PYQ – MZOE-001: Parasitology (Solved Q&A) | MZOE-001 | MSCZOO | M.Sc.Zoology | IGNOU | December 2024
M.Sc. (Zoology) (MSCZOO)
Term-End Examination
December, 2024
MZOE-001 : PARASITOLOGY
Time : 2 Hours| Maximum Marks : 50
Note: (i) Attempt any five questions.
(ii) All questions carry equal marks.
1. (a) What are endoparasites? Give any two examples. (2 Marks)
Endoparasites are parasites that live inside the body of their host. They usually infect internal organs like the intestine, liver, lungs, or blood. These parasites depend on the host for nutrients and often cause harm by damaging tissues, stealing nutrients, or releasing toxins. They are commonly found in vertebrates, including humans and may be transmitted through contaminated food, water, or direct contact.
Examples:
1. Taenia solium (pork tapeworm) – It lives in the human intestine and causes taeniasis.
2. Plasmodium vivax – A blood parasite that causes malaria in humans, transmitted by female Anopheles mosquitoes.
(b) What is the difference between mechanical vector and biological vector? Write one example for each. (2 Marks)
A mechanical vector is an organism that carries a pathogen from one place to another without the pathogen undergoing any development or multiplication inside the vector's body. The transmission is passive, usually through contamination. For example, a housefly can carry bacteria like Salmonella from feces to food surfaces.
A biological vector, on the other hand, is an organism in which the pathogen not only lives but also undergoes part of its life cycle, such as development or multiplication, before being transmitted to the host. The transmission is active and often through biting. For example, the female Anopheles mosquito acts as a biological vector for Plasmodium parasites which cause malaria. Inside the mosquito, the parasite undergoes important developmental stages before being passed to humans during a bite.
(c) What is Premunition? (2 Marks)
Premunition is a type of resistance or partial immunity in a host that already carries a low-level infection of a parasite. In this condition, the existing infection helps prevent a new or more severe infection by the same parasite. This condition does not remove the parasite from the body but keeps the infection under control so that it does not become dangerous. It is a form of partial immunity that works only when the parasite is still present in small numbers.
Premunition is commonly seen in diseases caused by protozoan parasites. A well-known example is malaria, where people living in endemic areas often develop premunition after repeated exposure. Their immune system does not fully clear the Plasmodium parasites but controls the infection to such a level that it prevents severe disease and also stops new infections from becoming too intense.
(d) List any two morphological adaptations of parasites. (2 Marks)
Parasites show many special structural features that help them survive inside or on the surface of their host. These features make it easier for them to attach, feed and protect themselves from the host's immune system.
Two important morphological adaptations are:
1. Suckers and Hooks: Many endoparasites like Fasciola hepatica (liver fluke) and Taenia solium (tapeworm) have strong suckers and hooks on their head or body. These help them to attach tightly to the walls of the host's internal organs such as the intestine or liver. This prevents them from being removed by the host's movements or digestion.
2. Body Flattening or Elongation: Flatworms such as tapeworms have a long and flattened body. This shape increases the surface area of their body, which helps them absorb nutrients directly from the host's body fluids. Since many parasites do not have a digestive system, this adaptation is very useful for nutrient absorption.
(e) Write the differences between incubation period and prodromal period of an infection. (2 Marks)
The incubation period is the time between the entry of a pathogen into the body and the appearance of the first symptoms of the disease. During this period, the pathogen multiplies silently and the infected person usually shows no signs of illness. The length of this period depends on the type of pathogen, the dose of infection and the host's immunity.
The prodromal period comes after the incubation period. It is a short phase when the first mild symptoms start to appear, such as fever, tiredness, or headache. These symptoms are general and not specific to the disease but signal that the illness is beginning to develop.
2. (a) Illustrate the life cycle of Plasmodium species with the help of a well labelled diagram. (5 Marks)
The life cycle of Plasmodium species, which causes malaria in humans, is complex and involves two hosts — the female Anopheles mosquito (definitive host) and the human (intermediate host). The cycle includes both asexual and sexual phases that occur in different hosts.
