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*mod i exam 3 > Parasites > Flashcards

Parasites Flashcards

1
Q

Outbreaks of Giardia lamblia occur when?

How is it transmitted?

A
  • When sewage contaminates drinking water
  • Transmitted through poorly purified water, often seen in travelers and campers
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2
Q

What occurs upon ingestion of Giardia lamblia?

What are the signs and symptoms?

A
  • After ingestion of the cyst, Giardia converts to the trophozoite form and cruises down and adheres to the small intestine wall, does NOT invade
  • Coats small intestine, interfering with fat absorption, leading to steatorrhea
  • Sx: bloating, flatulence, and foul-smelling diarrhea
  • Pt’s often experience significant weight loss and deficiencies in Vits A, D, E, and K
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3
Q

How is the Dx of infection with Giardia lamblia made?

A
  • Examination of stool for trophozoites
  • Can perform an ELISA stool antigen test
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4
Q

What are the symptoms of Entamoeba histolytic infection?

Where can it invade?

A
  • Abdominal pain, bloody diarrhea; can also cause intestinal amebiasis (ulceration along colon)
  • Can invade liver and form amoebic abscesses –> RUQ pain w/ hepatomegaly
  • May also invade lung and form pulmonary abscesses
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5
Q

How is Entamoeba histolytic transmitted; what forms does it take during its life cycle?

A
  • Cyst form can be transmitted fecal-orally or in contaminated water.
  • MSM are common carriers
  • Differentiates in trophozoite form which is the motile feeding form, that can cruise along intestinal wall and is invasive
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6
Q

How is Entamoeba histolytica diagnosed?

How can you tell if their is active disease or the person is an asymptomatic carrier?

A
  • Stool O and P looking for presence of cysts or trophozoites
  • Trophozoites w/ endocytosed RBCs in their cytoplasm suggest active disease
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7
Q

How is Cryptosporidium transmitted?

Describe its life cycle.

A
  • Fecal-oral route; contaminated water sources
  • Ingested as round cyst that contains 4 motile sporozoites, its life cycle occurs within intestinal epithelial cells
  • Creates oocysts which are then released into the feces
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8
Q

What are the signs and symptoms of Cryptosporidium?

Who is most at risk?

A
  • Watery diarrhea and abdominal pain in healthy individuals
  • Immunocompromised pts (AIDS, cancer, transplants): may develop severe, protracted diarrhea that is life-threatening
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9
Q

How is Toxoplasmosis gondii transmitted; who is most at risk?

A
  • Ingestion of cysts in undercooked meats (raw pork) or foot contaminatd with cat feces
  • Kitty litter boxes are MOST COMMON source for exposure in the U.S.
  • Pregant women and immunocompromised are most at risk
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10
Q

How does Toxoplasmosis gondii affect immunocompromise patients, especially those with AIDS?

A
  • Fever, LN, liver, and spleen enlargement and pneumonia
  • May also lead to Toxoplasma encephalitis: seizures, gait instability, weakness, or sensory losses
  • Infection of the retina, chorioretinitis, is also common
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11
Q

What is the most common CNS infection in AIDS patients?

A

Toxoplasma encephalitis

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12
Q

If a pregnant woman is infected with Toxoplasmosis gondii, she may transplacentally infect the fetus, what are the characteristics of congenital toxoplasmosis?

A
  • Chorioretinitis, blindness, hydrocephalus/seizures, mental retardation, microcephaly, and encephalitis
  • If infection is acquired early in gestation, may result in stillbirth
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13
Q

How can clinical reactivation of Toxoplasmosis gondii infection affect an infant later in life?

A
  • Most commonly results in retinal inflammation (chorioretinitis, which can cause blindness)
  • Peak incidence is the second or third decade of life
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14
Q

Diagnosis of Toxoplasmosis gondii in AIDS patients and fetuses can be done how?

What are the classic findings?

A
  • Ring (contrast)-enhancing lesions on CT or MRI
  • Examination of retina will reveal retinal inflammation
  • Serology will show elevated immunoglobulin titers
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15
Q

What does Trypansoma brucei rhodesiense and gambiense cause?

What is the vector?

Where is it endemic?

A
  • African sleeping sickness
  • Vector is Tsetse fly
  • Endemic to Western and SE Africa
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16
Q

After being bit by the Tsetse fly, how does the trypomastigo of Trypansoma brucei rhodesiense and/or gambiense cause infection?

