Module 7: Infectious Disease Medications

Tasks
Study tip: For each chapter, read "Special Concerns for Rehabilitation Patients" and "Case Study" prior to
chapter content. Answer the case study questions while you read the chapter, then compare your answers to
Appendix C.
Ch 33 (Treatment of Infections I: Antibacterial Drugs)
Ch 34 (Treatment of Infections II: Antiviral Drugs)

Medication Cabinet
Antibacterial drugs Antiviral drugs
amoxicillin (Amoxil) acyclovir (Zovirax)
cefazolin (Ancef) amantadine (Symmetrel)
vancomycin (Vancocin) famciclovir (Famvir)
piperacillin & tazobactam (Zosyn) indinavir (Crixivan)
gentamicin (Garamycin) zidovudine (Retrovir, AZT)
azithromycin (Zithromax) Alfa-2b (Intron A)
demeclocycline (Declomycin)
ciprofloxacin (Cipro)
levofloxacin (Levaquin)
silver sulfadiazine (Silvadene)
metronidazole (Flagyl)

Recall suffixes for infectious disease medications.

Suffix
1. Penicillin antibiotics -cillin
2. Tetracycline antibiotics -cycline
3. Various antibacterials -micin / -mycin
4. HIV protease inhibitors -avir
Assignment
Video case discussion applies to multiple modules and is due Nov. 20.
Assessment
Infectious Disease medications module is included in Examination 2 on Dec. 8. Practice questions are
available.

Learning Objectives
1. Differentiate clinical indications (medical diagnoses) for antibacterial vs. antiviral drugs.
a. Antibacterial drugs
i. Amoxicillin (Amoxil)
1. Otitis media, pneumonia, sinusitis, abscesses, bacteremia, meningitis, wound infections
(animal bites), Lyme disease, UTI; anthrax; blennorrhea; lymphogranuloma venereum;
nonspecific urethritis; trachoma
ii. Cefazolin (Ancef) (gram positive cocci and some gram negative cocci)
1. Generally, serves as an alternative agent to penicillins
2. Drug of choice in certain types of UTIs
3. Abscesses; bacteremia; cellulitis; endocarditis; osteomyelitis; pneumonia; arthritis, otitis,
sinusitis, others; gas gangrene
 iii. Vancomycin (gram positive bacilli and gram positive cocci)
1. Primarily serves as an alternative to the penicillins in treating a variety of infections,
including certain bacterial strains that are resistant to penicillin
2. Foodborne illnesses; antibiotic-associated colitis; Abscesses; bacteremia; cellulitis;
endocarditis; osteomyelitis; pneumonia; arthritis; otitis; sinusitis
iv. Piperacillin/tazobactam (Zosyn)
1. pneumonia, UTI; other systemic infections; various opportunistic & hospital-acquired
infections; abscesses, bacteremia, meningitis, wound infections (animal bites),
v. Gentamicin (Garamycin)
1. Variety of tissue and wound infections, bacteremia, pneumonia; UTI; endocarditis;
Listeriosis (meningitis, brain abscess, other CNS infections); hospital-acquired infection,
hospital-acquired infections;
vi. Azithromycin (Zithromax)
1. Legionnaires’ disease; “atypical” pneumonia, blennorrhea, lymphogranuloma venereum,
nonspecific urethritis, trachoma; otitis media; sinusitis; arthritis; otitis; Lyme disease
vii. Demeclocycline (Declomycin)
1. Anthrax, pneumonia, otitis media, sinusitis
viii. Ciprofloxacin (Cipro)
1. UTI (especially caused by E. coli, Klebsiella, Proteus, and Enterobacter aerogenes);
meningitis; GI infections, respiratory infections, osteomyelitis, and certain STD
(gonorrhea); Anthrax, “atypical” pneumonia, bacteremia, parathyroid fever, typhoid fever,
various opportunistic and hospital-acquired infections; otitis media; arthritis; sinusitis;
arthritis-dermatitis syndrome; genital infections; Legionnaires’ disease
ix. Levofloxacin (Levaquin)
1. bacteremia, parathyroid fever, typhoid fever, various opportunistic and hospital-acquired
infections; meningitis; UTI (especially caused by E. coli, Klebsiella, Proteus, and
Enterobacter aerogenes); arthritis-dermatitis syndrome; genital infections; GI infections,
respiratory infections, osteomyelitis, and certain STD (gonorrhea); anthrax; otitis media;
arthritis; sinusitis; Legionnaires’ disease; “atypical” pneumonia; blennorrhea;
lymphogranuloma venereum; nonspecific urethritis; trachoma
x. Silver sulfadiazine (Silvadene)
1. Applied topically to control bacterial infections in burns
xi. Metronidazole (Flagyl)-
1. used to treat serious infections caused by Bacteriodes and Fusobacterium
2. Antibiotic-associated colitis; gas gangrene;
3. Effective against certain protozoa
b. Antiviral drugs
i. Acyclovir (Zovirax)
1. Treatment of initial and recurrent herpesvirus infections (especially herpes simplex
related infections)
a. Genital and herpes simplex-related infections in other mucosal and cutaneous
areas (lips and face)
b. Varicella-zoster and related infections such as herpes zoster and chickenpox
c. Epstein Barr virus and related infections including infectious mononucleosis
ii. Amantadine (Symmetrel)
1. Prevention and treatment of influenza A infections (also used as an antiparkinsonism
drug)
iii. Famciclovir (Famvir)
1. Treatment and suppression of herpesvirus infections, including herpes simplex (genital
herpes) and herpes zoster (shingles)
iv. Indinavir (Crixivan)
1. Prevent synthesis and maturation of HIV, thus helping to prevent HIV replication and
progression of HIV-related disease
v. Zidovudine (Retrovir, AZT)
1. Inhibit the replication and proliferation of HIV type 1
vi. Alpha-2b (Intron A)
1. Hairy cell leukemia; Kaposi sarcoma (AIDS related); chronic hepatitis B and C; viral-
induced warts (condylomata acuminate infections); malignant melanoma
2. Explain concepts of "selective toxicity", "broad-spectrum", "bactericidal", and "bacteriostatic" for
antibacterial drugs.
a. Selective toxicity: drugs used to treat infectious diseases share a common goal of selective toxicity- must
selectively kill or attenuate the growth of the pathogenic organism without causing excessive damage to
the host (human) cells
i. In some cases, the pathogenic organism may have some distinctive structural or biochemical
feature that allows the drug to selectively attack the invading cell
ii. For instance, drugs that capitalize on certain differences in membrane structure, protein
synthesis, or other unique aspects of cellular metabolism in the pathogenic organism will be
effective and safe anti-infectious agents
b. Broad-spectrum: drugs that are effective against a variety of bacteria (gram-negative, gram-positive, and
various other types of bacteria)
c. Bactericidal: refers to drugs that typically kill or destroy bacteria
d. Bacteriostatic: drugs that do not actually kill bacteria but limit their growth and proliferation
i. Classification whether drug is bactericidal or bacteriostatic may depend on drug dosage