When an infected female Anopheles mosquito bites a human, it injects sporozoites into the bloodstream. These sporozoites travel to the liver, where they enter hepatocytes (liver cells) and multiply through asexual reproduction called exoerythrocytic schizogony. This leads to the formation of thousands of merozoites.
The liver cells eventually burst and release these merozoites into the bloodstream. Merozoites invade red blood cells (RBCs) and undergo further asexual reproduction known as erythrocytic schizogony. Infected RBCs burst at regular intervals, releasing more merozoites and causing the classical fever cycles seen in malaria. Some merozoites differentiate into gametocytes, the sexual stage of the parasite.
When another female Anopheles mosquito bites the infected human, it ingests the gametocytes. Inside the mosquito's midgut, male and female gametocytes fuse to form a zygote. The zygote becomes a motile ookinete, which penetrates the gut wall and forms an oocyst. Inside the oocyst, many sporozoites develop. These sporozoites travel to the mosquito's salivary glands, completing the cycle.
The mosquito can now infect another human through a bite, restarting the entire process.
(b) Which drugs are commonly used to treat malaria? Discuss their action. (5 Marks)
Malaria is treated using several antimalarial drugs depending on the Plasmodium species, severity of infection, and drug resistance patterns. The main drugs commonly used include Chloroquine, Artemisinin-based Combination Therapies (ACTs), Quinine, Mefloquine and Primaquine. These drugs work in different ways to kill the parasite during its life cycle inside the human body.
1. Chloroquine
Chloroquine works mainly against Plasmodium vivax, P. ovale and P. malariae. It stops the parasite from safely removing toxic heme, which comes from the digestion of red blood cell hemoglobin. As a result, toxic heme builds up and kills the parasite. However, in many areas, P. falciparum has developed resistance to chloroquine.
2. Artemisinin and Artemisinin-based Combination Therapies (ACTs)
ACTs are used as the first-line treatment for P. falciparum malaria. Artemisinin comes from a plant called Artemisia annua. Inside the parasite, it reacts with iron and forms free radicals. These radicals damage proteins and membranes of the parasite. Since artemisinin acts quickly but doesn't last long, it is given with a second drug like lumefantrine or mefloquine to fully clear the infection and avoid resistance.
3. Quinine and Mefloquine
Quinine is one of the oldest antimalarial drugs. Like chloroquine, it also affects heme detoxification inside the parasite. Mefloquine works in a similar way and is used where chloroquine resistance is found.
4. Primaquine
Primaquine is important for killing liver stages (hypnozoites) of P. vivax and P. ovale. It also kills gametocytes of P. falciparum, which helps stop the spread of malaria to mosquitoes. It affects the parasite’s mitochondria and energy metabolism.
3. (a) Explain the role of microbiota of sand fly in Leishmania development and transmission. (5 Marks)
Leishmania parasites are transmitted to humans by the bite of infected female sand flies. Inside the sand fly's gut, a complex community of microorganisms called microbiota lives, which plays an important role in the development and transmission of Leishmania. These gut microbes can either support or block the parasite's life cycle. Understanding this microbial interaction is essential for controlling the spread of leishmaniasis.
Role of Microbiota of Sand Fly in Leishmania Development
When a sand fly takes a blood meal from an infected vertebrate host, it ingests Leishmania amastigotes, which reach the midgut and convert into promastigotes. For this transformation and further development, the gut environment must be favourable. The gut microbiota affects this environment in the following ways:
- Supportive Role: Some bacteria help maintain the right pH, provide nutrients, and reduce immune reactions, helping the parasite survive and multiply.
- Defensive Role: Certain bacteria stimulate the sand fly's immune response, producing antimicrobial compounds that may damage Leishmania. Experiments show that when gut bacteria are removed using antibiotics, Leishmania often develops more easily, which proves that microbiota can act as a natural defense.
Role of Microbiota of Sand Fly in Leishmania Transmission
For transmission, Leishmania must reach the foregut and mouthparts of the sand fly so that it can enter the human body during the next bite. Microbiota helps in this step by:
- Providing surfaces or biofilms for parasite attachment, which prevents the parasite from being expelled from the gut.
