Anti-Infective Agents Flashcards
(89 cards)
1
Q
Parasitic worm infections are also called what?
A
helminth infections
2
Q
Parasitic Infections include what specifically?
A
- roundworms (flukes)
- tapeworms
3
Q
Where are parasitic infections common?
A
- common in tropical, poor rural areas
4
Q
How are specific diagnostics performed for parasitic infections?
A
- often involve evaluating stool/feces for eggs
5
Q
How do antihelmintics act in the body?
A
- act locally within the gut or systemically for those that infect other locations
- they expel parasitic worms and other internal parasites from the body by either stunning or killing them and without causing significant damage to the host
6
Q
Antihelmintic Agents
A
- Albendazole
- Ivermectin
- Nitazoxanide
- Praziquantel
- Pyrantel
7
Q
Side effects of Pyrantel
A
- nausea
- vomiting
- diarrhea
- abdominal pain
- heachache
- rash
8
Q
Antibacterial Agents
A
- development of new agents to keep up with patterns of resistance
- resistance develops as a “survival” mechanism for bacteria, disabling the antibiotic
- therapeutic drug monitoring can prevent toxicity and can ensure appropriate drug dose
- watch for avoidable food and drug interactions that may contribute to suboptimal therapy
9
Q
How do penicillins act in the body?
A
- can easily enter bacterial cell in case of gram-positive species
- gram-positive bacteria do not have an outer cell membrane and are simply enclosed in a thick cell wall
- PCN molecules are small enough to pass through the spaces of glycoproteins in the cell wall
- gram-positive bacteria are very susceptible to PCN
10
Q
Gram-positive bacterias
A
- Staphylococcus
- Streptococcus
- Enterococcus
11
Q
Characteristics of PCN
A
- 10% cross-sensitivity with cephalosporins
- low plasma protein binding capacity
- short half-life (requires multiple x/day dosing)
- excreted by the kidneys
12
Q
Side Effects of PCN
A
- diarrhea
- nausea
- rash
- superinfection (candidiasis)
13
Q
PCN Resistance
A
- E. coli produced specific enzymes that can break down pcn molecule “Penicillinase” aka B-lactamase
- B-lactamases is the most important mechanism of pcn resistance
- B-lactamase inhibitors prevent the bacterial degradation of beta lactam antibiotics and extend the rage of bacteria drugs are effective against
- B-lactamase inhibitors have little antibiotic activity on their own
14
Q
Characteristics of Cephalosporins
A
- beta-lactam antibiotic
- most commonly prescribed drugs
- broad-spectrum antibiotic coverage
- less susceptible to beta-lactamase
- disrupt the synthesis of the peptidoglycan layer forming the bacterial cell wall
15
Q
Side Effects of Cephalosporins
A
- N/V/D
- rash
- pain at the injection site
- superinfection (10% cross-sensitivity)
16
Q
1st Generation Cephalosporins
A
- oldest cephalosporins
- active against gram-positive cocci
17
Q
1st generation cephalosporins are not useful against what?
A
- enterococci
- listeria
- MRSA
- gram-negative cocci (gonococcus, meningococcus)
- H. influenza
18
Q
1st generation cephalosporins are effective against what?
A
- E. coli
- Proteus mirabilis
- Klebsiella pneumonia
19
Q
Examples of 1st generation cephalosporins
A
- Cefadroxil
- Cefazolin
- Cephelaxin
20
Q
2nd Generation Cephalosporins are less active against what?
A
- less active against staphylococci and enhanced activity against H-influenza
- weak gram-positive coverage
- strong gram-negative coverage
21
Q
2nd Generation Cephalosporins are active against what?
