Week 1: Medical Parasitology Flashcards
1
Q
Define: Saprophyte
A
A plant, fungus, or microorganism that lives on dead or decaying organic matter.
2
Q
What is a subclinical infection?
A
An illness that is staying below the surface of clinical detection. A subclinical disease has no recognizable clinical findings.
3
Q
T or F: Subclinical infection is more common than clinically apparent infection.
A
True
4
Q
Define: Virulence
A
The ability of an agent of infection to produce disease. The virulence of a microorganism is a measure of the severity of the disease it causes
5
Q
Define: Parasite
A
An organism that lives in or on an organism of another species (its host) and benefits by deriving nutrients at the other’s expense.
6
Q
Define: Opportunistic pathogen
A
An infection caused by pathogens that take advantage of an opportunity not normally available, such as a host with a weakened immune system, an altered microbiota, or breached integumentary barriers.
7
Q
Define: Compromised host
A
A patient with acquired or congenital immunologic deficiency at increased risk for infectious disease complications.
8
Q
Define: Pathogenesis
A
The pathogenesis of a disease is the biological mechanism (or mechanisms) progress of disease showing its morphological features or that leads to the diseased state. The term can also describe the origin and development of the disease, and whether it is acute, chronic, or recurrent.
9
Q
Define: Vertical transmission
A
transmission directly from parents to offspring via milk, blood, sperm, ova, placenta
10
Q
Define: Horizontal transmission
A
Individual infecting other individuals by contact, respiratory or faecal–oral spread
11
Q
Examples of virulence mechanisms of microorganisms that assist colonisation
A
Depression of mucociliary clearance Resisting stomach acid Resisting bile Motility promoted by flagellae Mucinase - penetration through mucous
12
Q
Define: Adhesin
A
Cell-surface components and virulence factors of bacteria that facilitate adhesion to other cells or to surfaces, usually the host they are infecting or living in.
13
Q
Define: Definitive host
A
The host where sexual reproduction occurs
14
Q
Define: Intermediate host
A
The host that supports development of asexual/larval stage
15
Q
Intermediate hosts that transmit the parasite hormone host to another are called _____.
A
vectors
16
Q
True or false:
Protozoa are multicellular organisms.
A
False. Protoza are single-celled.
17
Q
Protoza typically range from ___ to ___ in size.
A
10-52 micrometres
18
Q
Which organisms cause cryptosporidiosis?
A
Cryptosporidium hominis and Cryptosporidium parvum
19
Q
Which organisms cause giardiasis?
A
Giardia intestinales/lamblia/duodenalis
20
Q
The motile, feeding, asexual reproductive phase of protozoa is called _____.
A
trophozoite
21
Q
What is the process of asexual division of trophozoites called?
A
Schizogony
22
Q
Schizogony of the trophozoite produces ______.
A
merozoites
23
Q
Merozoites undergo a) _____ to produce b) _____.
A
a) gamogeny b) gametes (macro-/microgametes)
24
Q
Fertilisation of protozoan gametes leads to the production of ______.
A
oocysts
25
Oocysts contain _____ which can infect host cells.
sporozoites
26
What is the phylum of Cryptosporidium?
Apicomplexa
27
Parasitic protozoa that infect muscle tissue and brain
Toxoplasma gondii
28
Which organism causes toxoplasmosis?
Toxoplasma gondii
29
Which organism causes trichomoniasis?
Trichomonas vaginalis
30
How is Cryptosporidium spread?
It is spread through the faecal-oral route, often through contaminated earth, water, uncooked or cross-contaminated food.
31
Which anatomical part of the human body does Cryptosporidium colonise?
The brush border of the small intestine
32
True or false:
| Cryptosporidium usually results in relatively long-term infection.
False. Cryptosporidiosis is typically an acute short-term infection.
33
Life cycle of Cryptosporidium spp. including pathogenesis
1. Ingestion of food/water contaminated with oocyst-containing cattle or human faeces.
2. Acidity content of the gut causes the wall of sporozoite-containing oocysts to break down, causing the oocysts to excyst in small intestine and release sporozoites.
3. Released sporozoites invade epithelial cells of the small intestine and develop into trophozoites
4. Trophozoites undergo shizogony (asexual reproduction) to become Type I meronts which are called merozoites upon bursting out of the cell
5. As the merozoites burst out of the epithelial cells, this causes damage to the epithelium of the small intestine, causing diarrhoea as water enters the gastrointestinal lumen due to a leaky barrier.
