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283 Cards in this Set

  • Front
  • Back
definitive host
host undergoes Sexual Reproduction - humans and other animals
reservoir hosts
animals that harbor a parasite that is pathogenic for ANOTHER species
(is more difficult to eradicate)
intermediate host
animal in which larval or asexual stages are found
transfer host
a "not necessary" host but utilized host
incidental host
accidentally infected and not needed for the parasite's survival or development

may not allow the full development
vectors
usu. arthropod

carries an agent from one host to another
biologic vector
if parasite develops or multiplies in the vector

e.g.: mosquito in malaria
mechanical vector
just carries the organism from host to host
major routes of parasite transmission
oral fecal rout

vector borne

direct skin invasion

needle transfer
how are nematode eggs transmitted?
oral-fecal
structural characteristics of protozoa
flagella
nuclei
cilia
structural charcteristics of nematodes
cylindrical worms
structual characteristics of cestodes
elongate ribbone like
segmented body
structual characteristics of trematodes
flat or leaf-shaped
4 forms of protozoa
ameba

trypoanosome

malaria parasite

leishmania
sarcodina group

locomotion
diseases
ameboid like locomotion

amebic dysentery
mastigophora

locomotion
diseases
flagella locomotion

Chagas' disease, African sleeping sickness, giardiasis, trichomoniasis, leishmaniasis
Ciliata

locomotion
diseases
cilia locomotion

Balantidiasis
Sporozoa

locomotion
disease
no locomotion

malaria, babesiosis
3 types of helminths
nematodes

cestodes

trematodes
nematodes
elongate, cylindrical worms
stiff cuticle
pseudo-coelomic cavity
structures at both ends (mouth, uterus, uterine opening, anus)
digestive tract
separate sexes
cestodes
tape worms

elongate and ribbonlike
segmented body
segments have both male and female organs
scolex (attachment organ) with suckers around this structure
no digestive tract
eggs are operculated
trematodes
leaf-shaped
flat, bilaterally symmetrical bodies
most are hermaphroditic
have suckers
examples of trematodes
liver flukes - fasciola

lung flukes - paragonimus

blood flukes - schistosoma
5 types of ectoparasites
lice
mites
fleas
ticks
flies
crustacae
ecotoparasite
cyclops --> guinea worm
arachnida
ectoparasite

mites --> typhus
ticks --> many infections, eg: Rocky Mtn Spotted Fever
Insecta
ectoparasite

lice --> epidemic typhus
fleas --> plague
bugs --> Chagas' ds
beetles --> hymenolepis
flies --> onchocerciasis, loaisis, etc
5 factors in epidemiology
hygiene (oral-fecal transmission)
vector presence
human contact and closeness
environment (temp, moisture, etc.)
sexual contact (trich, crabs,etc)
2 examples of parasites that immunocompromised people are particularly susceptible to
strongloides

scabies
parasite leading to river blindness
onchocerciasis

if killed in the eye (rather than on the skin), then causes blindness
which worms tend to present such that they "make an agreement with the host," but the host reacts violently to anti-worm treatment?
helminths
types of GI tract parasite symptoms
diarrhea

blockage (worm moves from low to high part of bowel and curl up into a ball, blocking intestine)

irritation ("don't feel good" is common presentation)
allergic responses to parasites
cyst fluid released (cyst with parasite inside it)

responses to dead or dying parasites

hypersensitivity (reinfection, ascaris sensitivity)
parasitic cyst
egg w/ tough outer surface

can survive outside host
what cell type is central to allergic reaction at death of parasite?
eosinophils
3 major classes of parasite-related pathophysiological upsets
GI tract

allergic reaction

debility and malnutrition
pathogenic mechanisms of parasites
space occupying lesions (cysts)
degernative effects
irritation/psychological effects
tracking through the body
sclerosing (scarring)
blood vessel & blood pathology
cancer
immunological conditions
where do parasitic cysts tend to occur?
brain
chest
abdomen
muscle
describe parasitic degenerative effects
reactions to dying parasites

wearing out of host tissues due to repeated cycles
examples of clinical presentations of sclerosing conditions
nodules

liver fibrosis
two examples of conditions that include blood vessel and blood pathology
elephantiasis

