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Diagnostic Parasitology > (M) Coccidia (lecture-based) part 1 > Flashcards

(M) Coccidia (lecture-based) part 1 Flashcards

Coccidia, C. parvum, C. hominis, C. belli, T. gondii

1
Q
  • Largest group of apicomplexan protozoans
  • They are considered opportunistic in immunocompromised and immunodeficient
A

Coccidia

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2
Q

This is recognized as one of the major problems in animal farming and in zoo management

A

Coccidiosis

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3
Q

Eimeria

Phylum, Class, Subclass, Order, Genus

Familiarize

A

Apicomplexia
Conoidasida
Coccidiasina
Eucoccidiorida
Eimeria

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4
Q

All are true about the genera of coccidia, except:
A. Spore-forming
B. Single celled
C. Obligate intracellular parasites
D. Has an organelle of locomotion

A

D

rather movement is thru body flexion, gliding, or undulation of longitudinal ridges

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5
Q

3 phases of the life cycle

A
  • Sporogony
  • Schizogony (asexual stages)
  • Gametogony phase (sexual)
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6
Q

Life cycle

Forms a sporoblast, that will create a wall for itself by secreting materials, , at the same time the protoplasm forms two sporozoites within the sporocyst wall

A

SPOROGONY/SPORULATION PHASE

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7
Q

Life cycle

the development of an oocyst which came from a zygote.

A

SPOROGONY/SPORULATION PHASE

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8
Q

Life cycle

TOF. Thick shelled oocysts are passed unsporulated in the feces of the host, these consist of a single nucleus in a large pool of protoplasm.

A

T

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9
Q

Life cycle

Once the sporozoites have been formed, the oocyst is an infective sporulated oocyst that is ingested by the host for the life cycle to continue.

A

SCHIZOGONY/MEROGONY PHASE

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10
Q

Life cycle

When the sporozoites have invaded an epithelial cell they become rounded and are called?

A

trophozoites (merogony phase)

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11
Q

Life cycle

This trophozoite will then divide into a number of elongated nucleated merozoites, collectively known as a?

A

meront (merogony phase)

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12
Q

Life cycle

What type of meronts is recycled in the system to infect nother small intestinal ECs

A

Type 1

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13
Q

Life cycle

This type of meront is designated to undergo the gametogony phase

A

Type 2

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14
Q

Life cycle

Phase: Ends with the production of a zygote, which begins when the merozoites, type 2, will transform into undifferentiated gamete which will undergo sexual differentation to finally become a zygote.

A

GAMETOGONY

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15
Q
  • Causes diarrhea in animals (1971)
  • First case in humans (1976)
  • Frequent case of intractable diarrhea in immunocompromised patients
A

Cryptosporidium parvum

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16
Q
A
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17
Q
A
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18
Q

Cryptosporidium parvum

First observed in the gastric mucosal crypts of lab mice by

A

Tyzzer (1907)

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19
Q

Cryptosporidium parvum

Inhabits

A

small intestine, stomach, appendix, colon, rectum, biliary tree and pulmonary tree

sa module “brush borders of the mucosal epithelium of the stomach or the intestine” yan lang

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20
Q

Cryptosporidium parvum

Infective form

A

mature oocyst

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21
Q
A
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22
Q

Cryptosporidium parvum

causes auto infection

A

Thin-walled oocysts

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23
Q

Cryptosporidium parvum

passed out from the body through feces.

A

thick-walled oocysts

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23
Q
    • Worldwide distribution.
    • Common cause of diarrhea among travelers and patients of day-care centers more common among children than adults.
    • It can occur as water-borne infection or zoonotic.
    • In man, this parasite inhabits the brush borders of the mucosal epithelium of the stomach or the intestine. They may also inhabit the gall bladder and the pancreatic duct.
A

Cryptosporidium parvum

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24
Q

Causative agent of the disease Cryptosporidiosis

A

Cryptosporidium parvum

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25
Q

Cryptosporidium parvum

Host

A

Man

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26
Q

Cryptosporidium parvum

TOF. Heteroxenous.

