STEP 1 REVIEW:

VIROLOGY +
BACTERIOLOGY
By Meredith Greer
Important Thing
◻ The MOST important thing to learning
microbiology/infectious diseases is to
learn the EXCEPTIONS to the rules.
◻ Lots of things will be common, fewer
things will stand out…KNOW THE STAND
OUTS!
Classification of Viruses
◻ Viruses are either DNA or RNA, naked or
enveloped, icosahedral or helical, single
stranded or double stranded, linear or
circular, segmented or non-segmented,
and positive or negative (if they’re RNA).
◻ Sounds like a lot to memorize, but if you
an organize them into groups, it will be a
life saver on your Step 1.
DNA Viruses
◻ There are 7 DNA viruses, they are ALL
icosahedral!
◻ (Except Pox which is “complex”)
◻ But the point is that NONE are helical, so
if there is an answer choice that says
“helical DNA” it’s WRONG!!!
DNA Viruses
◻ So like I said, there are 7 DNA viruses, all
icosahedral (except Pox = complex)
◻ They are also all DS (except Parvo = SS)
…you will remember this bc parvus is
Latin for small and it’s the smallest DNA
virus bc it’s the only one that is single
stranded
DNA Viruses
◻ 4 DNA viruses are linear (HPAP:
Herpes and Poxvirus which are
enveloped and Adenovirus and
Parvovirus which are non-enveloped)
◻ 2 are circular (Polyoma and Papilloma
which collectively used to be called
Papova so remember that they go
together; they are also “supercoiled”
which I don’t think is important; they are
ALSO non-enveloped so that’s easy)
◻ 1 is “incomplete circular”:
HepaDNAvirus (gives you Hep B, all of
HepaDNAvirus Structure
RNA Viruses
◻ There are A LOT MORE RNA viruses!
About 15 that you need to know.
◻ ALL RNA viruses are SS!!!
 Except Reovirus/Rotavirus (10-11
segments!!!)
◻ 7 are icosahedral and linear w/ +
polarity:
 4 nakee: PicoRNAvirus, HepEvirus,
Calicivirus (Noro), Reo/Rotavirus (not +
bc DS)
 3 enveloped: Flavi, Toga, Retro (party
RNA Viruses
◻ 7 are helical (these are ALL enveloped)
 4 linear w/ neg polarity: Orthomyxo, Paramyxo,
Rhabdo, Filo
■ Note! Orthomxyo is the Flu and has 8
segments!
 1 linear w/ pos polarity: Corona
 3 circular w/ neg polarity:
■ Arena (2 segs)
■ Bunya (3 segs)
■ Delta (no segs)

◻ 1 is “uncertain” (Deltavirus AKA Hep D)

 This one is also enveloped, circular, and
negative
But what do all these
cause?!?
◻ Let’s do a brief overview of what all of
these cause, you should have already
learned this, so I’m not going into super
detail…
◻ We’ll start with the DNA viruses!
 Remember, 4 are naked, 3 are enveloped…
 Herpes, Hepadna, and Pox are
enveloped, those are all pretty big and
weird so you should be able to remember
that and then, the other ones are the other
ones!
BUT FIRST, A
PRACTICE
QUESTION!
Viral particles have been isolated from the blood of an
8 yo M. The particles are non-enveloped, SS DNA. The
pt most likely suffers from:

◻ Bronchiolitis
◻ Acute hepatitis
◻ Erythema infectiosum
◻ Rubella
◻ Chickenpox
◻ Mumps
Viral particles have been isolated from the blood of an
8 yo M. The particles are non-enveloped, SS DNA. The
pt most likely suffers from:

◻ Bronchiolitis
◻ Acute hepatitis
◻ Erythema infectiosum (Fifth disease)
◻ Rubella
◻ Chickenpox
◻ Mumps
Parvovirus B19
◻ Remember it’s genome?
 Naked, SS DNA (so obvi icosahedral then,
see?!)
◻ Replicates in upper resp tract or erythroid
precursor cells in BM (important to
know!)
◻ Causes? Erythema infectiosum (5th
disease)
 Symptoms? Common and then less
common…
■ Flu-like
illness w/ slapped cheek rash/lacey
body rash
■ Aplastic anemia! (will be person w/ sickle cell or
Papilloma Virus (HPV)
◻ Remember it’s genome?
 Naked, DS DNA (again, obvi icosahedral, duh!)
◻ Replication depends on HOST CELL polymerases
(what a bum)
◻ Causes?
 Warts, which serotypes?
■ 6 & 11
 Cervical cancer, which serotypes?
■ 16 & 18
◻ Big buzzword for this virus?
 Koilocytes! What are these?
■ Squamous epithelial cells w/: nuclear enlargement,
hyperchromasia (dark nucleus), and a “perinuclear halo”
Polyoma Virus
◻ Remember it’s genome? Hint: Same as
HPV!
 Naked, DS DNA (again, obvi icosahedral,
duh!)
◻ Who does this infect? (What pt
population?)
 Immunocompromised! (Transplant, HIV, etc)
◻ What 2 things can it cause?
 JC Virus, what’s this?
■ PML(progressive multifocal
leukoencephalopathy)
Adenovirus
◻ Remember it’s genome? Hint: Same as HPV
and Polyoma!
 Naked, DS DNA (again, obvi icosahedral, duh!)
◻ Remember that this one is spread by droplets,
close contact, and the oral-fecal route so…that
means it causes???
 Acute respiratory tract infections (RTIs)
 Gasteroenteritis and diarrhea
 And what other weirdo? Close contact? Eyeball?
■ Conjunctivitis!
 Also one more weirdo, (rare), usually seen in
kids…?
■ Hemmorhagic cystitis, eek!
Alright, on to the Herpes!
(8)
◻ It is IMPORTANT to know that all of the herpes
viruses can develop syncytia, can cause
viremia, and ALL become latent!
◻ Cell-mediated immune response is protective,
but the herps avoid the humoral
(antibody) immune response via these
syncitia…
◻ Syncitia: multinucleated giant cells that allow
viral spread from cell to cell. KNOW THIS!!!
◻ Test for this is the “Tzanck” test!
◻ Also…COWDRY TYPE A INCLUSION BODS!
(intraNUCLEAR)…
BZZZZZZZZZZZZZZZZZZZ!
Herpes Types…
◻ 3 types: alphaherpes, betaherpes,
gammaherpes
◻ Alpha: HSV1, HSV2, VZV
 Target mucoepithelial cells
 Latent in dorsal root ganglia
◻ Beta: CMV, HHV6 (roseola AKA exanthema
subitum AKA 6th dz), and HHV7 (don’t care)
 Lymphotrophic
 Latent in monocytes/lymphocytes
◻ Gamma: EBV and HHV8 (Kaposi’s
sarcoma)
 Lymphotrophic
 Latent in B cells!
HSV 1 & 2
◻ HSV 1: causes oral herpes and eye
herpes
 #1 cause of what (hint it’s a neuro dz)???
■ Viral encephalitis!!! Where is it?
■ TEMPORAL LOBE!  memory/confusion! What do we
give?
■ STAT IV ACYCLOVIR PLEASE!!!

 Also causes what random thingy? Fingers?

■ Herpetic whitlow
◻ HSV 2: causes genital herpes
VZV
◻ Starts in respiratory tract,
disseminates via viremia to skin, this
seems important!
◻ First timers get???
 Chicken pox!
◻ Reactivation leads to???
 Shingles! (Zoster)…signs/symptoms?
■ Dermatomally distributed vesicopapular rash!
■ Often can be preceded by pain for 4-7 days, if
lingers?
■ Post-herpetic neuralgia :/
QUICK SIDE NOTE!!!
◻ Reye’s syndrome: can happen after VZV,
but also can happen after the Flu, or
really any viral infection…what’s the buzz
association?
 ASPIRIN!
◻ What do you need to know about Reye’s?
 Affects brain and liver, causes
hypoglycemia
 CMV
◻ In healthy people, it can cause a picture similar to EBV
but heterophile ab (Monospot) test will be neg!
◻ MCC of what???
 Congential viral infection!!! What’s it look like?
■ At birth: Microcephaly, blue-berry muffin rash, HSM, seizures
■ First few yrs of life: Low vision, hearing loss, mental retardation
◻ What are some things it can cause in
immunocompromised pts? Name 5 things…
 Encephalitis
 Gastroenteritis
 Retinitis (tx w/ Cidofovir!...altho bad S/E prof so
Valgan also works)
 Hepatitis
 Pneumonia
◻ What are CMV’s inclusion bodies called?
 “owl eye” inclusions! (intranuclear)
HHV6 (Roseola)
◻ HHV6=6th dz=Roseola=exanthema
subitum…
◻ Looks like?
 Baby (usually 6 months – 2 years old)
 High fevers (like 102-104 F) for several
days, usually subsides BEFORE diffuse
macular rash which begins on the trunk
(and usually doesn’t affect the face like the
measles does)
 Beware, these fevers can  seizures!
EBV
◻ So this is mono (duh)…and will have a +
heterophile ab test (aka pt serum agglutinates
tube RBCs)
◻ Mono symptoms
 Pharyngitis, fever, lymphadenopathy, HSM
◻ EBV infects/is latent in which cells?
 B cells!
◻ EBV’s blood smear will show which cells?
 Atypical T lymphocytes!
◻ EBV is associated w/ a myriad of cancers! Which
ones?
 Lymphomas in immunocompromised pts
 Burkitt’s lymphoma in African children (on Step)
 Nasopharyngeal carcinoma in Chinese people (on
Step)
HHV8 (Kaposi’s)
◻ This will affect what patient population?
 AIDS pts! (really all pts w/ low CD4s)
◻ What’s it look like? (will likely be a pic)
Pox Viruses
◻ Variola (small pox): eradicated
◻ Vaccinia (cow pox): used in the small pox
vaccine
◻ Molluscum contagiosum: spread by
contact (including sexual transmission),
buzzwords will be small, pearl-like,
pink/skin-colored nodules or papules on
the skin, self-limiting dz
◻ NOT Chicken Pox (this is VZV, a herp,
DUH!)
 Hepatitis…es?
•HAV: (Picornavirus: naked icosahedral
+ssRNA)
•HBV: (Hepadnavirus: enveloped

icosahedral circular partially dsDNA)

•HCV: (Flavivirus: enveloped icosahedral -

ssRNA)
•HDV: (Deltavirus: dysfunctional, w/ HBV

only)
•HEV: (naked icosahedral RNA…
Hepatitis Exposure
Question!
THERE WILL
ALMOST
CERTAINLY BE A
QUESTION LIKE
THIS ON STEP 1!