anemia
cancers associated with pathogenic mechanisms
liver cancer - Asia

bladder cancer
examples of parasites tracking through the body
wandering larvae

eye-worms moving across conjunctiva
components of host responses and immunity to parasites
antibodies: IgE, IgG
cellular mechanisms
TH2 type responses (?)
mast cells, esoinophils, T cells
characteristics of host responses and immunity to parasites
allergies

acute inflammation - IgE (promote inflammation and healing) & IgG (attack parasites)

sclerosis and fibrosis
avoidance mechanisms of parasites
blocking antibodies
immunosuppression (T cell suppression)
proteolytic cleavage of antibody and complement
host antigen acquisition
what parasite turns muscle cells into nurse cells by taking over their genomes?
trichinella spiralis (nematode)
3 major anti-parasitic (anti-helminth) drugs
albendazole

praziquantel

ivermectin
diagnositic approaches to parasites
clinical presentation and knowledge of transmission (risk factors)

laboratory tests
- parasitological - find the parasite in stool/blood
- immunological/molecular - Ab or Ag presence & DNA presence
generic name for Flagyl
metronidazole
Human onchocerciasis
river blindness
nematode (filarial worm)
blindess b/c worm dying in eyes
dermiatitis due to inflammation

Mectizan is donated to rid endemic areas of this infection
drug used to treat river blindness
Mectizan
onchocerciasis vector
simulium - black fly vector
head nodules seen in onchocerciasis contain what?
adult worms
transmission of guinea worm
year long cycle

female emerges to spread new large in water for the intermediate host (IH)

person drinks water + IH

emerging of female causes secondary infections, pain, etc.
intermediate host of guinea worm
cyclops
clinical presentations of guinea worm
worm blisters in feet

dracunculiasis - rotting away around blister from immune response to breaking off part of worm (see CP 43)
control of guinea worm
filter water - linen material covered "pipe straws"

education

number dramatically dropping in all endemic countries (except Sudan)
most important waterborn pathogen in US
giardia lambila
structural characteristics of giardia lambila
flagellate protozoan parasite - 8 flagellae

"trophoozoite"

pear-shaped
in what human organ does giardia lambila reside?
small intestine (of mammals in general)

predilection for proximal jejunem
pathogenic mechanism of trophozoite
trophozoite adheres to enterocytes of small intesting by a sucking disk, producing low grade intestinal disease
how do giardia lambila multiply?
binary fission
giardia lambila trophozoites develop into...
oval cysts 10-12 um which are passed in feces
pathogenicity of giardia
10 cyst minimum required to produce an infection
TRUE/FALSE: giardia is commonly asymptomatic?
true
characteristics of giardia cysts
12 mm diameter
4 nuclei may be seen
gastric acid induces excystation
characteristics of giardia trophozoites
8 flagella per trophozoite

spiral motion, epithelium attaches by suction to villus
occurrence of giardia
all parts of the world

highest incidence where fecal contamination is common
transmission of giardia
ingestion of viable cysts
fecal-oral route

prepatent period 7.5 days

children are particularly susceptible (b/c of hygiene)
predisposing factors to giardia infection
children who are malnourished

day-care centers (contact-contact)

surgery

hypo-gammaglobulinemic individuals

NOT thought to be important in HIV diarrhea
stages of giardia infection
2-7 weeks incubation
diarrhea for 2 weeks
recovery

malabsorption, steathorrhea --> relapsing condition

stages: ingestion, colonization, adhesion
diarrhea of giardia infection
not well understood

damage to microvilli at enzymatic transport site
accumulation of active molcules in gut lumen
altered malabsoption of fat, microbial imbalance
clinical presentation of giardia
widely varied presentation, even within same strain

anorexia, nasuea, lassitude and diarrhea - offensive, frequent, yellow stools

abdominal distension, bad taste in mouth, flatulence

systemic upset does not generally occur
giardia complications or lack of recovery after 2 weeks generally relates to...
nutritional status of the host
3 severity levels of giardia presentations
asymptomatic - normal absorption and gut histology

mild - reduced xylose absorption and mild histological abnormalities

severe - malabsorption of fat, xylose, vit B12, villus hight down, interepithlial lymphocytes increased
TRUE/FALSE: in giardia, severe villus atrophy is rare
True
protective immunity against giardia
non-specific: a bile salt-dependent mild lipase is toxic to Giardia

