FUNGI:
cell wall: chitin
cell membrane: sterols (ie. ergosterol)
favored by heat and humidity
YEASTS
MOLDS
single cells (oval or round)
long filaments or hyphae (septate or nonseptate)
asexual budding
asexual spores (conidia)
pseudohyphae (clusters of buds)
mycelia (segments of hyphae)
humans
environment (ie. soil)
grows on 37C (blood agar, humans)
grows on 25 (Sabouraud’s agar)
CUTANEOUS FUNGI:
ORGANISM
Superficial fungal infections (dead skin):
PATHOGENESIS / CLINICAL FEATURES
cause pigment changes on surface of skin
lesions contain budding yeast cells and hyphae
Pityriasis (Tinea) versicolor (multi-colored)
Malassezia furfur
Tinea nigra (black-colored)
Cladosporium (Exophiala) werneckii
hypopigmented patches on the skin, especially on tanned skin in
the summer ( with hot, humid weather); scaling, itching
dark brown to black painless patches on palms and soles
found in soil and transmitted during injury (southern states)
Dermatophytes:
no yeast form
affect superficial keratinized structures
(scaly skin, hair loss, and brittle nails)
through action of keratinase
pruritic papules, vesicles
Microsporum (spiky, spindle-shaped,
thick-walled, single)
Trichophyton (cylindral, smooth, thinwalled, single)
Epidermophyton (club-shaped, smooth
moderately thick-walled, clusters of 2-3)
direct contact
fomites
animals: Microsporum also spread from dogs, cats
”Dermatophytid” reactions: hypersensitivity to fungal antigens
 no organisms found in granulomas
tinea capitis: scaly calp, hair loss (T. tonsurans, T. rubrum)
tinea corporis: ringworm of glabrous/smooth skin red, raised
tinea cruris (jock itch): red itchy patches on groin, scrotum
tinea pedis (athlete’s foot): toescracking, peeling of skin
tinea unguium (“onchomycosis”): thickened, discolored, brittle nails
tinea barbae: patches along beard distribution
DIAGNOSIS / TREATMENT
skin scrapings w/ KOH prep
selenium dandruff shampoo
topical imidazole
topical miconazole for Tinea
versicolor
keratolytic agent: salicylic acid
for Tinea nigra
skin scrapings w/ 10% KOH on
glass slide shows hyphae
macronidia or microconidia
ecothrix: hyphae around hair shaft
endothrix: hyphae w/in hair shaft
Wood’s light: fluorescence when
tinea capitis lesions caused by
Microsporum placed in UV light
topical imidazole
oral griseolfulvin (hair, nails)
Subcutaneous Mycoses:
Sporotrichosis: Sporotrix schenckii
dimorphic fungi in soil, plants (rose
thorns, splinters) enters via trauma
grow in soil, vegetation infect during trauma
subcutaneous nodule: local pustule or ulcer that spreads along
lymphatics more necrotic nodules along linear, lymphatic distribution
Chromoblastomycosis
(Phialophora, Cladosporium)
soil fungi in tropics: bare feet and legs
Mycetoma (Petriellidium, Madurella)
wounds on feet, hands, or back
slowly progessive granulomatous infection through skin trauma
cauliflower warts w/ crusting abscess along lymphatics: initially,
one violet-colored wartlike lesion more nodules over months/years
abscesses, with pus discharged through sinuses (pus has compact
colored granules similar to Actinomyces, Nocardia lesions
cigar-shaped budding yeasts
branching hyphae w/ oval conidia
at tips “daisy petals”
oral KI
itraconazole or amphotericin B
copper-colored sclerotic bodies:
dark brown, funus in WBC’s, M
local excision/ itraconazole
sulfonamides: actinomycotic form
no treatment for fungal form
SYSTEMIC FUNGI:
within lungs differentiate into yeasts
itraconazole for lung disease
Coccidiodes immitis
dimorphic (mold, spherule w/ endospores)
soil of arid regions: southwestern USA, Latin
America (Arizona, New Mexico, southern CA)
Filipinos
2nd most common opportunistic infection in
AIDS patients
Histoplasma capsulatum (nonencapsulated)
dimorphic (mold, yeast)
faculatative intracellular parasite
soil w/ bird droppings (ie. Starlings, bats)
Ohio, Mississippi River Valleys
mostly asymptomatic or mild pneumonia not contagious from person to person
amphotericin B for severe , disseminated disease
in soil, it forms hyphae with alternating arthrospores and
tissue: spherules w/ doubly
refractive walls filled w/ endospores
empty cells inhalation of arthrospores by humans
dissemination in IC: meningitis; bone and skin granulomas
erythema nodosum (red tender nodules on extensor surfaces)
and arthralgia “valley fever” (San Joaquin Valley, CA.) or