3. Explain clinical relevance of "resistance" to antibacterial and antiviral drugs.

a. Bacterial resistance
i. Most serious problems of antibacterial therapy is potential for the development of strains of
bacterium that are resistant to one or more antibacterial agents
1. Bacterial strains have natural acquired defense mechanismsàenables strain to survive
effect of drugsàcontinues to grow and reproduce similar resistant strains
2. Can cause a resistant strain bacteria if drugs not effective
ii. Bacterial resistance can occur because of several mechanisms
1. Certain bacteria strains may be able to enzymatically destroy antibacterial drug
2. The bacterial cell modifies or mask the site where the antibacterial drug typically binds on
or within a cell.
3. Bacteria may develop resistance through genetic mutations that change the enzymes
targeted by certain drugs
4. The drug's ability to penetrate the bacterial cell is reduced.
5. Certain bacteria may develop drug efflux pumps: expel drug from bacterial cell.
iii. Limit development of resistant strains
1. Antibacterial drugs should be used judiciously, not overused, a concept referred to as
antibiotic stewardship
b. Viral resistance
i. Viruses can mutate and alter their structural or functional characteristics so that previously
effective drugs will be unable to control specific viral infections adequately
ii. Efforts should be made to limit the inappropriate use of antiviral drugs and to contain the spread
of resistant viruses

