Tuesday, May 27, 2008


Lymphatic Filariasis (Philariasis) is a parasitic and infectious tropical disease, caused by three thread-like parasitic filarial worms called nematode worms, Wuchereria bancrofti, Brugia malayi, and Brugia timori, all transmitted by mosquitoes. It is extremely rare in Western countries. Loa loa is another filarial parasite of humans, transmitted by the deer fly.


The most spectacular symptom of lymphatic filariasis is elephantiasis—thickening of the skin and underlying tissues—which was the first disease discovered to be transmitted by a mosquito bite. Elephantiasis is caused when the parasites lodge in the lymphatic system. Elephantiasis affects mainly the lower extremities, whereas ears, mucus membranes, and amputation stumps are rarely affected; however, it depends on the species of filaria. W. bancrofti can affect the legs, arms, vulva, breasts, while Brugia timori rarely affects the genitals. Infection by Onchocerca volvulus and the migration of its microfilariae through the cornea is a major cause of blindness (Onchocerciasis). This disease is not known to be fatal, although it can obviously cause a fair amount of pain to the infected.


Filariasis is endemic in tropical regions of Asia, Africa, Central and South America with 120 million people infected. In endemic areas of the world (e.g., Malaipea in Indonesia), up to 54% of the population may have microfilariae in their blood.


Lymphatic Filariasis is thought to have affected humans since approximately 1500-4000 years ago, though an exact date for its origin is unknown. The first clear reference to the disease occurs in ancient Greek literature, where scholars discuss diagnosis of lymphatic filariasis vs. diagnosis of similar symptoms that can result from leprosy. The first documentation of symptoms occurred in the 16th century, when Jan Huygen Linschoten wrote about the disease during the exploration of Goa. Soon after, exploration of other parts of Asia and Africa turned up further reports of disease symptoms. It was not until centuries later than an understanding of the disease began to develop. In 1866, Timothy Lewis, building on the work of Jean-Nicolas Demarquay and Otto Henry Wucherer, made the connection between microfilariae and elephantiasis, establishing the course of research that would ultimately explain the disease. Not long after, in 1876, Joseph Bancroft discovered the adult form of the worm, and finally in 1877 the life cycle involving an arthropod vector was theorized by Patrick Manson, who proceeded to demonstrate the presence of the worms in mosquitoes. Manson incorrectly hypothesized that the disease was transmitted through skin contact with water in which the mosquitoes had laid eggs. In 1900, George Carmichael Low determined the actual transmission method by discovering the presence of the worm in the proboscis of the mosquito vector.


The diagnosis is made by identifying microfilariae on a Giemsa stained thick blood film. Blood must be drawn at night, since the microfilaria circulate at night, when their vector, the mosquito, is most likely to bite. There are also PCR assays available for making the diagnosis.


Medicines to treat lymphatic filariasis are most effective when used soon after infection, but they do have some toxic side effects. In addition, the disease is difficult to detect early. Therefore, improved treatments and laboratory tests are needed. Once Filaria is attacked, the patients are likely to get fever once in a year or two with shivering. They are also administered Florocid injections

Antibiotics as a possible treatment

In 2003 it was suggested that the common antibiotic doxycycline might be effective in treating elephantiasis. The parasites responsible for filariasis have a population of symbiotic bacteria, Wolbachia, that live inside the worm. When the symbiotic bacteria are killed by the antibiotic, the worms themselves also die. Clinical trials in June 2005 by the Liverpool School of Tropical Medicine reported that an 8 week course almost completely eliminated microfilariaemia. Diethylcarbamazine Citrate (Hetrazan) The good drugs of choice for killing adult filarial worm are Albendazole (broad spectrum anti-helminthic) and Ivermectin. A combination of DEC & Albendazole or DEC & Ivermectin is found more effective

Dengue Fever

Dengue fever and dengue hemorrhagic fever (DHF) are acute febrile diseases, found in the tropics and Africa, and caused by four closely related virus serotypes of the genus Flavivirus, family Flaviviridae.[1] The geographical spread is similar to malaria, but unlike malaria, dengue is often found in urban areas of tropical nations, including Singapore, Taiwan, Indonesia, Philippines, India and Brazil. Each serotype is sufficiently different that there is no cross-protection and epidemics caused by multiple serotypes (hyperendemicity) can occur. Dengue is transmitted to humans by the Aedes aegypti (rarely Aedes albopictus) mosquito, which feeds during the day.

Signs and symptoms

This infectious disease is manifested by a sudden onset of fever, with severe headache, muscle and joint pains (myalgias and arthralgias—severe pain gives it the name break-bone fever or bonecrusher disease) and rashes. The dengue rash is characteristically bright red petechiae and usually appears first on the lower limbs and the chest; in some patients, it spreads to cover most of the body. There may also be gastritis with some combination of associated abdominal pain, nausea, vomiting or diarrhea. Other symptoms include: fever;bladder problems;constant headaches;severe dizziness; and,loss of appetite. Some cases develop much milder symptoms which can, when no rash is present, be misdiagnosed as influenza or other viral infection. Thus travelers from tropical areas may inadvertently pass on dengue in their home countries, having not been properly diagnosed at the height of their illness. Patients with dengue can pass on the infection only through mosquitoes or blood products and only while they are still febrile. The classic dengue fever lasts about six to seven days, with a smaller peak of fever at the trailing end of the disease (the so-called "biphasic pattern"). Clinically, the platelet count will drop until the patient's temperature is normal. Cases of DHF also show higher fever, haemorrhagic phenomena, thrombocytopenia, and haemoconcentration. A small proportion of cases lead to dengue shock syndrome (DSS) which has a high mortality rate.


The diagnosis of dengue is usually made clinically. The classic picture is high fever with no localising source of infection, a petechial rash with thrombocytopenia and relative leukopenia. The WHO definition of dengue haemorrhagic fever has been in use since 1975; all four criteria must be fulfilled:[3] Fever, bladder problem, constant headaches, severe dizziness and loss of appetite.Hemorrhagic tendency (positive tourniquet test, spontaneous bruising, bleeding from mucosa, gingiva, injection sites, etc.; vomiting blood, or bloody diarrhea)Thrombocytopenia (<100,000>


The mainstay of treatment is supportive therapy. Increased oral fluid intake is recommended to prevent dehydration. Supplementation with intravenous fluids may be necessary to prevent dehydration and significant concentration of the blood if the patient is unable to maintain oral intake. A platelet transfusion is indicated in rare cases if the platelet level drops significantly (below 20,000) or if there is significant bleeding. The presence of melena may indicate internal gastrointestinal bleeding requiring platelet and/or red blood cell transfusion. It is very important to avoid aspirin and non-steroidal anti-inflammatory drugs; these drugs may aggravate the bleeding tendency associated with some of these infections. Patients should receive instead paracetamol preparations to deal with these symptoms if dengue is suspected.

Emerging treatments Emerging evidence suggests that mycophenolic acid and ribavirin inhibit dengue replication. Initial experiments showed a fivefold increase in defective viral RNA production by cells treated with each drug. In vivo studies, however, have not yet been done.