specific
- humoral antibody important
- IgM and IgA both kill Giardia
- surface antigens are called Giardins
4 methods of giardia diagnosis
stool examination

duodenal aspiration

tests

antibodies
diagnosis of giardia by stool examination
intermitten shedding occurs

tophozoites in stool
cysts in stool
antigen detection - IFA, ELISA
diagnosis of giardia by duodenal aspiration
micelles on biopsies
smears for trophozoites and cysts
diagnosis of giardia wrt antibodies
80% symptomatic patients have antibodies
persist 6 months after eradication
giardia treatment and recovery
Flagyl - metronidazole
- long course vs. short course
- alcohol contraindicated

diarrhea stops in 1-2 weeks
cyst exretion stops 2 days after tx begins
histology takes 1-2 months to restore
giardia prevention
clean drinking water
- not killed by normal water disinfection chloride concentrions

at 21*C, cysts reamin viable in water for 5 weeks

heating to 50*C kills encysted tophozoites

sterilze using tincture of iodine
cryptosporidia parasite
C. parvum - tiny intracellular parasite
4-5 mm oocytes
multiple fission, massive replication
destroys enterocytes
sporozoites: 1-2um: banana shaped
describe cryptosproridia life cycle
"Coccidian" type of life cycle
- sexual and asexual reproduction
- furable oocyst in environment
- zoonotic potential via an infective oocyst
cryptosporidia transmission
readily spread to contacts
important cause of infant diarrhea in developing countries
less common in breast fed children

NOT HOST SPECIFIC
disease caused by cryptosporidia
waterborne enteritis

paritcularly susceptible:
- immunocompromised - recovery requires T cells
- vet students interacting with calves

short incubation (2-4 days)
patent 10 days, then self cure
symptoms caused by cryptosporidia
intestinal infection - jejunum primary target

enterotoxic effect with weight loss

self-limiting to torrential diarrhea with malabsorption and severe wt loss in AIDS pts
No recovery from cryptosporidia with these factors
immunocompromised
AIDS
excessive weight loss
Cryptosporidia incidence
infections from calves

sewage-contaminated domestic water

daycare centers

cause of "Treveler's diarrhea" - when stressed
parasitology of cryptosporidia
no cilia or flagellae
oocysts 2-8 um (in enterocytes)
life cycle has 6 major stages
pathogenic dose: 10 oocysts
little host specificity
effects of cryptosporidia on host jejunum
villous atrophy
lamina propria infiltration of inflammatory cells

mechanism underlying malabsorption not clear
which two intestinal parasites are often transferred simultaneously?
giardia and cryptosporidia
for how long after cessation of diarrhea are cryptosporidia excreted in feces?
2 weeks
2 clinical statuses of cryptosporidia infection

usually, but not always, based on what?
acute vs. chronic diarrhea illness

usually related to host's immunostatus
cryptosporidia - acute diarrhea illness
self-limited attack 3-12 days
incubation: 1-2 weeks
no blood in stool
NO WBCs in stool
transient "flu-like" illness
abdominal cramps, N/V, low fever, HA
bloating and faltus less common than with giardia
shedding of oocytes 8-50 days
crytposporidia chronic diarrhea illness
AIDS or hypogammaglobulinemia

torrential diarrhea - major mortality factor

slim disease in African AIDS pts
extraintestinal cryptosporidiosis
seen in the immunocomprosmised

bilary tract disease (Gangrenous cholecystitis)

mixed cryptosporidium/CMV --> sclerosing cholangitis

respiratory tract involvement is reported in the immunocompromised
diagnosing cryptosporidiosis
oocysts seen or detected
stool oocytes need the right stain

diarrhea stools have more parasites than well formed stool
testing strategies for diagnosisng cryptosporidiosis
concentration techniques
IFA important
must be distinguished from yeasts
experienced technician needed
clinical management of cryptosporidiosis
with intact immune response - no Rx, only oral rehydration

AIDS pts - spiramycin (marcolide ABS)
sarcodina
amoebae (unicellular)
multiply by binary fissuion
tough cystic wall
pseudopod movement
most free living
most important sarcodina type
entamoeba