“desert rheumatism” (Arizona)
2 types of asexual spores: tuberculate macroconidia (thick
walled w/ fingerlike projections lab ID) and inhaled, infectious
microconidia (smaller, thin, smooth-walled spores)
calcification of small granulomatous foci in lungs/ spleen
AIDS pts: liver, spleen, and lymph nodes: hepatosplenomegaly
skin tests (spherulin or
cocciodin) DTH rxn
IgM/ IgG precipitin test
tissue: oval budding yeast cells
found in M
skin tests (histoplasmin)
 DTH rxn
complement fixation
chest X-ray (TB)
Blastomyces dermatitidis
dimorphic (mold, yeast)
moist soil rich in organic material
North America (east of Mississippi) and
Central America worldwide
Paracoccidiodes brasiliensis
endemic to rural Latin America
inhaled ovid conidia
also infects other animals (dogs)
rarest systemic fungal infection but also most severe and
rarely asymptomatic
ulcerated granulomas of skin, bone w/ weight loss, night sweats
inhaled spores
tissue: thin-walled round yeast
cells w/ single broad-based buds
and doubly refractive walls
tissue: thick-walled with multiple
buds
OPPORTUNISTIC FUNGI:
diabetes, lymphomas, broad spectrum antibiotics, immunosuppression (chemotherapy, AIDS pts)
Candida albicans
oral thrush (creamy white patches)
oval yeast w/ single bud; blastoconidium
diaper rash (skin folds: between fingers, groin)
budding yeast cells and pseudohyphae
vaginitis: vaginal itching and discharge ( risk during menses
and pregnancy, oral contraceptives, antibiotics, DM,  pH)
normal flora of mucous membranes of upper
IC: esophagitis (substernal chest pain and dysphagia)
respiratory, GI, and female genital tracts
dissemination (retinal exam shows multiple white fluffy candidal
normal flora, but never in blood
patches) sign of neutropenia
Cryptococcus neoformans
oval budding yeast (no mold form)
pigeon droppings eucalyptus tree
Aspergillus fumigatus aspergilloma
mold only: septate hyphae V-shaped
airborne conidia (inhaled, ingested, cut skin)
A. flavus on rice/grains mycotoxins (ie.
aflatoxin) toxic or carcinogenic to liver 
hepatocellular carcinoma
Mucormycosis (Mycor, Rhizopus)
saprophytic molds only: nonseptate hyphae
(root branches) w/ broad irregular walls and
right-angle branches
inhaled through lungs mostly asymptomatic
meningitis
pneumonia; bone and skin granulomas
4th cause of death in AIDS pts
dissemination: skin, CNS, heart, lung, nasa-orbital area, cornea
AIDS: hemoptysis and granulomas (lung cavitations)
allergic bronchopulmonary aspergillosis: type I
hypersensitivity reaction (IgE) resembling asthma
rhinocerebral mucormycosis: associated with diabetes
infection of nasal mucosa w/ invasion of sinuses and orbit
molds proliferate in walls of blood vessels (telangiectasia)
C. albicans: germ tube test at
37 C X 3hrs. and chlamydospores
oral thrush: ”swish and swallow”
nystatin
vaginitis: imidazole suppositories
amphotericin B (dissem. disease)
skin test w/ Candida: indicator of
competent cellular immunity
India ink: halo around organism
CSF: Ab to capsular antigen
flucytosine or amphotericin B
flat, velvety, bluish-green colony
fungus ball on chest X-ray
surgical removal, amphotericin B
endospores enclosed w/in a
sporangium
surgical resection
amphotericin B
PROTOZOANS:
eukaryotes with endoplasm, ectoplasm, and a cytosome
definitive host: harbors sexually reproducing stage
intermediate host: harbors asexually reproducing stage
Intestinal and Urogenital:
Entamoeba histolytica
invasion of intestinal epithelium and secrete enzymes localized trophozoites w/ RBC in
motile amoeba (trophozoite)
cytoplasm  active disease
necrosis “teardrop” ulcer erode and destroy intestines
cysts or trophozoites w/o
ingestion of nonmotile cyst (4 nuclei)
amoebic dysentery: bloody, mucus-containing diarrhea w/
internalized RBC carrier state
lower abdominal discomfort, flatulence, tenesmus, weight loss
differentiates into trophozoites in the ileum
diloxanide furoate to kill cysts
1 cyst=8 trophozoites colonize colon, cecum amoebic abscess of liver: RUQ pain, weight loss, fever, tender,
(luminal amebicide)
enlarged
liver
can
penetrate
diaphragm
and
cause
lung
disease
trophozoites (single nucleus) in diarrheal stool
metronidazole (Flagyl): luminal
E. coli: 8 nuclei
E. hartmani: 4 nuclei also, but smaller
cysts in formed stool
and systemic amebicide

E.
