Why it Itches when mosquitoes bites us and how to deal with it

Why it Itches when mosquitoes bites us?

Normally mosquito feed on nectar. They are found only female mosquitoes that suck blood. Various types of mosquitoes cause difference disease. However they cause itch on your skin. The female mosquitoes poke their proboscis through your skin so they can suck some of your blood to be later used to make eggs, they inject you with some of their saliva.

This saliva helps them to suck your blood more quickly, because it contains a cocktail of anticoagulants. It may function as blood anticoagulants so it won't clot during sucking. Once the female mosquito is full up of your blood or is disturbed, she flies away, leaving some of her saliva behind. Your body then kicks your immune system in gear as a response to the presence of this saliva.

It produces various antibodies which in turn bind to the antigens in the mosquito’s saliva. This then triggers the release of histamine.

Histamine is a nitrogen compound that, among other things, triggers an inflammatory response. It also helps white blood cells and other proteins to engage invaders in your body by making the capillaries of these cells more permeable. Bottom line, the histamine ends up making the blood vessels near the bite swell up. This produces a pink, itchy bump where the mosquito poked you.

Scratching the bump only makes this worse because it causes more irritation and inflammation of the sight, 

resulting in your immune system thinking it needs more antibodies to get rid of the foreign protein. So the more you scratch, the more it will swell; the itchier it will get; and the longer it will last.

Fit's Tips: After you realize that you've been bitten, try with all your might NOT to scratch that annoying itch - it'll only make it itch and swell more. Wash the area with soap and water, then apply calamine lotion, cortisone, or any other anti-itch cream to the infected area. An ice pack may also help.

For more way how health it see the link

Malaria vaccines could make the disease worse

Malaria vaccines could make malaria nastier. In mice given an experimental vaccine now in trials, the malaria parasite evolved to get round the immunity – and in the process caused more severe disease.

Malaria kills 2000 children every day, sickens millions repeatedly, and helps keep tropical nations in poverty. Yet there is still no vaccine, partly because the parasite takes different forms as it moves from mosquitoes to human blood, to liver cells, red blood cells and back to mosquitoes.

One malaria vaccine – RTS,S – is in large-scale trials. It targets the liver stage of the parasite. Other vaccines in trials target the blood-cell stage, and contain a parasite protein called AMA-1, meant to prime the body's immune system to attack it.

These vaccines all seem likely to be "leaky", allowing vaccinated people to still acquire and transmit some parasites. Parasites that pass through vaccinated people this way could start resisting the vaccine in two ways, says Andrew Read at Pennsylvania State University in University Park. The parasites' AMA-1 could change so that vaccine-induced immunity won't recognise it, a process called immune escape. Or parasites may emerge that dodge immunity in other ways, which could make the disease more virulent.

Rise in virulence

In 2004 Read tested this by passing mouse malaria repeatedly between mice made immune by natural infection. Those parasites indeed became more virulent, but it wasn't clear how.

Read has now repeated the experiment using an AMA-1 vaccine. His team passed blood-cell-stage malaria parasites 10 times between mice that had been given the AMA-1 vaccine. By the end, the parasites reached higher densities, and caused more anaemia, than those passed between unvaccinated mice. Parasites from vaccinated mice were more virulent in unvaccinated mice as well.

"The real eye-opener was that there was no immune escape," says Read. "Parasite AMA-1 was unchanged."

Boosted deadliness

Instead, the parasites had other changes in gene activity that allowed them to escape vaccine-induced immunity, and these changes also made them more virulent. A vaccine that did this in people would lose its effectiveness very quickly, says Read, while boosting the deadliness of local malaria, particularly for unvaccinated people.

Clinical trials test whether vaccines protect people from disease, but don't look for impacts on the actual pathogens, apart from some that have tracked immune escape. Read says that in future such trials should also track which genes are active in malaria parasites in vaccinated people.

Chris Plowe at the University of Maryland in Baltimore, who works on AMA-1 vaccines, agrees. It could be difficult, however, as agencies that fund vaccine trials do not normally fund such tracking.

