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CLINICAL MICROBIOLOGY > MT2 FUNGI/PARASITOLOGY > Flashcards

MT2 FUNGI/PARASITOLOGY Flashcards

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0
Q

How does YEAST divide?

A

by binary fission or budding

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1
Q

This type of FUNGI is a single celled eukaryote:

A

YEASTS

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2
Q

What do you call FUNGI that produce mycelia?

A

MOLDS

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3
Q

Describe the composition of MOLDS:

A

multicellular;

composed of HYPHAE

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4
Q

What is HYPHAE?

A

long, branching filament that, w/other hyphae, forms the feeding thallus of a fungus called the mycelium

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5
Q

What are the 2 types of HYPHAE?

A

septate,

aseptate

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6
Q

What is SEPTATE HYPHAE?

A

walls that divide hyphae into cells

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7
Q

What is ASEPTATE HYPHAE?

A

no walls

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8
Q

What are the 4 groups of FUNGUS?

A

PHYCOMYCETES,
ASCOMYCETES,
BASIDIOMYCETES,
DEUTEROMYCETES (FUNGI IMPERFECTI)

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9
Q

Describe the SEXUAL STAGES of PHYCOMYCETES:

A

SEXUAL SPORES - free zygotes;

ASEXUAL SPORES - enclosed in sac-like structures called SPORANGIUM

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10
Q

Describe the SEXUAL STAGES of ASCOMYCETES:

A

SEXUAL SPORES - enclosed in sacs called ASCI

ASEXUAL SPORES - exogenous, formed at the end of the hyphae

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11
Q

Describe the SEXUAL STAGES of BASIDIOMYCETES:

A

SEXUAL SPORES - found on BASIDIA

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12
Q

Describe the SEXUAL STAGES of DEUTEROMYCETES:

A

NO SEXUAL STAGE

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13
Q

Name 3 types of SYSTEMIC MYCOSES:

A

HISTOPLASMOSIS (SPELUNKER’S DZ),
COCCIDIOMYCOSIS (VALLEY FEVER),
BLASTOMYCOSIS

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14
Q

What causes HISTOPLASMOSIS?

A

HISTOPLASMA CAPSULATUM (ASCOMYCOTA)

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15
Q

Where is HISTOPLASMOSIS found? Where is the fungus found?

A

worldwide, concentrated in US in MIDWEST & EASTERN US;

in soil contaminated w/BAT & BIRD FECES (frequently in caves)

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16
Q

How is HISTOPLASMOSIS transmitted?

A

spores are inhaled

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17
Q

What causes BLASTOMYCOSIS?

A

COCCIDIOIDES IMMITIS

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18
Q

Where is COCCIDIOMYCOSIS found?

A

in SOUTHWESTERN US (NM/AZ)

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19
Q

How is COCCIDIOMYCOSIS transmitted?

A

ARTHROSPORES are inhaled

= spores united in the form of a string of beads, formed by fission

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20
Q

What symptoms present with COCCIDIOMYCOSIS?

A

most infections are ASYMPTOMATIC, maybe only a SLIGHT FEVER

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21
Q

What causes BLASTOMYCOSIS?

A

BLASTOMYCES DERMATITIS

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22
Q

How is BLASTOMYCOSIS transmitted?

A

spores are inhaled into lungs where they transform to a yeast form of the microbe

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23
Q

What symptoms present with BLASTOMYCOSIS?

A

50% of individuals are SYMPTOMATIC, with flu-like illness w/productive cough

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24
Q

What is AMPHOTERICIN B used to treat?

A

SYSTEMIC FUNGI

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25
Q

How does AMPHOTERICIN B work?

A

binds to STEROLS, preferentially to the primary fungal cell membrane sterol (ERGOSTEROL); disrupts cell causing LYSIS

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26
Q

Name a SUBCUTANEOUS MYCOSIS:

A

SPOROTRICHOSIS (ROSE HANDLER’S DZ)

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27
Q

What causes SPOROTRICHOSIS?

A

SPOROTHRIX SCHENCKII

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28
Q

Where is SPOROTRICHOSIS found?

A

as an OCCUPATIONAL HAZARD for GREENHOUSE WORKERS/GARDENERS

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29
Q

How is SPOROTRICHOSIS transmitted?

A

fungi enter via SKIN LESION, transform to yeast form

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30
Q

What symptoms present with SPOROTRICHOSIS?

A

nodules & skin lesions appear along LYMPHATIC SYSTEM

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31
Q

What part of the body is affected by DERMATOPHYTOSES?

A

they invade dead keratinized tissue (HAIR, NAILS);

aka SUPERFICIAL MYCOSES

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32
Q

What are 3 major genera of DERMATOPHYTOSES?

A

TRICHOPHYTON,
MICROSPORUM,
EPIDERMOPHYTON

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33
Q

What is a TINEA INFECTION? Is it CONTAGIOUS?

