Micro/simple/parasites

Front 1

What is Babesiosis?

Back 1

It is an infection very much like malaria. It is transmitted by the bite of a tick, and it invades and can be seen inside RBCs.
There are more than 100 species. They do not affect liver cells.

Front 2

What is babesia microti?

Back 2

It exists in the northeastern coastal US, and is spread by the bite of the same tick that spreads Lyme disease, (Ixodes scapularis).

Front 3

After biting the whitefooted mouse, the reservoir for B. microti, the tick will leap on the next human or animal passerby. TRUE/FALSE

Back 3

TRUE.

Front 4

What is the pathogenesis of Babesia?

Back 4

1. Babesia sporozoites exit from the ticks salivary glands into the blood of the the 2ary host.
2. The sporozoites invade RBCs and differentiate into pear or ring shaped trophozoites.
3. Trophozoites asexually bud and divide into 4 merozoites that stick together, forming a cross or x shaped tetrad(maltese cross).
4. RBC infection results in mild hemolysis so infection may be asymptomatic.
Asplenic patients are unable to clear the organisms as well and may have severe infection similar to falciparum malaria.

Front 5

How is babesiosis treated/

Back 5

Quinine and Clindamycin.

Front 6

Are Leishmania and Trypanosoma similar?

Back 6

Yes. They are both passed via a blood sucking insect, though they cause different diseases.
They can exist as rounded cells without flagella, called amastigotes, or as flagellated motile forms called promastigotes, epimastigotes and trypomastigotes. These are named according to the insertion site of their single flagellum.

Front 7

How is leishmania transferred?

Back 7

It is zoonotic, and carried by rodents, dogs and foxes and is transmitted to humans by the bite of a sandfly.
It is common in Central and South america, Africa and the Middle east.

Front 8

What happens following sandfly transmission?

Back 8

The promastigote invades phagocytic cells(macrophages) and transforms into the nonmotile mastigote.
The amastigote multiplies within macrophages, in the lymphnodes spleen liver and bone marrow.

Front 9

What are the three clinical forms of leishmaniasis?

Back 9

1. Cutaneous(simple and diffuse)
2. Mucocutaneous
3. Visceral

Front 10

A sandfly injects leishmania into the skin. TRUE/FALSE?

Back 10

TRUE. here they migrate to reticuloendothelial cells(fixed phagocytic cells in lymphnodes). A skin ulcer developscalled an oriental sore, it heals in a year, leaving a depigmented scar.

Front 11

Diagnosis of leishmania is made by observing the organism in stained skin scrapings from the ulcer base. TRUE/FALSE

Back 11

TRUE.

Front 12

What is the Leishmanin skin test?

Back 12

Because of the intact cell mediated immunity, this organism invokes a delayed hypersensitivity reaction.
Diagnosis can be made by injecting killed Leishmania intradermally. Just like the PPd test of tbc, a raised indurated papule 48 hrs later supports the presence of a leishmania infection.

Front 13

What is Diffuse Cutaneous Leishmaniais?

Back 13

A chronic form of cutaneous leishmaniasis occurs in patients with deficient immune systems. A nodular skin lesion arises, but does not ulcerate. It can last for 20 years.

Front 14

In Diffuse cutaneous leish., why is the leishmanin skin test often negative?

Back 14

The promastigotes are able to spread and infect the skin, causing diffuse nodular lesions. Due to the defect in cell mediated immunity, the Leishmanin skin test is negative.

Front 15

What is Mucocutaneous Leishmaniasis?

Back 15

A dermal ulcer arises at the site of the sandfly bite and soon heals. Months to years later, ulcers in the mucus membranes of the nose and mouth arise.
If untreated chronic erosion may occur, and death may ensue due to infection.

Front 16

What is Visceral leishmaniasis?

Back 16

Also known as Kala-Azar, the sandfly transmits Leishmania donovani to an individual, usually young malnourished children, who months later will complain of abdominal comfort and distension, low grade fevers and anorexias.

Front 17

What causes this abdominal distension?

Back 17

It is due to Leishmania donovani invasion of the reticuloendothelial cells of the spleen and the liver causing hepatomegaly and spleenomegaly.
90% of cases are fatal if untreated.

Front 18

How is this form treated?

Back 18

All forms of leishmaniasis can be treated with the pentavalent antimonial stibogluconate.

Front 19

What is African sleeping sickness?

Back 19

Trypanosoma rhodesiense and Trypanosoma gambiense are responsible for African sleeping sickness which is transmitted by the blood sucking bite of a tsetse fly.

