Parasitology Exam 1: Parasitic Diseases

Be precise and know, all free response: Terms, Drugs, Vector genus/species name (spelling matters), geography,

Parasite listing (Species name, genus, life cycle, reservoir hosts, diagnosis (what you do and what you look for), course of infection including vector, pathology/symptoms, epidemiology)

Be able to answer clinical case studies

What is the Trypanosomatidae genus that cause trypanosomiasis?

Trypanosoma

What is the Trypanosomatidae genus that causes Leishmaniasis?

Leishmania

What are the Trypanosome species that infects humans?

Trypanosoma brucei and Trypanosoma cruzi

What are the 3 Trypanosoma brucei subspecies that are the main causes of African Trypanosomiassis?

T.b. brucei → not infectious for humans, only livestock → causes Nagana disease

T.b. gambiense → infects humans, more common

T.b. rhodesiense → infects humans, rare

Characteristics of Trypanosomiasis from T.b. brucei

Acute → severe weight loss, equines, some ruminants, dogs, weeks, deathly

Chronic → severe weight loss, most common in cows, months, deathly

Swine usually recover from both.

T.b. gambiense Pathology/Symptoms

6 months → years

Most common form of Trypanosomiasis.

Pathology: invade central nervous system (enter spinal fluid), alters circadian rhythm causing sleeping sickness.

Symptoms: asymptomatic for months, after few months → intermitant high fever, swollen lymph nodes on neck and legs, lack of coordination, altered mental state

50% mortality of untreated patients

T.b. rhodesiense Pathology Symptoms

1-6 months

Symptoms: rapid weight loss, cardiac problems

100% mortality of untreated patients

Much more rare

T.b. gambiense Diagnosis/Treatment

Early stage → Pentamidine (intramuscular), Feximidazole (oral)

Late stage → Eflornithine (intravenous) normally co-administered with Nifurtinox (oral)

T.b. rhodesiense Diagnosis/Treatment

Early → Suramin (intravenous) serious side effects

Late → Melarsoprol (intravenous) horrible side effects

Tsetse fly ecology

Glossina morsitans → Diurnal, Sylvatic, Peri-domestic, domiciliary (factors vary by species)

Glossina palpalis and Glossina tachinoides → riverine/rainforest, peridomestic

What is the tsetse fly species that is a vector of T. rhodesiense?

Glossina morsitans

How could you control T.b. rhodesiense?

Vector control → removing brush where flies rest, arial spraying

• switch to night grazing

What are the tsetse fly species that are the vectors for T. gambiense?

Glossina palpalis and Glossina trachinoides

How could you control T.b. gambiense?

Can’t do vector control bc of rainforest habitat. Best way is to periodically test everyone and give medication

Life cycle of Trypanosoma brucei (subspecies have same life cycle)

1) fly takes blood meal by injection, and transmits metacyclic trypomastigotes

2) metacyclic trypomastigotes transform → bloodstream trypomastigote

3) multiply in bloodstream or spinal fluid

4) Many Trypomastigotes are now in blood

5) trypomasitgotes picked up by fly through bloodmeal

6) Now in the fly, bloodstream tryopomastigotes trasnform → procyclic trypomastigotes and multiply

7) Procyclic trypomastigotes leave mid gut and transform → epimastigotes

8) Epimastigotes multiply in salivary gland and transofrm → metacyclic trypomastigotes

Back to 1

Do the white blood cells attack the trypomastigotes while in bloodstream?

Yes, which is what causes the intermittent fever. But they don’t kill all of them because they have a Glycocalix (=surface coat with antigen proteins) that changes per individual. The one with the right protein slips past WBC.

How does the glycocalix work?

The surface is covered with millions of copies of one antigen protein. There are 100 different proteins that it could be, but only one gene (one protein) is expressed per individual. Expression is timed through generations, and is somewhat predictable.

What does VSG stand for?

Variant specific Glycoprotein. Mainly refers to the different proteins that could make up the glycocaliz in trypanosomes.

What’s another name for American Trypanosomiasis?

Chaga’s disease

What’s the species that causes Chaga’s disease?

Trypanosoma cruzi

Intermediate hosts of Trypanosoma cruzi?