A

TINEA = name given to a fungal skin infection (synonymous w/DERMATOPHYTE);
YES

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34
Q

Define TINEA PEDIS:

A

ATHLETE’S FOOT

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35
Q

Where does TINEA CORPORIS present?

A

TRUNK, EXTREMITIES

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36
Q

Where does TINEA CAPITIS present? What does it cause?

A

HEAD;

HAIR LOSS, RINGWORM

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37
Q

Where does TINEA UNGUIUM present?

A

NAILS

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38
Q

What causes TINEA VERSICOLOR?

A

YEAST (from normal flora)

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39
Q

What exacerbates T. VERSICOLOR?

A

heat, humidity, sweat (help it proliferate in some px)

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40
Q

Is TINEA VERSICOLOR contagious, like other TINEA INFECTIONS?

A

NO

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41
Q

How is T. VERSICOLOR diagnosed?

A

KOH wet mount (looking for yeast cells);

WOOD’S LAMP (if infection present where illuminated, area will fluoresce; no fluorescence/shine w/o infection)

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42
Q

What is a WOOD’S LAMP? What is it used for?

A

a lamp that emits UV light;

used to Dx TINEA VERSICOLOR

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43
Q

Name 2 conditions caused by PATHOGENIC YEAST:

A

CANDIDIASIS,

CRYPTOCOCCOSIS

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44
Q

What causes CANDIDIASIS?

A

CANDIDA ALBICANS

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45
Q

Where is CANDIDA ALBICANS found?

A

part of normal flora in mouth, gut, vagina; pathogenic when normal conditions are altered (antibiotics, depressed immunity)

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46
Q

What symptoms present with CANDIDIASIS?

A

THRUSH, skin/vaginal infections

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47
Q

What causes CRYPTOCOCCOSIS?

A

CRYPTOCOCCUS NEOFORMANS (a large, encapsulated yeast)

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48
Q

How is CRYPTOCOCCUS NEOFORMANS transmitted?

A

enters the host via respiratory route; after some time in the LUNGS, C. NEOFORMANS spreads to extrapulmonary tissues

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49
Q

To what site will C. NEOFORMANS often spread? Causing what?

A

the BRAIN;

infected px usually contract MENINGOENCEPHALITIS

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50
Q

What kind of organism is PNEUMOCYSTIS CARINII?

A

not yet established, bw FUNGUS (YEAST) or PROTOZOAN (antigenic differences have been found in strains derived from the various mammalian hosts)

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51
Q

Describe the PATHOGENESIS of PNEUMOCYSTIS CARINII:

A

in normal px, ASYMPTOMATIC infection of lungs occurs in early life –> organism persists in an INACTIVE/LATENT state unless the host becomes IMMUNOCOMPROMISED

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52
Q

What are the 3 life stages of a PARASITE?

A

EGG,
IMMATURE = LARVAE = NYMPH,
ADULTS

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53
Q

What is the surprising statistic about ASCARIS LUMBRICOIDES (a parasite/roundworm)?

A

> 1.4 billion people are currently infected with roundworm Ascaris lumbricoides, 20%of world’s population infected with this one eukaryotic parasite

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54
Q

What is a DEFINITIVE HOST?

A

one in which parasite reproduces

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55
Q

What is an INTERMEDIATE HOST?

A

one in which development occurs, but w/NO REPRODUCTION

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56
Q

How are INTESTINAL PARASITES Dx’d?

A

fecal specimens

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57
Q

How are BLOOD PARASITES Dx’d? Explain the 2 types:

A 
BLOOD FILMS (made from a drop of blood spread evenly on a slide and stained using Giemsa stain):
THICK FILMS (more sensitive for finding parasite in a thicker/more concentrated layer of blood);
THIN FILMS (more useful to ID parasites from a thin/monolayer blood specimen)
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58
Q

How are TISSUE PARASITES Dx’d?

A

biopsy, especially of muscle

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59
Q

What are PROTOZOA?

A

eukaryotic single celled parasites

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60
Q

Name an AMOEBA, & what it causes:

A

ENTAMOEBA HISTOLYTICA;

causes AMEBIC DYSENTERY

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61
Q

What are the 2 life stages of ENTAMOEBA HISTOLYTICA? Explain them:

A

TROPHOZOITE (the active, motile feeding stage, characterized by PSEUDOPODS);
CYST (similar to an ENDOSPORE, resistant to env’t, infective)

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62
Q

How is ENTAMOEBA HISTOLYTICA transmitted?

A

CYSTS ingested in contaminated water/food; use of NIGHTSOIL increases chance of contamination;
can be vectored by FLIES

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63
Q

Describe the pathogenesis of ENTAMOEBA HISTOLYTICA infection:

A

cysts EXCYST in intestine, causing bloody diarrhea; if TROPHOZOITES enter blood, they’ll move to liver, causing HEPATIC AMEBIASIS (collection of PUS in LIVER)

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64
Q

Name 7 types of FLAGELLATED PROTOZOA:

A

GIARDIA LAMBLIA, TRICHOMONAS VAGINALIS, TRYPANOSOMA BRUCEI, TRYPANOSOMA CRUZI, LEISHMANIA DONOVANI, LEISHMANIA TROPICA, LEISHMANIA BRAZILIENSIS

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65
Q

What does GIARDIA LAMBLIA cause?

