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 PATHOGENESIS / CLINICAL FEATURES DIAGNOSIS / TREATMENT
Superficial fungal infections (dead skin): cause pigment changes on surface of skin skin scrapings w/ KOH prep
lesions contain budding yeast cells and hyphae selenium dandruff shampoo
topical imidazole
Pityriasis (Tinea) versicolor (multi-colored) hypopigmented patches on the skin, especially on tanned skin in topical miconazole for Tinea
Malassezia furfur the summer ( with hot, humid weather); scaling, itching versicolor
Tinea nigra (black-colored) dark brown to black painless patches on palms and soles keratolytic agent: salicylic acid for
Cladosporium (Exophiala) werneckii found in soil and transmitted during injury (southern states) Tinea nigra

Dermatophytes: direct contact fomites skin scrapings w/ 10% KOH on

no yeast form glass slide shows hyphae
affect superficial keratinized structures animals: Microsporum also spread from dogs, cats macronidia or microconidia
(scaly skin, hair loss, and brittle nails) ”Dermatophytid” reactions: hypersensitivity to fungal antigens
through action of keratinase  no organisms found in granulomas ecothrix: hyphae around hair shaft
pruritic papules, vesicles endothrix: hyphae w/in hair shaft
Microsporum (spiky, spindle-shaped, tinea capitis: scaly calp, hair loss (T. tonsurans, T. rubrum)
thick-walled, single) tinea corporis: ringworm of glabrous/smooth skin red, raised Wood’s light: fluorescence when
Trichophyton (cylindral, smooth, thin- tinea cruris (jock itch): red itchy patches on groin, scrotum tinea capitis lesions caused by
walled, single) tinea pedis (athlete’s foot): toescracking, peeling of skin Microsporum placed in UV light
Epidermophyton (club-shaped, smooth tinea unguium (“onchomycosis”): thickened, discolored, brittle nails topical imidazole
moderately thick-walled, clusters of 2-3) tinea barbae: patches along beard distribution oral griseolfulvin (hair, nails)

Subcutaneous Mycoses: grow in soil, vegetation infect during trauma

Sporotrichosis: Sporotrix schenckii subcutaneous nodule: local pustule or ulcer that spreads along cigar-shaped budding yeasts
dimorphic fungi in soil, plants (rose lymphatics more necrotic nodules along linear, lymphatic distribution branching hyphae w/ oval conidia
thorns, splinters) enters via trauma at tips “daisy petals”
oral KI
itraconazole or amphotericin B
Chromoblastomycosis slowly progessive granulomatous infection through skin trauma copper-colored sclerotic bodies:
(Phialophora, Cladosporium) cauliflower warts w/ crusting abscess along lymphatics: initially, dark brown, funus in WBC’s, M
soil fungi in tropics: bare feet and legs one violet-colored wartlike lesion more nodules over months/years local excision/ itraconazole
Mycetoma (Petriellidium, Madurella) abscesses, with pus discharged through sinuses (pus has compact sulfonamides: actinomycotic form
wounds on feet, hands, or back colored granules similar to Actinomyces, Nocardia lesions no treatment for fungal form

SYSTEMIC FUNGI:
within lungs differentiate into yeasts mostly asymptomatic or mild pneumonia not contagious from person to person
itraconazole for lung disease amphotericin B for severe , disseminated disease
Coccidiodes immitis in soil, it forms hyphae with alternating arthrospores and tissue: spherules w/ doubly
dimorphic (mold, spherule w/ endospores) empty cells inhalation of arthrospores by humans refractive walls filled w/ endospores
soil of arid regions: southwestern USA, Latin
America (Arizona, New Mexico, southern CA) dissemination in IC: meningitis; bone and skin granulomas skin tests (spherulin or
Filipinos erythema nodosum (red tender nodules on extensor surfaces) cocciodin) DTH rxn
2nd most common opportunistic infection in and arthralgia “valley fever” (San Joaquin Valley, CA.) or IgM/ IgG precipitin test
