Parasites 1 Flashcards

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1
Q

Giardiasis Life Cycle and Transmission

A

Giardia lamblia

• Cysts spread by the fecal-oral route 
– Food or water supplies
– person-to-person
– Animal reservoirs ‘Beaverfever’
• Common in campers, groups of children, travelers returning from abroad
• Prevalence in the developing world may be as high as 10%.
• Cysts
– survive more than 2 months in cold water
– resistant to chlorine

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2
Q

Giardiasis Diagnosis

A

• O&P;microscopy 
– Cysts: 11-14 μm, oval, 4
nuclei
– Trophs: 12-15 μm, pear-shaped, 2 nuclei
• Antigen detection
- florescent stain
• Trophozoites may be obtained using the Enterotest kit or by duodenal aspiration, and detected in wet mounts

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3
Q

Giardia lamblia

A

Cyst: 4 nuclei; oval, 11- 14 x 7-10 um, prominent longitudinal fibers

Trophozoite: 2 nuclei;leaf-shaped longitudinal fibers

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4
Q

Things that look like Giardia lamblia but not pathogenic

A

Chilomastix mesnili
-Cyst: 7-9 x 4-6 um

-Trophozoite: Lemon-shaped with anterior hyaline knob and distinct cytosine near nucleus

Dientamoeba fragilis
Cyst: No cyst form

Trophozoite: 7-12 um; Usually binucleated; no peripheral chromatin; Vacuolated cytoplasm with debris, bacteria. nuclei can look like “die”

Endolimax nana
Cyst: 6-8 um ; 1-4 nuclei

Trophozoite: 7-12 um; One nucleus; No peripheral chromatin;Large karyosome

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5
Q

B. hominis

A

Cyst: 6-40 uM;Multiple, peripheral nuclei, large central body (similar to a large vacuole)

Trophozoite: Rarely present

May not be a pathogen

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6
Q

Cryptosporidium and Cyclospora

Coccidian Parasites

A

Same group as Plasmodium, Babesia, Toxoplasma

– Obligate intracellular pathogens; invade host cells with specialized organelles in the apical complex



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7
Q

Cryptosporidium

Life Cycle & Transmission

A

•ID = ~130 oocysts
• Person to person,animal to person, waterborne
• Day-care,nosocomial, other institutional
• Direct transmission– no intermediate hosts
• Worldwide distribution
- cysts immediately infective

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8
Q

Cryptosporidium

Diagnosis & therapy

A

• Directvmicroscopy
– Modified acid-fast (not standard stain)
– 4-6 um diameter
• Antigen detection–EIA/IFA
• PCR (investigational)
• Nitazoxanide used to treat, as well as anti-diarrheal agents

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9
Q

Cyclospora

Life cycle and transmission

A
• Oocysts shed in stool
– sporulate externally 8-11 days before infective
– resistant to formalin or chlorination
• Transmission by food or water, probably not person to person
• Seasonal, spring-summer
• Worldwide distribution


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10
Q

Cyclospora - Diagnosis and therapy

A

• Microscopy
– acid-fast staining • 7.5-10 um diameter
– autoflourescence
– safranin
- looks very much like crytospordium but twice the size
• Therapy
– responds to trimethoprim/sulfa
– long-term suppression for compromised hosts

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11
Q

Amebiasis - Life Cycle & Transmission

A

• Entamoeba histolytica
– Motile trophozoite reproduces and causes disease
– Entamoeba dispar is non-pathogenic but morphologically indistinguishable
- ingested red cells == histolytica
– Report as E. histolytica/dispar unless antigen or other testing done to distinguish
• Cysts spread by the fecal-oral route
– Food or water supplies
– person-to-person
• Cysts can survive for days or weeks, resistant to:
– drying
– gastric acidity
– chlorine
• 10% of the world population is colonized or infected

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12
Q

Amebiasis Diagnosis

A
•O&P; microscopy
• Serodiagnosis
- single nucleus, central karysome
- cysts 4 nuclei
– valuable in extraintestinal amebiasis, being positive in >90% of cases.
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13
Q

Microsporidia

A

•Protozoa (OOPS! Now they’re fungi!) belonging to order Microsporida, phylum Microspora
– >1000 species, 11 described in humans; newly described – many unknowns
• Obligate intracellular pathogens

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14
Q

Microsporidia Epidemiology

A

– Species involved in human disease
• Encephalitozoon, Enterocytozoon in GI disease
• Encephalitozoon, Nosema, Vittaforma, others, in ocular disease
– Immunosuppressed patients
• chronic diarrheal syndromes, esp. in HIV+ but also in other forms of immunosuppression
• disseminated disease with Encephalitozoon species
– Immunocompetent patients
• Diarrhea in travelers and others

