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Infectious Disease 2 > Exam Review 4 > Flashcards

Exam Review 4 Flashcards

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1
Q

What is the epi of toxoplasmosis?

A

Cosmopolitan distribution (worldwide); Generally causes very benign disease in immunocompetent adults

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2
Q

What are the intermediate hosts of toxoplasmosis? Definitive?

A

Felines are definitive host; Infects wide range of birds and mammals (intermediate hosts)

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3
Q

What is the pathogensis of toxoplasmosis?

A

Active invasion of host cells – Leads to their eventual death; Arrests the acute infection; Serious in immunocompromised and infants in utero

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4
Q

What is the life cycle of toxoplasmosis?

A
  1. From cats; 2. Ingestion of eggs from cat litter, sand, etc; 3. Released in intestine; 4. Multiply in all nucleated cells, released in blood causing lymphadenopathy, hepatosplen, CNS problems
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5
Q

How can toxoplasmosis be spread?

A

Ingesting eggs (from cat) through sandbox, cat litter, unwashed fruits and vegetables; vertically; from transplanted organs or blood

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6
Q

What is the tachyzoite stage of toxoplasmosis?

A

Rapid replication, Dissemination via macrophages, Reticuloendothelial cells, acute stage infection

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7
Q

What is the bradyzoite stage of toxoplasmosis?

A

Dormant, slowly replicating; Due to host immune response; Chronic or latent infection; Tissue cysts in brain and muscle

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8
Q

What causes transition from tachyzoite to bradyzoite stage of toxoplasmosis?

A

IL-2, IL-12 IFN-y; CD8+ Helper Cells; go from positive IgM and negative IgG to negative IgM and positive IgG

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9
Q

What are symptoms of acute toxoplasmosis?

A

When symptoms occur, can cause painless lymphadenopathy, w/ or w/o fever; Usually a single cervical node is enlarged; May persist for 4 to 6 weeks; Fever, headache, malaise, myalgia, lymphadenopathy, hepatosplenomegaly, and atypical lymphocytes

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10
Q

How should acute toxoplasmosis be diagnosed in immunocompetent host?

A

Serology, Parallel testing 4 wks apart (Seroconversion or 4fold rise in IgG titer), PCR, Histology

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11
Q

What occurs in congenital toxoplasmosis if it is acquired late in the pregnancy?

A

Appear normal at birth, but may have retinal scars or abnl CSF; Occasionally develop severe CNS and/or ocular findings; More common that the child has recurrent episodes of retinochoroiditis and impaired psychomotor development during the first 10-20 yrs of life (lower IQ than matched cohort)

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12
Q

What are distinctive ocular findings of congenital toxoplasmosis?

A

Healed scars are pale with distinct margins

and prominent black spots (classic “salt and pepper” lesions); NOTE: Recurrent retinochoroiditis leads to blindness

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13
Q

What is seen in HIV toxoplasmosis?

A

Multifocal necrotizing encephalitis; Altered level of consciousness, headache, focal neurologic deficits, seizures, fever; CT and MRI demonstrates low-density lesions at the corticomedullary junction/Basal ganglia

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14
Q

How should CNS toxoplasmosis be diagnosed?

A
  1. get serology - if positive, then treat; 
2. reimage in 2 weeks, if there hasn’t been any improvement, then biopsy; 
3. if serology is negative, then biopsy
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15
Q

What is the treatment for toxoplasmosis?

A

Sulfadiazine-pyrimethamine

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16
Q

What are the side effects of toxoplasmosis treatment?

A

Toxicity is to the bone marrow; Folinic acid given in conjunction with treatment; Hypersensitivity reactions common; Clindamycin or Atovoquone an alternative to sulfa

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17
Q

What is trichomonas vaginalis?

A

STD caused by trichomonads (3-5 anterior flagella); Trophozoite stage transmitted during sexual intercourse; often co-infection with other STDs; Associated with epithelium of uro-genital tract; both sexes equally susceptible but women more likely to be symptomatic

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18
Q

What are the symptoms of Trichomoniasis?

A

In females: Ranges from asymptomatic, to mild or moderate
irritation, to extreme vaginitis, Onset or exacerbation often associated with menstruation or pregnancy, Vaginal erythema, ‘strawberry cervix’ (in 2%); In males: 50-90% are asymptomatic, Mild dysuria or pruritus, Minor urethral discharge

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19
Q

How is Trichomoniasis diagnosed?

