Tuberculin Skin Test For Tuberculosis

What is a skin test?

tuberculin skin test (also known as the tuberculin skin test or PPD Mantoux) test can determine if a person has developed an immune response to bacteria that cause tuberculosis (TB).

The incubation period is two to 12 weeks is usually required after exposure to Mycobacterium tuberculosis PPD test positive.

How to administer TB skin tests?

Recommended standards for tuberculin test, known as the Mantoux test, is administered by injecting 0.1 ml volumes containing 5 TU (tuberculin units) PPD. PPD is injected just under the skin using a very small needle. Discreet, the elevation of pale skin (wheal) 6 to 10 mm is produced. This amount is generally rapidly absorbed.

What is a reading test TB skin?

"Read", a skin test for detecting elevated responses of the skin, hardening. Sclerosis is a key element to detect, not redness. Skin tests should be read in 48 or 72 hours after the test. Reading tests 48 hours before or after 72 hours are not accepted.

The diameter of induration should be measured for the palpable, raised, hardened around the injection site. Again, the redness is not measured.

tuberculin reaction is classified as positive according to the diameter of induration. The screening test, induration greater than or equal to 15 mm is considered a positive skin test. If you have personal contact with someone with active TB, 10 mm induration is considered a positive skin test. Induration of less than 2 mm (0-2mm) as a skin test negative.

The person who received the BCG vaccine (given in some countries but not in the U.S.) against tuberculosis may also have a positive skin test reaction of tuberculosis, although not always so. positive response, which is no vaccine can persist for years. Persons who were vaccinated after the first year of life or who have more than one dose of vaccine are more likely to have a lasting positive results than those who were vaccinated in infancy.

via web.njcu.edu

Our Attention to Disease Dengue Fever

Dengue fever is a disease that there are more mainstream in children and adolescents or adults with clinical signs include fever, muscle pain and / or joint pain, accompanied by leukopenia, with or without rash, and limfodenopati, bifasik fever, headache great, pain on eye movement, impaired taste on the tongue, mild thrombocytopenia, and spontaneous petekie. Dengue hemorrhagic fever or dengue hemorrhagic fever is a disease found in children and adults with primary symptoms of fever, muscle and joint pain, usually worse after the first two days. Spastic syndrome of dengue hemorrhagic fever is a disease accompanied by seizures.

Pathogenesis

Dengue virus is transmitted by Aedes aegypti and Aedes albopictus as a vector that will carry the virus into the human body through mosquito bites. The first infection can give symptoms as dengue fever. If that person gets repeated infections by different dengue virus type will cause a different reaction. Dengue Haemorrhagic Fever can occur when someone who has been infected with dengue the first time, had recurrent infections of other dengue virus. the virus to replicate in the regional lymph nodes and spread to other tissues, especially the reticuloendothelial system and skin as well as haematogenous bronkogen. The body will form virus-antibody complexes in blood circulation and therefore would lead to activation of the complement system resulting in the release of C3a and C5a anafiloksin thus increased permeability of blood vessel walls. Will occur also release ADP platelet aggregation, thrombocyte vasoaktif release that are increasing capillary permeability and the release of thrombocyte three factors that can stimulate intravascular coagulation. The occurrence of Hageman factor activation (factor XII) will cause widespread intravascular coagulation and increased permeability of blood vessel walls.

We Must Pay Attention to The Malaria Disease if it will go to Developing Countries

For those of us who like to go travel to a developing country or we will run the job then we must consider various aspects of safety factors other than the destination country we are. One aspect that is also very important for us to consider among other factors communicable diseases like malaria, filariasis, dengue fever, etc., which exist in the country. Especially for malaria, the disease is spread almost evenly in developing countries such as countries in the continent of Africa, Indonesia, India, and so forth. Malaria is a disease that can be either acute or chronic, caused by protozoa of the genus plasmodium characterized by fever, anemia and splenomegali.

                 figure via : uni-tuebingen.de

Etiology

Plasmodium malaria as a cause consists of four species, namely Plasmodium vivax, Plasmodium falciparum, Plasmodium malariae, and Plasmodium ovale. Malaria also involve an intermediary host, human or other vertebrate and definitive host is the mosquito.

Pathogenesis

The life cycle of malaria species consists of an exogenous sexual phase (sporogoni) in the body of the Anopheles mosquito and the asexual phase (skizogony) in the host body vertebra including humans.

a. Asexual Phase

Asexual phase is divided into phases and phase erythrocyte network. In the network phase, sporozoits enter the bloodstream into liver cells and multiply to form liver schizont containing thousands of merozoites. This process is called skizogony praeritrosit. Long this phase is different for each phase. At the end of this phase, schizont rupture and merozoites exit and enter the bloodstream, called sporulation. In P.vivax and P.ovale, partly hipnozoit sporozoits forming in the heart that can lead to long-term relapse and rekurens.