34
What is the main symptom of cryptosporidiosis in people with intact immune systems?
Self-limiting diarrhoea
35
What is the organism most commonly isolated in HIV positive patients presenting with diarrhoea?
Cryptosporidium
36
Cryptosporidium oocysts have a high resistance to _____.
disinfectants such as chlorine bleach.
37
Major hosts for C. parvum
Cattle
38
Immunocompromised patients cannot control which part of the Cryptosporidium life cycle?
Asexual cycle
39
Immunocompromised patients have ___ numbers of Cryptosporidium oocysts in the faeces.
high
40
Immunocompetent patients have ___ numbers of oocysts in the faeces.
low
41
Which stain is used to detect Cryptosporidium oocysts in faeces?
Ziehl-Neelsen
42
Symptoms of giardiasis
Severe diarrhoea and malabsorption of nutrients
43
Giardia intestinalis trophozoites reproduce via which mechanism?
Binary fission
44
Life cycle of Giardia intestinalis spp. including pathogenesis
1. Infections are passed between hosts by faecal-oral transmission of encysted parasite stage (hand to mouth contact)
2. Ingested cysts excyst (wall breakdown and release of trophozoites)
3. Trophozoites reproduce by binary fission, attach to the surface of the small intestine, interfering with absorption, triggering inflammation
4. When trophozoites pass through the colon, they form non-flagellated cysts which are excreted and contaminate the environment
5. Following their ingestion by a new host, they excyst in the small intestine releasing two trophozoites (stimulated by: bile salts, enzymes, pH, microaerophilic conditions, etc.), which live and propagate in the duodenum and jejunum.
45
What are the developmental stages of Giardia?
Trophozoites and cysts
46
Characteristics of Giardia trophozoites
1. Pear shaped
2. 10-30μm long
3. 8 flagella
4. Prominent ventral adhesive disc
5. 2 longitudinal axonemes (microtubules)
6. 2 tangential curved median bodies
47
Characteristics of Giardia cysts
- Ovoid to ellipsoid
- ~10 μm long
- Membrane-bound
- Contain 4 nuclei
48
How many trophozoites does each Giardian cyst contain?
Two
49
Giardia pathogenesis
1. Attached parasites may physically blanket the small intestinal mucosa significantly reducing the surface area for absorption
2. Infections damage and increase the turnover rate of epithelial cells culminating in villous atrophy which further reduces the surface area for absorption
3. Leads to malabsorption of fats and other nutrients resulting in watery diarrhoea accompanied by dehydration, intestinal pain and flatulence
50
Giardia lab diagnosis
Mainstay of diagnosis is immune-based detection of antigens (copro-antigen tests) however PCR methods are more sensitive.
For chronic cases, endoscopic techniques may be performed to detect trophozoites in intestinal biopsy material.
51
Treatment for giardiasis
Metronidazole is a drug of choice as it is cleaved to form active form under anaerobic conditions (such as in the intestine).
52
Organisms that cause malaria
Plasmodium spp.
53
Which mosquito is the most common vector for transmission of malaria?
Anopheles mosquito
54
Define: Merozoite
Merozoites are the daughter cells of protozoan parasites, produced via asexual reproduction (schizogony, merogony).
In malaria, these spores infect red blood cells and then rapidly reproduce asexually. These merozoites then can break and destroy the red blood cell hosts and infect others.
55
Define: Trophozoite
A trophozoite is the activated, feeding stage in the life cycle of protozoan parasites such as the malaria-causing Plasmodium falciparum (the opposite of the trophozoite state is the thick-walled cyst form).
The trophozoite develops into a schizont.
56
Define: Schizont
Mother cell which asexually produces daughter cells known as merozoites.
57
Plasmodium life cycle in the human host
In the human host:
1. The malaria parasite life cycle involves two hosts. During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host.
2. Sporozoites injected into the bloodstream leave the blood vasculature and invade hepatocytes. This begins the exo-erythrocytic stage of the life cycle during which asexual multiplication occurs.
3. Within hepatocytes the sporozoites undergo many nuclear divisions to mature into schizonts. This occurs over a period of 6 to 15 days, after which the schizonts burst and release thousands of merozoites into the circulation. P. vivax and P. ovale undergo a dormant stage, termed hypnozoites, that can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.