SORRY
A 45-year-old man was seen by his physician with a history of fever, loss of appetite,
nausea, and vomiting. He was also slightly jaundiced. A blood sample was drawn
and sent to the laboratory for a hepatitis screen. The following are the results:

HAV-IgM +
HAV-IgG -
HBsAg +
HBeAg +
HBcIgM -
HBcIgG +
Anti HCV (ELISA screen)+
Anti HCV (RIBA3) -

Which of the following states of infection(s)/exposure(s) do these results indicate?

HAV HBV HCV
A. Past Carrier/Chronic yes
B. Past Present/Acute no
C. Present Carrier/Chronic no
D. Present Carrier/Chronic yes
B. Present Present/Acute yes
A 45-year-old man was seen by his physician with a history of fever, loss of appetite,
nausea, and vomiting. He was also slightly jaundiced. A blood sample was drawn
and sent to the laboratory for a hepatitis screen. The following are the results:

HAV-IgM +
HAV-IgG -
HBsAg +
HBeAg +
HBcIgM -
HBcIgG +
Anti HCV (ELISA screen)+
Anti HCV (RIBA3) -

Which of the following states of infection(s)/exposure(s) do these results indicate?

HAV HBV HCV
A. Past Carrier/Chronic yes
B. Past Present/Acute no
C. Present Carrier/Chronic no
D. Present Carrier/Chronic yes
B. Present Present/Acute yes
A 45-year-old man was seen by his physician with a history of fever, loss of appetite,
nausea, and vomiting. He was also slightly jaundiced. A blood sample was drawn
and sent to the laboratory for a hepatitis screen. The following are the results:

HAV-IgM +
HAV-IgG -
HBsAg +
HBeAg +
HBcIgM -
HBcIgG +
Anti HCV (ELISA screen)+
Anti HCV (RIBA3) -

Which of the following states of infection(s)/exposure(s) do these results indicate?

HAV HBV HCV
A. Past Carrier/Chronic yes
B. Past Present/Acute no
C. Present Carrier/Chronic no
D. Present Carrier/Chronic yes
B. Present Present/Acute yes
A 45-year-old man was seen by his physician with a history of fever, loss of appetite,
nausea, and vomiting. He was also slightly jaundiced. A blood sample was drawn
and sent to the laboratory for a hepatitis screen. The following are the results:

HAV-IgM +
HAV-IgG -
HBsAg +
HBeAg +
HBcIgM -
HBcIgG +
Anti HCV (ELISA screen)+
Anti HCV (RIBA3) -

Which of the following states of infection(s)/exposure(s) do these results indicate?

HAV HBV HCV
A. Past Carrier/Chronic yes
B. Past Present/Acute no
C. Present Carrier/Chronic no
D. Present Carrier/Chronic yes
B. Present Present/Acute yes
A 45-year-old man was seen by his physician with a history of fever, loss of appetite,
nausea, and vomiting. He was also slightly jaundiced. A blood sample was drawn
and sent to the laboratory for a hepatitis screen. The following are the results:

HAV-IgM +
HAV-IgG -
HBsAg +
HBeAg +
HBcIgM -
HBcIgG +
Anti HCV (ELISA screen)+
Anti HCV (RIBA3) -

Which of the following states of infection(s)/exposure(s) do these results indicate?

HAV HBV HCV
A. Past Carrier/Chronic yes
B. Past Present/Acute no
C. Present Carrier/Chronic no
D. Present Carrier/Chronic yes
B. Present Present/Acute yes
A 45-year-old man was seen by his physician with a history of fever, loss of appetite,
nausea, and vomiting. He was also slightly jaundiced. A blood sample was drawn
and sent to the laboratory for a hepatitis screen. The following are the results:

HAV-IgM +
HAV-IgG -
HBsAg +
HBeAg +
HBcIgM -
HBcIgG +
Anti HCV (ELISA screen)+
Anti HCV (RIBA3) -

Which of the following states of infection(s)/exposure(s) do these results indicate?

HAV HBV HCV
A. Past Carrier/Chronic yes
B. Past Present/Acute no
C. Present Carrier/Chronic no
D. Present Carrier/Chronic yes
B. Present Present/Acute yes

How could you tell if HBV antibodies are from

immunization or infection?
A 45-year-old man was seen by his physician with a history of fever, loss of appetite,
nausea, and vomiting. He was also slightly jaundiced. A blood sample was drawn
and sent to the laboratory for a hepatitis screen. The following are the results:

HAV-IgM +
HAV-IgG -
HBsAg +
HBeAg +
HBcIgM -
HBcIgG +
Anti HCV (ELISA screen)+
Anti HCV (RIBA3) -

Which of the following states of infection(s)/exposure(s) do these results indicate?

HAV HBV HCV
A. Past Carrier/Chronic yes
B. Past Present/Acute no
C. Present Carrier/Chronic no
D. Present Carrier/Chronic yes
B. Present Present/Acute yes
Immunization only involves exposure and antibody
formation to surface antigen (HBsIg). This antibody is
to core protein. Plus you see Hbe in the blood….
A 45-year-old man was seen by his physician with a history of fever, loss of appetite,
nausea, and vomiting. He was also slightly jaundiced. A blood sample was drawn
and sent to the laboratory for a hepatitis screen. The following are the results:

HAV-IgM +
HAV-IgG -
HBsAg +
HBeAg +
HBcIgM -
HBcIgG +
Anti HCV (ELISA screen)+
Anti HCV (RIBA3) -

Which of the following states of infection(s)/exposure(s) do these results indicate?

HAV HBV HCV
A. Past Carrier/Chronic yes
B. Past Present/Acute no
C. Present Carrier/Chronic no
D. Present Carrier/Chronic yes
B. Present Present/Acute yes
Hepatitis C Testing
ELISA for anti-
HCV

RIBA
(recombinant immunoblot
assay)

RT-PCR for HCV RNA

A 45-year-old man was seen by his physician with a history of fever, loss of appetite,
nausea, and vomiting. He was also slightly jaundiced. A blood sample was drawn
and sent to the laboratory for a hepatitis screen. The following are the results:

HAV-IgM +
HAV-IgG -
HBsAg +
HBeAg +
HBcIgM -
HBcIgG +
Anti HCV (ELISA screen)+
Anti HCV (RIBA3) -

Which of the following states of infection(s)/exposure(s) do these results indicate?

HAV HBV HCV
A. Past Carrier/Chronic yes
B. Past Present/Acute no
C. Present Carrier/Chronic no
D. Present Carrier/Chronic yes
B. Present Present/Acute yes
RNA VIRUS
QUESTION!
Picornaviruses are small SS RNA viruses. Which of
the following picornavirus is the most acid-labile?

◻ A: Poliovirus
◻ B: Echovirus
◻ C: Rhinovirus
◻ D: Coxsackie A virus
◻ E: Hep A virus
Picornaviruses are small SS RNA viruses. Which of
the following picornavirus is the most acid-labile?

◻ A: Poliovirus
◻ B: Echovirus
◻ C: Rhinovirus (grows in 33C aka
COLD!)
◻ D: Coxsackie A virus
◻ E: Hep A virus
What (naked icosahedral) RNA
viruses cause:
◻ PicoRNAviruses: “PERCH”
 Polio, Echo, Rhino, Coxsackie A&B, Hep A
■ Polio: most infxns subclinical; flaccid paralysis
■ Echo: URIs, rash, infantile diarrhea, meningitis
■ Rhinovirus: common cold! (acid-labile!!!)
■ Coxsackie A: herpangina, hand/foot/mouth dz, acute
hemorrhagic conjunctivitis
■ Coxsackie B: pericarditis and myocarditis
■ Hep A: epidemic hepatitis (self-limiting illness w/
fatigue, weight loss,fever, abd pain, w/ or w/o
jaundice)
■ KNOW: usually caused by ingestion of contaminated food
(like shellfish) or water…it replicates in hepatocytes!!!
What (naked icosahedral) RNA
viruses cause:
◻ Calicivirus: Norovirus (epidemic
gastroenteritis)
 Hep E used to be Calici but is now
“Hepevirus”
■ Resembles HAV infxn-wise, high mortality
rate in preggies
◻ Reovirus: Rotavirus (11 SEGS!) replicates
in enterocytes, happens a lot in winter,
fever/vom/watery diarrhea in infants and
kids
◻ Astrovirus (need to know?):
What (env icosahedral) RNA
viruses cause:
◻ Flaviviruses:
 Hep C: can lead to chronic hep, cirrhosis, HCC
 Yellow Fever: spread by mosquitos (Aedes aegypti)
■ Sx: fever/n/v/GIT hemmorhage/jaundice
 Dengue: also spread by mosquitos (Aedes aegypti)
■ 1) asymptomatic
■ 2) dengue fever (breakbone, petechial rash)
■ 3) dengue hemorrhagic fever
■ 4) dengue shock syndrome (cross-reactive antibodytoo many
cytokines & complementDIC!)
 West Nile: also mosquitos (Culex)
■ Encephalitis and GBS-like syndrome
 St. Louis Encephalitis (Culex)
 Japanese encephalitis (Culex)
What (env icosahedral) RNA
viruses cause:
◻ Togaviruses: Alphavirus & Rubivirus
 Alphavirus: EEE and WEE
■ Spread by mosquitos! (Culex and Culiseta)
■ EEE worse (higher mortality) than WEE
■ EEE AKA “sleeping sickness” but NOT Trypanosoma
bruceii
 Rubivirus: Rubella!!!
■ Remember infxn of fetus in FIRST trimester!!!
■ Sx? MR, heart malformations, deafness, cataracts,
etc.
◻ Retrovirus: Oncovirus & Lentivirus
 Oncovirus: Human T-cell Leukemia
■ Tropical spastic paraparesis after >20 yr
latency
 Lentivirus: HIV (more on this later…)
What (env helical linear) RNA
viruses cause:
◻ Orthomyxoviruses: Flu A&B (8 segments), Flu
C (7 segments bc has HEF (hemagglutinin
esterase fusion) instead of HA+NA)
◻ Paramyxoviruses: Measles, Mumps
(parotitis, orchitis, aseptic meningitis),
Parainfluenza (Croup), RSV (bronchiolitis)
◻ Rhabdovirus: Rabies (MC from bats!!!)
◻ Filoviruses: Ebola and Marburg virus, eek!
◻ Coronavirus: common cold and SARS
 + polarity (it’s always positive to have a beer!)
What (env helical circular) RNA
viruses cause:
◻ Arenaviruses: 2 segments! LCMV
(lymphocytic choriomeningitis) and Lassa
fever virus
◻ Bunyaviruses: 3 segments! Encephalitis,
Korean hemorrhagic fever, Hantaviruses
(Sin Nombre virus)
◻ Deltavirus: No segs (covalently closed
circle), HDV (HBV required for infxn bc
HbsAg serves as the outer protein coat of
HDV)
An 8 yo Middle Eastern immigrant is brought to
clinic w/ low-grade fever and a skin rash that
started on his face and spread down his body. PE
reveals postauricular tenderness. Who am I?

