parasitology exam 1

list the three ways organisms interact

predation, competition, and symbiosis

list and describe the types of symbiosis

mutualism: both species has a net benefit (alligator and bird)

commensalism: one organism benefits and the other gains nothing, but is not harmed (pilot fish and shark)

parasitism: one organism benefits, and the other is harmed (tick and human)

obligate endoparasites

means "no other choice, lives inside" these parasites cannot live without a host

definitive host

all parasites had a definitive host at least during sexual maturity. supports the adult or sexually reproductive stage of a parasite, and this stage is necessary for parasite survival and life cycle completion

intermediate host

supports immature or non-sexual reproductive forms of a parasite; there may be asexual reproduction though. necessary for parasite survival and life cycle completion, but not all parasites have an intermediate host

transfer host

host that can move or relocate parasite stages from one location to another - most often reproductive stages such as eggs. insects such as flies and cockroaches are good transfer hosts. transfer hosts are not necessary for parasite survival but beneficial in spreading infection and repopulating

vector

host that acts as a definitive or intermediate host, but most importantly, transfers the parasite to the next host. good examples are mosquitos and flies.

life cycle stages take place in vector, then transfer to the next host

fomite

inanimate objects that can transmit eggs (doorknob most common)

Reservoir host

serves as a source of infection and reinfection of humans, and as a means of sustaining a parasite within a population and ecosystem. ex) primates on island of cypress

exposure

being in contact with an infectious organism. not all exposures lead to colonization

colonization

presence of infectious agent on/in a body surface without causing infection in the person

infection

invasion and growth of infectious agents, germs on/in the body

sign

objective evidence of a disease that can be observed by others. quantitative

symptom

subjective evidence of a disease, that is apparent only to the patient. qualitive

incubation period

time between exposure to an infection and the appearance of the first signs and symptoms

latency

the time from infection to infectiousness or being able to pass the infection

difference between infection and disease

infection is when there are infectious agents on/in your body and is multiplying. it only turns into disease when the cells in your body become damaged as a result of the infection, and a disease causes signs and symptoms

virulence factors influence disease and pathogenicity. what are virulence factors?

infectivity: ability of an organism to establish an infection

invasiveness: ability of an organism to spread to adjacent or distant tissues

pathogenicity: ability to produce substances that damage tissues (ex. toxins)

what does it mean to be a carrier?

has infection, but no disease and therefore no signs or symptoms. still infectious

pathogenic parasites

feed on YOU and cause signs and symptoms. most common parasite

intestinal parasites

feed on the food in your GI tract. this is still harmful because your body spends energy to digest food, but does not get the nutrient because the parasite eats it.

population burden

when there is a high population of parasites inside a host

trickling infection

the slow progression of an increase in population as the initial parasite(s) begin to reproduce

hyper-reproductivity

one of the main characteristics of parasites; can repopulate to insane levels. female giant roundworms can lay 2,000 eggs a day

helminths

nematodes: roundworms

cestodes: tapeworms

trematodes: flukes

common intestinal nematodes

enterobius vermicularis - pinworms

trichuris trichura - whipworm

ascaris lumbricoides - giant roundworm

geographic distribution of helminths infective in egg stage

tend to like tropical places, where the eggs in fecal matter stay warm and moist

colder regions, the eggs freeze.

low populations at the top of the african continent due to the sahara desert

enterobius vermicularis life cycle

-eggs are ingested

-larvae hatch in small intestine then migrate to colon

-adults mature in colon

-females migrate out of anus at night

-lay eggs on perineum; females uterus contracts and ruptures body wall, female dies

-eggs embryonate on perineum, causing itchiness

-fingers scratch the itch, get infected with eggs, and usually go to mouth

abnormal migrations:

vagina>uterus>fallopian tubes

from small intestine to appendix instead of colon

enterobius vermicularis general info

-to identify: eggs have a flat side, worm has cephalic swelling/expansion

-common in young children and group settings (family/school)

-sticky eggs

-actually reproduces better in colder climates

-transmission is direct: anus to mouth via fingers, or indirect: airborne eggs or fomites