What are the signs and symptoms?

A
  • Travels in blood stream to LNs and CNS
  • Recurrent fever, headache, dizziness, and LN swelling
  • CNS sx’s develop: drowsiness in daytime, behavioral changes, difficulty walking, slurred speech, and finally coma and death
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17
Q

What causes the intermittent (recurrent) fevers in African Sleeping Sickness?

A
  • Trypanosomes are covered with variable surface glycoprotein (VSG)
  • Undergoes constant antigenic variation - evades host immune system - thus there are waves of new Ags producing reccurent fevers
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18
Q

How is diagnosis of Trypansoma brucei rhodesiense and gambiense made?

A

- Blood smear w/ evidence of Trypomastigotes in peripheral blood

  • Can also test LNs, or spinal fluid
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19
Q

What is Naegleria fowleri associated with?

What kind of organism is it?

How does an infected patient present and what is the prognosis?

A
  • Fresh water (watersports, swimming, camping)
  • Is an amoeba
  • Pt presents with fever, headache, stiff neck, nausea and vomiting, which is similar to a bacterial meningitis; usually with a hx of swimming one week earlier

- RAPIDLY FATAL!

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20
Q

What is the CSF content of someone with acute meningoencephalitis caused by Naegleria fowleri?

How is the diagnosis made?

A
  • High neutrophil count, low glucose, and high protein, exactly like bacterial meningitis!!!
  • Lumbar puncture to dx; motile amoebas in CSF
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21
Q

Where is Trypansoma cruzi prevalent?

Which disease does it cause?

How is it transmitted and through what vector?

A
  • Southern U.S. (Texas), Mexico, South and Central America
  • Chagas disease
  • Transmitted through the vector, Reduviid bug (AKA “kissing bug), which bites around victims mouth anddeposits feces, which are introduced into the blood through scratching
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22
Q

How can acute Chagas disease be diagnosed?

A
  1. Blood smear to visualise motile trypanosomes
  2. Xenodiagnosis: sensitive test, grow bugs in lab and let feed on pt.
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23
Q

What occurs in Acute and Chronic Chagas’ Disease?

A
  • Acute: a hardened, red area, called a chagoma develops at site of parasite entry. Followed by fever, malaise, and swollen LNs
  • May result in tachycardia and ECG chagnes. CNS involvement can result in severe meningoencephalitis
  • Resolves in about a month and patients enter an asymptomatic, intermediate phase
  • Chronic: sets in 10-20 yrs later causing MEGAcolon, extreme constipation, MEGA-esophagus, anddilated cardiomyopathy
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24
Q

How is Babesia transmitted, what is the vector and the reservoir?

Where is it found?

What does infection cause?

A
  • Reservoir is the white-footed mouse
  • Carried by Ixodes tick, and spread to humans and farm animal through saliva of tick

- NE United States

  • Causes Babesiosis: malaria-like infection!
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25
Q

What are symptoms of Babesiosis?

Who is at high risk if infected?

A
  • Malaria-like sx’s including fever and hemolysis, as it invades RBCs
  • Asplenic and sickle cell disease pt’s are at greatest risk for severe infection
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26
Q

What visual characteristic allows for the diagnosis of Babesiosis and differentiation from Malaria?

Which lab technique used?

A
  • Maltese cross (X-shaped) appearance in RBCs formed by Tetrad of merozoites
  • Seen with wright-stained thick blood smears or Giemsa,
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27
Q

What is the vector for transmission of Plasmodium malariae, vivax, ovale, falciparum, and knowlesi?

Describe the events that occur once a person is infected and the life cycle of this protozoa?

A
  • Transmitted via Anopheles mosquitos carrying sporozoites in saliva; bites human host
  • Travel to liver where they mature to trophozoites –> schizont –> merozonites which burst liver cell causing release into the bloostream where they can infect RBCs
  • Some merozonites will change into male/female gametocytes. These cells circulate and will be taken up by a biting mosquito; continuing the cycle of infection
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28
Q

What type of fever cycle does Plasmodium malariae have?

A

Quartan fever cycle: causing a regular 3-day cycle of fevers and chills, followed by sweats as P. malariae bursts from RBCs every 72 hours

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29
Q

What type of fever cycle does Plasmodium vivax and ovale​ have?

What do they produce in the liver?