A
- cephamycins (subgroup) are active against Bacteroides
22
Q
Examples of 2nd generation cephalosporins
A
- Cefaclor
- Cefprozil
- Cefuroxime
- Cefotetan
- Cefoxtin
23
Q
3rd Generation Cephalosporins
A
- marked by stability to the common B-lactamases of gram-negative bacilli, and these compounds are highly active against Enterobacteriaceae, Neisseria, and H. influenza
24
Q
Examples of Enterobacteriaceae that 3rd generation cephalosporins are active against
A
- E. coli
- Proteus mirabilis
- indole-positive Proteus
- Klebsiella
- Enterobacter
- Serratia
- Citrobacter
25
4th Generation Cephalosporins
- has good penetration through outer membrane of gram-negative bacteria
- similar activity to cefotaxime and ceftriaxone
26
Example of 4th generation cephalosporins
- Cefepime
27
4th generation cephalosporins are active against what?
Pseudomonas aeruginosa
28
Side effects of 4th generation cephalosporins
Superinfection
- enterocci
- candida
29
Cholramphenicol
- useful against typhoid and conjunctivitis
- no longer recommended by WHO as first-line to treat meningitis
30
Side effects of cholramphenicol
- bone marrow suppression
- aplastic anemia
- leukemia
- N/V
31
Characteristics of Macrolides
- natural product consisting of a large macrocyclic ring
- are bacteriostatic in that they suppress or inhibit bacterial growth rather than killing bacteria completely
- are protein synthesis inhibitors
- wider antibiotic spectrum than penicillins
32
Macrolides are useful treating what?
- used to treat infections by gram-positive bacteria (PCN allergic patients), community acquired respiratory tract infections, and mycobacterial infections
33
Examples of Macrolides
1. Azithromycin
2. Clarithromycin
3. Erythromycin
4. Fidaxomicin
34
Side Effects of Macrolides
- clarithromycin and erythromycin are potent inhibitors of CYP3A4 and cause QT prolongation which can lead to Torsades de Pointes
- exhibit enterohepatic recycling
- can also cause cholestasis and Infantile pyloric stenosis
- given with colchicine may lead to colchicine toxicity
35
What is enterohepatic recycling?
- drugs absorbed by the gut sent to the liver, excreted into the duodenum in bile from the liver, leading to build up
36
Characteristics of Aminoglycosides
- display concentration-dependent bactericidal activity against "most gram-negative aerobic and facultative anaerobic bacilli"
- act by binding to aminoacyl site of ribosomal RNA
- require only short contact time, and are most effective against susceptible bacterial populations that are rapidly multiplying
- less toxic and do not require serum drug concentration monitoring
- 99% of the administered dose eliminated unchanged in the urine
37
When to prescribe aminoglycosides as monotherapy
- important as a second agent in treating serious infections
- sepsis
- osteomyelitis
- severe complicated UTI
- nosocomial respiratory infections
- abdominal infections
38
Peak serum concentration of aminoglycosides
30-90 minutes after IV/IM administration
39
Side Effects of Aminoglycosides
- nephrotoxicity varies widely but can be 10-20% and reversible in most cases
- ototoxicity may result in either vestibular or cochlear damage
- avoid in myasthenia gravis due to rare but serious neuromuscular blockade
40
Examples of Aminoglycosides
1. Amikacin
2. Gentamicin
3. Neomycin
4. Streptomycin
5. Tobramycin
6. Paromomycin
41
Characteristics of Fluoroquinolones
- are highly effective antibiotics with many advantageous pharmacokinetic properties including high oral bioavailability, large volume of distribution, and broad-spectrum antimicrobial activity
- are bactericidal that directly inhibit bacterial DNA synthesis
- food does not substantially reduce absorption
- renally eliminated
42
What are Fluoroquinolones useful against?
