Parasitology Flashcards
(104 cards)
1
Q
What is a definitive host for a parasite?
A
Host in which the sexual stage of a parasite life cycle occurs
2
Q
What is an intermediate host?
A
Host in which asexual reproduction or development occurs
3
Q
What is an incidental host?
A
A host that is not an obligate part of the parasite life cycle
4
Q
What is a cysticercus?
A
Encysted cestode larval form in tissues of infected intermediate host
5
Q
What is the class cestoda of worms?
A
No internal digestive system, include tapeworms;
transmission by ingestion of larval cysticeri or eggs
6
Q
What is the class Trematoda of worms?
A
Flukes of the lungs, liver and blood
broad flattened bodies witha simple digestive system
7
Q
What is the intermediate host of Taenia solium?
A
Pigs
8
Q
What is the pathology of taenia solium?
A
Taeniasis(adult worm in gut) often asymptomatic occasionally nausea, vomitting diahrrea weight loss
Cysitercosis ~1cm cysticeri located in any tissue causes
lumps and some inflammation neurocysticericosis is potentially dangerous
9
Q
How is Taenia solium diagnosed?
A
Active proglottids in feces, or eggs
contrast studies
10
Q
What is the treatment for Taenia solium?
A
Praziquantel, niclosamide or albendazole and dexamethasone is used to reduce inflammation
11
Q
What is dyphyllobothrium latum?
A
Fish tapeworm, similar to beef and pork versions
12
Q
What is the pathology associated with dyphyllobrothorium latum?
A
Fish tapeworm, like beef tapeworm. Adults absorb 80-100% dietary B12 leading to B12 defficiency and anemia
13
Q
What is used to treat dyphyllobrothorium latum?
A
Praiquantel or niclosamide (single dose)
14
Q
What is Echinococcosis?
A
Tapeworm in which dogs are definitive host and humans are incidental.
15
Q
What is the pathology associated with echinococcosis?
A
Hydatid cysts which can appear as tumors, Majority are in the liver and lungs
20 year latent period
disease can onset when it causes pain or ruptures
16
Q
What is the treatment of echinococcosis?
A
Percutaneous drainage with instillation of hypertonic saline or alcohol.
Surgical removal
Treat with albendazole but low cure rate
17
Q
What are schistosomiasis?
A
Blood flukes, 3 major that effect humans
18
Q
What are the intermediate hosts of shistosomiasis? And how are they transmitted?
A
The intermediate host is snails.
Invasive, aquatic free-living cercaria penetrate skine
19
Q
What are the morpohological differences between teh three schistosome eggs?
A
S. Mansoni have a lateral spike
S. haematobium have a terminal spike
S. Japonicum have no spike
20
Q
What is the pathology associated with schistosomiasis?
A
Early–no symptoms, possible rash, fever, headache, nausea as it migrates
Middle(onset 1-2 months)–from immune response to eggs
intense fever with oviposition, Katayama syndrome
abdominal pain, diarrhea, blood in stool
urogenital can cause blood in urine
Chronic (onset 5+ years)
eggs lodge in tissue
eosonic inflammation leading to granulomas
S. mansoni and S. japonicum go to severe liver disease and colon
S. haematobium go to extesnive fibrosis of bladder
21
Q
Where do the adult worms and eggs migrate to in each type of schistosomiasis?
A
Adult worms located in: S. mansoni--inferior mesenteric veins S. Japonicum--superior mesenteric veins S haematobium--venous plexus of bladder eggs migrate to: "-descending colon "-small intestine "-bladder
22
Q
What is the treatment for schistosomiasis?
A
Normally they are masked from immune system by absorption of host serum proteins
Praziquantel in either single or multiple doses potentiates active immunse system killing of adult worm
23
Q
What are the three different types of nematoda that act as parasites in humans/
A
lumenal[eneterobius vermicularis, trichuris trichiuria, ascaris lumbricoides]
hookworm[necator americanus, strongyloides stercoralis]
tissue worms[trichinell spiralis, toxocara canis]
24
Q
What is enterobius vermicularis?
A
Aka Pinworm
transmited by ingestion of eggs
25
What are some symptoms of enterobius vermicularis?
gravid female emerges from anus to lay eggs
perianal scratching facilitates transmission
perianal itch, restlessness, insomnia confirm by observation of eggs, scotch tape test
26
What is the pathology associated with enterobius vermicularis?
