Q.Malaria caused by Plasmodium is transmitted through-------- a) Air b) Contact c) Fleas on food d) Mosquito bites

Plasmodium completes its life cycle using humans as the intermediate host (asexual/liver and blood stages) and the female Anopheles mosquito as the definitive/primary host (sexual stage).

The malarial parasite Plasmodium multiplies asexually inside the human liver and red blood cells, causing the disease's symptoms, but its sexual cycle (production of gametes and sporozoites) occurs inside the gut of the female Anopheles mosquito. Both hosts — humans and the mosquito — are essential for Plasmodium to complete its full life cycle and be transmitted onward.

In the malaria parasite's (Plasmodium) life cycle, the sporozoite is the stage that develops in the mosquito's salivary glands and is infective to humans.

Within the female Anopheles mosquito, the malarial parasite undergoes sexual reproduction and sporogony, ultimately producing thousands of sporozoites that migrate to and accumulate in the mosquito's salivary glands. When the mosquito bites a human to take a blood meal, these sporozoites are injected into the bloodstream. They travel to the liver, invade liver cells, and multiply (forming merozoites), beginning the human phase of infection. Streptozoites and mesozoites are not real stages of the Plasmodium life cycle.

Sexual reproduction of Plasmodium (gamete formation and fusion) happens only inside the gut of the female Anopheles mosquito; in humans only asexual multiplication occurs.

The malarial parasite Plasmodium has two hosts:

• Human (intermediate host): only asexual reproduction (schizogony) takes place — first in liver cells, then repeatedly inside red blood cells. Rupture of infected RBCs releases merozoites and toxic haemozoin, producing the classic recurring chills and high fever of malaria.
• Female Anopheles mosquito (definitive host): when the mosquito bites an infected person, it takes up gametocytes along with the blood meal. Inside the mosquito's stomach, these gametocytes mature into male and female gametes, which fuse to form a zygote — this fusion is the sexual phase. The zygote becomes a motile ookinete, then an oocyst on the gut wall, which eventually produces thousands of sporozoites that migrate to the salivary glands, ready to infect the next person bitten.

Only the female Anopheles is involved because only females take blood meals (needed for egg development) and therefore only they can pick up and transmit gametocytes.

Haemozoin is a haemoglobin-breakdown pigment/toxin generated by the malarial parasite Plasmodium as it feeds on red blood cell contents.

When the malarial parasite (Plasmodium vivax, P. falciparum, etc.) infects red blood cells, it digests the host cell's haemoglobin as a nutrient source. This digestion releases free haem, which is toxic to the parasite; to detoxify it, the parasite polymerises the haem into an insoluble, inert pigment called haemozoin (also called malaria pigment). The periodic rupture of infected RBCs releases haemozoin along with other parasite metabolic products (collectively acting as toxins) into the bloodstream, which triggers the classic cyclical fever and chills of malaria. It is not a precursor of haemoglobin (it is a breakdown product), and it is not associated with Haemophilus or Streptococcus, which are unrelated bacterial genera.

Rupture of RBCs by the malarial parasite releases the toxic pigment haemozoin into the blood, triggering chills and high fever.

Malaria is caused by the protozoan parasite Plasmodium (e.g., P. vivax, P. falciparum), transmitted by the bite of an infected female Anopheles mosquito.

Inside the human body, the parasite multiplies within red blood cells (the erythrocytic cycle). When a large number of RBCs rupture simultaneously (synchronously) to release a new generation of merozoites, they also release a toxic substance called haemozoin (a haemoglobin-breakdown pigment) into the bloodstream.

Haemozoin is responsible for the classic paroxysm of malaria — a bout of chill (rigor), followed by high fever, that recurs every 48 or 72 hours depending on the Plasmodium species, coinciding with the synchronous rupture of infected RBCs.

The sporozoite, injected by the female Anopheles mosquito's bite, is the stage that infects humans with malaria.

The malarial parasite (Plasmodium) has a life cycle that alternates between the human host and the female Anopheles mosquito vector. When an infected female Anopheles mosquito bites a human, it injects thousands of sporozoites (formed in its salivary glands) into the person's blood. These sporozoites are the infective stage - they enter liver cells, multiply, and are then released into the blood as merozoites, which infect and rupture red blood cells (causing the recurring bouts of chill and high fever characteristic of malaria). Trophozoites and gametocytes are later intracellular stages within the RBC, not the stage that initiates infection.

