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Micro unit 2 > L10 > Flashcards

L10 Flashcards

1
Q

Parasitic infections are among the most prevalent diseases in

A

developing countries
• Also common in developed countries
• Typically cause no clinical infections

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2
Q

Parasitic infection is distinct from

A

parasitic disease

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3
Q

Toxoplasma gondii and hookworm infections are prevalent, but few

A

immunocompetent individuals develop disease

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4
Q

Parasitic Disease - Consequence of

A

prolonged, repeated, or high burden infection

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5
Q

Parasitic Disease - Usually

A

subacute or chronic
• Rarely fatal • Exceptions:
• Plasmodium falciparum (malaria) – may be rapidly fatal (3-5 days)
• Infections in immunocompromised individuals


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6
Q

Many parasitic infections are

A

zoonoses • Caused by agents that infect animals

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7
Q

Many human parasites require

A

human and nonhuman hosts to complete their life cycles • Humans are dead-end hosts for some parasites
• Infection occurs but no parasite developmental stage - life cycle not completed

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8
Q

• Two parasite types:

A

protozoa and helminths

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9
Q

Protozoa - single

A

celled orgs

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10
Q

Protozoa - Intracellular (red blood cells, macrophages)

•

A

Unable to withstand environmental dessication (drying)

• Life cycles do not include free environmental stage

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11
Q

Protozoa - Extracellular (lumen of GI tract)

•

A

Often transmitted by fecal-oral route
• Life cycles alternate between two forms
• Active trophozoite
• Dormant cyst – withstands environmental desiccation

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12
Q

Protozoa - Disease is consequence of

A

parasite replication to high numbers (small inoculum required to initiate infection)

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13
Q

• About 65,000 species of

A

protozoa

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14
Q

Most protozoa are

A

Most are harmless, free-living inhabitants
of water and soil

• Few are parasites

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15
Q

Mastigophora - • Motility primarily by

A

flagella

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16
Q

Mastigophora - • Single

A

nucleus

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17
Q

Mastigophora - • Sexual reproduction by

A

syngamy

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18
Q

Mastigophora - • Division by

A

longitudinal fission

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19
Q

Mastigophora - Parasitic forms tend to lack

A

mitochondria and Golgi

apparatus

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20
Q

Mastigophora - Most form

A

cysts and are free-living

• Most are solitary

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21
Q

Apicomplexa (Sporozoa) - • Most not motile except

A

male gametes

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22
Q

Apicomplexa (Sporozoa) - have Complex

A

life cycles

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23
Q

Apicomplexa (Sporozoa) - Produce

A

sporozoites following sexual reproduction

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24
Q

Apicomplexa (Sporozoa) - • Important in transmission of

A

infections

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25
Q

Apicomplexa (Sporozoa) - Most form

A

oocysts

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26
Q

Apicomplexa (Sporozoa) - Entire group is

A

parasitic

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27
Q

Helminths (worms) - are

A
  • Multicellular animals (metazoa)

* Roundworms, flatworms

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28
Q

Helminths (worms) - • Extracellular due to

A

large size

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29
Q

Helminths (worms) - • Protected by

A

cuticle

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30
Q

Helminths (worms) - Larvae can develop into

A

dormant

cysts

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31
Q

Helminths (worms) - Environmental and animal

A

reservoirs

• Do not typically complete life cycle in human

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32
Q

Helminths (worms) - Developmental stages take place

A

outside of human
(definitive hosts) in insect vectors or animal reservoirs (intermediate hosts)
Reproduce sexually

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33
Q

Helminths (worms) - • A few species (tapeworms) are

A

hermaphroditic

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34
Q

Helminths (worms) - Most helmiths cause

A

chronic infections that are tolerated by the human host

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35
Q

Helminths (worms) - Disease is not a consequence of

A

parasitic replication

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36
Q

Helminths (worms) - Parasitic burden due to

A

number of parasites that host initially acquires from environment

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37
Q

Helminths: Established infections not

A

eliminated by host response

• Spontaneously resolve when adult worms reach senescence

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38
Q

Parasitic Helminths: large

A

Tapeworms, flukes, and roundworms
• Adults large enough to be seen with the
naked eye

• From1mmto25minlength

Microscope is necessary to identify eggs and larvae

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39
Q

Parasitic Helminths: • Two major groups:

A

Flatworms and Roundworms

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40
Q

Flatworms - • Phylum

A

Platyhelminthes

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41
Q

Flatworms -

A

Thin

• Often segmented

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42
Q

Flatworms: Subdivisions

A

Cestodes (tapeworms)