4. Classify antibacterial drugs by mechanism of action: 1) inhibition of bacterial cell wall synthesis/function,
2) inhibition of bacterial protein synthesis, and 3) inhibition of DNA/RNA function.
a. Inhibition of bacterial cell wall synthesis/membrane function
i. Penicillins: Aminopenicillins
1. Amoxicillin (Amoxil)- also known as beta-lactam antibiotics because they share common
beta-lactam ring structure
a. Exert their effects by binding to specific enzymatic proteins within the bacterial
cell wall
i. These enzymatic proteins, known as penicillin-binding proteins (PBPs),
are responsible for normal synthesis and organization of the bacterial cell
wall
ii. In particular, PBPs help manufacture the peptidoglycans, which are
essential for normal membrane structure and function
iii. Penicillins attach to the PBPs and inhibit their function
1. Thus, construction of the bacterial cell wall is impaired, and the
cell dies from the membrane’s inability to serve as a selective
barrier and to contain the high internal osmotic pressure of the
bacterial cell
iv. Amoxicillin is a semisynthetic penicillin- has a broader antibacterial
spectrum; can be administered either orally or parenterally, depending
on the specific agent
 ii. Cephalosporins: First generation cephalosporins
1. Cefazolin (Ancef)
a. Classified as beta-lactam antibiotics, exert their bactericidal effects in a manner
similar to penicillins (inhibition of PBPs, resulting in inadequate peptidoglycan
production)
b. First generation cephalosporins are generally effective against gram-positive
cocci, and may also be used against some gram-negative bacteria
iii. Other Agents
1. Vancomycin (Vancocin)
a. Binds directly to bacterial cell wall precursors such as D-alanine and to impair the
incorporation of these precursors into the cell wall
b. Effective against gram-positive bacilli and cocci and primarily serves as an
alternative to the penicillins in treating a variety of infections, including certain
bacterial strains that are resistant to the penicillins
iv. Penicillin and Beta-Lactamase Combinations
1. Piperacillin and tazobactam (Zosyn)
a. Certain bacteria produce enzymes known as beta-lactamases which bind to
beta-lactam drug and destroy it before it can exert antibacterial effect
i. These bacteria are resistant to penicillin and other beta-lactam
antibacterial drugs
b. Certain drugs inhibit these beta-lactamase enzymes (Tazobactam) which prevent
the enzyme from destroying the penicillin, thus allowing the penicillin to remain
effective
i. These are typically combined with a specific type of penicillin
(Piperacillin) or other beta-lactam agent to treat infections caused by
bacteria that produce beta-lactamase enzymes
b. Inhibition of bacterial protein synthesis
i. Aminoglycosides
1. Gentamicin (Garamycin)
a. bind irreversibly to certain parts of bacterial ribosomes and cause several
changes in protein synthesis, including alterations in ribosome’s ability to read
mRNA genetic code
b. This misreading results in the improper synthesis of proteins that control specific
aspects of cell function, such as membrane structure and permeability
c. The lack of normal cell proteins leads to the bacterial cell’s death
d. Aminoglycosides have a very broad spectrum of antibacterial activity and are
effective against many aerobic gram-negative bacteria, including E. coli,
Pseudomonas, and Salmonella
i. They are also active against some aerobic gram-positive bacteria such
as certain species of Staphylococcus, and many anaerobic bacteria
ii. Consequently, aminoglycosides are used to treat a variety of tissues and
wound infections
ii. Macrolides
1. Azithromycin (Zithromax)
a. Inhibit bacterial protein synthesis by binding to specific parts of the 50S ribosome
in susceptible bacteria
i. This binding impairs protein synthesis primarily by interfering with the
function of transfer RNA (tRNA) at the ribosome
ii. Inhibits tRNA movement on the ribosome, thereby impairing amino acid
delivery and impairing elongation of polypeptide chain
iii. May also block the exit site (polypeptide tunnel) on the ribosome so that
the polypeptide chain cannot undergo further modification after this chain
has been synthesized
b. Exhibit a very broad spectrum of antibacterial activities and are active against
many gram-positive bacteria, as well as some gram-negative bacteria
i. Often used as the primary or alternative drug in a variety of clinical
conditions (especially useful in patients who are allergic to penicillin)
c. seem to have anti-inflammatory effects, especially in diseases associated with
airway inflammation
i. May be particularly useful in treating certain airway infections in people
with CF or other respiratory disorders associated with infection and
inflammation in airway tissues
 iii. Tetracyclines
1. Demeclocycline (Declomycin)
a. Inhibit protein synthesis by binding to several components of the ribosomal
apparatus in susceptible bacteria
i. May cause misreading of the mRNA code and may impair the formation
of peptide bonds at the bacterial ribosome
ii. Very effective in preventing bacterial protein synthesis
b. Active against a variety of bacteria including many gram-positive and gram-
negative bacteria, and other bacterial microorganisms (Rickettsia, spirochetes)
c. Their use as a broad-spectrum antibiotic has diminished somewhat, however,
because of the development of tetracycline-resistant bacterial strains
i. Currently tetracyclines are used to treat specific infections relating to
such bacilli as Chlamydia, Rickettsia, and certain spirochetes
ii. May also be used as alternative agents in treating bacterial strains that
are resistant to other drugs such as chloramphenicol, streptomycin, and
various penicillins
d. Have anti-inflammatory, neuroprotective, and immunomodulating effects
i. May protect cells from damage caused by harmful enzymes and free
radicals
c. Inhibition of DNA/RNA function
i. Fluoroquinolones
