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Unit 3 D&D > DD 02-28-14 11am-Noon Introduction to Parasites - Holmes > Flashcards

DD 02-28-14 11am-Noon Introduction to Parasites - Holmes Flashcards

1
Q

Parasite defn.

A

an organism which lives upon or within another living organism at whose expense it obtains some advantage

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2
Q

Parasitology’s concern

A

= pathogenic protozoa (unicellular eukaryotes) & metazoa (multicellular eukaryotes)

Includes:

  • helminths (worms)
  • arthropods (insects)
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3
Q

Life Cycles of human parasites

A

Complex life cycles

- some involve development in one or more additional host species (definitive host + intermediate hosts)

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4
Q

Definitive host of a parasite

A

= the species in which the parasite undergoes sexual replication

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5
Q

Intermediate host of a parasite

A

= other species besides the definitive host, in which asexual replication occurs

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6
Q

Important factors in parasite’s life cycle

A

Ability of parasites to infect specific tissues (tropism)

Geographic occurrence of parasitic diseases
- often restricted by availability of host species

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7
Q

Protozoan vs. Worm parasites

A

Most protozoan parasites can replicate and increase their numbers in humans.

In contrast, many worms undergo development but do not replicate in humans
- worm burden in humans reflects intensity of their exposure to infection

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8
Q

Parasites & the Immune system

A
  • Many parasites evade or subvert the protective immune responses of their hosts
  • Damage to host tissues is often result of host immune responses
  • Diseases caused by many parasites become clinically apparent when the number of parasites (the parasite burden) is high or when infection persists for long periods of time.
  • Development of effective vaccines against major human parasitic diseases has been difficult & remains an important goal for world health
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9
Q

Selective toxicity in parasitic disease

A
  • B/c parasitic diseases are caused by EUKARYOTIC pathogens, the biological bases for selective toxicity of anti-parasite drugs are quite different from anti-bacterial & anti-viral drugs
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10
Q

Dx of parasitic disease

A
  • often made by direct examination of parasites in specimens or biopsy materials collected directly from patients
  • Generally morphological criteria are much more helpful in parasitic disease than viral/bacterial disease
  • Immunological tests (detection of specific Ags & Abs) & molecular diagnostic tests (for specific nucleic acid sequences) are sometimes helpful
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11
Q

Helminth groups causing human disease

A
  1. Roundworms/Nematodes
  2. Flatworms/Trematodes/Flukes
  3. Tapeworms/Cestodes
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12
Q

Roundworms/Nematodes - examples

A 
Ascaris
Pinworms
Whipworms
Hookworms
Strongyloides
Echinococcus
Trichinella
Filarial worms
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13
Q

Flatworms/Trematodes/Flukes - examples

A

Schistosomes

Lung fluke

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14
Q

Tapeworms/Cestodes - examples

A

beef tapeworm
pork tapeworm
fish tapeworm

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15
Q

Protozoan groups that are human parasites

A
  1. Amebas
  2. Flagellates
  3. Ciliates (Balantidium coli)
  4. Sporozoa
  5. Microsporidia
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16
Q

Amebas - example

A

Entamoeba histolytica

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17
Q

Flagellates - examples

A

Giardia
Trichomonas
Trypanosoma
Leishmania

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18
Q

Ciliates - example

A

Balantidium coli

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19
Q

Sporozoa - examples

A

Cryptosporidium
Cyclospora
Plasmodium
Toxoplasma

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20
Q

Microsporidia - examples

A

Enterocytozoon

Septata

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21
Q

Schistosomiasis - paradigm of helminthic infection - Transmission, Basic course

A
  • transmitted to humans by exposure to contaminated fresh water
  • -> causes acute manifestations & progresses to chronic disease affecting intestinal or urinary system
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22
Q

Epidemiology of Schistosomiasis

A
  • affect ~200-300 million people a year globally
  • causes 200,000 deaths per year globally
  • 2nd only to malaria among parasitic diseases
    Among infected people,
  • 120 million are symptomatic
  • 20 million have severe disease
  • 85% live in sub-Saharan Africa
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23
Q

Schistosomes

A

= trematodes/flatworms

  • 3 species are widely distributed & cause most human infections
  • 2 species have more restircted distribution
  • Schistosomiasis in the US is only seen in immigrants or travelers
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24
Q

3 species of Schistosomes with wide distribution

A

Schistosoma mansoni
S. japonicum
S. haematobium

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25
Q

Schistosoma mansoni - location

A

primarily in Africa, South America and the Middle East

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26
Q

S. japonicum - location

A

primarily in China, the Philippines and Indonesia

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27
Q

S. haematobium - location

A

primarily in Africa and the Middle East

28
Q

2 species of Schistosomes with restricted geographic distribution

A 
Schistoma intercalatum (West Africa)
Schistoma mekongi (Southeast Asia)
29
Q

Life Cycle of Schistosomes

A

Complex life cycle

Eggs shed in feces/urine of infected humans

  • -> hatch in fresh water
  • -> release miracidia, which infect snails

Sporocysts develop in the snails

  • -> free-swimming cercaria are released
  • -> can penetrate human skin to initiate infection

Cercaria lose their tails & develop into schistosomulae in tissues of human host.

