Infectious Disease Lecture w/ Dr.

Lichtenberger 3 January 2012

The Topic of This Lecture Is: How to Differentiate Organisms

The cell wall structure determines whether bacteria stain blue (Gram+) or red (Gram-).
o Gram stains also reveal shape and arrangement, along with the presence of PMNs.
o Yeast can be seen on Gram stains. Theyre cigar-shaped, stain dark purple, and
larger than PMNs.
To differentiate Gram+ bacteria, incubate a culture on blood agar and confirm with
chemical tests.
o Staphylococci are catalase positive, such that they are able to break down
peroxide.
The only strain of Staph that is coagulase positive is S. aureus.
o All other Gram+ bacteria are catalase negative. Theyre differentiated by their type
of hemolysis.
-hemolysis is a mild amount of hemolysis. Do not confuse -hemolytic with
Group A Strep.
S. pneumoniae is capsule+ & optochin sensitive; S. viridans are
capsule- and resistant.
o The presence of a capsule is identified by the Quellung
reaction.
o Sensitivity to optochin is evaluated via a disc of the antibiotic on
the agar.
o S. pneumoniae form diplococci; S. mutans and other S. viridans
make chains.
All -hemolytics are bacitracin sensitive. Recent infections yield a
positive ASO titer.
-hemolysis is complete. Of these Streptococci, only S. pyogenes (GAS) is
bacitracin sensitive.
These bacteria are evidenced by yellowing of the agar around the cells.
-hemolytic Strep really like to infect infants. S. pyogenes is PYR+ (like
Enterococci).
The Lancefield classification system for Strep is based on C
carbohydrate differences.
o S. pyogenes is GAS; S. agalactiae is GBS; S. bovis is GDS. Know
that for Step 1.
Note that -hemolysis is a stupid, awful misnomer. Enterococci do NOT
hemolyze RBCs!
To differentiate from Strep, grow them on 6.5% NaCl. A Gram stain is
insufficient.
Under previous nomenclature, all Enterococci were labeled as Group D
Strep.
o The two spore-forming Gram+ organisms are Clostridium and Bacillus. Both are
rods.
Spores are resistant to destruction and are seen with a malachite green stain.
o The Gram+ rods we care about are Corynebacterium (diphtheria, motile) and
Listeria (non-motile).
There is only one Gram- coccus: Neisseria. The two strains are differentiated by maltose
fermentation.
o N. meningitides is able to ferment maltose, while N. gonorrhoeae cannot. Both
are diplococci.
Gram- rods (GNR) are first grouped by their ability to ferment lactose on a MacConkey
agar (not blood).
o Those that ferment lactose are Enterobacteriaceae, like E. coli, Klebsiella,
Citrobacter, and Serratia.
These are evidenced by pink colonies on the MacConkey agar.

Those that dont ferment lactose are differentiated by the presence of oxidase.
Pseudomonas is oxidase positive. Shigella, Salmonella, and Proteus are
oxidase negative.
Three Gram- bacteria have capsules (like S. pneumoniae): H. influenzae, K. pneumoniae,
and N. meningitides.
Special culture requirements! H. influenzae chocolate agar with factors V and X.
LEARN THESE
o Neisseria Thayer-Martin media; M. tuberculosis Lowenstein-Jenser agar.

AND THESE
Legionella charcoal yeast extract agar; All fungi Sabourauds agar.
THESE TOO, FUCK
India ink is a special stain, used primarily to identify Cryptococcus neoformans, whose
capsule blocks the ink.
Acid-fast stains work for mycobacteria (including Tb), which lack a cell wall.
The Giemsa stain is used to identify intracellular organisms: Plasmodium, Chlamydia,
Borrelia, Trypanosome.
Silver stains are used in tissue to identify fungi (like PCP in HIV patients), which stain
black.
Pigmented bacteria: S. aureus is gold; P. aeruginosa is blue-green; Serratia marcescens is
rust-colored.
Fungi are first divided into yeasts (Candida and Cryptococcus) or molds.
o C. albicans are the only germ tube+ organism. They like to form pseudohyphae.
o Molds are septate (Aspergillus and Fusarium), non-septate (Mucor and Rhizopus), or
dimorphic.
If it branches at 45, its probably Aspergillus. If it branches at 90, its
probably Mucor.
Susceptibility to antimicrobials is assessed by the MIC. One method is disk diffusion;
another is the E-test.
o The micro-dilution technique is pretty cool, as a color change from pink to purple
indicates the MIC.
o A number must be looked up in a reference book to determine if the strain is
resistant or not.
o