A
  • A tertian fever cycle: chills and fever, followed by sweats every 48 hours
  • Produce dormant hypnozoites in the liver, which can grow years later, causing relapsing malaria
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30
Q

What type of fever cycle does P. falciparum follow?

A
  • Is the most common and deadly of the Plasmodia, bursts red cells more irregularly, between 36-48 hours
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31
Q

P. falciparum causes the most severe form of malaria, what are some of the clinical manifestations of this infection?

A
  • Severe chills, high fevers, and profuse sweating
  • Continously bursting RBCs –> anemia and sticky RBCs
  • Sticky RBCs occlude post-capillary venules in organs such as kidney, lung, and even brain
  • Infected pt’s also get hepatosplenomegaly; spleen may rupture
  • Renal failure, lung edema, and coma may ensue, leading to death
32
Q

Who is resistant to some forms of Malaria and how?

A
  • Many African Americans and African blacks are resistant to P. vivax and P. falciparum infection due to absence of red cell membrane Ags Duffy a and b needed for binding
  • Sickle cell anemia trait appears to help protect the red cells from P. falciparum invasion

*This is awesome!

33
Q

How is diagnosis of Malaria made?

A
  • Examination of thin and thick blood smears, under oil-immersion magnification, revealing trophozoites and schizonts within RBCs
  • Characteristic banana shape
34
Q

How is Leishmania transmitted to humans?

Where is the disease leishmaniasis found?

What form does the vector carry and what occurs once someone is infected?

A
  • The vector is a sandfly
  • Carries the promastigote, which invades macrophages and transforms into the nonmotile amastigote, which multiplies within phagocytic cells in the LNs, spleen, liver, and bone marrow (reticulo-endothelial system)
  • South and Central America, Africa, and the Middle East
35
Q

What occurs in Visceral Leishmaniasis (Kala-azar)?

Characteristics of this disease.

A
  • Sandfly transmits Leishmania donovani or chagasi to an individual (most commonly young malnourished children), parasites invade macrophages
  • Causes severe systemic disease marked by hepatosplenomegaly, LAD, pancytopenia, fever, and weight loss (Severe anemia w/ massive splenomegaly!)
  • Often there is hyperpigmentation of the skin (dark and ashen skin)
36
Q

How is Visceral Leishmaniasis (Kala-azar) diagnosed?

A

Liver, spleen, marrow, LNs or skin lesion can be analyzed for amastigotes

37
Q

Trichomonas vaginalis is transmitted how?

What does it cause?

A
  • Transmitted sexually and hangs out in female vagina (vaginitis and cervicitis) and male urethra (usually asymptomcatic)
  • Female patient may complain of pruritis, burning on urination, and copious vaginal secretions; strawberry cervix
  • On PE you will find a thin, watery, frothy, malodorous discharge that is yellow-green in the vaginal vault
38
Q

How is the diagnosis of Trichomonas vaginalis made?

How can it be differentiated from Gardnerella and Candida infections?

A
  • Diagnosed w/ examination of vaginal discharge on a wet mount showing highly MOTILE trophozoites
  • Gardnerella shows “clue cells” and Candida shows pseudo-hyphae w/ budding yeast
39
Q

What is Enterobius vermicularis?

How are they transmitted?

Who is most affected and what are the signs?

How are they diagnosed?

A
  • Pin worms (Nematode)
  • Female pin worms migrate to anus and lay eggs, cause severe perianal itching, person scratches themselves and then reinfects himself or other (hand-to-mouth)
  • Typically affects children; very itchy anus typically at night
  • Diagnosed using scotch tape on anus, eggs will be deposited on the tape and can be viewed under microscope
40
Q

What are Ancyclostoma duodenale and Necator americanus?

How do they infect humans; describe their route through the body?

How are they diagnosed?

A
  • Hookworms (Nematode)
  • The larvae pentrate skin of soles of feet and move from blood stream —> lungs where they are coughed up and swallowed making their way to the small intestine where they mature into adults
  • Eggs in the stool and a high eosinophil count
41
Q

Once matured in the small intestine what do Ancyclostoma duodenale and Necator americanus do?

What are signs and symptoms and what serious risk do they pose to the host?

A
  • Attach to gut wall and feed from the capillaries of intestinal villi
  • May develop diarrhea, abdominal pain, and weight loss; local growth in the lung may result in a cough and infiltrate on CXR
  • Also an intense itching and rash at the site of penetration through the skin (between the toes)
  • Pt’s may develop severe iron deficiency anemia
42
Q

What is Ascaris lumbricoides and how is it transmitted?

