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Infectious Disease 2 > Exam Review 4 > Flashcards

Exam Review 4 Flashcards

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
Q

How is Fascioliasis diagnosed?

A

Egg in the stool, Serologic tests

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26
Q

How is Fascioliasis treated?

A

Triclabendazole 10mg/kg once - this is an orphan drug (must get it through CDC)

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27
Q

What is Paragonimiasis?

A

Get from gills and muscles of crustacea; causes granulomatous reaction, fibrosis & bronchiectasis, cyst – bronchiolar fistula

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28
Q

What are the symptoms of acute Paragonimiasis?

A

Diarrhea, abdominal pain, fever, chest pain, fatigue, urticaria, eosinophilia, cough, night sweats - looks like TB

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29
Q

How is Paragonimiasis diagnosed?

A

Eggs in sputum, Serology – Ectopic sites, Characteristic chest x-ray, biopsy

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30
Q

How is Paragonimiasis treated?

A

Praziquantel 75 mg/kg/d PO in 3 doses x 2d

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31
Q

How are flukes usually treated?

A

Praziquantel

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32
Q

What is Leishmania?

A

Promastigotes in sand fly; Intracellular amastigotes: macrophages in mammals

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33
Q

What are the 3 kinds of Leishmania?

A

Visceral Leishmaniasis, Cutaneous Leishmaniasis, Mucosal Leishmaniasis

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34
Q

What is the parasite burden vs the CMI burden for the 3 kinds of Leishmania?

A

Visceral Leishmaniasis: parasite; Cutaneous Leishmaniasis: both; Mucosal Leishmaniasis: CMI

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35
Q

What is Kala-Azar?

A

Visceral Lesihmaniasis

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36
Q

What is visceral Leishmaniasis?

A

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

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37
Q

What are the lab findings in Visceral Leishmaniasis?

A

Leukopenia, anemia, eosinopenia

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38
Q

How can Visceral Leishmaniasis be diagnosed?

A

Splenic Aspiration (NOT done in US), Liver Biopsy, Bone Marrow, Buffy Coat, Culture

39
Q

How is Visceral Leishmaniasis treated?

A

Liposomal amphotericin B

40
Q

What is cutaneous Leishmaniasis?

A

nodule that ulcerates and has “rolled up border”; self-healing (but takes a long time)

41
Q

What is Mucosal Leishmaniasis?

A

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
Q

What is “Old World” Leishmaniasis?

A

L. Major – Usually heals w/in 6 months; L. Tropica - Can visceralize or become chronic

43
Q

How is New World cutaneous Leishmaniasis treated?

A

Liposomal amphotericin B

44
Q

How is Old World cutaneous Leishmaniasis treated?

A

Topical paromomycin, self healing

45
Q

What are the types of intestinal amebas?

A

E. histolytica – invasive disease; E. dispar – non invasive; E. moshkovskii – non invasive

46
Q

What is the pathogenesis of E histolytica?

A

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
Q

What happens in the invasion of E histolytica?

A

lysis of tissue, PMNs, foci of necrosis-coalesce to form ulcer, deeper tissue invasion – vasculitis and
thrombosis

48
Q

What kinds of intestinal disease can you see in E histolytica?

A

Asymptomatic, Mucosal Disease (Acute rectocolitis (dysentary), Chronic nondysenteric colitis), Transmural Disease (Fulminant colitis with perforation, Toxic Megacolon); can also cause liver disease

49
Q

How is E histolytica diagnosed?

A

Intestinal Disease: Stool O and P – trophs or cysts, Stool Ag and PCR, Pathology; Liver Disease: ELISA postive by 7th day of illness

50
Q

How is amebiasis treated?

A

Tissue-Cidal (Kills trophs well): Metronidazole; Luminicidal (Kills cysts in the lumen): Paromoycin

51
Q

What is Diphyllobothrium latum?

A

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
Q

How do you get D latum?

A

Eating raw, insuffiently cooked or lightly pickled fish

53
Q

What are the clinical findings of D latum?

A

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
Q

How is D latum diagnosed?

A

Eggs in stool

55
Q

How is D latum treated?

A

Praziquantel

56
Q

What is Taeniasis?