(rare in US)
entamoeba histolytica
causes the disease "amoebiasis"

areas of high risk: Mexico, S. America
invasive forms of entamoeba histolytica cause...
flask-like ulcers
disease presentations of invasive entamoeba histolytica
intestinal - diarrhea
systemic
- liver abscesses
- lung, heart, others sites
amebiasis
fecal-oral transmission of tough cysts

humans = main reservoir
rate is LOWER in children
invasive form is seen more in males
pathology of amebiasis
lower bowel hemorrhage, dysentery

extraintestinal migration leads to hepatic abscesses, occasionally in the CNS

lungs involved in some cases
diagnosis of amebiasis
fetal microscopy
antigen detection
treatment of amebiasis
iodoquinol
boiling water kills cysts
(cysts live over a month at 4*C)
entamoeba coli
benign
colonic
normal flora
cyst transmission
coccidian protozoa
cryptosporidia
isospora
microsporidium
cyclospora
isospora
only has an enteric stage (small bowel mucosa)

causes disease in immunocompromised

persistent diarrhea and peripheral eosinophilia
microsporidium
usually only in the immunocompromised

peristent diarrhea, bronchiolitis

commonly parasitzes lower animals (silkworms, bees)

oral ingestion
cyclospora
may be common cause of diarrhea in travellers

outbreak from strawberries in MI
Life cycle of nematodes
5 stages:

L1 - newborn form
L2 - often in the vector
L3 - infective form (in human)
L4 - developing form in host
L5 - adult
Parasitology of nematodes
biggest class of helminths

multicellular

transmission by oral intake, skin or via vector
What stage of nematode life cycle is inside the human host?
L3
only nematode infection that is exacerbated in immunosuppression
strongyles
where are nematodes found in host?
adults in gut, blood/lymphatics or in subcutaneous tissues

usu. larvae cause pathology in various tissues
enterobiasis
enterobius vermicularis = "pinworms"

worldwide distribution

fecal/oral transmission
enterobiasis

what does it do in human host?
larvae mature in small intestine
adults live in colon and rectum
NO PATHOLOGY IN INTESTINE

females lay tough eggs on perianal skin

sticky eggs --> itchiness

successful transmission via durable eggs
conditions of enterobiasis transmission
1000 eggs/female

high density living conditions
greatest prevalence in children
handling kids' bedding/clothes --> risk infection

adult is small, whitish, pinshaped. lives 13 weeks

immunity is acquired
ascaris, aka:
human roundworms
largest parasitic nematode
ascaris
highest and second highest prevalence of ascaris (geographically)
Asia
Africa
where are ascaris eggs found?
soil

(eggs mature in soil)
Where are adult ascaris worms found?
small intestine
when are ascaris larvae released?
upon ingestion
pathogenesis of ascaris
larvae penetrate bowel, go to liver, lungs

larvae are coughed up from lungs and return to gut

larvae can generate allergic reactions

6-8 weeks until adulthood

symptoms produced by tissue invasion (wandering worms)
pulmonary phase of ascaris infection
migration of larvae through the lung
intestinal phase of ascaris infection
asymptomatic themselves except for:

gut interference
gut blockage
toxocara
dog and cat roundworms

zoonotic problem, primarily causing ocular and CNS problems in children

can't complete cycle in humans, but causes disease during migration phase

eggs present in moist soil
Mneumonic for toxocara
Remember: "all puppies infected"

(as a general rule. doesn't stand for anything)
toxocara in dogs
larvae hatch from infected eggs eaten by dogs

female dogs harbor larvae in tissue, pass to fetus to cause congenital infection

puppies release eggs in feces and children may ingest mature eggs
visceral larva migrans (VLM)
VLM

larvae migrating in body's tissues
ocular larva migrans (OLM)
larvae migrating in the eye (and CNS)
two types of hookworms
NECATOR americanus - New World Hookworm

ANCYLOSTOMA duodenale - Old World Hookworm
Hookworms
small intestinal NEMATODES
blood suckers
major cause of anemia, esp. in children

no autoinfection. eggs, once laid, hatch quickly.

