What are White Jaundice & Cerebral Malaria?

---

Two days back a girl in my hostel died from White Jaundice & Cerebral Malaria.. Ppl in my hostel are really scared.. I need to know bout these diseases as how they are transmitted or the reason for getting such diseases.. Pls let me know..
White Jaundice is just the fact that the whites of your eyes turn yellow instead of being white. And Cerebral Malaria can cause this jaundice. Cerebral Malaria is a severe form of Malaria, it attacks the blood vessels in the brain, and is more serious in children. You get Malaria from mosquitoes.




How do you catch malaria?

Malaria is passed on by the Anopheles mosquito biting a person who has malaria parasites in their blood.

The parasites develop in the intestine and salivary glands of the mosquito and can be passed on to other people the next time the mosquito bites.

In man, the parasite travels to the liver via the blood and then out into the bloodstream again where it invades the red blood corpuscles (the cells which carry oxygen in the blood). Malaria can also be passed on by blood transfusions and the use of infected needles
http://www.netdoctor.co.uk/travel/diseases/malaria_disease.htm


Cerebral malaria

Cerebral malaria can affect the brain and the rest of the central nervous system. It is characterised by changes in the level of consciousness, convulsions and paralysis.
http://www.netdoctor.co.uk/travel/diseases/malaria_disease.htm


MORE INFO.
Malaria, in the severe forms of cerebral malaria and acute anaemia, still kills over a million young children in Africa each year.

Malaria parasites live in red blood cells and cause them to stick to the inside of small blood vessels, particularly in the brain and eyes. This produces a 'whitening' of the blood vessels.

The disease also harms light-sensitive tissue in the eye because the parasites feed on the supply of oxygen and nutrients it needs.

St Paul’s has been involved with malaria research and how it affects the eye since 1995, mostly in Malawi and also in Kenya.

With our collaborators we have moved this field forward from interesting curiosity to vital diagnostic tool with unparalleled insight into how malaria becomes life-threatening when it infects the brain. In this disease the eye has truly been a “window on the brain”.

Ocular changes in severe malaria
In malaria, changes occur on the retina, the sensitive nerve tissue that detects light at the back of the eye. The retina develops white patches, multiple discreet haemorrhages and the retinal blood vessels, which are normally red, can become white. The optic nerve can become swollen, indicating increased pressure in the head. Remarkably the vision is rarely affected, but by investigating the nature of these changes we have shed light on disease mechanisms in the brain that lead to coma and death.
http://www.eyecharity.com/research_malaria.htm  (+ info)

Is cerebral Malaria curable?

---

One of my friends 3 year old son was affected with cerebral Malaria and Doctors are not giving a correct answer abt the Cure and if curable dos it come again?
HI, I copy - paste this articles for you, because it's way too long. Read them yourself ok ?

http://www.brown.edu/Courses/Bio_160/Projects1999/malaria/cermal.html

As cerebral malaria is the fatal within days of malaria infection if left untreated, immediate treatment is crucial. Because natural immunity to malaria is not fully understood (Immunity) and thus cannot yet be artificially imitated by drugs, control and prevention strategies are significant. Two of these are antimalarial chemotherapy and adjunctive measures. Public health interventions are also critical

Chemotherapy for cerebral malaria now primarily involves the use of quinine, for a patient with severe CM must be assumed to have chloroquine resistance. It is one of the four main alkaloids found in the bark of the Cinchona tree and is the only drug which over a long period of time has remained largely effective for treating the disease. Quinine has similar activity to chloroquine in that it is likely to interfere with the parasite’s enzymatic digestion.

Artemisinins have been shown in some clinical trials to clear parasitemia and fever faster than quinine or chloroquine, but they had no effect on mortality rates. Artemisinin has been used by the Chinese as a traditional treatment for fever and malaria. It is a sesquiterpene lactone derived from Artemisia annua. The two most widely used are artesunate and artemether. Because it is both cheap and effective, it is beginning to be included in treatment schedules. However, it is not yet licensed for use in Australia, North America or Europe. Its main value is in the treatment of multi-drug resistant falciparum malaria. As the possibility of quinine resistance looms, artemisinin and its derivatives may soon become the drugs of choice for CM treatment (Newton and Warrell).
Adjunctive measures for CM treatment exist, but they are debatable in both use and efficacy:

Anti-pyretics
Such as paracetamol to reduce fever. However, it is not clear if a reduction in core temperature benefits cerebral consequences.