dispar:
nonpathogenetic
1-2% of U.S. population (homosexual males)
Giardia lamblia
cysts differentiate to trophozoites in duodenum
filter water: chlorination does not
ingestion of cysts (4 nuclei)
kill; must boil and filter
no invasion: attachment to duodenal wall (surface of villi)
1 cyst = 2 trophozoites (pear-shaped w/ 4
string test: swallowing string into
inflammation of mucosa malabsorption of protein, fat
duodenum trophozoites adhering
pairs of external flagella w/ 2 anterior nuclei) nonbloody, foul-smelling diarrhea w/ nausea, anorexia,
camping, day-care centers, homosexuals
metronidazole (Flagyl)
flatulence, and abdominal cramps for weeks to months; no fever
Cryptosporidium parvum
mild diarrhea
attach to jejunum (no invasion)
acid-fast stain (modified Kinyoun
oocysts release sporozoites, which form
acid-fast stain) oocysts in feces
infants and AIDS patients: chronic, watery, nonbloody
trophozoites   oocysts passed out in feces diarrhea w/ large fluid loss (up to 3-17 liters of stool per day)
no effective drugs; purify water
ingested oocysts (4 motile sporozoites)
life-threatening; may also have fever, dehydration, weight loss
 try azithromycin
Cyclospora cayatanensis
1996 outbreak from contaminated raspberries
fluoresce blue under UV light
(Cyanobacterium-like body CLB)
disease similar to Cryptosporidium (up to 6 weeks)
Isospora belli
severe diarrhea in immunocompromised (AIDS) patients
trimethoprim + sulfamethoxazole
(invasion of small intestine mucosa destruction of brush border)
(Bactrim)
elliptical oocysts w/ 8 sporozoites
Microsporidia
severe, persistent, watery diarrhea in AIDS patients
albendazole
obligate intracellular replication
spores (spiral polar filaments)
Balantidium
diarrhea
large ciliated trophozoites or large
only ciliated protozoan
cysts w/ V-shaped nucleus in stool
main reservoir are domestic animals like pigs
Trichomonas vaginalis
watery, foul-smelling, greenish vaginal discharge w/ itching
pear-shaped motile trophozoites
on wet mount of vaginal secretions
pear-shaped w/ central nucleus and 4
and burning sensation
anterior flagella and undulating membrane
10% of men have urethritis (most are asymptomatic)
sexual contact (no cysts, only trophozoite)
metronidazole for both partners
very common cause of vaginitis may affect pregnancy
Naegleria fowleri
cysts (resistant to chlorine) and trophozoites
Acanthamoeba
cysts (resistant to chlorine) and trophozoites
Blood and Tissue Protozoa:
Malaria:
Plasmodium falciparum (common)
Plasmodium malariae (4%)
Plasmodium vivax (common)
Plasmodium ovale (very rare)
vector: female Anopheles mosquito
tropical, subtropical areas
300-500 million clinical cases/ year
1.5-2.7 million deaths (mostly children)
blacks w/ sickle cell more immune than whites
P. vivax, P. ovale, P. falciparum  48 hr. cycle
P. malariae 72 hr. cycle
schizogony: nuclear division w/o cell
division merozoites bud off from schizonts
P. vivax, P. ovale: hypnozoites latent in
liver reactivation
Toxoplasma gondii
cat feces w/ cysts eat undercooked pork
sexual reproduction in cats
transplacental transmission (TORCH)
infect any nucleated cell
most common CNS infection in AIDS patients
Pneumocystis carinii (classified as fungus)
mortality > 80% if untreated, 50% if treated
1st disease diagnosed in >50% of AIDS pts.
