Blood And Tissue Protozoa Flashcards
0
Q
Protozoa are classified as?
A
Single cell, eukaryotic organisms.
1
Q
What is the definition of ‘parasite’ ?
A
An organism that lives in or on the host by taking nourishment and protection from the host and consequently causing damage or disease.
2
Q
Name the four Protozoa.
A
Flagellates, Amoebae, Apicomplexans, Ciliates.
3
Q
Name three organs of motility for Protozoa.
A
Pseudopods, Flagella, Cilia.
4
Q
Protozoa only reproduce asexually (binary fission). True or False?
A
False.
They can also reproduce sexually via fusion of gametocytes.
5
Q
What is the actively feeding stage commonly referred to as?
A
Trophozoite.
6
Q
How do some pathogenic Protozoa protect themselves?
A
By protective membranes forming cysts.
7
Q
What is the name of the species that cause Malaria?
A
Plasmodium species.
Apicomplexa (sporozoan)
8
Q
How many people are at risk of developing Malaria?
A
3.4 billion people. Half the world’s population.
9
Q
What are the clinical manifestations of Malaria?
A
From asymptomatic parasitemia to severe complications.
10
Q
Malaria in pregnancy has what effect?
A
Can cause maternal anaemia, stillbirth, spontaneous abortion, low birth weight, and neonatal death.
11
Q
What is the name of the malarial vector?
A
Female Anopheles Mosquito.
12
Q
Name the five Plasmodium species.
A
1) P. vivax
2) P. ovale
3) P. malariae
4) P. falciparum
5) P. knowlesi
13
Q
Oocytes can be found where? And how do they come about?
A
In the midgut of Mosquitos via the fusion of gametocytes.
14
Q
Where can Sporozoites be found?
A
In the salivary gland of the Mosquito.
15
Q
How do they reach the host?
A
Injected into the bloodstream via blood meal.
16
Q
What cells do they infect first?
A
Hepatocytes.
17
Q
How many merozoites are released into the blood after multiplication within Hepatocytes?
A
20,000-40,000
18
Q
What type of red blood cell does P. vivax infect?
A
Young immature erythrocytes.
19
Q
What are some of the characteristics of P. vivax?
A
Form ring shaped immature trophozoite. Schuffner’s dots in RBC and schizogony (enlargement of cell due to production of merozoites).
20
Q
Incubation period?
A
10-17 days.
21
Q
List some of the symptoms.
A
Headache, muscle pains, photophobia, anorexia, nausea and vomiting.
22
Q
P. vivax infections if untreated can last for years and can lead to brain, kidney and liver damage. True or False?
A
True.
23
Q
What causes typical patterns of chills, fever and malarial rigours?
A
The rupture of RBCs which liberate merozoites and toxic cellular debris (haemoglobin).
24
When do paroxysms occur?
Every 48 hours or every third day.
25
Name a drug used for treatment.
Primaquine is used to eradicate the liver stage of the parasite and prevent relapse of the disease.
26
Describe the P. vivax life cycle.
Mosquito takes a blood meal injecting sporozoites.
Sporozoites infect liver cell.
Merozoites are released into bloodstream.
Immature trophozoite to mature trophozoite to schizont, to merozoite release or the immature trophozoite can form gametocytes.
Mosquito takes a blood meal and ingests gametocytes.
Microgamete enters macrogamete forming Oocyst.
Oocyst ruptures, releasing sporozoites.
27
What are the characteristics of P. ovale?
Forms schuffner's dots in young RBCs. As a consequence, the host cell becomes enlarged and the cell border is ragged.
28
What is the epidemiology?
Found in tropical Africa, Asia and South America.
29
How many years does untreated infection last?
One year. Relapse does not occur because there is no liver hypnozoites.
30
Name the drug used for treatment.
Primaquine.
31
When do paroxysms occur?
Every 48 hours or every third day.
32
What type of RBCs does P. malariae infect?
Mature ones with rigid cell membranes. Thus, parasite's growth is dictated by size and shape of RBC.
33
What are the characteristics of the parasite?
Forms typical band and bars in RBCs. Schizonts merozoites form rosettes.
34
What is the epidemiology?
Less prevalent than other plasmodia and is found in same subtropical regions.
35
What is the incubation period?
Longest incubation of 18-40 days to years.
36
When do paroxysms occur?
Every 72 hours or every fourth day.
37
How long can untreated infections last?
Roughly 20 years.
38
What is the epidemiology of P. falciparum?
Found in tropical and subtropical regions.
39
What type of RBCs does it infect?
Any.