warm, wet weather is favorable

bare feet = risk facctor
life cycle of hook worms
eggs in soil from fecal materal
infective larvae develop
larvae migrate through blood to lungs
larvae coughed up and swallowed
larvae develop in intestinal tract
strongyloides
threadworms

tiny, small intestine dweller

less common, but more severe than hookworm
can be life threatening

males mate with females, produce larvae that pass in feces

soil maturation can produce a free living cycle
pathogenesis of strongyloides
infective larvae penetrate skin

travel via venule, right heart and lungs to be coughed up and swallowed

mature in gut

larvae may penetrate lower bowel, enter venule (i.e.: autoninfection)

live for decades in humans

multiply indirectly outside host
two names for infective stronglyloides larvae pentrating skin
creeping urticaria

eosinophilic lung
3 pathologic events in strongyloides infection
skin penetration

pulmonary migration

intestinal penetration (minimal pathology)
causes of pathology in strongyloides infection
damage to tissues in migration

death of parasites --> inflammation
unique characteristic of strongyloides
only autoinfection phenomenon in helminths

can therefore persist for many years
what US population is most commonly seen with *old* strongyloides infections?
veterans of the Asian Wars (WWII, Vietnam)
diagnosing strongyloides infections
larvae in feces (intermittent output)

larvae in sputum

serology
treatment of strongyloides
thiabendazole, benzimidazoles

ALBENDAZOLE
trichuris, aka:
whipworms
trichuris
common, blood sucking, parasite of the large bowel, found in the tropics

host = humans, mostly seen in children

prevalent in Middle East

fecal/oral transmission
life cycle of trichuris
eggs commonly found in soil, on veggies

female worms 3.5cm, whiplike, lay eggs
eggs mature after 12-14 days in environment
ingestion --> larvae mature in bowel
uneven distribution in a community "wormy people"
clinical presentation of trichuris
well adapted. ergo, mostly asymptomatic, causing little pathology

attaches to wall of colon/rectum

blood suckers --> hemorrhagic diarrhea, anemia

damage to colonic mucosa - irritation/inflammation
diagnosis of trichuris
fecal microscopy
treatment of trichuris
benzimidazoles: ALBENDAZOLE
6 major groups of ectoparasites
lice
mites
fleas
bugs
ticks
flies
biting arthropods
transient (most), usually winged and highly mobile

hematophagous arthropods - piercing & sucking
- Diptera
- Bugs
- Fleas
- Soft ticks

Non-hematophagous arthropods - centipedes
ectoparasites with longterm host contact
fleas
hard ticks
lice
crab lice
endoparasites with longterm host contact
tungiasis

myiasis - Diptera
Pediculus, aka:
lice
pediculus
transmit many infectious diseases
diesase is called pediculosis
life cycle - only on host, 2 weeks
no metamorphosis, nymphs look like adults
mult feed daily to survive
lice structures
legs for clinging to hairs
blood feeding by three stylets
nits are glued to hair for some time
Vagabond's disease
pigmentation of the skin resulting from lice
insecticides used for treatment of headlice
Benzene Hexachloride/Pyrethins
Phthirius, aka:
crab lice
phtherius
venereal transmission
crab-like shape
people become sensitized to louse bites
no zoonotic lice
treatment of phthirius
clothes - 55*C for 20 minutes
sarcoptes, aka:
mites
burrowing mites cause...
mange
sarcoptes life cycle
male/females mate on skin and eggs laid in tunnels

nymphs hatch and burrow
sarcoptes clinical presentation
causes allergic sensitization, itchiness
regional preference (hands, elbows)
larvae migrate to skin surface
females feed on stratum corneum. secretions/exretions that cause irritations
sarcoptes mode of transmission
contact
scabies is caused by...
sarcoptes/mites
treatmetn of scabies
ivermectin/Stromectin,
acaricidal drugs
form of scabies that infects HIV+ patients
Norwegian scabies

extensive regions of scaling skin
demodex
follicle mite

species found on all animals, host specific

common on human face

hair follicles, sebaceous glands

disease reare, usually in females
fleas
blood suckers.