• Trematodes (flukes)

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43
Q

Roundworms - • Phylum

A

Aschelminthes

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44
Q

Roundworms - • Also known as

A

Nematodes

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45
Q

Roundworms -

A

Elongate
• Cylindrical
• Unsegmented

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46
Q

Epidemiology and Public Health

A
  • Transmission
  • Multiplication
  • Damage/disease
  • Treatment and Prevention
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47
Q

Parasite Vectors: Most are

A

arthropods

Involved in essential steps of parasitic life cycle

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48
Q

Female Anopheles mosquito –

A

malaria •

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49
Q

Tsetse flies –

A

sleeping sickness

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50
Q

• Black flies –

A

river blindness

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51
Q

• “Kissing” bugs –

A

Chagas’ disease

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52
Q

• Ticks –

A

babesiosis

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53
Q

Parasitic prevalence dependent on

A

local conditions favoring arthropod breeding

Stagnant water, foliage
• Suitable animal hosts

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54
Q

Reservoirs –

A

sources of parasites that do not participate directly in transmission

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55
Q

Parasite reservoirs: Humans

A

• Malaria parasites, amoebae

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56
Q

Parasite reservoirs: Animals

A
  • Pigs - trichinosis, pork tapeworm

* Cattle – beef tapeworm, cryptosporidiosis

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57
Q

Parasite Entry - Penetration of the - 2

A

skin (unbroken)

• Hookworm, schistosomes

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58
Q

Parasite Entry = Arthropod-borne

A
  • Bite wounds
  • Very efficient – malaria
  • Can be transmitted by blood transfusions
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59
Q

Parasite Entry - Oral /ingestion 1.

A

Oral/ingestion
• Contaminated food or water
• Inadequate control of human wastes
• Ascariasis, amebiasis

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60
Q

Dependent on parasitic life cycle and

A

presence or absence of intermediate hosts for trasnmission

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61
Q

Schistosomiasis –

A

snails required to allow parasite to mature
• Snails not present in North
America or Europe

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62
Q

Malaria

A

• Anopheles mosquitoes are present in US and indigenous mosquito pool can be infected

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63
Q

• Disease manifestation dependent on

A

size of inoculum that varies for different parasites

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64
Q

Amebiasis –

A

large inocula

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65
Q

Cryptosporidiosis –

A

few cysts

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66
Q

Helminths – directly proportional to initial

A

inoculum from environment

67
Q

Circumvent host

A

antibody and cell-mediated immune
responses for survival

  • Host plasma protein coatings (blood flukes)Surface antigen variation (trypanosomes)
  • Superoxide dismutase secretion (Leishmania) • Protection from host phagolysosome
68
Q

• Life cycles determined by

A

species and tissue tropisms

69
Q

• Strongyloides – attacks

A

intestinal wall

70
Q

• Hookworms – attack

A

intestinal lumen

71
Q

• A particular duffy factor antigen on red blood cell surface is required for

A

entry of P. vivax malaria parasites

72
Q

Leishmania donovani –

A

replicates at 37 oC

73
Q
  • Visceral leishmaniasis (bone marrow, liver, spleen)

* Leishmania tropica – replicates at also induce stage-specific transitions

A

25-30 oC
• Skin infections
• Temperature changes

74
Q

Deep tissue infections –>

A

chronic inflammation

75
Q

Cysticercosis – dead parasites leak

A

antigens that

trigger hypersensitivity in host

76
Q

• Both avenues of symptomology can be

A

concurrent

77
Q

Most clinical complications occur

A

years after initial infection

78
Q

Damage from parasitesClinical manifestations may be due to: •

A

Direct tissue damage by parasite

• Cytolysis  colonic ulcers, liver abscesses • Pathogenic amoeba

79
Q

• Effects of host immune response -

A

Schistosomiasis, cutaneous filariasis

80
Q

Schistosomiasis

A

GI or urinary tract bleeding for years
• Heavy, chronic infections can lead to hypertension,
obstructions and cancer

81
Q

• Pork tapeworm (Taenia solium)

A 
Adult parasite asymptomatic in intestine
• Larvae may enter blood and infect deep tissues as
cysts
• Asymptomatic in skeletal muscle
• Seizures or hydrocephalus in CNS
82
Q

Chagas’ disease (American trypanosomiasis)