- Maintaining gut health and conditions required for successful migration of Leishmania to the proboscis.
(b) Elaborate on the way of evading the action of host immune system of Leishmania. (5 Marks)
Leishmania is an intracellular protozoan parasite that causes leishmaniasis in humans. It mainly infects macrophages, which are the key immune cells responsible for killing foreign organisms. But instead of being destroyed, Leishmania survives and multiplies inside them. This is possible because the parasite has developed several smart strategies to avoid being attacked by the host's immune system. The immune evasion by Leishmania happens through the following four main mechanisms:
1. Blocking Phagolysosome Formation
Normally, after macrophages engulf microbes, they form a phagolysosome by fusing the phagosome with a lysosome. This leads to digestion of the microbe. Leishmania delays or blocks this fusion, so it avoids exposure to harmful enzymes and survives safely inside the macrophage.
2. Resistance to Oxidative Burst
Even if phagolysosome forms, macrophages release reactive oxygen species (ROS) and reactive nitrogen species (RNS) to kill pathogens. Leishmania produces enzymes like superoxide dismutase and trypanothione reductase that neutralise ROS, helping the parasite avoid damage.
3. Modulation of Host Immune Response
Leishmania interferes with cytokine signalling. It promotes anti-inflammatory cytokines like IL-10 and suppresses pro-inflammatory ones like IL-12. This reduces activation of T-cells and weakens the immune attack.
4. Antigenic Variation and Surface Molecules
The parasite changes its surface molecules like lipophosphoglycan (LPG), which helps it to avoid recognition by the host's immune system and continue infection undetected.
4. (a) Compare and contrast Stage I and Stage III of Trypanosoma. (5 Marks)
Trypanosoma brucei causes African sleeping sickness. The disease progresses through three main clinical stages after infection by the bite of a tsetse fly. Stage I (hemolymphatic stage) and Stage III (neurological stage) represent two important phases. Stage I is the early phase when the parasite stays in the blood and lymph. Stage III is the final and most dangerous phase when the parasite reaches the brain.
Here are the comparison between Stage I and Stage III of trypanosoma based on the following criteria:
1. Based on Site of Infection
In Stage I, the parasite stays in the blood and lymphatic system.
In Stage III, the parasite reaches the brain and spinal cord (central nervous system).
2. Based on Symptoms
Stage I shows fever, joint pain, headache, and swollen lymph nodes.
Stage III includes confusion, sleep problems, poor coordination, mood changes, and coma in severe cases.
3. Based on Immune Response
In stage I, Immune system attacks parasite in blood, but parasite escapes using antigenic variation
In stage III, Immune response becomes weaker and inflammation occurs in brain tissue
4. Based on Severity
Stage I is less dangerous and easier to cure.
Stage III is life-threatening and needs urgent treatment.
5. Based on Diagnosis
In Stage I, blood smear or lymph node aspirate is used for diagnosis.
In Stage III, cerebrospinal fluid (CSF) is tested after lumbar puncture.
6. Treatment
Stage I treated with Suramin or Pentamidine (do not cross blood-brain barrier)
Stage III treated with drugs like Melarsoprol or Eflornithine which can enter CNS
(b) Which preventive methods should be adopted for hookworm (Ancylostoma) infection? (5 Marks)
Hookworm infection is caused mainly by Ancylostoma duodenale and Necator americanus. These nematodes live in the small intestine and feed on blood. Infection occurs when the infective larvae in contaminated soil penetrate human skin, especially through bare feet. It is common in areas with poor sanitation, warm climate, and where people walk barefoot. Prevention mainly focuses on hygiene, sanitation and awareness to interrupt the life cycle of the parasite.
There are the following preventive methods that should be adopted to avoid hookworm infection:
1. Use of Proper Sanitation Facilities
Avoid open defecation (passing stool or waste from the body) and use proper latrines or toilets, especially in rural areas where hookworm is more common. This stops the contamination of soil with hookworm eggs and larvae.
2. Regular Use of Footwear
Since larvae enter through the skin of bare feet, wearing slippers or shoes while walking on soil is necessary, especially in endemic areas.