Describe its route once inside the body.

A
  • An intestinal NEMATODE (“large worm”) that is transmitted by ingestion of its eggs in contaminated food or water
  • Larvae emerge when the eggs reach the small intestine, penetrate intestinal wall, travel in bloodstream to the lung where they are coughed up, swallowed, and travel back to the small intestine where they mature.
43
Q

What are the signs and symptoms of infection by Ascaris lumbicoides?

Which organs can be affected?

A
  • Severe infection involve adult worm invasion into the bile ducts, gall bladder, appendix, and liver
  • Children with heavy worm loads may suffer from malnutrition and if the mass of worms is large enough can cause intestinal blockage (most often at ileocecal valve)
  • Larvae in the lung may lead to respiratory symptoms and a pulmonary infiltrate seen on CXR
44
Q

How is Ascaris lumbricoides​ infection diagnosed?

A
  • Eggs in the stool
  • Sputum exam may reveal larvae
  • Blood smear may also reveal eosinophilia
45
Q

How is infection with Strongyloides stercoralis (Nematode) acquired and describe its route through the body.

How is diagnosis made?

A
  • Acquired when larvae penetrate skin of soles of feet –> bloodstream –> lung–> coughed up and swallowed –> small intestine
  • Detection of larvae in the stool (no eggs) and eosinophilia in blood smear
  • May also do enterotest, where long nylon string is swallowed and later pulled back out the mouth, demonstrating larvae of Strongyloides
46
Q

What are the signs and symptoms of infection by Strongyloides stercoralis?

What if a person in immunocompromised?

A
  • Vomiting, abdominal bloating, diarrhea, anemia, and weight loss
  • May develop a pruritic rash, lung sx’s, and/or eosinophilia
  • If immunocompromised may lead to severe autoinfection as the filariform larvae invade the intestine, lung, and other organs –> pneumonia, ARDS, and multi-organ failure
47
Q

How does infection with Trichinella spiralis (Nematode) occur?

What occurs inside of the host?

A
  • Ingestion of encysted larvae in undercooked/raw PORK
  • Cysts travel to small intestine where the larvae leave the cysts and mature into mating adults.
  • Following mating, adult males are passed in the feces and the females penetrate intestinal mucosa, producing thousands of larvae
  • Larvae enter bloodstram and spread to organs and skeletal muscle where they become encysted and may last for decades
48
Q

What are the signs and symptoms of infection with Trichinella spiralis?

A
  • Abdominal pain, diarrhea, and fever as worms mature in small intestine
  • After migration into skeletal muscle, produce severe myalgias and fevers
  • In severe cases, may invade heart muscle and brain tissue
49
Q

How is diagnosis of Trichinella spiralis infection made?

Which values will be increased?

A
  • Serologic tests or muscle biopsy, revealing encyted larvae
  • Due to muscle invasion there will be a marked eosinophilia and also increased levels of serum muscle enzymes, such as creatinine phosphokinase (CPK)
50
Q

A person infected with Dracunculus medinensis (Nematode) will experience what symptoms?

How is this worm removed?

A
  • Allergic sx’s, including nausea, vomiting, hives and breathlesseness, during larval release
  • Common practice to remove worm invovles driving a small stick under the part of worm’s body that is looped out of skin and stick is slowly twisted each day to pull out the worm

*Think of a wooden stake being used to get ride of Dracula!

51
Q

What is Dracunculus medinensis and how is it transmitted?

What is the intermediate host?

Describe its life cycle.

A
  • The Guinea worm (tissue-invasive nematode)
  • Lives as a larval form in its intermediate host, the Copepods
  • Person drinks water containing Copepods, larvae penetrate the intestine and move deep into the subcutaneous tissue, where adults develop and mate
  • Females migrate to skin and a loop of her body pokes out and exposes her uterus; once in contact with water, thousands of motile larvae are released
52
Q

What is Onchocerca volvulus and where is this infection most commonly seen?

How is it transmitted?

Describe its life cycle

A
  • A tissue NEMATODE found in Africa and Central and South America
  • Larvae are transmitted to humans by bite of infected black flies
  • Larvae mature into adults, which can be found coiled up in fibrous nodules in the skin and subcutaneous tissue
  • After mating, the adults produce microfilariae, which migrate through dermis and CT
53
Q

What are the signs and symptoms of infection with Onchocerca volvulus?

