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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
Four species of Plasmodium that cause malaria in humans.
- P. falciparum *** <-- MOST CASES*** - P. malariae - P. ovale - P. Vivax
26
Plasmodium lifecycle
- 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)
27
special things that P vivax and P ovale can do?
-they can go into a dormant liver stage that sits around for years/decades and shows up way later
28
Plasmodium spp - transmission
bite of infected mosquito
29
(symptoms) characteristic clinical feature of malaria=
- 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
Duration and Pattern of paroxysm in P vivax
reoccurrence every 48 hrs
31
Duration and Pattern of paroxysm of P ovale
reoccurrence every 48 hrs
32
Duration and Pattern of paroxysm of P malariae
reoccurrence every 72 hrs
33
Duration and Pattern of paroxysm of P falciparum
reoccurrence every 48 hrs
34
malarial paroxysm stages:
- 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
common complication of malaria?
-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
highest level of infected RBC with which plasmodium species?
P Falciparum bc it can infect RBC of all ages
37
P vivax and P ovale can only infect what kind of RBC?
reticulocytes
38
P malariae prefers to infect what kind of RBC?
OLDER erythrocytes
39
severe anemia with whihc plasodium organism?
P Falciparum bc it can infect RBC of all ages
40
Other symptoms of Malaria?
- Splenomegaly - Hypoglycemia / lactic acidosis-P. falciparum - Microvascular sequestration-P. falciparum:Cerebral malaria
41
common complication of malaria?
-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
highest level of infected RBC with which plasmodium species?
P Falciparum bc it can infect RBC of all ages
43
purple banana looking thing in a blood smear w/ patient who has travel hisotry which organism
P. Falciparum - sexual form (gametocyte)
44
P malariae prefers to infect what kind of RBC?
OLDER erythrocytes
45
severe anemia with whihc plasodium organism?
P Falciparum bc it can infect RBC of all ages
46
Other symptoms of Malaria?
- Splenomegaly - Hypoglycemia / lactic acidosis-P. falciparum - Microvascular sequestration-P. falciparum:Cerebral malaria
47
Plasmodium diagnosis
- Recognize clinical syndrome (high fever that comes and goes in patterns) - Travel history - Blood smear positive for parasites
48
P. Falciparum under microscpoe:
tend to get RBC with mult rings
49
Babesiosis under the microscope?
parasites form a maltese cross
50
P Vivax and Ovale under microscpoe:
weird staining patterns with inclusions | -RBC have funny cells
51
Malaria- Control/Prevention/Treatment
- Eradicate insect vector / breeding grounds - Prophylaxis for travelers - Vaccine trials have been disappointing - Drug resistance is a major concern
52
Babesiosis - caused by? vector? Where are most cases?
- Babesia spp.- - bite of a tick - most cases reported New England, Upper Midwest and California
53
Babesiosis - symptoms
-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
Babesiosis - treatment
-atovaquone and azithromycin (quinine / clindamycin)
55
Babesiosis under the microscope?
parasites form a maltese cross
56
Filariasis - causes? what kind of worm? where do these cells live? vectors?
- 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
B. malayi causes and where found?
- Filariasis -lymphatic filariasis | - India, South East Asia, China, Korea, Japan.
58
W. bancrofti
- Filariasis -lymphatic filariasis - Central Africa, Mediterranean coast, Asia, Indonesia, New Guinea, the Caribbean, and parts of central and South America.
59
Filariasis - lifecycle:
- 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
Filariasis - diagnosis/presentation/treatment
look for larvae in blood smear collected at night - painful swelling may progress to elephantitis - eopsiophilia, asthma - drainage, surgery, drugs
61
Schistosomiasis - caused by? where found? transmitted how?
- Schistosoma spp - Africa and South America - eggs passed in poop
62
Schistosomiasis - lifecycle
- 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
Schistosomiasis - chronic symptoms?
Chronic infection results from the lodging of eggs in tissue, resulting in inflammation.
64
S. mansoni & S. japonicum - cause what? where do they liek to infect? consquences of infection
-Schistosomiasis -venous plexus of the small intestine -Chronic intestinal and hepatic dysfunction. Portal fibrosis, portal hypertension.
65
S. haematobium - causes what/ where does it like to live? consequences of infection?
-Schistosomiasis -venous plexus of the bladder -hematuria, dysuria, urinary frequency. loss of bladder function increased occurrence of squamous cell carcinoma of the bladder.
66
Schistosomiasis - dagnosis/treatment/control prevention
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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