Entamoeba histolytica

Giardia lamblia
(aka "G. duodenalis" or "G. intestinalis")
Cryptosporidium parvum
( aka C. hominis, C. felis, C muris, C. meleagridis )
Other Intestinal Protozoa
Epidemiology
Worldwide
1-2% asymptomatic in U.S
Worldwide.
Warm climate (as with most parasites)
Reportable to CDC
High incidence in AIDS patients
Most common in Children <5 years old
Transmission
Fecal/ oral via contaminated water/ food
Anal-oral sexual contact
Daycares, Hospitals, Prisons
Fecal/ oral via contaminated water/ food
Anal-oral sexual contact
Daycares, Hospitals, Prisons
Resists chlorine/ ozone used in water treatment plants
-Plants must have filtration step
Fecal/ oral via contaminated water/ food
Anal-oral sexual contact
Daycares, Hospitals, Prisons
Resists chlorine/ ozone used in water treatment
plants
-Plants must have filtration step
Pathology
Localized necrosis of large intestine due to cytotoxins
Infiltration of immune cells to ulcer site can lead to formation of palpable
masses (amebomas)- sometimes mistaken as intestinal carcinomas
Limited tissue destruction
Reduced absorption due to epithelial turnover
Moves via flagella
Mild & self-limiting in normal people
50% mortality in AIDS patients
Symptoms

Amebic Dysentery/ Colitis
Diarrhea
Bloody stool
Cramping & Abdominal pain
(No fever strictly intestinal)
Extraintestinal amebiasis (M > F adults)
Necrosis can provide route to blood stream
Liver abscess formation is common******
Fever, hepatomegaly, leukocytosis
Giardiasis
Mostly Asymptomatic
(Symptoms 1-3 weeks after exposure)
Malodorous, watery diarrhea
Abdominal distension & Cramps
Epigastric pain.
Low-grade fever
In severe cases:
Significant weight loss due to malabsorption
Symptomatic infections common in children
Death is extremely rare
Cryptosporidiosis
Mostly symptomatic >80%
(Symptoms 1 week after exposure)
Profuse watery diarrhea & cramps for ~2 weeks
Rare: Fever, Nausea, anorexia
Severe in immunocompromised (AIDS)****
Up to 50 large volume stools per day for months
Dehydration can be life-threatening
Infectious Form
Cysts in water
(circular w/ 1- 4 nuclei)
Cysts in water Oocysts in water
Intestinal Protozoa
Isospora belli / Cyclospora cayetanensis
Similar to Cryptosporidium in all ways
Increasing # of infections in AIDS patients
Diagnosis via Modified Acid-fast stain of Cysts
Treatment: SMX-TMP
-More receptive to treatment than crypto
Isospora is larger & more oblong
Cyclospora is also larger than cryptosporidium
Balantidium coli
Only ciliate pathogen of humans, rare in U.S.
Pigs are reservoir
Fecal oral-route- contamination w/ pig feces
Balantidiasis
Symptoms resemble those of amebiasis
Detect cyst or trophozoites in stool
Cysts are large and round with a dark, crescent
macronucleus visible
Trophozoites are even larger
Treatment: Tetracycline, Metronidazole,
Iodoquinol
Diagnosis
Microscopic detection: Cysts**** or trophozites in feces
-Tropozoite:
--> Rounded w/ a single dark nucleus (looks like an eye)
--> slowly motile in wet mounts of fresh stool, but destroyed by
preservatives
-Cysts:
--> Round
--> more stable in stained & preserved samples
--> best with iodine stains
EIA kits: commercially available for extraintestinal disease
Liver biopsy: extraintestinal spread
Endoscopy
Microscopic detection: Cysts**** or trophozites in feces
-Tropozoite:
--> Round to oval-shaped
--> stain TURQUOISE to GREY using Giemsa, trichrom, or Fe-hematoxylin
or saline-diluted wet mounts
-Cysts:
--> Oval
--> GREY with most stains
--> best with iodine stains
Fluorescently-conjugate Ab kits: commercially available
Duodenal aspirates: may detect flagellated trophozoites
Unlike other intestinals: DON'T stain well****
Modified acid-fast stain
Treatment
**Metronidazole or tinidazole**
-For both types of disease
-Not effective for carriers
-Can't give to pregnant women
Iodoquinol or paromycin
(for asymptomatic carriers)
-Paromomycin best for pregnant women, but NOT effective vs. invasice
dz
**Metronidazole or tinidazole**
-Can't give to pregnant women
Paromycin
-Best for pregnant women, but NOT effective vs. invasice dz
Nitazoxanide for kids??
Rehydration, supportive measures
Nitazoxanide for immunocompetent
Notes
Commensals Amoebas not involved in pathology:
E. dispar
-Morphologically indistinguishable from E. histolyticum
-Differentiate by Fecal Ag test or nucleic acid hybridization
Entamoeba coli (not to be confused with bacterial E.coli)
E. gigivalis
E. hartmanni
Isospora belli / Cyclospora cayetanensis
Similar to Cryptosporidium in all ways
Increasing # of infections in AIDS patients
Diagnosis via Modified Acid-fast stain of Cysts
Treatment: SMX-TMP
-More receptive to treatment than crypto
Isospora is larger & more oblong
Cyclospora is also larger than cryptosporidium
Balantidium coli
Only ciliate pathogen of humans, rare in U.S.