Journal reference: PLoS Biology, DOI: 10.1371/journal.pbio.1001368

Original from: http://www.newscientist.com/article/dn22125-malaria-vaccines-could-make-the-disease-worse.html

Malaria Parasite Life Cycle

Life Cycle of the Malaria Parasite

The malaria parasite requires specific human and mosquito to complete its life cycle. Once inside a human, the parasite develops and multiplies, causing periodic bouts of flu-like symptoms, including fever, headache, and chills. The developing parasites destroy red cells, which may cause death by severe anemia as well as by the clogging of capillaries that supply the brain or other vital organs with blood. The deadliest of the four species of the parasite is Plasmodium falciparum and Vivax, a species most likely to be transmitted by the mosquito Anopheles gambiae.

1. A female Anopheles mosquito carrying malaria-causing parasites feeds on a human and injects the parasites in the form of sporozoites into the bloodstream. The sporozoites travel to the liver and invade liver cells.
2. Over 5-16 days*, the sporozoites grow, divide, and produce tens of thousands of haploid forms, called merozoites, per liver cell. Some malaria parasite species remain dormant for extended periods in the liver, causing relapses weeks or months later.
3. The merozoites exit the liver cells and re-enter the bloodstream, beginning a cycle of invasion of red blood cells, asexual replication, and release of newly formed merozoites from the red blood cells repeatedly over 1-3 days*. This multiplication can result in thousands of parasite-infected cells in the host bloodstream, leading to illness and complications of malaria that can last for months if not treated.
4. Some of the merozoite-infected blood cells leave the cycle of asexual multiplication. Instead of replicating, the merozoites in these cells develop into sexual forms of the parasite, called male and female gametocytes, that circulate in the bloodstream. 
5. When a mosquito bites an infected human, it ingests the gametocytes. In the mosquito gut, the infected human blood cells burst, releasing the gametocytes, which develop further into mature sex cells called gametes. Male and female gametes fuse to form diploid zygotes, which develop into actively moving ookinetes that burrow into the mosquito midgut wall and form oocysts. 
6. Growth and division of each oocyst produces thousands of active haploid forms called sporozoites. After 8-15 days*, the oocyst bursts, releasing sporozoites into the body cavity of the mosquito, from which they travel to and invade the mosquito salivary glands. The cycle of human infection re-starts when the mosquito takes a blood meal, injecting the sporozoites from its salivary glands into the human bloodstream .

* Time-frame depends on the malaria parasite species. 

Plasmodium

Plasmodium is a genus of parasite infected on blood and known to spread by mosquito (Anophele types). Other genus of mosquito also carrier of malaria but not for other animals. There are about 200 genus kinds of plasmodium and 11 types infected humans. Other species infected other animals, monkeys, rodents, birds, and reptiles. The parasite always has hosts which is mosquito as a vector and a human, or animal host.

 Bellow are the picture of 5 genus of malaria parasite reported high risk to human:

Plasmodium Falciparum

Fig. 1:         Normal Red Cell

Fig. 2-10:    Young Trophozoites (Rings)

Fig. 11-18:   Trophozoites

Fig. 19-26:   Schizonts

Fig. 26:        Ruptured Schizonts

Fig. 27-28:   Mature Macrogametocytes (female)

Fig. 29-30:   Mature Microgametocutes (Male)

Plasmodium Vivax

Fig. 1:         Normal Red Cell

Fig. 2-6:      Young Trophozoites (Rings)

Fig. 7-18:    Trophozoites

Fig. 19-27:   Schizonts

Fig. 28-29:   Mature Macrogametocytes (female)

Fig. 30:        Mature Microgametocutes (Male)

 

Plasmodium Ovale

Fig. 1:          Normal Red Cell

Fig. 2-5:       Young Trophozoites (Rings)

Fig. 6-15:     Trophozoites

Fig. 16-23:    Schizonts

Fig. 24:         Mature Macrogametocytes (female)

Fig. 25:         Mature Microgametocutes (Male)

 

Plasmodium Malariae

Fig. 1:          Normal Red Cell

Fig. 2-5:      Young Trophozoites (Rings)

Fig. 6-13:     Trophozoites

Fig. 14-22:   Schizonts

Fig. 23:        Developing Gametocyte

Fig. 24:        Mature Macrogametocytes (female)

Fig. 25:        Mature Microgametocutes (Male)

Plasmodium Knowlesi

Fig. 1:          Normal Red Cell

Fig. 2-6:       Young Trophozoites (Rings)

Fig. 7-15:     Trophozoites

Fig. 16-23:   Schizonts

Fig. 24:        Mature Macrogametocytes (female)

Fig. 25:        Mature Microgametocutes (Male)