most people have been exposed
meningoencephalitis: just like bacterial meningitis
nausea/vomiting, fever, headache, stiff neck 95% die within 1 wk
chronic, granulomatous, brain infection in AIDS patients
keratitis: inflammation of cornea in contact lens wearers
 PMN,  protein,  glucose
amphotericin: poor results
 PMN,  protein,  glucose
amphotericin: poor results
asexual cycle/schizogony (in humans): sporozoites enter
humans during blood meal by mosquito enter hepatocytes within
30 minutes differentiate into schizonts rupture and release
merozoites into blood infect RBC’s differentiate into ringshaped trophozoites schizonts (16-32 nuclei) merozoites
sexual cycle/sporogony (in mosquitoes): some merozoites
develop into male and female gametocytes (one female
macrogamete or 8 sperm-like microgametes) diploid
zygote sporozoites salivary glands
thick and thin Giemsa stain of
blood smears: presence and ID
signet-ring trophozoites w/in
infected RBC’s
P. falciparum: crescent-shaped
gametocytes others: spherical
chloroquine: acute malaria kills
merozoites (in RBC’s)
primaquine: prevent relapses in P.
vivax, P. ovale by killing hypnozoites
mefloquine or (quinine +
Fansidar: sulfadoxine,
pyrimethamine) for chloroquineresistant strains of P. falciparum
chemoprophylaxis w/ chloroquine,
pyrimethamine bednets
avoid stagnant water
abrupt onset of fever/chills, headache, myalgia, arthralgia two
weeks after mosquito bite periodic cycle of chills, fevers, and
sweats (coincides w/ cycle between destruction of RBC’s)
fever spikes (up to 41 C) w/ splenomegaly, nausea/vomiting,
abdominal pain, and drenching sweat accompanying fever
brain/kidney involvement if P. falciparum untreated
hemolysis hemoglobiuria (dark urine = “blackwater fever”)
“sticky knobs” adhere and plug up capillaries brain necrosis
cell-mediated immunity
symptoms may resemble mononucleosis (heterophil-negative)
infection during pregnancy (new infection) abortion,
stillbirth, neonatal disease w/ encephalitis, chorioretinitis
(blindness), hepatosplenomegaly, fever, intracranial calcifications
IC: fatal encephalitis (reactivation of dormant cysts)
airborne inhalation (no person to person though)
sudden onset of fever, nonproductive cough, dyspnea,
tachypnea
cysts in alveoli: inflammation frothy exudate blocking gas
exchange
 no invasion of lung tissue
IF assay for IgM antibodies
crescent-shaped trophozoites in
Giemsa stain preps
sulfadiazine + pyrimethamine
pregnant should avoid emptying
litter boxes
Giemsa stain of lung smear:
trophozoites, intracystic bodies
(opposed comma-like particles)
bilateral rales and ronchi
TMP-SMZ or pentamidine
Trypanosoma cruzi (Chagas’ disease)
South and Central America
infected reduviid bug bites and defecates
trypomastigotes contained in feces enter host
bloodstream local replication in M and
infiltration chagoma
nonflagellated, round amastigotes w/in host
cells (myocardial, glial, reticuloendothelial)
Trypanosoma gambiense (Western Africa)
humans only (slower: kills in months-years)
Trypanosoma rhodesiense (Eastern Africa)
zoonotic (more severe: kills in weeks-months)
African Sleeping Sickness
painful bite of Tsetse fly
antigenic variation on surface glycoproteins
VSG: > 100 genes, but 1 expressed at a time
due to gene rearrangement
chagoma (Romana sign) near bite site: facial edema
(periorbital, perioral) + nodule
myocarditis/cardiomyopathy arrhythmia death
megasyndrome: megacolon, enlarged heart, enlarged esophagus
meningoencephalitis in AIDS patients
Leischmaniasis:
