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2025 SEM 2 CLINICAL PARASITOLGY (LEC) > plasmodium and babesia > Flashcards

plasmodium and babesia Flashcards

1
Q

what are the disease caused by plasmodium and babesia

A

parasitic infections
Plasmodium → Malaria
Babesia → Babesiosis

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2
Q

subkingdom, phylum and class of plasmodium and babesia

A

subkingdom: protozoa
phylum: apicomplexa
class: sporozoa (non-motile parasites )

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3
Q

how many known species are there in plasmodium and babesia and how many can infect humans

A

Plasmodium:
~200 known species, 10 can infect humans.
Babesia:
~100 known species, 4 can infect humans.

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4
Q

briefly explain the distribution of plasmodium species

▪ Plasmodium vivax
▪ Plasmodium ovale
▪ Plasmodium malariae
▪ Plasmodium falciparum
▪ Plasmodium knowlesi
▪ Babesia microti
▪ Babesia divergens

A

Plasmodium vivax:
Most predominant malaria parasite worldwide.

Plasmodium falciparum:
Confined to tropics & subtropics; causes malignant tertian malaria (most fatal).

Plasmodium malariae:
Found in subtropical & temperate areas, but less common.

Plasmodium ovale:
Limited to West Africa.

Plasmodium knowlesi:
Found in Southeast Asia; a zoonotic parasite from macaques.

Babesia microti → Most common in the USA.

Babesia divergens → More common in Europe.

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5
Q

Most predominant malaria parasite worldwide.

A

Plasmodium vivax

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5
Q

it causes malignant tertian malaria

A

Plasmodium falciparum

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6
Q

a zoonotic parasite from macaques

A

Plasmodium knowlesi
(macaques monkey to humans)

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7
Q

habitat and transmission of plasmodium

A

habitat:
- erythrocytes
- hepatocytes (liver cells)

vector:
- transmitted by over 60 species of female Anopheles mosquitoes

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8
Q

briefly explain the anopheles mosquitos’ resting place and breeding stage

A

transes

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9
Q

host of malaria parasite

A

it requires 2 hosts:

  1. definitive host - Female Anopheles mosquito (sexual reproduction)
    - producing sporozoites for transmission
  2. intermediate host - Humans (asexual reproduction)
    reproduction in:
    - liver cells (exoerythrocytic stage)
    - RBCs (erythrocytic stage)
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10
Q

mode of transmission of malaria parasite

A

▪ Mosquito bite (primary mode)
- pri and most common method
▪ Blood transfusion
▪ Congenital transmission (mother to fetus)
▪ Shared syringes

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11
Q

what are the morphological form of the stages of the plasmodium life cycle

A

[refer appearance to the transes]

Ring Forms (Early Trophozoites):
- earliest form after RBC invasion
- found in all plasmodium but varies slightly in shape

Developing Trophozoites:
- the parasite grows, consuming hemoglobin and producing hemozoin pigment.
- more RBC space occupied

Immature Schizonts:
- early stage of schizogony (asexual reproduction)
-expands and occupies more space within RBCs

Mature Schizonts:
- final stage before RBC ruptures, releasing merozoites
- leads to merozoite invasion of new RBCs, continuing the cycle

Gametocytes (Microgametocytes & Macrogametocytes):
Microgametocytes (male gametocytes)
Macrogametocytes (female gametocyte)

Instead of continuing the asexual cycle, some parasites differentiate into sexual forms. These gametocytes are picked up by mosquitoes, leading to transmission.

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12
Q

Male gamete precursor, essential for transmission to mosquitoes.

A

Microgametocytes (Male Gametocytes)

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13
Q

Female gamete precursor, essential for fertilization in mosquitoes

A

Macrogametocytes (Female Gametocytes)

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14
Q

Which Plasmodium species can form hypnozoites (dormant schizonts)?

A

Plasmodium vivax and Plasmodium ovale
hypnozoites = reactivate later and cause malaria relapses months or years after initial infection

*When P. vivax and P. ovale merozoites invade new liver cells after being released from the first liver schizont = secondary exoerythrocytic stage

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15
Q

true or false:
The cycle repeats whenever an infected mosquito bites a new human host.

A

true

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16
Q

asexual phase is also known as

A

schizogony

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17
Q

where does the sexual phase occurs in the mosquitoes

A

mosquito’s midgut
- gametocytes mature & fertilize = formation of sporozoites (sporogony)
- sporozoites travel to the salivary glands and enter human blood capillaries
- circulate in the bloodstream and reach the liver

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18
Q

briefly explain the human cycle (schizogony)

A

infection via mosquito bite
- sporozoites from the mo

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19
Q

briefly explain the liver stage and rbc stage

A

EXOERYTHROCYTIC CYCLE (LIVER STAGE)
within 30min, sporozoites invade hepatocytes
multiply and develop into schizonts
infected liver cell rupture, releasing the schizonts, now called merozoites
it is then released into the bloodstream infecting RBCs

ERYTHROCYTIC CYCLE (RBC STAGE)
merozoites invade RBCs and become young trophozoites
parasite feeds on hemoglobin, producing malaria pigment (hemozoin)
infected RBC ruptures again, releasing merozoites (the merozoites can)
- re-enters RBC to continue schizogony
- differentiate into immature sex cells (gametocytes)
▪ Male: Microgametocyte
▪ Female: Macrogametocyte

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20
Q

Which Plasmodium species do not have a secondary exoerythrocytic stage?

