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Clin Med - ID > Lecture 4 - Protazoan Infections > Flashcards

Lecture 4 - Protazoan Infections Flashcards

1
Q

A 28yo female present with fever of 39C and confusion. She returned 16 days ago from a 2 week trip to Kenya. Which of the following should be ordered immediately?

A

blood smear

looking for malaria parasite in the RBC

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2
Q

What are the most important intestinal protozoa?

A 
giardia intestinalis (chronic diarrhea) 
entamoeba histolytica (dysentery, liver abscess) 
cryptoporidium parvum (diarrhea in AIDS)
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3
Q

What are the most important tissue protozoa?

A 
Trypanosomiasis 
-African: T.b. rhodesiense, T.b. gambiense
-South American: T. cruzi 
Leishmaniasis (visceral vs cutaneous) 
Toxoplasmosis
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4
Q

What are the the most common blood protozoa?

A

Plasmoidum (malaria)

Babesia (transmitted by ticks)

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5
Q

What parasite most commonly causes malaria?

A

Plasmodium falciparum (the most common one to cause sxs d/t cytoadherence)

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6
Q

How is malaria transmitted?

A

Mosquito genus anapheles
females only

incubation is 1 week

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7
Q

Which two plasmodia can lay dormant in the liver for months to years?

A

P. ovale and P. vivax

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8
Q

Cytoadherence

A

seen in plasmoidum falciparum malaria parasite that causes the RBC to be sticky

this gums up the vasculature (ischemia –cerebral malaria)

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9
Q

What is the most common sx seen with malaria?

A

fever
episodic with very hight spikes (very high, like over 40)

the spikes in temp are d/t rupture of the RBCs

this leads to splenomegaly

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10
Q

What are common things you see on labs for pts with malaria?

A

anemia

thrombocytopenia (only 50% of pts with malaria have low platelets)

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11
Q

Plasmoidum falciparum results in what clinical manifestation?

A

cerebral malaria

severe anemia

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12
Q

What is the peak age for malaria infections?

A

young children (<5)

you have to have constant exposure to maintain immunity

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13
Q

Duffy antigen

A

is an antigen needed on the host RBC in order for P vivax parasite to enter the RBCs

evolution - no one in west Africa has duffy antigen so they do not get vivax

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14
Q

Sickle cell trait is protective against…

A

P. falciparum

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15
Q

Is malaria transmitted in the US?

A

No

We have about 1500 cases a year but they are from immigrants or travelers

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16
Q

How do you dx malaria?

A

Microscopy — thin and thick blood smears

RDTs (rapid diagnostic tests) using a drop of blood

Serology has NO place in dx of acute infection - since antibodies can be present for ~ 10 years after an infection

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17
Q

When using RDTs for malaria, where is it best to take blood from the pt?

A

Fingertips (using a lancet similar to glucose tests) because this is where the infected RBCs get stuck d/t cytoadherence

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18
Q

Which malaria parasite can result in coma due to ischemia induced cytoadherent infected erythrocytes obstructing circulation in the cerebral vasculature?

A

Plasmodium flaciparum

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19
Q

What is the management for malaria?

A

This is why it is so important to know which species is infecting the pt —done by the lab via blood smear

P.ovale/vivax —must treat liver hypnozoites to prevent relapse

There is now chloroquine drug resistance with p. Falciparum

Other: ACTs - artemesinin-based combination therapy

Can always call the CDC hotline for help

Typically these pts are admitted to the hospital and given IV meds

  • ICU
  • IV fluids +/- blood transfusion
IV quinidine
IV artesunate (From CDC)
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20
Q

How do you treat P. Vivax/ovale?

A

Must treat the liver hypnozoite stage with PRIMAQUINE x 14 days and then given chloroquine

MUST screen for G6PD deficiency first

Contraindicated in pregnancy —-the only option you have is to wait until the pt delivers and then treat the malaria

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21
Q

What prophylaxis is used for malaria prevention in travelers?

A

Reduce exposure:
DEET
Insecticide treated bednets
Cover skin

Chemoprophylaxis:
“Yellow book” from CDC to help guide drug based on location of travel

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22
Q

A 24 yo male with functional asplenia due to sickle cell disease goes to Cape Cod and develops a fever. The lab calls you to say there are funny looking things in his erythrocytes. The infection was likely transmitted by a …?

A

Tick

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23
Q

Babesiosis

A

Entraerythrocytic parasite transmitted in the US

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24
Q

Which species of babesiosis infects humans most commonly in the US?

A

B. Microti

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25
Q

How does babesiois microti infect humans?

A

Tick Ixodes scapularis (this is the same kind of tick that can transmit lyme disease)

The tick must be attached for >24 hours in order to transmit babesiosis microti

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26
Q

Where is babesiosis most commonly transmitted?

A

New england, wisconsin and minnesota

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27
Q

What is the clinical presentation of babesiosis?

