Parasitology Pt 2 Flashcards
3 Classes of Helminths
- Nematodes (roundworms)
- Cestodes (tapeworms)
- Trematodes (flukes)
Nematodes (Roundworms)
- Enterobius vermicularis
(human pinworm) - Ascaris lumbricoides & suum
(intestinal roundworms of humans & pigs) - Hookworms
- Toxocara canis & catti
- Ancylostoma braziliensis - Trichuris species
(whipworms) - Dracunculus medinensis
(Guinea worm) - Filariae
- Wuchereria bancrofti
- W. (Brugia) malayi
- Onchocerca volvulus
- Loa loa (eyeworm)
Cestodes (Tapeworms)
Flat/ribbon-shaped, segmented bodies
Proglottids
(reproductive segments containing both F & M sex organs)
No digestive system
(absorbs nutrients)
Transmitted via ingestion of contaminated undercooked meat OR fleas infected with dog/cat tapeworms
Taenia solium (pork tapeworm)
Taenia solium (pork tapeworm)
Pig = 1st intermediate host
1. Ingests embryonated ovum from human feces
2. Cysticercus develops in flesh (burrows/forms cysts in tissue)
Human = 2nd intermediate host
(definitive host)
3. Ingests pork containing cysticerci
4. Cysticercus develops into mature tapeworm in small intestine
5. Ova & ova-filled proglottids passed in human feces
Neurocysticercosis
- Eggs hatch & form cyst in brain
Trematodes (Flukes)
Bilaterally symmetrical flat/leaf-shaped
Suckers
(allow attachment while fluid withdrawn)
Can burrow through skin
Hermaphroditic
Life cycle includes 1 or more intermediate hosts (after escapes from egg )
- Larval form = within egg
- Cercariae = last stage
Schistosoma species
Schistosoma species
Hermaphroditic
Snail = 1st intermediate host
1. Miracidium hatches from eggs in freshwater & infects
2. Cercariae leave snail
Human = 2nd intermediate host
(definitive host)
3. Cercariae penetrates skin (in water)
4. Immature worm enters bloodstream & ends up in veins near intestine or bladder
5. Reach sexual maturity in veins of abdominal cavity
6. Females produce eggs
7. Eggs enter intestinal tract or bladder
8. Eggs passed in urine or feces into freshwater
Penetration of skin causes itching
Eggs become encapsulated in liver, lungs, brain
- Block portal veinous system
Molecular mimicry (adult worms)
- Incorporate host antigens on surface
Diagnosed by eggs in urine (S. haemotobium) or feces (S. mansoni or S. japonium)
High mortality rate
Enterobius vermicularis
Human pinworm
- Very common infection (North America & Europe)
Symptoms:
1. Mild GI upsets
2. Perianal itching
3. Irritability
4. Insomnia
5. Vaginal irritation (adult pinworms)
Diagnosed by eggs (scotch tape test) or worms (flashlight) on perianal area
Enterobius vermicularis:
Life Cycle
- Human infected when ingest eggs
- Eggs hatch in small intestine
- Worms migrate to large intestine & reach sexual maturity
- Females crawl out of anus & deposit eggs on perianal skin
- RETROINFECTION (eggs hatch & juveniles crawl back into anus to mature into adults) - Eggs become infective within 6 hrs
- Hands, bed clothing/linens, etc. contaminated with infective eggs
Ascaris lumbricoides & suum
Intestinal roundworms of humans & pigs
Most common nematode infection world-wide
Symptoms:
1. Ascaris pneumonia
2. Blockage of GI tract
3. Acute (fatal) peritonitis &/or blockage of bile/pancreatic duct
Diagnosed by eggs in feces of infected person
Ascaris lumbricoides & suum:
Life Cycle
- Eggs ingested by host
- Eggs hatch in small intestine
- Juveniles penetrate tissues of intestine & enter bloodstream
- Juveniles migrate to lungs & molt into 3rd stage juveniles
- 3rd stage juveniles migrate from pulmonary capillaries into alveoli
- “Coughed up” & swallowed
- Complete development into adults in small intestine
- Females produce eggs
- Eggs passed in host feces
- Juveniles within eggs mature to infective (2nd) stage
Toxocara canis & catti (hookworms)
Visceral larva migrans
Eggs from feces of infected dogs/cats ingested by human
- Hatch in intestine
- Can penetrate mucosa & enter circulation
Carried to:
- Liver
- Lungs
- Eyes
- Other organs
Cause inflammatory necrosis
Ancylostoma braziliense (hookworms)
Cutaneous larval migrans
- “Creeping eruption”
- Prevalent in tropical/subtropical countries & US
Filariform larvae in dog/cat feces infect humans
- Intestinal parasite of dogs/cats
- Contact with contaminated soil
Causes skin eruptions
- Migrates in skin (larvae move around)
Symptoms last 2-10 weeks (duration of larval persistence)
Prevention:
1. Treat pets
2. Wear shoes outside
3. Clean up after dogs/cats
Hookworms:
Life Cycle
(Necator spp. & Ancylostoma spp.)