Infectious Disease Lecture w/ Dr. Lichtenberger 3 January 2012

The Topic of This Lecture Is: Review of Antimicrobials

The first antibiotics were -lactams, which inhibit cell wall synthesis by blocking
peptidoglycan cross-linking.
o Penicillin resistance is conferred by a plasmid that carries -lactamase.
Clavulanic acid is a -lactamase inhibitor (ex. Clavamox). Others are
sulbactam/tazobactam.
o Penicillin treats Gram+ cocci & rods, and its still the first line treatment for
spirochetes like syphilis.
Oodles of people can have hypersensitivity reactions. Some develop
hemolytic anemias.
o Amoxicillin and ampicillin treat Enterococci, H. influenzae, E. coli, Listeria, and
Proteus.
Some Staph infections can be treated too, but most of them are resistant by
now.
o Some -lactams are penicillinase-resistant oxacillin, methicillin, nafcillin. They
treat most S. aureus.
For toxicity, interstitial nephritis is evidenced by a skin rash, elevated SCr,
fever, and WBC.
o Most penicillins dont treat P. aeruginosa, but piperacillin and ticarcillin are
effective.
Interestingly, they also work against GNRs and some anaerobes. I have no
idea why.
Cephalosporins are -lactams that are less susceptible to penicillinases. There are four
generations.
o 1st (cephalexin/cefazolin): Gram+ ONLY ||| 2nd (cefmetazole): Gram+, some Gram-,
and anaerobes
3rd gen (cefpoxidime): Mainly Gram- ||| 4th (cefepime): Gram+ and resistant
Gram Carbapenems are awesome due to their broad spectrum. They treat anything resistant to
other -lactams.
o Like cephalosporins, they can cross-react with PCN allergies. They dont work
against MRSA.
Monobactams like aztreonam treat Gram- bugs and nothing else. They dont cross-react
with PCN.
Glycopeptides like vancomycin inhibit cell wall formation by preventing D-AlaD-Ala
binding.
o They treat resistant Gram+, especially S. aureus (MRSA) and Enterococci. It is NOT
orally active.
They have absolutely no effect on Gram- bugs or anaerobes.
o Toxic effects include red man syndrome (just slow the infusion rate),
nephrotoxicity, and ototoxicity.
Aminoglycosides like gentamicin and tobramycin are protein synthesis inhibitors used for
resistant GNRs.
o They are well-renowned for their ability to cause ototoxicity, murdering innocent
hair cells.
Tetracycline and doxycycline cannot be used in children, as they stunt bone growth and
ruin enamel.
o They are used to treat Rickettsiae, spirochetes, Mycoplasma, and Chlamydia.
o Their absorption is minimized if taken with milk. Also, they can induce
photosensitivity.
Macrolides (erythromycin & azithromycin) treat atypical pneumonias, STDs, and Gram+
if PCN cant be used.

A lot of patients end up with GI discomfort or diarrhea. Serum levels of

anticoagulants may increase.
Lincosamides (clindamycin) are great for dental infections: Gram+ bugs and anaerobes
(NOT Gram-).
o If a patient develops diarrhea after taking clindamycin, suspect C. difficile colitis.
Sulfonamides (sulfamethoxazole) are great for treating UTIs, Nocardia, and Chlamydia.
They inhibit DHPS.
o Trimethoprim inhibits DHF reductase. It covers pneumocystis, Shigella, and
Salmonella.
o TMP-SMX (Bactrim) cant be given to those with G6PD deficiency. Theres risk of
nephritis or anemia.
The two drugs work together to completely inhibit bacterial folate synthesis.
Fluoroquinolones (ciprofloxacin) inhibit DNA gyrase. They mainly treat Gram- bugs
(Pseudomonas!).
o The most well-known side effect is tendonitis, which can lead to tendon rupture
(esp. Achilles).
Metronidazole creates metabolites toxic to bacteria. It works against anaerobes, like C.
difficile.
o It also treats parasites. As side effects, it can cause a metallic taste or nausea if
taken with EtOH.
It should only be given for short periods of time due to neurotoxicity.
When treating infections, hit early and hard with the appropriate antibiotic. Broader isnt
always better.
o Minimize the length of therapy, since toxic effects are more likely to appear over
time.
Any infection that involves pus is probably S. aureus. Try oxacillin, 1st gen cephalosporins,
or clindamycin.
o Fluoroquinolones are not effective at all. If its MRSA and in the blood, use
vancomycin.
Enterococcus infections can usually be treated with amoxicillin or ampicillin, not
cephalosporins.
Strep are usually treated by penicillins, followed by clindamycin. Dont use ciprofloxacin
or macrolides!
Except for Pseudomonas, Gram- infections are treated by FQs, Clavamox,
aminoglycosides, carbapenems
o Really, just dont use PCN alone, nor a 1st generation cephalosporin, vancomycin, or
metronidazole.
For Pseudomonas, go with ciprofloxacin, aminoglycosides, piperacillin, aztreonam, or
ceftazidime/cefepime.
o Drugs that dont work are macrolides, clindamycin, TMP-SMX, most cephalosporins,
and Clavamox.
For anaerobes, go with metronidazole or clindamycin. ||| If its PCP, the best choice is
Bactrim.
o

Infectious Disease Lecture w/ Dr. Lichtenberger 3 January 2012

The Topic of This Lecture Is: Ive Got a Fever, and the Only Prescription Is More Cowbell