Intesnse perianal pruritis
secondary infections due to scratching
urogenital invasion in female
no immunity
27
What is the treatment for enterobius vernicularis?
pyrantel pamoate, mebendazole, albendazole along with thorough housecleaning
28
What is trichuris trichiura?
Whipworm, adults attach to colonic mucosa
| definitive host is humans only
29
What is the lifecycle of trichuris trichiura?
Eggs are swallowed, hatch in intestine, adults mate and migrate to colon, eggs mature in soil
30
What is the pathology of the trichuris trichiura?
Worm Burden:
low to moderate: usually none, bleeding, bacteremia
high: disrupted colonic mucosa, bloody stool, prolapse
heavy burden in children leads to impaired growth and impaired cognitive ability
31
What is the treatment of trichuris trichiura?
3 days of ivermectin, mebendazole or albendazole
32
What is ascaris lumbricoides?
Definitive host humans, ingestion of eggs from soil. no person to person
33
What is the pathology of ascariasis lumbricoides?
Usually none with low to moderate worm bruden
heavy worm loads can lead to intestinal obstruction
stressed worms migration to other parts of body
chronic malnutrition
allergic inflammation from larval migration through lungs
34
What is the treatment for ascariasis lumbricoides?
MEbendazole, albendazole, ivermectin
35
What is necator americanus and ancylostoma duodenale?
Hookworm, with humans as a definitve host. Migrate to small intestine invasive contact through soil, no direct person to person contact
36
What is te life cycle of hookworm necator americanus?
Filariform larvae invade skin, go to circulation and lodge in lungs. Larvae coughed up and swalowed. Mature to adult in intestine, eggs to soil
37
What is the pathology associated with necator americanus?
Initial pruritis
bronchitis
exsanguination
anemia nd reduced mental and physical development in children
38
What is strongyloides stercoralis?
Small intestine located parasites with humans as their definitive host. Filariform penetrate skin, autoinfection
39
What is the treatment for strongyloides stercoralis?
pyrantel pamoate, albendazole and mebendazole
40
What is unique about the strongyloides stercoralis life cycle?
3 alternative pathways
direct: like hookworm, but no eggs, larvae in feces
indirect: sexual replication in soil
Autoinfection: larvae mature in host, enter through colonic mucosa
41
How is strongyloides stercoralis diagnosed?
Difficult because no eggs are excreted, iodine detection
fecal smear stianed with auramine O under UV light
Agar plate shows muiltile rhabditiform
Gram staining of a sputum can detect filariform
Serology sensitivity but lots of cross reactivity
42
What is teh pathology associated with strongyloides stercoralis?
Pulomonary manifestations
chronic inestinal malabsorption and dysentery
rash
autoinfection and immunosuppression can lead to hyperinfection
43
What is the treatment associated with strongyloides stercoralis?
ivermectin 1st choice, thiabenazole 2nd choice
44
What is trichinella spiralis?
Found in intestine and larvae in muscle, aka trichinosis
definitve host is swine and bears
humans area dead end incidental host
45
What is the pathology of trichinella spiralis?
Mild pathology from adult worms
localized inflammation around cysts adn degeneration of muscle
can have severe symptoms, cardiac adn nerual dysfunction, conjunctivitis, fever, muscle pain
46
What is the treatment and diagnosis for trichinella spiralis?
Treatment is mebendazole or albendazole as wella s corticosteroids for symptoms
serological test three weeks or longer after infection
47
What is toxocara canis?
```
Definitive host dogs
incidental host dogs
tocoariasis
ingestion of embryonated eggs from soil
most dogs infected
```
48
What is the the pathology of toxocara canis?
light infection; self-limiting pathology
heavy worm loads can lead to necrosis
enlarged liver, pulmonary complications neurological symptoms
immune hypersensitivity common
49
What is the Leishmania life cycle?
Sandfly ingest macrophages infected, transform in promastigote, divides in midgut of sandfly, and transfers to human where phagocytosed in macrophage and transformes into amastigotes inside macrophage
50
What is the pathology of cutaneous leshmaniasis?
Starts as bump, then an ulcerative sore, abundant amastigotes in lesions, spontaneous healing, strain-specific immunity
metastisis months to years after primary lesion heals, ulceration nasopharynx tissues
visceral leishmaniasis 2-12 months
fever adn wasting splenomegaly and hepatomegaly
51
What is the life cycle of African trypanosomes (sleeping sickness)
Testes fly bites human, inject trypomastigotes which transform and multiply by binary fisssion in various body fluids, taken up in blood by tsetse fly, transform again in midgut of tsetse fly
52
What is the pathology of african trypanosomiasis(sleeping sickness)?