a. Inhibit two specific enzymes (DNA-gyrase and topoisomerase IV) that affect DNA
function in certain bacteria
i. DNA gyrase is responsible for controlling the amount of DNA winding
(super coiling) in bacterial cells
ii. Topoisomerase IV enzymatically separates two new DNA strands that
form during bacterial cell division
b. Inhibit these enzymes, thereby impairing the normal DNA structure and function
that is needed for cell growth and replication
c. Effective against a wide range of gram-positive and gram-negative aerobic
bacteria and are especially useful in UTI caused by E. coli, Klebsiella, Proteus,
and Enterobacter aerogenes
d. Other indications include the treatment of GI infections, respiratory infections,
osteomyelitis, and certain STDs (gonorrhea)
2. Ciprofloxacin (Cipro)
a. Particularly effective against anthrax infections
3. Levofloxacin (Levaquin)
ii. Sulfonamides
a. Agents interfere with bacterial nucleic acid production by disrupting folic acid
synthesis in susceptible bacteria
b. Structurally like PABA, which is the substance used in the first step of folic acid
synthesis in certain types of bacteria
i. Either directly inhibit the enzyme responsible for PABA utilization or
become a substitute for PABA, which results in the abnormal synthesis
of folic acid (either way folic acid synthesis is reduced and bacterial
nucleic acid synthesis is impaired)
2. Silver sulfadiazine (Silvadene)
a. Combination of Sulfadiazine combined with silver nitrate and is often applied
topically to control bacterial infection in burns
iii. Others
1. Metronidazole (Flagyl)
a. Drug appears to be incorporated into bacterial cells, where it undergoes chemical
reduction
i. The reduced metabolite of metronidazole interacts with bacterial DNA
and causes it to lose its characteristic double-helix structure
1. leads to the disintegration of DNA molecules and loss of the
ability to replicate and carry out normal gene function
b. Effective against most anaerobic bacteria and is useful in treating serious
infections caused by Bacteroides and Fusobacterium
c. Effective against certain protozoa and has antiprotozoal effects
5. Identify adverse effects that are common across classes of antibacterial drugs.
Drugs that inhibit bacterial cell membrane synthesis/function
a. Penicillins- amoxicillin
i. Potential for allergic reactions
1. Hypersensitivity to penicillin (skin rashes, hives, itching, difficulty breathing)
2. Could be severe and lead to anaphylactic reaction (severe bronchoconstriction and
cardiovascular collapse)
3. Skin reactions can be life threatening (toxic-epidermal necrosis, Steven-Johnson
syndrome)
ii. Prolonged administration- may cause CNS problems (confusion, hallucinations) and certain blood
disorders (hemolytic anemia and thrombocytopenia)
iii. Other side effects: GI problems (N/V, diarrhea)
b. Cephalosporins- cefazolin
i. May cause allergic reaction similar to penicillin hypersensitivity
ii. Cross-sensitivity often exists- Patient allergic to penicillin will also display hypersensitivity to
cephalosporin agents
iii. GI problems (stomach cramps, diarrhea, N/V)
c. Vancomycin
i. Emergence of resistant bacteria is of concern
ii. Primary adverse effects (hypersensitivity- skin rashes); a bitter or unpleasant taste in the mouth,
and GI disturbances (N/V)
iii. Potential to cause nephrotoxicity and ototoxicity
d. Combination of piperacillin & tazobactam (Zosyn) beta-lactamase inhibitor
i. May produce side effects caused primarily by the penicillin component such as headache, GI
problems, allergic reactions
Drugs that inhibit bacterial protein synthesis
f. Aminoglycosides-gentamicin
i. Use is limited somewhat by problems with toxicity
1. Nephrotoxicity (bloody urine, acute renal tubular necrosis)- more common
ii. Ototoxicity (dizziness and ringing or fullness in the ears)- can be irreversible
iii. Toxicity may occur more frequently in patients with liver or kidney failure or elderly
iv. Other adverse effects: hypersensitivity (skin rashes, itching)
g. Macrolides- azithromycin
i. Various degrees of allergic reaction from mild skin rashes to acute anaphylaxis
ii. Liver toxicity (drug-induced hepatitis, liver failure)
iii. Cardiac arrhythmias in patients with risk factors that predispose them to cardiac irregularities
(electrolyte imbalances, latent arrhythmias; other pro-arrhythmic drugs)
h. Tetracyclines- demeclocycline
i. GI distress (N/V, diarrhea), hypersensitivity reactions (rashes); increased skin sensitivity to UV
light (photosensitivity)
ii. May affect bone growth (impair bone formation) somewhat in premature infants, but actually
have a positive effect on bone resorption in adults and may stabilize bone loss in conditions such
as RA, osteoporosis, and periodontal (gum) disease
iii. discoloration of the teeth and skin (could be permanent with high dosages used long duration)
iv. development of tetracycline-resistant strains and resulting superinfections
Drugs that inhibit bacterial DNA/RNA synthesis and function
i. Metronidazole
i. GI distress (nausea, diarrhea); allergic reactions (rashes), and CNS symptoms (confusion,
dizziness, mood changes)
ii. May also cause peripheral neuropathies (numbness and tingling in hands and feet)
j. Fluoroquinolones- ciprofloxacin, levofloxacin
i. Primary adverse effects: CNS toxicity (visual disturbances, headache, dizziness); GI distress
(N/V, diarrhea); allergic reactions (skin rashes, itching)
ii. Photosensitivity and increased skin sensitivity to UV light
iii. Rare but serious cases of nephrotoxicity
iv. May cause tendon pain and inflammation (tendinopathy) that can be severe and can ultimately
lead to tendon rupture
 k. Sulfonamides- silver sulfadiazine
i. GI distress, increased skin sensitivity to UV light, and allergic reactions
ii. Serious disturbances in the formed blood elements, including blood dyscrasias such as
agranulocytosis and hemolytic anemia may also occur during systemic therapy