A

> 25% are asymptomatic (especially in children)

Flu like illness: fever/chills, fatigue, HA (lasts weeks to months)

Complications:
ARDS, massive hemolysis, congestive heart failure, renal failure, death
-elderly, HIV+, and asplenic at higher risk

*absence of spleen means no way of controlling the growth of the parasite

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28
Q

How is babesiosis dx?

A

Microscopic exam of blood (giemsa stain)

PCR is most commonly used now d/t being more sensitive

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29
Q

Maltese cross

A

Classic finding (not always seen but when it is it is patognmonic for) babesia on blood smear

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30
Q

Which parasite can establish latency in the liver?

A

Plasmoidum vivax

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31
Q

Who is at greatest risk of malaria infections?

A

Children

Pregnancy

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32
Q

Beaver fever

A

Giardia intestinalis

Pear shaped flagellated protozoan

33
Q

How do pts with giardia intestinalis present?

A

> 50% are asymptomatic (esp. in children)

Acute:

  • 1 to 4 week incubation
  • loose, foul-smelling, pale stool
  • steatorrhea: fat malabsorption
  • cramping, bloating, nausea
  • anorexia, malaise, weight loss
  • NO blood in stool

Chronic:

  • steatorrhea
  • growth impairment

Even though it is called beaver fever you actually dont get a fever

34
Q

How do you dx giardia intestinalis?

A

PCR (mutiplex - GI FilmArray/BioFIre

35
Q

What is the treatment for giardia intestinalis?

A

Oral meds:

  • Metronidazole
  • tinidazole (single dose)
  • nitazoxanide
36
Q

Amoebiasis

A

From a burden of disease point of view, this is one of the most important parasites to know

Entamoeba histolytica
Entamoeba dispar (non-pathogenic species)
-cannot differentiate eachother microscopically

37
Q

Where is amoebiasis most common?

A 
Tropical areas with crowded living: 
Africa
Latin america
Southeast asia
India

US (immigrants —highest incidence in hispanic males 20-40 yo)

38
Q

How is entameobea histolytica transmitted?

A

Fecal-oral transmission as cysts

39
Q

Where in the body does entamoeba histolytic centralize to?

A

Colon and liver

Trphozolites invade the tissues of the colon (unlike giardia which just stays in the gut) and this can in turn get to the liver via portal flow and lead to liver abscess

40
Q

What are the clinical syndromes of ameobiasis?

A

Asymptomatic colonization
Ameobic dysentery (bloody diarrhea with fever)
Amoebic colitis
Liver abscess

41
Q

What is the onset of amoebic colitis?

A

Gradual (weeks)

42
Q

What is the clinical manifestation of ameobic colitis?

A 
Diarrhea 
Dysentery 
Abdominal pain 
Weight loss (if it goes on long enough) 
Fever
Heme-positive stool (GI bleeding)
43
Q

What is the clinical presentation for amoebic liver abscess?

A

This can be present without hx of intestinal sxs —dont let that fool you

Sxs >4 weeks 
Immigrant/traveler from endemic area
Fever
Abdominal pain 
Hepatomegaly 
Jaundice
Diarrhea
Weight loss
Cough (diaphragm irritation)
44
Q

“Anchovy paste”

A

The aspirate from the ameobic liver abscess

45
Q

How do you dx amoebiasis?

A

Stool PCR
Stool microscopy
Stool antigen detection
Serology (more sensitive for liver abscess than colitis)

46
Q

What is the treatment for amoebiasis?

A

Always treat active disease with metronidazole (kills trophoziotes) and give second drug to kill the cysts (luminal agent)

Asymptomatic colonization:
Treat with luminal agent

47
Q

Cryptosporidium parvum

A

Seasonal peaks in late summer and early fall

Person to person:
-outbreaks in day care centers

Zoonotic:
-farmers and animal handlers

Waterborne:

  • swimming pools
  • public drinking water
48
Q

What is the clinical picture for someone infected with crypotoporidiosis?

A

Watery diarrhea

Immunocompetent pts recover after 1-2 weeks

HIV (CD4<200): chronic diarrhea

49
Q

How is cryptosporidium parvum dx and treated?

A

Microscopy with modified acid fast stain
PCR

Treatment:
Reduce immunosuppresion (antivirals to get there CD4 count up)
50
Q

A 19 yo male presents with a 1 month hx of diarrhea and a 15 lb weight loss. He has mild, episodic and diffuse abdominal pain; no fevers or chills. On exam he has mild diffuse abdominal tenderness and is afebrile. He went camping 2 months ago but has not left north america. What is the most likely etiologic agent?

A

Giardia intestinalis

Not e. Histolytic d/t no outside country travel

Not cryptosporidum d/t not immunosupressed

51
Q

A pt with HIV and a CD4 count of 75 presents with weight loss and 3 months hx of watery diarrhea. A modified acid fast stain of a fecal sample is positive. What is the likely dx?