A
  • Pt’s develop a pruritic skin rash w/ darkened pigmentation
  • Skin may thicken w/ formation of papular lesions that are actually intraepithelial granulomas; thickened skin may appear dry and scaly
  • Microfilariae may also migrate to the eye causing blindness (“RIVER BLINDNESS”)

*There are villages in endemic area where most of the inhabitants are blind!!!

54
Q

How is diagnosis of Onchocerca volvulus made?

A
  • Demonstrating microfilariae in superficial skin biopsies, or adult worms in a nodule.
  • Microfilariae can often be seen in the eye (cornea and anterior chamber) by slit lamp examination!
55
Q

What do Wuchereria bancrofti and Brugia malayi (Nematodes) cause?

How are they transmitted?

A
  • A lymphatic infection which can result in chronic leg swelling
  • Transmission via bite by infected mosquito
  • Transmitted microfilariae mature into adults within lymphatic vessels and LNs of the genital and LEs
56
Q

What occurs after repeated exposure to Wuchereria bancrofti and Brugia malayi?

A
  • Frequent infections result in acute febrile episodes, associated w/ headaches and swollen inguinal LNs
  • Occasionally fibrous tissue will form around dead filariae that remain in LNs, the fibrous tissue plugs up lymph system, which results in swelling of the legs and genitals.
  • Swollen (edematous) areas become covered w/ thick, scaly skin and this chronic disfiguring manifestation is called elephantitis
57
Q

How is the diagnosis of infection w/ Wuchereria bancrofti and Brugia malayi made?

A
  • Identification of microfilariae in blood drawn at nighttime,due tonocturnal periodicity
  • Can also be made by identification of positive antibody titers via immunofluorescence
58
Q

How is Toxocara canis (Nematode) - dog roundworm transmitted and in what form?

What occurs during infection?

Diagnosis?

A
  • Ingesting of food contaminated w/ dog or cat feces containing eggs
  • Parasitic larvae inside human DO NOT mature into adults, instead continue to circulate body and cause toxocariasis (aka visceral larva migrans or ocular larva migrans)
  • Results in fever, diarrhea, wheezing, hepatitis, and visual loss (form chorioretinitis)
  • Dx: Serology or eosinophilia
59
Q

What is Taenia solium and what 2 ways can it be transmitted?

What occurs after ingestion of each form?

A
  • Pork tapeworm (Cestode), transmitted through ingestion of undercooked pork infected with LARVAE; pigsare theintermediate host
  • Larvae attach to mucosa of intestine via hooks on its scolex and grows to a length of 2-8 meters; usually cause minimal symptoms
  • If humans ingest eggs, they become the intermediate host and Cysticercosis occurs.
  • Eggs hatch within small intestine and the larvae migrate through the body, penetrating into tissue and encyst, most commonly in the brain and skeletal muscles –> Neurocysticercosis (seizures!)
60
Q

If Taenia solium eggs are ingested what occurs?

What are ths signs and symptoms?

Where is the infection endemic and is #1 cause of?

A
  • Eggs hatch in small intestne and larvae migrate throughout the body, penetrating into tissue and encyst, forming cysticerci (lesions)
  • Commonly in brain causing Neurocyticercosis causing seizures, obstructive hydrocephalus, or focal neuro defects
  • Endemic in areas such as Mexico, Central and South America, Philippines, and SE Asia, cysticercosis is the #1 cause of seizures
61
Q

How is the diagnosis of Cysticercosis caused by the Cestode, Taenia solium (pork tapeworm) made?

A
  • CAT scan or biopsy of infected tissue (brain or muscle), both of which may reveal calcified cysticerci (looks like swiss cheese on MRI)
  • Elevation of eosinophils in blood is a red flag!
62
Q

What is Diphyllobothrium latum and how it transmitted?

What clinical finding does it produce?

How is diganosis made?

A
  • The fish tapeworm (cestode), which is transmitted by ingesting larvae in raw freshwater fish
  • This large tapeworm provokes few abdominal symptoms, but can absrob vitamin B12 to a significant degree, leading to megaloblastic anemia!
  • Diagnosis of infection is made by identification of eggs in feces
63
Q

What is Hymenolepis nana and who is the intermediate host?