A

GIARDIASIS, aka BEAVER FEVER

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66
Q

What are 2 life stages of GIARDIA LAMBLIA?

A

TROPHOZOITE (active, motile feeding stage);

CYST (similar to endospore, resistant to env’t, infective)

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67
Q

How is GIARDIA LAMBLIA transmitted?

A

CYSTS ingested in contaminated water, particularly near beavers (reservoir)

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68
Q

Describe the pathogenesis of GIARDIA LAMBLIA:

A

CYSTS excyst in intestine, reproduce & cover intestinal wall;
this interferes w/FAT ABSORPTION, causing FATTY STOOLS/DIARRHEA

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69
Q

What causes TRICHOMONIASIS?

A

TRICHOMONAS VAGINALIS

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70
Q

What are the life stages of TRICHOMONAS VAGINALIS?

A

TROPHOZOITE (has 4 flagella);

NO CYST form

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71
Q

How is TRICHOMONAS VAGINALIS transmitted?

A

TROPHOZOITES passed sexually, causing UROGENITAL infections

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72
Q

What symptoms present with TRICHOMONIASIS?

A

green discharge, itching in females;

urethritis in males

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73
Q

What group of FLAGELLATED PROTOZOA cause TRYPANOSOMIASIS? Name 2 species:

A

TRYPANOSOMES;

T BRUCEI, T CRUZI

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74
Q

What disease is caused by TRYPANOSOMA BRUCEI?

A

AFRICAN TRYPANOSOMIASIS, aka AFRICAN SLEEPING SICKNESS

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75
Q

What are the life stages of TRYPANOSOMA BRUCEI?

A

TRYPANOSOME (protozoa form);

NO CYST form

76
Q

How is TRYPANOSOMA BRUCEI transmitted?

A

vectored by TSE-TSE fly

77
Q

Describe the pathogenesis of AFRICAN TRYPANOSOMIASIS:

A

(in VERTEBRATE hosts) trypanosomes live in BLOOD, LYMPH NODES, SPLEEN, CSF;
do NOT invade or LIVE IN cells, but rather in TISSUE SPACES (particularly in CNS);
within a few days animals become emaciated, uncoordinated, paralyzed –> death

78
Q

What symptoms (in humans) present w/AFRICAN TRYPANOSOMIASIS?

A

normally experience mental dulness, tendency to sleep, finally COMA & DEATH

79
Q

What disease is caused by TRYPANOSOMA CRUZI? Where is it seen?

A

CHAGAS’ DZ;

Mexico, South/Central America

80
Q

What are the life stages of TRYPANOSOMA CRUZI?

A

TRYPANOSOME (protozoa form);

NO CYST form

81
Q

How is TRYPANOSOMA CRUZI transmitted?

A

vectored by the REDUVIID BUG (aka KISSING BUG) via defecation into a wound

82
Q

What’s the pathogenesis of ACUTE CHAGAS’ Dz?

A

(from T. CRUZI) small red nodule (CHAGOMA) at bite site; heart, liver, spleen, lymph nodes are infected;
Sx include anemia, nervous disorders, muscle/bone pain, heart failure; death may ensue after 3-4 weeks;
most common in CHILDREN

83
Q

What’s the pathogenesis of CHRONIC CHAGAS’ Dz?

A

(from T. CRUZI) Sx are primarily nervous dysfunction which may continue for years; px may be virtually ASYMPTOMATIC & suddenly die of heart failure

84
Q

What disease is caused by LEISHMANIA DONOVANI?

A

VISCERAL LEISHMANIASIS, aka KALA-AZAR

85
Q

What are the life stages for LEISHMANIA DONOVANI?

A

PROTOZOA form;

NO CYST form

86
Q

How is LEISHMANIA DONOVANI transmitted?

A

vectored by SANDFLY

87
Q

What’s the pathogenesis of VISCERAL LEISHMANIASIS?

A

L. DONOVANI invades liver, spleen, kidney; causes enlarged liver, spleen, wasting, finally death (if untreated) in 2-3 years;

2-3 yrs following treatment, a condition called POST-KALA-AZAR DERMAL LEISHMANOID may develop (this is a GRANULOMATIS REACTION on the SKIN)

88
Q

What causes CUTANEOUS LEISHMANIASIS? What’s another name for this Dz?

A

LEISHMANIA TROPICA;

ORIENTAL SORE

89
Q

What are the life stages of LEISHMANIA TROPICA?

A

PROTOZOA form;

NO CYST form

90
Q

What is unique about the LIFE STAGES of TRYPANOSOMA & LEISHMANIA species? What’s a difference bw the 2?