AIDS patients “desert rheumatism” (Arizona)
Histoplasma capsulatum (nonencapsulated) 2 types of asexual spores: tuberculate macroconidia (thick tissue: oval budding yeast cells
dimorphic (mold, yeast) walled w/ fingerlike projections lab ID) and inhaled, infectious found in M
faculatative intracellular parasite microconidia (smaller, thin, smooth-walled spores) skin tests (histoplasmin)
soil w/ bird droppings (ie. Starlings, bats) calcification of small granulomatous foci in lungs/ spleen  DTH rxn
Ohio, Mississippi River Valleys AIDS pts: liver, spleen, and lymph nodes: hepatosplenomegaly complement fixation
chest X-ray (TB)
Blastomyces dermatitidis inhaled ovid conidia tissue: thin-walled round yeast
dimorphic (mold, yeast) also infects other animals (dogs) cells w/ single broad-based buds
moist soil rich in organic material rarest systemic fungal infection but also most severe and and doubly refractive walls
North America (east of Mississippi) and rarely asymptomatic
Central America worldwide ulcerated granulomas of skin, bone w/ weight loss, night sweats
Paracoccidiodes brasiliensis inhaled spores tissue: thick-walled with multiple
endemic to rural Latin America buds

OPPORTUNISTIC FUNGI:
diabetes, lymphomas, broad spectrum antibiotics, immunosuppression (chemotherapy, AIDS pts)
Candida albicans oral thrush (creamy white patches) C. albicans: germ tube test at
oval yeast w/ single bud; blastoconidium diaper rash (skin folds: between fingers, groin) 37 C X 3hrs. and chlamydospores
budding yeast cells and pseudohyphae vaginitis: vaginal itching and discharge ( risk during menses oral thrush: ”swish and swallow”
and pregnancy, oral contraceptives, antibiotics, DM,  pH) nystatin
normal flora of mucous membranes of upper IC: esophagitis (substernal chest pain and dysphagia) vaginitis: imidazole suppositories
respiratory, GI, and female genital tracts dissemination (retinal exam shows multiple white fluffy candidal amphotericin B (dissem. disease)
normal flora, but never in blood patches) sign of neutropenia skin test w/ Candida: indicator of
competent cellular immunity
Cryptococcus neoformans inhaled through lungs mostly asymptomatic India ink: halo around organism
oval budding yeast (no mold form) meningitis pneumonia; bone and skin granulomas CSF: Ab to capsular antigen
pigeon droppings eucalyptus tree 4th cause of death in AIDS pts flucytosine or amphotericin B
Aspergillus fumigatus aspergilloma dissemination: skin, CNS, heart, lung, nasa-orbital area, cornea flat, velvety, bluish-green colony
mold only: septate hyphae V-shaped fungus ball on chest X-ray
airborne conidia (inhaled, ingested, cut skin) AIDS: hemoptysis and granulomas (lung cavitations) surgical removal, amphotericin B
A. flavus on rice/grains mycotoxins (ie. allergic bronchopulmonary aspergillosis: type I
aflatoxin) toxic or carcinogenic to liver  hypersensitivity reaction (IgE) resembling asthma
hepatocellular carcinoma
Mucormycosis (Mycor, Rhizopus) rhinocerebral mucormycosis: associated with diabetes endospores enclosed w/in a
saprophytic molds only: nonseptate hyphae infection of nasal mucosa w/ invasion of sinuses and orbit sporangium
(root branches) w/ broad irregular walls and molds proliferate in walls of blood vessels (telangiectasia) surgical resection
right-angle branches 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 cytoplasm
motile amoeba (trophozoite) necrosis “teardrop” ulcer erode and destroy intestines  active disease
ingestion of nonmotile cyst (4 nuclei) amoebic dysentery: bloody, mucus-containing diarrhea w/ lower cysts or trophozoites w/o
differentiates into trophozoites in the ileum abdominal discomfort, flatulence, tenesmus, weight loss internalized RBC carrier state