-itching around anus, difficulty sleeping and restlessness

enterobius vermicularis pathology and diagnosis

large intestines/colon: attachment, irritation, inflammation, pinpoint necrosis

perianal area: itching, scratching, bacterial infection, benign tumors

toxic metabolites: nervousness, insomnia, irritability, and convulsions

diagnosis: anal swab with Qtip, or scotch tape test to the anus, or worms in feces preserved with alcohol

prevention: personal hygiene, mass chemotherapy, detergent, sunlight/UV light

enterobius vermicularis abnormal life cycle problems

migration to appendix: worm causes tissue decay, opportunistic bacteria causes bacterial infection, causes appendicitis

migration to vagina: in vagina has chance to migrate to fallopian tubes (usually don't make it that far). if worm lays eggs/ruptures in fallopian tubes, can cause salpingitis (scarring of fallopian tubes). if happening multiple times, the scarring can get so bad it can cause sterility or an atopic pregnancy

trichuris trichiura life cycle

whipworm

-eggs are ingested

-larvae hatch in small intestine

-adults in cecum (start of large intestine)

-embryonated eggs pass in feces

trichuris trichiura epidemiology

-southeastern US

-infection rates high in warm moist areas, eggs remain viable for long periods (5+ years)

-young children most susceptible

-common where night soil is processed

night soil

Human feces used as fertilizer

trichuris trichiura pathology

-burrowed into mucosa of large intestine/rectum

-attachment to gut wall; sews anterior end into gut wall and feeds on tissue

-must have decently large infection to reproduce

-tissue injury/necrosis, pinpoint hemorrhage, bacterial infection, loss of appetite

-heavy infections: anemia, dysentary, fever, rectal prolapse

trichuris trichiura diagnosis

-fecal smear

-proctoscopic exam

-colonoscopy

-eggs barrel shaped

prevention

-sanitary disposal of feces/night soil

-personal hygiene

ascaris lumbricoides life cycle

giant roundworm

-eggs are ingested

-larvae hatch in small intestine, then enter circulation system and migrate to lungs

-larvae are then coughed up and swallowed, re-entering the gastrointestinal tract

-mature in the small intestine, then reproduce in the small intestine

-eggs in feces

Ascaris lumbricoides epidemiology

-currently uncommon in US

-warm moist climate best for egg survival

-more common in areas using night soil for fertilizer

-most common host is pigs

ascaris lumbricoides pathology

lungs

-petechial hemorrhage

-sero cellular exodate

-cough

-allergic reactions to molting fluid

small intestine:

-resides in lumen of gut, no pathology/no tissue invasion

-swims against peristalic movement of gut

-feeds on intestinal contents

ascaris lumbricoides abnormal pathology

-intestinal obstruction

-appendicitis

-abnormal migrations to pancreatic duct, bile duct, esophagus, mouth, ears

-trachea to lungs (very dangerous)

-gut penetration (very dangerous)

ascaris lumbricoides diagnosis

-fecal smear

-female produces 200,000 eggs per day. human will pass 10,000,000 eggs a day

prevention:

-sanitation night soil disposal

-wash food

-personal hygiene

necator americanus / ancylostoma differences

necator americanus (new world hookworm)

-lunar cutting plates

ancylostoma duodenal (old worm hookworm)

-fangs or teeth

-produces more eggs

necator americanus / ancylostoma duodenal life cycle

-eggs enter soil via human feces

-larva emerge as rhabditiform form, free living

-will revert to thread like filariform larva and migrate to highest point in environment

-filariform make contact with a barefoot person and enter their skin and then circulation system

-larva move through the bloodstream to the lungs, where they are then coughed up and swallowed

-infection occurs in small intestine, eggs passed in feces

necator americanus / ancylostoma duodenal epidemiology

-mostly tropics/subtropics/temperate zones

-some mixing due to population migrations

-temperature and rainfall is important

-all ages susceptible

-spread through the silk road trade

-new world hookworm spread through slavery

necator americanus / ancylostoma duodenal pathology

skin

-papule, then vesicle, then lesion

-puritis (itching)

-edema (swelling)

-erthyema (redness)

lungs

-petechial hemorrhage

small intestine

-attachment and reattachment damage

overall

-anemia

-iron deficiency causing "pica" (urge to eat dirt)

necator americanus / ancylostoma duodenal diagnosis

-eggs in stool

prevention

-sanitation and disposal of feces

-proper treatment of night soil

-personal hygiene

-shoes

cutaneous larva migrans - "creeping eruption"

infection with larval stages of ancylostoma canium or ancylostoma braziliensis (dog and cat hookworms)

-pets are source of eggs; filariform larva penetrate skin and migrate subcutaneously but cannot complete their life cycle since they are in the wrong host

