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Phoresis
involves two organisms traveling together without any biological or physiological interdependence
Mutualism
both organisms benefit, often with a necessary physiological reliance; typically obligatory
Commensalism
one organism benefits while the other is unaffected
Parasitism
one organism either harms or lives at the expense of its host
Definitive Host
the host where the parasite achieves sexual maturity
Intermediate Host
necessary for the parasite’s developmental stages but without sexual maturation
Paratenic (transport) host
doesn’t support parasite development but can help bridge ecological gaps between hosts
Reservoir (amplifying) host
can carry a pathogen indefinitely without harm
Dead-end or Incidental hosts
don’t develop high parasite levels; unable to transmit the pathogen further
Hyperparasitism
a parasite hosting another parasite
Vector
an organism, often an arthropod, transmitting a pathogen from reservoir to host
Aberrant Host
an atypical host for the parasite it carries
Host Specificity
some parasites are specific to one host, while others can develop in multiple hosts
Ectoparasite
lives on the host’s surface
Endoparasite
resides inside the host
Facultative parasite
doesn’t rely on the host for survival; incidental
Obligate parasite
needs a host for survival and life cycle completion
Mechanical Damage
causes physical harm or obstruction in tissues
Physiologic damage
affects metabolism; consumes host’s nutrients
Direct Life Cycles
the parasite completes its life cycle within a single host species
Indirect life cycles
requires multiple host species for completion, typically involving 2-3 hosts: definitive, intermediate, and paratenic
Prevalence
proportion of a population infected at a specific time
calculation: number of existing cases/ total population
Incidence
rate of new infections in a population
calculations: number of new cases/ population at risk
Morbidity
refers to illness or disease state
Co-morbidities
presence of simultaneous illnesses
Mortality
incidence of death due to a disease
calculation: number of specific disease deaths/ total population
Focus
ecological aspects of disease transmission and prevalence
Sexual reproduction
increases disease resistance\
this process mixes genetic material from two parents to produce offspring
it increases genetic diversity and can enhance the host population’s resistance to diseases, including parasitic infections
can be resistant to anti parasitic by genetic recombination
Sexual selection
influence of parasites on mate choice
parasites can affect this process by influencing the host’s choice of mates
hosts often choose “healthy” mates over “unhealthy” ones based on indicators such as the quality of plumage in birds or body odors, which can signal good health and genetic fitness
Parasite reproduction types
asexual and sexual
Sexual dysfunction
some parasites may interfere with the host’s reproductive capabilities to their advantage
for example, a parasite may castrate the host, which diverts the host’s resources away from reproduction and towards sustaining the parasite
additionally, some parasites might suppress visible signs of infection, allowing the host to reproduce and spread the parasite to the next generation through offspring or contact with mates
Polyembro
development of many offspring from a single zygote
occurs in larval stages
ex: trematodes
Binary Fission
mitotic division of 1 cell into 2
ex: some protozoa
Internal Budding
new individual grows from somatic tissue of parent
ex: some larval cestodes
Schizogony ( multiple fission, merogony)
produces many daughter cells
nucleus divides (mitosis) many times before cytokinesis (cytoplasm division) occurs
ex: protozoa
Monoecious
hermaphroditism
single individual possesses gonads of both genders
self-fertilization
no need to find a mate
can mate with another individual or can self-fertilize
ex: cestodes, most trematodes (except Schistosomes)
Dioecious
each individual is a separate gender
sexual dimorphism
ex: nematodes, schistosomes (trematode)
Early Infection Phase of Trypanosoma brucei
trypanosomes in lymph and blood systems
Advantage Stage of Trypanosoma brucei
presence in brain parenchyma and cerebrospinal fluid
Heteroxenous Life Cycle
alternates between vertebrate blood/tissues and invertebrate gut
Hemoflagellates
require blood in laboratory culture media
one bite
several thousand metacyclic trypomastigotes transferred in ___________________
remain extracellular
trypomastigotes never enter the host cell
Trypanosoma brucei
infects animals only
affects various animals with distinct symptoms——
anemia, edema, watery eyes and nose, fever
emaciation, paralysis, death
horses, donkeys, ruminants (Nagana); acute: 2-4 months
cattle (infection lasts for months
dogs (blindness)
pigs (usually recover)
T.b. gambiense
characterized by chronic sleeping sickness symptoms such as disinterest, cognitive decline, unsteady movements, progressing to paralysis, seizures, escalating drowsiness, coma, and potentially death
is found in central and western Africa; it causes a chronic condition that can extend in a passive phase for months or years before symptoms emerge
T.b. rhodesiense
associated with an acute version of the disease marked by swift weight reduction and death within a few months
is found in southern and eastern Africa; its infection emerges in a few weeks and is more virulent and faster developing
T.b. gambiense (chronic form)
typical sleeping sickness
apathy, mental dullness, lack of coordination
paralysis, convulsions
increasing sleepiness
coma, death
T.b. rhodesiense (acute form)
rapid weight loss
death in a few months
Diagnosis of Trypanosoma brucei
identification is made by the detection of trypomastigotes in bodily fluids like blood, lymph, and CSF
serological testing can identify antibodies, particularly in T.b. gambiense infections, though it may result in false negatives
