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Micro 7 > Parasite Inf of Circ, Lymph, Res > Flashcards

Parasite Inf of Circ, Lymph, Res Flashcards

1
Q

African Trypanosomiasis - caused by? vector? intracellular?

A
  • T. brucei
  • Tsetse flies
  • NONE
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2
Q

Chagas’ Disease - caused by? vector? intracellular?

A
  • T. cruzi
  • Reduvid Bugs
  • Yes, skeletal and cardiac muscle cells; others
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3
Q

Leishmaniasis - caused by? vector? intracellular?

A
  • Leishmania sp.
  • Sandflies
  • Yes, macrophages
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4
Q

Malaria - caused by? vector? intracellular?

A
  • Plasmodium sp.
  • Mosquitoes
  • Yes, RBCs, hepatocytes
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5
Q

Babesiosis - caused by? vector? intracellular?

A
  • Babesia sp.
  • Ticks
  • Yes, RBCs
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6
Q

African Trypanosomiasis - casued by? found where? vector?

A
  • Trypanosoma brucei
  • Sleeping sickness
  • only in africa
  • tsetse fly
  • affects a lot of cattle in Africa
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7
Q

2 types of African Trypanosomiasis

A
  • West African – T. brucei gambiense = human to human spread

- East African – T . brucei rhodesiense = human to human, animal to human

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8
Q

African Trypanosomiasis presentation/symptoms

A

1) Early stage of infection:
- Organisms in blood and peripheral lymph nodes
- Fever, myalgia, chills, lymph node swelling (West)
2) Late stage of infection
- Invasion of CNS –> in CSF
- Headache, seizures, tremors, encephalitis, periods of sleeplessness and lethargy, coma and death.

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9
Q

African Trypanosomiasis - infectious process

A
  • tsetse fly takes a bite out of inf fly
  • some developmental process in the fly cut/saliva
  • bites human host
  • constant cycle of antigenic variation on surface of orgnaism = immune system can never clear all of them
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10
Q

Does east or west african form develop quicker?

A

east form is quicker both with incubation, easrly stage and late stage CNS involvement

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11
Q

African Trypanosomiasis - diagnosis/control

A
  • detection of parasites in blood smear, lymph node aspirates, or CSF
  • control disease by controlling flies
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12
Q

African Trypanosomiasis - treatment

A
  • melarsoprol - toxic-might kill host

- difluoromethylornithine (DFMO) - much better to use

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13
Q

Chagas’ Disease -casued by? found where? vector?

A
  • Trypanosoma cruzi
  • Reduvid Bugs
  • South and Cetnral America
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14
Q

Chagas’ Disease - infectious process

A
  • reduvid bugs bite infected animal
  • parasites develop in GI
  • bug bites human usually on face somewhere and poops where it feed
  • new parasites are in the POOP - and you rub the poop into your eye or some wound
  • in South & Central America
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15
Q

Chagas’ Disease - transmission

A
  • Bite /Defecation of infected reduviid bug.

- Blood Transfusion

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16
Q

Chagas’ Disease - symptomology

A
  • First sign of infection is development of chagoma - hard bump at site of bite
  • Romana’s sign =result of rubbing it into your eye
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17
Q

Chagas’ Disease - presentation

A

1) Acute phase=Fever, malaise, myalgia and hepatosplenomegaly
2) Indeterminate (Asymptomatic phase)= Few parasites in blood. High level of Ab.
Most individuals remain in this phase for life.
3) Chronic disease (10-30% individuals)= Infection of cardiac muscle and myenteric plexus.
Develops years to decades after infection.
Cardiac and GI involvement.
Congestive heart failure / Megacolon, Megaesophageous (loss of perstalsis)

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18
Q

T. cruzi vs T. brucei

A

T Cruzi can get into cells like heart and stuff

T. Bruzi cant get into cells- mostly in blood

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19
Q

Chagas’ Disease - diagnosis

A
  • need a good travel history’
  • Acute phase-detection of parasites in peripheral blood.
  • Chronic disease-serology
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20
Q

Leishmaniasis -casued by? vector?