1 cyst=8 trophozoites colonize colon, cecum amoebic abscess of liver: RUQ pain, weight loss, fever, tender, diloxanide furoate to kill cysts
trophozoites (single nucleus) in diarrheal stool enlarged liver can penetrate diaphragm and cause lung disease (luminal amebicide)
cysts in formed stool E. coli: 8 nuclei E. hartmani: 4 nuclei also, but smaller metronidazole (Flagyl): luminal
1-2% of U.S. population (homosexual males) E. dispar: nonpathogenetic and systemic amebicide
Giardia lamblia cysts differentiate to trophozoites in duodenum filter water: chlorination does not
ingestion of cysts (4 nuclei) no invasion: attachment to duodenal wall (surface of villi) kill; must boil and filter
1 cyst = 2 trophozoites (pear-shaped w/ 4 inflammation of mucosa malabsorption of protein, fat string test: swallowing string into
pairs of external flagella w/ 2 anterior nuclei) nonbloody, foul-smelling diarrhea w/ nausea, anorexia, duodenum trophozoites adhering
camping, day-care centers, homosexuals flatulence, and abdominal cramps for weeks to months; no fever metronidazole (Flagyl)
Cryptosporidium parvum mild diarrhea attach to jejunum (no invasion) acid-fast stain (modified Kinyoun
oocysts release sporozoites, which form infants and AIDS patients: chronic, watery, nonbloody acid-fast stain) oocysts in feces
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
elliptical oocysts w/ 8 sporozoites (invasion of small intestine mucosa destruction of brush border) (Bactrim)
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 main reservoir are domestic animals like pigs cysts w/ V-shaped nucleus in stool
Trichomonas vaginalis watery, foul-smelling, greenish vaginal discharge w/ itching pear-shaped motile trophozoites
pear-shaped w/ central nucleus and 4 and burning sensation on wet mount of vaginal secretions
anterior flagella and undulating membrane 10% of men have urethritis (most are asymptomatic)
sexual contact (no cysts, only trophozoite) very common cause of vaginitis may affect pregnancy metronidazole for both partners
Naegleria fowleri meningoencephalitis: just like bacterial meningitis  PMN,  protein,  glucose
cysts (resistant to chlorine) and trophozoites nausea/vomiting, fever, headache, stiff neck 95% die within 1 wk amphotericin: poor results
Acanthamoeba chronic, granulomatous, brain infection in AIDS patients  PMN,  protein,  glucose
cysts (resistant to chlorine) and trophozoites keratitis: inflammation of cornea in contact lens wearers amphotericin: poor results
Blood and Tissue Protozoa:
Malaria: asexual cycle/schizogony (in humans): sporozoites enter thick and thin Giemsa stain of
humans during blood meal by mosquito enter hepatocytes within blood smears: presence and ID
Plasmodium falciparum (common) 30 minutes differentiate into schizonts rupture and release signet-ring trophozoites w/in
Plasmodium malariae (4%) merozoites into blood infect RBC’s differentiate into ring- infected RBC’s
Plasmodium vivax (common) shaped trophozoites schizonts (16-32 nuclei) merozoites P. falciparum: crescent-shaped
Plasmodium ovale (very rare) sexual cycle/sporogony (in mosquitoes): some merozoites gametocytes others: spherical
vector: female Anopheles mosquito develop into male and female gametocytes (one female chloroquine: acute malaria kills
tropical, subtropical areas macrogamete or 8 sperm-like microgametes) diploid zygote merozoites (in RBC’s)
300-500 million clinical cases/ year sporozoites salivary glands primaquine: prevent relapses in P.
1.5-2.7 million deaths (mostly children) vivax, P. ovale by killing hypnozoites
blacks w/ sickle cell more immune than whites abrupt onset of fever/chills, headache, myalgia, arthralgia two mefloquine or (quinine + Fansidar:
P. vivax, P. ovale, P. falciparum  48 hr. cycle weeks after mosquito bite periodic cycle of chills, fevers, and sulfadoxine, pyrimethamine) for