A

NO CYST forms for either T or L species;

T species life in TRYPANOSOME (which is a protozoa form), while L species live in PROTOZOA form

91
Q

What species of FLAGELLATED PROTOZOA DOES have a CYST form?

A

only GIARDIA LAMBLIA

92
Q

How is LEISHMANIA TROPICA transmitted?

A

vectored by the SANDFLY

93
Q

Describe the pathogenesis of CUTANEOUS LEISHMANIASIS:

A

red papule from sandfly bite; slow to heal, scars

94
Q

What causes MUCOCUTANEOUS LEISHMANIASIS? What’s another name for this Dz?

A

LEISHMANIA BRAZILIENSIS;

aka ESPUNDIA

95
Q

What are the life stages of LEISHMANIA BRAZILIENSIS?

A

PROTOZOA form;

NO CYST form

96
Q

How is ESPUNDIA transmitted?

A

vectored by SANDFLY

aka MUCOCUTANEOUS LEISHMANIASIS

97
Q

Describe the pathogenesis of MUCOCUTANEOUS LEISHMANIASIS:

A

lesions in the junction of the PHARYNX result in the break down of the PALATE of the MOUTH & NOSE

98
Q

Name a type of CILIATED PROTOZOA:

A

BALANTIDIUM COLI

99
Q

What causes CILIARY DYSENTERY?

A

BALANTIDIUM COLI

100
Q

What are the life stages of BALANTIDIUM COLI?

A

large, ciliated TROPHOZOITE form;

CYST form

101
Q

How is CILIARY DYSENTERY transmitted?

A

fecal-contaminated water, particularly ass’d w/infected PIG feces

102
Q

What symptoms present w/BALANTIDIUM COLI infection?

A

abdominal pain; watery, bloody stools

103
Q

What is the TREATMENT for all LEISHMANIASES?

A

antimony compounds like meglumine antimonate (Glucantime);

also, more recently tx’d w/ORAL MILTEFOSINE

104
Q

What are SPOROZOA? Name 2 genera:

A

eukaryotic single celled parasites;
characterized by complex life cycles;
Genera PLASMODIUM & TOXOPLASMA

105
Q

Which GENUS causes MALARIA?

A

PLASMODIUM

106
Q

What are the life stages of PLASMODIUM?

A

SPOROZOITES (released from MOSQUITO into human host, go to LIVER) –> undergo ASEXUAL reproduction (SCHIZOGONY) –> produce MEROZOITES (infect & destroy RBCs causing Sx of MALARIA) –> GAMETOCYTES (produced as result of erythrocytic stage in RBC, taken up by FEMALE MOSQUITO)

107
Q

Describe the 2 cycles (within a vertebrate host) of PLASMODIUM:

A

EXOERYTHROCYTIC STAGE (in LIVER);

ERYTHROCYTIC STAGE (in RBCs) - MEROZOITES in RBCs produce waste product called MALARIAL PIGMENT; LYSIS of RBCs cause anemia & jaundice of malaria

108
Q

How is PLASMODIUM transmitted?

A

vectored by ANOPHELES MOSQUITO

109
Q

Name 4 species of PLASMODIUM:

A

P. VIVAX;
P. MALARIAE;
P. FALCIPARUM;
P. OVALE

110
Q

Which PLASMODIUM species is most commonly the cause of MALARIA? Name the malaria type:

A

PLASMODIUM VIVAX;

called BENIGN TERTIAN MALARIA

111
Q

What symptoms present in BENIGN TERTIAN MALARIA?

A

SCHUFFNER’S DOTS (infected RBCs have unique PINK dots); fevers that typically occur every other day; relapse from LATENT LIVER INFECTION is common

112
Q

What distinctive characteristic is seen in RBCs infected by PLASMODIUM VIVAX?

A

ring-shaped (referring to TROPHOZOITE stage within RBC); RBC is large when infected

113
Q

What causes QUARTAN/MALARIAL MALARIA?

A

PLASMODIUM MALARIAE

114
Q

What distinctive characteristics present with P. MALARIAE infections?

A

NO enlarged RBCs; a distinctive BANDING PATTERN; ASEXUAL forms in RBCs appear as ROSETTES; fever occurs in 72 hr pattern; no relapses occur

115
Q

Which is more common bw P. VIVAX & P. MALARIAE?

A

P. VIVAX

116
Q

What symptoms & pathologies result from PLASMODIUM FALCIPARUM infections?

A

daily fever, becoming TERTIAN (36 to 48 hours); chills, nausea;

BLACKWATER FEVER (characterized by intravascular hemolysis, 
hemoglobin and kidney failure. When RBCs burst, hemoglobin leaks into blood plasma, damages the glomerulus in the kidney,  begins to leak into the urine, causing further damage to kidney tubules);

CEREBRAL MALARIA can ensue (mental status changes, coma, death)

117
Q

Where is PLASMODIUM FALCIPARUM common? How does it compare to the other PLASMODIUM infections?