A

P. falciparum and P. malariae.

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21
Q

briefly explain sporogonic cycle

A
  1. When a female Anopheles mosquito bites an infected human, it sucks up blood containing the sexual forms of the parasite (gametocytes).
  2. Inside the mosquito’s stomach, the male gametocyte (microgametocyte) splits into 8 tiny sperm-like cells (microgametes).
  3. The female gametocyte (macrogametocyte) matures into an egg-like cell (macrogamete).
  4. A microgamete fertilizes a macrogamete, forming a zygote (like a baby parasite).
  5. The zygote changes into a wiggly form called an ookinete, which moves through the mosquito’s stomach lining.
  6. The ookinete sticks to the mosquito’s stomach wall and turns into a protective sac called an oocyst.
  7. Inside the oocyst, thousands of tiny sporozoites (infectious stage) grow.
  8. When the oocyst bursts, sporozoites spread inside the mosquito’s body.
  9. 20% of the sporozoites move to the mosquito’s salivary glands, ready to infect a new person.
    10.When the mosquito bites another human, it injects the sporozoites, starting a new malaria infection.
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22
Q

Most pathogenic & responsible for most malaria deaths.

A

Plasmodium falciparum (Malignant Tertian Malaria)
- infects all ages of RBC (young and old)

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23
Q

How long does sporogony take?

A

1–4 weeks
depending on the Plasmodium species and environmental temperature.

