Chapter 54 Chemotherapy of Protozoal Infections Flashcards

1
Q

Best agents for treating sleeping sickness and chronic Chagas disease

A

None existent

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2
Q

Problems with antiprotozoal drugs

A

most are toxic at therapeutic doses and increasing drug resistance of parasites

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3
Q

Prevalence of Amoebiasis

A

10% or Worlds population about 50 million people and mortality rate of 100,000 annually

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4
Q

Amoebiasis is commonly seen in:

A

individuals living in poverty, crowded conditions and in areas with poor sanitation

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5
Q

what are the three morphologically identical Entamoebas?

A

E. histolytica, E. dispar and E. moshkovskii

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6
Q

the recently discovered Entamoeba that may be pathologic

A

E. bangladeshi

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7
Q

Entamoeba that requires treatment

A

E. histolytica

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8
Q

The third leading cause Of mortality by parasitic infection

A

E. histolytica

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9
Q

Route of transmission of Entamoebas?

A

fecal-oral, ingestion of cysts (infective stage)

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10
Q

Outcome of E. histolytica infection

A

Most are asymptomatic, but when trophozoites invade the colonic mucosa, it may cause colitis and bloody (amebic) diarrhea; trophozoites may also travel to the liver causing amebic liver abscess (ALA)

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11
Q

the cornerstone of therapy for amebiasis is

A

metronidazole or its analogue tinidazole

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12
Q

T/F: Metronidazole is effective against entamoeba cysts?

A

False. Thats why you should add luminal agents (paromomycin or iodoquinol) together with metronidazole to eradicate the entamoeba especially in individuals with amebic colitis or amebic liver abscess

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13
Q

A drug that is used primarily for treatment of kf cryptosporidiosis and giardiasis that showed effectivity against E. histolytica

A

nitazoxanide

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14
Q

Is the most common reported intestinal protozoan infection in the US

A

Giardiasis

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15
Q

Giardiasis is caused by

A

flagellated protozoan G. intestinalis

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16
Q

giardiasis infection is via

A

ingestion of cyst form of the parasite found in fecally contaminated water or food, or through anal sex (male homosexuals)

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17
Q

Hosts of entamoeba parasites?

A

Only humans

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18
Q

Giardiasis infection may result to?

A

asymptomatic carrier state, acute self-limited diarrhea, and chronic diarrhea with signs of malabsorption (steatorrhea) and weight loss

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19
Q

Treatment for giardiasis?

A

metronidazole, 5-7 days may be repeated or prolonged or

tinidazole, single dose (may be superior to metronidazole) or

nitazoxanide for adults and immune-competent children <12 Y.O

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20
Q

treatment of giardiasis in pregnant women?

A

paromomycin to avoid mutagenic effects of other drugs

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21
Q

this organism inhabits the genitourinary tract where it causes vaginitis in women and urethritis in men

A

T. vaginalis

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22
Q

The most common nonviral sexually transmitted disease

A

trichomoniasis

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23
Q

what form of the parasite is seen in infected secretion in trichomoniasis?

A

Trophozoite forms

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24
Q

DOC for trichomoniasis?

A

Metronidazole, but Tinidazole is better tolerated and can be used to treat metronidazole-resistant T. vaginalis

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25
Q

is a zoonotic infection caused by an obligate intracellular protozoam T. gondii

A

toxoplasmosis

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26
Q

the natural host of T. gondii

A

Cats and other feline species (showing tissue cyst/bradyzoites which are also seen in other mammals)

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27
Q

routes of infection of toxoplasmosis in humans:

A

ingestion of undercooked meat with tissue cysts,
ingestion of contaminated vegetable matter containing infective oocytsts,
Direct contact with the faces of cat shedding oocysts,
Transplacental fetal infection with tachyzoites from acutely infected mothers

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28
Q

Tissue cyst of T. gondii

A

bradyzoites

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29
Q

form of T. gondii that causes transplacental fetal infection

A

tachyzoites

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30
Q

T/F acute illness of toxoplasmosis requires immediate treat & intervention?