4. After this initial replication in the liver (exo-erythrocytic schizogony), released merozoites infect red blood cells and undergo asexual multiplication in the erythrocytes (erythrocytic schizogony).
5. During the erythrocytic cycle, the merozoites develop to form immature or ring stage trophozoites which then progress to mature trophozoites. The erythrocytic cycle results in the formation of 4 to 36 new parasites in each infected cell within a 44 to 72 hour period 6.
6. The mature ring stage trophozoites mature into schizonts, which rupture releasing merozoites. Blood stage parasites are responsible for the clinical manifestations of the disease due to the rupture of erythrocytes.
7. Released merozoites can infect new erythrocytes to begin the erythrocytic cycle again or differentiate into sexual erythrocytic stages (gametocytes).
58
Define: Sporozoite
In the life-cycle of apicomplexan protozoa, sporozoites are cells that infect new hosts.
Sporozoites are formed by sporogony, a type of sexual or asexual reproduction by multiple fission of a spore or zygote, characteristic of many sporozoans.
59
Schizogony produces daughter cells known as a) _____, which can develop in to b) ______ or enter new host cells and undergo another cycle of schizogony.
a) merozoites b) gametocytes
60
Gametocytes, which are derived from a) _____, are cells that are capable of developing into b) ______
a) merozoites b) gametes
61
The most commonly encountered malarial parasites
Plasmodium falciparum and plasmodium vivax
62
Within RBCs, malarial protozoan parasites are contained within a vacuole called ______.
Parasitophorous vacuole.
63
The classic "quaternary fever" in malaria is due to _____
merozoites bursting out of RBCs during the erythrocytic stage.
64
Plasmodium spp. life cycle in the mosquito
In the mosquito:
1. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal from an infected host. The parasites’ multiplication in the mosquito is known as the sporogonic cycle C.
2. While in the midgut of the mosquito, the microgametes fertilise the macrogametes, forming a zygote.
3. The zygotes becomes elongated and motile, now termed ookinetes, which invade the midgut wall where they develop into oocysts.
4. The oocysts grow and rupture to release sporozoites, which make their way to the mosquito's salivary glands.
5. Inoculation of the sporozoites into a new human host during the mosquito's next blood meal perpetuates the malaria life cycle.
65
True or false:
| Malaria can be spread transplacentally.
True.
66
Sporozoites are formed by _______.
sporogony (sexual or asexual reproduction by multiple fission of a spore or zygote).
67
Disease and symptoms of malaria
* Classical “ quaternary fever”
| * Anaemia (due to damage to RBC and metabolism of haemoglobin) and jaundice (due to increased haemoglobin)
68
Pathogenesis of fever and chills in malaria
Fever coincides with rapid release of merozoites and parasite material, triggering inflammatory response. This leads to production of TNFα, IL-1 which cause the symptoms of fever and chills.
69
Diagnosis of malaria
Mainstay of diagnosing malaria is by blood smear
70
True or false:
| Immunochromatographic rapid testing for malarial parasites has high specificity and sensitivity relative to PCR testing.
False. Immunochromatographic testing has high specificity but poor sensitivity. PCR tests detect a much lower parasite load.
71
Drugs used to treat malaria
Chloroquine and Artemesin
72
Malarial treatment to alleviate symptoms
Therapy for symptoms involves schizonticidal drugs e.g. chloroquine, quinine, artemisinin combinations which terminate clinical malarial attacks
73
Malarial treatment to prevent relapses
Therapy involves tissue schizonticidal drugs (e.g. Primaquine) act on hypnozoites in the liver that cause relapse of symptoms on reactivation
74
Malarial treatment to prevent spread
Therapy to prevent spread includes:
- Gametocytocidal drugs e.g. Primaquine for P. falciparum, Chloroquine for all other
- Sporontocides drugs prevent the development of oocysts in the mosquito thereby preventing transmission (e.g. Primaquine and chloroguanide)
75
Most effective methods for prevention of malaria
Vector control e.g. bed nets treated with insecticide
76
Platyhelminthes are commonly known as what?
Flatworms
77
Nematoda are more commonly known as what?
Roundworms
78
What are the two main subgroups of platyhelminthes?