“Kissing bugs”, most common → subfamily Triatomine: Rhodnius prolixus, Triatoma infestans

Life cycle of Trypanosoma cruzi

1) Triatimine bug takes bloodmeal from human and poops, dropping trypomastigotes

2) T. cruzi travels into a cell at bite site and transform → amastigotes

3) Amastigotes multiply in the cell and burst out

4) Now intracellular amastigotes transofmr → trypomastigotes and enter bloodstream (could go back to 3rd step at this point)

5) Get picked up by fly

6) Trypomastigotes transform → epimastigotes in midgut

7) Multiply in midgut

8) epimastigotes → Metacyclic trypomastigotes now in hindgut, waiting to be pooped out (back to 1)

Phases of American trypanosomiasis

1) Acute

2) Late acute

3) Chronic

T. cruzi acute pathology/symptoms

Pathology: Most common in children under 5, localized inflammation.

Symptoms: persistent fever/chills, fatigue, swollen lymph nodes, anemia, nervous disorders

May resolve sponraneously

T. cruzi late acute pathology/symptoms

Pathology: pseudocyst in heart whose rupture causes inflammation. Death in 3-4 weeks

Symptoms: local inflammation, heart failure

T. cruzi chronic pathology symptoms

Arises if acute left untreated

Pathology: Heart, digestive tract swell, creating swollen abdomen. Results in heart failure

T. cruzi diagnosis/treatment

Diagnosis: look for trypanosomes in blood during early stage (during fever). Test for antibodies, xenodiagnosis → use bugs to feed and bring up tryps

Drugs: Acute → Benznidazole and nifurtinox (both serious side effects)

Chronic → treat symptoms

T. cruzi epidemiology

Sylvatic, peridomestic through rats/opossoms, domiciliary from Rhodnius prolixas and Triatoma infestans (nocturnal and prefer houses with cracks (i.e. thatch roofs and log/stick walls)). More severe in people from South America.

What hemoflagellate causes Leishmaniasis?

Leishmania genus

What are the 3 forms of leishmaniasis?

1) Visceral (most severe/deadly)

2) Cutaneous (most common)

3) Mucocutaneous (most disfiguring)

Leishmania life cycle

1) Sandfly takes blood meal by tearing into skin and promastigotes fall into wound site

2) Promastigotes phagocytized by macrophages (White blood cells)

3) Promastigotes transform → amastigotes inside macrophage

4) Amastigotes multiple and burst out of cell (cell lysis)

5) Sandfly takes blood meal and picks up macrophages with the amastigotes

6) ingests and destroys the macrophages, leaving amastigotes in the midgut

7) amastigote transform → promastigote in midgut

8) multiply and migrate to proboscis (back to 1)

Main species that cause Visceral Leishmoniasis

in Eastern Hemisphere (EH) → Leishmania donovani

in Western Hemisphere (WH) → Leishmania chagasi

What are the main species that cause Cutaneous Leishmaniasis?

EH → L. tropica, L. major

WH → L. mexicana

What are the main species that cause Mucocutaneous Leishmaniasis?

WH → L. braziliensis (more common), L. mexicana

Pathology/Symptoms of Visceral Leishmaniasis

Pathology: Move from skin to other tissues (lymph nodes, spleen, liver). The amastigotes kill the WBC so bone marrow makes more WBCs than RBCs, causing lack of RBCs (anemia)

Symptoms: Anemia, fever malaise, heplatosplenomegaly (spleen and intestine grow very large, showing swollen abdomen)

Diagnosis/Treatment of Visceral Leishmaniasis

Look for trypomastigotes internal tissues

Drugs: Pentostam (injection), glucantine (injection), miltefosine (better side effects and oral)

What does a relapse of visceral leishmaniasis appear as, and what causes it?

Caused by incomplete treatment the first time. Shows as Post-kala-azar dermal leishmanoid

Visceral Leishmaniasis epidemiology

common countries: Brazil, Kenya

dogs are the reservoir host

Cutaneous Leishmaniasis pathology/symptoms

Skin ulcer localized to bite site.

Cutaneous Leishmaniasis diagnosis/treatment

diagnose by ulcer, taking sample and looking for amastigotes (few → L. major, lots → L. tropica)

Treatment: natural healing is normally best

Drugs: Pentostam, glucantine

Cutaneous Leishmaniasis epidemiology

• Most important fly genus is Phlebotomus

• L. mexicana appears in northern South America

• L. tropica in Eastern Europe. Domiciliary, many amastigotes in ulcer

• L. major in West Africa, Saudi Arabia, Middle East. Sylvatic, few amastigotes in ulcer

Mucocutaneous Leishmaniasis pathology/symptoms

Initial: lesions at bite site

Secondary: lesions/infection spreads to buccal and nasal openings

Mucocutaneous Leishmaniasis epidemiology

Common countries: Brazil

small rodents main reservoir. L. braziliensis is sylvatic so hard to control.