Pigs are reservoir
Fecal oral-route- contamination w/ pig feces
Balantidiasis
Symptoms resemble those of amebiasis
Detect cyst or trophozoites in stool
Cysts are large and round with a dark, crescent
macronucleus visible
Trophozoites are even larger
Treatment: Tetracycline, Metronidazole,
Iodoquinol
Trichomonas vaginalis Toxoplasma gondii
Naegleria fowleri,
Acanthamoeba spp.
Epidemiology
2-3 million cases per year in the U.S.
Carriage:
-F: 5-20%; M: 2-10%
Very common (many exposed, but asymptomatic)
Encephalitis primarily AIDS related****
"Free-living"
NO definite host
Transmission
Sexual contact (STD)******
Humans the only reservoir
Urogenital parasite***
Oocytes in Feces of CATS******
Swimming in contaminated
fresh & brackish water
(sewage, lakes, swimming pools)
Symptoms
-Urethritis in MEN
-Homogenous, watery vaginal discharge
-Irritation & inflammation can occur
Toxoplasmosis
Exposure is asymptomatic 90%of time
Acute:
Cervical lymphadenopathy
HA, Night Sweats, Chorioretinitis
Encephalitis:
AIDS patients***** (esp. Haitian)
Occurs often fromlatent reactivation
-AMS, chorioretinitis, seizures, sensory abnormalities,
hemiparesis, coma
-PNA-like
Acute Congenital:
Less likely to acquire early in gestation
Exposure EARLY = more dangerous
Exposure in LATER gestation = wide range of effects
-Severe neuro problems
Primary amebic meningoencephalitis (PAM)
N. fowleri & Acanthamoeba
Rare, but VERY HIGH mortality (>95%) w/i 72 hours
Hemorrhage & necrosis of brain tissue
AMS & Severe HA
Altered taste & smell*****
Sensitivity to light
Amebic keratitis
ONLY Acanthamoeba
-Usually starts from trauma or contact lens use
-Corneal ulcers
-Granulomatous skin lesions also seen
Pathophysiology
&
Lifecycle
Endemic Extraintestinal Protozoa
Domestic cat= definitive host
Mammals, birds = intermediate host
--> bug divides intracellularly in any host tissue
After ingestion oocytes hatch in gut to formtachyzoites
Tissue cysts can persist INDEFINITELY
-Destruction of host cells during acute infection -->
necrotic lesions
-Immunosuppressed pts: brain involvement w/ large
necrotic abcesses
-Congenital infections: retinal foci involvement -->
impair vision

Trophozoite = infectious form
Free living amoeba- no definitive host
N. floweri:
-Enters via olfactory epithelium****
(goes fromnose to brain)
-3 forms all found in environment:
--> Cyst, Trophozite & Flagellated
Acanthamoeba:
-Enters via respiratory tract or cut skin
-2 forms in environment: Cyst & Trophozoite
(both forms infectious)
No cyst form
Trophozoite infective!
50% have colpitis macularis "strawberry cervix"
-Characterized by patchy erythmatous lesions on
cervix
Infected pregnant women at risk for pre-term, low
birth weight.
Diagnosis
NO CYST FORM***
Detect mobile trophozoites
(polar flagella, 1 nucleus "eye")
in PAP smear, urethral or vaginal discharge
Serology****
Rising IgG titers over days to weeks= Diagnostic
Elevated IgM = Acute infection
IgM NOT seen w/ reactivation (so not good for AIDS)
DNA PCR: dx in utero infections
-Trophozoites in wet mount microscopy CSF or brain
biopsies
-Amoeba destroyed during staining
Keratitis: Scrapings of cornea/ skin lesion
Serology NOT useful b/c no bloodstreamphase
**Considered in those with meningitis where CSF
does NOT show bacteria or fungus**
Treatment
Metronidazole & Tinidazole
Treat both partners***
Not needed in immunocompetent patients
AIDS: Pyrimethamine + sulfadiazine + leucovorin
Pregnant women (1st & 2nd trimester):
Spiramycin
Pregnant women (later):
Pyrimethamine + sulfadiazine + leucovorin
PAM = Ampho B, miconazole, rifmapicin??