Tsetse fly
large, brown, and stealthy
while taking blood from a mammalian host, an infected one injects metacyclic trypomastigotes into skin tissue
the parasites enter the lymphatic system and pass into the bloodstream
Amastigote
kinetoplast and kinetosome above the nucleus, flagellum short and confine in pocket
cell is globular
Promastigote
kinetoplast and kinetosome at anterior end of cell, flagellum free and lone
cell is elongated
Epimastigote
kinetoplast and kinetosome close and anterior to the nucleus
there is a short undulating membrane before the flagellum emerges at the anterior of the cell
cell is elongated
Leishmaniasis Vector
female sand flies
Phlebotomus spp (Old World)
Lutzomyia spp (New World)
Leishmaniasis Distribution
1 million cases worldwide
distribution depends on species complex
poverty-related disease
malnutrition
displacement
poor housing
illiteracy
comprised immune systems
environmental changes
deforestation
dam construction, irrigation schemes
urbanization
migration of native people to endemic areas
serious impediment to socioeconomic development
Cutaneous Leishmaniasis ulcers
oriental sore, Jericho boil
on exposed parts of the body (face, arms, legs)
L. tropica
distributed throughout asia, africa, mediterranean, russia, densly populated areas
definitive host is human
vector is phlebotomus sand fly
dogs and foxes are reservoir hosts
L. major
distributed throughout the middle east, russia, brazil and rural areas
humans are the definitive host
the phlebotomus sand fly is the vector
rodents are the reservoir host
causes ulcers
L. mexicana
distributed throughout central and south america, bolivia, brazil, colombia, peru and north america
causes chiclero ulcers, bay sores, cartilage ulcers, ulcers can last for up to 40+ years
Leishmania braciliensis
known as Espundia or Uta
humans are definitive host
Lutzomyia sand flies are the vectors
sloths and anteaters are the reservoir hosts
found in central and south america
Northern range of Leishmania baziliensis
ulcer
self limiting
itchy
flat
open
oozing
similar to cutaneous Leishmaniasis
appears in 1-4 weeks
heals within 6-15 months
Leishmania braziliensis Southern Range
begins as cutaneous leishmaniasis
ulcer metastasizes to mucocutaneous zones
occurs before primary ulcer heals or up to 30 years later
nose, mouth, lips, trachea, pharynx
destroys cartilage and soft tissues
necrosis
secondary bacterial infection
ulcers may last for years
death— secondary infections, respiratory problems
Leishmania donovani
known as dum dum fever and kala-azar
humans are the definitive host
Phlebotomus spp and Lutzomyia spp are the vectors
found throughout asia, africa, south and central america
Giardia intestinalis
most common flagellate of human GI tract
discovered by Anton van Leeuwenhoek
40+ species descriptions
now only 5 valid species
mammals
G. duodenalis
G. muris
birds
G. ardeae
G. psittacii
amphibians
G. agilis
Giardia oral infection
ingestion of cysts; contaminated water
feal-oral
hands
Giardia zoonosis
risk of humans acquiring this infection from dogs or cats is small
exact type of this that infects humans is usually not the same type that infects dogs and cats
Giardia triggers
resorption of locomotor organelles
adverse environmental conditions
low food
desiccation, low O2, pH
temperature change
osmotic change
Giardia mechanisms
secretion of cyst wall
storage of food, e.g. glycogen, starch
Giardia intestinalis— cysts
found in feces (diagnostic stage)
stage found most commonly in non-diarrheal feces
responsible for transmission of giardiasis
infectious when passed in stool or shortly afterward
resistant forms
hardy; can survive several months in cold water
excystation
in small intestine
each cyst produces two trophozoites
Giardia intestinalis— Trophozoites
found in feces (diagnostic stage)
active feeding stage
multiply by longitudinal binary fission
remain in lumen of proximal small bowel
free or attached to the mucosa by a ventral sucking disk
encystation occurs as parasites transit toward the colon
Giardia Life cycle
direct life cycle
mammals are definitive hosts
beavers, dogs, cats, horses, humans, cattle, and birds are the reservoir hosts
molecular characterization
Morphology— trophozoites
pyriform— pear shaped
2 nuclei with karyosomes
8 flagella— 4 pairs
2 median bodies
function unknown
possible metabolic rule
adhesive disc on ventral surface
Morphology— cysts
8-12 μm long
4 nuclei
4 median bodies
6 flagella (in mature cysts)
Giardia distribution
very common worldwide
warm climates
children most affected
fecal-oral transmission
prevalence rates
2-7% in developed countries
20-30% in most developing countries
Giardia distribution in the United States
2011, a total of 16,868 giardiasis cases were reported
2019, total cases = 14,887
CDC estimates upwards of 2.5 million cases annually
Giardia Pathology
enteritis
mechanical damage to intestinal villi
damage caused by adhesive disc and large number of parasites
shortening and blunting of villi and epithelial cells
malabsorption
fat, fat soluble vitamins, Folic acid
incubation period: 8 days
prepatent period: 10-36 days
self limiting
range of symptoms
all age class, but especially children
Giardia Diagnosis
presence of trophozoites or cysts
feces
cysts shed intermittently— must take several samples over a period of days
duodenal aspiration or biopsy
immunodiagnostics
ELISA
immunofluoresence
PCR
Giardia Treatment
Atabrine
may cause unwanted symptoms in children
Metronidazole (Flagyl)
less toxic to children
all members of household must be treated
Control the spread of Giardia
reduce fecal contamination of water
can be resistant to filtration and chlorination
portable water filtration systems— iodine (for campers)
travelers to endemic areas are advised to avoid uncooked foods that might have been grown, washed, or prepared with water that was potentially contaminated
sanitation!