- Infective juveniles penetrate skin
- Migrate via blood to lungs (coughed up & swallowed) - Juveniles enter small intestine
- Attach to surface
- Mature to adult forms - Adult hookworms attach to lining of small intestine
- Feed on blood - Females produce eggs
- Eggs passed in feces - Eggs hatch in soil
- Juveniles develop into infective (3rd) stage
Trichuris species (whipworm)
Live in large intestine
- Anterior end embeds in cells of lining
Can live long time
- Constant reinfection & heavy worm burdens
Symptoms:
1. Diarrhea
2. Dysentery
3. Anemia
Heavy worm infection in children lead to mental & physical retardation
Diagnosed by eggs in feces
Trichuris species:
Life Cycle
- Eggs ingested by host
- Eggs hatch in small intestine
- Juveniles migrate to large intestine
- Males & females reach sexual maturity & mate
- Adults in large intestine
- Eggs passed in feces
- Juveniles within eggs mature into infective juveniles
Dracunculus medinensis (Guinea worm)
Host infected by drinking water containing infected copepods (intermediate host)
Can live in body 1-2 years
Dies & causes little reaction if doesn’t reach skin
In superficial tissue:
- Liberates toxic substance that produces local inflammatory reaction (sterile blister)
- Worm lies beneath blister
Contamination of blister produces:
- Abscesses
- Cellulitis
- Ulceration
- Necrosis
Removal strategy = pour water on blister
Dracunculus medinensis:
Life Cycle
- Human drinks unfiltered water containing copepods with L3 larvae
- L3 larvae released when copepods die
- Penetrate host’s stomach & intestinal wall
- Mature & reproduce - Fertilized female worm migrates to skin surface
- Causes blister
- Discharges larvae - L1 larvae released into water from emerging female worm
- Female worm begins to emerge 1 yr after infection - L1 larvae consumed by copepod
- Undergoes 2 molts & becomes L3 larvae
Filariae
Major blood & tissue parasites of humans
- Thread-like roundworms
- Belong to family Filarioidea
Spread by bite of arthropod
Adult filariae live in lymphatic tissue & give birth to prelarval forms (microfilariae)
- Microfilariae burrow through tissue & circulate in blood/lymphatic system
- Blocks lymphatics (swelling)
Wuchereria bancrofti & W. (Brugia) malayi
W. bancrofti = Pacific islands & Africa
W. malayi = SE Asia
Transmitted by bite of infected mosquito
- Microfilariae mature into adults & mate in lymphatics of genitals/lower extremities
- Offspring enter nearby blood vessels
Symptoms:
1. Fever
2. Swollen lymph nodes
3. Elephantiasis (swelling of legs/genitals)
Elephantiasis
- Formation of fibrous tissue around dead filariae plugs up lymphatic system
Wuchereria bancrofti:
Life Cycle
- Mosquito takes blood meal
- L3 larvae enter human skin - Adults in lymphatics
- Adults produce sheathed microfilariae
- Migrate into lymph/blood channels - Mosquito takes blood meal
- Ingests microfilariae - Microfilariae shed sheaths, penetrate midgut, & migrate to thoracic muscle
- L1 larvae
- L3 larvae
- Migrate to head & proboscis
Onchocerco volvulus
River blindness (blinding filariasis)
Vector = female black fly
Onchocerciasis
- Nodular & erythematous lesions in skin & subcutaneous tissue
(chronic inflammatory response to infection)
- Microfilariae migrate through dermis, CT, & eye
Loa loa (eyeworm)
Filarial infection that may lead to blindness
Vector = deer fly
Migrates under skin
(up to 1in every 2 min)
Swelling appears spontaneously
- Fugitive/Calabar swelling
- Persists 4-7 days & disappears
Usually no serious problems
- EXCEPT: passing through orbital conjunctiva or nose bridge
4 Groups of Fungi
(based on sexual reproduction)
- Zygomycetes (zygospores)
- Basidiomycetes (basidiospores)
- Ascomycetes (ascospores)
- Deuteromycetes (or fungi imperfecti)
- Sexual reproduction not observed
4 Ways Fungi Cause Disease
- Allergic reaction (inhaling spores)
- Reaction to fungal toxin (mycotoxins)
- Mycoses (fungi grow in/on body)
- Economic impact (destroys food supply & leads to starvation)
Superficial Mycoses
- Pityriasis versicolor (tinea versicolor)
- Tinea nigra
Pityriasis versicolor (tinea versicolor)
Malassezia species
Chronic superfical fungal infection
Leads to hypo/hyper-pigmented patches on skin (do not tan in sunlight)
Tinea nigra
Exophiala weneckii
Dark brown/black painless patches on soles of hands/feet
Superfical Cutaneous Mycoses