A

common in the tropics;

MOST serious dz

118
Q

Describe the infection by PLASMODIUM FALCIPARUM:

A

multiple SPOROZOITES infect 1 RBC –> creates ‘SIGNET RING’ formation;
infection restricted to LIVER & SPLEEN

119
Q

What are the similarities & differences bw P. VIVAX & P. OVALE?

A

(similarities) similar infection to P. VIVAX, common in AFRICA, commonly RELAPSE
(difference) produces FEWER MEROZOITES

120
Q

What causes TOXOPLASMOSIS?

A

TOXOPLASMA

121
Q

Name a species of TOXOPLASMA:

A

TOXOPLASMA GONDII

122
Q

What animals are susceptible to TOXOPLASMA GONDII infection?

A

(very LOW host specificity) rodents, mammals, birds;

DEFINITIVE HOST - domestic & wild CATS

123
Q

What are the life stages of TOXOPLASMA GONDII?

A

SPOROZOITES are the INFECTIOUS form, they are within OOCYST that passes out in FECES

124
Q

How is TOXOPLASMA GONDII transmitted?

A

ingestion of undercooked, infected meat, containing TOXOPLASMA OOCYSTS;
ingestion of OOCYST from fecally-contaminated HANDS/FOOD;
TRANSPLACENTAL TRANSMISSION

125
Q

Describe the pathogenesis of TOXOPLASMOSIS in an IMMUNOCOMPETENT px:

A

(generally) cats shed OOCYSTS for only 1-2 weeks, but large #s may be shed; OOCYSTS can survive in env’t for several months, are remarkably resistant to disinfectants, freezing, drying, but are killed by heating to 70°C for 10 min;
(immunocompetent px) generally an asymptomatic infection; ~10% experience acute dz w/flu-like Sx (self-limiting)

126
Q

Describe TOXOPLASMOSIS in an IMMUNOCOMPROMISED px:

A

(generally) px often have CNS dz, may have RETINOCHOROIDITIS or PNEUMONITIS;
(in AIDS px) TOXOPLASMIC ENCEPHALITIS is the most common cause of INTRACEREBRAL MASS lesions, thought to be caused by reactivation of CHRONIC infection

127
Q

Describe CONGENITAL TOXOPLASMOSIS:

A

results from an acute primary infection acquired by the mother during pregnancy; incidence/severity varies w/the trimester during which infection was acquired (1st trimester is most damaging); invades CNS, may cause blindness, encephalitis, mental retardation

128
Q

What species of SPOROZOA resembles a GIARDIA LAMBLIA infection? Describe it:

A

CRYPTOSPORIDIUM PARVUM;

difficult to detect in water (during water treatment); ingestion of CYSTS cause WATERY DIARRHEA

129
Q

What are NEMATODES?

A

ROUNDWORMS; multicellular parasites

130
Q

What are 3 broad categories of NEMATODES?

A

ROUNDWORMS transmitted by INGESTION of OVA;

ROUNDWORMS transmitted by DIRECT PENETRATION of INFECTIOUS LARVAE;

ROUNDWORM TISSUE PARASITES

131
Q

Name 3 species of ROUNDWORMS transmitted by OVA INGESTION:

A

ASCARIS LUMBRICOIDES;
TRICHURIS TRICHIURA;
ENTEROBIUS VERMICULARIS

132
Q

What’s the largest species of NEMATODE to parasitize the human intestine?

A

ASCARIS LUMBRICOIDES (also the most COMMON helminthic infection)

133
Q

Describe the life cycle of ASCARIS LUMBRICOIDES:

A

OVA are ingested –> LARVAE hatch in DUODENUM, move into BVs –> LARVAE move to LUNGS to molt & mature –> in 3 wks, LARVAE are coughed up & swallowed –> once in SMALL INTESTINE, develop into ADULT worms

FEMALES produce ~200,000 eggs DAILY; eggs pass out w/FECES; eggs in SOIL are viable for up to 3 yrs

134
Q

What symptoms present w/ASCARIS LUMBRICOIDES infections?

A

may cause STUNTED GROWTH, but ADULT worms usually cause NO ACUTE Sx;
high worm burdens may cause ABDOMINAL PAIN & INTESTINAL OBSTRUCTION;
MIGRATING ADULT worms may block BILE DUCT;
during LUNG PHASE of larval migration, PULMONARY Sx possible

135
Q

Which nematode is known as the WHIP WORM?

A

TRICHURIS TRICHIURA

136
Q

Describe the life cycle of TRICHURIS TRICHIURA:

A

eggs ingested (oral-fecal route) –> hatch in SMALL INTESTINE –> LARVAE migrate to CECUM, mature into ADULTS –> ADULTS live in CECUM & ASC COLON (fixed in this location, w/anterior portions threaded into MUCOSA)

ADULT FEMALES produce up to 10,000 eggs daily; shed in FECES

137
Q

What symptoms present w/TRICHURIS TRICHIURA infection?