A
  • Leishmania sp.
  • Sandflies
  • Lives inside macrophages
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21
Q

Leishmaniasis - lifecycle

A
  • sandflies get and bite human
  • flagellated forms in host –> into macrophages
  • differentiates into a amastegotes and lives in a macrophage
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22
Q

Leishmaniasis - 3 clinical presentations

A
  • Cutaneous – (L. major, L. tropica, L. mexicana)
  • Mucocutaneous – (L. braziliensis)
  • Visceral – (L. donovani, L. infantum, L. chagasi)
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23
Q

Visceral Leishmaniasis orgnaisms and infectious process

A
  • L. donovani, L. infantum, L. chagasi
  • Involves the dissemination of parasites throughout the reticuloendothelial system. -Parasites can be found in macrophages of the liver, spleen, bone marrow, etc.
  • Initial cutaneous lesion may or may not be seen.
  • Symptoms are thought to develop months (possibly years) after inoculation.
  • Initial presentation is usually an irregular low grade fever.
  • Most infections are asymptomatic and resolve.
  • Full blown disease presents as fever, weight loss, hepato-splenomegaly, a “wasting “ appearance.
  • Systemic immuno-suppression is common.
  • Secondary bacterial and viral infection is the typical cause of death
  • Fulminate visceral leishmaniasis typically occurs in the very old, very young, or malnourished.
  • Disease is fatal (90%) if untreated.
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24
Q

killing Leishmaniasis organims that are in macrophages

A

gamma interferon to activate macropages - cell mediated immunity

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25
Q

Four species of Plasmodium that cause malaria in humans.

A
  • P. falciparum * <– MOST CASES*
  • P. malariae
  • P. ovale
  • P. Vivax
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26
Q

Plasmodium lifecycle

A
  • moswqito picks up parasite
  • deveolpment into mature-er parasites in mosquito GI
  • mosquito biteshuman and injects via salivary glands
  • parasites clearedin the liver and infect hepatocytes - differentiation and replication process
  • after development released from liver into circulation (all signs of disease start showing)
  • start infecting RBC (and hepatocyte)
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27
Q

special things that P vivax and P ovale can do?

A

-they can go into a dormant liver stage that sits around for years/decades and shows up way later

28
Q

Plasmodium spp - transmission

A

bite of infected mosquito

29
Q

(symptoms) characteristic clinical feature of malaria=

A
  • malarial paroxysm=This is associated with the synchronous release of merozoites, and the lysis of RBCs. This presents with flu-like symptoms, most notably fever, chills, headache, and muscle ache.
  • This process of symptoms goes through cycles as RBC are destroyed (ANEMIA) due to increasing numbers of plasmodium inside - depends on species
30
Q

Duration and Pattern of paroxysm in P vivax

A

reoccurrence every 48 hrs

31
Q

Duration and Pattern of paroxysm of P ovale

A

reoccurrence every 48 hrs

32
Q

Duration and Pattern of paroxysm of P malariae

A

reoccurrence every 72 hrs

33
Q

Duration and Pattern of paroxysm of P falciparum

A

reoccurrence every 48 hrs

34
Q

malarial paroxysm stages:

A
  • Cold Stage (15-60 min)-rigors, cold dry skin, high core temperature, rapid pulse, nausea, vomiting
  • Hot Stage (2-6 hrs)-severe headache, palpitations, confusion, delirium.
  • Sweat Stage (8-12 hrs)–perspiration, exhaustion, sleep
35
Q

common complication of malaria?

A

-Anemia!!!
-The asexual stage of the parasite destroys RBCs each time it completes a cycle of replication.
Three mechanisms involved in the pathogenesis of anemia:
1. RBC lysis by mature asexual intra-erythrocytic parasites.
2. Suppression of erythropoiesis by cytokines (TNF-a, IL-1). (loosing red cells and cant make more!)
3. Destruction of RBCs by the spleen.

36
Q

highest level of infected RBC with which plasmodium species?

A

P Falciparum bc it can infect RBC of all ages

37
Q

P vivax and P ovale can only infect what kind of RBC?

A

reticulocytes

38
Q

P malariae prefers to infect what kind of RBC?

A

OLDER erythrocytes

39
Q

severe anemia with whihc plasodium organism?

A

P Falciparum bc it can infect RBC of all ages

40
Q

Other symptoms of Malaria?

A
  • Splenomegaly
  • Hypoglycemia / lactic acidosis-P. falciparum
  • Microvascular sequestration-P. falciparum:Cerebral malaria
41
Q

common complication of malaria?

A

-Anemia!!!
-The asexual stage of the parasite destroys RBCs each time it completes a cycle of replication.
Three mechanisms involved in the pathogenesis of anemia:
1. RBC lysis by mature asexual intra-erythrocytic parasites.
2. Suppression of erythropoiesis by cytokines (TNF-a, IL-1). (loosing red cells and cant make more!)
3. Destruction of RBCs by the spleen.