A

False, the disease is usually self-limiting and doesn’t require treatment

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31
Q

most common finding of congenital toxoplasmosis

A

chorioretinitis

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32
Q

primary treatment for toxoplasmic encephalitis

A
  1. antifolates (pyrimethamine) + sulfadiazine + folinic acid (leucovorin)
    but is toxic due to the SULFA compound
  2. pyrimethamine+clindamycin is comparable but with substantial toxicity
  3. alternative regimens combi drug (azithromycin + clarithromycin+ atovaquone or dapsone) is less toxic but less effective
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33
Q

drug for preventing toxoplasma transmission to the fetus, used in early pregnancy

A

spiramycin

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34
Q

treatment for fetal toxoplasmosis infection?

A

antifolates (pyrimethamine) + sulfadiazine + folinic acid (leucovorin) to the mother (after 12-14 weeks of gestation) and postnatally given to the newborn for 1 year

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35
Q

caused by coccidian protozoan parasite that causes diarrhea

A

cryptosporidiosis

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36
Q

cryptosporidia species accountable to almost all infections in humans

A

C. parvum and C. hominis (newly named)

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37
Q

Mode of infection of cryptosporidiosis?

A

ingestion of infectious oocyst in feces spread by human to human contact or by contaminated water

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38
Q

form of cryptosporidia parasite that invade host epithelial cells?

A

sporozoites

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39
Q

cryptosporidiosis is usually ________ in immunocompetent individuals

A

self-limiting

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40
Q

treatment of cryptosporidiosis and immunocompetent children and adults

A

Nitazoxamide

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41
Q

treatment of cryptosporidiosis and immunocompromised patients

A

restoration of immune function

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42
Q

causes african sleeping sickness or trypanosomiasis

A

T. brucei,
west african type: gambiense causing later CNS involvement and long-term course
east african type: rhodesiense causing progressive and rapidly fatal CNS involvement with terminal cardiac failure

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43
Q

vector for T. brucei

A

Tsetse flies of genus Glossina

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44
Q

trypanosomiasis is restricted to

A

sub-Saharan africa, causing serious infection and may also cause protein malnutrition by threatening the livestock (nagana)

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45
Q

Stage 1 of trypanosomiasis

A

earliest stage, replicating parasites is seen in the bloodstream or lymph without CNS involvement

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46
Q

Stage 2 of trypanosomiasis

A

characterized by CNS involvement with symptoms including febrile illness, lymphadenopathy, splenomegaly and occasional myocardiris

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47
Q

treatment for early stage of trypanosomiasis west african type?

A

pentamidine, parenteral for long periods but ineffective against late-stage disease

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48
Q

treatment for early stage of trypanosomiasis east african type?

A

suramin, parenteral for long periods but ineffective against late-stage disease

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49
Q

traditional treatment of trypanosomiasis with CNS involvement

A

melarsoprol, but causes fatal reactive encephalitis

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50
Q

only agent for late stage of trypanosomiasis

A

eflornithine (inhibitor or ornithine decarboxylase, a key enzyme for polyamine metabolism) but is only effective against T. brucei gambiense early and late stages of the disease with less side effects than melarsoprol
but INEFFECTIVE monotherapy against T. brucei rhodisiense

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51
Q

treatment of choice for late-stage T. brucei gambiense

A

NECT (Nifurtimox+Eflornithine)Combination Therapy with good efficacy and less side effects than melarsoprol

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52
Q

also known as American trypanosomiasis

A

Chagas Disease

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53
Q

a zoonotic infection caused by T. cruzi

A

Chagas disease

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54
Q

Chagas’ disease is primarily confined to

A

Latin America

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55
Q

common vector to chagas disease

A

bloodsucking triatomid bugs

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56
Q

other route of transmission of Chagas disease?

A

blood transfusion and organ transplantation

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57
Q

chronic form of Chagas disease causes

A

cardiomyopathy,
megaesophagus,
megacolon,
death

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58
Q

Chagas heart disease follows what guidelines?