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15
Q

Microsporidia Diagnosis – Stool Microscopy

A
• GI Infection
– Stool exam
• Weber’s trichrome & other stains
• E. bineusi: 1.5x.9 um
• E. intestinalis: 2.5-3.0 um
• Size, shape similar to many bacteria
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16
Q

Microsporidia Diagnosis – Cytology

A

• Ocular, urinary/renal, biliary, pulmonary infections
– Require special stains
• H&E/Pap insensitive
• Chromotrope or Gram-based stains

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17
Q

Microsporidia Diagnosis – Histology

A
  • Can visualize intracellular spores with appropriate stains
  • May be present in small numbers – serial sections may be required
  • EM provides species diagnosis
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18
Q

Microsporidia Diagnosis – The Future

A

• Antibody-based methods
– Available for Encephalitozoon species only
• Nucleic acid-based methods

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19
Q

Malaria Life Cycle & Transmission

A

• Four species of Plasmodium
– P. falciparum
– P. vivax
– P. malariae
– P. ovale
• Primarily insectborne; Anopheles mosquitoes
• Malaria is also transmitted by blood transfusion, needle sharing, and congenitally

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20
Q

Malaria Epidemiology

A
  • Worldwide prevalence of >100 million cases
  • kills over 1 million people per year, mostly children, in Africa alone.
  • Half of all human deaths since the Stone Age have been due to malaria
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21
Q

Malaria - P. falciparum

A
Worldwide in the tropics & subtropics
• The deadliest form
• A medical emergency
– very high parasitemias
– parasitized cells stick to the capillary endothelium, causing renal, pulmonary, and cerebral complications
– resistance to chloroquine
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22
Q

Malaria - P. vivax

A

• Widely prevalent in tropics, subtropics, & temperate regions
– Not found in West Africa
• Less severe than P. falciparum
• Requires treatment of latent form in liver

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23
Q

Malaria - P. malariae

A
  • Widely prevalent in tropics, subtropics, & temperate regions – Not as common as vivax and falciparum
  • No latent form in liver
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24
Q

Malaria - P. ovale

A
  • Most common in tropical Africa, but also found rarely in Asia and South America
  • Requires treatment of latent form in liver
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25
Q

Malaria - P. ovale

A
  • Most common in tropical Africa, but also found rarely in Asia and South America
  • Requires treatment of latent form in liver
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26
Q

P. knowlesi

A
  • Primarily a rhesus monkey pathogen; emerging in humans in southern Asia.
  • Resembles P. malariae morphologically; more severe clinically.
  • Overall importance still being assessed.
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27
Q

How To Remember Which Is

Where

A

• Two types of malaria that don’t recur from the liver:
– P. falciparum – high incidence and severity
– P. malariae – lower incidence and severity
– Both worldwide in the tropics
• Two types of malaria that do recur from the liver divide the world between them:
– P. vivax – high incidence, most of the world except Western Africa
– P. ovale – lower incidence, occupies the niche in Western Africa

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28
Q

Babesia -Life Cycle & Transmission

A

• A tick-borne illness
– Ixodes spp.
• Endemic to US Northeast, and other areas where vector is found
• Organism related to Plasmodium

29
Q

Babesia - Clinical Illness

A

• Incubation period: 1-4 weeks
• Fever, malaise, headache, chills, fatigue
• Anemia, possible renal failure
• Hepatosplenomegaly
• Asplenic and HIV(+) patients at increased risk
– Many asymptomatic infections in normal hosts

30
Q

Malaria - Diagnosis

A
  • Microscopy
  • QBC
  • Antigen detection
  • Molecular methods
31
Q

Malaria Antigen Test

A
  • Binax NOW approved 2007
  • Detects P. falciparum (HRP2) and common malarial antigen separately
  • Microscopy detection limit is ~5-20 parasites/ul
  • Negative results must be confirmed by thick and thin smears
32
Q

Microscopy

A

• Let’s face it, that’s how most of us diagnose malaria
• MIC.52200 Are both thick and thin films (routine blood films and/or buffy coat films) made to provide thorough examination for blood parasites?
• Thick smears
– More sensitive than thin smears
– Complicated for most of us unskilled folks
– Identification difficult
• Thin smears
– Less sensitive but superior morphology
– Allows quantitation