Leishmania donovani visceral leishmaniasis
attachment to M mediated by 2 molecules on parasite:
 1) gp 63 (glycoprotein)
2) LPG (lipophosphoglycan)
and several molecules on M C3 receptor, LFA1, p150,95
visceral leishmaniasis (Kala-azar): double peak (diurnal) fever,
hepato-splenomegaly, pancytopenia, immunosuppression,  IgG
 affect organs of reticuloendothelial system (liver, spleen, BM)
 hyperpigmentation of light-skinned patients
Leishmania tropica (Old World)cutaneous
Leishmania mexicana (New World)cutaneous
Leishmania braziliensis mucocutaneous
painless bite of sandfly
ingestion of amastigotes in M of host
amastigotes able to live at pH=4 (cytoplasm)
differentiate to promastigotes migrate to
pharynx of sandfly infect on next bite
reside in phagolysosome of M
reservoir: forest rodents
trypomastigotes multiple and differentiate into epimastigotes in
insect gut become trypomastigotes passed in insect feces
metacyclic trypomastigotes ingested in blood meal by tsetse fly
procyclic stage: multiplication in insect midgut migrates to
salivary glands transforms to epimastigotes multiply more and
forms metacyclic trypomastigotes carried by fly bite host
enter bloodstream and become blood-form trypomastigotes
hard, red painful skin ulcer: heals within 2 weeks
lymphadenopathy and intermittent weekly fever; dizziness
demyelinating encephalitis: daytime drowsiness, dysarthria,
muscle tremors, apathy coma and death (usu. from pneumonia)
cutaneous: initially, red papule at bite site enlarge satellite
nodules that coalsce & ulcerate Oriental sore, Chiclero’s ulcer
  in CMI large areas of skin affected (leprosy)
mucocutaneous: papule at bite site metastatic lesions at
mucocutaneous junction of nose-mouth destroy nasal cartilage
 death 2 to infection, starvation, aspiration pneumonia
blood smear trypomastigotes
xenodiagnosis: reduviid bug bites
host look for epimastigotes in gut
nifurtimox or benznidazole: kill
trypomastigotes in blood; less
effective against amastigotes in tissue
no effective therapy for chronic
disease
blood smear trypomastigotes
aspirate of chancre or enlarged
LN parasites
suramin: curative if given before
onset of encephalitis (does not cross
BBB no CNS penetration)
melarsoprol: extremely toxic but
used if CNS involvement
pentamidine: alternative drug
presence of amastigotes in skin
lesion or BM, spleen, LN biopsy
skin test (using leischmanin: crude
homogenate of promastigotes)
sodium stibogluconate
HELMINTHS (WORMS):
Cestodes: Tapeworms
Taenia solium (pork tapeworm)
ingestion of raw, cured, undercooked pork
containing larvae (cysticerci)
cysticercus: pea-sized fluid-filled bladder
scolex has 4 suckers and circle of hooks
attach to gut wall
worldwide, but endemic in Mexico, Latin
America, Spain, Portugal, Africa, SE Asia
Taenia saginata (beef tapeworm)
ingestion of raw or undercooked beef
containing larvae (cysticerci)
scolex had 4 suckers and NO hooklets
worldwide, but endemic in Africa, S. America,
Europe
Diphyllobothrum latum (fish tapeworm)
ingestion of undercooked fish containing
larvae (plerocercoid or sparganum larvae)
no suckers; 2 elongated suckling grooves
Scandinavia, Japan, northern Russia, Canada
Echinococcus granulosus (dog tapeworm)
ingestion of eggs by humans
dog=definitive host sheep=intermediate host
human=dead end intermediate hosts
sheep-raising areas: CA, AZ, NM, Alaska,
Canada, S. America, Africa, Mediterranean
scolex w/ hooks, but only 3 proglottids (one
of smallest tapeworm)
Hymenolepis nana (dwarf tapeworm: smallest)
most frequently found tapeworm in U.S.