A

ACC and AHA for treatment of heart failure (using ACE inhibitors and beta adrenergic blockers, with downward adjustment-but still debated)

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59
Q

treatment for Chagas disease

A

Either of the two nitroheterocyclic drugs- nifurtimox ans benznidazole.
Both can suppress parasitemia and cure acute phase Chagas disease, and also deemed beneficial to intermediate and late stages of Chagas disease.
Both are TOXIC and must be taken for long periods

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60
Q

a complex vector-borne zoonotic disease caused by 20-species of intramacrophage protozoa of genus Leishmania

A

Leishmaniasis

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61
Q

reservoir of leishmania

A

small mammals and canines

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62
Q

vector of leishmania

A

female phloebotomine sandflies

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63
Q

transformation cycle of leishmania

A

flagellated free PROMASTIGOTES from infected feeding sandflies is regurgitated and enter the human host where they are engulfed by macrophage and then becomes AMASTIGOTES then multiply within the phagolysosomes until the macrophages burst and the amastigotes invades more macrophages and taken up by feeding sandflies where they transform back to promastigotes

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64
Q

Classification of Leishmaniasis in increasing order of systemic involvement and severity

A
  1. Cutaneous - (self-limiting, cured after 3-18 months but can leave dysfuguring scars)
  2. Mucocutaneous
  3. Diffuse Cutaneous
  4. Visceral (Kala Azar) - (fatal unless treated)

2-4 don’t resolve without therapy

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65
Q

the leishmaniasis disease syndrome manifested depends on?

A
  1. species or subspecies of infecting parasite
  2. distribution of infected macrophages
  3. host immune response
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66
Q

Classic therapy for all species of Leishmania is

A

Pentavalent antimony compounds (sodium stibogluconate or sodium antimony gluconate),

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67
Q

FDA-approved first orally active agent for treatment for cutaneous, mucocutaneous, and visceral leishmaniasis

A

miltefosine but TERATOGENIC, also should promising results as treatment for animal reservoirs like dogs

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68
Q

alternative drug for miltefosine in treating visceral leishmaniasis

A

liposomal amphotericin B, highly effective agent

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69
Q

used with some success as a parenteral agent for visceral leishmaniasis

A

Paromomycin

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70
Q

drug with topical formulations used in cutaneous leishmaniasis

A

paromomycin

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71
Q

babesiosis, a tick-borne zoonotic disease, is caused by

A

B. microti or B. divergens

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72
Q

babesiosis resembles what parasite

A

malaria, invading the RBCs

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73
Q

babesiosis presents with

A

febrile illness, hemolyis and hemoglobinuria, is usually mild and self-limiting but may be severe or fatal un ASPLENIC and severely immunocompromised

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74
Q

therapy for severe babesiosis

A

Combi of Clindamycin + Quinine

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75
Q

therapy for mild to moderate babesiosis

A

combi of Azithromycin + Atovaquone

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76
Q

Balantidiasis is an infection of LARGE INTESTINE is caused by what parasite

A

B. coli, ciliated protozoan

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77
Q

Theraphy for balantidiasis

A

Tetracycline

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78
Q

a coccidia that causes self-limited diarrhea in normal hosts or
prolonged diarrhea in immunocompromised patients

A

Cyclospora cayetanensis

79
Q

a coccidia that causes diarrhea in patients with AIDS

A

Cycloisospora belli, formerly known as Isospora belli

80
Q

treatment for Cyclospora and Cycloisospora infections?

A

trimethoprim-sulfamethoxazole

81
Q

a spore-forming, unicellular, eukaryotic organisms that were once considered to be parasites

A

Microsporidia

82
Q

A drug that is highly effective against visceral leishmaniasis (90% cure rate) and used for antimonial-resistant cases, can be also be used for cutaneous and mucosal leishmaniasis,
effective for immunocompromised patients

A

Amphotericin B, lipid preparations have reduced toxicity but costly and difficult to administer

83
Q

Leishmania has similar _______ composition to fungi

A

sterol

84
Q

MOA of Amphotericin B

A

forms complexes with ergosterol precursors forming pores in the cell membrane allowing ions to enter

85
Q

typical regimen for visceral leishmaniasis using Amphotericin B

A

10-20 mg/kg total dose over 10-20 days by IV infusion (95% cure rate)