carrier of major diseases: Y. pestis, rickettsia, murine typhus, tapeworms

voracious blood suckers, will feed on any host in environment

jumps from host/host

flea bite hypersensitivity - sensitization to salivary allergens
most problematic flee
cat flea
prevention of flea infections
vacuuming, insecticides, growth regulated
flea life cycle
larvae, pupate, hatch to form adults - free living, eyeless & wormlike

normally lives on cat/dogs, eggs hatch in coat or in environment
ticks
periodic blood suckers, usually on mammals, birds

head parts inserted deep, anticoagulant injected

engorged ticks drop off, lay eggs in environment

most populous in summer
type of tick that infests houses in winter
Rhipicephalus - borwn dog tick
ticks cause...
irritating skin lesions

spread of infectious diseases
- Lyme disease
- Rocky Mountain Spotted Fever
Bugs
insects, blood suckers, wingless or prefer not to fly

mouth parts - piercing sucking type
Cimex
Bug
NOT a vector of HIV (contrary to rumor)
bed bug
feed on blood at night
irritating bites (sheet stains and papule irritation)
sensitization to salivary antigens
Triatoma
kissing bugs, "Reduvid" bugs
feed on other bugs - "assassin bugs"
blood suckers, transmit protozoa (Chagas' disease)
Parasite in hindgut --> feces --> infection "Romana's sign" swelling
Romano's sign
indicative of Chagas' disease

unilateral, painless, periorbital swelling
Myiasis
larvae of flies in the tissues

secondary infections common
Myiasis
see lecture for details
Nematodes with dermatological presentation
pinworms
onchocerciasis
guinea worm --> dracunculiasis
loa loa --> loiasis
Protozoa with dermal presentation
leishmaniasis
Leishmaniasis - the disease
arthropod transmitted flagellate
intracellular replication
chronic disease, organism replicates in macrophages
Forms of leishmaniasis
Cutaneous - disfiguring

Visceral - fatal (often even if treated)

Mucocutaneous - disfiguring
Diagnosis of leishmaniasis
biopsy
culture
treatment of leishmaniasis
antimonials (Pentostam)
protracted, toxic regimes
leismaniasis life cycle
infected female sand fly bites and injects promastigotes into skin

amastigotes form in cells, reproduce and invade tissue

sand fly bites and ingests amastigotes

promastigotes develop in sand fly
trichomoniasis
venereal transmission only

symptomatic in female - usu. asymptomatic in male

symptoms of allergic inflammation

highly site specific pathogen
trichomonas vaginalis
oval 10-20um diameter organisms

4 anterior flagella with undulating membrane (twitching motion)

no cystic forms occur

many are actively phagocytic
moderately anaerobic conditions for optimal growth
binary fission
what cell type is infected in trichomoniasis?
squamous cells - almost always in vagina - NOT columnar
trichomonas vaginitis
discharge contains large numbers of PMNs

organisms are free in vagina or adhering to epithelium, but no tissue invasion

micrscopic hemorrhages in 50% cases

microulceration occurs under clumps of organisms

PMNs & macrophages are capable of killing trichomonads. local IgA response occurs
clinical presentation of trichmonas in women
up to 90% clinically symptomatic
many symptomatic women have other infections
vaginal discharge in 65% of women
50% have vulvar irritation/pruritis
abdominal discomfort occurs in 10%
symptoms exacerbated following menstrual period
vulva is erythematous in 30% of patients
clinical presentation of trichomonoas in men
nearly always asymptomatic
cause of nongonoccocal urethritis
diagnosis of trichomonas
microscopic examination of a fresh sample

large numbers of PMN (yellow discharge supports diagnosis)

pH < 4.5 supports diagnosis

pungent odor supports diagnosis

motile trichomonads sometimes detectable

DDX: candidiasis (no yellow discharge, no change in pH, no pungent odor)
treatment of trichomonas
5-nitroimidazoles

Metronidazole: 2.0gm single oral dose cures

7-day regimen for men is used
prevention of trichomonas
nonoxynal G - spermatoxide is effective, but has not been studied in detial

condoms
what organisms undergo initial development in snails?
trematodes
schistosomiasis
flatworms - blood flukes
waterborne, via snails
adults in visceral blood vessels, eggs shed in feces or urine
types of schistosome that sheds eggs in feces
schistosomiasis mansoni
types of schistosome that sheds eggs in urine
schistosomiasis haematobium
bird schistosomes in Michigan
contaminate fresh water

penetrating larvae of these cause swimmer's itch
pathogenesis of schistosomiasis - overview
dermatitis
migratory phase --> pulmonary lesions
hepatic, urinary or pulmonary stages (vascular system)(
acute phase (antigen Ab complexes)
chronic phase (granulomas, cancer)
schistosomiasis pathogenesis
skin penetration on water contact