Trematodes: Flukes
pig ingests egg-infested human feces eggs develop into larvae
that disseminate through intestine into muscle of animal and
develop into cysticercus uncooked pork with larvae eaten by
humans cysticercus attach to gut wall: anorexia, mild diarrhea
larvae take 3 months to grow to adult size (5 m)
ingestion of eggs cysticercosis: eggs hatch into larvae in gut
and penetrate into tissue and encyst usually asymptomatic until
larvae dies in 4-5 years inflammatory response: anaphylactic
shock, retinitis/uveitis, seizures, meningitis, death
cattle ingest gravid proglottids detached daily and passed in
human feces embryos (oncospheres) emerge from egg and
burrow into cow’s intestine larvae in muscle of cattle
larvae take 3 months to grow to adult size (10 m)
most are asymptomatic: anorexia and mild diarrhea
do not cause cysticercosis in humans
larvae attach to gut wall and become adult worms gravid
proglottids release fertilized eggs and passed in stool fresh water
eggs eaten by crustaceandifferentiate to larvae eaten by fish
most are asymptomatic: abdominal discomfort and diarrhea
absorb vitamin B12: megaloblastic anemia
1000’s of worms in dog’s intestineseggs passed out in feces
and contaminate environment and ingested by sheep (or humans)
oncosphere embryos emerge migrate to liver (or lungs, bones,
brain) large fluid-filled hyatid cysts
cyst rupture anaphyaxis
liver cyst hepatic dysfunction lung cyst bloody sputum
brain cyst headache, focal neurologic signs
no intermediate hosts: humans ingest eggs reinfect humans
abdominal discomfort and nausea/vomiting
gravid proglottids w/ 5-10 primary
uterine branches in stools
(T. saginata has 15-20 branches)
calcified cysticerci on CT scan
larvae floating in vitreous
niclosamide
praziquantel for cysticercosis
( Ca++ permeability paralyze
worm; Ab-mediated WBC killing)
gravid proglottids w/ 15-20
primary uterine branches in stools
niclosamide for intestinal worms
(uncouples oxidative phosphorylation
immobilizationexpulsion)
oval (other tapeworms are round)
eggs w/ lidlike opening (operculum)
longest tapeworm (up to 13 m)
niclosamide
brood capsules containing
multiple protoscoleces
CT scan and tissue biopsy
surgical removal of cysts
hypertonic saline kill organism
albendazole
niclosamide
8-10 polar filaments between hooks
praziquantel
Schistosomiasis (blood flukes):
S. mansoni (African, Middle East, S. America),
S. japonicum (Orients, water buffalo, pigs)
affect GI system (live in mesenteric veins)
in definitive venos site, female lays fertilized eggs penetrate
vascular endothelium enter gut or bladder lumen eggs
excreted in stools or urine hatch in fresh water ciliated larvae
penetrate snailsdevelop & multiplemany cercariae
S. haematobium (Africa, Middle East) affects
urinary tract (adults live in urinary bladder)
most pathologic findings from presence of eggs in liver, spleen,
or wall of the gut or bladder
acute phase: itching, dermatitis, fever/chills, diarrhea,
lymphadenopathy, hepatosplenomegaly, eosinophilia
free-swimming, fork-tailed cercariae
penetrate the skin  “Swimmer’s Itch”
adults exist as separate sexes but live attached
to each other: female resides in a groove in the
male, “the schist”, where he continously
fertilizes her egg
Clonorchi sinensis (Oriental liver fluke)
ingestion of undercooked fish w/ cercaria
snail is intermediate host (ingests eggs)
Paragonimus westermani (lung fluke)
ingestion of raw crab meat w/ larvae
penetrate GI wall migrate thru diaphragm
Fasciola hepatica (sheep liver fluke)
sheep and other domestic animals in Latin
America, Africa, Europe, and China
eating watercress (or other aquatic plants)
contaminated by larvae
Fasciolopsis buski (intestinal parasite of
hymans and pigs)
endemic to Asia, India
Heterophyes heterophyes
eating raw fish (Africa, Asia) w/ cysts
Nematodes (Intestinal): Roundworms
S. mansoni, S. japonicum: GI hemorrhage, hepatosplenomegaly
(eggs in liver granulomas fibrosis, hepatomegaly, portal
hypertension splenomegaly), death from exsanguination from