86
Q

FDA recommendation regimen for VISCERAL leishmaniasis using Amphotericin B

A

21 mg/kg total dose

given in 3 mg/kg IV on first 1-5 days, day 14 and day 21

87
Q

FDA recommendation regimen for CUTANEOUS leishmaniasis using Amphotericin B

A

at least 21 mg/kg total dose

given in 3 mg/kg/d IV for 7-10 days

88
Q

these are molecules that are required for cell division that is inhibited by eflornithine

A

polyamines (putrescein, spermidine, and spermine)

89
Q

irreversible catalytic (suicide) inhibitor of ornithine decarboxylase

A

eflornithine (DFMO)

90
Q

the enzymes that catalyzes the first and the rate-limiting step in polyamine biosynthesis

A

ornithine decarboxylase

91
Q

a polyamine that is required in the synthesis of trypanothione

A

spermidine

92
Q

trypanothione is a conjugate of

A

spermidine and glutathione that replaces that function of glutathione in trypanosomes

93
Q

eflornithine is transported into the cell via

A

amino acid transporter (Tb AAT6)

94
Q

NECT (Nifurtimox+ Eflornithine Combi Therapy) is the DOC for

A

late-stage West African (Gambian) Trypanosomiasis

95
Q

is a cytostatic agent that depletes polyamine

A

eflornithine, given IV

96
Q

T/F: both human and parasite enzymes are susceptible to eflornithine?

A

True, but mammalian enzymes are turned over rapidly while parasite enzymes is stable-SELECTIVE TOXICITY

97
Q

minimum eflornithine CSF concentration for parasite clearance

A

50 μM

98
Q

T/F: eflornithine binds well with plasma proteins and doesn’t penetrates the CSF

A

False, eflornithine does not bind to plasma proteins and well-distributed and penetrates into the CSF

99
Q

half-life of eflornithine and renal clearance

A

3-4 hours, renal clearance 2 ml/min/kg ( >80% of unchanged drug)

100
Q

NECT vs Eflornithine alone

A

higher cure rate, easier to administer

101
Q

NECT dosing for late-stage West African Trypanosomiasis

A

Nifurtimox (oral)
15 mg/kg/d
divided doses every 8 hours for 10 days
+
Eflornithine (IV infusion)
200 mg/kg IV every 12 hours by 2-hour infusion for 7 days
with coadministration of substantial volumes of IV fluid leads to limitation of use posed by fluid overload

102
Q

Eflornithine adverse reactions are generally reversible on drug withdrawal including

A

abdominal pain and headache - chief complaints
local reactions at injection site
fever peaks , seizures and diarrhea - most severe reactions
hearing loss (reversible) after prolonged therapy

103
Q

luminal agents for E. histolytica in amebic colitis and amebic liver abscess

A
  1. halogenated 8-hydroxyquinolines:
    iodoquinol (diiodohydroxyquin) SAFER than clioquinol and
    clioquinol (iodochlorhydroxyquin)
  2. paromomycin - preferred since less adverse-effects
104
Q

most important toxic reaction to clioquinol

A

subacute myelo-optic neuropathy

105
Q

Administration of iodoquinol in children with chronic diarrhea may cause

A

optic neuropathy and permanently vision loss

106
Q

less severe manifestation of neurotoxicity of hydroxyquinolines

A

Peripheral neuropathy

107
Q

dosing of iodoquinol in adults

A

650 mg/day oral, 3 times daily for 20 days

108
Q

dosing of iodoquinol in children

A

30-40 mg/kg/d (not exceeding 1.95 g/d)

divided three times daily for 20 days

109
Q

drug that is supplied as a 3.6% solution in PEG for slow IV administration (since drug is intensely irritating)

A

melarsoprol

110
Q

only drug effective against late-stage (CNS) East African Trypanosomiasis,
also effective against late-stage (CNS) West African Trypanosomiasis

A

melarsoprol

111
Q

the active drug of melarsoprol

A

melarsen oxide,

melarsoprol is rapidly metabolized (<30 minutes) to melarsen oxide

112
Q

melarsen oxide binds with

A

trypanothione resulting in adduct formation and inhibition of tryoanothione reductase