3. Maintenance of Personal Hygiene
Washing hands with soap after defecation and before eating, cleaning the feet properly and cutting nails regularly reduce chances of infection.
4. Access to Clean Water and Food
Using safe drinking water and properly washed vegetables helps avoid indirect ingestion of infective stages of the parasite.
5. Periodic Deworming
Drugs like Albendazole and Mebendazole are effective in killing adult worms. Regular deworming (giving medicine to remove intestinal worms) is important in areas with high prevalence to control spread and reinfection.
6. Community Health Education
Educating people about transmission and preventive steps improves public cooperation in controlling infection.
5. Differentiate between any two pairs of terms: (5+5 Marks)
(a) Invasive and Non-invasive trophozoites of Entamoeba histolytica
Entamoeba histolytica is a protozoan parasite that infects the human large intestine. Its trophozoite is the active, feeding and motile stage. Inside the host, trophozoites can behave in two different ways depending on how deep they go in the host tissue. Based on this, they are classified into invasive and non-invasive forms. These two forms differ in their behaviour, enzyme production, pathogenicity and interaction with the immune system.
The following are the differences based on important aspects:
1. Location and Movement
In invasive type, trophozoites actively penetrate the mucosal lining of the intestine and may reach deeper tissues like submucosa and even enter the bloodstream to reach organs such as the liver.
In non-invasive type, they remain restricted to the intestinal lumen and do not invade the epithelial barrier.
2. Pathogenic Effect
Invasive trophozoites damage host tissue and cause serious conditions like amoebic dysentery, intestinal ulcers and liver abscess.
Non-invasive forms are mostly non-pathogenic or cause only mild and self-limiting symptoms.
3. Enzyme Production
Invasive forms release tissue-destructive enzymes such as cysteine proteinases and histolysin, which help them in tissue penetration.
Non-invasive forms do not produce such enzymes and cannot cross tissue layers.
4. Immune Response
Invasive forms trigger a strong immune reaction with inflammation and tissue destruction.
Non-invasive trophozoites avoid immune detection as they do not invade tissues.
5. Diagnostic Features
Invasive forms are found in stool or tissues containing ingested RBCs, which is a key sign of invasion.
Non-invasive forms are seen in stool without RBCs.
6. Clinical Outcome
Invasive trophozoites lead to serious illness that needs medical treatment.
Non-invasive ones may stay harmless or get naturally cleared from the body.
(b) Acute and Chronic amoebic dysentery
Amoebic dysentery is caused by Entamoeba histolytica, which infects the colon. Based on how fast and how long the symptoms appear, the disease is classified into acute and chronic forms. These forms differ in symptoms, tissue damage and long-term effects.
The following are the differences based on important aspects:
1. Based on Onset and Duration
Acute dysentery starts suddenly and lasts for a few days to weeks.
Chronic dysentery develops slowly and continues for months or even years, often in cycles.
2. Based on Nature of Symptoms
Acute form has severe symptoms like frequent blood-filled and mucus-filled stools, abdominal pain and urgency.
Chronic form has milder symptoms like loose stool, weakness and weight loss that appear on and off.
3. Based on Intestinal Damage
In acute cases, deep ulcers form quickly in the intestinal wall due to active tissue destruction.
In chronic cases, repeated damage and healing lead to thickening and fibrosis of the intestinal lining.
4. Based on Nutritional Effect
Acute cases cause temporary dehydration and fatigue.
Chronic cases lead to long-term malnutrition, especially in children, along with anaemia.
5. Based on Risk of Complications
Acute dysentery may cause fulminant colitis or perforation if untreated.
Chronic cases can result in liver abscess due to slow spread of the parasite to the liver.
(c) Brugian and Occult filariasis
Filariasis is a parasitic disease caused by filarial worms, mainly Wuchereria bancrofti and Brugia malayi. Based on clinical presentation and underlying cause, it is broadly divided into Brugian filariasis and Occult filariasis. These two types show key differences in their symptoms, parasite presence and immune response.
1. Based on Causative Species
Brugian filariasis is caused mainly by Brugia malayi, sometimes Brugia timori.