P. malariae 72 hr. cycle sweats (coincides w/ cycle between destruction of RBC’s) chloroquine-resistant strains of P.
fever spikes (up to 41 C) w/ splenomegaly, nausea/vomiting, falciparum
schizogony: nuclear division w/o cell abdominal pain, and drenching sweat accompanying fever chemoprophylaxis w/ chloroquine,
division merozoites bud off from schizonts brain/kidney involvement if P. falciparum untreated pyrimethamine bednets
P. vivax, P. ovale: hypnozoites latent in hemolysis hemoglobiuria (dark urine = “blackwater fever”) avoid stagnant water
liver reactivation “sticky knobs” adhere and plug up capillaries brain necrosis
Toxoplasma gondii cell-mediated immunity IF assay for IgM antibodies
cat feces w/ cysts eat undercooked pork symptoms may resemble mononucleosis (heterophil-negative) crescent-shaped trophozoites in
sexual reproduction in cats infection during pregnancy (new infection) abortion, Giemsa stain preps
transplacental transmission (TORCH) stillbirth, neonatal disease w/ encephalitis, chorioretinitis sulfadiazine + pyrimethamine
infect any nucleated cell (blindness), hepatosplenomegaly, fever, intracranial calcifications pregnant should avoid emptying
most common CNS infection in AIDS patients IC: fatal encephalitis (reactivation of dormant cysts) litter boxes
Pneumocystis carinii (classified as fungus) airborne inhalation (no person to person though) Giemsa stain of lung smear:
mortality > 80% if untreated, 50% if treated sudden onset of fever, nonproductive cough, dyspnea, trophozoites, intracystic bodies
1st disease diagnosed in >50% of AIDS pts. tachypnea (opposed comma-like particles)
most people have been exposed cysts in alveoli: inflammation frothy exudate blocking gas bilateral rales and ronchi
exchange  no invasion of lung tissue TMP-SMZ or pentamidine
Trypanosoma cruzi (Chagas’ disease) chagoma (Romana sign) near bite site: facial edema blood smear trypomastigotes
South and Central America (periorbital, perioral) + nodule xenodiagnosis: reduviid bug bites
infected reduviid bug bites and defecates myocarditis/cardiomyopathy arrhythmia death host look for epimastigotes in gut
trypomastigotes contained in feces enter host megasyndrome: megacolon, enlarged heart, enlarged esophagus nifurtimox or benznidazole: kill
bloodstream local replication in M and meningoencephalitis in AIDS patients trypomastigotes in blood; less
infiltration chagoma effective against amastigotes in tissue
nonflagellated, round amastigotes w/in host trypomastigotes multiple and differentiate into epimastigotes in no effective therapy for chronic
cells (myocardial, glial, reticuloendothelial) insect gut become trypomastigotes passed in insect feces disease
Trypanosoma gambiense (Western Africa) metacyclic trypomastigotes ingested in blood meal by tsetse fly blood smear trypomastigotes
humans only (slower: kills in months-years) procyclic stage: multiplication in insect midgut migrates to aspirate of chancre or enlarged
Trypanosoma rhodesiense (Eastern Africa) salivary glands transforms to epimastigotes multiply more and LN parasites
zoonotic (more severe: kills in weeks-months) forms metacyclic trypomastigotes carried by fly bite host suramin: curative if given before
African Sleeping Sickness enter bloodstream and become blood-form trypomastigotes onset of encephalitis (does not cross
painful bite of Tsetse fly hard, red painful skin ulcer: heals within 2 weeks BBB no CNS penetration)
antigenic variation on surface glycoproteins lymphadenopathy and intermittent weekly fever; dizziness melarsoprol: extremely toxic but
VSG: > 100 genes, but 1 expressed at a time demyelinating encephalitis: daytime drowsiness, dysarthria, used if CNS involvement
due to gene rearrangement muscle tremors, apathy coma and death (usu. from pneumonia) pentamidine: alternative drug

Leischmaniasis: attachment to M mediated by 2 molecules on parasite: presence of amastigotes in skin

Leishmania donovani visceral leishmaniasis  1) gp 63 (glycoprotein) 2) LPG (lipophosphoglycan) lesion or BM, spleen, LN biopsy
and several molecules on M C3 receptor, LFA1, p150,95
Leishmania tropica (Old World)cutaneous visceral leishmaniasis (Kala-azar): double peak (diurnal) fever, skin test (using leischmanin: crude
Leishmania mexicana (New World)cutaneous hepato-splenomegaly, pancytopenia, immunosuppression,  IgG homogenate of promastigotes)
 affect organs of reticuloendothelial system (liver, spleen, BM)
Leishmania braziliensis mucocutaneous  hyperpigmentation of light-skinned patients sodium stibogluconate