A

F (mono)

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27
Q

Cryptosporidium parvum

Reservoirs

A

Cattle, cat, dog

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28
Q

Cryptosporidium parvum

Mode of Transmission

A
  • Ingestion of contaminated food and water (water-borne is most common)
  • Autoinfection
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29
Q

Cryptosporidium parvum

Incubation period

A

2-14 (7 average) days

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30
Q

Clinical manifestation: Biliary tract can be involved: RUQ pain, sclerosing cholangitis, cholecystitis

A

Cryptosporidium parvum

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31
Q

Clinical manifestation: chronic, persistent profuse diarrhea, weight loss, electrolyte imbalance, emaciation, and abdominal pain

A

Cryptosporidium parvum

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32
Q
  • Depend on the immune status
  • Immunocompetent: asymptomatic or self-limiting febrile illness with diarrhea, abdominal pain, nausea, and weight loss
  • Immunocompromised: chronic, persistent profuse diarrhea, weight loss, electrolyte imbalance, emaciation, and abdominal pain
A

Cryptosporidium parvum

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33
Q

Cryptosporidium parvum

TOF. Stool can be voluminous (1 - 25 L/day).

A

T

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34
Q

Cryptosporidium parvum

Diagnosis to demonstrate colorless, spherical oocysts (4-5 um) with small and large granules

A

Stool Examination (DFS)

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35
Q

Cryptosporidium parvum

Diagnosis:
- Method of choice
- Oocysts appear as red acid-fast spheres against a blue background

A

Modified acid-fast stain of stool samples

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36
Q

Cryptosporidium parvum

May may also be done to recover the oocyst.

other than DFS and modified acid-fats stain

A

enterotest

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37
Q

Cryptosporidium parvum

What are the available serologic tests?

A
  • Fluorescent staining: auramine-phenol or acridine orange
  • Indirect IF: definitive identification
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38
Q

Cryptosporidium parvum

If oocysts are not demonstrable in the previous diagnosis, what can be done?

A

Sheather’s sugar flotation and zinc sulfate flotation can be done

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39
Q

Cryptosporidium parvum

Diagnosis: antibody against parasite is seen within 2 months of acute infection

A

Serodiagnosis

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40
Q

Cryptosporidium parvum

Diagnostic tool: using light and EM at the apical surface of intestinal epithelium (jejenum is preferred)

A

Histopathological examination

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41
Q

Cryptosporidium parvum

Diagnostic: lasts for 1 yr and seen using ELISA (highly sensitive and specific) or IF

A

Anti-oocyst ab

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42
Q

Cryptosporidium parvum

this diagnostic dentifies 17 kDa and 27 kDa sporozoite agn

A

Western blot

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43
Q

Cryptosporidium parvum

Self limiting typically within?

A

2-3 weeks

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44
Q

Cryptosporidium parvum

has approved for treatment of diarrhea in people with healthy immune systems, however, its effectiveness among immunosuppressed is still unclear.

A

Nitazoxanide

Nitazoxanide 500 mg BD x 3 day — effectiveness is still unclear

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45
Q

Cryptosporidium parvum

an antimicrobial used to treat a number of parasitic infections

A

Paromomycin

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46
Q

Cryptosporidium parvum

What are the Supportive management?

A

fluid, electrolyte and nutrient replacement

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47
Q

Cryptosporidium parvum

TOF. No chemotx effective.

A

T

di ko gets

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48
Q

1. Cryptosporidium parvum

TOF. Chlorination does not affect the parasite.

A

T

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49
Q

Cryptosporidium parvum

Prevention

A
  • Synergistic effect of multiple disinfectants and combined water treatment processes may reduce C. hominis oocysts in drinking water
  • Natural water and swimming pool water should not be swallowed
  • Contamination of drinking water by human and animal feces should be prevented.
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49
Q
  • Found mainly in humans
  • It has a universal distribution with infections reported worldwide
  • Most epidemics are associated with water usually with calf feces
  • An additional species identified through genetic analysis
  • All stages of development are completed in the host GI tract (monoxenous life cycle)
  • It was not well recognized prior to AIDS; Nosocomial infections have been reported among health workers caring for AIDS pts
A

Cryptosporidium hominis

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49
Q

Cryptosporidium hominis

Prevelence in the Ph

A

2.6%

49
Q

Cryptosporidium hominis

A study in San Lazaro Hospital attempted to describe Cryptosporidium among diarrheic pts and reported a prevalence of? and in PGH>

A

SLH = 8.5%
PGH = 1.7%

as if lalabas ‘to

49
Q

Cryptosporidium hominis

Infective stage

A

Unsporulated oocyst

Oocysts are already infective when passed out

Should be sporulated kasi thick walled siya sa tae, mb mb

50
Q

Cryptosporidium hominis

may become heavily infected and lead to acute and gangrenous cholecystitis

organs (2)

A

bile duct and gall bladder

51
Q
  • Described by Rudolf Virchow (1860) but was named only in 1923
  • Was first seen in troops in the Middle East during WWI
  • More common in the tropical and subtropical regions than temperate region
  • The other previously known species Isospora hominis is now taxonomically grouped under Sarcocystis
A

Cystoisospora belli

52
Q

Cystoisospora belli

Hetero or monoxenous

A

mono

ata

53
Q

Cystoisospora belli

This parasite was described by?