Keratitis - 0.1%propamidine isethionate +/-
miconazole +/- itraconazole
Possible cornea replacement
Plasmodium
(P. falciparum, vivax, malariae, ovale)
Babesia
(B. microti most common in USA)
Leishmania
(L. donovani, L. tropica, L. braziliensis, L. major)
Epidemiology
Sub-Saharan Africa
Endemic in most tropical countries
Almost all U.S. cases are from travelers/ immigrants
Most deaths are in children <5 years old
Heterozygous sickle cell anemia: resistant to ALL forms of Malaria
Most Blacks of African origin are resistant to P. vivax d/t genetic lack of the Duffy antigens
on RBC's that are required for entry
Northeastern seaboard
(Martha's Vineyard, Nantucket, Long Island)
Babesia is similar to malaria BUT IN AMERICA
Flagellate parasite similar to trypanosomes
Worldwide in temperate & tropical climates
Transmission
-Infected through bite of FEMALE Anopheles mosquito carrying Plasmodium
-Transfusions-associated malaria also occurs via Merozoites in blood
Life cycle
-Mosquito = definitive host
--> where sexual reproduction occurs
-Differentiation into sexually competent forms occurs in human
--> Mosquito-human transmission required for completion of life cycle
Vector = Ticks
Reservoirs = Voles & small mammals
Vector = sandly
Reservoirs = RATS
Symptoms
All symptoms most severe with P. falciparum infection
Some patients may have mixed infections
Cyclical fever - corresponds with cycle of parasite replication and RBC lysis
Sx
Myalgia, Malaise, Fatigue, Nausea/ Diarrhea,
Anemia--> ***pancytopenia***
Hepatomegaly, Splenomegaly
Neurologic symptoms/ AMS
Mostly in P. falciparum, P. vivax rarely
Headaches, confusion, lethargy, multiple convulsions, coma
Organ failure:
Caused by anemia, reduced oxygen delivery, capillaries occlude,
***Blackwater fever*** (dark urine from excretion of Hg d/t kidney malfunction)
Pregnancy- Associated Malaria
Pregnant women lose resistance (less loss the more times pregnant; resistance returns
post-partum & increases during pregnancy as a function of parity)
Parasite attachment to capillaries in placenta---> decreased blood flow to fetus --->
miscarriage
Uncomplicated falciparummalaria: Defined as having no organ failure or neurological
problems
Severe falciparummalaria (MEDICAL EMERGENCY) is dx'ed by having any one of:
Pulmonary edema, Respiratory distress, AMS, Seizures, Severe anemia, Jaundice,
Hemoglobinuria, Renal impairment
Babesiosis
(Incubation: 1-4 wks)
-Malaise, Fever, Chills, weakness
-Severe cases: Hepatosplenomegaly, Renal failure,
Anemia
Those with **splenectomy** are susceptible to severe
disease.
Cutaneous Leishmaniasis
"Oriental sore" "Delhi or Alppo boil" "uta" "chiclero ulcer"
-Caused by L. major, L. braziliensis, L. mesicanii, L. tropica
-Sx:
--> RED PAPULE @ bite site 2 wks - 2 months after infection
--> Lesion ulcerates & becomes crusted & hyperpigmented
--> Ulcers painless, but may itch intensely
-Dx:
--> microscopic exam of Giemsa-stained scrapings from lesions
Mucocutaneous Leishmaniasis
"Espundia"
-Caused by L. viannia braziliensis
-Sx:
--> Like previous, but can METS to MUCOSAL SURFACES, including nasopharynx
-Dx:
--> microscopic exam of Giemsa-stained scrapings from lesions
Visceral Leishmaniasis
"Kala-azar Fever" "Dumdum fever"
-Caused by L. donovani
- Mostly in S. Asia, Brazil, Sudan
-Infected bites usually unapparent; Primary Sx develop after a few wks to year
-Sx:
--> Fever, chills, hepatosplenomegaly, pancytopenia, renal dysfcn,
hypergammaglobinemia
-Dx:
--> microscopic exam of Giemsa-stained scrapings from lesions
Malaria & Babesia
Diagnosis
-Exclusively diagnosed by microscopic examination of thin blood smears
--> Morphology of erythrocytes (shizont) & parasites are diagnostic for species ID
-Enzyme-linked assays for parasite Ag
In highly endemic areas can diagnose based on history of fever & epidemiology
Children less than age 5 fever = malaria till proven otherwise, treat immediately!
Blood film
Similar morphology to Plasmodium but Larger and darker
Maltese cross (x-shape)*****
Correlate travel history to rule out Malaria
Treatment
Endemic falciparum malaria nearly completely resistant to Chloroquine
Uncomplicated P. falciparum
Endemic areas: Artesiminin-based (artemether or aretsunate) combination (PO, PR, IV)
--> Drug 1: artemesinins (artemether, artesunate, artemotil, dihydroartemisinin)
--> Drug 2: mefloquine, lumefantrin, amodiaquine, sulfadoxin-pyrimethamine
Non-endemic areas (US)- 1 out of 4 options:
1. Malarone
2. Artemether-lumefantrin (Coartem)
3. Quinine + clindamycine/tetracyline/doxycycline
4. Mefloquine
Severe P. falciparum malaria
-Main concern to keep pt. alive
-Monotherapy of either:
1. Artemesinin-based (IV or PR)
2. Quinine (IV or IM)
3. Quinidine (IV)
Vivax, Malariae, Ovale:
- Chloroquine, mefloquine, or amodiaquine
--> (still responsive to Chloroquine, but increasing resistance)
-Primaquine MUST be used to kill off hynozoites in P. Vivax & Ovale
Usually unnecessary & Mild cases resolve spontaneous.