113
Q

resistance to melarsoprol is due to

A

defects linked to aquaglyceporin pore-forming protein

114
Q

terminal half-life of melarsen oxide

A

43 hours

115
Q

fatality rate for untreated East African (Rhodesian) Trypanosomiasis

A

~100% fatality rate

116
Q

T/F: for T. brucei rhodesiense relapse, you can still use melarsoprol as second course

A

True

117
Q

T/F: for T. brucei rhodesiense uncured with melarsoprol, you can still use melarsoprol as second course

A

False, use eflornithine instead

118
Q

Melarsoprol dosing

A

2.2 mg/kg/d IV for 10 days

119
Q

what is employed/added throughout the treatment course to reduce the prevalence of encephalopathy caused by melarsoprol?

A

prednisolone

120
Q

most often adverse reaction to melarsoprol?

A

febrile reaction after drug administration, especially if parasitemia is high

121
Q

most serious complication of melarsoprol, occuring in 5-10% of patients after 9-11 days of treatment

A

reactive neuropathy

122
Q

adverse effects of melarsoprol such us vomiting and abdominal colic is reduced by?

A

slow IV injection, with patient supine and fasting

123
Q

melarsoprol administration in leprous patient may cause?

A

the precipitation of erythema nodosum

124
Q

contraindications in melarsoprol use

A

influenza epidemics and G6PD deficiency (causing hemolytic anemia)

125
Q

T/F: melarsoprol can be given to pregnant patients?

A

True

126
Q

Metronidazole had especially high activity in vivo or in vitro against anaerobic protozoans

A

T. vaginalis and E. histolytica

127
Q

Oral doses of metronidazole imparted____ activity to semen and urine with high cure rate of the disease ____.

A

trichomonacidal activity, trichomoniasis

128
Q

1-( beta-hydroxyethy)-2-methyl-5-nitroimidazole

A

metronidazole

129
Q

True or False
Metronidazole had extremely useful clinical activity against a variety of anaerobic pathogens both gram (-) and gram (+) bacteria including the protozoan _____

A

True

G. lamblia

130
Q

Other clinically effective 5-nitroimidazoles closely related in structure and activity to metronidazole

A

tinidazole

ornidazole

131
Q

Metronidazole has potent amebicidal activity against

A

E. histolytica

132
Q

phase of life cycle in G. lamblia that is affected by metronizadole at ____ concentrations

A

Trophozoites

1-50microgram/mL (in vitro)

133
Q

studies in drug-sensitive and drug-resistant protozoan parasites indicates that the nitro group on __of metronidazole is essential for activity and substitution at the ___ enhance the resonance conjugation of the chemical structure increases protozoal activity

A

C5

2 position

134
Q

What will happen if 2 position is substituted by an acyl group of metronidazole?

A

it ablates the conjugation thus reduces antiprotozoal activity

135
Q

True or false

Metronidazole manifests antibacterial activity against all anaerobic cocci and both anaerobic gram- and gram+ bacilli, including Bacteroides speciesand, anaerobic spore-forming gram+ bacilli and nonsporulating gram+ bacilli

A

False

Nonsporulating gram+ bacilli are often resistant, as are aerobic and facultatively anaerobic bacteria

136
Q

Metronidazole is clinically effective in infections such as

A

trichomoniasis, amebiasis, giardiasis and variety of infections caused by obligate anaerobic bacteria including Bacteroides, Clostridium, Fusobacterium, Peptococcus, Peptostreptococcus, Eubacterium, and Helicobacter

137
Q

Metronidazole is clinically effective in microaerophilic bacteria such as

A

Helicobacter and Campylobacter species

138
Q

Metronidazole may facilitate extraction of this parasite in but has no direct effect on the parasite

A

adult guinea worms in dracunculiasis

139
Q

The selective toxicity of metronidazole toward anaerobic and microaerophilic pathogens derives from their____, this considers metronidazole as ____

A

metabolism

prodrug

140
Q

anaerobic and microaerophilic pathogens reactive to metronidazole contains electric transport component that have a sufficiently negative redox potential to donate electrons to the drug

A

ferredoxins (small Fe-S proteins)

141
Q

What will happen to the action of metronidazole if there’s an increasing levels of O2