Occult filariasis is usually linked to Wuchereria bancrofti, especially when there is no microfilaria in the blood.
2. Based on Microfilaria in Blood
Brugian filariasis is typically microfilaremic, meaning microfilariae are present in peripheral blood, especially at night (nocturnal periodicity).
Occult filariasis is amicrofilaremic. Microfilariae are absent in blood due to immune destruction or tissue entrapment.
3. Based on Immune Response
Brugian filariasis shows a typical parasitic infection with less severe immune response.
Occult filariasis involves a strong hypersensitive immune response, with eosinophilia and allergic features.
4. Based on Clinical Symptoms
Brugian filariasis causes classical symptoms like lymphadenitis, lymphangitis and in chronic cases like elephantiasis.
Occult filariasis presents with tropical pulmonary eosinophilia (TPE), coughing, wheezing, weight loss and high eosinophil count, often without lymphatic symptoms.
5. Based on Diagnostic Indicators
Brugian filariasis cases can be diagnosed by detecting microfilariae in night blood smear.
Occult filariasis requires serological tests or detection of antifilarial antibodies since microfilariae are not seen in blood.
6. Based on Tissue Involvement
In Brugian filariasis, adult worms reside in lymphatic vessels causing local swelling.
In occult filariasis, immune complexes affect lungs, lymph nodes or other tissues without direct parasite detection.
(d) Sandflies and Tse-tse flies
Sandflies and tsetse flies are medically important insects that act as vectors for serious parasitic diseases in humans. They differ in morphology, habitat, feeding behaviour and the diseases they transmit. Their comparison can be made based on the following aspects:
1. Based on Taxonomy
Sandflies belong to the family Psychodidae and genus Phlebotomus (Old World) or Lutzomyia (New World).
Tse-tse flies belong to the family Glossinidae and genus Glossina.
2. Based on Size and Appearance
Sandflies are small, about 2–3 mm long, with hairy bodies and long legs. Their wings are held in a V-shape at rest.
Tse-tse flies are larger, about 6–14 mm long, with a robust body. Their wings rest flat over the abdomen and have a characteristic hatchet-cell venation.
3. Based on Habitat Preference
Sandflies prefer dark, humid places such as rodent burrows, cracks and crevices.
Tse-tse flies are found in tropical forests, savannahs and riverine vegetation of sub-Saharan Africa.
4. Based on Feeding Time and Behaviour
Sandflies are nocturnal feeders, biting mostly during night.
Tse-tse flies are diurnal and feed during the daytime.
5. Based on Biting Mechanism
Sandflies have piercing and sucking mouthparts but are weak fliers, so they hop around while feeding.
Tse-tse flies are strong fliers with powerful proboscis to pierce skin and suck blood.
6. Based on Diseases Transmitted
Sandflies transmit Leishmania species causing leishmaniasis and Bartonella bacilliformis causing Carrion's disease.
Tse-tse flies transmit Trypanosoma brucei species causing African sleeping sickness (trypanosomiasis)
6. (a) How does immunotherapy with 45 kDa antigen of Trichinella spiralis work in the murine model? (2 Marks)
The 45 kDa excretory-secretory (ES) antigen of Trichinella spiralis muscle larvae has shown promising effects in immunotherapy, especially in murine (mouse) models. When this antigen is injected into infected mice, it stimulates the immune system to produce protective responses. It mainly triggers a Th2-type immune reaction, which includes secretion of IL-4, IL-5, IL-10 cytokines and high levels of IgG1 antibodies. These responses help in limiting larval migration and reducing their encystment in muscle tissues. Though the antigen does not directly kill the larvae, it creates an unfavourable environment for their survival. Mice treated with this antigen show significantly fewer muscle larvae, indicating that the 45 kDa antigen can protect against the chronic stage of trichinellosis. This supports its potential use as an effective vaccine or therapeutic tool in future studies.
