability is usually several months(occasionally years in chronic carriers) or until disappearance of HBsAg and appearance of surface antibody.
Host factors:
a) Age:
In countries in which infection with HBV is relatively uncommon, the highest prevalence of the surface antigen is found in the 20-40 year age group. In countries, where infection with HBV is common, much infection occurs perinatally or during early childhood.
b) High risk groups:
Certain groups carry higher risks. For example, in USA., the annual incidence of HBV infection in surgeons is estimated to be 50 times greater than that in the general population, and is more than twice that of other physicians. Other high risk groups comprise recipients of blood transfusions, health care and laboratory personnel, homosexuals, prostitutes, percutaneous drug abusers, infants of HBV carrier mothers and patients who are immuno-compromised.
c) Humoral and cellular responses:
Antibodies form in a week or two after onset of jaundice- the order being, first core antibody, then “e” antibody and much later surface antibody.
Mode of transmission
a) Parenteral route:
HBV is essentially a blood-borne infection. It is transmitted by infected blood and blood products through transfusions, dialysis, contaminated syringes and needles, pricks of skin, handling of infected blood, accidental inoculation of minute quantities of blood such as may occur during surgical and dental procedures, immunization, traditional tattooing, ear and nose piercing, acupuncture, etc.
b) Perinatal transmission:
Spread of infection from HBV carrier mothers to their babies appears to be an important factor for the high prevalence of HBV infection in some regions, particularly China and SE Asia.The mechanism of perinatal infection is uncertain. Infection of the baby is usually anicteric and is recognized by the appearance of surface antigen between 60-120 days after birth.
c) Sexual transmission:
The sexually promiscuous, particularly male homosexuals, are at very high risk of infection with hepatitis B.
d) Other routes:
Transmission from child to child, often called horizontal transmission. The researchers believe that the spread occur through physical contact between children with skin conditions such as impetigo and scabies, or with cuts or gazes. Often transmission occur when children play together or share the same bed.
Phases of HBV infection:
There are three phases of HBV infection:
1. The incubation period for HBV is 4 to 10 weeks during which patients are highly infective.
2. This is followed by a symptomatic phase with intermittent flares of hepatitis and marked increases in aminotranferase serum levels.
3. The final phase is seroconversion to anti-hepatitis B core antigen(anti-HbcAg).
• Patients who continue to have detectable hepatitis B surface antigen (HbsAg) and a high serum titer of HBV DNA for more than 6 months have chronic HBV.
Clinical Presentation:
• Easy fatigability, anorexia, anxiety and malaise
• Ascites, jaundice, variceal bleeding, and hepatic encephalopathy can manifest with liver decompensation
• Hepatic encephalopathy is associated with hyper-excitability, impaired mentation, confusion, obtundation( altered level of consciousness) and eventually coma
• Vomiting and seizures
Physical Examination:
• lcteric sclera, skin and secretions.
• Decreased bowel sounds, increased abdominal girth, and detectable fluid wave.
• Asterixis(flapping tremor or liver flap)
•Spider angioma( collection of small, dilated arterioles clustered very close to the surface of the skin).
Laboratory tests:
• Presence of hepatitis B surface antigen for at least 6 months.
• Intermittent elevations of hepatic transaminase(alanine transaminase and aspartate transaminase) and
• Hepatitis B virus DNA>105 copies/mL.
• Liver biopsies for pathologic classification as chronic persistent hepatitis, chronic active hepatitis, or cirrhosis.
Prevention:
• Prophylaxis of HBV can be obtained by vaccination or by passive immunity in post-exposure cases with hepatitis B immunoglobulin.
• 2 products are available for prevention of hepatitis B infection:
- Hepatitis B vaccine
- Hepatitis B immunoglobulin (HBIg)
• Goals of immunization against viral hepatitis include prevention of the short- term viremia that can lead to transmission of infection, clinical disease and chronic HBV infection
Hepatitis B vaccine
• Engerix- B:
Vaccine indicated for immunization against infection caused by all known subtypes of hepatitis B virus
Dosage and administration:
• IM administration
• Persons from birth through 19 years of age: A series of 3 doses(0.5ml each) on a 0-,1-,6-month schedule
• Persons 20 years of age and older: A series of 3 doses(1ml each) and a 0-,1-,6- month schedule
• Adults on hemodialysis: A series of 4 doses(2ml each) as a single 2 ml dose or as two 1ml doses on a 0-,1-,6-month schedule
Dosage form and strength:
• 0.5ml(10mcg) single-dose vials and prefilled syringes
•1ml(20mcg) single-dose vials and prefilled syringes
Hepatitis B immunoglobulin:
Used only for post-exposure for HBV for
• Perinatal exposure of infants of HBV- carrier mothers
• Sexual exposure to HBsAg positive persons
• Percutaneous or permucosal exposure to HBsAg-positive blood
• Exposure of an infant to a care giver who has acute hepatitis
Brands available in Pakistan:
• BEHRIN
• HEP-GLOBIN
•HEPATECT and
• HEPUMAN
TREATMENT :
Treatment of chronic HBV with cirrhosis
• Compensated cirrhosis: Treat with Adefovir or entecavir
• Decompensated cirrhosis: Lamivudine+ adefovir or Entecavir + adefovir
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What is hepatitis e? hepatitis e vaccine? hev virus?
Classical dengue fever or”break-bone fever” is an acute viral infection, caused by at least 4 serotypes(1,2,3 and 4) of dengue virus. Dengue fever can occur epidemically or endemically. Epidemics may be explosive and often start during the rainy season when the breeding of the vector mosquitoes (e.g., Aedes aegypti) is generally abundant. Temperature also plays an important role in the transmission of dengue virus by mosquitoes. Mosquitoes kept at 26 C fail to transmit DEN-2 virus. Hence, the low incidence of DHF in certain seasons could be explained by this observation.