A

ANEMIA (consume blood cells w/anterior end buried in mucosa), damage to epithelial layer (can lead to secondary bacterial infection), PROLAPSED RECTUM possible (in extreme cases)

138
Q

What’s a PINWORM, and what’s its only HOST?

A

ENTEROBIUS VERMICULARIS;

humans

139
Q

Describe the life cycle of ENTEROBIUS VERMICULARIS:

A

GRAVID (pregnant) ADULT FEMALE worm (is NOCTURNAL) migrates out of INTESTINE to lay up to 20K eggs on PERIANAL skin at night –> eggs transferred to FINGERNAILS BY SCRATCHING –> eggs are ingested –> LARVAE hatch in SMALL INTESTINE, migrate to COLON where they mature into ADULTS

140
Q

Where are PINWORMS found?

A

worldwide, more common in TEMPERATE (than tropical) climates;
most COMMON helminthic infection in the US (~40 mil px);
infections more frequent in SCHOOL/PRESCHOOL CHILDREN & in CROWDED conditions

141
Q

What symptoms present w/ENTEROBIUS VERMICULARIS infections?

A

often ASYMPTOMATIC;
most typical Sx is PERIANAL ITCHING (esp @ night) which may lead to secondary infection;
occassionally, female genital tract invasion –> VULVOVAGINITIS

142
Q

Name 4 nematodes transmitted by DIRECT PENETRATION of INFECTIOUS LARVAE:

A

ANCYLOSTOMA DUODENALE & NECATOR AMERICANUS;
ANCYLOSTOMA BRAZILIENSE;
STRONGYLOIDES STERCORALIS

143
Q

What 2 species are nicknamed (together) as the AMERICAN HOOKWORM?

A

ANCYLOSTOMA DUODENALE & NECATOR AMERICANUS

144
Q

Describe the life cycle of the AMERICAN HOOKWORM:

A

ADULT FEMALE in small intestine lays 10-20K eggs daily –> eggs in FECES –> LARVAE hatch, feed on bacteria –> RHABDITIFORM LARVA molts to FILARIFORM LARVA (infective) –> FILARIFORM LARVA penetrate bare skin –> moves to LUNG, are SWALLOWED

145
Q

What symptoms present w/AMERICAN HOOKWORM infection?

A

larval penetration of skin usually does LITTLE damage, DERMATITIS possible;
LARVAE may cause PULMONARY Sx (rarely PNEUMONITIS);
ADULT worms in SM INT attach to MUCOSA w/strong cutting plates, begin feeding on BLOOD –> ANEMIA, MALNUTRITION

146
Q

What’s known as the DOG & CAT HOOKWORM?

A

ANCYLOSTOMA BRAZILIENSE

147
Q

Describe the life cycle of ANCYLOSTOMA BRAZILIENSE:

A

LARVAE penetrate SKIN & wander –> (life cycle not complete in humans) continue to wander aimlessly –> CREEPING ERUPTION (VISCERAL LARVAL MIGRANS) in humans –> intense ITCHING & EOSINOPHILIA

148
Q

Describe the life cycle of STRONGYLOIDES STERCORALIS:

A

(alternates bw FREE-LIVING & PARASITIC forms) –> FEMALE in SM INT is OVOVIVIPAROUS (eggs remain w/in mother up until they hatch), eggs are deposited in MUCOSA, hatch & move to LUMEN –> LARVAE excreted in FECES (or cause AUTO INFECTION) –> become FREE-LIVING ADULTS in SOIL, produce eggs that develop into infectious FILARIFORM LARVAE –> LARVAE penetrate skin –> thru BLOOD to LUNGS –> molt in LUNGS, are swallowed, become ADULTS in SM INT

149
Q

Name 4 species of NEMATODE TISSUE PARASITES:

A

ANISAKA;
TRICHINELLA SPIRALIS;
WUCHERERIA BANCROFTI;
ONCHOCERCA VOLVULUS

150
Q

What is ANISAKA?

A

they are parasites in the stomachs of MARINE FISH & BIRDS

151
Q

Describe the life cycle of ANISAKA:

A

LARVAE ingested by humans (from raw fish) –> produce INTESTINAL OBSTRUCTION, PAIN, NAUSEA, VOMITING

152
Q

Where is ANISAKA commonly seen? How is it TREATED?

A 
where raw fish is eaten more commonly (Japan, Pacific coast of S Am., Netherlands);
SURGERY ONLY (no effective drug tx)
153
Q

Describe the life cycle of TRICHINELLA SPIRALIS:

A

ENCYSTED LARVAE are ingested & during digestion reach SM INT where molt to become ADULTS –> ADULT FEMALES produce 100’s of LARVAE –> just after copulation, MALE dies; following larval production FEMALE dies –> LARVAE carried via BLOOD to MUSCLE where they ENCYST –> if host is not consumed by another host, larvae calcify & die (humans are a dead end host)

154
Q

What animals will TRICHINELLA SPIRALIS infect?