A fever is defined as a core body temperature of > 100.4 F, though temperature varies
with time of day, anatomic site, physical or emotional activity, and gender (esp. during
ovulation).
o It is often, but not always, a sign of infection. Alleviation of fever signifies
appropriate therapy.
Microorganisms can release exogenous pyrogens or toxins (LPS/endotoxin, Shiga toxin,
etc).
o Cytokines are endogenous pyrogens. Examples are IL-1, IL-6, TNF-, and IFB-.
o The hypothalamus receives these signals and causes vasoconstriction, which
conserves heat.
Heat is also retained by pilo-erection and voluntary activities.
The body produces additional heat by increasing metabolism and shivering.
Fevers can be treated by antipyretics, as they are a response to cytokines. Theyre not
hyperthermia!
o Hyperthermia is unregulated, excessive production of heat. Antipyretics are
useless to treat it.
o Theres feedback for fevers, so temperature rarely exceeds 105.8 F.
In hyperthermia, the temperature frequently exceeds 107.6 F, so the patient
fries to death.
A single temperature measurement is not clinically useful. The acuity and pattern are way
more helpful.
o Characteristic patterns on a temperature curve can suggest particular diagnoses.
Fevers can be managed with ice packs or sponges with cool water. Ice baths are not
recommended.
o Or, use drugs like APAP, aspirin, NSAIDs, or corticosteroids.
o Its probably a good idea to let the fever go for a bit to establish a pattern and fight
infection.
Fever of unknown origin (FUO) defies diagnosis is 5-15% of cases. Its a diagnosis of
exclusion.
o Physical exams look at the temperature curve, skin, mucous membranes, lymph
nodes, organ size
Initial labs look at CBC, LFTs, ESR, UA, blood cultures, and CXR.
o If still nothing is found, do CTs, ultrasounds, MRIs, and hell, maybe even a nuclear
medicine scan.
o The definition of a classical FUO is a temp of > 38 C for at least 3 weeks with > 2
hospital visits.
Ask about travel, contacts, animals, medications, and immunizations.
It could be cancer, infection, inflammation, etc. Just observe! Dont waste
antibiotics.
o A hospitalized patient who gets a fever after admission likely has a nosocomial
infection or drug fever.
o Patients who are immune-deficient probably have an infection. Start
antimicrobials ASAP.
o If a definitive diagnosis cant be reached and the condition is chronic, mortality
rates are low.
The longer the presence of fever, the less likely its an infection (higher
chance of cancer).
Survival rates are quite poor if the only sign of a neoplasm is a FUO.
Infectious Disease Lecture w/ Dr. Lichtenberger 4 January 2012
The Topic of This Lecture Is: Infections Characterized by Fever and Lymphadenopathy

Mononucleosis-like syndrome involves fever, fatigue, lymphadenopathy (esp. in the

neck), and pharyngitis.

This usually affects young patients. The differential includes infections, lymphoma,
and leukemia.
Infectious mononucleosis is caused by EBV, but most people infected by EBV do not
develop symptoms.
o Kids in daycares and college-aged folks (15-24) are the most likely to get the
symptomatic disease.
It is probably spread by saliva exchange, not by fomites. That isnt hard data.
o The virus doesnt have to spread from symptomatic patients. Healthy people shed
the virus.
o One of the biggest risks is splenomegaly, as an enlarged spleen can rupture with
physical activity.
o CBCs will hopefully show > 50% mononuclear cells and > 10% atypical
lymphocytes.
Early on, there are transient VCA-IgMs (heterophile). Later, permanent IgGs
are developed.
The test used most commonly is a rapid agglutination test called
Monospot.
LFTs may be mildly elevated, while in cases of CMV, they may be severely
elevated.
o Antivirals dont work, so just treat the symptoms and ensure the patient doesnt
rupture a spleen.
Cytomegalovirus (CMV) is the largest virus that can infect humans. Infection rates are
pretty high.
o Like mono, kids that go to daycare tend to get it. Sheltered kids will get it as
adolescents.
It can be passed vertically. And, in IC patients, prophylaxis is needed to avoid
encephalitis.
o Serology does not reveal heterophiles. The FUO lasts longer, and a sore throat is
less common.
Theres also less splenomegaly, and atypical lymphocytosis is not expected.
o Like mono, we dont know how its transmitted. It can be by saliva and by blood
(transfusions).
o

 A primary HIV infection presents however it wants. The most common are those in this
lectures topic.
o In the first few weeks, HIV RNA PCR is far, far superior to the ELISA serology (only
positive in 50%).
o In acute retroviral syndrome, antiretrovirals is a good idea, but the symptoms are
self-limited.
It is possible to notice abnormalities in lymph tissue on a colonoscopy.
Toxoplasmosis is caused by a protozoon. Humans are an intermediate host for a parasite
that likes cats.
o The disease is caused by touching cat feces (or soil that s been soiled HAR HAR)
and then eating.
o Only 10-20% of cases are symptomatic, producing mono-like syndrome, at times
with chorioretinitis.
o During pregnancy, acute toxoplasmosis is bad. Its totally fine to have it before
pregnancy (IgG+).
Fetuses get intracerebral calcifications, hydrocephalus, and chorioretinitis.
o Diagnosis is by serology in healthy patients. In IC patients, toxoplasmosis can
reactivate in the brain.
AIDS patients that get seizures will have ring-enhancing lesions on MRI
(biopsy confirms).
o Only IC patients (WBC < 200) require treatment. Use sulfadiazine and
pyrimethamine.
Cat-scratch fever is caused by Bartonella henselae. The vector is a flea, but a cats
scratch is required.
o In this disease, theres a primary cutaneous papule 3-10 days after the scratch that
lasts 1-3 weeks.
Azithromycin decreases the duration of the lymphadenopathy. Rarely,
resection is needed.
o Atypically, theres Parinauds oculoglandular syndrome. Think eye problem +
lymphadenopathy.
o Antibiotics dont really help, especially in atypical disease. Prevent it by keeping
cats flea-free.
Infectious Disease Lecture w/ Dr. Lichtenberger 4-5 January 2012
The Topic of This Lecture Is: Infections Characterized by Fever and Rash