A

high levels of O2 can both inhibit the action of metronidazole-induced toxicity (decreases the reductive activation) and increases recycling of the activated drug

O2 competes with metronidazole for electrons generated by energy metabolism

142
Q

Anaerobic and microaerophilic organisms that are susceptible to metronidazole derive energy from

A

oxidative fermentation of ketoacids such as pyruvate

143
Q

produces electrons that reduce ferredoxin and catalytically donates electrons to metronidazole or to biological electron acceptors

A

Pyruvate decarboxylation

144
Q

Catalyst of Pyruvate decarboxylate

A

pyruvate:ferredoxin oxidoreductase

145
Q

PFOR

mechanism in metronidazole metabolism

A

pyruvate:ferredoxin oxidoreductase

catalyzes pyruvate decarboxylate

pyruvate decarboxylate produces electrons that reduce ferredoxin and catalytically donates electrons to metronidazole or to biological electron acceptorsthat

146
Q

Shows resistance to metronidazole

A

T. vaginalis
G. lamblia
E. histolytica

147
Q

Two major types of abnormalities that lead to resistant strains of T. vaginalis to metronidazole

A

impaired oxygen-scavenging capabilities

lowered levels of PFOR

148
Q

Why infections with resistant strains to metronidazole responds to higher doses or prolonged therapy of the said drug?

A

PFOR and ferredoxin are not completely absent although lowered

149
Q

in amebic trophozoites, metronidazole resistance is mediated primarily by increase expression of what enzymes

A

superoxide dismutase and peroxiredoxin

150
Q

Bacteroides spp resistance in metronidazole is linked to what family of genes?

A

nitroimidazole(nim) resistance gene

nimA, -B, -C, -D, -E, -F

151
Q

The mean effective concentrations of metronidazole for most susceptible protozoa and bacteria

A

≤ 8microgram/mL

152
Q

plasma concentration of a single 500mg dose of metronidazole after 0.25-4hrs

A

8-13microgram/mL

153
Q

half-life of metronidazole in plasma

A

~8hrs

154
Q

Less than 20% of metronidazole is bound to plasma proteins with the exception of the

A

placenta

155
Q

metronidazole penetrates well into body tissues and fluids including

A
vaginal secretions
seminal fluids
saliva
breast milk
csf
156
Q

Major oxidative metabolites of metronidazole

A

hydroxy and acetic acid

157
Q

Preparations of metronidazole for administration

A

oral
iv
intravaginal
topical

158
Q

The main site of metabolism of metronidazole and accounts for ___ of the systemic clearance

A

Liver

50%

159
Q

___ of labeled metronidazole is pass in the urine after an oral dose and ___ is recovered as unchanged drug

A

75%

10%

160
Q

metabolite of metronidazole that has a longer half-life of ___ and has ___ of antitrichomonal activity

A

hyroxy
~12hrs
~50%

161
Q

Urine color of patients taking metronidazole

A

reddish brown

162
Q

Oxidative metabolism of metronidazole is induced by drugs and compound such as (4)

A

phenobarbital
prednisone
rifampim
ethanol

163
Q

this drug appears to inhibit hepatic metabolism of metronidazole

A

cimetidine

164
Q

metronidazole preferred treatment regimen to genital infections with T. vaginalis in both m and fm

A

2-g single oral dose

165
Q

this drug alternative has longer half-life than metronidazole and appears to have better response in curing genital infections

what is the dosing

A

tinidazole

2-g single dose

166
Q

treatment regimen for patients who cannot tolerate a single 2-g dose or 1-g BID of metronidazole

A

250-mg TID or 375-mg BID for 7 days

167
Q

treatment regimen for repeated courses or higher doses of metronidazole for uncured or recurrent infections

A

250-mg TID or 375-mg BID for 7 days with intervals of 4-6 weeks elapse between courses

168
Q

should be considered prior to treating recurrent or uncured genital infections caused by T. vaginalis with metronidazole

A

leukocyte count

169
Q

a measure used to successfully treat resistant strains of T. vaginalis

A

2-g dose to both patient and sexual partner

170
Q

dose of topical gel and vaginal suppository given in addition to oral therapy of metronidazole that will increase the chance of drug concentration and beneficial in refractory cases.

