“ The greatest harm to the greatest number “
Bangar raju Dept of Microbiology KMC-IC
IMPORTANCE
Important of all protozoal diseases Occurs mainly in tropics and subtropical countries being highly endemic in Sub Sharan Africa 200-300 million cases annually 1-2 million people die of malaria Caused by a blood protozoan belonging to genus Plasmodium
Malaria
Plasmodium falciparum Plasmodium vivax Plasmodium ovale Plasmodium malariae
Malaria
geographic distribution
Reported malaria cases in 2006
USA: 844 South Carolina: 8 South-East: 41
Reported indigenous malaria cases in the US (1957-2003)
Reported indigenous malaria cases in the different states (1957-2003)
Species of indigenous malaria cases reported in the US (1957-2003)
Encounter and entry:
Transmitted to humans by mosquito vector, female Anopheles After 9 to 17 days after a female anopheles ingest blood from a person Develops malaria symptoms 8 to 30 days later Most of the cases in USA are imported cases Anopheles exist in United states Can also be transmitted by sharing needles among intravenous drug users- induced malaria
Spread and multiplication:
Life cycle comprises two stages Asexual phase- in humans (Intermediate host) In Asexual phase- parasite divides by fissionschizogony Schizogony in humans occurs in two places- in liver cells and in RBCs In liver the cycle is called is Pre erythrocytic cycle and in RBCs it is called as Erythrocytic cycle The products of these two cycles are called as merozoites.
Sexual phase- in mosquito (Definitive host) Sexual phase takes place in female anopheles mosquito Cells required for this phase are formed in human Only maturation and fertilization takes place in mosquito Products of this cycle are called as sporozoites Hence called as sporogony Thus showing alternation of generation- asexual and sexual phases alternatively
Malarial parasites
life cycle
Features of pre-erythrocytic schizogony in humans
P. vivax Pre erythrocytic stage (days) Diameter of pre erythrocytic schizont No of merozoites in PES 8 P. falciparum P. malariae 5.5 15 P. ovale 9
45
60
55
60
10,000
30,000
15,000
15,000
Malarial parasites
morphology
Malignant tertian
Benign tertian Ovale tertian
Quartan
PATHOGENESIS AND CLINICAL PICTURE
Characterized by fever, head ache and prostration and often serious complications Classified by the interval between fever attacks With each attack of fever the patient feels shivering, then hot and dry then drenching sweats Headache is usually severe with myalgia- misdiagnosed as only influenza All malaria causes red cell destruction with anemia and splenomegaly Falciparum malaria causes red cell sludging and cytokine release causing cerebral malaria Immune glomerulonephritis is common, hematuria, renal failure can occur as complications
Malarial symptoms
type
tertian (vivax and ovale)
organ Involved
spleen, liver, erythrocytes systemic
symptoms
headache, lassitude, vague aching of bones and joints, chills and high fever (103-106 F), nausea and vomiting, convulsion, euphoria, profuse sweating. Symptoms every other day and last 812 hours . Spontaneous recovery same as above but no tertian pattern: there may be daily spiking; no spontaneous recovery and ultimately fatal. Renal & CNS involvement same as tertian, but paroxysm occurs every three days (2 clear days)
falciparum (malignant tertian) quartan (malariae)
Malarial paroxysm
Malarial diagnosis
Travel history symptoms Blood smear thick and thin smear
f
v
o
m
THICK AND THIN SMEAR
DIPSTICK TEST FOR MALARIA
Quantitative blood count (QBC)
Malaria
control and treatment
Control Control mosquito population Mosquito netting Treatment: Quinine derivatives P. falciparum often drug resistant Quinine can be use prophylactically
Blackwater Fever
Black-water fever is a rare but deadly form of malaria. In some cases, it can kill a person within a few hours of being infected. In Black-water fever, Plasmodium falciparum parasites cause the break-down of a huge number of red blood cells at the same time. Hemoglobin from these broken-down cells is passed from the body mostly in the urine
The victim's urine turns such a deep red that it is almost black. The effects of Blackwater fever come on so fast that drug therapy may not be effective. Instead, people with Blackwater fever are given exchange blood transfusions in an effort to get rid of infected red blood cells and replace them with healthy cells.
What is Cerebral Malaria?
Cerebral malaria is a rapidly developing encephalopathy, but much pathology of is not clearly understood. Malaria occurs in millions of people, but only 2050 % of the cases develop into cerebral malaria. It is unclear why some people develop it and others do not. Cerebral malaria develops when parasitized red blood cells (PRBCs) adhere to the cerebral microvasculature, causing blockage of the blood's pathway
This blockage stops blood flow, leading to a shortage of oxygen and nutrients those areas of the brain. The occlusion of the small vessels occurs diffusely throughout brain. This phenomenon seems to occur in all patients with cerebral malaria, although there are numerous other complications that occur as a result of this disease.
Approximately half of the patients with cerebral malaria have elevated intercranial pressure and seizures. On rare occasions, the parasite causes cerebellar ataxia, but no loss of consciousness. The ataxia can occur up to 4 weeks after a malaria attack occurs, but will disappear after 1-2 weeks. Physical manifestations of the disease may be an abnormal EEG resulting from the lack of oxygen, loss of sulci, and a MRI may show hemorrhagic lesions and infarction.
A common cause of death for patients with cerebral malaria is acute respiratory arrest, may be a result of the intracranial pressure causing a fatal brain stem herniation. Most people who survive cerebral malaria have no residual neurologic problems. Only about 10 % of patients surviving cerebral malaria suffer from neurologic deficits such as hemiparesis, hypotonia, or spasticity
Have an unclear understanding of the disease because so many people survive the disease without any neurologic problems. This fact leads us to believe it is unlikely that there is complete obstruction of blood flow. One hypothesis is that the parasite indirectly causes an abnormally high release of nitric oxide in the brain, which changes brain function in the same way as ethanol. This would result in a unconscious state. This hypothesis explains the reversibility of the coma state, it does not explain many of the other problems associated with the disease, such as the blocked microvasculature.