Causes what?

Diagnosis how?

A
  • The dwarf tapeworm (cestode), which has NO intermediate host
  • Humans ingest eggs that grow into adult tapeworms and adult tapeworms pass more eggs that are again ingested by humans
  • Causes abdominal discomfort and occasionally nausea and vomiting
  • Diagnosis made by eggs in stool
64
Q

What does Echinococcus granulosus and multilocularis infection cause?

What are the hosts and how is it spread?

A
  • Hydatid disease and Extra-intestinal Tapeworm Infection (cestodes)
  • Dogs are definitive host, sheep are intermediate host, humans are incidental host after ingesting eggs that were in dog feces that contaminated food or water
  • Hatch in the intestine and larvae penetrate intestinal wall disseminating through the body. Most larvae concentrated in the liver, but may also infect lungs, kidney, and brain
65
Q

After ingesting the eggs of Echinococcus granulosus and multilocularis what occurs inside the body?

How can they cause symptoms and what may they be mistaken for?

A
  • Each larvae forms a single, round fluid-filled “hydatid” cyst, which may causes symptoms as they compress the organs around them
  • Humans are extremely allergic to the fluid within the cyst, and if cyst burst, the allergic rxn (anaphylactic reaction) may be fatal

- E. multilocularis cysts undergo lateral budding and can be misdiagnosed as slowly growing tumors!

66
Q

If a surgeon is to remove a Hydatid cyst what technique is employed prior to operation?

A

Saline, iodophore, or ethanol is instilled into the cyst to make sure the contents are dead before removing the cyst

67
Q

If you suspect a diagnosis of infection by Echinococcus granulosus causin a hydatid cyst where would you take a tissue biopsy or employ a CAT scan to?

A

Most commonly the liver, but can also be seen in the brain

68
Q

Where are Trematodes (AKA flukes) - more speicifically Schistomas (blood flukes found?

How common are infections by these organisms?

How do they infect?

A
  • Free living acquatic organisms that penetrate through exposed skin and invade the venous system, where they mate and lay eggs
  • Infections are extremely common worlwide, second only to malaria as a cause of sickness in the tropics
69
Q

How is the diagnosis of Taenia solium made?

A

Demonstration of proglottids and/or eggs in a fecal sample

70
Q

How are the adult Schistomas (blood flukes) able to survive and release eggs inside the human for years?

A

Practice molecular mimicry, tricking the host’s immune system into thinking that the schistosomes are NOT foreign!

71
Q

Schistosoma japonicum and schistosoma mansoni (Trematodes) release eggs into portal circulation, which can lead to what detrimental effects?

A
  • Can cause severe chronic inflammation in the liver
  • Immune response to the eggs leads to liver fibrosis and blockage of the portal venous system, leading to backup of venous pressure into the spleen and mesenteric veins (portal HTN)
  • Pt’s may be jaundiced, have abdominal pain, and eventually succumb to liver failure
72
Q

Adult Schistoma haematobium (Trematode) reside where in the body and infection has what signs and symptoms?

What malignancy is this fluke associated with?

A
  • Veins surrounding the bladder
  • Cause inflammatory cystitis and granulomas, eventually leading to mucosal eruptions and hematuria.
  • Most frequent complication is inflammation and fibrosis of the ureteral walls, leading to obstruction, hydronephrosis, and chronic pyelonephritis
  • Association with squamous cell carcinoma of the bladder!
73
Q

What are part of the Trematode family?

Cestode family?

A
  • Trematodes (aka flukes) include the freshwater-dwelling schistosomes
  • Cestodes are also known as tapeworms!
74
Q

What are the intermediate hosts of the Trematodes, Schistosomas?

A

Snails

75
Q

After penetration of the skin by a Schistosoma larvae what occurs at the site of penetration?

What symptoms are seen 4-8 weeks later?

A
  • Dermatitis at the site of penetration, known as swimmers itch
  • Between 4-8 wks later Katayama fever follows, with symptoms including fever, hives, headache, weight loss, and cough
  • LN, liver, and spleen enlargement w/ eosinophilia are common
76
Q

What is the Geographic distribution of the Trematodes: Schistoma japonicum, mansoni, and haematobium

A
  • Japonicum = Eastern Asia
  • Mansoni = South America, Africa, and Middle East
  • Haematobium = Africa

*mod i exam 3 (16 decks)

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