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Microbiology > Infections of the Circulatory, RES & Lympahtics-Parasitic > Flashcards

Infections of the Circulatory, RES & Lympahtics-Parasitic Flashcards

1
Q

Agent of African Trypanosomiasis

A

T. brucci

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2
Q

Agent of Chagas’ Disease

A

T. cruzi

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3
Q

Leishmaniasis agent

A

Leishmania sp.

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4
Q

Malaria agent

A

Plasmodium sp.

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5
Q

Babesiosis agent

A

Babesia sp.

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6
Q

T. brucci (African Trypanosomiasis) vector

A

Tsetse flies

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7
Q

T. cruzi (Chagas’ Disease) vector

A

Reduvid Bugs

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8
Q

Leishmania sp. (Leishmaniasis) vector

A

Sandflies

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9
Q

Plasmodium sp. (Malaria) vector

A

Mosquitoes

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10
Q

Babesia sp. (Babesiosis) vector

A

Ticks

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11
Q

Sleeping sickness (African Trypanosomiasis) is caused by

A

Trypanosoma brucei

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12
Q

causes wasting disease in cattle called “Nagana”

A

Trypanosoma brucei

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13
Q

causes west african sleeping sickness (human to human)

A

T. brucei gambiense

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14
Q

causes east african sleeping sickness (human to human, animal to human)

A

T. brucei rhodesiense

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15
Q

Early stage of African Trypanosomiasis infection

A

organisms in blood and peripheral lymph nodes, also fever, myalgia, chills, lymph node swelling (West)

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16
Q

Late stage of African Trypanosomiasis infection

A

Invasion of CNS, headache, seizures, tremors, encephalitis, periods of sleeplessness and lethargy, coma and death

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17
Q

This form of African Trypanosomiasis (sleeping sickness) has a longer incubation period of weekts to months and CNS involvement after weeks or years as opposed to the other form which develops both within a month

A

West African form

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18
Q

Dx: African Trypanosomiasis

A

detection of parasites in blood smear, lymph node aspirate, or CSF

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19
Q

Control of African Trypanosomiasis

A

control tsetse fly populations

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20
Q

African Trypanosomiasis is the classical example of this immune defense

A

Antigenic variation

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21
Q

Tx of African Sleeping Sickness

A

melarsoprol (80% effective, but 5% or more develop encephalopathy due to drug-replaced now by DFMO)
difluoromethylornithine (DFMO)

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22
Q

First signs of Chagras’ disease

A

fever, local swelling, periorbital edema, myocarditis myalgia, malaise, hepatosplenomegaly

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23
Q

Once in the human host Trypanosoma cruzi takes on this form which spread systemically over many years

A

amastigote

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24
Q

Chronic Chagras’ disease- due to infection of cardiac muscle and myenteric plexus

A

dysrhythmias, cardiomyopathy, megaesophagus, megacolon (death from heart attack)

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25
Q

Reduvid bugs pass Trypanosoma cruzi to humans by

A

through the feces left on the skin after biting the human

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26
Q

What is one resevoir for Chagras’ disease in the lower US?

A

animal vectors (raccoons, opossums)

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27
Q

periorbital edema caused by Chagras’ disease-first sign

A

Romana’s sign

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28
Q

most individuals remain in this stage for life where there are few trypanosoma cruzi in the blood and a high level of Ab

A

Indeterminate (Asymptomatic phase)

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29
Q

What is the biggest difference between African and American Trypanosomiasis

A

African Trypanosomiasis is extracellular, American is intracellular

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30
Q

Dx: acute phase of American Trypanosomiasis

A

detection of parasites in peripheral blood

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31
Q

Dx: chronic disease

A

serology

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32
Q

has a single flagella

A

Leishmania spp.

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33
Q

intracellular in macrophages

A

Leishmania spp

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34
Q

transmitted by flies which pick up blood from an infected individual including infected macrophages and spreads it to another individual

A

Leishmania spp.

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35
Q

opportunistic pathogen in HIV + individuals, primarily in the mediterranean

A

Leishmaniasis

36
Q

important resevoirs of Leishmaniasis

A

Canines, rodents

37
Q

3 forms of Leishmaniasis

A

cutaneous, mucocutaneous, visceral

38
Q

Visceral form of Leishmaniasis is caused by

A

L. donovani, L. infantum, L. chagasi

39
Q

parasites are found in the reticuloendothelial system-macrophages of liver, spleen, bone marrow, etc

A

Leishmaniasis

40
Q

full blown disease presents as fever, weight loss, hepato-splenomegaly, a “wasting” appearance, systemic immuno-suppression

A

Leishmaniasis-visceral

41
Q

common cause of death is secondary bacterial and viral infection

A

Leishmaniasis visceral

42
Q

Why do antibodies afford little or no protection against Leishmaniasis?

A

Leishmaniasis have only intracellular amastigotes-so antibodies won’t work!