wash hands, food, water, fomites contaminated with infective cysts
Giardia presentation in animals
dogs/cats
diarrhea
cattle (calves)
chronic diarrhea
death uncommon
lambs
neonatal infections
low weight gain
periparturient rise (PPR)
PPR of excretion of cysts in ewes— major source of giardiasis in lambs
wild animals
especially beavers
The periparturient egg rise
is a well-documented phenomenon in small ruminants: a temporary loss of naturally-acquired immunity to gastro-internal parasites that begins approximately two weeks before parturition and continues for up to eight weeks after
Parturition
the action of giving birth to young
Trichomonads
3 flagella= tritrichomonas
4 flagella= trichomonas
5 flagella= pentatrichomonas
undulating membrane
axostyle
median tube-like organelle
Distribution of Trichomonas vaginalis
worldwide
definitive hosts
humans
reproductive tracts of males and females
most are asymptomatic
females— vagina, urethra
males— prostate, seminal vesicles, urethra
morphology
4 anterior flagella
undulating membrane
7-32 μm long, 5-12 μm wide
Trichomonas vaginalis life cycle
direct life cycle
sexual transmission
extracellular
no cyst stage
parasites attach to epithelial cells with cytoplasmic extensions
transmission
primarily sexual
possible by artificial insemination
congenital— documented in newborns
young children— contaminated clothing
Trichomonas vaginalis— diagnosis
presence of parasite
in secretions or urine— wet mount
in culture of vaginal secretions
good for detecting low numbers of parasites
time-consuming
molecular diagnosis
DNA hybridization
PCR
Trichomonas vaginalis female pathology
inflammation, itching, leukorrhea (white, green with trichomonads)
frequent and painful urination
during pregnancy
premature births
low birthrate
Trichomonas vaginalis male pathology
usually asymptomatic
inflammation of urethra, prostate
painful urination, thin discharge
may enhance HIV transmission
Trichomonas vaginalis treatment
metronidazole (flagyl)
cures in ~5 days
some strains are resistant
sexual partners should be treated as well
Tritrichomonas foetus distribution
United States
Europe
Tritrichomonas foetus definitive hosts
cattle, horse, other large mammals
cats
Tritrichomonas foetus life cycle
sexual transmission, no cyst stage
asymptomatic male (penis sheath) infects female (asymptomatic in vagina)
pregnancy triggers systemic infection
trophozoites invade uterus
Tritrichomonas foetus morphology
3 anterior flagella
undulating membrane
nucleus
axostyle
Tritrichomonas foetus diagnosis
presence of parasites
smears— amniotic fluid, vaginal/uterine secretions, placenta, fetal tissues, preputial secretions
PCR
IFA
Tritrichomonas foetus bull pathology
occur in preputial cavity, also in testes, epididymus, seminal vesicles
asymptomatic carriers
cannot be used for breeding
Tritrichomonas foetus cow pathology
occurs in vagina, uterus
abortion
Control Tritrichomonas foetus
proper herd management
use artificial insemination only for breeding infected cows
check bulls before purchase
cull infected bulls
vaccine
given to cows
does not prevent infections
may increase number of viable offspring
Tritrichomonas foetus in cats
diarrhea
giemsa-stained fecal smear
characteristic appearance of Tritrichomonas foetus
3 anterior flagella and long, undulating membrane
Entamoeba
vesicular nucleus
small endosome near center
amoebic dysentery
ameobiasis
infects 10% of world population
100,000 deaths per year
caused by crowding, poor santitation
People at Risk for Entamoeba
immigrants/travelers
people in institutions, daycares
refugees
people engaging in anal-oral sexual practices
soldiers
night soil users (human feces used as fertilizer)