A

Demonstration of parasite - direct observation or in vitro culture

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20
Q

How is Trichomoniasis treated?

A

Metronidazole (Flagyl) and simultaneous treatment of partner

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21
Q

What is Fasciola?

A

Sheep liver fluke found in sheep and herbivore raising

areas

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22
Q

What is the life cycle of Fasciola?

A

eggs go through snails, attach to watercress, penetrate intestine, cause symptoms, eggs are excreted

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23
Q

What is the acute hepatic stage of Fasciola?

A

Within 6 to 12 weeks of ingestion of
metacercariae; Symptoms reflect larval migration (thru small intestinal wall, peritoneal cavity, and liver capsule); Acute stage can last for 2-4 months w/ marked eosinophilia, abdominal pain, intermittent fever, malaise and weight loss, urticaria; Abdominal pain – right hypochondrium; Hepatomegaly – liver may be tender to palpation; liver cyst on MRI

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24
Q

What is chronic Fasciola?

A

F. hepatic migrate to lumen of common bile duct - matures; Eggs appear in the stool after a prepatent period of 3 to 4 months; The patient may become asymptomatic; Symptoms: Intermittant biliary obstruction – mimics biliary colic/acute cholecystitis, Ascending cholangitis – fever, jaundice, and upper abdominal pain