What are the main Amoeba genera that’s parasitic?

Entamoeba, Iodamoeba, Endolimax

What are the 2 common, parasitic Entamoeba species?

Entamoeba histolytica, Entamoeba coli

Entamoeba histolytica course of infection

1) Ingest Metacyst (mature cyst, immature cysts are not infectious)

2) Excyst (transform → trophozoite) in small intestine

3) Multiply, feeds onlarge intestine

3a) gets into bloostream and travels to brain, liver, lungs and forms ulcers

3b) Form a cyst in large intestine to get pooped out

Entamoeba histolytica pathology

broken (eaten) intestinal lining, ulcers, perforated colon

Entamoeba histolytica symptoms

• Light infection → asymptomatic (epidemiologically most worrisome)

• Moderate infection → intermittent diarrhea, no fever, loose stool

• High infection → high abdominal pain/cramps, lots of loose stool per day, ulcers in blood vessels

Entamoeba histolytica diagnosis/treatment

1) look for cysts and/or trophozoites in fecal

2) might need to sample blood if spread

Drugs: Metronidozole, If in liver → Trinidazol, ornidazole

Entamoeba histolytica epidemiology

Metacyst is the only one that’s infectious and survives (Trophozoites die)

• Reservoir host → asymptomatic humans, sometimes dogs/pigs

• Location → tropics

• Mechanical vectors → roaches or flies walking through feces

People with diarrhea are not passing cysts, they’re passing throphozoites, so they can’t infect anybody else.

Naegleria fowleri is an __________, ________parasite.

opportunistic, free-living

Naegleria fowleri pathology

cyst travels up nasal to brain and starts eating. Death within a week.

Naegleria fowleri symptoms

vomitting, high fever

Naegleria fowleri treatment

Drugs: miltefosine

Naegleria fowleri epidemiology

aerobic in soil and water. Rapid proliferationin high heat. People get infected during water activities in high heat, when water gets up the nose.

The acanthomoeba genus are ________, _________ parasites

opportunistic, free-living

How do people get infected with Acanthomoeba species?

infects the eye, normally through contact solution

Acanthomoeba symptoms

Immunocompitent → may become blind in infected eye

Immunocompromised → eye and skin infections, other bad internal things

What’s the difference Diplomonada and Parabasalia?

Diplomonada: at least 2 nuclei, multiple symmetrical flagella

Paranasalia: 1 nucleus, rigid axostyle, undulating membrane connected to flagella

Is Giardia duodenalis diplomonada or parabasalia?

diplomonada

Giardia duodenalis life cycle

1) human consumes infectious cyst through contaminate water/food

2) Cyst transform to → trophozoite and split in 2 in small intestine and starts feeding

3) Trophozoite Encysts when it gets close to the colon

4) cyst gets pooped out (back to 1). If trophozoite gets pooped out through diarrhea it dies quickly in environment

Giardia duodenalis pathology/symptoms

Pathology: inflammation, irritation

Symptoms: diarrhea, abdominal pain

Giardia duodenalis diagnosis/treatment

Diagnosis: trophs/cysts in fecal

Drugs: metronidazole or quinacrine

Giardia duodenalis epidemiology

Most common intestinal parasite in U.S.

Can be found in many mammals, common in pets, and obviously zoonotic.

Is Trychomonas vaginalis a diplomonada or parabasalia?

Parabasalia because of its undulating membrane

Trichomonas vaginalis course of infection

vagina, urethra, prostate, seminal vesicles. Feeds on bacteria, leukocytes, and cell exudates

Trichomonas vaginalis epidemiology

Sexually transmitted

Trichonomas vaginalis diagnosis/treatment

Diagnosis: take pap smear and look for trophozoites

Drugs: Metronidazole

Balantidium coli is the only ______ parasite of humans, and is the _____-est protozoan

ciliate; largest

Balantidium coli course of infection

1) Cyst is ingested by human

2) Excyst and travel to colon and lumen of large intestine where they multiply

3) Encyst and are passed in feces

Balantidium coli pathology/symptoms

Usually asymptomatic, mild-moderate chronic diarrhea, or acute dysentery (bloody diarrhea).

Deep intestinal ulcers and occasional perforation on large intestine → abdominal pain.

Balantidium coli diagnosis/treatment

Diagnosis: Take fecal and look for trophs/cysts

Drugs: Tetracycline

Balantidium coli epidemiology

Rare

reservoir host → swine

Trophs cannot last long in environment