- Dermaphytosis
(normal skin = resistant to dermaphytes) - Candida albicans
(overgrowth of normal flora)
Dermatophytosis
Excessive moisture allows invasion of keratinized layers of tissue
- Infection of hair, skin, nails
Caused by dermatophytes
(keratinophilic fungi of 3 specific genera):
1. Trichophyton
2. Epidermophyton
3. Microsporum
Dermatophytes produce keratinase
- Allow destruction of keratin
(byproducts used as nutrients)
Dermatophyte Infections
- Tinea corpis (ringworm)
- Mycoses of body - Tinea capitis
- Mycoses of scalp - Tinea axillaris
- Mycosis of underarm - Tinea cruris (jock itch)
- Mycosis of groin - Tinea pedis (athlete’s foot)
- Mycosis of foot - Tinea unguium (onychomycosis)
- Mycosis of nails
Candida albicans
Overgrowth of natural commensal fungi (mainly located in GI tract)
- Oral thrush (mouth)
- Heavy duty antibiotics - Diaper rash (groin)
- Candida vaginitis (vagina)
Subcutaneous Mycoses
Caused by saprophytic fungi
- Normal soil inhabitants
Enter following trauma to skin
Remain localized to subcutaneous tissue OR spread along lymphatics to local nodes
- See track (line)
- Local necrosis
- Sporothrix schenckii
- Phialophora & Cladosporium
Sporothrix schenckii
Sporotrichosis
- Local pustule or ulcer with nodules draining lymphatics
Dimorphic fungus
Hazard for gardeners
Phialophora & Cladosporium
Chromoblastomycosis
- Wart-like lesions with crusting abscesses extending along lymphatic system
Systemic Mycoses by Dimorphic Fungi
- Coccidioides immitis
- Histoplasma capsulatum
- Blastomyces dermatitids
Coccidioides immitis
Coccidioidomycosis (Valley Fever)
- Endemic in SW USA & Latin America (arid regions)
- Mild pneumonia/flu-like symptoms
(Often asymptomatic)
Dimorphic
- Mold in soil
- Spherule (containing endospores) in tissue
Transmitted via inhalation of arthrospores
- May spread from lungs to bones & CNS
- Dissemination more often in immunocompromised
Resolution of disease results in long-term immunity against reinfection
Johny Moore (SA spur infected & 2 yr treatment - ended career )
Histoplasma capsulatum
Histoplasmosis (Spelunker’s Disease)
- Endemic in central & eastern states
Dimorphic fungus
- Mold in soil
(contaminated with bat/bird droppings)
- Yeast in tissue
(tuberculate macro or microconidia multiplying within macrophages)
Transmitted via inhalation of conidia (spore)
Mild respiratory symptoms
(often asymptomatic)
Spreads through body within macrophages
- Dissemination most often in immunocompromised
Small granulomatous foci of infection heals by calcification
Blastomyces dermatitids
Blastomycosis
- SE USA & Ohio-MS River Valley area
Dimorphic fungus
- Mold in soil
- Yeast in tissue (broad-based bud)
Transmitted via inhalation of conidia
Symptoms:
1. Primary pulmonary stage
2. Chronic granulomatous disease
3. Dissemination may result in ulcerated granulomas of skin, bone, & other sites
4. Destruction of nasal passages
Systemic “Opportunistic” Mycoses
- Cryptococcus (Filiobasidiella) neogormans
- Candida albicans
- Asperigillus fumigatus/flavus
Cryptococcus (Filiobasidiella) neogormans
Cryptococcosis
Present in soil
- Pigeon droppings
Transmitted by inhalation of minimally encapsulated spores (basidiospores)
Usually asymptomatic or pneumonia
Can spread to CNS in immunocompromised
- Cryptococcal meningitis/meningoencephalitis
Most often occurs in individuals with suppressed cell-mediated immunity (ex: AIDS)
Virulence factors:
1. Capsule
2. Melanin production
3. Growth within macrophages
Candida albicans
Normal flora (present in body)
- Upper respiratory tract
- GI tract
- Female genital tract
Occurs when local/systemic host defenses impaired
- Overgrowth of normal flora
Clinical presentation:
1. Thrush
2. Esophageal
3. Disseminated candidiasis (bloodstream infection)
4. Chronic mucocutaneous candidiasis
Diagnosed by pseudohyphae & germ tube formation
Vaccine studies underway at UTSA
- Dr. Jose Lopez-Ribot & Stepgen Saville (MBT laboratory)
Asperigillus fumigatus/flavus
Aspergillosis
Exists ONLY as molds
- Soil, decomposing organic materials, fruits, nuts, grains
Occurs most often in neutropenic patients
Growth in pulmonary cavities
- Fungus ball
- Invades lungs & other organs
Allergic bronchopulmonary aspergillosis (ABPA)
- Fungal infection of the lung due to a hypersensitivity reaction to antigens of A. fumigatus
Aflatoxin production (A. flavus)