Anti-convulsants
Such as phenobarbital sodium for seizures. It is crucial to control or prevent seizures, as they can cause neuronal damage and are associated with a fatal outcome.

Reduce intracranial pressure
Using agents such as osmotic diuretics.

Hypoglycemia correction
Using hypertonic glucose. However, theoretically, correcting hypoclycemia in the presence of tissue hypoxia can worsen tissue acidosis.

Exchange transfusion
Generally only been justified when peripheral parasitemia exceeds 10% of circulating erythrocytes. The role of these blood transfusions remains highly controversial, as they are both expensive and potentially dangerous in many malaria-endemic areas.

Anti-Inflammatories
Such as corticosteroids. However, there have been few controlled studies demonstrating benefit.

Desferrioxamine
An iron-chelating adjuvant agent with antimalarial properties. Reduces formation of reactive oxygen species by reducing amount of free iron.

Microcirculatory Flow ­
Such as pentoxifylline. Reduces red cell deformability and blood viscosity, decreases systemic vascular resistance, and impairs platelet aggregation, thus improving microcirculatory flow.

Hope this help.  (+ info)

Had Cerebral Malaria in 1951.Recovered then .Could it return?

---

Malaria was in West Africa .and was very serious.
im not 100% sure and in particular about cerebral but i thought that malaria was something that could return. if ur worried tho i think u should speak to yr doctor  (+ info)

why do people with cerebral malaria talk so much and become so powerful?

---

They are not powerful, they are suffering from dimentia read on -

Severe Malaria
Severe malaria occurs when P. falciparum infections are complicated by serious organ failures or abnormalities in the patient's blood or metabolism. The manifestations of severe malaria include:

Cerebral malaria, with abnormal behavior, impairment of consciousness, seizures, coma, or other neurologic abnormalities

Severe anemia due to hemolysis (destruction of the red blood cells)

Hemoglobinuria (hemoglobin in the urine) due to hemolysis

Pulmonary edema (fluid buildup in the lungs) or acute respiratory distress syndrome (ARDS), which may occur even after the parasite counts have decreased in response to treatment

Abnormalities in blood coagulation and thrombocytopenia (decrease in blood platelets)

Cardiovascular collapse and shock  (+ info)

what are the neurological complications of cerebral malaria?

---

1)What are the neurological complications of Cerebral Malaria?
It was Four years back since I have suffered from an attack of malaria.And, the onset of illness was a week back with complaints of headache,fever,nausea and vomiting. Then, I was admitted to hospital and I had been stayed in Coma for seven days. Blood smears confirmed infestation by falciparum malaria.
And its complications followed by Acute Renal Failure then immediate hemodialsis treatment started with all supportive care, after third session my condition markedly improved but I have developed psycho-neurological symptom complex.
After three weeks of stay in the hospital, Liver and renal function tests markedly reduced, then I was partially recovered and discharged.
Although, EEG and MRI imaging four weeks after the onset of illness have shown normal findings, I was told by the doctor as I have brain stem encephalopathy and peripheral neuropathy.
I am now a 36 years old man having difficulty in walking as well as writing. And also I have minimal difficulty to talk. I have visited so far to notable neurologists in this country, but all recommend me one thing ‘’physical exercise’’ however, my conditions get worsening while I started to exercise. Now, I have stopped all exercises except the occupational therapy and walking using a standing frame.
2)What will you recommend me to be able to walk again and work independently?
habtu - Neurologic effects have been reported in children but have not been described in detail in adults. The most striking findings were neuropsychological disorders, in particular memory impairment and diffuse white matter damage on magnetic resonance imaging. Only three of the patients had made a full recovery after 6 months.
In adults, sequelae are less common, and range from 3–10% in prevalence in India, 10% of adults had neurological sequelae on discharge, including psychosis (4%), cerebellar ataxia (3%), and extrapyramidal rigidity or hemiplegia.45 The depth and duration of coma and multiple convulsions were independent risk factors for neurological sequelae.