42
Q

highest level of infected RBC with which plasmodium species?

A

P Falciparum bc it can infect RBC of all ages

43
Q

purple banana looking thing in a blood smear w/ patient who has travel hisotry which organism

A

P. Falciparum - sexual form (gametocyte)

44
Q

P malariae prefers to infect what kind of RBC?

A

OLDER erythrocytes

45
Q

severe anemia with whihc plasodium organism?

A

P Falciparum bc it can infect RBC of all ages

46
Q

Other symptoms of Malaria?

A
  • Splenomegaly
  • Hypoglycemia / lactic acidosis-P. falciparum
  • Microvascular sequestration-P. falciparum:Cerebral malaria
47
Q

Plasmodium diagnosis

A
  • Recognize clinical syndrome (high fever that comes and goes in patterns)
  • Travel history
  • Blood smear positive for parasites
48
Q

P. Falciparum under microscpoe:

A

tend to get RBC with mult rings

49
Q

Babesiosis under the microscope?

A

parasites form a maltese cross

50
Q

P Vivax and Ovale under microscpoe:

A

weird staining patterns with inclusions

-RBC have funny cells

51
Q

Malaria- Control/Prevention/Treatment

A
  • Eradicate insect vector / breeding grounds
  • Prophylaxis for travelers
  • Vaccine trials have been disappointing
  • Drug resistance is a major concern
52
Q

Babesiosis - caused by? vector? Where are most cases?

A
  • Babesia spp.-
  • bite of a tick
  • most cases reported New England, Upper Midwest and California
53
Q

Babesiosis - symptoms

A

-Symptoms develop 1-8 weeks after bite.
fever, chills, myalgia, hemolytic anemia-replication of parasites in RBCs
-Many infections are asymptomatic
-The elderly, asplenic, and immunosuppressed are at highest risk of symptomatic infection.

54
Q

Babesiosis - treatment

A

-atovaquone and azithromycin (quinine / clindamycin)

55
Q

Babesiosis under the microscope?

A

parasites form a maltese cross

56
Q

Filariasis - causes? what kind of worm? where do these cells live? vectors?

A
  • lymphatic filariasis) is caused by the filarial nematodes Wuchereria bancrofti and Brugia malayi.
  • NEMATODES - transmitted by mosquito
  • adult forms reside within the lumen of lymphatic vessels.
57
Q

B. malayi causes and where found?

A
  • Filariasis -lymphatic filariasis

- India, South East Asia, China, Korea, Japan.

58
Q

W. bancrofti

A
  • Filariasis -lymphatic filariasis
  • Central Africa, Mediterranean coast, Asia, Indonesia, New Guinea, the Caribbean, and parts of central and South America.
59
Q

Filariasis - lifecycle:

A
  • mosquito gets
  • dev in mosquito
  • bite human and move into lymphatics-(lymphatics of the upper and lower extremities and male genitalia.) where it lives
  • more microfilariae released into blood stream
60
Q

Filariasis - diagnosis/presentation/treatment

A

look for larvae in blood smear collected at night

  • painful swelling may progress to elephantitis - eopsiophilia, asthma
  • drainage, surgery, drugs
61
Q

Schistosomiasis - caused by? where found? transmitted how?

A
  • Schistosoma spp
  • Africa and South America
  • eggs passed in poop
62
Q

Schistosomiasis - lifecycle

A
  • eggs passed in poop
  • snails are intermediate host
  • snails release infectious form
  • infectious form can penetrate skin (swimmin in dirty ass water literally)
  • get into bladder and colon = in poop and pee
63
Q

Schistosomiasis - chronic symptoms?

A

Chronic infection results from the lodging of eggs in tissue, resulting in inflammation.

64
Q

S. mansoni & S. japonicum - cause what? where do they liek to infect? consquences of infection

A

-Schistosomiasis
-venous plexus of the small intestine
-Chronic intestinal and hepatic dysfunction.
Portal fibrosis, portal hypertension.

65
Q

S. haematobium - causes what/ where does it like to live? consequences of infection?

A

-Schistosomiasis
-venous plexus of the bladder
-hematuria, dysuria, urinary frequency.
loss of bladder function
increased occurrence of squamous cell carcinoma of the bladder.

66
Q

Schistosomiasis - dagnosis/treatment/control prevention

A

Diagnosis : Eggs in feces or urine

Control / Prevention :
Control snail population
Limit exposure to water
Improve sanitation

Micro 7 (6 decks)

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