Phase erythrocytes and merozoites in the blood begins to attack trophozoit erythrocyte shape. The process continues to be trophozoit-schizont-merozoites. After 2-3 generations of merozoites formed, some merozoites turn into sexual forms. The period between the beginning of infection until the discovery of parasites in peripheral blood is prapaten period, while the shoots / incubation sporozoits intrinsic starts from the entry in the host body until the clinical symptoms of fever.

b. Sexual Phase

Sexual parasites in the stomachs of female mosquitoes enter. These forms have become micro and makrogametosit maturation and fertilization occurs, called the zygote (ookinet)). Ookinet then penetrate the mosquito stomach wall and into oocysts. When oocyst rupture the thousands sporozoits be released and reach the salivary glands of mosquitoes.

Pathogenesis of malaria are two ways:

1. Naturally, through the bite of mosquitoes to the human body.

2. Induction, if the asexual stage in erythrocytes into human blood through transfusions, injections or in the

    newborn through the placenta of infected mothers (congenital).

Clinical Manifestations

To find or make a diagnosis of malaria is the most basic necessary information from the disease. symptoms and signs that can be found are fever, splenomegali, anemia, and jaundice. Fever generally occurred periodically since the outbreak associated with the mature schizont (sporulation). In malaria tertiana (P.vivax and P.ovale), schizont maturation occurs every 48 hours so the periodicity of the fever every third day. While on malaria kuartana (P.malariae) maturation occurs every 72 hours so that the periodicity of fever occurs every four days. Each attack is marked by periodic fever attacks. Fever typical of malaria consists of three stages, namely shivering (15-1 hours) with the peak of fever (2-6 hours), and diaphoretic patients (2-4 hours). Fever will decrease gradually because the body can adapt to the parasites in the body and there is immune response.

Examination Support

Peripheral blood examination can still be done and how this is the most suitable although there are other ways ie using rapid test kits (Rapid Diagnostic Test) to detect malaria.

Treatment

Use of antimalarial drugs used not only for curative treatment alone but more than that, it can be used as:

1. Preventive treatment (prophylaxis) which aims to prevent infection or clinical symptoms. Healing can be obtained with this type of therapy on infection by P. falciparum malaria because it does not have parisit eksoeritrosit phase.
2. Curative treatment can be done with malaria drug skizontisid types.
3. Prevention of transmission useful for preventing infection in mosquitoes or mosquito sporogonik influence. Antimalarial drugs that can be used like a type of gametosid or sporotosid.

Filariasis is Still Happening in Developing Countries

Preview Filariasis

Lymphatic filariasis (elephantiasis disease) is a chronic infectious disease caused by the filaria worm. The disease is transmitted by various species of mosquitoes. In 2004, an estimated one-fifth of the world's population or 1.1 billion people in 83 countries at risk of filariasis, particularly in tropical and subtropical areas. This disease can cause disability, social stigma, psychosocial barriers and decreased productivity of patients, families and communities, causing substantial economic losses. Patients with a burden of family and country.

Lymphatic filariasis elimination of global agreements have been reached with recommended resolutions by the World Health Assembly (WHA) on May 13th 1997 is "... ... Elimination lymphatic filariasis as a public health problem ... ... ..". Follow up the resolution, the WHO declared in 2000 the Global Goal Of Elimination Lymphatic Filariasis as a Public Health Problem by 2020. To achieve these objectives the need for epidemiologic picture that includes knowledge about the causes of disease (agent), humans susceptible (host) animals (reservoir hosts), the vector, the environment that influence the development of the disease, the chain of transmission and the situation of filariasis in Indonesia.

Although filariasis does not cause death but it is one cause of disability, poverty and other social problems. This is because in case of permanent disability is lifelong sufferer unable to work optimally, so that it can be a burden his family, to the detriment of society and state. The frequency of acute attacks in patients with filariasis is lowered work productivity so it can also harm the public. In addition, patients will experience an economic loss of approximately 17.8% of household expenses, or 32.3% of the cost of family meals.

Defect in patients with a clinical filariasis due to poor treatment of injured limbs or suffered swelling. Clinical filariasis patients affordable health services are usually no symptoms and severe disability, therefore, patients with chronic clinically severe and permanent disability bias is a poor, remote and inaccessible health services adequately.

The Cause of Filariasis

Indonesia's Filariasis caused by three species of filaria worms:

1. Wuchereria bancrofti

2. Brugia malayi

3. Brugia timori.

Microfilariae have a certain periodicity, that is, microfilariae in peripheral blood at certain times only. For example in W. Bancrofti are periodic nocturnal means numerous in the microfilariae in peripheral blood at night, while by day there are many capillaries in organs such as lung, heart and the kidney.