43
Q

Tx: Leishmaniasis

A

gamma-interferon mediated activation of macrophages, heavy metal compounds (considerable toxicity)

44
Q

Eliminated malaria from the US in 1940s using

A

DDT, draining swamps and wetlands, and screens for windows/air conditioning-reduced exposure tme

45
Q

Why do competent vector mosquitoes in the US typically not spread malaria

A

there are few individuals to transmit it from, can happen if an infected traveler returns to the US

46
Q

4 species of Plasmodium that cause malaria in humans

A

P. falciparum, P. vivax, P. malariae, P. ovale

47
Q

Species that take on a form called a hypnozoite that can stay dormantin the liver for decades and then can cause malaria (common in vietnam vets)

A

P. vivax, P. ovale

48
Q

characteristic clinical feature of malaria

A

malarial paroxysm-merozoites lysing RBCS when replicating, causes flu-like symptoms (fever, chills, headache, muscle ache)

49
Q

flu-like patterns recur every 48 hrs

A

P. vivax, ovale

50
Q

flu-like patterns recur every 72 hrs

A

P. malariae

51
Q

flu-like patterns recur every 48 hrs

A

P. falciparum

52
Q

malarial paroxysm stages

A

cold stage, hot stage, sweat stage

53
Q

common complication of malaria

54
Q

waste products of plasmodium replication can stimulate TNF-alpha, IL-1 and other cytokine release from the immune system causing

A

suppression of erythropoiesis

55
Q

plasmodium infected RBCs are

A

destroyed by the spleen

56
Q

highest number of RBC lysis in malaria is seen in infections with

A

P. falciparum (infects both mature and young erythrocytes)

57
Q

can only infect older erythrocytes

A

plasmodium malariae

58
Q

can only infect young RBCs (reticulocytes)

A

P vivax (Duffy +) P. ovale (Duffy -/+)

59
Q

complication of malaria from consumption of glucose by plasmodium falciparum that causes lactic acidosis that may affect CNS function

A

hypoglycemia

60
Q

RBC infected by P. falciparum get bumps on their surface and stick together blocking microvasculature in the brain

A

cerebral malaria

61
Q

Dx: malaria

A

recognize clinical syndrome, travel history, blood smear positive for parasites

62
Q

rodents and cattle serve as reservoirs

A

Babesia spp. (Babesiosis)

63
Q

symptoms develop 1-8 weeks after bite: fever, chills, malgia, hemolytic anemia (many infections are asymptomatic-symptomatic more in elderly, asplenic, immunosuppressed)

A

Babesiosis

64
Q

Tx: Babesiosis

A

atovaquone, azithromycin (quinine/clindamycin)

65
Q

maltese cross in RBCs is a distinguishing characteristic of

A

Babesiosis

66
Q

Wuchereria bancrofti and Brugia malayi cause

A

Filariasis (lymphatic filariasis)

67
Q

Wuchereria bancrofti and Brugia malayi exert their effects by

A

infecting lymphatic vessels and obstructing flow causing elephantiasis

68
Q

Filariasis is transmitted by

A

the bite of infected mosquitoes

69
Q

high IgE, eosinophilia, asthma associated with filariasis

A

Tropical Pulmonary Eosinophilia

70
Q

acute infection indicated by fever, chills, and lymphadenitis-painful swelling may last for weeks and recur frequently

A

Filariasis

71
Q

Dx: Filariasis

A

observation of microfilariae in blood smears

72
Q

Tx: Filariasis

A

microfilariae killed and adults damaged by DEC

73
Q

used to counteract allergic response to dying worms in Filariasis

74
Q

Caused by schistosoma spp.

A

Schistosomiasis

75
Q

snails are part of the life cycle

A

Schistosoma spp.

76
Q

swimming in water contaminated with human sewage allows cercariae to penetrate the skin in this disease

A

Schistosomiasis

77
Q

Are shed in both feces and urine due to migration of schistosomulae

A

Schistosoma eggs (Shistosomiasis)

78
Q

inhabits venous plexus of the large intestine

A

Schistosoma mansoni

79
Q

inhabits venous plexus of the small intestine

A

Schistosoma japonicum

80
Q

inhabits the venous plexus of the bladder

A

Schistosoma haematobium

81
Q

lodging of eggs causes inflammation and possible fibrosis/cirrhosis resulting in loss of bladder and liver function

A

Shcistosomiasis Chronic Infection

82
Q

Dx: of Schistosomiasis

A

eggs in feces or urine

83
Q

Control or prevention of Schistosomiasis

A

control snail population, limit exposure to water, improve sanitation

84
Q

cause chronic intestinal and hepatic dysfunction-portal fibrosis and hypertension

A

S. japonicum and S. mansoni

85
Q

causes hematuria, dysuria, urinary frequency, loss of bladder function, increased occurrence of squamous cell carcinoma of the bladder

A

S. haematobium

Microbiology (8 decks)

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