```
self healing chancre
hematogenous dissemination to lymphatics and tissues
waves of parasitemia with fever
lymphadenopathy (winterbottom's sign)
CNS infection, sleeping, dementia
death trhough coma or 2ndary infection
immune evasion by antigen variation
always fatal if untreated
```
53
What are the treatments for trypanosomias?
First stage treatments: early on drugs are good
Pentamidine, Suramin
Second stage treatments( late they must cross blood brain barrier
melarsoprol
eflornithine and nifurtiox
54
What is south american trypanosomiasis?
trypanosoma cruzi
vector borne by reduvid bugs
transfusion
endemic in South america
55
What is the pathology of chagas disease, Trypanosomiasis?
```
Acute 2-4 mos fever, chagoma (Romana's sign)
hematogenous spread
sever in children
chronic: onset at 10-20 yers
peristant amastigotes
damage to nerve/muscle cells of heart esophogaus
inflammation and autoimmunity
death from sudden heart attack
no Tx for chronic Chagas
```
56
hat is trichomonas vaginalis?
luminal or urogenital, no free living or encysted state, stable 24 hours out,
57
What is the pathology of Trichomoniasis?
not life threatening, 70% asymptomatic
vaginits, burning adn itching, inflammation, frothy vaginal discharge
male:
itching or irritation, burning after urination or ejaculation
increase risk of acquiring HIv
58
What are the differences between fungi and higher eukaryotic cells?
contain ergosterol rather than cholesterol
antifungal drug amphotericin B binds it, and azole and allylamine interfere w/ biosynth
fungal cellsare usually surrounded by a rigid cell wall composed of carbohydrate polymers and proteins
59
What are the two fungi that require interaciton with humans to live and are natural part of flora?
Candida albicans and Malassexia furfur
60
What are two pathogenic yeasts?
Cryptococcus neoformans, and histoplasma capsulatum which is dimorphic
61
What are the defining charactersitics of yeast?
unicellular, spherical or ellipsoid, reproduce by budding or fission
62
What is hyphae/mycelium?
Also refured to as mold, hyphae is branching tubules, 3 types
mycelium is a mass of intertwine hyphae
Rhizoids , rootlike structures
63
What are pathogenic molds?
Aspergillus which exists only as mold
| candida albican which is dimorphic but mold morphotype is pathogenic
64
What are condidiospores?
asexual reproductive elements taht can be borne naked on specialized structures, macroconidia large multicellular and micrcondia-small single celled
65
What are sporangiospores?
Single celled spores that are formed within sacs called sporangea from the hyphae
66
What are the problems from gneral funcal infections?
hypersensitivity, opportunistic infection mytotoxins
67
What does Amanita cause when ingested?
severe or fatal liver and kiney damage inhibiting RNA polymerase 2
68
What is produced by Aspergillus flavus taht causes what?
aflatoxin, mutagenic carcinogenic in contaminated grains
69
What are some ways of diagnosing?
KOH-technique, direct microscopic exam, cultivation on blood agar, Serological methods, PCR, mass spec, FISH
70
What are the targets of antifungal drugs?
ergosterol
cell wall syntehsis
nucleic acid synthesis
disruption of microtubules
71
What are the four resistance mechanism to the azoles?
efflux pumps
decrease affinity of target enzyme for drug
increase expression of target enzyme
alternative metabolic pathway leading to ergosterol
72
How does polyene cause resistance?
resistance to polyenes and amphotericin B is not common, mechansim of resistance is related to reduction of ergosterol in resistant organism or by masking it
73
How does allyamines-terbinafine resistance occurs?
Clinical failure is not b/c of resistanc ebut due to CDR1 multidrug efflux pump
74
HOw does echinocandins resistance occurs?
resistant organisms have point mutations in subunits of glucan syntehsis targets
75
How does resistance to flucytosine occur?
alteration in permease that reduces uptake
| alteration in enzymes necessary for conversion to active metabolites
76
What type of helper t cells are important for immunocompetent individuals to clear fungal infections?
neutrophils, TH1 mediated resposne, humoral and cellular immunity
IL12 and IFNgamma
77
What are the superficial mycoses?
Malassexia furfur
hortaea werneckii/exophiala werneckii
piedraia hortae
Trichosporon
78
What are the cutaneous mycoses?