(b) Describe any four methods by which filariasis can be diagnosed in human beings. Which is considered most accurate and why? (5 Marks)
Filariasis is diagnosed mainly by detecting microfilariae or antigens of adult filarial worms in human samples. There are several diagnostic methods, but the following four are most commonly used:
1. Microscopic Examination of Peripheral Blood
This is the classical and most commonly used method. A thick smear is prepared from night blood because Wuchereria bancrofti and Brugia malayi show nocturnal periodicity. The smear is stained with Giemsa stain and examined under the microscope. Microfilariae are identified based on features like sheath, tail nuclei and length.
2. Circulating Filarial Antigen Detection (CFA Test)
This is done using immunochromatographic card tests (ICT) or ELISA (Enzyme-Linked Immunosorbent Assay). It detects antigens from adult female Wuchereria bancrofti worms, even in the absence of microfilariae. It is useful in day-time sampling and for detecting occult infections.
3. Polymerase Chain Reaction (PCR)
PCR detects specific DNA sequences of filarial parasites. It is highly sensitive and specific. It can detect very low parasite loads and is effective in both symptomatic and asymptomatic cases. It is ideal for surveillance and mapping during control programs.
4. Ultrasonography
In lymphatic filariasis, especially in men, adult worms can be visualized in scrotal lymphatics using Doppler ultrasound. The "filarial dance sign" is a characteristic indication of motile adult worms.
Most Accurate Method
Among all, Polymerase Chain Reaction (PCR) is considered the most accurate due to its extremely high sensitivity and specificity. However, it requires advanced lab setup, so antigen detection (CFA test) is often preferred in field conditions.
(c) Discuss the pathogenicity of guinea worm (Dracunculus). (3 Marks)
Guinea worm causes a parasitic infection known as dracunculiasis in humans. The disease begins when a person drinks water containing infected copepods (Cyclops) that harbor the third-stage larvae of Dracunculus medinensis. Once inside the human host, the larvae are released in the stomach, penetrate the intestinal wall and migrate to subcutaneous tissues.
After about a year, the gravid female worm moves toward the skin surface, usually on the lower limbs and causes the formation of a painful blister. This blister eventually ruptures, allowing the worm to emerge. The contact with water triggers the release of thousands of larvae into the water, continuing the cycle.
The blister and worm emergence cause intense burning pain, swelling and secondary bacterial infections. Inflammation can lead to abscesses and ulcerations. In severe cases, it may result in septic arthritis, cellulitis and even disability, especially if the worm dies inside the tissues and calcifies.
Though the adult male worm dies soon after mating and causes no harm, the female worm's migration and emergence are responsible for the major pathological effects in dracunculiasis.
7. (a) Why is plague also called 'black death' ? Explain the transmission of plague in animals and its different forms. (7 Marks)
Plague is a deadly zoonotic disease caused by the bacterium Yersinia pestis. It is historically known as the "Black Death" because of the large pandemic that occurred in Europe between 1347 and 1351, killing nearly one-third of the population. The term "black" refers to the dark discoloration of the skin, especially in the extremities like fingers and toes, caused by tissue necrosis due to septicemia. This blackening of skin, along with the high death rate, gave it the name "Black Death."
Transmission of Plague in Animals
Plague is a vector-borne disease and primarily affects wild rodents such as rats, squirrels, and prairie dogs. The transmission mainly occurs through the bite of infected fleas, especially Xenopsylla cheopis. These fleas act as vectors and carry the Yersinia pestis bacteria from infected rodents to healthy animals or humans. When a flea feeds on an infected rodent, the bacteria multiply inside the flea's gut. When the flea bites another host, it regurgitates the bacteria into the bloodstream, causing infection. Sometimes, direct contact with infected tissues or inhalation of respiratory droplets can also spread the disease among animals.
Carnivorous animals may also become infected by consuming infected rodents. Domestic animals such as cats and dogs can become infected too and may transmit the disease to humans in rare cases.
Forms of Plague in Animals
There are mainly three forms of plague seen in animals:
1. Bubonic Plague – This is the most common form. It is characterized by swollen lymph nodes (buboes), fever and lethargy. It usually results from flea bites.
2. Septicemic Plague – This form occurs when the bacteria enter the bloodstream directly. It can be primary or secondary to bubonic plague. Symptoms include bleeding, shock and necrosis of body tissues.