◻ Herpesvirus
◻ Togavirus
◻ Reovirus
◻ Paramyxovirus
◻ Parvovirus
An 8 yo Middle Eastern immigrant is brought to
clinic w/ low-grade fever and a skin rash that
started on his face and spread down his body. PE
reveals postauricular tenderness. Who am I?

◻ Herpesvirus
◻ Togavirus (Rubella…postauricular
tenderness!!!)
◻ Reovirus
◻ Paramyxovirus
◻ Parvovirus
LIGHTNING ROUND…EASY
◻ Koplik’s spots:
 Measles…Where?
 Buccal mucosa @ 3rd molar
◻ Negri bodies:
 Rabies!!!
◻ Slapped-cheek syndrome:
 Parvovirus B19
◻ Owl-eye inclusions:
 CMV
◻ Sterility secondary to bilateral orchitis:
 Mumps
LIGHTNING ROUND…EASY
◻ Hairy leukoplakia:
 EBV…How do you test for EBV?
 Heterophile antibody test (Monospot)
◻ Motor neuron destruction paralysis:
 Poliovirus…What else can Poliovirus cause?
 Aseptic meningitis
◻ Hemagglutinin and neuraminidase:
 Influenzas/Orthomyxovirus…AND?
 Mumps and Parainfluenza (but both
activities on same spike)
LIGHTNING ROUND…EASY
◻ Maculopapular rash
 Measles
◻ Dumbbell shaped core:
 Poxvirus
◻ Prairie dogs:
 Monkeypox
◻ Culex mosquitoes:
 West Nile & St. Louis Encephalitis
◻ Breakbone fever:
 Dengue.
■ Four dengue clinical syndromes?
■ 1) asymptomatic 2) dengue fever (breakbone,
petechial rash) 3) dengue hemorrhagic fever 4)
dengue shock syndrome (cross-reactive antibody)
LIGHTNING ROUND…EASY
◻ Most common viral respiratory infection amongst
infants:
 RSV.
■ Treat with?
■ Aerosolized ribavirin
◻ Viral croup (laryngotracheobronchitis):
 Parainfluenza
◻ Acid labile & replication @ 33°C:
 Rhinovirus
◻ Acid stable & replication @ 37°C:
 Enteroviruses
◻ Enterovirus causing pericarditis/myocarditis:
 Coxsackie B
◻ Shellfish/cruise ship gastroenteritis:
 Norovirus (a Calicivirus)
LIGHTNING ROUND…EASY
◻ Latency associated transcripts:
 Herpes!
◻ Heterophile antibody negative
mononucleosis:
 CMV
◻ Risk of transmission increased w/
membrane rupture >6 hrs before
delivery:
 HSV-2
◻ Trigeminal ganglia latency:
 HSV-1, VZV
◻ Dermatomal pruritic rash:
LIGHTNING ROUND…
MEDIUM
◻ Macularpapularvesicularcrusts @
mucocutaneous borders:
 HSV-1
◻ Endothelial cell cancer:
 Kaposi’s Sarcoma (HHV-8)
◻ Progressive Multifocal Leukoencephalopathy:
 JCV (Polyomavirus)…What cells are infected?
 Oligodendrocytes and astrocytes
◻ Eczema as contraindication for vaccination:
 Vaccina
 What pox doesn’t cross-immunize with the
rest? Molluscum contagiosum
LIGHTNING ROUND…
MEDIUM
◻ Tropical spastic paraparesis:
 HTLV, What else does HTLV cause?
 ATL (Adult T-cell Lymphoma)
◻ Lumbosacral ganglia latency:
 HSV-2
◻ Burkitt’s lymphoma:
 EBV. What oncogene gets activated?
 c-myc
◻ Limbic system infection:
 Rabies
◻ Dane particles:
 Hep B!
 LIGHTNING ROUND…HARD
◻ Epidemic non-bacterial gastroenteritis (90%):
Norovirus…What family?
 Calicivirus…What’s the genome?
 Naked, icosahedral, +ssRNA
◻ Acute hemorrhagic conjunctivitis:
 Enterovirus (Coxsackie A)
◻ Zoonotic virus w/ near 100% mortality:
 Filoviridae (Ebola and Marburg) & Rhabdovirus
◻ Arbovirus w/ 50% mortality:
 Eastern equine encephalitis. Which is in what family?
■ Togaviridae
◻ NSP4 enterotoxin:
 Rotavirus…Affects flow of what ion?
 Calcium
 LIGHTNING ROUND…HARD
◻ Shepherd’s crook structure:
 Filoviridae
◻ Hemagglutinin, w/o neuraminidase:
 Measles
◻ Genes: pol, env, pre-core, X:
 Hepatitis B. Genome?
 Comedy central logo! (Partially dsDNA)
◻ Penton:
 Adenovirus. Does what?
 Triggers endocytosis by binding integrins
◻ E6 & E7:
 HPV. Do what?
 E6 destroys p53; E7 binds pRbs releasing E2F repair
and replication proteins
 LIGHTNING ROUND…HARD
◻ DC-SIGN:
 HIV. What’s this?
 Gp120’s receptor on dendritic cells
◻ Koilocytes:
 HPV! Which serotypes can lead to cancer?
 16 & 18!
◻ Zoonotic virus associated w/ abortions?
 LCMV (Lymphocytic choriomeningitis virus) What
family?
 Arenavirus…What’s the genome?
 Enveloped, helical, -ssRNA, 2 segments!
◻ Erythroblast P antigen:
 Parvovirus B19!!!!!
NOW FOR MORE ON
HIV…
HIV Classification and
Structure

◻ A pathogenic
human retrovirus
 Lentiviruses:
■ HIV-1 and HIV-2
 Oncoviruses:
■ HTLV-I and HTLV-II
HIV Lifecycle – Early Events
◻ Cells targeted
 CD4+ T cells,
macrophages,
microglial cells
◻ Viral attachment
 Viral gp120 binds to
CD4+ molecule
 CCR5 or CXCR4
coreceptor binding
◻ Viral fusion
 Gp41
transmembrane
protein

J Ctr Cancer Res, NCI

2008
HIV Lifecycle – Early Events
(cont)
◻ Disassembly
◻ Reverse
transcription
◻ Nuclear Transport
◻ Integration

AIDSInfoNet.org;
Mandell, Principles and Practice of Infectious Diseases. 7 th Ed.
HIV Lifecycle – Late Events
◻ Transcription
◻ Assembly
◻ Budding
◻ Maturation

Proteas
e

AIDSInfoNet.org
Consequences of HIV
infection
◻ HIV Targets specific cells
 CD4+ receptor is present on:
■ CD4+ T helper cells – critical for presentation and
elimination of intracellular pathogens
■ Macrophages, monocytes, dendritic cells, microglial
cells, neurons
◻ Combination of direct infection and killing of
CD4+ cells and host inflammatory response
leads to gradual depletion of immune system
 Death from AIDS without therapy
◻ Integrated virus lasts for the life of the cell
 Infection for life in the case of neurons
 HIV- specific targets
Integrase Protease
Inhibitors Inhibitors

Reverse
Attachmen Fusion Transcriptase
t (CCR5) Inhibitor Inhibitors (NRTI,
Inhibitors s NNRTIS)
ANTI-VIRAL
QUESTION!
A patient stumbles into the ER with history of new onset seizure,
memory loss and worsening confusion. You are worried that this
patient’s state may progress to coma so you begin empiric
treatment with:

◻ Ribavirin
◻ Amantidine
◻ Lamivudine
◻ Efavirenz
◻ Acyclovir
A patient stumbles into the ER with history of new onset seizure,
memory loss and worsening confusion. You are worried that this
patient’s state may progress to coma so you begin empiric
treatment with:

◻ Ribavirin
◻ Amantidine
◻ Lamivudine
◻ Efavirenz
◻ Acyclovir!!! Since HSV-1 is the most
common cause of viral encephalitis,
you should treat with Acyclovir to
avoid coma/death!
Antivirals
◻ A-, gan-, fam-, valacyclovir: guanosine
analogues, prodrugs, P’d by thymidine
kinase
 Val’s cost more $$$ than others but work
better!
 Give Val’s if your pt has good insurance!
◻ Foscarnet: pyrophosphate analogue,
inhibits HSV DNA pol; for Acyclovir-
resistant infections!
◻ Oseltamivir & zanamivir: block
Neuraminidase (prevents budding)
Antivirals
◻ Cidofovir: Cytosine analogue
 For CMV patients w/ HIV associated retinitis
◻ Hep B: interferon alpha and Entecavir
◻ Hep C: pegylated interferon-alpha w/ oral
Ribavirin!!!
◻ Be sure you know that interferon’s side
effect is depression that can lead to
suicide!!!
Overview of ARTs…
◻ mArAviroc: AttAchment inhibitor (CCR5)
◻ enFuvirtide: Fusion inhibitor
◻ NRTI/NNRTIs: reverse transcriptase
blockers
◻ Raltegravir: “teg” blocks inTEGrase
◻ Things that end in “navir”: Protease
inhibitors
ART – Entry Inhibitors
◻ CCR5 Receptor Antagonist
 Maraviroc
 Binds to the transmembrane coreceptor cavity,
which prevents interaction of the V3 loop of
gp120 with the CCR5 coreceptor
◻ Fusion Inhibitors
 Enfuvirtide
 Binds to gp41
 Inhibits fusion blocking the conformational
change in gp41 required for membrane fusion
and entry into CD4 cells
 ART –
Reverse Transcriptase Inhibitors
◻ Nucleoside/Nucleotide Reverse
Transcriptase Inhibitors
 Zidovudine, stavudine, tenofovir,
lamivudine, emtricitabine,
didanosine, abacavir
 Nucleoside or nucleotide
analogues
■ Compete with naturally occurring
nuceloside/tide for inclusion in chain
■ Serve as chain terminators
◻ Non-nucleoside reverse
transcriptase inhibitors
 Efavirenz, delavirdine, nevirapine,
etravirine, rilpivirine
 Bind to hydrophobic pocket of RT
changing confirmation and
inhibiting DNA polymerization
ART – Protease Inhibitors
◻ Saquinavir, ritonavir,
indinavir, nelfinavir,
amprenavir, lopinavir,
atazanavir, fosamprenavir,
tipranavir, darunavir
◻ Competitively inhibit
protease:
 Bind to the active site by
mimicking the transition state
of protease’s actual substrates
ART – Integrase Inhibitors
◻ Raltegravir, Elvitegravir
◻ Integrase performs two functions
 3’ end processing of viral DNA
 DNA strand transfer
 Current ARV
Medications
NRTI PI Integrase Inhibitor
▪ Abacavir (ABC) ▪ Atazanavir (ATV) (II)
▪ Didanosine (ddI) ▪ Darunavir (DRV) ▪ Raltegravir (RAL)
▪ Emtricitabine (FTC) ▪ Fosamprenavir (FPV) ▪ Elvitegravir* (EVG)
▪ Lamivudine (3TC) ▪ Indinavir (IDV)
▪ Stavudine (d4T) Fusion Inhibitor
▪ Tenofovir (TDF) ▪ Lopinavir (LPV) ▪ Enfuvirtide (ENF, T-20)
▪ Zidovudine (AZT, ZDV) ▪ Nelfinavir (NFV)
▪ Ritonavir (RTV) CCR5 Antagonist
NNRTI ▪ Saquinavir (SQV) ▪ Maraviroc (MVC)
▪ Delavirdine (DLV) ▪ Tipranavir (TPV)
▪ Efavirenz (EFV)
▪ Etravirine (ETR)
▪ Nevirapine (NVP)
▪ Rilpivirine (RPV)
SWITCHING TO
BACTERIA NOW…
WE’LL START WITH
STAPHY!
(My fav)
BUT FIRST, A
PRACTICE
QUESTION!
A 24 yo F presents to your office w/ burning urination,
urgency and frequency. She is sexually active. UCx shows
catalase-pos, gram-pos cocci. The organism responsible
for this pt’s sx is most likely:

◻ Coagulase positive
◻ Hemolytic
◻ Novobiocin resistant
◻ DNase positive
◻ Yellow pigment producer
A 24 yo F presents to your office w/ burning urination,
urgency and frequency. She is sexually active. UCx shows
catalase-pos, gram-pos cocci. The organism responsible
for this pt’s sx is most likely:

◻ Coagulase positive
◻ Hemolytic
◻ Novobiocin resistant (Staph sapro!!!)
◻ DNase positive
◻ Yellow pigment producer
Staphylococcus aureus
◻ Coagulase +, Catalase +
◻ Other important things it has:
 Surface Protein A (SPA)
■ Binds Fc portion of IgG
 Alpha toxin (not a superantigen!)
■ Creates pores causing hemolysis and tissue
damage
 Lipases = promote abscess formation!
Important!
 Staphylokinase = a fibrinolysin
 Hyaluronidase = hydrolyzes connective
tissue matrix
Staphylococcus aureus
◻ Before you start thinking about the crazy
things it causes, remember its primary
skin diseases…
 Folliculitis – hair follicles (gross)
 Furuncles – a deep folliculitis (grosser)
 Carbuncles – bunch o’ furuncles connected
(grossest)
 Impetigo – epidermis (honey crusted
lesions!!!)
 Erysipelas – dermal lymphatics (well
demarcated)
 Cellulitis – subcutaneous fat layer
Staphylococcus aureus
◻ Staph can spread through blood and
lymphatics to cause:
 Osteomyelitis (and possibly bone
abscesses)
 Septic arthritis
 Myositis
 Meningitis
 Endocarditis
 AND MORE!!!
Staphylococcus aureus
◻ But the most fun thing about Staph is its
TOXINS!!!
◻ The following toxins are
SUPERANTIGENS!!!
 TSST-1Toxic Shock Syndrome (a toxemia)
■ High
fever! HoTN! Sun burn! Desquamating
palms/soles!
 ExfoliatinScalded Skin Syndrome
■ Peely baby!
 EnterotoxinFood poisoning
■ Be sure to r/o the viruses: Noro! Rota! Astro!
Staphylococcus aureus
◻ Final thought…Staph is very resistant!
◻ PRSA (Penicillin resistant) =
production of Beta-lactamases via
plasmid…do you remember how Penicillin
works?
 Inhibits production of peptidoglycan cross-
links in the cell wall
◻ MRSA (Methicillin resistant) = altered
target (PBP2a) via mecA gene
Staphylococcus epidermidis
◻ Coagulase – (duh, Staph aureus is the
ONLY Coag + bacteria that you know!!!)
◻ Catalse +
◻ Novobiocin susceptible (zone of
inhibition!)
◻ Bacteria forms biofilms on medical
devices and prosthetic
implantsendocarditis!
◻ Normal flora!
◻ Vanc it!
Staphylococcus
saprophyticus
◻ Coagulase –, Catalase +
◻ Novobiocin resistant
◻ UTI (cystitis) in young, sexually active
females
 Pt complains of: frequency, urgency, and
dysuria (burning pain on urination)
 Urine is cloudy (pyuria)
◻ Please don’t get this question wrong! So
easy!
A 34 yo HIV+ M presents w/ sudden-onset fever, chills,
cough, and L-sided CP that worsens w/ deep breathing. PE
w/ bronchial breath sounds over LLL. CD4 is 800. Who am
I?

◻ Streptococcus pneumoniae
◻ Mycoplasma pneumoniae
◻ Pneumocystis jiroveci
◻ Staphylococcus aureus
◻ Legionella pneumophila
◻ Moraxella catarrhalis
◻ Mycobacterium tuberculosis
A 34 yo HIV+ M presents w/ sudden-onset fever, chills,
cough, and L-sided CP that worsens w/ deep breathing. PE
w/ bronchial breath sounds over LLL. CD4 is 800. Which is
the MOST LIKELY cause of his symptoms?

◻ Streptococcus pneumoniae
(COMMON THINGS ARE COMMON!!!)
◻ Mycoplasma pneumoniae
◻ Pneumocystis jiroveci
◻ Staphylococcus aureus
◻ Legionella pneumophila
◻ Moraxella catarrhalis
◻ Mycobacterium tuberculosis
STREPPY!
Streptococcus pyogenes
◻ Catalase –, Beta-hemolytic!, Bacitracin
susceptible
◻ Other important things it has:
 M Protein
■ Binds to factor H, destroying C3-convertase, prevents
opsonization by C3b!
 F protein – binds fibronectin on pharyngeal epithelial
cells
 Lipoteichoic acid – binds fibronectin on epithelial cells
 Hyaluronic acid capsule = not immunogenic so can be
very virulent! But also means can’t make vax
against.
 C5a peptidase – degrades C5a (chemotaxi!)
 Streptokinase = a fibrinolysin
 Hyaluronidase = hydrolyzes connective tissue matrix
 DNase = protect bacteria from being trapped in
neutrophil extracellular traps (NETs)…not that
important…
Streptococcus pyogenes
◻ So same as Staph, remember its primary skin
diseases…
 Impetigo – epidermis (honey crusted lesions!!!)
 Erysipelas – dermal lymphatics (well demarcated)
 Cellulitis – subcutaneous fat layer
 NECTROTIZING FASCIITIS WEE!!!
■ Exotoxin B…it’s a protease!!! KNOW!!!
◻ Other toxin-mediated diseases caused by Strep:
 Scarlet fever – strawberry tongue and red rash!
■ Via Erythrogenic toxin via lysogenic conversion!!!
 Strep TSS
■ Via Pyogenic Exotoxin A
◻ Oops I almost forgot! #1 cause of pharyngitis!
DUH!
Streptococcus pyogenes
◻ Sequelae?
 Acute rheumatic fever = carditis,
polyarthritis
■ After Strep throat only!
 Acute glomerulonephritis = immune
complex disease
■ After
Strep throat (1-2 weeks) or impetigo (3-4
weeks)
 Can test for anti-Streptolysin O (ASO)
■ Streptolysin O = inactivated by high O2 (needs
low levels)
■ Streptolysin S = not inactivated by O2
Streptococcus agalactiae
◻ Catalase – (duh!!!), B-hemolytic,
Bacitracin resistant!
◻ Hydrolyzes hippurate, + CAMP test
◻ Early onset: neonatal sepsis and
pneumonia
◻ Later onset: neonatal sepsis and
meningitis
◻ Screen baby-mama at 34-37 weeks!!!
 NOTE: baby w/ lethargy, poor muscle
tone, & respiratory stress could be from
botulism, GBS or Herpesvirus! Lots o’
floppy bebes!
Streptococcus pneumoniae
◻ Cat –, A-hemolytic (green), Optochin
susceptible, Souble in bile!, + Quellung rxn!
◻ Other important things it has:
 IgA protease
 Polysaccharide capsule – Major virulence
factor! Conjugate vax against 7 serotypes
(kids) or 23 serotypes (adults)…kids vax
coupled to carrier protein (diphtheria
toxoid) b/c kids can’t recognize T-cell ind.
antigens???
◻ Causes: pneumonia, meningitis, and otitis
media!
◻ Be aware that Influenza, Parainfluenza,
Rhinovirus, etc. can cause similar sx!
Viridans Strep
◻ Cat –, A-hemolytic, Optochin resistant,
NOT soluble in bile
◻ Normal flora in nasopharynx
◻ Causes: dental caries and endocarditis!
◻ Test question = patient who recently
underwent dental work presents to ER w/
heart probs…DUH!
Enterococcus…Group D
Strep?
◻ Cat –, miscellaneous-hemolytic, Optochin
resistant, hydrolyzes esculin, can
grow in bile and NaCl!!!
◻ Causes: UTI, endocarditis, wound infxns,
bacteremia, intra-abdominal abscesses
◻ VRE!!! D-ala, D-ala  D-ala, D-lac
 Gives this resistance to VRSA via
conjugation!
A 33 yo F presents to a fertility clinic for assessment. She has been attempting to
coneive for one yr w/o success and her monogamous male partner has been found to
have an adequate sperm count and motility. PMH sig for 15 yrs OCP use prior to 2 yrs
ago, purulent urethritis 5 yrs ago treated promptly w/ ceftriaxone, and HTN controlled
w/ methyldopa. Which of the following is the most likely major contributing factor in
her ability to conceive?