Dermatophytes:
Trichophyton
Epidermophyton
microsporum
79
What are the subcutaneous mycoses?
sporothrix schenckii
80
What is Malassezia furfur?
superficial, responsible for versicolor
lipophilic yeast, growth requires oil
small hypo or hyperpigmented macules that don't tan
spontaneous resolution not likely, fluoreces
81
What is hortaea werneckii
tinea nigra
dematiaceous frequenly branched septate hyphae
solitary irregular pigmented macule
can resemble malignant melinoma
82
What is Piedraia hortae?
responsible for black piedra
brown to reddish-black mold
presence of dark nodules that surround hair shaft
cured witha hair cut
83
What are the three endemic fungi pathogens?
```
Histoplasma capsulatum(yeast))
Blastomyces dermatidis (yeast)
Coccidoides immitis (endospores)
they are dimorphic have different morphologies in environement as opposed to body mold in environemtn
can infect immunocompetend individuals
```
84
How does infection occur most often from endemic environmentsal molds?
inhalation
85
For endemic molds where is the usual primary infection and how else does it often present?
lungs, can disseminate and some poeple present with cutaneous lesions as a result of dissemination with blastomyces dermatidis
86
What is the main diagnostic method?
microscopic ezamination
87
Where are the endemic regions of each of hte endemic fungi?
cocci-->southwest
blastomyces midwest and ollowing the missippi and its tributaries
histoplasmosis--directly on mississippi
88
Histoplasma capsultam is located where?
acidic soil, soil containing hig nirogen content, in those geographic regions 85% skin immunological activity indicating previous infection
89
In host what is histoplasma capsulatum present as?
oval budding yeast with narrow bud head, insode mononuclear phagocytes and extracellular
90
What is the hallmark of histoplasma capsulatum infection?
requries CD4+ T cells to control and produces granulomas containing phagocytes and lymphocytes to control fungal gowth
usually asymptomatic infection or flu like symptoms
91
What are the clinical syndromes associated with histoplasma capsulatum?
pulmonary can resemble miliary tb on xray
acute pericarditis in 5% of symptomatic patients
disseminated in 1/2000 pts spread to blood
ocular histoplasmosis syndrome
fibrosing mediastinitis
92
How does blastomyces appear in the body?
Large budding yeast witha large broad bud neck, 1/100000 in endemic areas
93
How long is the incubation period for blastomyces?
4-6 weeks, trauma can lead to deep cutaneous infection
94
What are the clinical syndromes of blastomyces?
Can present is a bening and self-limiting granulomatous
can present as TB like
has skin subcutaneous nodule or papule as most common extra pulmonary dissemination
can bind macrophage integrins
95
Coccidoides present as what in humans?
Large spherules, that contain numerous small endosphores
96
Coccidoides is usually acquired by what route?
respiratory route, after soild disrution in late summer and early fall, can have granulomatous infection
97
What is the clinical syndrom of coccidoiides?
60 % asymptommatic, mild flu like syndrome 7-21 days after exposure
dissemination in 1% of cases can result in severe symptoms such as meningitis often fatal and dark skinned individuals are susceptible to disseminated disease
pregnancy a periilous time forinection
cocci most virulent fungal infection but 95% resolve iwthout therapy
98
What is the role of cocci in AIDS patients?
25% develop it and third most common life threatening infection in AIDS pateints
99
What are the mian treatments for endemic fungi?
in mild to moderate pulmonary diseae no treatment or itraconazole
in severe disseminated diseae Amphotericin B
100
What are the most common causes of fungal infection pateint in hematopoietic stem cell and organ transplant pateints?
Candida and aspergillus
101
What is the morphology associated with canddia?
complex morphology and yeast and hyphae morphologies are seen adn psuedohyphae, the pseudohyphae is the most frequently tissue invasive
102
C. Albicans have what as virulence determinants?
invasive psuedohyphae
adhesion complex molecules, CR3 adn CR4 are targets and surfavce hyphal wall protein
hydrolytic enzyme
103
Where are common sites for infection of opportunisitic myocytes?
skin, nail and mucosal can occr in immunocompetent bc of compromised local host
sites of surgical procedures and indwelling catheters
moist fat folds or abraded skin
broad spectrum antibiotics open up mucosal esp vagina to canidas
104
Cryptococcus i swhat type of fungus?
monomorphic budding yeast
worldwide distribution
obreaks only observed in gattii