40
What structures can be seen in blood films?
Ring forms mainly. Growing trophozoite and Schizont stages are rarely seen in blood films. Reddish granules called maurer's dots can be seen in host cells. P. falciparum is often seen at the very edge of the cell membrane. This is called the accole position.
41
What is the incubation period?
Shortest incubation of 7-10 days.
42
List some of the symptoms.
Chills, fever, nausea, vomiting and diarrhoea.
43
When do paroxysms occur?
Every 48 hours or every third day.
44
What happens if infection is untreated?
Causes cerebral malaria, blackwater fever due to kidney damage, liver involvement leads to bile vomiting and serious dehydration.
45
What type of RBCs does P. knowlesi infect?
Any.
46
What animals are affected?
Macaque monkeys. Hundreds of human cases reported from Malaysia.
47
What percentage of patients experience no complications?
94%.
48
Can be asymptomatic. True or False?
True.
49
What drugs are used for treatment?
Chloroquine (P. falciparum is sometimes resistant) and primaquine.
50
Name the three life threatening plasmodium species.
P. falciparum.
P. knowlesi.
P. vivax.
51
Name the three plasmodium species that do not form liver hypnozoites (sleeping forms).
P. falciparum.
P. knowlesi.
P. malariae.
52
How would diagnosis be made?
Travel history.
53
What are the methods for diagnosis?
Microscopic examination of thin films (giemsa staining) and thick films (concentration method) of blood. PCR and serology.
54
List a few features used to identify a malarial parasite.
Morphology of gametocytes- round or crescent shaped (P. falciparum).
The quality of malarial pigment- coarse pigment is suggestive of P. malariae.
The level of parasitaemia and presence of multiple infections of red cells, suggestive of P. falciparum.
55
Is there a vaccine available?
No. This is because of developed resistance to a number of malaria medicines.
56
What are some of the preventative measures?
The use of insecticidal nets and insecticides.
57
What makes primaquine an effective drug?
It acts by interfering with a part of the parasite (mitochondria) that is responsible for supplying it with energy.
It kills gametocytes.
58
What is the downfall of this drug?
It has insignificant activity against the asexual blood forms of the parasite and therefore it is always used in conjunction with a blood schizonticide and never as a single agent.
59
How do the malarial parasites escape from the host immune response?
Through polymorphism of dominant surface antigens and by living within host red blood cells where there is no antigen presentation pathway.
60
When is the best time for blood films to be taken?
Between paroxysms of chills and fever, when the greatest numbers of intracellular organisms are present.
61
What is the effective way of treating malaria caused by P. falciparum?
Combinations of the rapid-acting artemisinins with an existing or newly introduced antimalarial compound have been shown to be highly effective in both treatment and control whereby artemesinins leave a relatively small number of organisms for the second agent to clear which reduces the chances of an escape-resistant mutant arising from the infection.
62
What are the two types of trypanosomiasis?
African (sleeping sickness) and American trypanosomiasis (Chagas' disease).
63
What is the vector for African trypanosomiasis?
The tsetse fly vector.
64
What are the two subtypes?
Slowly developing disease caused by trypanosoma brucei gambiense, western and central regions of Africa.
Rapidly progressing disease caused by T. brucei rhodesiense: Eastern and Southern parts of the continent.
65
What is the life cycle?
Tsetse fly takes a blood meal, injecting metacyclic trypomastigotes. They transform into blood trypomastigotes which are carried to other sites. Trypomastigotes multiply by binary fission in various body fluids e.g blood, lymph and spinal fluid. Tsetse fly takes another blood meal and ingests the bloodstream trypomastigotes which then turn into procyclic trypomastigotes in tsetse flys midgut. They multiply by binary fission and transform into epimastigotes. Epimastigotes multiply in salivary gland, transform into metacyclic trypomastigotes. Cycle starts again.
66
What is the trypanosoma morphology?
A posterior kinetoplast, centrally located nucleus, an undulating membrane and an anterior flagellum. Two sub species are indistinguishable morphologically. The outer surface of the organism is coated with variable surface glycoprotein (VSG).
67
What is the only stage that reproduces in the human host?
Trypomastigote stage.
68
How does VSG help with escaping the immune system?
Numerous switching of VSG (antigens) accounts for antigenic variation. T. brucei contains hundreds of VSG genes, accounting for about 10% of all it's genes.
69
What are the three stages of African trypanosomiasis?
Bite reaction (chancre)
Parasitaemia (blood and lymphoid tissues)
CNS stage
70
Describe what a chancre is.