Can use a combo of Clindamycin + Quinine
**Pentavalent antimonies**
--> mainly Na stibogluconate
Miltefosine
--> CI in pregnancy
Triazole antifungals??
Findings P. falciparum P. vivax
multiply infected
RBC
often occasionally
age of infected RBC
any young
Schuffner's dots no yes
RBCs enlarged no yes
Merozoites per
shizont (mean)
12 16
Crescent Shaped
gametocytes
yes no
Trypanosoma brucei
ss gambiensis- West African
ss rhodensiensis - East African
Trypanosoma cruzi
(American Trypanosomiasis)
Epidemiology
&
Characteristics
Africa
-Vector-borne flagellated bloodstream pathogens
-Kinetoplastids (unique darkly staining organelle - kinetoplast)
Endemic to Central and South America
-ASx/Acute/Chronic forms
Transmission Vector: Tsetse fly
Vector: Reduviid Bug - "kissing bug"
Bug feces get in the bite site w/ infectious form
Symptoms
Trypanosomiasis (African Sleeping Sickness)
Acute phase: [few days - weeks after exposure]
Ulcer at bite site (Trypanosomal chancre)
Systemic phase: "Hemolymphatic Stage"
-Fever
--> often unresponsive to antimalarials
-Lymph node enlargement
-Myalgia, Arthalgia
Winterbottom's sign = West African Disease***
-Enlarged posterior cervical lymph nodes
Generalized lymphadenopathy = East
-East is worse then west****
CNS involvement (chronic) phase:
-HA, lethargy, tremors,
-Wasting syndrome
-Ataxia, personality changes, meningoencephalitis
-Sleep abnormalities- insomnia @ night, daytime sleep
-Progresses to coma and death
East = 9-12 months
West= 2-5 yrs
Chagas Disease (American Trypanosomiasis)
Inflamed lesion (Chagoma) at bite site
Acute phase: [7-20 days post-infection]
-Fever, Lymphadenopathy (especially around eyes) Hepato-/ spleno-
megaly
-Subcutaneous edema
-Rash
rare (10%) : acute myocarditis or meningoencephalitis
Indeterminant/Asymptomatic Chronic: 20-40% of cases, [may last
decades]
-Little to no signs of infection
-May or may not progress to 3rd phase
Systematic chronic phase: "Chronic Chaga's Dz"
-Cardiac Enlargement (Chronic Chagasic Cardiomyopathy)
--> w/ heart enlargement & defects in conduction
-Arrhythmias, Blockages & Thromboembolisms
-Involv. of esophagus or colon (Chronic Chagasic Megaesophagus)
Deaths due to Chagas = Cardiac related
(death from acute phase rare)
Diagnosis
Acute phase:
Blood & Lymph Smears showing parasites
(thick or thin films)
CNS/ Chronic Phase:
Parasites in CSF(elevated lymphocytes & IgM)
Microscopy:
-parasites can be seen in thick or thin blood films, but can be hard to
detect, esp. in later stages
- [ ] of blood samples may be necc.
Xenodiagnosis:
-very slow
ELISA or EIA
Imaging studies:
-can be used for heart function & morphology, but not diagnostic
Treatment
Acute/Systemic phases:
Pentamidine
or
Suramin (West African only!)
CNS involvement:
TB gambiensis: eflornithine (qid)
+/- nifurtimox (for less frequent dosing)
TB rodesiensis : Melarsoprol (an arsenic)
[Only acute phase can be treated!]
-Benznidazole or Nifurtimox
Pathophysiology
&
Lifecycle
Extraintestinal Protozoans cont.

-Difference vs. T. brucei : presence of "amastigote" phase
--> penetrates tissue & divides intracellularly by fission
--> stage can be source of reinfection
Metacyclic trypomastigote = infectious from
Metacylcic Trypomastigotes injected by fly during feeding
Metacylcic Trypomastigote --> Bloodstream Trypomastigote
Blood Trypomastigote undergoes binary fission in the blood & lymph
These eventually invade the CNS
Bloodstream Trypomastigote taken up when fly bites
In fly:
-Transform into procyclic trypomastigote in FOREGUT
-Migrate to the salivary glands
-In salivary glands become epimastigotes then metacylcic trypomastigote
Visceral larval migrans
Enterobius vermicularis
(Pinworms)
Ascaris lumbricoides
Tricuris trichiura
(Whipworms)
Ancylostomaduodenale
Necator americanus
(Hookworms)
Strongyloides sterocoralis
(Threadworms)
Trichenellaspiralis Toxocaracani/ cati Ancyclostomabraziliensis
("Creeping Eruption")
Epidemiology
Worldwide
Humans only host***
VERY COMMON IN CHILDREN ****
Daycares*** & hospitals
Extremely common & worldwide
-In places with inadequate sanitation
-Children are more likely to be symptomatic
-No animal reservoir
-A. suum is a related zoonotic pig parasite that can infect
humans
Extremely common & worldwide
Mainly in SE United States
Mostly asymptomatic, kids may be symptomatic
Tropical & Sub-tropical climates
Ancylostoma duodenale
-Mnemonic: A.D. (like after death) = Old world
Necator americanu
-Mnemonic: NA = North America (Newworld)
-Fromsoil contaminated with feces
-Fewzoonotic species can infect humans
-Endemic in tropical areas
(Africa, Caribbean, SE Asia)
-Small endemic foci in rural SE United States Worldwide (rarer in U.S.)