6. Identify adverse effects for specific antiviral drugs.

a. Acyclovir (Zovirax)
i. Topical application may produce local irritation of cutaneous and mucosal tissues
ii. Prolonged systemic administration of acyclovir may cause headaches, dizziness, skin rashes,
and GI problems (N/V, diarrhea)
b. Amantadine (Symmetrel)
i. CNS symptoms such as confusion, loss of concentration, mood changes, nervousness,
dizziness, and light-headedness; overdose can cause seizures
c. Famciclovir (Famvir)
i. Well tolerated; Minor side effects: headache, dizziness, and GI disturbances (N/V)
d. Indinavir (Crixivan)- Protease Inhibitors
i. Alterations in fat deposition in the body (lipodystrophy)- fat deposits atrophy in the limbs, but
excess fat is deposited in the abdomen
ii. Blood lipids may also be adversely affected, resulting in increased plasma cholesterol, increased
triglycerides, and decreased HDL
iii. Other metabolic disturbances: insulin resistance
iv. Metabolic syndromeàincreased risk of CVD
v. Other side effects: diarrhea, headache, fatigue
e. Zidovudine (Retrovir, AZT)- nucleoside reverse transcriptase inhibitors (NRTIs)
i. Blood dyscrasias, such as anemia and granulocytopenia
ii. Fever, chills, nausea, diarrhea, dizziness, headache, and excessive fatigue
iii. Myopathy, as indicated by skeletal muscle tenderness, weakness and atrophy; peripheral
neuropathies, liver dysfunction, and lactic acidosis
iv. Pancreatitis, CNS toxicity (headache, irritability, insomnia); and GI disturbances (nausea,
diarrhea)
f. Alpha-2b (Intron A)
i. Flulike symptoms, including fever, chills, muscle aches, and general malaise
ii. Loss of appetite, nausea, vomiting, diarrhea, and unusual tiredness
iii. Behavioral side effects such as depression,
iv. When injected IM or Sub-Q: may get irritation around injection site
v. Immune system may produce anti-interferon antibodies, especially with prolonged administration