◻ Methyldopa oocyte toxicity

◻ Inadequate time of attempted conception
◻ Inappropriate abx therapy
◻ OCP-induced ovarian failure
◻ Advanced maternal age
A 33 yo F presents to a fertility clinic for assessment. She has been attempting to
coneive for one yr w/o success and her monogamous male partner has been found to
have an adequate sperm count and motility. PMH sig for 15 yrs OCP use prior to 2 yrs
ago, purulent urethritis 5 yrs ago treated promptly w/ ceftriaxone, and HTN controlled
w/ methyldopa. Which of the following is the most likely major contributing factor in
her ability to conceive?

◻ Methyldopa oocyte toxicity

◻ Inadequate time of attempted conception
◻ Inappropriate abx therapy
(Chlamydia!!!)
◻ OCP-induced ovarian failure
◻ Advanced maternal age
NEISSERIA!
Neisseria gonorrhoeae
◻ Gonorrhea
 Presents with:
■ Dysuria
■ Purulent,
“coffee cream-colored” urethral
discharge
 Sexually active patient (they will usually tell
you this in the case)
 Usually late teens to 30’s, but not
necessarily
Neisseria gonorrhoeae
◻ Disseminated gonococcal infections
 Strains resist complement lysis
■ Sialic acid added to gonococcal lipooligosaccharide
(similar to LPS, but shorter) makes it “look” like a
host molecule
 Gonococcal arthritis
■ Leading cause of septic arthritis in adults!!!
■ Spreads to joints via the blood (transient
bacteremia)
 Ophthalmia neonatorum
■ Gonococcal infection of the eyes in a newborn of a
mother with gonorrhea
■ Standard treatment of newborns’ eyes with
erythromycin ointment
Neisseria meningitidis
◻ Septic Meningitis
 Presents with:
■ Fever, malaise
■ Nuchal rigidity
■ Petechial rash and purpura (due to
meningococcemia)
■ LP shows cloudy CSF (mostly neutropils)
 Usually high school student at camp, or a
college student who lives in a dorm, or military
barracks
■ Associated with poor hygiene and communal living
areas
◻ Meningococcal vaccine produces protective
antibody against the polysaccharide
Neisseria meningitidis
◻ Meningococcemia = N. meningitidis in
the blood
 Encapsulated, so hard to clear from the
blood (“serum resistant”)
 Usually occurs with meningitis
 Can cause Disseminated Intravascular
Coagulation (DIC), which leads to:
■ Cortical necrosis of the kidneys
■ Can affect the brain and lungs
■ Causes infarction of the adrenal glands which
leads to adrenal insufficiency
■ A.k.a – Waterhouse-Friderichsen Syndrome!!!
Identification of Neisseria
◻ Cultured on Thayer-Martin Medium
 A specially formulated chocolate agar
■ (w/ factors V: NAD+ and X: hematin)
◻ All Neisseria are Gram negative diplococci
◻ All Neisseria are oxidase-positive
◻ Sugar metabolism (positive = production of
acid turns the medium yellow)
 N. gonorrhoeae = glucose only
 N. meningitidis = glucose + maltose
 N. sicca = glucose + maltose + sucrose
Bacteriology Round, Easy
◻ Coagulase +:
 Staph aureus…Breaks through clot with?
 Staphylokinase (a fibrinolysin)
◻ Can grow in bile:
 Enterococcus spp.
◻ Enzyme that promotes abscess formation:
 Lipase…What bacteria caries this?
 Staph aureus
◻ Cytokines responsible for fever, rash, vomiting, HoTN,
shock, & multiple organ failure:
 IL-1, IL-2, TNF (stimulated by superantigens…cytokine
storm!)
◻ Enzyme that confers Penicillin resistance:
 B-lactamase…This is transferred via:
 Plasmids!
An indigent alcoholic came to the ER with a fever
of 102, dyspnea, rales, and reduced lung sounds.
A smear made from fluid collected was loaded
with gram-positive, lancet-shaped diplococci.
The isolate was mucoid on blood agar, as well as
alpha-hemolytic. The isolate was susceptible to
optochin. A characteristic of this pathogen:

A. causes scarlet fever

B. leads to glomerulonephritis
C. is catalase positive
D. outer membrane protein
E. Undergoes autolysis when in bile salts
An indigent alcoholic came to the ER with a fever
of 102, dyspnea, rales, and reduced lung sounds.
A smear made from fluid collected was loaded
with gram-positive, lancet-shaped diplococci.
The isolate was mucoid on blood agar, as well
as alpha-hemolytic. The isolate was susceptible
to optochin. A characteristic of this pathogen:
A. causes scarlet fever
B. leads to glomerulonephritis
C. is catalase positive
D. outer membrane protein
E. Undergoes autolysis when in bile
salts –
S. pneumo!
An indigent alcoholic came to the ER with a fever
of 102, dyspnea, rales, and reduced lung sounds.
A smear made from fluid collected was loaded
with gram-positive, lancet-shaped diplococci.
The isolate was mucoid on blood agar, as well
as alpha-hemolytic. The isolate was
susceptible
A. causestoscarlet
optochin. A characteristic
fever- S. pyogenesof
this pathogen:
B. leads to glomerulonephritis- S. pyogen
C. is catalase positive- Staph spp. &
Neisserias
D. outer membrane protein- N. gonorrhea
E. Undergoes autolysis when in bile
salts –
S. pneumo!
Bacteriology Round,
Medium?
◻ LPS: Gram – …Components?
 Lipid A, O Ag, Core
◻ Alpha-hemolysis:
 Strep pneumo…and?
 Viridans Strep
◻ Optochin resistant:
 Viridans Strep…and?
 Enterococcus!
◻ IgA Protease:
 Strep pneumo & Neisserias…major virulence factor of Strep pneumo?
 POLYSACCHARIDE CAPSULE!
◻ Acute urethritis:
 N. gonorrhoeae
◻ Acute cystitis:
 Staph sapro
◻ Utilizes glucose AND maltose:
 N. meningitidis
A college student went to the campus clinic
complaining of sores on his arm. A smear was
made from one of the lesions exuding pus and
material was sent to the lab for culture. An
important virulence trait of the coagulase-
positive coccus identified in the lab is its
antiopsonic activity due to:

A. fibronectin-binding protein
B. hyaluronic acid capsule
C. M protein
D. outer membrane protein
E. protein A
A college student went to the campus clinic
complaining of sores on his arm. A smear was
made from one of the lesions exuding pus and
material was sent to the lab for culture. An
important virulence trait of the coagulase-
positive coccus identified in the lab is its
antiopsonic activity due to:

A. fibronectin-binding protein
B. hyaluronic acid capsule
C. M protein
D. outer membrane protein
E. protein A – Staph aureus!
A college student went to the campus clinic
complaining of sores on his arm. A smear was
made from one of the lesions exuding pus and
material was sent to the lab for culture. An
important virulence trait of the coagulase-
positive coccus identified in the lab is its
antiopsonic activity due to:
A. fibronectin-binding protein – Strep pyo
B. hyaluronic acid capsule – Strep pyo
C. M protein – Strep pyo
D. outer membrane protein – Neisseria
gonorrhoeae
E. protein A – Staph aureus!
Bacteriology Round, Hard?
◻ Hemorrhaging in adrenal glands:
 Waterhouse-Friderichsen syndrome…caused by?
 N. meningitidis…mechanism?
 Endotoxin…Shock-inducing component of endotoxin
 Lipid A!
◻ Altered PBP2a:
 Methicillin resistance…Who?
 MRSA…how?
 Chromosomal gene:
 mecA
◻ Acute glomerulonephritis:
 Strep pyo…What is it?
 Immune complex disease…comes after?
 Pharyngitis or impetigo
Cumulative Round, Hard?
◻ Baby meningitis:
 Strep agalactiae…but following diarrhea?
 Echovirus (an Enterovirusa Picornavirus)
◻ Gastroenteritis:
 Staph aureus…mechanism?
 Exotoxin…infection or intoxication?
 Intoxication…if cultures come back negative?
 Think: Astrovirus, Norovirus…Norovirus family?
 Calicivirus…genome?
 Naked, icosahedral, +ssRNA, non-seg!
◻ Arthritis in a 28 y/o P1G1 female:
 N. gonorrheoaea…Gram stain?
 G – diplococci…if cultures come back negative?
 Think Parvovirus B19
◻ Pharyngitis:
 Strep pyo!!!...if cultures come back neg?
 Think ICARE (Influenza, Corona, Adeno, Rhino, EBV)
Practice Question…
◻ A 3 year old toddler cries, pulls on his L
ear, and tells his mother it hurts. You
swab and plate on blood agar, and
expect to see…Associated with…
Practice Question…
◻ A 3 year old toddler cries, pulls on his L
ear, and tells his mother it hurts. You
swab and plate on blood agar, and
expect to see: Beta-hemolysis.
Associated with: Strep pneumo.
But wait…
◻ But, three days later, the mother calls
you stating her son has a fever,
wheezing, and a seal-bark cough. You
should shift your differential towards…
But wait…
◻ But, three days later, the mother calls
you stating her son has a fever,
wheezing, and a seal-bark cough. You
should shift your differential toward…
◻ HINT: the blood agar comes back with no
growth, and no hemolysis
But wait…
◻ But, three days later, the mother calls
you stating her son has a fever,
wheezing, and a seal-bark cough. You
should shift your differential towards…
◻ HINT: the blood agar comes back with no
growth, much less any hemolysis
◻ PARAINFLUENZA!
But wait…
◻ But, three days later, the mother calls
you stating her son has a fever,
wheezing, and a seal-bark cough. You
should shift your differential towards…
◻ HINT: the blood agar comes back with no
growth, much less any hemolysis
◻ PARAINFLUENZA!
◻ Strep pneumo can cause pneumonia
(wheezing, fever), but not really known
for croup (seal-bark cough). Classic
Parainfluenza in kids.
Rapid Review Charts!
◻ Coming up…in 3…2…1…!
 Staphylococcus
Staph aureus Staph epidermidis Staph saprophyticus
carotenoid pigment- creamy
Colonies yellow (pig X neut superoxides) white (no pig, not as virulent)