33
Q

Malaria Microscopy - P. falciparum

A
Diagnosis: ‘P. falciparum or not.‘
• The banana-shaped  gametocyte is diagnostic if seen.
• Early rings, no trophs
– Applique’ forms
– Dual infected cells
– Dual chromatin dots
34
Q

Microscopy: P. vivax

A
  • Amoeboid trophozoites
  • Schuffner’s granules
  • 12-20 merozoites/schizont
35
Q

Microscopy: P. malariae

A
  • Heavy, blocky trophs
  • ‘Band forms
  • 8-12 merozoites/ schizont
  • Heavy malarial pigment
  • ‘Rosette’ forms
36
Q

Microscopy: P. knowlesi

A
  • Rings resemble falciparum

* Later stages resemble malariae

37
Q

Microscopy: P. ovale

A
  • Oval, sometimes fimbriated RBC containing troph
  • Compact, less ameboid than vivax
  • Prominent, dark Schuffner’s granules
  • 6-14 merozoites per schizont
38
Q

Microscopy: Babesia

A
• Diagnosis
– Blood smears
– Serology / PCR
• Morphology
– Small, pleiomorphic rings
• <1/5 diameter of RBC
– Streak and ‘Maltese Cross’ forms
– Many extracellular  merozoites
– Rings predominant!
39
Q

Quantitation of Malaria

A

• When blood films are positive for malaria parasites (Plasmodium spp.), it is the percentage parasitemia reported along with the organism identification
• Used to determine treatment, primarily for P. falciparum but occasionally for vivax.
• Also used to determine response to treatment; parasitemia should drop within 24h, but resistance can be expressed after days of therapy.
• Reproducibility is important
– Usually expressed as parasites / 100 RBC

40
Q

African Trypanosomiasis

Life Cycle & Transmission

A
  • Dwell extracellularly in bloodstream
  • Transmitted by Tsetse fly (Glossina spp.)
  • T. brucei rhodesiense
  • T. brucei gambiense
41
Q

African Trypanosomiasis

Clinical Illness

A
• Triphasic disease
– Chancre at site of bite
– Hemolymphatic stage
• Fever, lymphadenopathy, pruritis
– CNS disease ‘Sleeping sickness’
• Meningoencephalitis
• Headaches, somnolence, altered mental status
42
Q

African Trypanosomiasis

Diagnosis

A
• T. b. gambiense
– in large areas of West and Central Africa.
• T. b. rhodesiense much more limited
– found in East and Southeast Africa.
• Flagellates found in blood, marrow, node aspirates, CSF
– Concentration methods
– Antigen detection, PCR
– Small posterior kinetoplast
– Dividing forms – not seen in T. cruzi
43
Q

Chaga’s Disease

Life Cycle & Transmission

A

• Spread by Reduviid or
‘Kissing’ bug
• Shed in bug feces and scratched into the skin by the host
• Trypanosomes reproduce intracellularly, released into circulation

44
Q

Chaga’s Disease - Epidemiology

A
  • Found in large areas of Latin America
  • Associated with thatched-roof housing
  • Many animal reservoirs
  • Vectors and organism found in southern and southeastern US
  • Transmitted by transfusion and congenitally
45
Q

Chaga’s Disease

Clinical Illness

A
• Local lesion at site of infection (chagoma)
• Acute phase
– Many cases asymptomatic
– Fever, lymphadenopathy, myocarditis
• Chronic disease
– Cardiomyopathy
– GI tract; megacolon, megesophagous
• Intracellular amastigotes
46
Q

Chaga’s Disease - Diagnosis

A
• Acute illness
– Microscopic exam of blood or buffy coat
– Culture in special media
– Xenodiagnosis
• Chronic illness
– Serology, CDC IFA/EIA
– Xenodiagnosis
• Morphology
– Curved, often C-shaped
– Prominent subterminal kinetoplast
– Never dividing in blood
47
Q

Leishmania - Life Cycle & Transmission

A
  • Transmitted by sandflies
  • Injected promastigote transforms to amastigote within macrophages
  • Cutaneous and visceral forms
48
Q

Leishmania – Clinical Disease

A

• Cutaneous
– Single or few chronic, ulcerating lesions; many species
– Latin America, southern Europe, Middle east, southern Asia, Africa
– Mucocutaneous in Latin America
• Visceral
– primarily L. donovani complex (Asia), L. infantum/chagasi (Africa and Latin America), others
– Hepatosplenomegaly, anemia, cytopenias, systemic symptoms
– India, Bangladesh, Nepal, Sudan, and Brazil
– Important OI in HIV infection

49
Q

Leishmania – Diagnosis

A
  • Serology of limited value
  • Biopsy followed by impression smears with cultural identification
  • Molecular diagnosis
50
Q