Macules are flat, non-palpable lesions in the plane of the skin. Think early chicken pox.
o Papules are palpable and raised. If they are large enough, theyre called nodules.
o Pustules are papules that are full of pus. Vesicles are small blisters and bullae
are large blisters.
Vesiculo-bullous lesions include HSV, varicella zoster, and vibrio vulnificus (this one is
more bullous).
Humans are the only reservoir for HSV. HSV-1 presents in the oral cavity; HSV-2 hangs out
in your pants.
o IC patients can have disseminated disease. A fever blister might be a precursor to a
fatal disease.
o In additional to fever and lymphadenopathy, the rash for HSV is grouped vesicles
that are painful.
o Diagnosis is made by the Tzanck test (smear the opened vesicle), a culture/PCR, or
just a history.
Treatment is anything in the family of acyclovir. If its severe (like, in the
eyes), go IV.
These drugs work by competing with d-GTP on the viral DNA polymerase.
Varicella zoster (VZV) only affects humans. Its spread by airborne droplets, so it
replicates in the nose.

The first infection causes chicken pox, but reactivation for whatever reason causes
singles.
o The disease starts out maculopapular. Soon after, vesicles form in a dermatomal
distribution.
Unlike smallpox, these lesions will be in different stages of healing (mixed
presentations).
o If shingles presents in on CN V1, eyesight can be destroyed. This necessitates IV
antivirals.
Ramsay-Hunt Syndrome refers to involvement of CN VII, causing Bells
palsy.
Vibrio vulnificus is acquired by eating raw shellfish or oysters, or warm ocean water with
these critters.
o It pretty much only hits patients with underlying liver disease (excess iron).
o Symptoms have abrupt onset of fever accompanied by hypotension and severe
cellulitis.
There is no diarrhea! Treat immediately with debridement, ciprofloxacin,
and ceftazidime.
Necrotizing fasciitis is an immediate emergency, as both fascia and fat are
progressively destroyed.
o Type I is a mix of aerobic and anaerobic bacteria. It happens in IC patients or after
surgery.
o Type II is from S. pyogenes. This can affect otherwise healthy patients and kill within
hours.
o In necrotizing fasciitis, the lesion is painful (out of proportion), as is the surrounding
area.
A bulla is just the tip of the iceberg. Debridement is absolutely
necessary.
Neisseria meningitides can cause bacteremia, causing disseminated intravascular
coagulation (DIC).
o The fibrin thrombi can then occlude arterioles, leading to infarcts. This is purpura
fulminans.
This disease is extremely contagious. Close contacts need prophylactic
antibiotics.
o Cultures reveal Gram- diplococci that ferment maltose and glucose
(meningococcemia).
A few hemorrhagic pustules at small joints can be from disseminated N. gonorrheae.
Treat with ceftriaxone.
o Rather than getting a culture at the pustule, get it from the source of entry (mouth
or genitals).
Infective endocarditis from S. viridans or Staph may be evidenced by painless
hemorrhagic macules on the palms or soles (Janeway lesions) or painful purpuric nodules
on the pulp of the digits (Oslers nodes).
Capnocytophaga canimorusus is found in the mouths of dogs. It causes severe disease
in asplenic patients.
o There is a disseminated purpuric rash. Treat these patients with Clavamox.
S. aureus can cause soft tissue infections, like cellulitis. It really likes to form pus-filled
abscesses.
o Treat with Bactrim, clindamycin, or doxycycline. If its MRSA, use vancomycin.
Secondary syphilis involves fever, headache, myalgia, lymphadenopathy, and a
characteristic rash.
o The rash is maculopapular and erythematous or brown. Its on the palms, soles, and
trunk.
o Get a FTA on these patients to confirm the diagnosis. Treat with benzathine or
penicillin G.
o

 Eschars are necrotic lesions that grow. In Pseudomonas, there bacteria invades arteries
and veins.
o There is ischemic necrosis termed ecthyma gangrenosum. Culture and treat
accordingly.
Cutaneous anthrax is from Bacillus anthracis, a Gram+ spore-forming aerobic rod.
o Patients contact spores from animals that feed on grass. The ulcer is painful and
edematous.
o Treat this with ciprofloxacin or doxycycline, unless its susceptible to amoxicillin.
IC patients or diabetics can get mucormycosis in their nasal cavities. It makes broad
hyphae at 90.
Infectious Disease Lecture w/ Dr. Lichtenberger 5 January 2012
The Topic of This Lecture Is: Travelers Diseases