In epidemiological filaria worms were divided into 6 types, namely:

1. Wuchereria bancrofti urban types (urban)

Found in urban areas such as Jakarta, Bekasi, Tangerang, Semarang, Pekalongan, Indonesia and surrounding countries have a periodicity nokturna, transmitted by Culex quinquefasciatus mosquitoes are breeding in household waste water.

2. Type of rural Wuchereria bancrofti (rural)

Found in rural areas outside Java, particularly widespread in Papua and East Nusa Tenggara, the Indonesian state has periodicity nocturnal transmitted through a variety of mosquito species Anopheles, Culex and Aedes.

3. Type of periodic Brugia malayi nocturnal

Microfilariae are found in peripheral blood at night. Anopheles mosquitoes that spread it are found in areas barbirostis paddy fields.

4. Brugia Malay sub periodic type nocturnal

Microfilariae found in the peripheral blood on day and night, but were more common at night. Mosquitoes that spread it are Mansonia spp found in swamp areas.

5. Non-periodic Brugia malayi type

Microfilariae are found in peripheral blood both night and day. Mansonia mosquitoes transmitted is bonneae and Mansonia uniformis found in the jungle.

6. Timori type of periodic Brugia nocturnal

Microfilariae are found in peripheral blood at night. Anopheles mosquitoes that spread it are barbirostis found in rice cultivation areas in East Nusa Tenggara, Maluku Tenggara, Indonesia country.

Filaria worm morphology

In general, the three species of worm life cycle is no different. Parasite life cycle occurs in the human body and the bodies of mosquitoes. Adult worms (called makrofilaria) living in the tract and lymph nodes, while his son (called microfilariae) in the circulatory system.

1. Makrofilaria

Makrofilaria (adult worms) of cylindrical-shaped, smooth as creamy white yarn and live in the lymph system. Female worms are ovovivipar and measuring 55-100 mm x 0.16 mm, can produce millions of microfilariae. Smaller male worms  55 mm x 0.09 mm with a circular tail.

2. Microfilaria

Female adult worms after fertilization spend millions of children of worms called microfilariae. Microfilaria size 200-600 μm x 8 μm and have a glove. Microscopically, the morphology of microfilariae of species can be distinguished based on: the size and color gloves headroom on Giemsa staining, the core body composition, number and location of the core at the tip of the tail.

Brugia malayi

Wuchereria bancrofti

Brugia timori

Chain Transmission of Filariasis

Filariasis transmission can occur when there are three elements, namely:

1. A source of transmission, is human or host reservoir containing the microfilariae in the blood.

2. The existence of a vector, is mosquitoes that can transmit filariasis.

3. Humans are susceptible to filariasis.

Someone can be infected with filariasis, where a person gets a bite of infective mosquitoes, the mosquitoes containing infective larvae (larval stage 3 - L3). At the time of infective mosquito bites humans, the L3 larvae will exit from the proboscis and live in the skin surrounding the hole mosquitoes. At attract mosquitoes proboscis, L3 larvae will go through a mosquito bite wounds and move toward the lymph system. In contrast to the transmission of malaria and dengue, see the cause of filariasis transmission chain is not easily transmitted from one person to another in a particular area, so it can be said that a person can be infected with filariasis, if he gets a mosquito bite a thousand times.

L3 larvae Brugia malayi and Brugia timori will become adult worms in the period of approximately 3.5 months, while Wuchereria bancrofti takes approximately nine months.

Besides difficult occurrence of mosquito-to-human transmission, real ability to get the microfilariae when mosquitoes suck blood containing the microfilaria is also very limited, the mosquitoes that suck too much microfilaria can experience death, but if microfilariae are sucked too little can minimize the number of microfilariae that L3 larva will be transmitted.

Vector density, temperature and humidity affect the displacement of filariasis. Temperature and humidity affect the life of a mosquito, so that existing microfilaria in mosquito body is not enough time to grow into infective larvae L3 (extrinsic incubation period of parasites). Extrinsic incubation period of Wuchereria bancrofti to between 10 -14 days, while Brugia malayi and Brugia timori between 8 -10 days.

Periodicity of microfilariae and mosquito biting behavior influence infection risk. Microfilariae that are periodically nocturnal (microfilaria only found in the peripheral blood at night) has a vector that actively seek out the blood at night, so that transmission also occurs at night. In regions with sub-periodic microfilariae nocturnal and non-periodic, transmission can occur day and night.

In addition to the above factors, population mobility from filariasis-endemic areas to other areas or vice versa, the potential to become the media of inter-regional spread of filariasis.