Schistosomulae gain access to circulation

  • -> migrate to portal blood
  • -> mature into adult worms

Adult worms migrate to mesenteric veins or venous plexus of bladder (depending on species)
–> mating –> eggs

Eggs produced circulate in venous blood to the liver & are also released into intestine or urinary bladder, depending on the anatomic location of adult worms.
–> Release of eggs into environment perpetuates infection cycle

(see pic in notes)

30
Q

Schistosomes that migrate to & mate in the mesenteric vein

A

S. mansoni
S. japonicum
S. intercalatum
S. mekongi

–> eggs produces are released into intestines (or circulate to liver)

31
Q

Schistosomes that migrate to & mate in the venous plexus of the bladder

A

primarily S. haematobium

–> eggs produces are released into urinary bladder (or circulate to liver)

32
Q

Cercarial invasion into the skin

A

can cause dermatitis (swimmers itch) within 2-3 days

33
Q

Acute phase of schistosomiasis

A
  • aka Katayama fever
    = a serum-sickness like illness
  • occurs 4-8 weeks after skin invasion
    = occurs coincident w/ worm maturation & onset of oviposition
  • often accompanied by lymphadenopathy & hepatosplenomegaly
34
Q

chronic stage of schistosomiasis

A
  • involves granulamatous & fibrotic changes in liver or bladder (site depending on species)
    = consequences of host rxns to deposited eggs
    –> leads to formation of infiltrates containing large numbers of eosinophils & eventually to scarring
35
Q

Severity of Schistosomiasis & Symptoms

A 
Light infestations = may be asymptomatic
Heavier infestations = often symptoms such as...
For intestinal schistosomiasis:
- diarrhea
- abdominal pain
- ascites 
For urinary schistosomiasis:
- bloody urine (hematuria) 
- bladder cancer
36
Q

Dx of Schistosomiasis

A
  • microscopic examination of stool or urine for schistosome eggs w/ characteristic sizes & shapes
  • detection of similar schistosome eggs in tissue biopsies
37
Q

Major strategies for controlling schistosomiasis:

A

Public health education

  • avoid contact w/ infected water
  • build wells & latrines to provide potable water
  • avoid contamination of environmental water sources

Molluscicides & environmentasl modification to control snail intermediate

Mass treatment of populations w/ anti-schistosome drugs (such as praziquantel, etc.),

Research on diagnostic tests, improved therapeutics, & vaccines for schistosomiasis

Even in regions where control of schistosomiasis has been effective, parasite has not been eliminated & transmission continues, albeit at lower frequency

38
Q

Malaria as an important paradigm of protozoan infection - Overview

A

= the most important parasitic disease

- 4 species of protozoa in genus Plasmodium cause malaria in humans

39
Q

Malaria - Epidemiology

A
  • affects > 1 billion people a year
  • causes 1-3 million deaths/year
  • eliminated from US, Canada, Europe, Russia (except imported cases)
  • Global malaria & resistance to anti-malarial drugs are still major problems
40
Q

Four species of protozoa causing malaria in humans

A

Plasmodium genus

  • P. vivax
  • P. ovale
  • P. malariae
  • P. falciparum
41
Q

Plasmodium vivax

A

widely distributed, from tropical to temperate zones

42
Q

Plasmodium falciparum

A
  • causes most of the malaria deaths

- primarily in tropics / subtropics

43
Q

Life cycle of malaria parasites - Asexual Phase of Development

A

Infected mosquitos bite humans & inject sporozoites into the blood

After primary replication in liver…

  • -> merozoites are released into blood
  • -> infect erythrocytes
  • -> undergo additional asexual replication

Gametes (macro- & micro-gametocytes) are
formed in some infected erythrocytes.