egg - granulomas, biliary passage, bladder

granulomatous changes around eggs in tissues

gastrointestinal disease, cirrhosis (S. mansoni)

bladder bleeding, thickening, cancer
schistosomiasis diagnosis
eggs in feces
schistosomiasis treatment
parziquantel treatment
no vaccine as yet
5 parasites with pulmonary presentations
malaria
paragonomiasis
trichinella
nematodes
filariasis
Pneumocystis carinii
4-6mm cyst
multiple fission - no resistant cysts known
lung inhabitant, intracellular or free in superficial cells of airway
immunity to PCP
70% of children have serum Abs to PCP by 4 years
pathogensis of PCP
usu. well controlled in normal host
diagnosis of PCP
microscopy, PCR, DFA - silver stains
treatment of PCP
aerosolized pentaminidine

without tx, fatal in immunocompromised hosts
Paragonamiasis
trematode

living predominantly in the lungs

Latin America and Asia
House dust mites
allergies

asthma
Trichinella
zoonotic infection passed by carnivorism
tiny enteric nematode
larvae migrate and invade muslce cells (nurse cells), lives here for years
exposure by eating poorly cooked pork or other carnivores
pigs get infected from garbage feeding - contains infected meat
trichinosis
disease caused by trichinella
clinical picture of trichinosis
larvae mature quickly
enteritis symptoms, followed by muscle invasion, muscle pain, periodic fever
hx of exposure, gut pain, diarrhea, muscle pain
CNS and mycardial complications
convalescent phase in 2nd month
larvae lie for years, then die and calcify
disease severity proportional to number of larvae ingested
allergic reactions complicate the disease
diagnosing trichinosis
biospy (muscle - intercostal, diaphragm are highest)

serology

radiology
treatment of trichinosis
Mebendazole, Thiabendazole

anti-inflammatory agents
parasites that present in CNS
cysticercosis
malaria
acanthamoeba
naegleria
toxoplasma
coccidian parasite
common infection, BUT uncommon as disease (except in immunocompromised)
about 35% US pop. infected
toxoplasmosis life cycle
infection occcus either w/ fecal oocysts or with ingestion of tissue stages

intracellular replication. replication in enterocytes of cats results in resistant oocysts

predator/prey cycle keeps organism going everywhere

ingested oocysts produce sporozoites in humans, then tissue stages
transmission of toxoplasmosis
transplacental
oral ingestion of oocytes from cats
oral ingestion of tissue cysts (eg: meat)
3 important reservoirs:
- cats
- soil
- intermediate host

uncontrolled proliferation occurs in AIDS cases
pathogenesis of toxoplasmosis
all cells can be infected, including macrophages and neurocytes

rapid proliferation occurs until immunity sets in
initiating event for inflammation in toxoplasmosis
rupturing of toxoplasma cyst
toxoplasma disease
invation of maternal tissues during pregnancy --> invasion of fetus --> congenital abnormalities

toxoplasma gondii - most important infectious cause of congenital abnormalities

primary infection in normal people --> flu like symptoms and cervical lymphadenitis

pet cats and meat are major sources of infection
diagnosis of toxoplasma
tests - serological tests as indicators of infection
- seropositive = immune or infected
- DNA probe tests, biopsy also used
treatment of toxoplasma
treatment difficult
sulfonamides/pyrimethamine
fetotoxicity
prevention of toxoplasma
hygiene
cooking of meat
Naegleria
free-living amoebae, prevalent in US water
warm fresh water or brackish water
highly motile, has flagellate stage. thermophilic, tough cysts.
5-7 day incubation
invades via olefactory epithelium --> olfactory nerve --> brain, inducing purulent meningitis
causes PAM
fata, no treatment
PAM
primary amebic meningoencephalitis

caused by naegleria
Acanthamoeba
Acanthamoeba castellani common in water

free living in water as trophs or cysts
v. sluggish - no flagellate stage
invasive usu. only in immunocompromised
affects the CNS and other tissues
ocular infection
ocular infection of acanthamoeba
invasive to cornea --> amoebic keratitis