A

Cryptosporidium parvum

52
Q

Sleeping sickness

A

Human Afriocan Trypanosmiasis (HAT)

Two morphologically identical subspecies of trypanosmoes:
Gambian HAT: trypanosoma brucei gambiense
Rhodesian HAT: trypansosoma b. Rhodesiense

Transmitted by tsetse flies

These flies are attracted to blue and their bites hurt

53
Q

Tsetse flies

A

Transmit human african trypanosmoiasis (HAT)

54
Q

What are the clinical manifestations of human african trypanosmiasis?

A

Early: asymptomatic: tryps in blood and lymph nodes

Late: CNS involvement and tryps in CNS —BAD - leads to coma and death “sleeping sickness”

55
Q

Where are the two african trypanosmes commonly seen?

A

Tryposoma brucei gambiense (west african)
Trypanosma brucei rhodesiense (east african)

These are NOT intracellular
They’re swimming amongst the RBCs

56
Q

Primary chancre is seen with what?

A

Trypanosma brucei gambiense and rhodesience

Develops at bite wound

57
Q

What are the main differences between gambian and rhodesian HAT?

A

Time of incubation

Gambian is months to years

Rhodesian is weeks

58
Q

Winterbottom’s sign

A

Posterior cervical adenopathy seen with gambian HAT

Not many things cause posterior cervical lymphadenopathy

59
Q

What are the clinical manifestations of HAT/

A 
Gambian:
WInterbottom’s sign: posterior cervical adenopathy 
Asymptomatic for months or years 
Intermittent fever: due to antigenic variation 
CNS involvement: 
Diurnal somnolence, nocturnal insomnia 
Constant HAs 
Behavioral changes 
DEATh

Rhodesian:
Develops over weeks

60
Q

How do you dx HAT?

A

Microscopy with giemsa staining

  • lymph node aspirate
  • blood
  • late stage disease: CSF
61
Q

Chagas Disease

A

tripanisoms transmitted by kissing bug

62
Q

How do people get Chagas Disease?

A

the parasite is in the feces of the kissing bug
when the kissing bug is feeding on your blood it poops
when you scratch the bug bite you get the feces into the bite

63
Q

Which organs are affected by the parasite transmitted from the kissing bug?

A

parasite: trypanosma cruzi

affects cardiac and GI

64
Q

What is the clinical manifestation of Chagas disease?

A

t.cruzi parasite

acute chagas disease:

  • Chagoma: indurated lesion at site of parasite entry
  • Romana’s sign: when conjunctiva is port of entry
  • fever, facial edema
  • severe myocarditis with ECG changes

Chronic chagas disease:

  • dilated cardiomyopathy
  • GI: megacolon and megaesophagus

this infection lasts YEARS

65
Q

Chagomas sign

A

seen with chagas disease (t. cruzi)

indurated lesion at site of parasite entry

66
Q

Romanas Sign

A

seen with chagas disease when conjunctiva is port of entry of feces from t. cruzi

67
Q

How is chagas disease dx?

A

acute:
parasite seen microscopically in blood or other specimen (CSF, bone marrow, lymph node biopsy)
PCR

Chronic:
T. cruzi specific IgG (serology)
PCR

68
Q

What is the treatment for chagas disease?

A

antiparasitic drugs not very effective

pacemaker (cardiomyopathy)

cardiac transplantation (reactivation of acute disease may occur so follow these pts with PCR)

69
Q

Leishmaniasis

A 
Visceral Leishmaniasis (VL) 
-Kala-azar

Cutaneous Leishmaniasis (CL)

Mucocutaneous Leishmaniasis

70
Q

Sandfly

A

vector of the leishmania parasite

71
Q

Kala-azar

A

visceral leishmaniasis

seen in NE India and South Sudan

opportunistic infection in AIDS infections

72
Q

Leishmania parasite is intracellular or extracellular?

A

intracellular

it preferentially likes phagocyte cells –bone marrow, liver, and spleen

73
Q

What are the clinical features seen with Kala-azar?

A

visceral leishmaniasis

majority of infections self-resolving 
full blown Kala-azar: 
-fever
-weight loss
-hepatosplenomegaly 
-pancytopenia
-hypergammaglobulinemia
-hyperpigmentation ("black fever") 
children <5 years old are most susceptible age group
74
Q

How is Kala-azar dx?

A

PCR of blood or biopsy material

75
Q

Cutaneous Leishmaniasis

A

chronic ulcerating lesion that heals after weeks to months but leaves scar

76
Q

How is CL dx?

A

cutaneous leishmaniasis

biopsy and PCR

the ulcer develops at site where parasite are inoculated

77
Q

Mucocutaneous Leishmaniasis

A

Leishmaniasis braziliensis (central/south america)

destructive mucosal lesions

78
Q

A 56 yo immigrant from Bolivia presents with worsening dyspnea x 6 months, fatigue and exercise intolerance. Cardiac echo shows a dilated heart with EF of 10%. What other organ system is likely to be affected by the causative infection?

A

GI system

chagas - kissing bug

Clin Med - ID (9 decks)

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