Trematoda (flukes) and Cestoda (tapeworms)
79
The most common intestinal helminth in humans
Nematoda (roundworms)
80
Trematoda is divided into which two groups?
Digenea and Aspidogastrea
81
Digenea are commonly known as what?
Flukes
82
Characteristics of trematoda
- Adults are usually hermaphrodites
| - Two suckers, one around the mouth and a larger sucker midway along the underside
83
Definitive host of trematoda
a land vertebrate
84
Intermediate host of trematoda
Usually a mollusc, and in many cases a fish or arthropod is a second intermediate host
85
Infection with schistosoma causes which disease?
schistosomiasis
86
Diagnosis of T. saginata and T. solium infection
Intestinal infections in humans are diagnosed by the detection of gravid segments or eggs in faecal samples.
87
Life cycle of T. saginata and T. solium
1. Humans infected by ingesting raw or undercooked infected meat containing oncospheres.
2. Once ingested, the eggs excyst and scolex attaches to the intestinal wall and proglottids develop.
3. Eggs or gravid proglottids in faeces and passed into environment
4. Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated by eggs or gravid proglottids
5. Oncospheres hatch, penetrate intestinal wall, and circulate musculature
6. Oncospheres develop into cysticerci in muscle and the cycle is when ingested by humans
88
Pathogenesis of T. saginata and T. solium infection
Cysticerci may develop in virtually every organ and tissue of the human body. Humans are susceptible to pressure necrosis, particularly when cysticerci develop in the brain or eyes. Degenerating cysticerci may elicit severe acute, and even fatal, inflammatory responses before their eventual calcification.
89
Life cycle of E. granulosus
The adult Echinococcus granulosus (sensu lato) (2—7 mm long) image resides in the small intestine of the definitive host. Gravid proglottids release eggs image that are passed in the feces, and are immediately infectious. After ingestion by a suitable intermediate host, eggs hatch in the small intestine and release six-hooked oncospheres image that penetrate the intestinal wall and migrate through the circulatory system into various organs, especially the liver and lungs. In these organs, the oncosphere develops into a thick-walled hydatid cyst image that enlarges gradually, producing protoscolices and daughter cysts that fill the cyst interior. The definitive host becomes infected by ingesting the cyst-containing organs of the infected intermediate host. After ingestion, the protoscolices image evaginate, attach to the intestinal mucosa image , and develop into adult stages image in 32 to 80 days.
Humans are aberrant intermediate hosts, and become infected by ingesting eggs image . Oncospheres are released in the intestine image , and hydatid cysts develop in a variety of organs image . If cysts rupture, the liberated protoscolices may create secondary cysts in other sites within the body (secondary echinococcosis).
90
Pathogenesis of E. granulosus
- E. granulosus-pathogenic only in human ”accidental” intermediate host. The adult stages are considered benign and do not cause disease in dogs, as the worms do not invade or feed on host tissues. Significant pathological changes occur in humans when the slowly-growing cysts put pressure on surrounding tissues and produce chronic space-occupying lesions.
- Clinical signs include compression of liver resulting in jaundice, portal hypertension and abdominal distention. Cysts in the lung may cause haemoptysis, dyspnoea and chest pain.
- Cyst rupture and sudden release of hydatid fluid may cause severe allergic reactions (e.g. asthma and anaphylactic shock)
91
Nematodes are commonly known as
roundworms
92
Enterobius vermicularis is commonly known as
pinworm
93
Ascaris lumbricoides is commonly known as
roundworm
94
Diagnosis of E. vermicularis
Worm eggs are rarely found in faeces so conventional coprological examination techniques are not used.
Instead, infections are best diagnosed by the macroscopic detection of adult worms or the microscopic detection of eggs on the perineum. Sticky-tape may be applied to the perianal skin first thing in the morning and then stuck onto a glass slide for microscopic examination of adherent eggs
95
Life cycle of E. vermicularis:
Gravid adult female Enterobius vermicularis deposit eggs on perianal folds, which develop and become infective in 4-6 hours under optimal conditions
Infection occurs via self-inoculation (transferring embryonated eggs to mouth with hands that have scratched perianal area) or through exposure to eggs in the environment. Larvae inside eggs mature within 4-6 hours.
Following ingestion of infective eggs, larvae hatch in small intestine. The adults establish themselves in the colon, usually in the cecum.
Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area
The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions
Alternatively, eggs trapped in perianal folds may hatch and the larvae may enter the intestines directly via the anus (process called retro-infection)
96
Pathogenesis of E. vermicularis including symptoms
Pulmonary migration by larvae may cause haemorrhages, oedema, inflammation, and pulmonary congestion with cough, chest pain and difficulty breathing
Migrating larvae often die causing focal inflammation
Adult worms developing in the gut feed on luminal content, contributing to protein energy malnutrition and impaired carbohydrate absorption
Moderate-heavy infections may cause a variety of digestive disorders, poor growth and development in small children, abdominal pains, restlessness, insomnia and allergic responses (rashes, asthma)
Heavy infections may also cause life-threatening gut obstructions where tangles of worms block the gut
Infections by small numbers of worms may remain asymptomatic
97
Pathogenesis of Ascaris lumbricoides including symptoms
Pulmonary migration by larvae may cause haemorrhages, oedema, inflammation, and pulmonary congestion with cough, chest pain and difficulty breathing
Migrating larvae often die causing focal inflammation
Adult worms developing in the gut feed on luminal content, contributing to protein energy malnutrition and impaired carbohydrate absorption
Moderate-heavy infections may cause a variety of digestive disorders, poor growth and development in small children, abdominal pains, restlessness, insomnia and allergic responses (rashes, asthma)
Heavy infections may also cause life-threatening gut obstructions where tangles of worms block the gut
Infections by small numbers of worms may remain asymptomatic
98
Life cycle of Ascaris lumbricoides
Adult worms live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the faeces. Unfertilised eggs may be ingested but are not infective. Larvae develop to infectivity within fertile eggs after 18 days to several weeks, depending on environmental conditions.
After infective eggs are swallowed, the larvae hatch, invade the intestinal mucosa and are carried via portal, then systemic circulation to the lungs
The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed
Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years
99
Schistosomiasis pathogenesis
Migration of eggs through the wall of the intestine causes inflammation and formation of pseudopapillomas in the colon, leading to obstruction of, and bleeding into the gut.
Migration of parasite eggs to the liver leads to an inflammatory response, leading to formation of granulomas which destroy the organ tissue
Chronic infection can lead to liver fibrosis and cirrhosis, as well as schistosomal myelopathy, which may result in permanent neurological damage
Damage to the liver causes changes in blood circulation and leads to hepatosplenomegaly through increased portal blood pressure
Increased portal blood pressure results in formation of ascites und changes in vein structure leading to formation of varicose veins in stomach and oesophagus, which can rupture and be fatal
Schistosomiasis does not have high mortality but causes chronic debilitating infection
100
Diagnosis of schistosomiasis
- Chief method of diagnosis is to locate parasite eggs in faeces (S. mansoni and S. japonicum), or urine (S. haematobium). Eggs may not be present in high numbers in urine or faeces; concentrating eggs by centrifugation of urine or faeces often a part of diagnostic procedure.
- Serological test are possible e.g. indirect immunofluorescence (IIF), ELISA, circumoval precipitin test (COPT), circulating antigens (e.g. circulating anodic antigen)
- Questionnaire - travel history, frequency of exposure to water etc.
- Interpretation of clinical symptoms
- Ultrasound examinations can reveal enlargement of the liver
101
Schistosoma spp life cycle
Schistosoma spp. life cycle:
1. The intermediate host (water-living mollusc e.g. snail) release cercariae into its aqueous environment.
2. Cercariae are free-swimming and secrete enzymes to burrow into the host. Human exposure is through fresh water contact with cercariae (penetrate skin). Cercariae lose their tail during penetration through tissue and become schistosomulae.
3. Schistosomulae migrate through the tissues, enter the circulation, and migrate to portal blood in liver where they mature into adults.
4. Paired adult worms migrate to the mesenteric venules of bowel/rectum (S. Japonicum and S. mansoni), laying eggs that circulate to the liver and shed in stool, and venous plexus of the bladder (S. haematobium). Migration of the worms causes damage to tissue, leading to pathology of infection.
5. Once the eggs reach the urine or faeces, they are excreted in fresh water. In water, the eggs hatch, releasing ciliated miracidia which penetrate the tissues of snails.
6. Within the snail, miracidia undergo development and asexual replication, until the cercariae burst out into the aqueous environment after the right developmental period