Meat products Pork or Beef
Could be wild game (look out for a hunter)
Worldwide
Associated w/ dogs & cats contact
Humans = accidental hosts
Infection w/ hookwormspp. not native to
humans
Infects other mammals (dogs & cats)
Transmission
Eating raw undercooked meat
w/ encysted larvae
Ingestion of eggs via material
contaminated by animal (pet) feces
Filariformlarvae in contaminated soil
Pathophysiology
Ingest eggs & eggs hatch in small intestine
Adults inhabit cecum, appendix, & ascending colon
Females migrate out anus at night to deposit eggs in
perianal mucosa***
--> then retreat into lower GI
Eggs are mature & hatch w/i hours
--> can reinfect via larva re-entering the anus
[Adult worms: 2-13 mm, females 2x bigger than males]
Ingest eggs
Eggs develop in small intestine into 2nd stage larvae
Escape intestine & carried by circulatory systemand
spread to lungs
Mature larvae are coughed up and reswallowed
Develops into adult in small intestine
Eggs are then passed in feces & are infectious after 1-3
weeks developing in the soil.
[Largest nematode in humans: 20-35 mm]
Humans ingest eggs --> formlarvae in small
intestine --> larvae develop into adults in colon -->
eggs excreted in feces & require 2-3 wks before
they are infective
Adults formin colon
**Human stage confined only to GI tract**
Eggs in feces deposited into soil
Eggs hatch into non-infective rhabditiformlarvae
Larvae become infective filariformlarvae in 2 weeks
--> penetrate skin directly & migrate to lungs
Coughed up & swallowed --> adults develop in small intestine
--> attach to intestinal mucosa & suck blood fromintestinal
walls
Females pass 10,000 - 20,000 eggs/day in feces
Worms can live 1-5 years, but CANNOT reproduce in host
Has both a free living & parasitic cycle
--> Males only free-living
--> Female can be either
Larvae become infective filariformlarvae in 2 weeks
--> penetrate skin directly & migrate to lungs
Coughed up & swallowed --> adults develop in small intestine
--> attach to intestinal mucosa & suck blood fromintestinal walls
Females reproduce asexually in colon
--> hatch into rhabditiformlarvae --> passed in feces or
develop into Filariformlarvae can reinfect host -("autoinfection")
-Sexual reproduction occurs in soil
Encysted larvae are ingested
Excystation occurs in small intestine
--> Larvae penetrate mucousa and develop into
adults
Adults expelled in feces
Larvae go to striated muscle and formcysts
("nurse cells") that survive for years
In animals larvae can infect another animal when
host eaten
Ingest eggs (contact with material contaminated w/ feces)
Eggs hatch in small intestine
Larvae migrate to various tissues
Life cycle CANNOT be completed in humans
-Humans terminal host
-Filariformlarvae penetrates skin, but
does NOT migrate to lungs
Disease
Enterobiasis
Look for kid scratching bottom****
-Perianal itching due to irritation fromeggs
-Diarrhea can occur in acute infection
-Can develop allergies to secretions of worms
-Rarely extracolonic infections in patients w/
compromised bowel integrity
--> ex: IBD
Ascariasis
(Adults are normally asymptomatic)
Acute symptoms
-Children: can exacterbate malnutrition
-High wormload: abdominal pain & intestinal obstruction
Loeffler's syndrome (Pneumonitis)
-Due to pulmonary migration
-Coughing, dyspnea, Eosinophilia
Rarely can spread and cause substantial tissue damage
(Liver, Bile duct, Gall Bladder)
Tricuriasis
Usually asymptomatic
-Abdominal pain
-Secondary bacterial infection frompenetration of
mucosa.