A nonpustular, painful, itchy chancre, forms 1-3 weeks after the bite and lasts 1-2 weeks. It leaves no scar.
71
What is parasitaemia?
It is marked by attacks of fever which starts 2-3 weeks after the bite and is accompanied by malaise, sweating, pain in the joints, insomnia, headache and oedema.
```
Rhodesian disease (acute): febrile episodes may last few weeks to several months.
Gambian disease (chronic): lasts for several years. Often ends fatally with CNS involvement.
Parasitaemia is more prominent during the acute stage than during the recurrence episodes.
```
72
Describe the winterbottom sign.
Characteristic of Gambian disease, visible enlargement of the glands of the posterior cervical region.
73
How does the CNS stage come about and what are the symptoms?
With time the parasite crosses the blood-brain barrier and migrates to the CNS causing neurological changes which include psychiatric disorders, seizures, coma and ultimately death. Other signs include, lack of interest and disinclination to work, low and tremulous speech, males become impotent.
74
What are the methods used for diagnosis?
Detection of parasite in bloodstream, lymph secretions and enlarged lymph node aspirate provides a definitive diagnosis in early (acute) stages.
The parasite in blood can be concentrated by centrifuging or by the use of anionic support media. Cerebrospinal fluid must be examined for organisms. ELISA for definite diagnosis.
75
What is the downside to diagnosis?
Early diagnosis is difficult because of the lack of specific signs or symptoms in the first stage of the disease and also because of the lack of sensitivity of the parasitological methods available.
76
Name drugs used for treatment.
Pentamidine and Suramin. CNS involvement should be treated with Melarsoprol. They all have a certain level of toxicity.
77
How to control and prevent.
Avoid contact with tsetse flies. It is said that immunisation has not been effective due to antigenic variation.
78
What is the epidemiology for Chagas' disease?
Central and South America stretching from parts of Mexico to Argentina.
79
What is the name of the vector and how does it transmit?
Riduvid bug bites in the facial area and defecates during feeding. The metacyclic trypomastigotes contained in the faeces gain access to the mammalian tissue through the wound which is often rubbed by the individual.
80
What are the reservoirs for T. cruzi?
Raccoon, possum, cattle, pigs, cats and dogs.
81
What is the life cycle?
Riduvid bug takes blood meal, trypomastigotes enter bite wound or mucosal membranes such as the conjunctiva, metacyclic trypomastigotes penetrate various cells at bite wound site, transform to amastigotes which multiply by binary fission in cells of infected tissues. Intracellular amastigotes transform into trypomastigotes then burst out of the cell and enter the bloodstream, bug takes blood meal, forms epimastigote stage in midgut, multiplies in midgut, metacyclic trypomastigotes in hindgut. Cycle starts again.
82
What are the three forms of T. cruzi?
The Trypomastigote; found in mammalian blood, morphologically similar to African trypanosomes.
The epimastigote form is found in the insect intestine.
The amastigote form is found intracellularly or in pseudocysts in mammalian viscera (particularly in myocardium and brain) is round or oval in shape, and lacks a prominent flagellum.
83
How does T. cruzi escape the host immune system?
Binding; trypomastigotes bind to the cell surface (e.g a monocyte) via a variety of receptor proteins including fibronectin. Sialic acid is important as cells deficient in sialic acid are not penetrated. But T. cruzi has an enzyme called trans-sialidase which puts more sialic acid onto cells, enhancing uptake.
Entry into the cell; uptake is by process of induced phagocytosis. Lysosomes migrate to the cell surface when cells come in contact with T. cruzi and the parasite enters a cytoplasmic vacuole, the parasitophorous vacuole, that is formed from a lysosome. T. cruzi releases a protein toxin that inserts into the membrane of the lysosome. As a result T. cruzi escapes into the cytoplasm as the lysosomal membrane is destroyed.
84
What are the three stages of Chagas' disease?
Primary lesion (chagoma)
Acute phase
Chronic phase
85
What is a chagoma?
Appears soon after bite as raised, erythematous plaque surrounded by hard oedema. Usually found on the face, eyelids, cheek, lips or the conjunctiva. Infection in the eyelid, resulting in a unilateral conjunctivitis and orbital oedema (Ramana's sign).
86
What is the acute phase?
Appears 7-14 days after infection. Characterised by restlessness, malaise, increasing exhaustion, chills, fever, bone and muscle pains. Other manifestations include hepatomegaly, acute myocarditis. In children, the disease may cause meningo-encephalitis and coma. Death occurs in 5-10% of infants.
87
What is the chronic phase?