painless bite of sandfly cutaneous: initially, red papule at bite site enlarge satellite
ingestion of amastigotes in M of host nodules that coalsce & ulcerate Oriental sore, Chiclero’s ulcer
amastigotes able to live at pH=4 (cytoplasm)   in CMI large areas of skin affected (leprosy)
differentiate to promastigotes migrate to
pharynx of sandfly infect on next bite mucocutaneous: papule at bite site metastatic lesions at
reside in phagolysosome of M mucocutaneous junction of nose-mouth destroy nasal cartilage
reservoir: forest rodents  death 2 to infection, starvation, aspiration pneumonia
HELMINTHS (WORMS):
Cestodes: Tapeworms
Taenia solium (pork tapeworm) pig ingests egg-infested human feces eggs develop into larvae gravid proglottids w/ 5-10 primary
ingestion of raw, cured, undercooked pork that disseminate through intestine into muscle of animal and uterine branches in stools
containing larvae (cysticerci) develop into cysticercus uncooked pork with larvae eaten by (T. saginata has 15-20 branches)
cysticercus: pea-sized fluid-filled bladder humans cysticercus attach to gut wall: anorexia, mild diarrhea calcified cysticerci on CT scan
scolex has 4 suckers and circle of hooks larvae take 3 months to grow to adult size (5 m) larvae floating in vitreous
attach to gut wall ingestion of eggs cysticercosis: eggs hatch into larvae in gut niclosamide
and penetrate into tissue and encyst usually asymptomatic until praziquantel for cysticercosis
worldwide, but endemic in Mexico, Latin larvae dies in 4-5 years inflammatory response: anaphylactic ( Ca++ permeability paralyze
America, Spain, Portugal, Africa, SE Asia shock, retinitis/uveitis, seizures, meningitis, death worm; Ab-mediated WBC killing)
Taenia saginata (beef tapeworm) cattle ingest gravid proglottids detached daily and passed in gravid proglottids w/ 15-20
ingestion of raw or undercooked beef human feces embryos (oncospheres) emerge from egg and primary uterine branches in stools
containing larvae (cysticerci) burrow into cow’s intestine larvae in muscle of cattle
scolex had 4 suckers and NO hooklets larvae take 3 months to grow to adult size (10 m) niclosamide for intestinal worms
worldwide, but endemic in Africa, S. America, most are asymptomatic: anorexia and mild diarrhea (uncouples oxidative phosphorylation
Europe do not cause cysticercosis in humans immobilizationexpulsion)
Diphyllobothrum latum (fish tapeworm) larvae attach to gut wall and become adult worms gravid oval (other tapeworms are round)
ingestion of undercooked fish containing proglottids release fertilized eggs and passed in stool fresh water eggs w/ lidlike opening (operculum)
larvae (plerocercoid or sparganum larvae) eggs eaten by crustaceandifferentiate to larvae eaten by fish longest tapeworm (up to 13 m)
no suckers; 2 elongated suckling grooves most are asymptomatic: abdominal discomfort and diarrhea
Scandinavia, Japan, northern Russia, Canada absorb vitamin B12: megaloblastic anemia niclosamide
Echinococcus granulosus (dog tapeworm) 1000’s of worms in dog’s intestineseggs passed out in feces brood capsules containing
ingestion of eggs by humans and contaminate environment and ingested by sheep (or humans) multiple protoscoleces
dog=definitive host sheep=intermediate host oncosphere embryos emerge migrate to liver (or lungs, bones, CT scan and tissue biopsy
human=dead end intermediate hosts brain) large fluid-filled hyatid cysts surgical removal of cysts
sheep-raising areas: CA, AZ, NM, Alaska, cyst rupture anaphyaxis hypertonic saline kill organism
Canada, S. America, Africa, Mediterranean liver cyst hepatic dysfunction lung cyst bloody sputum
scolex w/ hooks, but only 3 proglottids (one brain cyst headache, focal neurologic signs albendazole
of smallest tapeworm) niclosamide
Hymenolepis nana (dwarf tapeworm: smallest) no intermediate hosts: humans ingest eggs reinfect humans 8-10 polar filaments between hooks
most frequently found tapeworm in U.S. abdominal discomfort and nausea/vomiting praziquantel
Trematodes: Flukes
Schistosomiasis (blood flukes): in definitive venos site, female lays fertilized eggs penetrate molecular mimicry: incorporating
S. mansoni (African, Middle East, S. America), vascular endothelium enter gut or bladder lumen eggs host antigens onto surface fool
S. japonicum (Orients, water buffalo, pigs) excreted in stools or urine hatch in fresh water ciliated larvae host’s immune system
affect GI system (live in mesenteric veins) penetrate snailsdevelop & multiplemany cercariae
S. mansoni: prominent lateral spine
S. haematobium (Africa, Middle East) affects most pathologic findings from presence of eggs in liver, spleen, or S. japonicum: small lateral spine