-dog and cat skin is a lot thinner than human skin, so the parasites cannot penetrate human host skin deeper

creeping eruption pathology

-confined to the skin with damage cause by the migration of the filariform larva

-tunnels is where worm was, will not be able to see where worm currently is under skin

creeping eruption diagnosis

-observation of surpegenous tunnels

prevention

-do not allow pets in sandboxes or on the beach

-take care when working/playing around animals

-use plastic drop cloth in crawl spaces under house

trichinella spiralis life cycle

pork worm, aka "the great imitator"

-mouse has trichinella

-pig eats mouse

-pig has encysted larva in striated muscle

-human eats undercooked pig

-larva released in small intestine

-adults mature in small intestine, females give LIVE BIRTH

-larva then penetrates blood vessel but then breaks out in muscle

-lay dormant in muscle as encysted larva

-larva favor well oxygenated muscles like eye muscles, diaphragm, larynx, tongue, intercostal, biceps/triceps,pecs

trichinella spiralis stage one

time period: 1-10 days post infection

immune system response to tissue damage and metabolites causes a severe inflammatory response promoting the worm to move down the gut to normal tissue. inflammation follows and worm continue to move until it runs out of small intestine and is eventually expelled. this self cure is beneficial to host and to worm

-ingestion of larva with maturation into adults in small intestine

-necrosis and panmucosal inflammation begins at 72 hours and peaks at 8 days

-nausea

-vomiting

-diarrhea

-fever

trichinella spiralis stage two

time period: 7-14 days post infection

adults expelled from intestines, where self cure happens. larva are migrating to muscles via the circulation . larva migrate from gut to muscles

-small capillary hemorrhage from larva rupturing smallest capillaries as they pass through vessels (will see in fingernails)

-bilateral ocular edema as eye muscles are invaded

-hyper eosinophilia

trichinella spiralis stage three

time period: approx 3 weeks post infection

larval encystment

-myositis (muscle inflammation)

-myalgia (muscle pain)

-degeneration of muscle fibers

trichinella spiralis stage four

calcification of larva

-symptomless

trichinella spiralis diagnosis

-muscle biopsy: new infection won't be calcified, old infection (21+ days) calcified

-hard to diagnose, adult worms gone by day 14

prevention

-freeze/cook pork

-remove rodents from pig farms

-cook garbage if used to feed pigs

strongyloides stercoralis direct life cycle

thread worm

-infective filariform penetrate intact skin, initiating the infection

-filariform larva enter circulation system, break out in lungs, coughed up, and swallowed into small intestine

-mature and reproduce in small intestine

-eggs are deposited in intestinal mucosa, they hatch in tissue of intestine, and then the larva migrates to the lumen

-rhabditiform larva in the intestine are excreted in feces

strongyloides stercoralis autoinfection

internal autoinfection

-rhabditiform larva in the large intestine can become filariform larva

-penetrate intestinal mucosa or perianal skin

-follow normal infective life cycle

-(more common for immunosuppressed people)

external autoinfection

-when someone is bedridden and can't clean up their own feces, rhabditiform larva sit in feces

-larva reenter person through perianal skin

-follow normal infective life cycle

strongyloides stercoralis indirect cycle

-rhabditiform larva pass in stool

-larva develop into free living adult worms

-reproduce and lay eggs

-eggs hatch into rhabditiform larva

-either become infective filariform larva, or develop into free living adult worms

strongyloides westeri and strongloides stercoralis

S. westeri infects horses, S. stercoralis infects humans

strongloides stercoralis epidemiology

-mostly tropics/subtropics/temperate zones

-new parasite, strongloides species has many hosts. human worm is indistinguishable; can form infections in dogs, cats, and horses

strongloides stercoralis pathology

skin

-less mechanical damage than hookworm, but still forms papule>vesicle>lesion

lungs

-petechial hemorrhages

intestines

-adults deep in mucosa. migrating female lays eggs, larva migrate out of mucosa and into lumen of gut

-cavitation

-muscosal sloughing

-fluid and blood loss

-dysentary

-secondary bacterial infection

-duodenal ulcers

strongloides stercoralis internal autoinfection pathology

-parasites do not undergo self cure in immunosuppressed people

-larva hatch and do not leave gut, penetrate blood vessels

-break out in lungs and cause massive pulmonary damage

-travel to gut and cause more mechanical damage

-population increases dramatically

strongloides stercoralis diagnosis

-continuous mucoid diarrhea changing to dysentery

-rhabditiform larva in fresh stool

-filariform larva in older stool

-lung aspirations

-larva in sputum

prevention

-shoes

-same as hookworm

ivermectin

2015 nobel prize given to William Campbell and Satoshi Omura for creating ivermectin

tissue nematodes

cause more damage than intestinal nematodes

-dracunculus medinensis

-wucheria bancrofti

-loa loa

-onchocerca volvulus

dracunculus medinensis life cycle

guinea worm, "fiery serpent"