3. Pneumonic Plague – This is the most dangerous and contagious form. It involves the lungs and can spread through respiratory droplets. It may develop from septicemia or can be primary if inhaled.
(b) How do root knot nematodes and cyst nematodes parasitize their hosts?(3 Marks)
Root knot nematodes (Meloidogyne spp.) and cyst nematodes (Heterodera and Globodera spp.) are two major types of endoparasitic nematodes that attack plant roots and cause significant crop damage. Both weaken the host plant, reduce yield and can make it more vulnerable to other infections.
Root knot nematodes penetrate the root tip and migrate intercellularly to the vascular cylinder. There, they establish feeding sites by inducing the formation of giant cells through nuclear division without cytokinesis. These giant cells provide a continuous supply of nutrients to the nematode. As the nematode feeds, it causes characteristic root swellings or galls which impair water and nutrient uptake.
Cyst nematodes follow a different strategy. The infective second-stage juveniles penetrate the root and migrate intracellularly to the vascular tissue, where they induce the formation of a specialized feeding structure called a syncytium by dissolving cell walls between adjacent cells. This multinucleated feeding site provides nutrition throughout the nematode's life. As the female matures, her body becomes lemon-shaped and eventually turns into a hardened cyst filled with eggs, which remains in the soil after her death.
8. Explain different types of vaccines against parasitic diseases. (10 Marks)
Parasitic diseases like malaria, leishmaniasis, schistosomiasis and filariasis affect millions of people, mostly in tropical and subtropical countries. Developing vaccines against parasites is more difficult compared to bacteria and viruses. This is because parasites are bigger, have complex life cycles and can escape from the immune system by changing their surface antigens. Still, different types of vaccines have been developed or are under development to fight these infections.
There are the following main types of vaccines used or studied for parasitic diseases:
1. Live Attenuated Vaccines
These vaccines use live parasites that are made weak in the laboratory so that they cannot cause full disease. When injected, they stimulate the immune system to recognise the parasite. They give strong and long-lasting protection but may not be safe for people with weak immunity or chronic illness.
Example: Attenuated Plasmodium falciparum sporozoites for malaria have been tested in clinical trials. Also, irradiated cercariae of Schistosoma mansoni were used in experimental vaccines.
2. Killed or Inactivated Vaccines
These vaccines are made by killing the parasite using heat, radiation or chemicals like formalin. The dead parasites are then used in the vaccine. Since they are not alive, they cannot multiply or cause infection in the body, which makes them safe for use. However, because they do not grow or spread inside the body, they produce a weaker immune response compared to live vaccines. That is why such vaccines usually need to be given in multiple doses or with the help of adjuvants to improve their effectiveness.
Example: Heat-killed Leishmania major parasites were tested in vaccine trials for cutaneous leishmaniasis. However, the results were not very successful because the immune protection was not strong enough.
3. Subunit Vaccines
These vaccines contain only important parts of the parasite such as surface proteins or antigens. These do not cause infection and are easy to prepare. But they produce a limited immune response and need adjuvants to increase their effect.
Example: RTS,S/AS01 is a licensed malaria vaccine that contains a recombinant protein from Plasmodium falciparum combined with hepatitis B surface antigen.
4. DNA Vaccines
In this method, small circular DNA (plasmids) containing genes of the parasite are injected into the host. The host cells produce parasite proteins, which trigger immune response. DNA vaccines are stable and low-cost but not yet widely approved for humans.
Example: DNA vaccines are under research for Toxoplasma gondii, Trypanosoma cruzi and Leishmania donovani.
5. Recombinant Vector Vaccines
These use a harmless virus or bacterium as a carrier to deliver parasite genes into the host. These mimic infection and stimulate both antibody and cell-mediated responses.
Example: Modified vaccinia virus Ankara (MVA) and adenovirus vectors for malaria antigens are under trial.
6. Multi-epitope or Conjugate Vaccines
These vaccines use several small antigenic parts from different life stages of the parasite. Sometimes they are linked to a carrier protein to make them more immunogenic. This approach gives broader protection.
Example: Conjugate vaccines using synthetic peptides are being tested against Schistosoma haematobium and Leishmania infantum.
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