A

(low host specificity) bears, bigs, rats

155
Q

What Sx present w/TRICHINELLA SPIRALIS infections?

A

LIGHT infections - may be ASYMPTOMATIC;
larval migration into muscle tissues can cause FACIAL EDEMA, CONJUNCTIVITIS, FEVER, MYALGIAS, RASHES, BLOOD EOSINOPHILIA;
occasional life-threatening manifestations - MYOCARDITIS, CNS involvement, PNEUMONITIS

156
Q

What are 2 types of FILARIAL WORMS?

A

WUCHERERIA BANCROFTI;

ONCHOCERCA VOLVULUS

157
Q

What causes ELEPHANTIASIS & what is another name for this condition?

A

WUCHERERIA BANCROFTI;

BANCROFTIAN FILARIASIS

158
Q

How is BANCROFTIAN FILARIASIS transmitted?

A

vectored by MOSQUITO

159
Q

Describe the life cycle of WUCHERERIA BANCROFTI:

A

females in LYMPH DUCT are OVOVIPAROUS, produce 1000s of immature LARVAE (aka MICROFILARIAE) –> MICROFILARIAE released into lymph, swept into blood thru THORACIC DUCT –> MOSQUITOES ingest MICROFILARIAE in BLOOD MEAL –> MICROFILARIAE mature in MOSQUITO to final infective LARVAL stage

160
Q

What Sx present w/BANCROFTIAN FILARIASIS?

A

(when females release MICROFILARIAE) intense lymphatic inflammation occurs w/CHILLS & FEVER –> lymph nodes become obstructed –> SWEATING;
(M) SCROTUM/LEGS;
(F) LEGS;

161
Q

How can a clinician Dx WUCHERERIA BANCROFTI infections?

A

MICROFILARIAE exhibit PERIODICITY in the blood (they can be demonstrated during certain times of the day, other times seem to disappear from peripheral circulation;
draw blood at NIGHT to observe MICROFILARIAE

162
Q

What dz is caused by ONCHOCERCA VOLVULUS?

A

RIVER BLINDNESS

163
Q

How is ONCHOCERCA VOLVULUS transmitted?

A

vectored by a BLACK FLY (SIMULIUM)

164
Q

Describe the life cycle of ONCHOCERCA VOLVULUS:

A

ADULT worms locate under skin, become encapsulated by host reactions to form NODULES –> adult FEMALE releases MICROFILARIAE –> MF migrate thru skin to EYES

165
Q

What Sx present w/RIVER BLINDNESS?

A

LIZARD SKIN - inflammation from larvae migrating thru skin;

BLINDNESS - when larvae migrate to eyes from skin

166
Q

PLATYHELMINTHES are also known as what? And what are 2 broad groups?

A

FLAT WORMS;

TREMATODA (FLUKES), CESTODA (TAPEWORMS)

167
Q

Name 6 types of FLUKES:

A 
FASCIOLA HEPATICA (LIVER FLUKE);
CLONORCHIS SINENSIS (CHINESE LIVER FLUKE);
FASCIOLOPSIS BUSKI (GIANT INTESTINAL FLUKE);
SCHISTOSOMA MANSONI, S. HAEMATOBIUM, S. JAPONICUM (BLOOD FLUKES)
168
Q

Describe a LIVER FLUKE:

A

large, leaf-shaped parasites of HERBIVORES, can infect humans accidentally

169
Q

Describe the life cycle of a LIVER FLUKE:

A

(ADULTS live in BILE DUCT) eggs passed out of LIVER w/BILE, into INT to be voided w/FECES –> LARVAE penetrate SNAILS –> CERCARIAE (motile larvae) leave snail, ENCYST as METACERCARIAE on water plants –> METACERCARIAE ingested by animal, migrate to LIVER

170
Q

What Sx present w/LIVER FLUKE infection?

A

LIVER is damaged (by fluke migration);

worms in BILE DUCTS cause INFLAMMATION, PAIN, CHILLS, FEVER

171
Q

Describe the life cycle of the CHINESE LIVER FLUKE:

A

eggs excreted in FECES –> eggs hatch in water, LARVAE penetrate snails –> larvae mature in snails, CERCARIAE leave snail to penetrate FISH –> METACERCARIAE encyst in fish flesh –> humans consume undercooked/raw fish –> worms mature in BILE DUCTS, produce up to 4K eggs/day for at least 6 months

172
Q

Describe the life cycle of the GIANT INTESTINAL FLUKE:

A

eggs in FECES hatch in WATER –> LARVAE penetrate SNAILS –> CERCARIAE move to plants (usually WATER CHESTNUTS) –> METACERCARIAE encyst under leaves –> humans/pigs eat water chestnuts

173
Q

What’s unique about SCHISTOSOMES?