A

Rudolf Virchow (1860)

54
Q

Cystoisospora belli

TOF. Rudolf Virchow (1860) named the disease.

A

F (described lang)

was only named in 1923

55
Q

Cystoisospora belli

host

A

humans

56
Q

Cystoisospora belli

What takes place in vitro within 48 hours after stool passage?

A

sporulation

57
Q

Cystoisospora belli

Diagnostic stage

A

recovery of unsporulated oocyst in the stool

58
Q

Cystoisospora belli

Infective stage

A

sporulated oocyst

59
Q

Cystoisospora belli

  • Size: 20 - 33um x 10 - 19pm
  • Shape: elongate ovoid, one end is narrowed as compared to the other that results to a “neck-like” appearance.
A

oocyst

60
Q

Cystoisospora belli

thin smooth two-layered, colorless

A

Cyst wall

61
Q

Cystoisospora belli

contains 1-2 sporoblasts

A

Immature unsporulated oocyst (diagnostic stage)

62
Q

Cystoisospora belli

contains 2 sporocyst each containing 4 crescent-or banana shaped sporozoites with a single nucleus (infective stage)

A

Mature sporulated oocyst

63
Q

Cystoisospora belli

Infection is confined to the intestinal epithelial cells, and cause destruction of the?

A

surface layer of the intestine

64
Q

What species

There is profuse watery diarthea, malabsorption, markedly abnormal intestinal mucosa with short villi, hypertrophied crypts, and infiltration of the lamina propia with eosinophils, neutrophils, and round cells.

A

Cystoisospora belli

65
Q

Cystoisospora belli

Causative parasite of

A

Human Coccidiasis.

66
Q
  • It has a worldwide distribution, although rare, it is more common in tropical than temperate region.
  • More common in tropical and subtropical countries with poor sanitary conditions The disease is common among pts with AIDS; also reported among those with lymphoma, leukemia, and organ transplant
    • Incidence:
      • In Africa, 2-3% with AIDS were infected
      • South America: 10%
      • Haiti and Africa: 7-20%
      • Endemic: Africa, Australia, Caribbean Islands, Latin America, Southeast Asia
  • Seen in both adults and children (day care centers and mental institutions); causes severe diarrhea among infants
  • Humans are its only host; both the sexual and asexual process occurs in man.
A

Cystoisospora belli

67
Q

Cystoisospora belli

incubation period

A

1-4 days

68
Q

Cystoisospora belli

This produces pale yellow and foul-smelling stools that may suggest malabsorption process.

A

mild gastrointestinal distress to severe dysentery

69
Q

Cystoisospora belli

contains undigested food, mucus, and Charcot-Leyden crystals

A

stool

70
Q

Cystoisospora belli

(Immunocompromised/immunocompetent) self-limiting enteritis to severe diarrheal illness resembling that of cryptosporidiosis, giardiasis, or cyclosporiasis;

A

compromised

71
Q

Cystoisospora belli

(Immunocompromised/immunocompetent) asymptomatic or self-limiting AGE

A

Immunocompetent

72
Q

Cystoisospora belli

Poop has high fecal fat content due to

A

malabsorption

73
Q

Cystoisospora belli

  • Demonstration of the oocyst stage in fecal smears (few in numbers)
  • Charcot-Leyden crystals may be seen in the specimen
  • Does not contain blood and pus
A

Stool Examination

74
Q

Cystoisospora belli

Concentration procedures

A

formalin-ether, ethyl acetate, zinc sulfate and sugar

75
Q

Cystoisospora belli

This maybe employed to increase the yield of positive results.