urinary tract (adults live in urinary bladder) wall of the gut or bladder S. haematobium: terminal spine
acute phase: itching, dermatitis, fever/chills, diarrhea,
free-swimming, fork-tailed cercariae penetrate lymphadenopathy, hepatosplenomegaly, eosinophilia praziquantel: initial exacerbation
the skin  “Swimmer’s Itch” of symptoms (death evokes vigorous
 S. mansoni, S. japonicum: GI hemorrhage, hepatosplenomegaly immune response)
adults exist as separate sexes but live attached (eggs in liver granulomas fibrosis, hepatomegaly, portal
to each other: female resides in a groove in the hypertension splenomegaly), death from exsanguination from
male, “the schist”, where he continously ruptured esophageal varices
fertilizes her egg
S. haematobium: hematuria; superimposed bacterial UTI’s;
granulomas, fibrosis of bladder carcinoma of the bladder
Clonorchi sinensis (Oriental liver fluke) excystation in duodenumenter biliary ducts bile duct typical small, brownish, operculated
ingestion of undercooked fish w/ cercaria fibrosis/ hyperplasiabile duct carcinoma (cholangiocarcinoma) eggs in stool
snail is intermediate host (ingests eggs) upper abdominal pain, anorexia, hepatomegaly, eosinophilia praziquantel
Paragonimus westermani (lung fluke) enters the lung parenchyma hermaphroditic adults produce typical operculated eggs in sputum
ingestion of raw crab meat w/ larvae eggs that enter bronchioles chronic cough w/ bloody sputum or feces
penetrate GI wall migrate thru diaphragm TB-like: pleuritic chest pain, dyspnea, recurrent bact. pneumonia praziquantel
Fasciola hepatica (sheep liver fluke) larva excyst in duodenum penetrate gut wall reach liver praziquantel
sheep and other domestic animals in Latin RUQ pain, fever, hepatomegaly obstructive jaundice
America, Africa, Europe, and China halzoun: painful phayngitis from adult flukes on posterior wall surgically remove adult flukes in
eating watercress (or other aquatic plants) flukes acquired from eating raw sheep liver pharynx and larynx
contaminated by larvae
Fasciolopsis buski (intestinal parasite of eating aquatic vegetation carrying cysts typical eggs found in feces
hymans and pigs) pathology due to damage of intestinal mucosa by adult fluke praziquantel
endemic to Asia, India most asymptomatic; may have ulceration, abscesses, hemorrhage
Heterophyes heterophyes inflammation of intestinal epithelium: abdominal pain, typical eggs found in feces
eating raw fish (Africa, Asia) w/ cysts nonbloody diarrhea praziquantel
Nematodes (Intestinal): Roundworms
Enterobius vermicularis (pinworm) lifecycle confined to humans: eggs hatch in small intestine, ”Scotch tape” of perianal skin
ingestion or inhalation of worm eggs where larvae differentiate to adults and migrate to colon and mate eggs not found in stools
most common helminth in U.S. (mostly female migrates to anus at night and releases 1000’s of eggs mebendazole or pyrantel pamoate
affects children < 12) (only kill adult worms, not eggs)
majority: asymptomatic, some perianal pruritus may require retreatment
Trichuris trichiura (whipworm) eggs hatch in GI migrate to cecum and ascending large typical eggs (barrel-shaped w/ plugs
ingestion of eggs in soil contaminated w/ feces intestinemature adult produces 1000’s of eggs/day for 6-8 yrs at each end) in stool
slow life cycle (incubate 3-6 wks in soil) abdominal pain and diarrhea mebendazole
Ascaris lumbricoides (largest intestinal: >25cm) larvae migrate through gut wall into bloodstream into the lungs transient pulmonary infiltrates and
ingestion of eggs in soil contaminated w/ feces up bronchi and trachea and swallowed become adults in SI eosinophilia (Loeffler’s syndrome)
very common (esp. in tropics, and southern live in lumen, does not attach to wall 1000’s of eggs/ day oval eggs with irregular surface in
states in the U.S.) stools; occasionally, adult worms
major damage occurs during migration rather ascariasis: pneumonia w/ fever, cough, and eosinophilia
than presence of adult worms in the intestine adult worms can cause abdominal pain and obstruction mebendazole or pyrantel pamoate
Ancylostoma duodenale (Old World) larvae carried by blood to lungsmigrate into alveoli and up transient pulmonary infiltrates and
Necator americanus (New World hookworm) bronchi and trachea swallowed become adults in SI eosinophilia (Loeffler’s syndrome)
filariform larva in moist soil penetrate skin attach to wall (cutting plates: Necator or teeth: Ancylostoma) eggs in stool