A

Trivial skin lesion  asymptomatic or mildly
symptomatic
• Acute infections  swollen eyelid (Romaña’s Sign),
lymph node swelling (young children and immunocompromised susceptible to more severe illness and death)
• Indeterminate, symptom-less stage that can last
months to years
• Named after Cecilio Romaña, Argentinian who
described the phenomenon
• Chronic infectionslesions on various organs
(e.g., heart, esophagus, colon or peripheral nervous system); the damage done to organs during this phase is irreversible and tends to weaken the body, sometimes fatally

83
Q

Eradication is successful only when more

than one of the following are employed:

A
  1. Chemoprophylaxis – preventative drugs
    • Chloroquine effective against all 4 species of Plasmodium (but, some becoming resistant)
    • Ivermectin for onchocerciasis (river blindness) 2. Immunization
  2. Field control measures
    • Insecticides (e.g., DDT) sprayed on mosquitoes that rest under eaves after biting
    • Sanitation - Potable water
84
Q

• Many parasites masquerade as ‘self’ by coating themselves in

A

host antigens

85
Q

Some parasites (trypanosomes) continually alter

A

surface antigens

86
Q

Different proteins/polysaccharides displayed on surfaces at different life stages

A

Need polyvalent vaccine that contains major

antigens from all each stage of life cycle

87
Q

Malaria - most important of all protozoan diseases •

A

“The greatest harm to the greatest number”

Approximately 156 named species of Plasmodium protozoa that infect various species of vertebrates
• Four are known to infect humans and vary in virulence due to red blood cell age preference:
• P. falciparum – all ages of rbcs (greatest mortality)
• P. vivax/P. ovale – reticulocytes and young rbcs
• P. malariae – older rbcs

88
Q

Infected humans are the only reservoir for

A

Plasmodium that infect humans

89
Q

Malaria: Transmission occurs

A

9-17 days

after bite of infected female Anopheles mosquitoes • Symptoms develop 8-30 days later

90
Q

Imported malaria

A

• Endemic area infection - travelers import parasite to

nonendemic areas during incubation

91
Q

Induced malaria

•

A

Transmission via blood transfusions or needles

92
Q

• Sporozoites inhabit

A

mosquito salivary glands

93
Q

After mosquito bite, sporozoites travel through bloodstream and enter

A

liver cells within 30 minutes
• Hepatocellular cycle
• Multiply and mature
• 2 weeksmonths (sometimes years)

94
Q

Release to blood as merozoites

A

Invade red blood cells, divide and mature (erythrocytic cycle) into trophozoite • Nuclei and organelles
replicate (schizont) • 2-3 days: red blood
cells burst and liberate more merozoites

95
Q

Parasites multiply asexually (

A

binary fission) in liver and red blood cells

96
Q

Some plasmodia in blood may develop into

A

gametocytes capable of sexual reproduction in mosquitoes.

97
Q

• Parasite replication can be

A

synchronous

98
Q

Typical paroxysm

A

Simultaneous lysis of many RBCs and release of large number of merozoites and other parasitic molecules every 48 -72 hours
• GPI (glycophosphatidylinositol)
• Stimulates tumor necrosis factor (TNF) and IL-1 from macrophages
• Fever, edema, anemia, shock

99
Q

Glycophorin A/Duffy blood group antigen on RBC surface

A

Black Africans – often Duffy negative

100
Q

• Sickle cell anemia

A 
Defective sickle cell hemoglobin
• Red blood cells shaped like a "C"
• Genetic mutation of a single nucleotide
of the β-globin gene
• Glutamate  valine
101
Q

• Heterozygous individuals (carriers)

A

Disease less acute
• Malaria parasite causes RBCs to rupture
prematurely, making the plasmodium unable to reproduce

102
Q

Chloroquine - Target parasite’s food vacuole where

A

hemoglobin is degraded

Toxic heme detoxified
• Chloroquine blocks detoxification and kills parasite

103
Q

• Chloroquine was once the most widely used

A

drug for chemoprophylaxis and treatment

Now, P. falciparum resistant strains widespread
• Mutation of vacuolar membrane protein that pumps drug out of food vacuole

104
Q

Chloroquine Not effective against

A

P. vivax/P. ovale liver stages (must employ primaquine)
• P. falciparum/P. malariae do not produce dormant liver
stages

105
Q

Babesia - Destroy

A

red blood cells

• Easily confused with P. falciparum

106
Q

Babesia - Babesiosis is endemic in

A

US

• Illness nonspecific/difficult to recognize

107
Q

Babesia - B. microti concentrated in same areas as

A

endemic Lyme disease

Animal reservoir same – white footed mouse
• Transmitted by deer tick (Ixodes scapularis)