The most common food-related illnesses are travelers diarrhea, Hepatitis A, typhoid fever,
and giardiasis.
o Travelers should bring alcohol-based hand sanitizer and use it damn near constantly.
Only eat freshly cooked food thats still hot (not a buffet), or commercially
wrapped food.
They should boil water for > 10 minutes, and they should avoid ice made
from tap water.
o The risk of food-borne illness is increased simply because meals arent homecooked.
Most cases of travelers diarrhea are caused by Enterotoxigenic E. coli (ETEC),
yielding watery diarrhea.
o The disease is self-limited to 3-4 days, although in rare cases, theres post-infectious
irritable bowel.
Bloody stool and more severe diarrhea are associated with EAEC and C.
jejuni.
Treat with oral rehydration and a dose or two of fluoroquinolones or
azithromycin (C. jejuni).
o The onset may be more insidious and associated with gas if its a parasite, like
giardia or E. histolytica.
o Rarely, the cause is rotavirus or norovirus (cruise ships!). There will be more
nausea and vomiting.
These viruses are extremely contagious, and outbreaks are hard to contain.
o Symptomatic treatments are antidiarrheals (bismuth) and antimotility agents
(loperamide).
People who are at high risk for infection (IC) can take prophylactic rifaximin.
Later, she said that rifaximin is a good alternative to bismuth. Its just
more costly.
Hepatitis A is caused by an ssRNA virus. Its preventable by vaccine. Its transmitted by
the oral-fecal route.
o The incubation period is about a month. Symptoms are fever, malaise, anorexia,
and nausea.
The disease is more severe with increased age, leading to hepatitis (jaundice
and dark pee).
o If travel will begin shortly after vaccination, hepatitis A immunoglobulins are given
instead.
Typhoid fever is caused by S. typhi. Its seen everywhere but first-world countries, except
for travelers.
o The bug can remain in a gallbladder, shedding bacteria chronically and affecting
close contacts.
o Symptoms are high fever (> 103 F), headache, malaise, anorexia, splenomegaly,
and a faint rash.

The vaccine is not 100% effective, but its recommended to be given 2 weeks before
travel.
If exposed, diagnosis is made by culturing the stool, due to bacterial
shedding.
For Entamoeba histolytica, mature cysts are ingested, but trophozoites are what cause
disease.
o The parasites can travel to the lungs or form abscesses in the liver with chocolatecolored pus.
o This is a large bowel diarrhea (colitis) many small amounts of painful, bloody
diarrhea.
Contrast this to small bowel diarrhea, which is explosive, large amounts of
watery diarrhea.
o Like most parasites, onset is insidious. Cysts in stool or positive serology appear
before symptoms.
If a biopsy is done, flask-shaped ulcers will be seen due to invasive
amoebiasis.
o If theres no invasion, treat the diarrhea with paramomycin. If its invasive, use
metronidazole.
Paramomycin is an aminoglycoside that is not absorbed from the GI tract
(lumenal).
Giardia is a protozoon that is not invasive. The trophozoites just attach to the duodenum.
o As a small bowel issue, there are foul-smelling, greasy stools with a lot of flatulence
and cramps.
o Diagnosis is made by an ELISA test on the stool. Treat this parasite with
metronidazole.
o

 Arthropod-related infections include those from mosquitoes, sandflies (Leishmaniasis),

ticks, and fleas.
o Minimize risk by wearing proper attire, inspecting for ticks, and avoiding activity
from dusk to dawn.
Repellants like DEET help, as do bed nets or clothes that have been treated
with permethrin.
In any patient that has come from an endemic area and has a FEVER, suspect malaria as
a cause.
o Only a few areas in the world have malaria that can be treated by chloroquine
(Haiti is one of them).
o Disease is caused by sporozoites that mature in the liver and leave as merozoites.
They mature in RBCs, which eventually lyse (anemia!) and release
gametocytes.
o The mosquitoes that carry the disease are Anopheles, which are nocturnal (thats
important).
The first symptoms are FEVER, headache, and malaise. Later, theres
hemolytic anemia.
o The Plasmodium species that kills people is P. falciparum. Others are P. vivax and
P. ovale.
The latter patients require primaquine to treat the liver hypnozoites.
o Chemoprophylaxis is only given to travelers whose itinerary puts them at risk.
If chloroquine can be given, its a weekly drug given 1-2 weeks before to 4
weeks after.
If not, try mefloquine, but it has some pretty awful psychiatric side effects.
Drugs that must be taken daily include atovaquone (Malarone) and
doxycycline.
Dengue fever is transmitted by Aedes aegypti, which is a diurnal mosquito that loves
stagnant water.
o There are four serotypes. An initial infection yields immunity for one but not the
others.
But, a second infection by another serotype increases risk for hemorrhagic
fever (DHF).
o Initial symptoms are fever, retro-orbital headache, myalgia, and a rash on days 3-5.
o In cases of DHF, there are leaky capillaries and thrombocytopenia, necessitating
medical care.
Anyone with a diagnosis of dengue fever should avoid aspirin for this reason.
The same mosquito for dengue caries yellow fever, transmitted by a flavivirus for which
we have a vaccine.
o Early symptoms are flu-like, but a toxic phase follows with liver failure and
hematemesis.
o The vaccine for yellow fever has a chance of inducing neurotropic disease. That
sucks.
Rickettsiae africae is carried by ticks. Its an intracellular pathogen that hangs out in
sub-Saharan Africa.
o Most patients will develop a fever, rash, and maybe other benign symptoms. Treat
with doxycycline.
Leptospirosis is caused by a spirochete that hangs out in water that infected animals
piss in.
o First, there are flu-like symptoms, followed by liver damage.
LFTs are very high, but total bilirubin only mildly elevated.
o The spirochetes can be identified by serology or IG fluoroscopy. Treat with
doxycycline.
Syphilis is caused by Treponema pallidum. It can imitate many diseases due in its later
stages.