7. Describe strategies for pharmacological management of HIV, including HAART.

a. Drugs can inhibit replication of HIV and are usually specific for HIV1 form of the virus because HIV1 is
more prevalent in people infected by HIV
b. First strategy was using Zidovudine (Retrovir, AZT) as an anti-HIV agent followed by NRTIs (nucleoside
reverse transcriptase inhibitors) that act like zidovudine to prevent HIV replication.
i. These drugs inhibit the reverse transcriptase enzyme that HIV uses to synthesize viral DNA from
viral RNA which impairs one of the early steps in viral replication, thus slowing the progression of
HIV infection
c. Protease inhibitors: indinavir (Crixivan) were second breakthrough
i. These drugs impair the HIV protease enzyme that is responsible for several steps in HIV
replication
ii. Like NRTIs, these drugs do not kill the virus but can slow its replication and prevent the spread of
HIV to noninfected cells
rd
d. NNRTI (nonnucleoside reverse transcriptase inhibitors) were the 3 strategy to inhibit HIV replication
i. Inhibit reverse transcriptase enzyme’s ability to perform one of the initial steps in HIV replication
ii. NNRTIs however directly inhibit the active (catalytic) site on the enzyme, whereas zidovudine and
other NRTIs serve as false substrates that take the place of the substance (thymidine) normally
acted on by this enzyme
iii. Patient can use these drugs with other agents (NRTIs, protease inhibitors) to provide optimal
benefits in preventing HIV replication and proliferation
e. Newer strategies are HIV entry inhibitors
i. which impair the virus’s ability to attach to the host cell’s surface, thereby inhibiting HIV entry into
the susceptible lymphocytes (can’t begin process of replication)
f. Lastly, integrase inhibitors have been developed
i. Inhibit a key enzyme (HIV integrase) that enables HIV to splice its viral DNA into the host cell
chromosome
ii. By inhibiting this enzyme, these drugs limit the ability of HIV to integrate its genetic code into the
host cell DNA, thus preventing the virus from
inducing the host cell to manufacture new viral
components
g. Several anti-HIV drugs are often administered
simultaneously to provide optimal inhibition of HIV
replication and proliferation
i. Combining several agents is referred to as highly
active antiretroviral therapy (HAART) and often
involves the simultaneous use of at least three anti-
HIV agents
ii. Typical HAART strategy for initial treatment of HIV
infection involves the use of two nucleoside RTIs
and one nonnucleoside RTI
iii. HAART can prevent the progression of HIV
infection and help sustain immune function by
allowing increases in the number of functioning
CD4 lymphocytes
iv. Use of HAART is associated with a substantial
reduction in the incidence of AIDS and with
improved clinical outcomes (fewer infections, decreased cancers, prolonged survival) in people
infected with HIV
v. Adherence to HAART is often difficult because of potential for side effects with these drugs and
the difficulties in remembering the complicated dosages regimens
vi. HAART does not completely eliminate the virus from the infected host (even though HIV is no
longer traceable in blood levels) because some of the viral components remain sequestered
within tissues, where they remain hidden from HAART drugs
vii. Simultaneous use of several drugs during HAART increases risk for drug-drug interactions,
increased likelihood of metabolic disorders that affect lipid and glucose metabolism, and may
cause toxicity to the liver, kidney, and other organs
viii. If HIV is not treated successfully, the body is open to infection from various other microorganisms
(opportunistic infections) because microorganisms take advantage of the chance to infect people
who lack normal immune defenses
1. The best prevention against these infections is aggressive anti-HIV treatment that
promotes T lymphocyte survival and helps maintain a functioning immune system
2. Treatment of opportunistic infections in patients with AIDS
a. Acyclovir (Zovirax) and famciclovir (Famvir)
i. Unusually severe vesicular and necrotizing lesions of mucocutaneous
areas (mouth, pharynx) and GI tract (Herpes simplex organism)
ii. Painful, vesicular eruption of skin according to dermatomal boundaries
(shingles) (Varicella-zoster organism)
b. Ciprofloxacin (Cipro)
i. Enterocolitis and bacteremia (salmonella organism)