108
Q

Babesia Life Cycle - Merozoites injected under skin by

A

tick

RBCs invaded

109
Q

Babesia Life Cycle - NO intermediate

A

liver stage

110
Q

Babesia Life Cycle - Replication via

A

binary fission

111
Q

Babesia Life Cycle - Lyse

A

RBCs
• Ticks feed on
infected RBCs to keep cycle

112
Q

Toxoplasma

A

Infection common in humans, but disease rare

• Disease can be severe for immunocompromised patients and developing fetuses

113
Q

Toxoplasma three symptoms

A 
Three syndromes:
Mononucleosis-like
• Congenital infection
• Brain/heart (immunocompromised)
• Association with schizophrenia?
114
Q

Toxoplasma: Survive in

A

macrophages

• Prevent acidification and phagolysosome fusion

115
Q

Toxoplasma: Consumption of inadequate

A

cooked meat (tissue cysts) or food contaminated with cat feces (oocysts)
• Cats harbor sexual cycle
(similar to mosquitoes in malaria)

116
Q

Cysts penetrate

A

ntestinal wall, enter bloodstream and disseminate

117
Q

Pregnant women are warned not to come into contact with

A

Toxoplama

-Toxoplasma can cause miscarriage

118
Q

Toxoplasma in cat feces is eaten by

A

rats, and affects the amygdala of rats. This changes rat behavior.

Infected rats are attracted to cats, and get eaten

119
Q

Infected humans may also affect human behavior. There is some evidence that Toxoplasma infection is linked to

A

schizophrenia

Surge in schizoprenia occurs in human population at the same time as an 1800s surge in cat popularity as pets

120
Q

Persons infected by Toxoplasma are

A

three times more likely to die in a car accident

121
Q

Leishmania -

A

Small protozoans (flagellates)

122
Q

Leishmania - Transmitted by

A

sandflies (Phlebotomus)
• Tropical/subtropical areas
• Rare in North America/Europe

123
Q

Leishmania - Reservoirs

A

• Rodents, dogs, other animals, humans

124
Q

Leishmania - Several species

•

A

Different tissue tropisms and clinical displays
• Skin ulcers, cutaneous and subcutaneous lesions, and
disseminated visceral leishmaniasis (“Kala azar”)
• Different temperature preferences (25-30 oC vs 37 oC)

125
Q

Leishmania = Promastigote (flagellated) binds to

A

macrophages
• Superoxide dismutase
produced

126
Q

Leishmania - Converts to

A 
amastigote
(no flagella)
• Resistant to lysosomal
enzymes
• Requires low pH for
nutrient uptake (glucose
and proline)
127
Q

Leishmania - Antimony-containing

compounds useful for

A

treatment

128
Q

• Trypanosoma cruzi

A

Chagas’ disease (American trypanosomiasis)
• Latin America and southern US • Transmission
• Reduviid (“kissing”) bug
• Grows in intestine, bug bites
and deposits feces, scratching introduces organism into bite
• Illness
• Mild usually, complications 10-20 years later
• Nerve, GI, heart damage

129
Q

• Trypanosoma brucei

A 
African sleeping
sickness
• Transmission – tsetse
flies (Glossina)
• Transmitted directly via
bite
• Main reservoirs:
• East Africa – wild game animals
• West Africa – humans and domestic animals (cattle)
130
Q

Trypanosomes Illness

A

Systemic (fever and swollen lymph nodes) and chronic in bloodstream
• Dominant surface antigen (variable surface
glycoprotein) changes to avoid immune system • Antigenic variation via genetic rearrangement (one
expressed locus, multiple ‘silent’ loci that can recombine)
• Months/years later – infect CNS, brain, spinal fluid

131
Q

• Giardia lamblia, Trichomonas vaginalis – flagellates

A

Frequent in US

• Waterborne and sexual transmission

132
Q

• Entamoeba histolytica – amoeba

A

• Common in developing countries

133
Q

• Cryptosporidium, Cyclospora, Isospora – apicomplexans

A

Non-motile, reproduce by alternating sexual/asexual cycles

• Foodborne

134
Q

• Microsporidia – not true protozoa (like bacteria)

A

• Obligate intracellular parasites – small

135
Q

Giardia lamblia and Giardiasis Worldwide zoonosis

A

Ingestion of water contaminated by feces from animal carriers
• Cysts highly resistant
• Chlorine – waterborne
outbreaks
• Stomach acid –
stimulates cysts to transform to vegetative trophozoites