44
Q

Asexual phase of development for malaria parasites occurs in…

A
  • aka schizogony

- occurs in humans

45
Q

Dormant phase of malaria in humans

A
  • Sporozoites of all malaria parasites can infect liver cells & replicate
  • BUT only P. vivax & P. ovale can establish a dormant hepatic phase w/ non-dividing
    forms called hypnozoites that can initiate late relapses.
46
Q

Life cycle of malaria parasites - Sexual Phase of Development

A
  • aka sporogony
  • occurs in infected mosquito
  • Gametes fuse in intestine to form zygotes.
  • Development of parasite in mosquitoes eventually leads to production of sporozoites in salivary gland.
  • Introduction of sporozoites into susceptible human by bite of an infected mosquito initiates a repetition of the life cycle of the parasite.
47
Q

Acquire immune response to malarial parasites

A
  • Acquired immune responses that help to control the development of malaria parasites in humans are also shown.
48
Q

Symptoms of malaria – associated with…

A
  • primarily associated w/ rupture of infected RBCS & release of merozoites
49
Q

P. falciparum – malaria pathogenesis

A
  • invades erythrocytes of all ages & can therefore achieve highest parasitemia & mortality
50
Q

P. vivax & P. ovale – malaria pathogenesis

A
  • invade only young erythrocytes
51
Q

P. malariae – malaria pathogenesis

A
  • invades only old erythrocytes
52
Q

Untreated patients with malaria & periodicity

A

Process often becomes synchronized

Fever paroxysms may have regular periodicity

  • 48 hr for benign tertian malaria caused by P. vivax or P. ovale
  • 72 hr. for quartan malaria caused by P. malariae
  • 36-48 hr. for malignant tertian malaria caused by P. falciparum
53
Q

Anemia in malaria

A

May be disproportionate to parasitemia

Results from…

  • RBC lysis
  • RBC phagocytosis by stimulated reticuloendothelial system
  • RBC sequestration in enlarged spleen
  • Depressed bone marrow function

Hemolysis can be extreme, resulting in hemoglobinuria (blackwater fever)

54
Q

Physical examination findings in malaria patient

A
  • jaundice
  • hypotension
  • tachycardia
  • fever
  • hepatosplenomegaly
55
Q

P. falciparum infections – symptoms & mechanism

A
  • vasodilation causes hypotension & inadequate blood supply to vital organs
  • P. falciparum-infected RBCs bind to microvascular endothelium, which is especially significant in cerebral malaria (up to 50% mortality)
56
Q

Malarial death - major cause in adults

A
  • Multi-organ failure
57
Q

With P. malariae infections – symptoms & mechanism

A
  • immune complex deposition leading to glomerulonephritis is common
58
Q

Immunity to malarial infection

A
  • pt mounts immune response that makes subseqent episodes of symptomatic disease less severe
  • Both B & T cell responses are involved
  • W/in a few weeks of infection, stage specific anti-plasmodium antibodies are produced
  • Natural immunity is short-lived
  • Continual re-infection is required to maintain it
  • People returning to endemic areas following long absence may thus be quite susceptible to re-infection
59
Q

Diagnosis of malaria

A
  • Usually by detection of asexual forms of parasites in stained thick or thin blood films
  • Morphological features of intracellular parasites & infected erythrocytes are used to differentiate the 4 species from each other & from other protozoan that also can replicate in erythrocytes
  • Rapid monoclonal Ab-based tests for the PfHRP2 antigen or for Plasmodium LDH antigens are also useful in diagnosis of P. falciparum infections
60
Q

Splenic enlargement in malaria

A
  • common in apparently healthy individuals w/ repeated infections
  • often used to estimate prevalence of malaria in populations in endemic areas
61
Q

Malaria & Selection of traits

A
  • widespread & lethal nature of malaria has apparently selected for traits that protect against plasmodia but are otherwise undesirable

Includes:

  • sickle cell anemia
  • thalassemias
  • glucose-6-phosphate dehydrogenase deficiency
62
Q

Malaria & HbS (Sickle Cell)

A
  • Parasites do not appear to thrive in Hb S associated w/ sickle cell disease, nor in certain other abnormal Hgb’s
63
Q

Thalassemia & Malaria

A
  • In thalassemia, there is increased production of fetal hemoglobin
  • -> retards maturation of P. falciparum
64
Q

G6PD deficiency & Malaria

A
  • the oxidative stress may inhibit parasite growth
65
Q

HLA-B53 & Malaria

A
  • associated w/ recovery from falciparum malaria

- very common in West Africa

66
Q

Prevention of malaria

A
  • Minimize mosquito contact in endemic areas
  • Efforts at mosquito control & malaria eradication during 1950’s & 1960’s by using DDT & drugs were eventually frustrated by concurrent appearance of DDT-resistant mosquitoes, cessation of DDT use due to its environmental effects, & development of drug resistant plasmodia
  • Array of drugs for prophylaxis & treatment
  • Extensive efforts to develop effective vaccines against various forms of malaria

Unit 3 D&D (18 decks)

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