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CP Board Review - Microbiology > Parasites 1 > Flashcards

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
Malaria - P. ovale
* Most common in tropical Africa, but also found rarely in Asia and South America * Requires treatment of latent form in liver
26
P. knowlesi
* Primarily a rhesus monkey pathogen; emerging in humans in southern Asia. * Resembles P. malariae morphologically; more severe clinically. * Overall importance still being assessed.
27
How To Remember Which Is | Where
• 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
28
Babesia -Life Cycle & Transmission
• A tick-borne illness – Ixodes spp. • Endemic to US Northeast, and other areas where vector is found • Organism related to Plasmodium
29
Babesia - Clinical Illness
• 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
Malaria - Diagnosis
* Microscopy * QBC * Antigen detection * Molecular methods
31
Malaria Antigen Test
* 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
Microscopy
• 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
Malaria Microscopy - P. falciparum
``` 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
Microscopy: P. vivax
* Amoeboid trophozoites * Schuffner’s granules * 12-20 merozoites/schizont
35
Microscopy: P. malariae
* Heavy, blocky trophs * ‘Band forms * 8-12 merozoites/ schizont * Heavy malarial pigment * ‘Rosette’ forms
36
Microscopy: P. knowlesi
* Rings resemble falciparum | * Later stages resemble malariae
37
Microscopy: P. ovale
* Oval, sometimes fimbriated RBC containing troph * Compact, less ameboid than vivax * Prominent, dark Schuffner’s granules * 6-14 merozoites per schizont
38
Microscopy: Babesia
``` • 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
Quantitation of Malaria
• 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
African Trypanosomiasis | Life Cycle & Transmission
* Dwell extracellularly in bloodstream * Transmitted by Tsetse fly (Glossina spp.) * T. brucei rhodesiense * T. brucei gambiense
41
African Trypanosomiasis | Clinical Illness
``` • Triphasic disease – Chancre at site of bite – Hemolymphatic stage • Fever, lymphadenopathy, pruritis – CNS disease ‘Sleeping sickness’ • Meningoencephalitis • Headaches, somnolence, altered mental status ```
42
African Trypanosomiasis | Diagnosis
``` • 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
Chaga’s Disease | Life Cycle & Transmission
• 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
Chaga’s Disease - Epidemiology
* 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
Chaga’s Disease | Clinical Illness
``` • 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
Chaga’s Disease - Diagnosis
``` • 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
Leishmania - Life Cycle & Transmission
* Transmitted by sandflies * Injected promastigote transforms to amastigote within macrophages * Cutaneous and visceral forms
48
Leishmania – Clinical Disease
• 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
Leishmania – Diagnosis
* Serology of limited value * Biopsy followed by impression smears with cultural identification * Molecular diagnosis
50
Leishmania vs. Histoplasma
• Leishmania – Discrete organisms with nucleus and kinetoplast PAS(-) • Histoplama – Yeast, often budding Parent and bud not within a discrete membrane PAS(+)
51
Toxoplasma | Life Cycle & Transmission
* Acquired by contact with cat feces or undercooked meat * Transplacental transmission * Benign disease in normal hosts
52
Toxoplasma | Clinical Illness – Normal Hosts
• Acute mononucleosis – Chills, fever, headaches, myalgias, lymphadenitis & fatigue – Lifetime carriage of latent organisms
53
Toxoplasma - Clinical Illness – Congenital | Toxoplasmosis
• 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
Toxoplasma | Clinical Illness – Compromised Hosts
• 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
Toxoplasma Diagnosis
``` • Primarily Serological – IgM for acute infections – IgG for exposure status – Combine with clinical syndromes • Histopathology • PCR (experimental) ```
56
Filaria | Epidemiology & Types
• 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
Lymphatic Filaria | Life Cycle & Transmission
* Spread by mosquito/insect vectors * Adults live in lymph nodes * Juveniles (microfilaria) in blood
58
Onchocerca volvulus | Life Cycle & Transmission
• Spread by black fly vectors • Adults live in subcutaneous nodules • Juveniles (microfilaria) migrate through skin & subcutaneous tissues
59
Loa Loa | Life Cycle & Transmission
* Spread by horse fly or deer fly vectors * Adults live in cornea or subcutaneous tissues * Juveniles (microfilaria) in blood
60
Lymphatic Filaria | Clinical Presentation
• Lymphatic filariasis – lymphatic obstruction by adults, lymphedema – pulmonary eosinophilia as reaction to microfilariae
61
Onchocerca volvulus | Clinical Presentation
``` • Onchocerciasis • skin -- chronic inflammation, thinning and atrophy • eyes – anterior punctate keratitis – uveitis and retinal lesions ```
62
Loa loa | Clinical Presentation
``` • Loasis – eye worm • passage of adult across the eye – Calabar swellings • 5-10 cm areas of edema and angioedema ```
63
Filaria | Diagnosis
• Detecting microfilaria – Blood: lymphatic filariasis and loasis – Skin snips for Onchocerca • Antigen test for Wuchereria bancrofti is gold standard for this disease
64
Filaria – the Blood Smear
• 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
Filaria | Identification
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
Parasites in GI Tract
``` Giardia Cryptosporidium Cyclospora Entamoeba Microsporidia ```
67
Parasites in Blood
Plasmodium Babesia Trypanosoma
68
Parasites in Skin/Tissue
Toxoplasma | Leishmania
69
Parasites in Genital Tract
Trichomonas

CP Board Review - Microbiology (6 decks)

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