A

Concentration procedures

76
Q

Cystoisospora belli

What method produces granular red color against a green background

A

Modified Ziehl-Neelsen method

77
Q

Cystoisospora belli

this method may reveal flattened mucosa, damaged villi, infiltration of the lamina propria with lymphocytes, plasma cells, and eosinophils

A

Mucosal bowel biopsy

78
Q

Cystoisospora belli

TREATMENT

FAMILIARIZE NLANG PSL

A
  • Asymptomatic infections are self-limiting and no treatment needed
  • Mildly symptomatic may be managed with bed rest and bland diet
  • Trimethoprim-sulfamethoxazole or Cotrimoxazole 160/800 mg QID × 10 d then BID × 21 d
  • Combination therapy with pyrimethamine (50-75 mg/day) and sulfadiazine for 7 weeks
  • Relapses occur in AIDS pts hence maintenance dose: TMP-SMX 1 tablet 3х a week

as if lumabas

79
Q
  • Worldwide distribution seen in many animal species
  • Has cosmopolitan distribution and although the infection is quite common, the disease is rare.
  • Endemic worldwide in humans and in domestic and wild animals
A

Toxoplasma gondii

80
Q

Toxoplasma gondii

Causative agent of

A

toxoplasmosis

81
Q

Toxoplasma gondii

higher prevalence of positive titers

A

Pigs (19%) and rats (8.1%)

82
Q

Toxoplasma gondii

TOF. Available in the PH.

A

F (Not available in the Philippines due to lack of demand since clinical toxoplasmosis is not common)

83
Q

Toxoplasma gondii

They showed that only 2.4% of the population is seropositive for Toxoplasma gondii

A

Cross and Basaca-Sevilla (1984)

84
Q

Toxoplasma gondii

Infective stages

A
  • Tachyzoites (in groups or clones)
  • Bradyzoites (in tissue cysts)
  • Sporozoites (in oocyst)

pero sa mdoule its Trophozoites, cysts and oocysts (ingested)

85
Q

Toxoplasma gondii

Definitive host

A

Cat (complete life cycle occurs only in the cat family Felidae)

86
Q

Toxoplasma gondii

Intermediate host

A

Man, animals, birds, rodents

87
Q

Toxoplasma gondii

What stages occur in the intestinal epithelium

A

Schizogony, gametogony and sporogony

88
Q

Toxoplasma gondii

Extraintestinal stages (asexual)

A

tachyzoites, bradyzoites

89
Q

Toxoplasma gondii

Hetero/monoxenous

A

heteroxenous

90
Q

Toxoplasma gondii

sporozoites enters the cell and transforms into?

A

tachyzoite

91
Q

Toxoplasma gondii

rapidly growing trophozoites or endozoites that multiply in many types of host cell by?

A

endodyogeny

92
Q

Toxoplasma gondii

What is this reproduction called whereby 2 daughter trophozoites are formed within the parent cell

A

endodyogeny

93
Q

Toxoplasma gondii

In the intermediate host (man), T. gondi undergoes 2 stages of development:

A

ACUTE PROLIFERATIVE STAGE
CHRONIC CYSTIC STAGE

94
Q

Toxoplasma gondii

STAGE: Sporozoites enter the cell and transforms into a tachyzoite, the rapidly growing trophozoites or endozoites that multiply in many types of host cell by ENDODYOGENY (is a form of asexual reproduction that involves the development of two daughter cells within a mother cell, which is consumed by the offspring upon their maturation).

A

ACUTE PROLIFERATIVE STAGE.

95
Q

Toxoplasma gondii

STAGE: As host immunity develops antibodies, the fast multiplying tachyzoites give rise to slow multiplying bradyzoites that form cysts which are found in visceral organs, including the lungs, liver, and kidneys but are more prevalent in the neural and muscular tissues, including the brain, eyes, and skeletal and cardiac muscles.

A

CHRONIC CYSTIC STAGE

96
Q

Toxoplasma gondii

Through what host is where ingestion of cysts that leads to a stage of endodyogeny.

A

definitive host (cat)

97
Q

Toxoplasma gondii

Endodyogeny is immediately followed by a stage of repeated ?

A

endopolygeny

98
Q

Toxoplasma gondii

this is an asexual reproduction in which several, more than two daughter cells are formed within a mother cell via internal budding, in the cat small intestine epithelial cells, producing merozoites

A

endopolygeny

99
Q

Toxoplasma gondii

Merozoites multiply (schizogony stage) and some undergo gametogenesis resulting to production of?

A

micro- and macrogametocytes (gametogony/gamogony)

100
Q

Toxoplasma gondii

Fertilization of the macrogamete results to the formation of?

A

unsporulated oocysts

then expelled in the feces of the definitive host to the external environment.

101
Q

Toxoplasma gondii

In the environment, sporulation of the oocyts occurs and completed within how many days?

A

3-4 days

102
Q

T. gondii

are present in humans and other intermediate hosts. Schizogony and sporogony both occur in cat.