- gram positive
- gram negative
- anaerobes
- atypicals
- mycobacteria
- GU infections
- hospital-acquired CAUTI
- pneumonia
- pyelonephritis
- prostatitis
43
Adverse Effects of Fluoroquinolones
- C. difficile
- tendinopathy
- neuropathy
44
Black Box Warning for Fluoroquinolones
- tendon rupture (higher among people > 60 years old)
- aortic dissection
- C. dificille colitis
- worsening of myasthenia gravis symptoms
45
Fluoroquinolone Toxicity
- blockade of GABa receptor complex in the CNS
46
Examples of Fluoroquinolones
1. Ciprofloxacin
2. Finafloxacin
3. Gemifloxacin
4. Levofloxacin
5. Maxifloxacin
6. Ofloxacin
47
Fluoroquinolones Contraindications
- epilepsy
- Marfan's syndrome
- Ehlers-Danlos Syndrome
- QT prolongation
- pre-existing CNS lesions or inflammation
- prior CVA
- avoid in pregnancy
48
Characteristics of Sulfonamides
- act as competitive inhibitors dihydropteroate synthase (DHPS) involved in folate synthesis
- are bacteriostatic inhibiting growth and multiplication of bacteria but not killing them
- allergies to sulfonamides are common (3%)
49
Sulfonamides that are devoid of antibacterial activity
- the anticonvulsant sultiame
- sulfonylureas
- thiazide diuretics
50
Examples of Sulfonamides
1. Sulfadiazine
2. Sulfamethoxazole/trimethoprim
3. Sulfasalazine
51
Sulfonamides are effective against what kind of microorganisms?
- gram-positive bacteria
- gram-negative bacteria
- some protozoa
- toxoplasma species
- chlamydia
- nocardia
52
Sulfonamides are effective against what diseases?
- staph aureus
- strep pneumonia
- strep pyogenes
- proteus mirabilis
- E. coli
- Salmonella
- klebsiella
- pseudomonas
- N. gonorrheae
- listeria
53
Side Effects of Sulfonamides
- Stevens-Johnsons syndrome
- toxic epidermal necrolysis
- the DRESS syndrome
54
Miscellaneous Urinary Anti-Infectives
1. Fosfomycin
2. Methenamine
3. Nitrofurantoin
4. Trimethoprim (but most often in conjunction with sulfamethoxazole and has a synergistic effect causing it to be bacteriocidal
55
Antifungal Agents
- fungal infections becoming more common with increasing states of immunosuppression (chemotherapy, HIV, etc.)
- opportunistic fungal infections have also demonstrated resistance and mutation
- multiple agents with different mechanisms of action are available for use
- many agent are susceptible to drug interactions involving liver metabolism and competition with other drugs using same "hepatic" pathway
56
Allylamines
- antifungal that are used to kill fungi to treat athlete's foot, jock itch, ringworm, and nail fungus (dermaphytes)
- topical activity working to inhibit fungal growth
57
Dermaphytes
- microsporum
- trichophyton
- molds (aspergillus)
58
Examples of Allylamines
1. Terbinafine
59
Side Effects of Allylamines
- rash
- diarrhea
- vomiting
- increased liver enzymes
- hepatic failure
- headache
- cough
- ototoxicity
60
Azoles
- antifungal
- blocks CYP450 dependent enzymes interrupting the cellular membrane of fungi
61
What do azoles treat?
- candidiasis
- aspergillosis
- cryptococcosis
- histoplasmosis
- blastomycosis
- coccidioidmycosis
62
Examples of Azoles
1. Fluconazole
2. Itraconazole
3. Voriconazole
4. Posaconazole
63
Side Effects of Azoles
- GI (N/V/D, abd pain)
- hepatotoxicity
64
Echinocandins
- antifungal
- inhibits enzyme activity in the fungal cell wall
- synergistic with amphotericin B and additive activity with fluconazole
65
What do Echinocandins treat?