A

mature in blood stream of DEFINITIVE HOST;

unlike other FLUKES) are DIOECIOUS (separate genders

174
Q

What are the 3 SCHISTOSOMES & describe their similar life cycle:

A

SCHISTOSOMA MANSONI, S. HAEMATOBIUM, S. JAPONICUM;
M/F live in host BVs (each species prefer different vv.) –> F release 3K eggs/day –> eggs pass thru tissue to reach INT/BLADDER –> eggs reach fresh water in URINE/FECES –> eggs hatch in fresh water –> infective LARVAL stage penetrates snail –> snail excretes infective CERCARIAE form w/a FORKED TAIL –> CERCARIAE penetrate skin of a vertebrate host, mature into ADULTS, reside in vv. –> adults may live 20-30 years

175
Q

What Sx present w/SCHISTOSOMA infections?

A

SWIMMER’S ITCH - dermatitis from penetration of skin by CERCARIA;
w/in 1-2 months, develop FEVER, CHILLS, COUGH;
(most serious damage done by EGGS) eggs lodged in VENULES & TISSUE cause immune system to respond –> as eggs accumulate –> SPLENOMEGALY, ASCITES (fluid in ABD cavity) –> high eosinophilia

176
Q

Name 4 kinds of TAPEWORMS:

A 
TAENIA SAGINATA (BEEF TAPEWORM);
TAENIA SOLIUM (PORK TAPEWORM);
DIPHYLLOBOTHRIUM LATUM (FISH TAPEWORM);
ECHINOCOCCUS GRANULOSUS
177
Q

What is a SCOLEX?

A

the HEAD of an ADULT tapeworm, used to attach to human intestinal wall (SM INT)

178
Q

What is a PROGLOTTID?

A

a segment of a tapeworm’s body;

each contains a set of M & F organs that produce eggs

179
Q

Describe the life cycle of TAENIA SAGINATA:

A

cattle consume GRAVID PROGLOTTIDS or EGGS in contaminated feed –> eggs hatch & LARVAE migrate to muscle –> larvae encyst in muscle as CYSTICERCI

180
Q

What Sx present w/TAENIA SAGINATA infection?

A

only produce MILD abdominal Sx; most striking feature is PASSAGE of PROGLOTTIDS

181
Q

Describe the life cycle of the PORK TAPEWORM:

A

(morphology & life cycle similar to BEEF T.W.) proglottids & eggs eliminated in FECES –> PIGS consume gravid proglottids or eggs in contaminated feed –> eggs hatch & larvae migrate to muscle –> larvae encyst in muscle as CYSTICERCI

182
Q

What is CYSTICERCUS?

A

consists of SCOLEX within a large BLADDER, so CYSTICERCI aka BLADDER WORMS

183
Q

What conditions arise from TAENIA SOLIUM infection?

A

CYSTICERCOSIS - only occurs w/T. SOLIUM; infective larvae migrate into mm/tissue of human host & develop into CYSTICERCI (can develop in BRAIN or EYE –> MENINGITIS, VISUAL DISTURBANCE, ACUTE INFLAMMATION);
ADULT worms rarely cause Sx (main Sx often the PASSAGE of PROGLOTTIDS)

184
Q

Describe the life cycle of the FISH TAPEWORM:

A

eggs eliminated in FECES –> eggs hatch in water, LARVAE called CORACIDIUM –> coracidium ingest by COPEPODS –> copepods eaten by FISH –> larvae mature to SPARGANUM, encyst in fish mm –> human infection from undercooked fish

185
Q

What Sx present w/FISH TAPEWORM infection?

A

(infections can be long-lasting, like DECADES) most are ASYMPTOMATIC; may include abdominal discomfort, diarrhea, vomiting, weight loss; VIT B12 deficiency w/ANEMIA may occur (tapeworm absorbs large amounts of B12)

186
Q

Describe the life cycle of ECHINOCOCCUS GRANULOSUS:

A

adult worms infect CANINES & release eggs in SM INT –> eggs eliminated in FECES, ingested by SHEEP/CATTLE/PIGS/etc –> humans are accidental hosts, transmission usually by contact w/infected DOG (dogs may be infected by eating VISCERA of LIVESTOCK) –> larvae move into LIVER/LUNG, form HYDATID CYST (contains infectious worms called HYDATID SAND)

187
Q

What Sx present w/ECHINOCOCCUS GRANULOSUS infection?

A

can remain SILENT for years before enlarging cysts cause Sx in affected organs;
HEPATIC involvement can result in abdominal pain, a mass in the hepatic area, biliary duct obstruction;
PULMONARY involvement can produce chest pain & cough;
RUPTURE of cysts can produce fever, eosinophilia, anaphylactic shock, cyst dissemination;
other organs (BRAIN, BONE, HEART) can also be involved, w/resulting Sx

CLINICAL MICROBIOLOGY (1 decks)

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