What is classical dengue fever? dengue fever vaccine? dengue fever

 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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What is trachoma? Trachoma?eye diseases

 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”. 

what is hepatitis e? hepatitis e vaccine?hev virus

                                       

                     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 c? hepatitis c vaccine schedule?hep c vaccine?

What is hepatitis d? hepatitis d vaccine? hdv virus?

        

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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                     What is hepatitis b?hepatitis b vaccine schedule?hep b vaccine ?
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                    What is hepatitis e? hepatitis e vaccine?hev virus?

What is Alpha Blockers? Side effects of alpha blockers? Alpha blockers

     

 ALPHA ADRENERGIC RECEPTOR  BLOCKING AGENTS

              (ALPHA BLOCKERS)

Drugs with diverse chemical structures block alpha adrenergic receptors and inhibit their responses.The blockade is reversible except in case of  phenoxybenzamine which causes irreversible blockade  due to its covalent biding to alpha receptors.
  These drugs differ regarding their capability of blocking the two subtypes of alpha receptors i.e. postsynaptic alpha 1 receptors and presynaptic alpha 2 receptors. Prazosin is a selectoive blocker of postsynaptic alpha 1 receptors.Phenoxybenzamine is more potent in blocking postsynaptic alpha 1 receptors than in blocking presynaptic alpha 2 receptors. Phentolamine and tolazoline are nonselective blockers of alpha receptors. On the other hand yohimbine is a selective alpha 2 blocker.

CLASSIFICATION OF ALPHA BLOCKERS:

1. CHEMICAL CLASSIFICATION:

• BETA-Halokylamines

           Phenoxybenzamine
           Dibenamine

• Substituted Imidazolines

           Phentolamine

           Tolazoline

• Phenoxyalkylamines

          Thyroxamine

• Ergot alkaloids

           Ergotamine

           Dihydroergotamine

• Dibenzapines

           Azapetine

• Benzodioxans

           Piperoxan

• Indolealkylamines

           Yohimbine

• Phenothiazines

           Chlorpromazine

• Miscellaneous

           Prazosin

           Indoramine

           Labetalol

   
      2.  CLASSIFICATION BASED  ON DURATION OF ACTION:

• Reversible 

           Phentolamine

           Tolazoline

           Prazosin

• Irreversible

           Phenoxybenzamine

           Dibenamine

      3..CLASSIFICATION BASED ON SELECTIVITY OF ACTION:

• Selective alpha 1 Postsynaptic blocking agent

           Prazosin

• Predominantly aplha 1 Postsynaptic blocking agent

           Phenoxybenzamine

• Selective alpha 1 Presynaptic blocking agent

          Yohimbine

• Non-selective( Blocks both alpha 1 and alpha 2)

          Phentolamine

 PHARMACOLOGICAL ACTIONS OF ALPHA BLOCKERS

    These drugs bind to alpha adrenergic receptors and interfere with the capacity of sympathomimetic amines to initiate action at these sites.They prevent the response of effector organs to adrenaline,nonadrenaline and other sympathomimetic amines whether released in the body or injected. Circulating catecholamines are antagonized more readily than are the effects of sympathetic nerve stimulation. Phenoxybenzamine binds covalently to the alpha receptors and produce irreversible blockade. Other drugs bind reversibly and antagonize the action of sympathomimetic amines competitively.

Vasodilation:

  The principal action of all alpha blackers is to produce peripheral vasodilation, with the exception of ergotamine which possesses a direct vasoconstrictor action.

Vasomotor Reversal:

   Alpha blockers reverse the pressor effect of adrenaline due to the unmasking of beta effects producing vasodilation of skeletal muscle vessels and hypotension. These drugs abolish the pressor effect of nonadrenaline which possesses mainly alpha effects.

Miosis:

  These drugs constrict pupil of eyes by blocking the action of fibres of iris.

THERAPEUTIC USES OF ALPHA BLOCKERS:

Peripheral Vascular Spastic Disease:

   With the exception of the ergot alkaloid,alpha blockers have been used in the treatment of peripheral vascular spastic diseases for such conditions as thromboangitis obliterans(Buerger's disease) and Raynaud's syndrome. It is assumed that sympathetic hyperactivity contributes in part to these conditions and that this component is eliminated by alpha receptors blockade. Alpha blockers are used for treatment of chillblains and intermittent claudication.

Phaeochromocytoma:

   Alpha blockers are used in the investigation and in the preoperative treatment of phaechoromocytoma which is a rare hyperfunctioning tumour of adrenal medulla. It is composed of chromaffin tissue and secreates large quamtutues of adenaline and nonadrenaline, alpha adrenergic blockade transiently lowers the elevated arterial pressure that is characteristic of this tumour.

Hypertension:

  Treatment of hypertension with alpha blockers except prazosin has been rather disappointing due to reflex tachycardia and palpitation produced by them. Usefulness of prazosin in hypertension may be due to its lack of potency in inhibiting presynaptic alpha 2 receptors. Phenoxybenzamine and phentolamine have been used successfully to control acute hypertensive episodes due to symparhomimetics,amd to certain foods and drugs in the presence of MAO inhibition.

Autonomic Hyperreflexia:

   It follows high spinal cord transection and is associated with paroxysmal elevation in blood pressure. These pressor episodes and associated signs ans symptoms are well controlled by relatively small oral doses of phenoxybenzamine,

Glaucoma:

    Alpha blockers may be use in glaucoma.

Migraine:

   Ergotamine is of particular value in migraine due to its direct vasoconstrictor effects.

Shock:

 In certain types of shock when reflex neurogenic vasoconstriction due to hyperactivity of compensatory mechanisms is a prominent feature, the judicial use of alpha blockers can increase local blood flow in important areas, kidney and mesenteric bed, where local anoxia is relieved and recovery facilitated. These drugs should not be given unless the central venous pressure has been elevated by fluid administration without an adequate circulatory response. However use of dopamine is preferred in such situations.

ADVERSE EFFECTS OF ALPHA BLOCKERS:

• Postural Hypotension
• Tachycardia
• Nasal Stuffiness
• Sedation
• Diarrhoea
• Failure of ejaculation

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