The initial presentation chancre is a painless chancre, seen on whatever touched a

vagina.
The secondary stage is condylomata lata (rash), along with systemic signs.
The tertiary stage is Argyll-Robertson pupil, neurosyphilis (ataxia), and
whatever else.
o VDRL is a non-specific test. Confirm the diagnosis with FTA (both positive means an
active infection).
If the VDRL is + but FTA is -, its a false positive. If only FTA is +, its been
treated.
o Again, the first-line treatment for syphilis is an injection of penicillin G.
These are spirochetes, so dont get these mixed up with the arthropod-mediated diseases.
o

Infectious Disease Lecture w/ Dr. Lichtenberger 5 January 2012

The Topic of This Lecture Is: Geographic Diseases of the U.S. of A

Rocky Mountain spotted fever is caused by Rickettsia rickettsii. It is NOT found in

states near the Rockies.
o A special stain is needed to identify this intracellular pathogen indigenous to the
Atlantic coast (NC).
The tick has to be attached for several hours before R. rickettsii is
transmitted.
o Initial symptoms are flu-like, but later theres abdominal pain with arthralgia.
Rash starts after fever. Its petechial, with small, flat, pink, non-itchy macules
on distal joints.
Severe symptoms of RMSF are pneumonitis and vasculitis.
Diagnosis is by symptoms and the epidemiological clues (near tall grass,
woods, etc).
o On serology, IgM titers appear first, then IgG antibodies after 2 weeks (like
everything else).
The antibody assay is for Weil-Felix. Learn that name. Treat this with
doxycycline.
Ehrlichia chaffeensis is a small Gram- bacteria that clusters inside of macrophages.
o Its carried by the Lone-star tick or dog tick, which hang out in Texas and the
Southeast U.S.
o As opposed to RMSF, the rash is maculopapular, and its also less likely to be seen.
Vasculitis is rare.
Diagnosis is made by elevated IgG and a blood smear for the pathogen (or
PCR).
o Contrast this bug with Anaplasma phagocytophilim, which is from Ixodes in the
Northeast U.S.
Also, A. phagocytophilim invades granulocytes like PMNs rather than
macrophages.
Lyme disease is caused by the spirochete Borrelia burgdorferi, via the tick Ixodes
scapularis.
o The most prominent epidemiological sites are Minnesota, Wisconsin, and the
Northeast U.S.
The disease is transmitted by nymph-stage ticks that feed for 24-36 hours.
o The pathognomonic sign is the bulls-eye rash, which has the fancy name
erythema migrans.
Early Lyme titers are probably negative, so just diagnose via the clinical
picture.
o Later signs are fever, AV nodal block, mononeuritis, hepatitis, ophthalmitis, and
arthritis.
The arthritis is seen in stage 3 (persistent), along with encephalopathy or
polyneuropathy.
o The cornerstone of treatment is doxycycline. Later-staged disease requires
ceftriaxone too.
Another disease carried by Ixodes is Babesia microtii, which forms a Maltese cross within
cells.
o Its not a huge deal except in patients without spleens. It presents a lot like malaria.
Theres fever, chills, headache, myalgia, anemia, etc. But, theres no history
of travel.
Patients without spleens will die from cardiorespiratory failure or renal failure.
o This is the only tick-related disease not treated with doxycycline! Instead, treat it
like malaria.
Go with atovaquone and azithromycin. Give blood transfusions for severe
anemia.

The three endemic mycoses are dimorphic, in that they are molds in nature but yeast in
tissue.
o The clues for diagnosis are the geographic distribution and the smear.
o They all cause progressive fever, dyspnea, and cough with oral ulcers and
organomegaly.
Histoplasma capsulatum is found in the Mississippi River Valley. Think bats, cave
exploration, and Tennessee.
o Sputum cultures are rarely positive. They look like little suns or like fish eggs.
If in the lungs, antigens are obtained on lavage. If disseminated, antigens are
in the urine.
o If the disease is progressive or chronic, use itraconazole. In IC patients, use
amphotericin B.
Blastomyces dermatitidis also likes the MRV. It prefers the lungs, but has the potential
to infect bones.
o Cultures of skin lesions and biopsy are much better than serology.
o As opposed to histoplasmosis and coccidiomycosis, treat EVERYONE, not just
complicated cases.
For Coccidiodies immitis, its found in the soil of the Southwestern deserts and San
Joaquin River Valley.
o Dissemination is rare in an immunocompetent host. Pulmonary symptoms are just
flu-like.
o The mainstay of diagnosis is serology (or biopsy), not blood culture. There is
eosinophilia!
o In most cases, just observe. But, pregnant or IC patients require fluconazole.
Paracoccidiomycosis presents the same way, but its found in Brazil and South America.
o It can cause chronic pulmonary symptoms. Diagnose by biopsy of a bug that looks
like a ships wheel.