Leishmania vs. Histoplasma

A

• Leishmania
– Discrete organisms with nucleus and kinetoplast PAS(-)

• Histoplama
– Yeast, often budding Parent and bud not within a discrete membrane PAS(+)

51
Q

Toxoplasma

Life Cycle & Transmission

A
  • Acquired by contact with cat feces or undercooked meat
  • Transplacental transmission
  • Benign disease in normal hosts
52
Q

Toxoplasma

Clinical Illness – Normal Hosts

A

• Acute mononucleosis
– Chills, fever, headaches, myalgias, lymphadenitis & fatigue
– Lifetime carriage of latent organisms

53
Q

Toxoplasma - Clinical Illness – Congenital

Toxoplasmosis

A

• Occurs in infants born to mothers during pregnancy
– Most SEVERE if infection occurs early in pregnancy
– Most LIKELY if infection occurs late in pregnancy
• Chorioretinitis, encephalitis, hydrocephalus, microcephaly, retardation, blindness
• Delayed presentations - months to years

54
Q

Toxoplasma

Clinical Illness – Compromised Hosts

A

• Most commonly reactivation in previously infected patients
– HIV-infected
– Others; transplants, etc.
• Single or multiple CNS lesions
– Ring-enhancing Toxoplasma brain abscesses
• Occasional eye or lung disease
• Carditis in heart transplant patients

55
Q

Toxoplasma Diagnosis

A
• Primarily Serological
– IgM for acute infections
– IgG for exposure status
– Combine with clinical syndromes
• Histopathology
• PCR (experimental)
56
Q

Filaria

Epidemiology & Types

A

• Lymphatic filariasis
– 120 million infected
–Wuchereria bancrofti - 90% - worldwide tropics
– Brugia malayi 10% - E and S Asia

• Onchocerciasis
– 17 million infected with Onchocerca volvulus, mostly in sub-Saharan Africa

• Loasis
– 12 million infected with Loa loa, mostly in west & central African rain forests

57
Q

Lymphatic Filaria

Life Cycle & Transmission

A
  • Spread by mosquito/insect vectors
  • Adults live in lymph nodes
  • Juveniles (microfilaria) in blood
58
Q

Onchocerca volvulus

Life Cycle & Transmission

A

• Spread by black fly
vectors
• Adults live in subcutaneous nodules
• Juveniles (microfilaria) migrate through skin & subcutaneous tissues

59
Q

Loa Loa

Life Cycle & Transmission

A
  • Spread by horse fly or deer fly vectors
  • Adults live in cornea or subcutaneous tissues
  • Juveniles (microfilaria) in blood
60
Q

Lymphatic Filaria

Clinical Presentation

A

• Lymphatic filariasis
– lymphatic obstruction by adults, lymphedema
– pulmonary eosinophilia as reaction to microfilariae

61
Q

Onchocerca volvulus

Clinical Presentation

A
• Onchocerciasis
• skin -- chronic inflammation, thinning and atrophy
• eyes
– anterior punctate keratitis
– uveitis and retinal lesions
62
Q

Loa loa

Clinical Presentation

A
• Loasis
– eye worm
• passage of adult across the eye
– Calabar swellings
• 5-10 cm areas of edema and angioedema
63
Q

Filaria

Diagnosis

A

• Detecting microfilaria
– Blood: lymphatic filariasis and loasis
– Skin snips for Onchocerca
• Antigen test for Wuchereria bancrofti is gold standard for this disease

64
Q

Filaria – the Blood Smear

A

• Collection depends on the organism
– Wuchereria bancrofti commonly 9PM-3AM for most strains
– Brugia malayi normally during evening
– Loa loa during daylight
– Periodicity adjusts to a new time zone over ~1 week
– Subperiodic forms of Wuchereria and Brugia exist
• Preparation
– Thin smears
– Concentration and thick smears

65
Q

Filaria

Identification

A

Wuchereria bancrofti
• Sheathed, nuclei stop short of end of tail

Brugia malayi
• Sheathed, two small nuclei in tail

Onchocerca vovulus
• Unsheathed, from skin, not blood

Loa loa
• Sheathed, nuclei to continue to end of tail

66
Q

Parasites in GI Tract

A
Giardia
Cryptosporidium
Cyclospora
Entamoeba
Microsporidia
67
Q

Parasites in Blood

A

Plasmodium
Babesia
Trypanosoma

68
Q

Parasites in Skin/Tissue

A

Toxoplasma

Leishmania

69
Q

Parasites in Genital Tract

A

Trichomonas