High parasite burden:
Diarrhea, weight loss, appendicitis***
Mnemonic: Whip worms whip the appendix
Ancyclostomiasis
Chronic infection/ High wormBurdens: Hypochromic anemia
--> Growth retardation in malnourished children
Other symptoms:
Abdominal pain, diarrhea, malnutrition
-Loeffler's syndrome (during lung phase)
-Rash @penetration site
"Ground Itch"- Rash at penetration site
Loeffler's syndrome (during lung phase)
Strongylodiasis
Often asymptomatic
Loeffler's syndrome (during lung phase)
Heavy wormburden:
-Occlusion of bile or pancreatic ducts, malabsorption, bloody
diarrhea, epigastric pain
--> w/ Peripheral eosinophilia (vs. PUD)
Hyperinfection Syndrome:
-Fromrepeated cycles of autoinfection
-Usually Immunosupressed (esp. hematological cancer or with
steroid tx)
-Larvae migrate to most organ systems
-High mortality
Trichinosis
Symptoms highly DOSE DEPENDENT
<10 larvae = Asymptomatic
>100 is significant
>1000 = death
Fever, abdominal pain, myalgias
Splinter hemorrhages under nails
Lethal infections are due to Myocarditis,
Encephalitis & Pneumonitis
Visceral Larval Migrans
Most asymptomatic
Heavy burdens (esp in kids):
Cough, rash, anorexia, hepatosplenomegaly, pneumonitis
CNS involvement seen and rare deaths due do encephalitis
Ocular larval migrans: LOVES THE EYES
Red eye & Visual Impairment
Can be mistaken for retinoblastoma
Cutaneous Larval Migrans
-Intense RED rash
--> can sometimes be traced as SC
migration pattern of larvae
--> very itchy & uncomfortable
Diagnosis
Detection of eggs in perianal area= Diagnostic
"Scotch tape" test
-Eggs are oval, double layered & flattened
--> Mnemonic: flattened shape = kid sat on them
(Eggs rarely seen in actual feces)
-Eggs are visualized in formalin-fixed fecal samples
--> usually stained with iodine
-Eggs are oval, 50 mwide & 50-75 mlon
--> thick-walled
--> amber in color w/ iodine-staining
-Occasionally, patients will present after passing an adult in
the feces which, at 20-35 cm, can be disconcerting
-Larvae might be seen in sputumin transient lung phase
Detect eggs in feces
Eggs are Oval & yellowish (bile-stained)
w/ thick white caps on both ends
Detect eggs in feces
Eggs: oval, thin-shelled & non-bile stained
Detect rhabditiformlarvae in feces
--> larvae transparent
(Eggs rarely seen in stool)
Examination of multiple samples needed
Difficult (fecal samples no good)
Muscle biopsies to ID encysted larvae
Clinical signs + Eosinophilia = clue
Serology (ELISA) + Eosinophilia
&
Look for eggs in animal feces = confirmatory
(human feces not useful)
Clincal presentation (mostly)
Serology: esoinophilia & elevated IgE
Treatment
Mebendazole
or Pyrantel pamoate
2-3 rounds of tx. due to high reccurence rate
Whole family should be treated
[Even ASx should be treated!!!]
**Albendazole + Pyrantel pamoate**
Alternatives:
Mabendazole
Ivermectin
No treatment needed for mild infections
Mebendazole for severe burdens
-Don't use in pregnancy
Alternatives:
Albendazole
Ivermectin
Mebendazole
-Highly effective & is ovicidal
-Prevents transmission
Alternatives:
Purantel pamoate
Albendazole
Ivermectin
Alternatives:
Albendazole
GI Phase (vs. adults):
Albendazole or Mabendazole
Severe Sx:
Corticosteroids
Albendazole
Severe Sx:
Corticosteroids
Alternatives:
Mebendazole
Thiabendazole
Albendazole
Mabendazole
Nematodes (Roundworms)
Fecal-oral (via ingestion of eggs) FilariformLarvae penetrate skin directly
STRONG ASS HOOKERS = Worms that go through the lungs
Strongyloides, Ascaris, Hookworms
Agent
Wuchereria bancrofti
Brugia malayi/ timori
(Filariasis)
Onchocerca volvulus
(River Blindness)
Dracunculus medinensis
("Guinea Worm")
Loa loa
Dirofilaria immitis
(Dog heartworm)
Epidemiology
Set of extraintestinal infections caused by vector-borne,
threadlike worms
Wuchereria bancrofti [Bancroft's filariasis]
- Tropical areas worldwide
Brugia malayi/Brugia timoria [Brugian or Malyan filariasis]
-SE Asia
Endemic to Africa
Sudan, Ethiopia, Ghana, Mali
(near eradication)
Endemic in Africa rain forests
Transmission
Vector: Mosquitos w/ larvae
(Aedes, Anopheles, Culex)
--> non-endemic in US
Vector: Blackfly w/ larvae
Drinking water contaminated with
Copepod (water flea) w/ larvae
Vector: Chrysops fly Vector: Mosquito
Pathophysiology
Larvae transmitted via mosquito bite
Larvae migrate to lymphatics & mature into adults
Microfilariae are then released into bloodstream
--> DIAGNOSTIC!