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25
How is Fascioliasis diagnosed?
Egg in the stool, Serologic tests
26
How is Fascioliasis treated?
Triclabendazole 10mg/kg once - this is an orphan drug (must get it through CDC)
27
What is Paragonimiasis?
Get from gills and muscles of crustacea; causes granulomatous reaction, fibrosis & bronchiectasis, cyst – bronchiolar fistula
28
What are the symptoms of acute Paragonimiasis?
Diarrhea, abdominal pain, fever, chest pain, fatigue, urticaria, eosinophilia, cough, night sweats - looks like TB
29
How is Paragonimiasis diagnosed?
Eggs in sputum, Serology – Ectopic sites, Characteristic chest x-ray, biopsy
30
How is Paragonimiasis treated?
Praziquantel 75 mg/kg/d PO in 3 doses x 2d
31
How are flukes usually treated?
Praziquantel
32
What is Leishmania?
Promastigotes in sand fly; Intracellular amastigotes: macrophages in mammals
33
What are the 3 kinds of Leishmania?
Visceral Leishmaniasis, Cutaneous Leishmaniasis, Mucosal Leishmaniasis
34
What is the parasite burden vs the CMI burden for the 3 kinds of Leishmania?
Visceral Leishmaniasis: parasite; Cutaneous Leishmaniasis: both; Mucosal Leishmaniasis: CMI
35
What is Kala-Azar?
Visceral Lesihmaniasis
36
What is visceral Leishmaniasis?
Spectral syndrome in which most infections are self-limited; If symptomatic: Onset usually insidious – can be abrupt, Characterized by fever, weight loss, abdominal enlargement, weakness, loss of appetite; Spleen is firm, nontender b/c massively enlarged, hepatomegaly is seen; can cause death – associated with superinfection
37
What are the lab findings in Visceral Leishmaniasis?
Leukopenia, anemia, eosinopenia
38
How can Visceral Leishmaniasis be diagnosed?
Splenic Aspiration (NOT done in US), Liver Biopsy, Bone Marrow, Buffy Coat, Culture
39
How is Visceral Leishmaniasis treated?
Liposomal amphotericin B
40
What is cutaneous Leishmaniasis?
nodule that ulcerates and has "rolled up border"; self-healing (but takes a long time)
41
What is Mucosal Leishmaniasis?
Nodular and ulcerative lesions of the oral-nasalpharyngeal mucosal surfaces; occurs days to years (43!) following primary infection with L. braziliensis; Nasal septum lesion or horseness often first symptom or sign
42
What is "Old World" Leishmaniasis?
L. Major – Usually heals w/in 6 months; L. Tropica - Can visceralize or become chronic
43
How is New World cutaneous Leishmaniasis treated?
Liposomal amphotericin B
44
How is Old World cutaneous Leishmaniasis treated?
Topical paromomycin, self healing
45
What are the types of intestinal amebas?
E. histolytica – invasive disease; E. dispar – non invasive; E. moshkovskii – non invasive
46
What is the pathogenesis of E histolytica?
Killed instantly at 100ºC, Lives at 4ºC for months, Resistant to chlorine, Survives for many days on salads, cheese, yogurt, flies and cockroaches; Trophozophoites have the ability to colonize or invade the large bowel while cysts are never found within invaded tissues.
47
What happens in the invasion of E histolytica?
lysis of tissue, PMNs, foci of necrosis-coalesce to form ulcer, deeper tissue invasion – vasculitis and thrombosis
48
What kinds of intestinal disease can you see in E histolytica?
Asymptomatic, Mucosal Disease (Acute rectocolitis (dysentary), Chronic nondysenteric colitis), Transmural Disease (Fulminant colitis with perforation, Toxic Megacolon); can also cause liver disease
49
How is E histolytica diagnosed?
Intestinal Disease: Stool O and P – trophs or cysts, Stool Ag and PCR, Pathology; Liver Disease: ELISA postive by 7th day of illness
50
How is amebiasis treated?
Tissue-Cidal (Kills trophs well): Metronidazole; Luminicidal (Kills cysts in the lumen): Paromoycin
51
What is Diphyllobothrium latum?
Broad or Fish Tapeworm; Inhabits the ileum and jejunum; Large tapeworm - 3000 to 4000 proglottids measuring from 3 to 12 m; Scolex – attachment organ contains 2 sucking grooves; D. Latum proglottid – note the rosette shape of the uterus
52
How do you get D latum?
Eating raw, insuffiently cooked or lightly pickled fish
53
What are the clinical findings of D latum?
Few symptoms/pathologic changes in bowel, so often picked up incidentally; Vague abdominal pain – Sensation “something moving inside”; Diarrhea; NOTE: Proglottids do not crawl out anus; causes B12 anemia
54
How is D latum diagnosed?
Eggs in stool
55
How is D latum treated?
Praziquantel
56
What is Taeniasis?
T soleum and T saginata; Worm can push its way out of the anus and move down the patient's leg
57
What are the symptoms of Taeniasis?
Proglottids migrating out of anus, abdominal pain
58
How is Taeniasis treated?
Praziquantel
59
What is Neurocysticercosis?
Caused by T solium; can cause intense inflammation, seizures; can obstruct the ventricles and cause hydrocephalus
60
What happens in the vesicular stage of Neurocysticercosis?
Little inflammatory reaction; formation of a collagen capsule around the parasite
61
What are the stages of Neurocysticercosis?
vesicular, colloidal, granular, calcified
62
How is Neurocysticercosis diagnosed?
CT scan/MRI, Western Blot, eye exam, stool for ova and parasites
63
How is Neurocysticercosis treated?
Albendazole and steroids; add praziquantel if 2+ lesions
64
What is Echinococcus granulosus?
tapeworm that has dog as definitive host and goes through sheep
65
How is Echinococcus treated?