Blood Agar Hemolysis beta hemolyzes no no (grows on!)

Random ferments mannitol

Catalase/Coagulase yes/yes yes/no yes/no

Specialty Testing for ID sensitive to novobiocin resistant to novobiocin

Nose is main site, skin also,
occasionally vagina, rectum,
Source/Reservoir perineum)
hand contact, fomites (towels,
Transmission Modes lesions)

food poisoning, abscesses,

septicemia, endocarditis,
osteomyelitis, pyogenic (no food poisoning
impetigo/pyoderma,wound or TSS); 50% of artificial
infection, pneumonia, possibly device infections (skin
necrotizing fascitis (usually source)--> biofilm formation, pyogenic (no food poisoning
Pathology strep) bacteremia or TSS);
heavily contaminated
environment,
immunocompromised, esp. reduced humoral immunity; young
Predisposing Factors diabetes, IV use, CGD reduced humoral immunity; sexually active women
 Streptococcus
Strep.
Strep. pyogenes agalactiae Enterococcus Viridans
(Group A) (Group B) Strep Pneumococcus (Group D) Streptococci
Culture Stuff beta hemolyzes alpha, beta, or
(due to streptolysin gamma (no)
O and S) beta hemolyzes alpha hemolysis hemolysis alpha hemolysis
Capsule

polysaccharide capsule
(most important
virulence factor),
capsules swell
sialic acid rich w/specific antiserum
hyaluronic acid capsule (Quellung rx)
Antibiotic
Testing for bacitracin bacitracin optochin
ID susceptible resistant optochin susceptible optochin resistant resistant
Specialty
Testing for not bile-soluble ;
ID ASO assay (no can hydrolyze
lysis is positive, lysed by esculin (makes
two well change in bile/deoxycholate crystalline
Todd units, or a hydrolyzes (because of amidase in can hydrolyze glycoside black).
titer greater than hippurate; cell membrane esculin(makes Grows in 6.5%
240 @ time of positive CAMP activation)--> BILE crystalline glycoside NaCl or 40% bile
disease) test SOLUBILE black) slats
Source/ genital tract of
Reservoir skin, some in women (and
 Streptococcus
Strep. pyogenes Strep. agalactiae Strep Enterococcus Viridans
(Group A) (Group B) Pneumococcus (Group D) Streptococci
Transmission
Modes since lots of people usually originates
have it, not from own colonies
considered but can spread
respiratory droplets birth communicable nosocomially
Pathology
Neonatal Most common
pharyngitis, meningitis/sepsis, bacterial
cellulitis, impetigo, neonatal pneumonia pneumonia.
necrotizing fascitis, (early & late). Can Bacteremia, Nosocomial UTIs, Most common
strep TSS, cause endocarditis, meningitis, URI, endocarditis, urinary, cause of
rheumatic fever, arthritis, otitis media, biliary, CV infections; endocarditis.
acute osteomyelitis, sinusitis (esp. intra-abdominal or Dental caries,
glomerulonephritis; postpartum community aq), pelvic infections, brain
scarlet fever. endometriosis. pericarditis, sepsis. bedsores. abscesses.
Predisposing/
Resisting Factors

Intoxication,
aspiration,
respiratory tract
>18 hours of abnormalities/obstr
membrane rupture uctions, irritants;
ab to M protein, during birth; birth heart failure;
type-specific <37 weeks gestation; splenectomy, sickle
immunity (80 moms w/o ab to cell, nephrosis; urinary catheters/UT
serotypes) Group B elderly instrumentation
 Neisseria
N. gonorrhoeae N. menigitidis N.sicca
Culture grown on "chocolate" heated blood agar
and Thayer-Martin (chocolate + vanc, grows on Thayer-Martin inhibited on Thayer-
colistin, trimethoprim, nystatin) medium Martin medium
Endotoxins lipooligosaccharide,sialic acid (N
acetylneuraminic acid) can resist MAC ;
outer membrane proteins, this endo lipopolysaccharide in outer
weaker than m type, bacteremia not as membrane, causes fever and
severe here shock
Other Virulence pili mediate attachment to mucosa,
Factors antiphagocytic, associated with
virulence; opacity-associated outer
memrane protein (Opa); IgA protease IgA protease
Capsule polysaccharide capsule,
antiphagocytic. Causes at
no polysaccharide capsule least 13 serologic groups.
Specialty Testing glucose, maltose,
for ID maltose, glucose fermentation; and sucrose
Glucose fermentation only latex agglutination test fermentation
Source/Reservoir only humans, reproductive tract; only humans; membranes of
anorectal and pharyngeal too nasopharynx and flora of URI
Transmission
Modes sex, newborns at birth airborne droplets
Pathology Gonorrhoea (urethristis, dysuria,
purulent discharge, epididymitis in men) Meningitis, meningococcemia.
(women: purulentdischarge, PID, Purpura fulminans from DIC.
sterility, ectopic pregnancy). Septic Cortical necrosis in kidneys.
arthritis. Neonatal conjunctivitis Adrenal infarction--> death is
GRAM + RODS!
Healthy volunteers orally inoculated w/
pathogenic strains of C. dif do NOT develop
signs of infection. Why?
◻ Cell-mediated immunity
◻ Mucosal IgA abs
◻ Gastric acidity
◻ Intestinal biomass
◻ Rapid GI transit
Healthy volunteers orally inoculated w/
pathogenic strains of C. dif do NOT develop
signs of infection. Why?
◻ Cell-mediated immunity
◻ Mucosal IgA abs
◻ Gastric acidity
◻ Intestinal biomass
◻ Rapid GI transit
Clostridia
◻ Spore Formers
 Important because? – Spores are SUPER
hard to kill
◻ Obligate Anaerobes
 Important because? – They can live in
canned food!
◻ Ubiquitous in the soil
Clostridium tetani
◻ Local infection with systemic spread of
toxin
◻ Causes Tetanus
 Buzz words: spastic paralysis, trismus
(lockjaw), opisthotonus, risus sardonicus (a
characteristic grimace), terminal spore =
“tennis racket appearance”
◻ Tetanospasmin
 Blocks release of inhibitory
neurotransmitters GABA and glycine 
constant activation of motor neurons
◻ Typical presentation: Pt steps on a rusty
nail, Pt is a drug user doing “skin-popping”, Pt
is a neonate with an infected umbilical stump
Clostridium botulinum
◻ Can be an intoxication OR a local
infection with systemic spread of
toxin
 Foodborne botulism = intoxication
■ Typical
Presentation: Pt ate home-canned food
that was not cooked/improperly cooked
 Wound botulism = local infection w/ toxin
spread
■ Typical
Presentation: Pt is a drug-user who was
skin-popping black tar heroin
 Infantile botulism = local infection w/ toxin
spread
Clostridium botulinum
◻ Botulinum toxin
 Blocks release of acetylcholine
 Encoded by a lysogenic phage
◻ Buzz Words: flaccid paralysis,
descending weakness/paralysis,
diplopia, dysphagia, respiratory
muscle failure (IMPORTANT
COMPLICATION!!! BE READY TO
INTUBATE!)
Clostridium perfringens
◻ Causes Food Poisioning
 Enterotoxin action in the small intestine
■ Superantigen
■ Watery diarrhea, little vomiting, resolves in 24 hours
◻ Causes Gas Gangrene (Clostridial myonecrosis)
 Local infection with systemic toxin spread
 Alpha toxin: lecithinase, damages cell membranes
causing necrosis
 Typical presentation: War wound, or pt stepped on a
rusty nail
■ Puncture wounds are more likely to lead to gas gangrene
than open wounds (goes deeper and creates an anaerobic
environment)
 Buzz Words: CREPITUS!!!, double zone
hemolysis, Naegler test, hyperbaric oxygen
treatment
Clostridium difficile
◻ Most common cause of diarrhea in
hospitalized patients!
◻ Pseudomembranous colitis
 Pseudomembrane = yellow-white plaques
on colonic mucosa
 Associated with antibiotics, particularly
Clindamycin
■ C.
diff is carried in the GI tract, Clindamycin
wipes out the normal flora, then C. diff has a
chance to set up an infection
 Toxin A: causes diarrhea (fluid production
and mucosal damage)
 Toxin B: causes pseudomembrane
Bacillus anthracis
◻ Spore former
 Spores can be inhaled (pulmonary disease),
ingested (GI disease), or inoculated into a cut
(cutaneous disease)
◻ Cutaneous disease
 painless ulcer with black eschar (scab) and
edema, called a malignant pustule
◻ Pulmonary disease
 “wool-sorter’s disease”, hemorrhagic
mediastinitis, mediastinal widening shown
on chest x-ray (no classical features of
pneumonia)
Bacillus anthracis
◻ Toxins: encoded by plasmid pXO1
 Protective Antigen (PA) = forms pores to allow
entry of EF and LF into cells
 Edema Factor (EF) = Increases cAMP  fluid loss
from cells  edema
 Lethal Factor (LF) = protease that cleaves
activator of MAPK pathway  inhibits cell growth
◻ Poly-D-glutamic acid capsule: plasmid
pXO2
 Protein capsule, NOT polysaccharide
■ Antiphagocytic
■ Antibodies against the capsule are NOT protective
◻ Buzz Words: “Boxcar-shaped”
Bacillus cereus
◻ Spore former
◻ Causes food poisoning in two forms:
 Emetic Form
■ Heat-stable toxin (superantigen similar to S.
aureus)
■ Nausea and vomiting 1-5 hours after ingestion
■ Associated with fried rice!