Ingestion of microfilariae by mosquito feeding completes
the cycle
Same cycle as lymphatic filariasis
Tissue preference for skin & eyes
Ingest larvae in copepods (water fleas)
Larvae penetrate gut & mature in peritoneum
--> eventually mates
--> Mate, male dies, female lives
Female can grow to 1 m+ & penetrates connective
tissues
After a year female migrates to lower extremity & forms
a blister
Blister ruptures & female peaks out to deposit larvae in
-Microfilariae migrate throughmuscle, SC tissue
& eye
Transmitted to humans by mosquito
Disease
Lymphatic Filariasis
-Primarily infects lymphatic system, causing enlargement of
tissues & susceptibility to other bacterial infections
-Extreme manifestation: Filarial elephantitis
-Lymphadenopathy
-Recurrent fever
-Abscesses form sometimes
-Chronic infection --> elephantitis
Onchocerciasis (River blindness)
-Ocular lesions*****
--> Conjunctivitis --> keratitis
--> Blindness in 5% of affected
-Dermatitis
-Skin nodules ("onchocercomas")
Dracunculiasis
Excruciating & Debilitating pain due to migration of
worms through SC tissues
Blister on lower extremity when worm is about let loose
eggs in water
Loaisis
Transient "Calabar swellings" of extremities +
eosinophilia +
microfilariae in eye
Dirofilariasis
"Coin lesion" in lung
Diagnosis
Detection of microfilariae in blood*****
Marked eosinophilia
Detect microfilariae in skin snips or biopsies of
nodules
Marked eosinophilia
Patient history & symptoms sufficient in endemic areas
Calibar swellings
+
Eosinophilia + Microfilariae in eye
Thoaracotomy specimens
Treatment
Early:
Diethylcarbamazine
--> good vs. adults & microfilariae
--> CI: concurrent Onchocerca infection
Ivermectin
-Kills microfilariae, but NOT adults!
-Chronic filariasis RESISTANT to Tx
-Surgery can reduce physical signs of elephantitis
Ivermectin
Mnemonic: rIVER blindness, IVERmectin
Possible surgical removal of lesions
Wrap around stick & slowly roll worm out over weeks
very painful!
Metronidazole
--> may accelerate extraction, but can promote worm
migration
Diethylcarbamazine
Corticosteroids for allergic response
Filariasis
(Threadlike worms)
Nematodes (Roundworms) continued
Schistosoma spp.
(Blood flukes /"Snail Fever"/ "Bilharziasis")
Paragonimus westermani
(Lung fluke)
Fasciolopsis buski
(Giant intestinal fluke)
Fasciola hepatica
(Liver fluke)
Opisthorchis sinesis
(Chinese Liver fluke)
Epidemiology
Tropical areas (including Mexico & Caribbean)
Second only to malaria in incidence
All cases in U.S. are imported (Travelers & Immigrants)
Exception: Swimmers itch (Great lakes)
SE Asia (primarily)
Africa, Latin America
High incidence rate
Endemic in SE Asia Worldwide Endemic in SE Asia

Free-living Cercariae
penetrate skin directly in fresh water (also beachs/ shallow water)
Raw/ Undercooked Seafood (crustaceans
especially)
Eating aquatic plants
(especially water chestnuts)
Eating aquatic plants
Undercooked fish
(Intermediate host = freshwater fish)
Pathophysiology
Eggs excreted in human feces or urine
Eggs hatch in fresh water & form miracidia that penetrate snails
Snails = intermediate host****
In snails sporocysts form then become cercariae (infectious form)****
Cercariae penetrate skin and lose their tail to become schistosomulae.
Enter blood, mature in liver
Adults mate in characteristic circulatory sites (worms bisexual)
-Worms are not immunogenic due to molecular mimicry (eggs are though)
Larval migration and growth in lung
Destruction of lung tissue occurs
Rarely invades CNS
Similar life cycle to Schistosoma
(except for skin penetration)
Similar life cycle to Schistosoma
(except for skin penetration)
Freshwater fish is intermediate
host
Similar life cycle to Schistosoma
(except for skin penetration)
Symptoms

Schistosomiasis
Many asymptomatic
Acute Schistosomiasis (Katayaman's Fever) [few weeks after exposure]
Fever, cough, abdominal pain, diarrhea
Rash @ penetration site
Hepatosplenomegaly, eosinophilia
Liver granulomas****
S. hematobium: [urinary localization]
-Urinary frequency, hematuria, bacteriuria (and GI symp. still)
Chronic Schistosomiasis
Deposited eggs cause granulomatous immunologic response
Fibrosis and obstruction also occur
Swimmer's Itch (Schistosomal or Cercarial Dermatitis)
Skin rash from larval penetration
Species can't reproduce in humans
Larvae penetrate skin & cannot progress further & die
Great lakes region*****
Paragonimiasis
Cough, fever
"Rusty sputum"- colored with w/ blood &
eggs
Increased susceptibility to bacterial infection
Chronic infection:
Bronchitis & pleural effusions
CNS spread:
Seizures, visual defects, motor weakness
Mnemonic: cowboys/ westerners smoke so
therefore westermani = lung fluke
Heavy worm burden:
Abdominal pain
Diarrhea
Malabsorption
Intestinal obstruction
Hepatomegaly
RUQ pain
Fever, Chills
Eosinophilia
Hepatitis & Biliary obstruction if worms
occlude bile duct
****Mnemonic: hepatica = liver
Usually asymptomatic
In severe infections:
Epigastric pain
Fever
Diarrhea
Hepatomegaly
Jaundice
Diagnosis
Detect eggs in feces
Detect eggs in urine for S. hematobium
S. mansoni: Lateral spine (Charles Manson dagger on SIDE)
S. hematobium: Terminal spine at end, circular, small
S. japonicum: Circular & small (like a ying-yang symbol)
Detect eggs in sputum**** Detect eggs in stool Detect eggs in stool Detect eggs in stool
Treatment Praziquantel
Praziquantel
Alternative:
Bithionol
Praziquantel Triclabendazole Praziquantel
Trematodes (Flukes/ flatworms)
Taenia solium (PORK tapeworm)
Taenia sagnita (BEEF tapeworm)
Echinococcus granulosus
(also E. multilocularis, E. vogeli)
Diphyllabothriumlatum
(Fish tapeworm)
Hymenolepis nana (dwarf tapeworm)
Hymenolepis diminuta (rat tapeworm)
Epidemiology
Worldwide
Common in U.S.