ruptured esophageal varices
S. haematobium: hematuria; superimposed bacterial UTI’s;
granulomas, fibrosis of bladder carcinoma of the bladder
excystation in duodenumenter biliary ducts bile duct
fibrosis/ hyperplasiabile duct carcinoma (cholangiocarcinoma)
upper abdominal pain, anorexia, hepatomegaly, eosinophilia
enters the lung parenchyma hermaphroditic adults produce
eggs that enter bronchioles chronic cough w/ bloody sputum
TB-like: pleuritic chest pain, dyspnea, recurrent bact. pneumonia
larva excyst in duodenum penetrate gut wall reach liver
RUQ pain, fever, hepatomegaly obstructive jaundice
halzoun: painful phayngitis from adult flukes on posterior
wall flukes acquired from eating raw sheep liver
eating aquatic vegetation carrying cysts
pathology due to damage of intestinal mucosa by adult fluke
most asymptomatic; may have ulceration, abscesses, hemorrhage
inflammation of intestinal epithelium: abdominal pain,
nonbloody diarrhea
molecular mimicry: incorporating
host antigens onto surface fool
host’s immune system
S. mansoni: prominent lateral spine
S. japonicum: small lateral spine
S. haematobium: terminal spine
praziquantel: initial exacerbation
of symptoms (death evokes vigorous
immune response)
typical small, brownish, operculated
eggs in stool
praziquantel
typical operculated eggs in sputum
or feces
praziquantel
praziquantel
surgically remove adult flukes in
pharynx and larynx
typical eggs found in feces
praziquantel
typical eggs found in feces
praziquantel
Enterobius vermicularis (pinworm)
ingestion or inhalation of worm eggs
most common helminth in U.S. (mostly
affects children < 12)
Trichuris trichiura (whipworm)
ingestion of eggs in soil contaminated w/ feces
slow life cycle (incubate 3-6 wks in soil)
Ascaris lumbricoides (largest intestinal: >25cm)
ingestion of eggs in soil contaminated w/ feces
very common (esp. in tropics, and southern
states in the U.S.)
major damage occurs during migration rather
than presence of adult worms in the intestine
Ancylostoma duodenale (Old World)
Necator americanus (New World hookworm)
filariform larva in moist soil penetrate skin
worlwide distribution, esp. tropical areas
endemic in southern states
major damage occurs during migration rather
than presence of adult worms in the intestine
Strongyloides stercoralis (small roundworm)
2 distinct life cycles:
1) w/in human body 2) free-living in soil
penetration of skin by infectious (filariform)
larvaemigration up trachea and swallowed
major damage occurs during migration rather
than presence of adult worms in the intestine
Trichinella spiralis
eating undercooked pork (U.S.: home-made
sausages) w/ larvae encysted in striated muscle
Nematodes (Tissue): Roundworms
lifecycle confined to humans: eggs hatch in small intestine,
where larvae differentiate to adults and migrate to colon and mate
female migrates to anus at night and releases 1000’s of eggs
majority: asymptomatic, some perianal pruritus
eggs hatch in GI migrate to cecum and ascending large
intestinemature adult produces 1000’s of eggs/day for 6-8 yrs
abdominal pain and diarrhea
larvae migrate through gut wall into bloodstream into the lungs
up bronchi and trachea and swallowed become adults in SI
live in lumen, does not attach to wall 1000’s of eggs/ day
ascariasis: pneumonia w/ fever, cough, and eosinophilia
adult worms can cause abdominal pain and obstruction
larvae carried by blood to lungsmigrate into alveoli and up
bronchi and trachea swallowed become adults in SI
attach to wall (cutting plates: Necator or teeth: Ancylostoma)
eggs develop 1st into noninfectious, feeding (rhabditiform) larvae
 then into 3rd stage, infectious, nonfeeding (filariform) larvae
”Ground itch”: pruritic papule or vesicle at entry site
loss of blood microcytic anemia (weakness and pallor)
larvae molt into adults in small intestine eggs hatch in mucosa
rhabditiform larvae passed in feces entire life cycle in soil
or filarial larvae, which penetrates intestinal wall directly w/o
leaving host and migrate to lungs (autoinfection)