Infectious Disease Lecture w/ Dr. Lichtenberger 5 January 2012

The Topic of This Lecture Is: Zoonoses

Again, Cat-scratch fever is caused by Bartonella henselae. Cats are bacteremic but
asymptomatic.
Plague is caused by Yersinia pestis, transmitted by a flea bite from those that live on
prairie dogs, rats, etc.
o A bubonic lymph node is painful and extremely swollen, localized near the bite.
o Pulmonic plague is a rapid pneumonia that can spread through blood or an
aerosol (dear God).
It can cause septicemia and necrosis of distal extremities. Treat with
aminoglycosides.
Brucella is found in many animals, but we care about livestock, since its transmitted in
unpasteurized dairy.
o Its a widespread zoonosis mediated by a Gram- intracellular bacteria. Dont eat
fancy French cheese.
o Theres an insidious onset of fatigue, weight loss, anorexia. Patients just feel unwell
for months.
There may be sacroiliitis, epididymitis, orchitis, and so on. It involves many
organs.
o Diagnosis requires a history of consuming unpasteurized dairy. Serologic testing
confirms.
Monotherapy doesnt work often, so we go with a tag-team of doxycycline
and gentamicin.
Francisella tularensis is a Gram- intracellular bug that causes tularemia. Its carried by
bunnies and squirrels.
o The animals get it from ticks. We get it being near infected rabbits or eating poorly
cooked bunny.
The epidemiological areas for the boards are Missouri, Arkansas, and
Marthas Vineyard.
o Six forms: ulceroglandular, glandular, oculoglandular, oropharyngeal, typhoidal,
pulmonary.
o Tularemia can be obtained by aerosol, so be careful when culturing it for diagnosis
(PCR works too).
If the lungs are affected, mortality rates are high. Treatment is always by
aminoglycosides.
R. ricketsii causes RMSF (ticks), R. typhi is from fleas, R. prowazekii is from lice. All are
Weil-Felix positive.
o While RMSF has a petechial rash that affects palms and soles (joints!), the other two
do not.
Also note that endemic typhus causes a more maculopapular rash (esp. on
the back).
o All of these are treated by doxycycline. Note that only R. prowazekii is not endemic
(its epidemic).
Coxiella burnetii is transmitted by aerosol. It does not cause a rash; rather, it causes Q
fever.
o Diagnosis is by serology and a history of being near pregnant livestock or pets.
o Its part of the workup for FUO, although there may also be headache and
pneumonia.
Hantavirus is transmitted by aerosols from dried rat feces from a chronically infected rat.
o It presents with severe pneumonia along with fever, myalgia, and cough.
o Diagnose it by IgM serology or PCR. Since its a virus, theres no treatment but
support.
Lymphocytic choriomeningitis (LCM) is an ssRNA virus transmitted by rats. Close
contact is required.

IC patients (transplant recipients) are at risk too. Its from inhaling excreta or being
scratched.
o The flu-like symptoms subside after 2-4 days, then come back (hopefully not as
encephalitis).
West Nile Virus is a RNA virus transmitted by mosquitoes. If it gets into birds, the birds
die rapidly.
o Humans and other animals are incidental hosts. Almost everyone is fine within a
week.
o But, < 1% of folks get meningoencephalitis, fever, ataxia, and muscle weakness
(flaccid paralysis).
o Diagnosis is by IgM in the serum or CSF. Note that PCR is not helpful.
o

Infectious Disease Lecture w/ Dr. Lichtenberger 5 January 2012

The Topic of This Lecture Is: Infectious Diarrheal Illnesses

The incubation period for norovirus is about 48 hours. Vomiting and diarrhea persist for
about 2 days as well.
o Rotavirus also causes viral enteritis. Pretty much every kid will get it by the time
theyre 5 years old.
For food-borne diseases, incubation periods provide clues to diagnosis. If its < 2 hours, its
a chemical agent.
o If its 2-7 hours, its a preformed toxin (like S. aureus). If its 8-14 hours, its
Clostridium perfinges.
Anything more than 14 hours is a viral or bacterial pathogen doing its thing.
o Do not give antibiotics for S. aureus food poisoning! Also, the keyword is
mayonnaise.
o For C. perfinges, theres watery diarrhea and no vomiting. The keyword is reheated
meat.
o For Bacillus cereus, theres an emetic form with a short incubation and an enteric
form thats longer.
The keyword for B. cereus mediated food poisoning is fried rice.
Non-invasive diarrhea is caused by ETEC or EAEC. This is travelers diarrhea or
persistent diarrhea in kids.
o Treat this with Bactrim or fluoroquinolones, and itll resolve without sequelae.
Invasive diarrhea is dysentery. Theres fever, abdominal pain, and bloody diarrhea with
mucus.
Enterohemorrhagic E. coli (EHEC) secretes a toxin like Shigella. It contaminates leafy
green veggies.
o It also affects undercooked meats. A tiny amount of bacteria can cause symptoms.
Theres no fever.
o There is hemorrhagic colitis without fever, but theres a risk for hemolytic uremic
syndrome.
HUS is evidenced by hemolytic anemia, renal failure (high SCr), and
thrombocytopenia.
o Do NOT give antibiotics or antimotility agents because this is mediated only by a
toxin!
Shigella is similar, but it also causes a fever. It CAN be cured by antibiotics: FQ, Bactrim,
and ceftriaxone.
Non-typhoid Salmonella infects poultry (eggs!). It induces bloody diarrhea and can
cause bacteremia.
o As opposed to Shigella, it has a high inoculum, and it is motile. Both of them are
lactose fermenters.
Campylobacter jejuni causes the same symptoms. It can be cultured at higher
temperatures (42 C).
o So, symptoms are usually not enough to differentiate causes of invasive diarrhea.
Get a culture.
o Treat C. jejuni with azithromycin. Complications include GBS or reactive arthritis.
Clostridium difficile is an anaerobic Gram+ bug that forms spores and produces a toxin.
o It is the usual cause of antibiotic-associated diarrhea. Its diagnosed by seeing
toxin in the stool.
Because it makes spores, its hard to kill. This is why it spreads in hospitals.
o Pseudomembrane colitis can worsen into TOXIC MEGACOLON with certain
strains of C. difficile.
Not everyone with CDAD presents with diarrhea. Most dont have fever, just
leukocytosis.
Imaging may show dilation of the colon. If it gets to > 10 cm, holy shit cut out
the colon.