If calcified: watch and wait; if young cyst and no daughter cyst: PAIR; if daughter cysts: surgery and Albendazole
66
What are the stages of Echinococcus?
CE1: Unilocular, simple cyst - PAIR; CE2: Multivesicular, multiseptated cysts in which the daughter cysts may partly or completely fill mother cyst with “wheel-like” structure - surgery and Albendazole; CE4/CE5: calcified - watch and wait
67
What are potential complications of Echinococcus?
Rupture into the biliary tree, the lung, or the peritoneal cavity; Pulmonary Hydatid Disease (after rupture in lung); bone involvement (pain, swelling, pathological fracture)
68
What is Dientamoeba fragilis?
Originally classified as an ameba, but in flagellate group; Exists only in trophozoite form; Difficult to identify in stool; causes GI symptoms
69
How is Dientamoeba fragilis treated?
Metronidazole
70
What are the 2 forms of giardia?
Cyst (infectious) and trophozoite (disease-causing)
71
What is the pathogenesis of giardia?
Attaches to Small Intestine; inflammatory response is minimal; interferes with Brush Border enzymes
72
How is giardia spread?
Waterborne (not killed by chlorination), Direct fecal-oral, Foodborne
73
What are the symptoms of giardia?
Diarrhea w/foul smelling stool, Gas bloating, and abdominal cramps, Malaise and anorexia; Incubation 1-2 weeks; symptoms can last longer than 10 days
74
How is giardia diagnosed?
Stool examination for ova and parasites, ELISA
75
How is giardia treated?
Metronidazole and Tinidazole – Tinidazole most effective, long half life
76
When can you get cryptosporidium?
Endemic childhood diarrhea in developing areas, Traveler’s diarrhea - visitors to developing areas, Protracted diarrhea in immunocompromised patients, Waterborne outbreak in developed countries
77
What are the symptoms of cryptosporidium?
Onset is usually acute, Generally self limited; Diarrhea – Watery, voluminous, and occasionally explosive, abdominal cramps weight loss, nausea, low grade fever, sweats, myalgias, and headache; Illness can last 10-14 days
78
What happens when AIDS patients get cryptosporidium?
Severe persistent diarrhea - may be cholera-like; Lungs, middle ear, biliary tract, pancreas and stomach may be involved; occurs when CD4 is under 100
79
How is cryptosporidium diagnosed?
Stool examination - up to 3 samples may be necessary; immunoflouresence and EIA
80
How is cryptosporidium treated?
Nitazoxanide - treat children and patients with HIV
81
Who gets Cyclosporiasis?
Worldwide distribution – outbreaks in Nepal, Haiti, Peru associated with rainy season; US peak incidence May to July; Assoc w/ various foods (imported and domestic), e.g. raspberry; Waterborne outbreaks have occurred; Can be seen in travelers; person-to-person transmission unlikely
82
What are the clinical manifestations of Cyclosporiasis?
Diarrhea may not be initial symptom, but does cause watery diarrhea-relapsing, cyclical pattern that alternates with constipation; Profound fatigue; Indigestion or heartburn; Anorexia, weight loss; Flulike prodrome may precede diarrhea
83
How is Cyclosporiasis treated?
Trimethoprim-Sulfamethoxazole (Bactrim); Ciprofloxacin alternative
84
What is the life cycle of American Trypanasomiasis?
1. bug sucks blood and ingests the trypomastigotes; 2. replication and fecal excretion; 3. trypomastigotes excreted with feces enter through bite wound or mucous membrane; 4. invade nucleated cells; 5. differentiate into amastigotes and replicate; 6. transform into trypomastigotes and enter bloodstream
85
Where is American Trypanasomiasis found?
New World Disease
86
How is Chagas transmitted?
Bite of kissing bug, blood transfusion, vertically, breast milk, organ transplant, oral (accidentally pulverize and eat the bug)
87
How does Chagas invade?
Trypomastigotes invade Cardiac Muscle (CM), vascular | smooth muscle, interstitial areas of smooth muscle/vascular and myocardium; CM’s are invaded & destroyed
88
What are signs of Chagas?
Romana's sign (Nonpainful unilateral edema of the upper and lower eyelids that lasts for several weeks), Chagoma
89
What is the acute stage of Chagas?
Very rarely diagnosed and often mild; may have signs at portal of entry; High parasitemia; Fever, systemic symptoms, hepatosplenomegaly (last up to 3 mo.), atypical lymphocytosis; EKG abnl common, acute meningoencephalitis and myocarditis rare, but associated with high mortality
90
How is American Trypanasomiasis treated?
Benznidazole, Nifurtimox; lots of side effects; available from CDC; Reduces the severity of symptoms and shortens the clinical course and duraJon of detectable parasitemia
91
How does Chagas progress?
Acute, then chronic phase, then indeterminate form (no signs or symptoms) but can reactivate
92
What are the complications of reactivated Chagas?
cardiomyopathy, GI - can cause dilation and thickening of gut wall
93
When should American Trypanasomiasis be treated?
Should be treated if: acute, early congenital, children, reactivation in immunosuppressed; generally offered if: adults 19 – 50 years old without advanced cardiomyopathy; Individualized decision/not necessarily recommended in: Adults over 50 without advanced cardiomyopathy
94
What happens if immunocompromised patient gets Chagas?
Febrile episodes, apparent organ rejection and inflammatory panniculitis, skin nodules; HIV patients can get CNS disease

Infectious Disease 2 (6 decks)

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