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

(66 cards)

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
Schistosoma mansoni - location
primarily in Africa, South America and the Middle East
26
S. japonicum - location
primarily in China, the Philippines and Indonesia
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S. haematobium - location
primarily in Africa and the Middle East
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2 species of Schistosomes with restricted geographic distribution
``` Schistoma intercalatum (West Africa) Schistoma mekongi (Southeast Asia) ```
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Life Cycle of Schistosomes
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
Schistosomes that migrate to & mate in the mesenteric vein
S. mansoni S. japonicum S. intercalatum S. mekongi --> eggs produces are released into intestines (or circulate to liver)
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Schistosomes that migrate to & mate in the venous plexus of the bladder
primarily S. haematobium | --> eggs produces are released into urinary bladder (or circulate to liver)
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Cercarial invasion into the skin
can cause dermatitis (swimmers itch) within 2-3 days
33
Acute phase of schistosomiasis
- 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
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chronic stage of schistosomiasis
- 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
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Severity of Schistosomiasis & Symptoms
``` 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
Dx of Schistosomiasis
- microscopic examination of stool or urine for schistosome eggs w/ characteristic sizes & shapes - detection of similar schistosome eggs in tissue biopsies
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Major strategies for controlling schistosomiasis:
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
Malaria as an important paradigm of protozoan infection - Overview
= the most important parasitic disease | - 4 species of protozoa in genus Plasmodium cause malaria in humans
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Malaria - Epidemiology
- 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
Four species of protozoa causing malaria in humans
Plasmodium genus - P. vivax - P. ovale - P. malariae - P. falciparum
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Plasmodium vivax
widely distributed, from tropical to temperate zones
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Plasmodium falciparum
- causes most of the malaria deaths | - primarily in tropics / subtropics
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Life cycle of malaria parasites - Asexual Phase of Development
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
Asexual phase of development for malaria parasites occurs in...
- aka schizogony | - occurs in humans
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Dormant phase of malaria in humans
- 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
Life cycle of malaria parasites - Sexual Phase of Development
- 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.
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Acquire immune response to malarial parasites
- Acquired immune responses that help to control the development of malaria parasites in humans are also shown.
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Symptoms of malaria – associated with…
- primarily associated w/ rupture of infected RBCS & release of merozoites
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P. falciparum – malaria pathogenesis
- invades erythrocytes of all ages & can therefore achieve highest parasitemia & mortality
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P. vivax & P. ovale – malaria pathogenesis
- invade only young erythrocytes
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P. malariae – malaria pathogenesis
- invades only old erythrocytes
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Untreated patients with malaria & periodicity
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
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Anemia in malaria
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)
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Physical examination findings in malaria patient
- jaundice - hypotension - tachycardia - fever - hepatosplenomegaly
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P. falciparum infections – symptoms & mechanism
- 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)
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Malarial death - major cause in adults
- Multi-organ failure
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With P. malariae infections – symptoms & mechanism
- immune complex deposition leading to glomerulonephritis is common
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Immunity to malarial infection
- 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
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Diagnosis of malaria
- 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
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Splenic enlargement in malaria
- common in apparently healthy individuals w/ repeated infections - often used to estimate prevalence of malaria in populations in endemic areas
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Malaria & Selection of traits
- 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
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Malaria & HbS (Sickle Cell)
- Parasites do not appear to thrive in Hb S associated w/ sickle cell disease, nor in certain other abnormal Hgb’s
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Thalassemia & Malaria
- In thalassemia, there is increased production of fetal hemoglobin - -> retards maturation of P. falciparum
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G6PD deficiency & Malaria
- the oxidative stress may inhibit parasite growth
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HLA-B53 & Malaria
- associated w/ recovery from falciparum malaria | - very common in West Africa
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Prevention of malaria
- 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