Front 20

What happens after the tsetse fly bites its victim?

Back 20

The motile flagellated form of these 2 organisms, called a trypomastigote, spreads via the blood to lymphnodes and CNS.

Front 21

The first manifestation is a hard red painful skin ulcer that heals in 2 weeks. The patient then experiences fever, headache, dizziness and lymphnode swelling. TRUE/FALSE

Back 21

TRUE. Drowsiness and difficulty walking ensues. Slurred speech, coma and death may result as well.

Front 22

What are the 2 forms of African sleeping sickness?

Back 22

1. West African sleeping sickness-caused by T. brucei gambiense. It is noted for slow progressing fevers and late neurologic symptoms.
2. East African- caused by T. brucei rhodesiense, is more severe with death occuring within weeks to months.

Front 23

What causes the intermittent fevers of Trypanosomiasis?

Back 23

The trypanosomes are covered with about 10 million molecules of a repeating single glycoprotein called the VSG(variable surface proteins).
Trypanosomes possess genes that can make thousands of different VSGs. Every time the human host develops antibodies directed against the VSG, the trypanosomes produce progeny with a new VSG coat.

Front 24

Regarding VSGs, these are similar to the antigenic variation of the spirochete Borrelia recurrentis, which causes relapsing fever. TRUE/FALSE

Back 24

TRUE.

Front 25

How isdiagnosis acheived and what is the treatment if any?

Back 25

Diagnosis consists of visualization of trypomastigotes in peripheral blood, lymph nodes or spinal fluid.
patients are treated with Suramin, if the CNS is not involved. If the CNS is involved melarsoprol, which is very toxic, is employed.

Front 26

What is Chagas' disease?

Back 26

This is truly a disease of the Americas. It is caused by TRYPANOSOMA CRUZI AND IT SURVIVES IN WILD ANIMAL RESERVOIRS SUCH AS RODENTS, OPPOSUMS AND ARMADILLOS.

Front 27

Is there a vector for T. cruzi?

Back 27

Yes. The vector is the reduviid bug also called the kissing bug. It feeds on humans while they sleep and defecate whilr it eats.

Front 28

What is its pathogenesis?

Back 28

T. cruzi trypomastigotes, which are present in the bugs feces tunnel into the human host.
The trypomastigote loses its undulating membrane and flagellum and rounds up to form the amastigote which rapidly multiplies. organisms invade the skin, macrophages, lymphnodes and spread in the blood to organs.

Front 29

What is acute Chagas' disease?

Back 29

At the skin site of parasite entry, a hardened, red area develops called a chagoma.
This is followed by systemic spread with fever, malaise and swollen lymph nodes. The heart and CNS can be infected.

Front 30

What is the intermediate phase of acute Chagas' disease?

Back 30

The acute illness resolves in about a month and patients enter the intermediate phase. There are no symptoms but there are low levels of parasites in the blood as well as antibodies against T. cruzi.

Front 31

What is chronic Chagas' disease?

Back 31

The organs primarily affected are the heart and some hollow organs such as the colon and esophagus.
Strangely, intracellular T. cruzi amastigotes are not found.

Front 32

How is the heart affected?

Back 32

Arrythmias are an early sign, as well as heart block(1st and 2nd) and V. tach. Dilated cardiomyopathy may also be a sequela.

Front 33

A big dilated poorly functioning esophagus develops with symptoms of difficulty and pain in swallowing with regurgitation. TRUE/FALSE

Back 33

TRUE. Megacolon can result in chronic constipation.

Front 34

What is diagnosis of acute Chagas' disease?

Back 34

Direct exam of the blood for motile trypomastigotes.
Xenodiagnosis-40 lab grown reduviid bugs are allowed to feed on the patient, and one month later, their intestinal contents are examined for the parasite.

Front 35

Is there a treatment regimen?

Back 35

Although nifurtimox and benznidazole can be used for acute cases, there is currently no effective therapy for the chronic manifestations.

Front 36

What is Balantidium coli?

Back 36

Food or water contaminated with pig feces is the usual cause. The cysts mature into ciliated trophozoites and travel to the intestine tract. They dig into the intestinal wall where they easily exist cosuming native bacteria. Some patients develop diarrhea.

Front 37

Balantidium Coli trophozoites are noted for being the largest parasitic protozoans in the intestine. TRUE/FALSE

Back 37

TRUE. Diagnosis is made by identifying the ciliated trophozoites or cysts in stool specimens.

Front 38

What is the treatment?

Back 38

Tetracycline is effective.