A

0.75% and 500-1000-mg

171
Q

dose of oral preparation of metronidazole to adult and children infected with amebic colitis and amebic liver abscess

A

500-750-mg TID for 7 to 10 days for adults

35-50mg/kg/day given in 3 divided doses for 7 to 10 days for children

172
Q

How many days is the standard recommendation for the duration of metronidazole therapy?

A

7-10 days

173
Q

Period and duration of treatment for amebic liver using metronidazole or tinidazole?

A

short course, -2.4-g OD as single oral dose for 2 days

174
Q

in patients with E. histolytica who recovered from acute amebiasis after metronidazole treatment, it is highly recommended that they should also be treated with what? give examples of such drugs.

A

luminal amebicide

diloxanide furoate

metronidazole is less effective in treating organisms that thrives in bowel lumen such as luminal amebiasis

175
Q

First-line therapy against giardiasis aside from metronidazole that is yet to be approved in U.S for this infection, give the dosing

A

tinidazole single 2-g dose

176
Q

Metronidazole also achieves clinically effective levels to this parts of the body

A

bones
joints
cns

177
Q

appropriate IV dosing for metronidazole when oral administration is not possible

A

15mg/kg is followed by 6hrs later by a maintenance dose of 7.5/kg every 6hrs, usually for 7-10days

178
Q

Metronidazole is used as a component of prophylaxis for ____ and is employed as a single agent to treat ____

A

colorectal surgery

bacterial vaginosis

179
Q

Metronidazole is also used in combination with other antibiotics and a proton pump inhibitor in regiments to treat this infection

A

H. pylori

180
Q

Metronidazole is used as a primary therapy for infection to this spore-forming gram+ pathogen which is also the major cause of pseudomembranous colitis. Give the appropriate dosing

A

C. difficile

250-500 mg orally TID for 7-14days (or even longer)

181
Q

This drug is an alternative treatment to C. diff. infection than oral vancomycin therapy because its efficacy and cost-saving. Give its downside effects comparted to oral vancomycin.

A

Metronidazole

reported cases on increase treatment failures and higher rates of disease recurrence

182
Q

This antiprotozoal drug is also used in treatment for patients with Crohn’s disease who have perianal fistulas, it can also help control colonic (but not small bowel) Crohn’s disease. Give the drug and its dosing

A

metronidazole

(high doses) 750mg TID for prolonged periods may be necessary and neurotoxicity may be limiting

183
Q

This antiprotozoal drugs can sentisize hypoxic tumor cells to the effects of ionizing radiation but are not used clinically for this purpose.

A

metronidazole and other nitroimidazoles

184
Q

Most common side-effects of metronidazole

A

headache
nausea
dry mouth
metallic taste

185
Q

Occasional side-effects of metronidazole

A

vomiting
diarrhea
abdominal distress

186
Q

This side-effects to metronidazole may be associated with an exacerbation of candidiasis

A

furry tongue
glossitis
stomatitis

187
Q

common and very rare neurotoxic effects from metronidazole

A

Common:
dizziness
vertigo

very rare:
encephalopathy
convulsions
incoordination
ataxia
188
Q

cutaneous signs that are indicative of drug sensitivity to metronidazole that requires withdrawal of the treatment

A

urticaria
flushing
pruritus

189
Q

What will happen if patient taking metronidazole imbibes alcohol within 3 days of therapy?

A

this drug has disulfiram-like effect and some patients experience abdominal distress, vomiting, flushing and headache

190
Q

What will happen if metronidazole and any disulfiram-like or drugs are taken together? why.

A

confusional and psychotic states may occur

191
Q

Metronidazole, although seen not teratogenic to humans, it is not advised to take this drug in what stage of pregnancy?

A

1st trimester

192
Q

What will happen to patients taking metronidazole and coumadin at the same time?

A

prolonged PT

193
Q

This drug can elevate plasma levels of metronidazole. Why.

A

Cimetidine

it inhibits hepatic microsomal metabolism

194
Q

Does metronidazole linked to any forms of cancer to humans?

A

No current evidence but only carcinogenic in rodents (given high doses and prolonged periods)