Cardiac arrhythmia is common. Chronic disease results in an abnormal function of the hollow organs (heart, oesophagus and colon). The cardiac changes include myocardial insufficiency, cardiomegaly. Disturbances of peristalsis lead to megaesophagus and megacolon.
88
What methods are used for diagnosis?
Definitive diagnosis requires the demonstration of trypanosomes by microscopy or biological tests (in the insect or mice). Antibodies are often detectable by complement fixation or immunofluorescence and provide presumptive diagnosis.
Clinical diagnosis is usually easy among children in endemic areas.
89
Treatment and prevention.
No cure is available. Benznidazole and nifurtimox have been used for acute stage with good results however their side effects limit their prolonged use in chronic cases.
90
What disease is caused by sand flies?
Leishmaniasis.
91
Name the four species of leishmania (hemoflagellates).
L. donovani
L. mexicana
L. tropica
L. viannia
92
What is the epidemiology for leishmania species?
Prevalent in tropics and subtropics, South America, west Asia.
Associated with malnutrition, population displacement, poor housing, a weak immune system and lack of resources.
93
Leishmaniasis is a zoonosis. What does this mean?
A disease that can be transmitted to humans from animals. Natural reservoirs include foxes, dogs, jackals, cats and rodents.
94
What is the chronic and life threatening aspects of the disease?
Chronic slow to heal diseases: symptoms localised. Cutaneous leishmaniasis (the most common), mucocutaneous or diffuse cutaneous leishmaniasis.
More life threatening disease:
Visceral leishmaniasis: dissemination to internal organs such as liver, spleen, bone marrow.
95
Which of the species are chronic?
L. tropica: cutaneous leishmaniasis (oriental sore, Delhi boil)
L. braziliensis (sub genus L. viannia): mucocutaneous leishmaniasis (American leishmaniasis, espundia, chiclero ulcer)
96
Which of the species are visceral?
L. donovani (kala-azar, dumdum fever).
97
What is the life cycle?
The promastigote stage (long, slender form with a free flagellum) is present in the saliva of infected sand flies. Human infection is initiated by the bite of an infected sandfly, which injects the promastigotes into the skin, where they lose their flagella, enter the amastigote stage, and invade reticuloendothelial cells. Ingested amastigotes transform in the sandfly into the promastigote stage, which multiplies by binary fission in the fly midgut. After development, this stage migrates to the fly proboscis (mouth), where new human infection can be introduced during feeding.
98
Promastigotes are injected by insect bite, lose flagella and enter amastigote stage that invade reticulo-endothelial cells (macrophages). What then happens to the macrophage?
Cell rupture releasing the amastigotes
99
What are the clinical symptoms?
Gradual onset of fever, diarrhoea, chills, anemia, marked enlargement of liver and spleen, weight loss, persistence of disease causes deeply pigmented granulomatous areas of skin (post kala-azar dermal leishmaniasis)
100
When does death occur if left untreated?
Within 1-2 years.
101
How is cutaneous leishmaniasis characterised?
One or more cutaneous lesions (sores) on areas where sand flies have fed. The sores can change in size and appearance over time. May look like a volcano, with a raised edge and central crater. Can be painful or painless.
102
What symptoms does L. tropica cause (cutaneous leishmaniasis)?
L. tropica multiplies locally, producing of a papule, 1-2 weeks or months after the bite. The papule gradually grows to form a relatively painless ulcer. The centre of the ulcer encrusts while satellite papules develop at the periphery.
103
How is mucocutaneous leishmaniasis characterised? (L. braziliensis)
Initial symptoms are similar to cutaneous leishmaniasis, except that the parasite can metastasise. Lesions spread to mucoid tissues (oral, pharyngeal and nasal) and lead to their destruction and hence sever deformity. Partial or total destruction of mucous membranes of the nose, mouth and throat.
104
How is visceral leishmaniasis characterised?
L. donovani in visceral leishmaniasis are rapidly eliminated from the site of infection, hence there is rarely a local lesion. Parasites localise and multiply in the mononuclear phagocytic cells of spleen, liver, lymph nodes, bone marrow, intestinal mucosa and other organs. This causes splenomegaly, distended abdomen and severe muscle wasting.
105
When can the amastigote and promastigote stage be seen for leishmaniasis?
Amastigote stage can be demonstrated in tissue biopsy, bone marrow examination, lymph node aspiration.
Blood culture can show promastigote stage - a small dark staining kinetoplast can be seen next to the spherical nucleus in some parasites.
106
Kala azar: treatment, prevention and control.
Amphotericin B, success with oral miltefosine. Protection from sand flies and insect repellents.