 Diarrheal Form
■ Heat-labile toxin (AB-exotoxin similar to
Cholera toxin)
■ Watery, non-bloody diarrhea and abdominal
pain 8-16 hours after ingestion, lasts 20-36
Corynebacterium
diphtheriae
◻ Transmitted by airborne droplets
 Pseudomembrane in the oropharynx
■ Fibrinous exudate caused by local inflammation
 Bleeds when scraped or removed (so
don’t!)
◻ Diphtheria toxin
 ADP-ribosylation of EF2  stops protein
synthesis
■ Same mechanism as Pseudomonas’ Exotoxin
A!
 Lysogenic conversion by a phage
 Strains that lack the toxin gene are NOT
pathogenic
◻ Toxoid vaccine
Listeria monocytogenes
◻ High-risk groups
 Pregnant women, newborns,
immunocompromised
■ Causes meningitis and sepsis in these patients
■ Note: in healthy pts, causes mild gastroenteritis

◻ Typical presentation: Pregnant woman in

the 3rd trimester who ate/drank unpasteurized
cheese/milk or ate contaminated deli meat
◻ Internalin (produced by Listeria) binds E-
cadherin (on human cells) and causes
endocytosis
◻ Listeriolysin = allows escape from endosome
into cytosol
◻
GRAM NEG RODS
Why so many?
A 39 yo paraplegic M w/ an indwelling bladder catheter
presents to the ED w/ rigors, n/v. Temp 102. UA w/ 3+
leukocyte esterase, many WBCs. U and BCx show non-
lactose fermenting Gram neg bacilli. Who am I?

◻ E coli
◻ Pseudomonas aeruginosa
◻ Klebsiella pneumoniae
◻ Staph sapro
◻ Enterococcus cloacae
◻ Ureaplasma urealyticum
A 39 yo paraplegic M w/ an indwelling bladder catheter
presents to the ED w/ rigors, n/v. Temp 102. UA w/ 3+
leukocyte esterase, many WBCs. U and BCx show non-
lactose fermenting Gram neg bacilli. Who am I?

◻ E coli (lactose ferm)

◻ Pseudomonas aeruginosa (non-
lactose ferm)
◻ Klebsiella pneumoniae (lactose ferm)
◻ Staph sapro (Gram pos)
◻ Enterococcus cloacae (Gram pos)
◻ Ureaplasma urealyticum (requires fancy
Cx)
Random Gram – Facts
◻ Strict anaerobe = Bacteroides
◻ Strict aerobe = Pseudomonas = blue-
green!
◻ MacConkey’s agar = who ferments
lactose?
 E. coli! (pink to red colonies)
 Klebsiella is L+ too!
◻ Serratia marcescens is L- but produces
red colonies on blood agar
◻ Don’t forget: endotoxin = LPS = all Gram
–s!
GI Gram –s…diarrhea fun!
◻ Know the dif between secretory diarrhea and
dysentery!
 Secretory = watery = tissue invasion is ABSENT =
copious amounts of watery diarrhea with no blood
or pus (duh) = small intestine = V. cholerae &
ETEC
 Dysentery = scantier volume = probs tissue
invasion PRESENT = blood, mucus, pus = large
intestine = Shigella
◻ Hemorrhagic colitis diarrhea = tissue invasion
ABSENT = copious amounts of fluid w/ RBCs
but NO LEUKOCYTES = EHEC
◻ Bloody watery diarrhea = tissue invasion
PRESENT = stools w/ copious amts of fluid,
bloody, pus = Salmonella, Campy, & YP
E. coli
◻ Most common cause of uncomp. UTI!
◻ ETEC – heat-labile and heat-stable toxins
 Traveler’s diarrhea & childhood diarrhea
◻ EHEC – Shiga-like toxin!
 Buzzword = CONTAMINATED BEEF!
 Hemorrhagic colitis, HUS, TTP, NON-febrile,
watery & bloody diarrhea
Random slide of nosocomial
infxns.
◻ Klebsiella pneumoniae = L+ = CHUBBY
CAPSULE!
◻ Enterobacter = L+
◻ Citrobacter = slow L+
◻ Serratia marcescens = slow L+ = RED @
25C!
◻ Proteus = L– = swarming motility!
 Produces urease!  kidney stone formation
 Staghorn calculi?
Salmonella
◻ Motile, produces H2S, invasive!
◻ Salmonella typhi = gallbladder carrier
state!
 Typhoid fever = chronic fever, headache,
weakness
■ Blood culture becomes positive (day 10-14)
■ THEN…Rose spots…spreads back to GI…stool
positive
 M-cells, Peyer’s patches
◻ Salmonella enteritidis & typhimurium
 Gastroenteritis (fever, N/V, cramps, diarrhea)
■ 24-48 hours after ingestion of contaminated food
(poultry, eggs, dairy products)
 Post-infxn. Reiter’s may occur!!! (assoc w/ HLA-
B27)
■ Can’t see, can’t pee, can’t climb a tree!
Shigella
◻ Non-motile, do NOT produce H2S
◻ Also invade M-cells of Peyer’s patches
◻ Post-infxn. Reiter’s may occur! (same as
Salmonella)
◻ S. dysenteriae = more serious form of
dysentery
 Lower ab cramps, tenesmus, stools w/ blood
and pus
 Shiga toxin (duh) = enterotoxic, cytotoxic,
neurotoxic
■ Inhibits protein synth by inactivation of 60S…
ultimately blocks electrolyte transportfluid
accumulation in GI tract lumen
■ HUS can occur w/ high levels! Eek!
Vibrio
◻ Grown on TCBS (thiosulfate-citrate-bile salts-
sucrose agar)
 V. cholerae = yellow; V. para & vulnificus =
green
◻ V. cholerae
 NO fever, rice-water stools
 Tx: fluid + electrolyte replacement!
◻ V. parahaemolyticus = marine life!
 Gastroenteritis w/ bloody diarrhea
 Also…wound infxns? Dangers of the open sea?
Who knows…
◻ V. vulnificus = also marine
 Also gastroenteritis & wound infxns. but can
lead to sepsis  fasciitis and myonecrosis…don’t
be an alcoholic! (@ greater risk)…alcoholic
Yersinia enterocolitica
◻ Cramps, diarrhea, fever = MIMICKS
APPENDICITIS!
◻ Reiter’s syndrome possible
◻ Can grow in refrigerated foods
◻ Produces a toxin similar to heat-stable
ETEC toxin (Step asks a lot of “similar
toxin” questions for some reason…)
Bacteroides fragilis
◻ Anerobe! Normal flora! Most common
microbes in the large intestine!
◻ Causes: pleuropulmonary infxns and
peritoneal abscesses
◻ Tx: Metronidazole!
Campy!
◻ Zoonotic; primary reservoir = poultry!
◻ Spread by ingestion of contaminated
milk, water, meat or poultry
◻ Bloody diarrhea! (RBCs & PMNs)
◻ Can also be assoc w/ Reiter’s!
◻ AND GUILLAN-BARRE!
KNOWTHISKNOWTHIS!!!
H. pylori
◻ Person-to-person spread!
◻ Produces: UREASE!!! Cytotoxin!
Mucinase!
◻ Causes: gastritis; gastric & duodenal
ulcers
◻ Associated w/: gastric
adenocarcinomas!
 This is the only cancer that can be tx’d
w/ abx!
 Triple therapy: 2 abx (Metronidazole
and Amoxicillin or Clarithromycin) + 1
List o’ Urinary Tract Dudes
◻ Gram –s (Be able to differentiate! Buzzwordz!)
 E. coli (MCC uncomplicated UTI, lactose ferm)
 Klebsiella pneumoniae (big capsule, lactose
ferm)
 Proteus spp. (kidney stonez!)
 Pseudomonas aeruginosa (non-lactose
fermenting)
 Serratia marcescens (red on blood agar at 25C)
◻ Non-Gram –s
 Enterococcus (Gram +)
 Candida albicans (fungus w/ pseudohyphae…in
immunocompromised)
 Staphylococcus saprophyticus (Gram +)
A 35 yo F presents to the ER w/ a diffuse pruritic papulopustular
rash. Her friend was brought to the ER 2 days ago w/ similar
symptoms. Pustular fluid demonstrates oxidase+ Gram neg rods
that produce pigment on culture medium. Which of the following
is the most likely source of this pt’s infxn?

◻ Human contact
◻ Insects
◻ Food
◻ Water
◻ Soil
◻ Pets
A 35 yo F presents to the ER w/ a diffuse pruritic papulopustular
rash. Her friend was brought to the ER 2 days ago w/ similar
symptoms. Pustular fluid demonstrates oxidase+ Gram neg rods
that produce pigment on culture medium. Which of the following
is the most likely source of this pt’s infxn?