A

T soleum and T saginata; Worm can push its way out of the anus and move down the patient’s leg

57
Q

What are the symptoms of Taeniasis?

A

Proglottids migrating out of anus, abdominal pain

58
Q

How is Taeniasis treated?

A

Praziquantel

59
Q

What is Neurocysticercosis?

A

Caused by T solium; can cause intense inflammation, seizures; can obstruct the ventricles and cause hydrocephalus

60
Q

What happens in the vesicular stage of Neurocysticercosis?

A

Little inflammatory reaction; formation of a collagen capsule around the parasite

61
Q

What are the stages of Neurocysticercosis?

A

vesicular, colloidal, granular, calcified

62
Q

How is Neurocysticercosis diagnosed?

A

CT scan/MRI, Western Blot, eye exam, stool for ova and parasites

63
Q

How is Neurocysticercosis treated?

A

Albendazole and steroids; add praziquantel if 2+ lesions

64
Q

What is Echinococcus granulosus?

A

tapeworm that has dog as definitive host and goes through sheep

65
Q

How is Echinococcus treated?

A

If calcified: watch and wait; if young cyst and no daughter cyst: PAIR; if daughter cysts: surgery and Albendazole

66
Q

What are the stages of Echinococcus?

A

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
Q

What are potential complications of Echinococcus?

A

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
Q

What is Dientamoeba fragilis?

A

Originally classified as an ameba, but in flagellate group; Exists only in trophozoite form; Difficult to identify in stool; causes GI symptoms

69
Q

How is Dientamoeba fragilis treated?

A

Metronidazole

70
Q

What are the 2 forms of giardia?

A

Cyst (infectious) and trophozoite (disease-causing)

71
Q

What is the pathogenesis of giardia?

A

Attaches to Small Intestine; inflammatory response is minimal; interferes with Brush Border enzymes

72
Q

How is giardia spread?

A

Waterborne (not killed by chlorination), Direct fecal-oral, Foodborne

73
Q

What are the symptoms of giardia?

A

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
Q

How is giardia diagnosed?

A

Stool examination for ova and parasites, ELISA

75
Q

How is giardia treated?

A

Metronidazole and Tinidazole – Tinidazole most effective, long half life

76
Q

When can you get cryptosporidium?

A

Endemic childhood diarrhea in developing areas, Traveler’s diarrhea - visitors to developing areas, Protracted diarrhea in immunocompromised patients, Waterborne outbreak in developed countries

77
Q

What are the symptoms of cryptosporidium?

A

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
Q

What happens when AIDS patients get cryptosporidium?

A

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
Q

How is cryptosporidium diagnosed?

A

Stool examination - up to 3 samples may be necessary; immunoflouresence and EIA

80
Q

How is cryptosporidium treated?

A

Nitazoxanide - treat children and patients with HIV

81
Q

Who gets Cyclosporiasis?

A

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
Q

What are the clinical manifestations of Cyclosporiasis?

A

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
Q

How is Cyclosporiasis treated?

A

Trimethoprim-Sulfamethoxazole (Bactrim); Ciprofloxacin alternative

84
Q

What is the life cycle of American Trypanasomiasis?

A
  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
Q

Where is American Trypanasomiasis found?

A

New World Disease

86
Q

How is Chagas transmitted?

A

Bite of kissing bug, blood transfusion, vertically, breast milk, organ transplant, oral (accidentally pulverize and eat the bug)

87
Q

How does Chagas invade?

A

Trypomastigotes invade Cardiac Muscle (CM), vascular

smooth muscle, interstitial areas of smooth muscle/vascular and myocardium; CM’s are invaded & destroyed

88
Q

What are signs of Chagas?

A

Romana’s sign (Nonpainful unilateral edema of the upper and lower eyelids that lasts for several weeks), Chagoma

89
Q

What is the acute stage of Chagas?

A

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
Q

How is American Trypanasomiasis treated?

A

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
Q

How does Chagas progress?

A

Acute, then chronic phase, then indeterminate form (no signs or symptoms) but can reactivate

92
Q

What are the complications of reactivated Chagas?

A

cardiomyopathy, GI - can cause dilation and thickening of gut wall

93
Q

When should American Trypanasomiasis be treated?

A

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
Q

What happens if immunocompromised patient gets Chagas?

A

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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