Subtle deficits (for example, cognitive difficulties, language and behavior problems) are increasingly recognized, and have been documented in 24% of children after recovery from cerebral malaria. The prevalence of these impairments in adults or after other forms of severe malaria is not known, because of lack of long-term follow-up studies with neuropsychological examinations.
Continue to exercise and remain active.  (+ info)

what causes cerebral malaria?

---

am doing medica researh........
pliz help me with your view.
The cause of cerebral malaria is not well understood. Currently, there are two major hypotheses explaining its etiology. They are the mechanical and the humoral hypotheses.

The mechanical hypothesis asserts that a specific interaction between a P. falciparum erythrocyte membrane protein (PfEMP-1) and ligands on endothelial cells, such as ICAM-1 or E-selectin, reduces microvascular blood flow and induces hypoxia. This selective cytoadherence of PRBCs and non-PRBCs, also known as rosetting, can apparently better account for CM’s histopathological hallmark and its characteristic coma condition. However, this hypothesis is inadequate in explaining the relative absence of neurological deficit even after days of unconsciousness.

The humoral hypothesis suggests that a malarial toxin may be released that stimulates macrophages to release TNF-a and other cytokines such as IL-1. The cytokines themselves are not harmful, but they may induce additional and uncontrolled production of nitric oxide. Nitric oxide would diffuse through the blood-brain barrier and impose similar changes on synaptic function as do general anesthetics and high concentrations of ethanol, leading to a state of reduced consciousness. The biochemical nature of this interaction would explain the reversibility of coma.  (+ info)

how do you contract cerebral malaria?

---

Malaria(specially Flciparum type)if not diagnosed and treated promptly can invade Cerebral cortex and cause cerebral Malaria.Deaths in Malaria are always due to cerebral type.  (+ info)

What happened to malaria in the American colonies?

---

I tell my students that early colonists in the Chesapeake suffered from malaria. One asked me why we don't have malaria anymore. Ideas?
Quinine, from the bark of South American Cinchona trees, protected millions of people from malaria in colonial times, enabling exploration and colonization in areas otherwise habitable but for this deadly disease. When administered promptly, quinine has the ability to halt malaria symptoms in just a few days (Garrett, 1994). Qunine has significantly affected the earth's population, for better or worse, by greatly reducing malaria's ability to control populations, especially in cities where large numbers of people were in constant close contact with each other. Before quinine was introduced to India in the 1850s, malaria was killing 1.3% of the population annually. Quinine has allowed India's population to grow to 700 million, whereas without it, India's population would be about 7 times less (Hobhouse, 1986). Populations of natives from western Africa had a high frequency of sickle cell anemia, which has deleterious symptoms, but had the great benefit of rendering afflicted persons largely immune to malaria. For many centuries, blacks from western Africa were preffered slaves because they could work in areas where other people would contract malaria, an  (+ info)

Is it possible to have Malaria for 3 months and a low grade fever?

---

I have been running a fever for about 3 months.
and I have nearly all the symptoms of malaria but my fever is never super high its anywhere from 99 to 100.8 might have been 100.9 before.

there are times I feel almost normal then always get worse again,
is it possible to have malaria this time and it be mild?
If you have been exposed to mosquitoes, it is possible. You need to go for a blood test to find out if you have the malaria virus.  (+ info)

How has Malaria effected the net growth in Africa over the last 50 years?

---

How has Malaria effected the net growth in Africa over the last 50 years?
Probably not too much because malaria is easily treated. Many people in africa take anti-malarials when they develop fever.  (+ info)

---

---

• Home
• Our method
• Usage examples
• Index

• Statistics
• Contact

---