contact lens users

if no tx, is fatal in all cases
cestodes
ribbon-like segmetned tabeworms of small intesting
do not have body cavity
complex life cycles - worm stage and cyst stage
4-30 meters in length
sometimes egresses from body
scolex of tapeworm
attachment organ on the head associated with 2 or 4 suckers
TRUE/FALSE: most tapeworms that infect humans require at least one intermediate host
TRUE
symptoms associated with infection by tapeworm in the adult stage
symptomless, only causing nutrient deprivation in the host
symptoms associated with infection by tapeworm in the larva stage
serious or fatal pathology
tapeworms - life cycle
Definitive host: adult worm in gut lumen
--> ingestion of eggs in feces --> Intermediate host

Intermediate host: larval cyst in viscera
--> ingestion of tissue cyst--> Definitive host
Beef tapeworm
taenia saginata
large, 25-30 feet, lives in small bowel
distal segments shed in feces, contain eggs
eggs eaten by cattle
larval form encysts in mucle
humans infected by eating beef
Diagnosis of taenia saginata/beef tapeworm
segments visible
fecal microscopy
treatment for cestods
praziquantel

albendazole
taenia solium
pork tapeworm
large worm in small bowel (<40ft)
segments exit, shedding eggs
eggs hatch in pig gut - larvae encyst in pork muscles
transmission via rare pork
serious CNS problem caused by taenia solium
Neurocysticerosis
What happens when taenium solium eggs hatch in humans?
larvae invade eye, CNS, muscle, skin
neurocysticercosis diagnosis
space occupying CNS lesion
images
seroloyg
treatment for neurocysticercosis
surgery
chemotherapy
albendazole
Trypanosomiases - two types
Trypsansoma brucei

Trypanosoma cruzi
Trypanosoma brucei
tsetse fly vector
transmitted, AFrica
sleeping sickness, replication in CNS tissues
trypanosoma cruzi
triatomic bug vector
transmitted in S. America
replication in heart muscle, nerves
chronic heart disease, bowel disease
3 parasites that present vascularly
malaria
schistosomiasis
lymphatic filariasis
Elaphantiasis
skin changes caused by Wuchereria, Brugia infections - FILARIAL WORM

general term to cover range of disease presentations seen in lymphatic filariasis
Filariasis
mosquito borne nematodes
live in lymphatics; microfilariae in blood
lymphadenopathy, lymphedema
lymphedema
seen in filariasis
accumulation of lymph fluid in tissue of limbs, etc.
hydrocele
accumulation of lymph in scrotal sac
seen in filariasis
parasites with systemic presentations
strongyloides
hookworm
malaria
toxoplasmosis
two parasites that cause anemia
hookworm
malaria
malaria's life cycle
coccidian
mosquito borne
intracellular replication, RBCS, hepatocytes
plasmodium falciparum
most important malaria species

periodic fevers, debilitation
cerebral syndrome - can be fata
anemia
chronic attacks lead to renal complications
malaria is most severe in what demographics?
children from endemic areas
adults from non-endemic areas
diagnosis of malaria
blood stages
serology, DNA probes
treatment of malaria
primaquine, cholorquine
fancidar, mlarone, artemesin
immunity to malaria
controversial - parital in endemically exposed
malaria vaccine available?
no
malarial pathogenesis of anemia
autoimmune
2 parasites that cause hepatosplenomegaly and corresponding abdominal distention
malaria
leishmaniasis
parasites that present general multi-organ
leishmaniasis
amebiasis
ecchinococcus
cysticercosis
what condition is correlated with a high seroconversion rate to Toxocara?
epilepsy
Echinococcus granulosus
tapeworm
causes "Hydatid disease"
small tapeworms fo dog gut, eggs hatch in herbivores and invade viscera
cystic form, proliferative, "hydatids"
cystic larvae eaten by dog, to complete the cycle
eggs will hatch in human gut, cycsts form in internal organs
space occupying lesions
treatment for echinococcus
surgery
antihelminthics
echinococcus multilocularis
zoonotic disease
adult form in foxes, cats
larvae in rodents
cystic larval stages can infect humans, grow fast, rapidly fatal

treatment requires surgery
Chagas' disease, aka:
American trypansomiasis

trypanosoma cruzi
Triatomid bugs, aka:
reduvid or kissing bugs

cause Chagas' disease