pneuminitis w/ coughing and wheezing
if high worm burden female worms: inflammation of mucosa
hyperinfection ( damage) in immunocompromised: bloody,
watery diarrhea and sepsis from infiltration of enteric bacteria
gastroenteritis a few days after eating undercooked pork
1-2 weeks later: fever, muscle pain, periorbital edema,
eosinophilia
CNS, cardiac symptoms frequent
”Scotch tape” of perianal skin
eggs not found in stools
mebendazole or pyrantel pamoate
(only kill adult worms, not eggs)
may require retreatment
typical eggs (barrel-shaped w/ plugs
at each end) in stool
mebendazole
transient pulmonary infiltrates and
eosinophilia (Loeffler’s syndrome)
oval eggs with irregular surface in
stools; occasionally, adult worms
mebendazole or pyrantel pamoate
transient pulmonary infiltrates and
eosinophilia (Loeffler’s syndrome)
eggs in stool
occult blood in stool frequent
mebendazole or pyrantel pamoate
larvae in stool
striking eosinophilia (seen in all
migratory nematode infections)
thiabendazole or mebendazole
larvae w/in striated muscle
steroids plus mebendazole
(not very effective)
Wuchereria bancrofti (Pacific Islands, Africa)
Brugia malayi (Malay Peninsula, SE Asia)
female mosquito (Anopheles, Culex) bites and
deposits infective larva (L3) that penetrates skin
and enters lymph node
Onchocerca volvulus
female blackfly Simulium deposits infective
larvae while biting subcutaneous tissue
Loa loa
bite of deer fly Chrysops deposits infective
larva on skin wander in body become adults
Dracunculus
tiny crustaceans w/ infective larvae
swallowed in drinking water
Nematode Larvae Diseases:
Toxocara canis
major cause of visceral larva migrans
definitive host is dog; humans: dead-end hosts
young children (more likely to ingest soil)
Ancylostoma caninum (dog hookworm)
Ancylostoma braziliense (cat hookworm)
children, construction workers exposed to
infected soil (mainly southern U.S.)
Anisakis
ingested in raw seafood (sushi, sashimi)
After 1 year: mature to adults that produce microfilaria (L1)
circulate in blood (mainly at night) ingested by mosquito
microfilaria produce infective larva (L3) transferred w/ next bite
early: asymptomatic late: fever, lymphangitis, cellulitis
obstruction of lymphatics edema of legs and genitalia
(elephantiasis)
differentiate into adults, usually within dermal nodules
”river blindness” (infection rate > 80% in endemic areas)
disease: cellular immune response to death of microfilariae
females release microfilariae that enter blood (daytime)taken
up by fly during bloodmealdifferentiate to infective larvae….
thick blood smears from patient at
night reveal microfilariae
Calabar swellings: hypersensitivity rxn causing transient (2-3
days), localized, erythematous, subcutaneous edema
adult worm crawling across the conjuctiva (harmless)
larvae released in small intestine and migrate to body adults
adult females cause skin to ulcerate and release motile larvae
burning, itching inflamed papule w/ ulceration
diethylcarbamazine (microfilariae
only)
surgical excision of worms in eyes
head of worm in the skin ulcer:
worm looped out under the skin and
slowly pulled out over course of days
adult female in dog intestine produces eggs that are passed in
feces into the soil human ingest soil w/ eggs larvae in SI
migration to many organs (liver, brain, and eyes)
granulomas form around dead larva (delayed hypersensitivy)
blindness due to retinal involvement; fever, hepatomegaly
larvae penetrate skin and migrate through subcutaneous tissue
causing an inflammatory response prurutic lesions (“creeping
eruption”) similar eruptions w/ Strongyloides and Necator
eosinophilia (larval migration)
hypergammaglobulinemia
can penetrate submucosa of stomach or intestine
gastroenteritis, eosinophilia, and occult blood in stool
no effective drugs
diethylcarbamazine (against
microfilaria only paralyze)
ivermectin (microfilaria only 
GABAmuscle paralysis)
suramin (kills adults, but toxic)
visualization of microfilariae in a
blood smear
diethylcarbamazine
oral or topical thiabendazole