- Most species of Candida but not cryptococcus, trichosporon, and rhodotorula
66
Examples of Echinocandins
1. Anidulafungin
2. Caspofungin
3. Micafungin
67
Side Effects of Echinocandins
- fever
- rash
- nausea
- phlebitis
- histamine-like reaction (flushing)
** Overall well-tolerated
68
Polyeyens
- antifungal
- antimicrobial polyene compounds target fungi
- obtained from streptomyces bacteria
- little is known about PK
- bind and extract ergosterol directly from the cellular membrane of fungi
- high protein binding (up to 95%)
- primary route of elimination is unknown
69
What do Polyeyens treat?
- treats most Candida species
70
Examples of Polyeyens
1. Amphotericin B
2. Nystatin
71
Side Effects of Polyeyens
- N/V
- chills
- rigors common
- nephrotoxicity
- electrolyte imbalances
72
Pyrimidines
- antifungal
- combination therapy with amphotericin B for severe cryptococcal pneumonia, meningoencephalitis, and select invasive candida infections
- interferes with DNA and protein synthesis
- serum monitoring and renal dosing are necessary
73
Examples of Pyrimidines
1. Flucytosine (5-FC)
74
Side Effects of Pyrimidines
- hematologic toxicity
- hepatic toxicity
- GI toxicity
- leukopenia
- thrombocytopenia
75
Misc. Antifungal Agents
- inhibits fungal cell mitosis
- deposited in karatin layer of skin, hair, nails
- useful for dermaphyte infections (tinea capitus, cruris, pedis, unguium)
76
Misc. Antifungal Agents Contraindications
- hepatic failure
- porphyria
- pregnancy
77
Examples of Misc. Antifungal Agents
1. Griseofulvin
2. Potassium iodide
78
Side Effects of Misc. Antifungal Agents
- hepatotoxicity
- nephrosis
- N/V/D
- rash
- photosensitivity
- (PCN allergy)
79
Mycobacterial Infections
1. TB
2. leprosy
3. nontuberculosis mycobacteria (NTM)
80
Antimycobacterial Agents
- generally include multiple drug regimens and prolonged courses due to slow growth organisms
- high rate of intrinsic resistance mutations and those that develop during treatment
- typically 3-6 months of treatment required for drug susceptible TB
- latent vs. active infection are treated differently
81
Examples of Antimycobacterial Agents
1. Antituberculosis agents
2. Antimycobacterials (misc.)
82
Antiviral Agents
- viruses replicate within cells and often use host cells, enzymes, and other macromolecules to make viral particles
- effective antivirals inhibit virus specific replication and/or inhibit virus directed protein synthesis
83
What are viruses?
- are microorganisms made up of single or double-stranded DNA or RNA in a protein coat (capsid)
84
Examples of Antiviral Agents
1. Adamantanes
2. Antiretrovirals
3. Interferons
4. Monoclonal antibodies
5. Neuroaminidase inhibitors
6. Nucleosides and nucleotides
7. HCV antivirals
8. Antivirals (misc.)
85
Examples of Protozoal Infections
- Giardiasis
- Trichomoniasis
- Malaria
86
Antiprotozoal Agents
- used to treat infections caused by protozoa (single cell organisms) that act as parasites
- protozoal infections often requires treatment using multiple drugs; vaccines are unavailable
- many agents have potentially severe toxicity
87
Examples of Antiprotozoal Agents
1. Atovaquone
2. Metronidazole
3. Nitazoxamide
4. Pentamidine
5. Tinidazole
6. Dapsone
7. Amebicides
8. Antimalarials
9. Antiprotozoals (misc.)
88
Side Effects of Antiprotozoal Agents
- nausea
- vomiting
- disulfiram-like reaction
- vaginitis
- peripheral neuropathy
- ataxia
- confusion
89
Clinical Pearls
1. Confirm presence of infection
2. Identify predisposing factors
3. Identify the pathogen
4. Collect infected material
5. Perform gram stain
6. Perform serologies
7. Perform C & S
8. Select empiric therapy considering every infected site
9. Monitor therapeutic response
10. Assess for therapeutic failure
11. Assess host/drug factors