Mnemonic: T. sOlium = pOrk
Worldwide
North & West U.S. (upper plains, Alaska, Prar)
Worldwide
Largest human parasite
Worldwide
H. nana is most common tapeworm in U.S.
H. dimunta is rare in humans
Transmission
Eating contaminated pork or beef
w/ larva (cysticerci)
Cysticercosis: Ingestion of eggs
(Human feces or autoinfection via reverse peristalsis in already infected)
Contact with dog/canine (foxes, wolves)
feces containing eggs
Eating raw/ undercooked fish containing larva Eating Beetles/ Mealworms in grain
Pathophysiology
Taeniasis
Pigs & cows ingest eggs in environment
Eggs hatch in animals & form oncospheres whcih migrate to tissues
Oncospheres develop into cysticerci in muscle in animals
Humans eat meat containing cyticerci which contain an immature scolex
Scolex attaches to small intestine & adults develop
-T. solium (2-7m), T. saginata (~5m with cases up to 25m)
Adults release eggs & gravid (fertile) proglottids
Cysticercosis
Ingest eggs (NOT cysticerci)
Eggs hatch in stomach instead of small intestine
Larva then mimic life cylce in animals (like cows & pigs)
Develop oncospheres, penetrate stomach & migrate to muscles & other
tissues
Dogs are definitive host*****
Humans are accidental*****
After ingestion eggs hatch and form oncospheres
Oncospheres migrate all over body (Lung & Liver)
Oncosphere then develops into a cyst that slowly grows as it
fills w/ scolices
E. granulosus : cystic echinococcosis (most common form)
E. multilocaris - alveolar echinococcosis (prefers lungs)
E. vogel i- polycystic echinococcosis
Eggs in freshwater hatch to become free swimming larvae
(coracidium)
Larva are eaten by crustaceans & develop into proceroid
stage
Fish eat the crustaceans, larvae develop to plerocercoid
stage
Humans eat the undercooked fish
Larvae then develop in intestine
Tapeworms are HUGE (10 meters)
Intermediate host = rats, beetles
Cysticercoid live in beetles/mealworms. Humans
ingest these bugs in grain, etc, and the larva
develop into adults in our intestines. Eggs in our
feces are eaten by the beetles = new cycle.
H. nana eggs in our feces are immediately
infective - can reinfect other humans or autoinfect.
Symptoms
Taeniasis
(Usually asymptomatic)
Vague abdominal complaints
Chronic indigestion
Cysticercosis
******T. solium only******
Inflammation following cysticerci here causes pathology
Form cysts in tissues
****Brain: Hydrocephaly, nerve damage, seizures, meningitis
Eye infections: Vision Problems
Hydatidosis
Cyst can mimic a slow growing tumor
-Especially in lungs & liver
Can put pressure on surrounding tissues with symptoms
dependent on region of body
-In liver: Hepatitis & Jaundice
-In lung: Difficulty breathing
Cysts can get huge (liters volume)
Fish tapeworm infection
Usually asymptomatic
Vague abdominal complaints
Vitamin B12 decificency
Hymenolepsosis
Usually asymptomatic
Vague abdominal complaints
Nause & Diarrhea
Headache
Diagnosis
**Detect eggs or proglottid segments in feces**
Uterine structure of proglottids
is different between the species
-T. sOlium = round/ Oval proglottids
-T. saginata = rectangular proglottids
Cysticercosis: Imaging (CT, MRI, X-ray)
Serology &
Imaging: CT, MRI, X-ray
Look for "Hydatid sand"
(grainy appearance of images)
Oval, Operculated, bile-stained eggs
in feces
O & P exam on feces
to detect eggs
Treatment
Taeniasis:
Niclosamide
Alternative:
Praziquantel, Paromycin, Quinacrine
Cysticercosis:
** Praziquantel**, Albendazole
Surgical removal of cyst
+
Mebendazole or Albendazole
Praziquantel or Niclosamide or Paromycin,
B12 supplements
Praziquantel or Niclosamide
Cestodes (Tapeworms)