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24
When does the mosquito become infective?
when sporozoites reach the mosquito’s salivary glands = ready to transmit malaria to humans - when the mosquito bites a human, it injects sporozoites, restarting the infection cycle
25
How does Plasmodium falciparum appear in a blood smear?
Small rings (1/6 of RBC size) Multiple rings per RBC (appliqué form) Double chromatin dots Schizonts hidden in capillaries Crescent (banana)-shaped gametocytes Mature schizont has 8–24 merozoites (usually 16). Maurer’s clefts (coarse dots) visible on staining.
26
How long is the erythrocytic cycle for 1. Plasmodium falciparum? 2. Plasmodium vivax? 3. Plasmodium malariae? 4. Plasmodium knowlesi? 5. Plasmodium ovale?
36–48 hours 48 hours 72 hours 24 hours (fastest replication cycle) 48 hours
27
Which Plasmodium species prefers reticulocytes (young RBCs)?
Plasmodium vivax key features: All parasite stages visible in blood Enlarged RBCs Schüffner’s dots present Amoeboid trophozoite 12–24 merozoites in schizont
28
Which Plasmodium species infects older RBCs?
Plasmodium malariae key features: Thicker ring stage (compared to P. vivax) RBCs remain normal or slightly smaller Ziemann’s stippling (fine granules) present Trophozoite stretches across RBC (band form) 8 merozoites in schizont (rosette formation)
29
Which zoonotic Plasmodium species infects humans?
Plasmodium knowlesi (transmitted from monkeys) key features: Looks like P. falciparum in the ring stage Multiple rings per RBC Accole form & double chromatin dots Band-form trophozoite (like P. malariae) 10–16 merozoites per schizont
30
What is the rarest Plasmodium species in human
Plasmodium ovale key features: Similar to P. vivax but more compact Less amoeboid in shape Schüffner’s dots present in RBCs
31
what is the origin of the word malaria
From Latin: "Mal" = bad "Aria" = air it was also known as Paludism or Paludismo, form the word "palus" meaning miasma or mist
32
What are the general symptoms of malaria?
headache lassitude (tiredness) bone and joint paint chilly sensation fever
33
The release of merozoites, pigment, and RBC debris into circulation at the end of schizogony.
triggers malarial paroxysm - the patient feels normal or well until the next paroxysms occurs
34
briefly explain the three stages of malarial (febrile) paroxysm?
Cold stage (up to 1 hour): - Chills, shivering that processes to a teeth-chattering - Peripheral vasoconstriction (lips/nails turn cyanotic) Hot stage (6-12 hours): - High fever (39-41°C) - Flushed skin, nausea, vomiting, headache - Rapid pulse - Possible convulsions in children Sweating stage (several hours): - Profuse sweating - Temperature falls, headache disappears - Exhaustion but symptom-free afterward
35
what are the pathogenesis of malaria
1. liver - enlarged, congested, with haemozoin pigment deposits. 2. spleen - Acute phase → Soft, enlarged, congested. - Chronic phase → Fibrosis & dilated sinusoids. (vessels becomes wider than normal) 3. bone marrow - decreased erythropoiesis, leading to anemia. - causes of anemia: ▪ RBC rupture. ▪ Autoimmune hemolysis (complement-mediated). ▪ Hypersplenism (excess RBC destruction).
36
What is the most serious complication of P. falciparum malaria?
Cerebral malaria – it can be fatal. mechanism: Schizonts secrete surface proteins (knobs). Infected RBCs stick to uninfected RBCs & capillary walls. Leads to blockage, anoxia, ischemia, and hemorrhage in the brain.
37
What are the pulmonary complications of malaria?
1. Pulmonary edema - fluid overload or hypoxia 2. Acute Respiratory Distress Syndrome (ARDS) - fluid in lungs due to increased alveolar-capillary permeability - plasmodium spp that can cause ARDS: P. falciparum, P. vivax, P. knowlesi.
38
Seen in patients with repeated malaria infections & inadequate quinine treatment.
Blackwater Fever (P. falciparum) Massive hemolysis → Anti-RBC antibodies → Hemoglobin in urine (black-colored) complications: - renal failure - liver failure - circulatory collapse.
39
What causes acute renal failure (ARF) in malaria?
Tubular necrosis from ischemia & hemoglobinuria.
40
Which Plasmodium species is associated with nephrotic syndrome?
P. malariae - immune complex-mediated glomerular damage
41
Genetic resistance mechanisms that naturally protect against malaria.
innate immunity to malaria genetic traits that protect against malaria: HbE → Protection against P. vivax. HbS (Sickle cell trait) → Impairs P. falciparum multiplication. HbF (Fetal hemoglobin) → Protects newborns from malaria. G6PD Deficiency → Increases RBC resistance to P. falciparum.
42
How do Duffy-negative RBCs provide malaria resistance?
they prevent P. vivax and P. knowlesi from entering RBCs.
43
Immunity developed after repeated exposure, offering partial protection against severe disease.
acquired immunity to malaria
44
A state of asymptomatic infection that prevents superinfection but disappears once malaria is cleared.
premunition in malaria immunity
45
How do maternal antibodies protect infants from malaria?
IgG antibodies from the mother provide protection for the first 3 months in endemic areas. *young children are highly susceptible, acquire immunity as they grow
46
Why are young children highly susceptible to malaria?
lose maternal antibodies and need repeated exposure to develop immunity. hence, to imrove immunity w age: Frequent exposure helps older children & adults develop resistance to severe disease.
47
A malaria relapse due to low-level persistent parasitemia that remains undetectable but continues at subclinical levels.
recrudescence - typically occur within 8 weeks after the primary infection due to waning immunity or antigenic variation *all malaria species can cause recrudescence
48
Which malaria species can cause recrudescence?
All malaria species can cause recrudescence.
49
A recurrence caused by the reactivation of dormant hypnozoites in the liver.
Relapse - after primary infection, it can occur from 24 weeks to 5 years * P. vivax and P. ovale. can cause relapse
50
What is the gold standard for diagnosing malaria?
Microscopic examination of thin and thick blood smears. 1. Thin smear – number of infected red blood cells divided by 1000 X 100 2. Thick smear – number of parasites per 100 white blood cells X 100
51
What are other methods of malaria diagnosis?
Rapid Diagnostic Tests (RDTs) Molecular Diagnosis Serodiagnosis Culture
52
main drugs used to treat malaria?
Chloroquine Quinine Amodiaquine Pyrimethamine-based combinations Primaquine (for hypnozoites of P. vivax & P. ovale)
53
How can malaria be prevented?
1. Chemoprophylaxis (e.g., chloroquine, mefloquine, doxycycline) for travelers. 2. Vector control through: Insecticide residual spraying (IRS) - spraying of the indoor surfaces of house with residual insecticides Insecticide-treated bed nets (ITNs) Use of repellents, protective cloting, mosquito coils and screening of house 3. Anti-lavarl measures
54
The use of antimalarial drugs to prevent infection in travelers visiting endemic areas.
chemoprophylaxis recommended drugs: Proguanil Chloroquine Mefloquine (weekly) Doxycycline (daily) Start: 1 week before traveling to an endemic area. Continue: While staying in the endemic area. Stop: 4–6 weeks after leaving the endemic area.
55
What type of parasite is Babesia?
Intraerythrocytic sporozoan parasite - similar in morphology to Plasmodium falciparum.
56
How is Babesia transmitted?
Tick bite (Ixodes species – primary mode). Blood transfusion (human-to-human).
57
host and transmission of babesia
HOSTS Definitive Host: Ixodid ticks (Ixodes species). Intermediate Hosts: Humans and rodents. TRANSMISSION Bite of infected Ixodid ticks (primary mode). Blood transfusion (human-to-human transmission).
58
What is the key morphological feature of Babesia inside RBCs?
"Maltese cross" formation (tetrads of parasites).
59
Does Babesia have a liver stage like Plasmodium?
No, Babesia lacks a liver stage.
60
What happens during sporogony (sexual reproduction) in ticks?
Ticks ingest infected blood containing Babesia gametocytes. Sexual reproduction occurs inside the tick. Sporozoites form and migrate to the tick’s salivary glands. The tick bites a new host, transmitting sporozoites.

2025 SEM 2 CLINICAL PARASITOLGY (LEC) (8 decks)

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