Treatment is metronidazole is if its mild or ORAL vancomycin if its severe (maybe

with IVIG).
An odd treatment that actually works very well is a fecal transplant.

Infectious Disease Lecture w/ Dr. Lichtenberger 6 January 2012

The Topic of This Lecture Is: Respiratory Viral Infections: Influenza

Influenza A infects oodles of animals and humans, so it causes epidemics and

pandemics.
o Influenza B only infects people and parrots. Influenza C only infects humans and
swine.
o The antigen glycoproteins in influenza are hemagglutinin and neuraminidase
(H#N#).
Within the viral capsid, there are multiple RNA segments. They are able to
mutate.
o The viruses that can infect humans are H1-H3 and N1-N2, but dramatic drifts are
possible and deadly.
Its nave viruses that cause major issues, as people develop antigens if
theyre exposed.
Influenza A tends to start in wild aquatic birds, then gets to poultry, then pigs
or people.
o Pandemics tend to occur when an avian virus undergoes genetic reassortment with
a human virus.
The most important symptom of influenza is a very high fever, plus chills, bone pain,
myalgia, and nausea.
o Infants, old people, and pregnant chicks can end up with pneumonia, myocarditis,
or encephalitis.
o When a patient with influenza is in the hospital, an N95 mask is not needed, just a
regular one.
It is spread by droplets that do not remain as an aerosol. The virus hangs out
on surfaces.
o A rapid antigen test is obtained by jamming a swab into the nasopharynx (not the
mouth).
While the test is pretty specific, it is not sensitive. Preferably, just use the
clinical picture.
One should test hospitalized patients, pregnant women, and cases outside of
outbreaks.
Tamiflu is only given if the flu is caught within the first 48 hours. Otherwise, just provide
supportive fluids.
o The exception to this rule is pregnant women. In clinical practice, they get meds no
matter what.
Others include kids under 5, people over 65, and those with chronic medical
conditions.
o Oseltamivir (Tamiflu) and zanamivir are neuraminidase inhibitors that prevent
release of virions.
o If there are pulmonary symptoms, treat the patients for CAP, which may be from
secondary bacteria.
Influenza can be prevented by vaccination and frequent hand-washing. Also, sneeze into
your damn elbow.
o Dont touch your mucous membranes after touching other stuff. Stay home if youre
sick.
Infectious Disease Lecture w/ Dr. Lichtenberger 6 January 2012
The Topic of This Lecture Is: HIV and Primary Care

Antigenicity to HIV is mediated by the surface glycoprotein gp120, along with gp41.
o HIV likes to infect CD4 T-cells, macrophages, and dendritic cells. It binds to the host
at CCR5.
People who are homozygous for a CCR5 variant are immune to HIV.
o After binding, RNA is injected into the cell. Its reverse transcribed to DNA, then
integrated.

Once integrase does its thing, new viral RNA and HIV proteins can be
transcribed.
o The turnover of the virus is unbelievably fast. Over 1010 virions are produced and
destroyed daily.
o Reverse transcriptase is a pretty awful enzyme, but its mistakes provide
heterogeneity for the virus.
In dudes, the incidence of HIV from heterosexual contact is increasing toward that of gay
men.
o For women, the second most likely cause of HIV other than sex is IV drug abuse.
o But, on a case by case basis, the highest risk is from needle-sharing or receiving
buttsex.
Immediately after exposure, theres an extremely high viral load. It then drops to a
relatively stable set point.
o Similarly, the T-cell count drops acutely, then returns to baseline. It then steadily
declines.
o AIDS is defined as a CD4 count below 200. At that point, viral load starts increasing
sharply.
At a CD4 count below 500, theres increased risk of infections and neoplastic
events.
If CD4 drops below 50, then patients can get stuff like CMV, MAI, or
lymphoma.
The other definition of AIDS is the presence of an opportunistic infection.
o The most common pneumonia in AIDS patients is still S. pneumoniae, even though
they can get PCP.
The normal test for HIV is ELISA, confirmed by Western blot, since theres a risk of false
positives.
o Because of false positives, never report ELISA as positive! It is termed reactive or
non-reactive.
If there is a reactive ELISA, the first step is to repeat it. Then, do a Western
blot.
False negatives can be due to a window period (~2 weeks), recent
transfusion, or transplant.
o A positive Western blot is any 2 of p24, gp41, or gp160/120. Negative = no bands,
else indeterminate.
Indeterminate tests can be interpreted with regard to viral load (positive if >
1000).
Western blots will be negative at later evaluation if antiretrovirals are started
early.
o The other test is for the HIV RNA viral load, which is the nucleic antigen test (NAT
HV-1).
Always get informed consent before an HIV test and only disclose results in person.
o Go over the last three slides, since its stuff that needs to be regurgitated on the
exam.