-parasite larva consumed by a copepod (vector)

-human drinks unfiltered water containing copepods

-larva are released when copepods die

-larva penetrate hosts stomach and intestinal wall

-mature and reproduce

-fertilized female worm migrates to surface of the skin, causes a blister, and larva discharges from blister when person comes into contact with worm

dracunculus medinensis epidemiology

almost eradicated! 13 cases in 2024. only in africa

common source is stepwells

dracunculus medinensis pathology and diagnosis

-lesions on foot or ankle

-sometimes, worm grows up leg and can damage knee joint

treatment

-medicine

-matchstick

prevention

-treat carriers

-kill copepods

-filter water

-education

Wuchereria bancrofti life cycle

bancroft's filariasis, "elephantiasis"

-mosquito bites host, infection occurs because microfilaria are present in vector's saliva/on proboscis

-mature in lymphatic system

-adults produce sheathed microfilaria that migrate into lymph and blood channels

-mosquito bites host, ingests microfilaria

-microfilaria shed sheaths, then undergo different larval stages

Wuchereria bancrofti epidemiology

-mosquito vector, common in tropics and subtropics

-wide range of intermediate hosts due to different species of mosquitos

Wuchereria bancrofti pathology

asymptomatic: 70%

-adult worms cause little or no blockage

-mild inflammation

acute filariasis: 25%

-adult worms cause pathology

-peri endo lymphatic inflammation

-inflammation causes scarring and narrowing of lymph lumen

chronic filariasis: 5%

-results from repeated infections

-increased worm burdens and blockage of collateral lymph circulation

-hypersensitivity to worm metabolites

-intense peri endo lymphatic inflammation leading to lymphatic scarring

-severe tissue swelling

-elephantine skin due to lack of nourishment (blood vessels and lymph channels restricted)

Wuchereria bancrofti diagnosis

-microfilaria in blood

-presence of antibody to worm

when treated with medicine and worms die, it will not cause a blockage since there will be no inflammation due to no worm metabolites

also treated with compression bandages, surgery, lymphatic bypass surgery

prevention

-mosquito control

-mass chemotherapy

-supportive treatment

loa loa life cycle

eye worm

-chrysops sp. (deer fly) bites host, larva from vector enters host

-adults live in subq tissue

-produce sheathed microfilaria, found in spinal fluid, urine, sputum, peripheral blood, and in the lungs

-fly bites host and becomes infected

-microfilaria shed sheaths and undergo different larval stages in vector

loa loa epidemiology

- Distributed in rain forest areas of Central and West Africa

- Several species of deer fly, genus Chrysops, serve as vectors

loa loa pathology

-worms move freely through subq tissue

-attracted to warmth

-can wander across eye

-form subq nodules, growth of entwined worms

-if host forms a capsule around nodule due to hypersensitivity reaction, it is called a calabar swelling

loa loa diagnosis

-observation

-history of exposure

-microfilaria in blood

treatment

-surgical removal of calabar swelling THEN medicine

onchocerca volvulus life cycle

river blindness

-simuliun damnosum (vector, blackfly), bites host and infects

-larva in subq tissue

-adults in subq nodule

-adults produce UNsheathed microfilaria that are typically found in skin and lymphatics, but also occasionally blood, urine, peripheral blood, and sputum

-blackfly bites host, becomes infected

-microfilaria undergo different larval stages in vector

onchocerca volvulus epidemiology

-Significant public health problem in Africa and South America

-Black fly larval stages only in clear, fast-running streams

-Adult flies survive in high humidity and plenty of streamside vegetation

onchocerca volvulus pathology

-benign tumors (similar to calabar swelling)

-microfilaria migrate under skin and can cause hanging groin, or across the eye and cause corneal damage

-migrating microfilaria cause skin to be detached and lose elasticity. results in parchment skin, this can also lead to severe bacterial infections between layer of skin and tissue

wolbachia

a genus of bacteria which infects arthropod species, including onchocerca volvulus. this bacteria is responsible for the inflammatory reaction that causes river blindness

also means that a person who has onchocerca volvulus, can take antibiotics and get rid of the worms since the worm and bacteria have a mutualistic relationship

onchocerca volvulus diagnosis

-skin biopsy looking for microfilaria

treatment

-remove benign tumor, THEN ivermectin and/or antibiotic

prevention

-remove vector and treat carriers