136
Q

Giardia lamblia

A 
Intestinal protozoan
"African shield" morphology
http://web.indstate.edu
Mild, persistent diarrhea
• Not bloody like Entamoeba
• Asymptomatic carriers can
pass cysts for years.
• Daycare & mental institution
epidemics are common.
• Trophozoites attach in the
duodenum using ventral sucking disk, but do not invade • Inflammation leads to
maladsorption of proteins & fat (greasy, foul smelling stools)
137
Q

Trichomonas vaginalis

A 
Common vaginal flagellate (15% or more of women)
• Occasionally causes vaginitis
• Transmitted by sexual contact
• Men are usually asymptomatic
• Less common, less pathogenic species are
found in:
• GI tract (T. hominis)
• Mouth (T. tenax)
138
Q

Entamoeba histolytica

A 
Amoebiasis
• Destruction of host tissue (colon)
• Flask-shaped ulcers
• Can spread via bloodstream and produce
abscesses in liver, brain, other organs
• Many humans carry non-pathogenic amoebas
that are indistinguishable (E. dispar)
• Transmitted via fecal-oral route
• Vegetative trophozoite
• Highly resistant cyst

139
Q

Entamoeba histolytica

A 
Adhere to host cell receptors containing digalactose residues • Attachment via lectin
surface protein • Damage
• Attachment
• Contact-killing
• Pore-forming proteins
(amoebapores)
• Ingestion of killed host cell by ameba
140
Q

Entamoeba histolytica • Non-immune hosts

A

Pathogenic amoebas destroy host phagocytic cells

neutrophils, non-activated macrophages

141
Q

Entamoeba histolytica • Immune hosts

A

• Cell-mediated immunity required
• Circulating antibodies not likely important
• Amoebas produce cysteine protease that digests
IgA, IgG and other proteins

142
Q

Cryptosporidium

A

• Zoonosis
• Often in rural areas but can be spread person to person in crowded urban environments (day care centers)
• Outbreaks with public water systems (ie. Milwaukee, 1993)
• Found in most surface
waters that utilities draw from

143
Q

Cryptosporidium resembles Toxoplasma

A
  • Infectious oocysts produced in intestine and spread to other animals
  • Highly resistant to chlorine
  • Expelled in huge numbers in watery stools
  • Do not invade intestinal epithelial cells or disseminate
  • Stay within microvilli of small intestine
  • Single episode of diarrhea that lasts ≤ 2 weeks
  • Common in Great Britain and United States
144
Q

• Roundworms (nematodes)

A

Fewmmto20cm

• No visible body segmentation

145
Q

Ascaris – most frequent infections (Southern US)

A 
Eggs require several weeks in
environment to mature to infective
stage
• Eggs are ingested
• Hatch in small intestine and release
larvae that penetrate mucosa • Travel to lung, then to
trachea/pharynx and swallowed
• Mature in GI lumen and eggs released in stool
146
Q

• Pinworms (nematodes)

A

Common in temperate and tropical areas

• Prevalent in small children and in institutions

147
Q

Enterobius

A

Eggs do not require maturation stage outside of body
• Transmitted readily by fecal-oral route (ingestion)
• Eggs resist drying and can be transmitted from clothes
or dust
• Hatch in small intestine and larvae mature in large
intestine
• Females travel perianal skin, lay eggs (perianal itching symptom, which facilitates spread)

148
Q

A Helminth Cycle: The Pinworm

A

Person swallows microscopic eggs
• Picked up from another infected person by direct contact
• Or by touching articles an infected person has touched
• Eggs hatch in the intestine
• Release larvae that mature in to adult worms (about 1
month)
• Male and female worms mate
• Female migrates out of the anus to deposit eggs
• Causes intense itchiness
• Relieved by scratching
• Scratching contaminates the fingers which transfer the eggs
• Eggs spread to others or the original host reinfects him or herself

149
Q

• Hookworms (nematodes)

A 
Necator americans, Ancylostoma duodenale
• Penetrate skin as filariform larvae
• Soil contaminated with human, cat or dog stools
and larvae
• Do not require ingestion
• Fecal-cutaneous route
150
Q

Distribution and Importance of Parasitic Worms

A

About 50 species parasitize humans
• Distributed in all areas of the world
• Yearly estimate of worldwide infections- in the billions

