Malaria parasite belongs to

Phylum: ApicomplexaClass: SporozoaOrder: HaemosporidaGenus: Plasmodium.

Calassification of Malaria

Malaria remains the world's mostdevastating human parasitic infection.Malaria affects over 40% of the world'spopulation. WHO, estimates that thereare 350 - 500 million cases of malariaworldwide. In India 2 million cases and1000 deaths annually

Distribution of Malaria

Protozoan parasites characterized by the productionof spore-like oocysts containing sporozoites wereknown as sporozoa.They live intracellularly, at least during part of theirlife cycle.At some stage in their life cycle, they possess astructure called the apical complex, by means of whichthey attach to and penetrate host cells.These protozoa are therefore grouped under thePhylum Apicomplexa.The medically important parasites in this group arethe malaria parasites, Coccidia, and Babesia.The Phylum Apicomplexa includes 2 classes viz.haematozoa and coccidia and 3 orders—eimeriida,haemosporida, and piroplasmida.

Characteristics of Malaria

Plamodium vivax: Benign TertianMalaria.Plasmodium falciparum: MalignantTertian Malaria.

Plasmodium malariae: Benign QuartanMalaria.Plasmodium ovale: Benign Tertian Malaria.

Causative Agents of Human Malaria

Malaria parasites—Erythrocytic stages of the four species (Giemsa stain. Magn × 2000)

The malaria life cycle is a complex systemwith both sexual and asexual aspects . cycleof all species that infect humans is basicallythe same. There is an exogenous sexualphase in the female Anopheles mosquito (thedefinitive host) called sporogony during whichthe parasite multiplies. There is also anendogenous asexual phase that takes placein the vertebrate or human(the intermediatehost) host that is called schizogeny

The malaria life cycle

life cycle of malaria

occurs due to enhanced phagocytosis ofremnants of ruptured red cells and debris ofschizont.

Remnants

Pathogenesis and Clinical Picture

Enlargement of liver and spleen.

The common first symptoms – fever, headache,chills and vomiting – usually appear 10 to 15 daysafter a person is infected. If not treated promptlywith effective medicines, malaria can cause severeillness and is often fatal.

Stage1 (cold stage): Chills for 15 mt to 1 hourCaused due to rupture from the host red cells escapeinto Blood Preset with nausea, vomitting,headache.

Stage 2 (hotstage): Fever may reach upto 400c may last for several hours starts invading newer red cells.

Early symptoms

Stage3: (sweating stage) Patent starts sweating,concludes the episode Cycles are frequentlyAsynchronous Paroxysms occur every 48 – 72 hoursIn P.malariae pyrexia may last for 8 hours or moreand temperature my exceed 410c

More commonly, the patient presents with a combinationof the following symptoms

Fever Chills Sweats Headaches Nausea and vomiting Body aches General malaise.

Complications

• Vivax, ovale & malariae malaria Relatively benign.

• Chronic malariae malaria Nephrotic syndrome.

Parasite produces increased amount of antigens

Immune system produces increased amount of antibodies.

Antigens attach to antibodies producingimmune-complex in blood.

Immune-complexes are deposited on the glomerular walls activating the complement

Child has

nephrotic syndrome

C1, 4, 2,3, 5, 7, 96, 8, MAC

Kidney tissue damage.

Complications of falciparum malaria

1- Knobs develop on surface of infected RBCs

Knobs are parasite antigens expressed on the surface of infected red cells containing trophozoites and schizont stages.

They adhere to receptors found on endothelium of blood capillaries of blood supply internal organs

anoxia and necrosis. Normal RBC

Infected RBC

Parasite antigens

Blood capillary

In brain : cerebral malaria. Headache, drowsiness, convulsions & coma

In GIT : ischaemia in capillary bed of intestinal wall.

Diarrhoea, dysentery, gastrointestinal bleeding

In liver : impaired glycogenolysis, Hypoglycaemia.

In the kidney: acute renal failure.

In the lung : Pulmonary oedema, difficulty in breathing.

Hypotension, circulatory collapse & chock

,

Complications of falciparum malaria

2- Hyper-reactive malarial splenomegalyThe spleen is markedly enlarged with increased IgMproduction. This is due to reduction of T-suppressorcells that control B-cell activation.

3- Black water fever

Occurs: when?

- Repeated attacks of P.falciparum infection.

- Incomplete quinine therapy.

Pathogenesis

Massive intravascular haemolysis occurs producing

Anaemia, haemoglobinuria, jaundice.

Cause This is autoimmune with development of antibodies to infected red blood cells.

Pathogenesis of Black Water Fever

Normal urine

Haemoglobinuria Jaundiced patient

Blood Vessel of the infected patient

Normal RBCs Infected RBCs

Auto-antibodies

1- Thin and thick blood films to demonstrate the parasite.

Thin blood film

Thick blood film

5-Giemsa stained blood films

Microscopic Diagnosis

3-One drop of blood spread on a

slide

4- drops of blood spread in a small circle on a slide

1-Finger prick

2-put drop of blood on slide

Buffy Coat Method

RBCs

Plasma

WBCs, platelets, parasite

Patient’s

blood

Buffy coat

Centrifugation of

blood sample

A technique used for collection of parasite from blood sample

P. vivax P. ovale P. malariae P. falciparum

♂♀ ♀ ♀♀ ♂

♂♂

Schuffner’s dots Ziemann’s dots Maurer’s clefts

Malaria pigments (Haemozoin)

X

X

Enlarged,

rounded

Enlarged,

oval Normal size & shape

Ring 1/6

RBC size

Ring 1/3

RBC size

Ring 1/3

RBC size

Ring 1/3

RBC size

Multiple rings

Not seen in

peripheral blood

Band-

shaped

Diagnosis

2- Detection of circulating parasite antigen using monoclonal antibodies.

3- Detection of parasite DNA and RNA in patient’s blood using DNA and RNA probes.

Malaria pigments = HaemozoinIt is the remnants of haemoglobin that

was digested by Plasmodium parasiteSchuffner’s dots

Ziemann’s dots

Maurer’s clefts It is degeneration process

occurring in Plasmodium

infected RBCs

Called: Stippling

TC

Control

• Treatment of cases.

• Mosquito control.

• Chemoprophylaxis.

• Vaccination trials:

The problem is antigenic variation. A synthetic

vaccine with separation of the gene responsible forantigenic variation.

Chrooquine sulfadoxine, and pyrimethaminealong with primaquine. In chlroquineresistance, quinine or artemesinin are used.

Treatment

Babesia species causes Babesiosis

Hard tick

القراد

Geographical Distribution: North and South America and Europe.

Babesia is an animal parasite that causes Texas cattle fever. It affects humans in contact with animals.

Mode of Infection

• Through the bite of hard ticks.

• Through blood transfusion.

buddingmerozoites

Sporozoites

infective stage

Hard tick

Rings

diagnostic

stage

Rupture

Pathogenesis and Clinical Picture

Asymptomatic.

Malaria-like picture with haemolytic anaemiabut NO periodicity.

Fulminant disease that may end fatally in: Splenectomized OR Immunodefficientpatients.

Babesia is an opportunistic protozoan

Diagnosis

1- Blood film

2- Serology

3- PCR

Prevention and Control

Measures to control ticks

Treatment

Clindamycin + Quinine

Compare between

Blood picture of falciparum malaria and babesia

infected patient.

Ring stage

Gametocyte stage

Ring stage

P.falciparum Babesia

Malaria pigments: present

No malaria pigments