Exo-erythrocytic schizogony of Plasmodium — the asexual multiplication stage occurring outside red blood cells — takes place in the liver.

When an infected female Anopheles mosquito bites a human, it injects sporozoites into the bloodstream. These sporozoites travel to and invade liver cells (hepatocytes), where they undergo asexual multiple fission called exo-erythrocytic schizogony, producing large numbers of merozoites. This 'exo-erythrocytic' (outside-RBC) stage is distinct from and precedes the erythrocytic cycle. Option (b) RBC is where the subsequent erythrocytic schizogony occurs (merozoites released from the liver invade red blood cells and cause the cyclical fever of malaria), not the exo-erythrocytic stage asked about here. Option (a) Stomach and (d) Leucocytes are not sites of Plasmodium schizogony in the human host — the stomach is relevant to the mosquito's sexual (sporogonic) cycle, and leucocytes are immune cells, not typically invaded by schizogony stages.

Haemozoin is the pigment/toxin produced by Plasmodium (the malaria parasite) as a by-product of haemoglobin digestion, and its periodic release causes the characteristic fever of malaria.

When Plasmodium (the causative organism of malaria) multiplies inside human red blood cells, it digests the host cell's haemoglobin for nutrition; the leftover heme component is polymerised into an insoluble, dark pigment called haemozoin (also historically called malarial pigment). When the infected RBCs rupture to release a new brood of merozoites, haemozoin and other toxic metabolic products are released into the bloodstream, triggering the immune/febrile response responsible for the classic recurring chills and high fever of malaria. It is not a precursor of haemoglobin (b) -- it is a breakdown product/waste, not something built into new haemoglobin. It is not associated with Haemophilus (c) or Streptococcus (d) bacteria; those genus names are unrelated to the malarial parasite Plasmodium.

The rupture of red blood cells by the malarial parasite releases a toxin that triggers the body's fever response, producing malaria's classic cyclical chills and fever.

Plasmodium, the causative protozoan parasite of malaria, invades and multiplies inside the host's red blood cells (RBCs) in a repeating cycle. At the end of each cycle, the infected RBCs rupture synchronously, releasing newly formed parasites (merozoites) to infect fresh RBCs, along with a toxic pigment substance called haemozoin (a byproduct of the parasite's digestion of haemoglobin) and other cellular debris into the bloodstream. This sudden release triggers a strong immune/inflammatory response from the host's body, which manifests as the characteristic high fever accompanied by chills and shivering, recurring at regular intervals that correspond to the parasite's synchronised reproductive cycle inside the RBCs (e.g., roughly every 48 or 72 hours depending on the Plasmodium species).

Plasmodium vivax is genuinely digenetic and its cycle has three named phases (schizogony, gamogony, sporogony), but statements (iii) and (iv) contain factual errors.

(i) True -- Plasmodium vivax is a digenetic parasite, needing two hosts (the Anopheles mosquito and humans) to complete its life cycle. (ii) True, reading 'polygony' as the intended term 'gamogony' (gametocyte formation) -- the life cycle is classically described in three phases: schizogony (asexual multiplication in the human liver and red blood cells), gamogony/gametogony (formation of male and female gametocytes, beginning in humans), and sporogony (the sexual cycle completing in the mosquito's gut, producing sporozoites). (iii) False -- the yellowish-brown pigment granules seen in an infected red blood cell/schizont are malarial pigment (hemozoin), a haem-breakdown by-product; Schuffner's granules/dots are a separate, fine pink-red stippling seen in the cytoplasm of P. vivax-infected red blood cells, not the pigment inside the schizont itself, so labelling the schizont's pigment granules 'Schuffner's granules' is incorrect. (iv) False -- Plasmodium multiplies inside and ruptures (lyses) red blood cells, not white blood cells; it is this cyclical lysis of infected RBCs, releasing merozoites and toxic metabolic waste, that produces the periodic fever characteristic of malaria.

Black water fever is a dangerous complication of Plasmodium falciparum malaria.

P. falciparum causes the most severe form of malaria; in some cases massive destruction of red blood cells releases so much haemoglobin that it darkens the urine — the condition called black water fever, which can also involve kidney damage. P. vivax, P. malariae and P. ovale cause milder forms of malaria and are not typically associated with black water fever.