151
Q

Intestinal Helminths -

A

Human hookworm larvae move from skin to heart via blood or lymphatics and become trapped in lung
• Dog/cat hookworms are relegated to skin
• Break through lungs, coughed up, swallowed
• Life cycle continues in small intestine and eggs
released (10,000 – 20,000 eggs/day)
• Chronic anemia
• Hookworms hang onto intestinal mucosa with teeth,
secrete anticoagulant, and suck host’s blood
• Severity proportional to worm burden

152
Q

• Strongyloides stercoralis

A

Mostly tropical areas but can be anywhere
• Causes intestinal malfunction by perforating intestinal wall producing septicemia
• Can reinfect same host – lethal systemic disease in immunocompromised hosts (kidney transplants)

  • Does not require external soil phase
  • Direct penetration through skin via feces
  • Migration to intestines identical to hookworms
153
Q

Tapeworms

A

Long, ribbonlike with rectangular segments
(proglottid) that are self-contained units
• Attach to intestinal wall by a head
(scolex) with sucking discs or grooves
• Can penetrate deep tissues and form
infective, cystic larvae
• Acquired by eating raw or undercooked meat
or fish
• Taenia saginata (beef)
• Taenia solium (pork)
• Diphyllobothrium latum (fish)

154
Q

Tapeworm Life Cycle

A

Life cycle depends on humans (definitive host) and animals (intermediate host)
• Cattle infected by ingesting human feces with eggs
• Eggs hatch, enter bloodstream, lodge in tissues
• Humans infected by eating beef containing larvae
(cysticerci)
• Worms can live in intestine for decades and grow up to
10 m in length
• Fish tapeworm associated with B12 deficiency
• All human infections correlate with consumption of undercooked or raw meat • Cooking destroys larvae

155
Q

Tapeworm Tissue Infections

A

Deep tissue infections can produce severe disease
• Cysticercosis – T. solium eggs hatches into invasive larvae
• Usually acquired from ingestion of tissue cysticerci from
infected pork
• May be acquired endogenously by autoinfection from
host’s own feces or regurgitation of eggs
• Echinococcosis (cystic hydatid disease)
• Echinococcus granulosus
• Ingestion of infectious eggs rather than tissue cysticerci
• Source – carnivore feces (e.g., dogs, wolves, coyotes)
• Transmission via fecal-oral route, not from
contaminated meat
• Hydatid cysts form in many organs


156
Q

Tissue and Blood Helminths

A

Ingestion Acquired
• Trichinella spiralis –
trichinosis
• Most infections are
asymptomatic
• Larvae hatch, cross
mucosa, enter lymphatics and blood • Diarrhea/pain
• Encysted larvae in striated/cardiac muscle produce inflammation
• Cysts calcify, but worms can be viable for 30 yrs


157
Q

Tissue and Blood Helminths

A

Skin Acquired
• Schistosomes (blood flukes)
• Each species has unique geographic distribution,
dependent on snail intermediate host • Schistosomiasis
• Symptoms depend on location of the adult worms and the type of eggs released
• S. haematobium – bladder (eggs released in urine)
• S. mansoni – large intestine (eggs released in stool)
• S. japonicum – small intestine (eggs released in stool)

158
Q

Tissue and Blood Helminths

A
  • Infective cercariae released from snails
  • Burrow through skin of people in infected water
  • Lose tails and change to schistosomulae that enter blood
  • Pass to portal venous system to mature
  • Move in pairs (male/female) to small/large intestine, bladder, sexually reproduce and eggs released
159
Q

Schistosomiasis

A

Eggs trapped in host tissues induce formation of granulomas that undergo fibrosis that can produce disease symptoms years later
• Pathogenesis anomalies:
• Fibrotic reactions to eggs mediated by cytokines and
long-term complications
• Lack of effective immune response to male and female
worms that reside in vascular system for decades
• Worms employ camouflage with host proteins (serum albumin, HLA antigens)

160
Q

Filariasis - Onchocerciasis

A

(‘river blindness’)

• Transmission via Simulium black flies

161
Q

Filariasis - Lymphatic filariasis (elephantiasis)

A

• Transmission via mosquitoes
• Nocturnal microfilarie – more prevalent in blood at
night

162
Q

Filariasis - Geographic distribution limited by

A

vectors
• Not within the United States
• Humans are not reservoirs

163
Q

Filariasis - Adult filarial worms live in

A

subcutaneous
tissues
• Microfilariae offspring travel through lympatics
(lymphatic filariasis) or subcutaneous tissue (onchocerciasis)

Micro unit 2 (12 decks)

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