worlwide distribution, esp. tropical areas eggs develop 1st into noninfectious, feeding (rhabditiform) larvae occult blood in stool frequent
endemic in southern states  then into 3rd stage, infectious, nonfeeding (filariform) larvae
major damage occurs during migration rather ”Ground itch”: pruritic papule or vesicle at entry site mebendazole or pyrantel pamoate
than presence of adult worms in the intestine loss of blood microcytic anemia (weakness and pallor)
Strongyloides stercoralis (small roundworm) larvae molt into adults in small intestine eggs hatch in mucosa larvae in stool
2 distinct life cycles: rhabditiform larvae passed in feces entire life cycle in soil striking eosinophilia (seen in all
1) w/in human body 2) free-living in soil or filarial larvae, which penetrates intestinal wall directly w/o migratory nematode infections)
penetration of skin by infectious (filariform) leaving host and migrate to lungs (autoinfection)
larvaemigration up trachea and swallowed pneuminitis w/ coughing and wheezing thiabendazole or mebendazole
major damage occurs during migration rather if high worm burden female worms: inflammation of mucosa
than presence of adult worms in the intestine hyperinfection ( damage) in immunocompromised: bloody,
watery diarrhea and sepsis from infiltration of enteric bacteria
Trichinella spiralis gastroenteritis a few days after eating undercooked pork larvae w/in striated muscle
eating undercooked pork (U.S.: home-made 1-2 weeks later: fever, muscle pain, periorbital edema, steroids plus mebendazole
sausages) w/ larvae encysted in striated muscle eosinophilia CNS, cardiac symptoms frequent (not very effective)

Nematodes (Tissue): Roundworms

Wuchereria bancrofti (Pacific Islands, Africa) After 1 year: mature to adults that produce microfilaria (L1) thick blood smears from patient at
Brugia malayi (Malay Peninsula, SE Asia) circulate in blood (mainly at night) ingested by mosquito night reveal microfilariae
female mosquito (Anopheles, Culex) bites and microfilaria produce infective larva (L3) transferred w/ next bite
deposits infective larva (L3) that penetrates skin early: asymptomatic late: fever, lymphangitis, cellulitis diethylcarbamazine (against
and enters lymph node obstruction of lymphatics edema of legs and genitalia microfilaria only paralyze)
(elephantiasis)
Onchocerca volvulus differentiate into adults, usually within dermal nodules ivermectin (microfilaria only 
female blackfly Simulium deposits infective ”river blindness” (infection rate > 80% in endemic areas) GABAmuscle paralysis)
larvae while biting subcutaneous tissue disease: cellular immune response to death of microfilariae suramin (kills adults, but toxic)
Loa loa females release microfilariae that enter blood (daytime)taken up visualization of microfilariae in a
bite of deer fly Chrysops deposits infective by fly during bloodmealdifferentiate to infective larvae…. blood smear
larva on skin wander in body become adults
Calabar swellings: hypersensitivity rxn causing transient (2-3 diethylcarbamazine (microfilariae
days), localized, erythematous, subcutaneous edema only)
 adult worm crawling across the conjuctiva (harmless) surgical excision of worms in eyes
Dracunculus larvae released in small intestine and migrate to body adults head of worm in the skin ulcer:
tiny crustaceans w/ infective larvae adult females cause skin to ulcerate and release motile larvae worm looped out under the skin and
swallowed in drinking water burning, itching inflamed papule w/ ulceration slowly pulled out over course of days
Nematode Larvae Diseases:
Toxocara canis adult female in dog intestine produces eggs that are passed in eosinophilia (larval migration)
major cause of visceral larva migrans feces into the soil human ingest soil w/ eggs larvae in SI hypergammaglobulinemia
definitive host is dog; humans: dead-end hosts migration to many organs (liver, brain, and eyes)
young children (more likely to ingest soil) granulomas form around dead larva (delayed hypersensitivy) diethylcarbamazine
blindness due to retinal involvement; fever, hepatomegaly
Ancylostoma caninum (dog hookworm) larvae penetrate skin and migrate through subcutaneous tissue oral or topical thiabendazole
Ancylostoma braziliense (cat hookworm) causing an inflammatory response prurutic lesions (“creeping
children, construction workers exposed to eruption”) similar eruptions w/ Strongyloides and Necator
infected soil (mainly southern U.S.)
Anisakis can penetrate submucosa of stomach or intestine no effective drugs
ingested in raw seafood (sushi, sashimi) gastroenteritis, eosinophilia, and occult blood in stool