A

tachyzoites and bradyzoites

103
Q

T. gondii

TOF. Endodyogeny in the definitive host, while endodyogeny, endopolydeny and gamogony in the intermediate host.

A

F (opposite)

Endodyogeny - intermediate - man

Endodyogeny, endopolygeny gamogony - definitive - cat

104
Q

T. gondii

  • are rapidly dividing trophozoites seen during the acute phase of the infection.
  • Crescent shaped, approximately 2 by 6 um, with a pointed anterior (conoidal) end and a rounded posterior end.
  • Spherical to ovoid nucleus that is usually nearer the blunt end.
A

TACHYZOITES

105
Q

T. gondii

are the slow multiplying forms within the cyst during the chronic cystic phase of the infection

A

BRADYZOITES/CYSTOZOITES

106
Q

T. gondii

Transmission

A

Horizontal and vertical transmission

107
Q

T. gondii

Transmission: via pocyts (consuming food or water contaminated with mature oocysts shed into the environment by cats feces, eating undercooked meat of animals harboring tissue cysts containing tachy/bradyzoites

A

Horizontal

108
Q

T. gondii

Transmission: via tissue cysts (Blood transfusion, organ/BM transplantation)

A

Horizontal

109
Q

T. gondii

transmission: via oocysts (Transplacental transfer from the mother to the fetus during pregnancy

A

Vertical transmission

110
Q

T. gondii

Incubation period

A

2-14 days

111
Q

T. gondii

TOF. Most cases are asymptomatic; only manifests as a disease in immunodeficiency or suppression.

A

T

112
Q

T. gondii

often severe and even fatal manifesting with the so-called Sabin syndrome, which consists of chorioretinitis, cerebral calcification, convulsion or psychomotor disturbance, and hydrocephalus or microcephalus.

A

Congenital toxoplasmosis

113
Q

T. gondii

may result in mothers acquiring the infection during first trimester

A

Stillbirth and abortion

114
Q

T. gondii

the most common form of the disease.

A

Acquired toxoplasmosis

115
Q

T. gondii

the most common type, resembles infectious mononucleosis, characterized by cervical and axillary lymphadenopathies, malaise, muscle pain, and irregular low-grade fever

A

mild lymphatic form of Acquired toxoplasmosis

116
Q

T. gondii

often with skin rashes, chills, high grade fever, and prostration which may be associated with encephalitis, myocarditis and focal pneumonia, retinochoroiditis, hepatitis, splenomegaly, extramedullary hematopoiesis, failure to gain weight

A

Acute fulminating disseminated infection of Acquired toxoplasmosis

117
Q

T. gondii

diagnostic diagnosis

A

Biopsy of lymph nodes, bone marrow, spleen, brain and other tissues to demonstrate the organisms

118
Q

T. gondii

DIAGNOSIS

familiarize

A
  • Demonstration of the oocyst in fecal smear.
  • Biopsy of lymph nodes, bone marrow, spleen, brain and other tissues to demonstrate the organisms (tissue cyst) is diagnostic.
  • Serologic tests are used to detect antibodies:
    • Complement Fixation test, Double Sandwich ELISA test, Indirect Immunofluorescent antibody test., Indirect Hemagglutination test, Sabin-Feldman dye test, and Frenkel skin test, which is a type of delayed hypersensitivity reaction.
    • A seroconversion to a positive titer of 4-fold increase is indicative of an infection
    • High titers (>1,024) may also be seen in chronic cases hence the need for IgM antibody detection via IgM indirect fluorescent ab technique or a sandwich ELISA
  • Polymerase Chain Reaction for detection of the parasites
    • DNA can be used in serum, amniotic fluid, CSF and brochioalveolar lavage
119
Q

T. gondii

Persons who are ill and immunocompromised can be treated with:

A

Pyrimethamine 25-100 mg OD and Sulfadiazine 1-1.5 g QID in combination for 1 month (can keep Toxoplasma under control but do not kill it)

120
Q

T. gondii

Pyritethamine can lower blood counts in most people. It should be given with?

A

Leucovorin (folinic acid)

121
Q

T. gondii

may cause serious allergic actions (fever, rash)
Can be substituted with Clindamycin, Azithromycin, Clarithromycin, Dapsone, Atovaquone

A

Sulfadiazine

122
Q

T. gondii

used to prevent hypersensitivity reactions

A

steroids

123
Q

T. gondii

treatment for for immunocompromised

A

Prophylaxis with TMP/SMX

Diagnostic Parasitology (36 decks)

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