◻ Human contact
◻ Insects
◻ Food
◻ Water (Pseudomonas! Hot tub
folliculitis!)
◻ Soil
◻ Pets
Pseudomonas
◻ Pseudomonas aeruginosa = aerobe,
duh!
 Blue-green!
■ Pyocianin

 Polysaccharide capsule
 Exotoxin A
 Causes: wound infxns, meningitis, UTI!,
pneumonia, eye/ear infxns, & ecthyma
gangrenosum (sepsis w/ hemorrhagic
necrosis of skin…ew), also hot foot
syndrome (yum), #1 cause of
chronic pulm infxn in CF pts!!!
Haemophilus influenzae
◻ NOT the cause of the flu!
◻ Fastidious! Must grow on chocolate agar!
◻ Requires both X & V factors for growth
◻ Polysaccharide capsule!
◻ IgA1 protease; Catalase + & Oxidase +
◻ Type B (Hib) is invasive! Most virulent!
 Ye olde cause of meningitis but now less
common bc of the Hib conjugate vaccine
◻ Also causes: epiglottitis (Hib), non Hib
strains cause otitis media (vax not
preventative of this)
◻ PS: H. ducreyi = chancroid = gross.
Catalase –
Bordatella pertussis
◻ Whooping cough (duh)
◻ Pertussis toxin  lymphocytosis
 A subunit catalyzes ADP-ribosylation of an
inhibitory G protein…blahblahblah inhibits
neutrophil activation!
◻ Bvg encodes 2-component system…
 BvgS (sensor) catalyzes phosphorylation of
BvgA (response activator)  activates
transcription of virulence genes!
◻ Prevented by vax!
 DTaP (Diphtheria toxoid, Tetanus toxoid,
Acellular pertussis toxoid)
A 63 yo M has been brought to the ER w/ recent
onset of high fever, confusion, HA, watery diarrhea,
and productive cough. He has been smoking two
packs of cigarettes daily for more than 30 yrs and
has been dx w/ chronic bronchitis. BP 100/70, HR 90,
RR 34, T 105F. Gram stain w/ no bacteria but
numerous neutrophils. Which of the following is the
most likely cause of this pt’s dz?
◻ Mycoplasma pneumoniae
◻ Klebsiella pneumoniae
◻ Steptococcus pyogenes
◻ Legionella pneumophila
◻ Mycobacterium kansasii
◻ Coccidioides immitis
A 63 yo M has been brought to the ER w/ recent
onset of high fever, confusion, HA, watery diarrhea,
and productive cough. He has been smoking two
packs of cigarettes daily for more than 30 yrs and
has been dx w/ chronic bronchitis. BP 100/70, HR 90,
RR 34, T 105F. Gram stain w/ no bacteria but
numerous neutrophils. Which of the following is the
most likely cause of this pt’s dz?
◻ Mycoplasma pneumoniae
◻ Klebsiella pneumoniae
◻ Steptococcus pyogenes
◻ Legionella pneumophila
◻ Mycobacterium kansasii
◻ Coccidioides immitis
Legionella
◻ BCYE (charcoal-yeast) culture w/ L-
Cysteine
◻ Spread by aerosolized contaminated
water!!!
◻ Causes: fever, chills, NON-productive
cough, severe pneumonia, and
DIARRHEA!!!
 Will likely be an old man who has a
pertinent hx of tobacco use who lives in a
ye olde nursing home w/ a bad air
conditioning system…hopefully?
All I have to say about CNS
infxns is…
◻ Memorize based on age group/where/how acquired!
◻ Infants < 2 mos
 Strep. agalactiae (GBS)
 E. coli – both GBS and E. coli K1 have sialic acid capsules!
 NOTE: sialic acid-rich capsules are NOT immunogenic! They inhibit
opsonization tho.
 Listeria monocytogenes
◻ Childhood (community acquired)
 N. meningitidis (duh)
 S. pneumo (duh)
 Hib (duh) DUH!
◻ Older children – adults (comm acquired)
 S. pneumo
 N. meningitidis
 Listeria monocytogenes
◻ Nosocomial
 E. coli, Pseudomonas, Klebsiella, S. pneumo, S. aureus, S. epidermidis
◻ NOTE: The most likely organism causing meningitis in
presence of otitis media = S. pneumo; w/ petechiae and
purpura it will probs be N. meningitidis. KNOW!
Zoonoses, finally!
◻ For the most part I remember these as
the drag queens bc they have boy names
but added an “ella” to the end of all of
them…kinda…
◻ Gram –s:
 Brucella abortus, Francisella tularensis,
Pasteurella multocida, Salmonella
enteritidis, Bartonella henselae and
quintana, Campy, E. coli, Yersinia pestis
◻ Gram +s:
 Bacillus anthracis, Listeria mono,
Bartonella
◻ Short, G- rods, aerobic & capnophilic
(need CO2)
◻ Bartonella henselae = cat scratch
fevaaa!
 Or bacillary angiomatosis (vascular
disorder of skin & viscera) in
immunocompromised individuals
◻ Bartonella quitana = trench fevaaa!
 Spread by body louse
 Sx = severe headache, fever, weakness,
pain in tibia?
Brucella
◻ Brucellosis = undulating fever!
(pattern of periodic night sweats & fever
w/ headache and joint pain due to
recurrent invasion of the blood stream)
 Other Sx = granulomas in liver, bone &
spleen
◻ Brucella abortus = in cows
◻ B. melitensis = goats and sheepies
◻ B. suis = swine
◻ B. canis = dogs
Francisella tularensis
◻ BUNNIES! (handling or eating)
 Can also be from ticks, deerflies, or
mosquitos
◻ Tularemia = ulcer, lymphadenopathy,
granulomas in lung, liver, & spleen, and
FEVER!
Yersinia pestis
◻ Plasmids! = carry yad, yops, fra, and pla
◻ Bubonic plague = buboes…
 Transmitted by fleas!
 Death in hours to days of bubo development
 Can also cause pneumonic plague
Borrelia burgdorferi
◻ Lyme Disease!!!
 Erythma migrans (targetoid skin lesion)
 Neurologic (Bell’s palsy, bilat!)
 Cardiac (AV nodal block!)
 Recurrent arthritis
 Tick borne (Ixodes…same tick as Babesia)…on
white-footed mouse or white-tailed deer
 Note: Borellia needs darkfield microscopy!!!
◻ Borrelia recurrentis & hermsii
 Relapsing fever NOT undulating (that’s Brucella)
 Recurrentis = epidemic = human reservoir =
Africa
 Hermsii = endemic = rodent reservoir = US
Rickettsiaceae
◻ Rickettsia rickettsii = Rocky Mtn. spotted
fever
 By ticks
◻ Rickettsia prowazekii = epidemic typhus
= lice
◻ Rickettsia typhi = murine typhus = fleas
◻ Rickettsia tsutsugamushi = scrub typhus
(eschar @ bite site…) = By
mites/chiggars
Some rando’s…
◻ Bacillus anthracis = spores from wool &
hides!!!
◻ Pasturella multocida = cellulitis! Animal bite!
◻ Erysipelothrix = purplish-red, well-def skin
lesions; from handling swine, poultry, or fish
◻ Coxiella burnetii = Q fever! Milk from
infected cows or if you’re delivering cow
placenta…?
 Or you can inhale dried poops from
cows/sheep/goats
◻ Listeria mono = contaminated vegetables,
water, ice cream, cheese, and other dairy
products
CHLAMYDIA
Kind of its own thing…
Chlamydia
◻ Obligate anaerobes, can’t make their
own energy (ATP), can’t be Gram stained
◻ Chlamydia trachomatis causes: urethritis
(often w/ gonorrhea) which can  PID 
sterility, reactive arthritis, and
conjunctivitis
◻ Chlamydia pneumo and psittaci 
atypical pneumonia (may now be
“Chlamydiophila”)
◻ Tx w/ Doxy (like Rickettsias bc
intracellular)
SYPHILLIS
Also kind of its own thing.
Syphillis
◻ Caused by Treponema pallidum (a spirochete)
◻ Primary: painless chancre
◻ Secondary: flu-like sx, rash on palms/soles,
condyloma lata (gross)
◻ Tertiary: in your brain!
 Gummas
 Tabes dorsalis (dorsal column destruction  ataxia
and + Romberg bc no proprioception, Charcot
joints = buzzword!)
 Argyll Robertson pupil AKA light-near dissociation
AKA accommodate but do not react to light
◻ Don’t forget about congenital syph!
 Saber shins, saddle nose, deafness, Hutchinson’s
teeth, mulberry molars
MYCOBACTERIA!
Do NOT confuse w/ Mycoplasma!
Mycobacterium tuberculosis
◻ Acid-fast
 Not Gram + or Gram –
 Stains with carbolfuchsin
 Waxy coat of mycolic acid
◻ Humans are the reservoir, spread by
respiratory droplets
◻ Symptoms: fever, weight loss, chills,
night sweats, cough, usually over
several weeks/months
Mycobacterium tuberculosis
◻ Lab Tests
 Culture on Lowenstein-Jensen agar
■ Mycobacteriagrow slowly, so you have to wait
6-8 weeks before you call it negative
 Cord factor (a virulence factor)
■ Trehalose6,6, dimycolic acid
■ Allows bacilli to grow in parallel cords 
increased virulence
■ Inactivates neutrophils, damaging
mitochondria and inducing release of TNF
■ Mycobacteria w/o cord factor can NOT
cause dz
Mycobacterium tuberculosis
◻ Tuberculin Skin Test
 Type IV (delayed-type) hypersensitivity
reaction
 + test means there has been exposure, doesn’t
necessarily mean there is an active infection
◻ Granuloma Formation
 Activated macrophages form giant cells that
“wall off” the infection
 Caseous necrosis in the center
 Ghon Complex = single parenchymal
lesion in the lung, calcified bronchial
lymph nodes visible on X-ray
Mycobacterium tuberculosis
◻ Treatment (RIPE)
 Rifampin (Rifabutin in an AIDS pt)
 Isoniazid
 Pyrazinamide
 Ethambutol
◻ MDR TB = TB resistant to at least
Isoniazid and Rifampin
◻ Drug resistance = due to point
mutations in bacterial genes, NOT from
acquiring resistance genes from
plasmids, phage, etc.
Mycobacterium tuberculosis
◻ BCG Vaccine
 Attenuated strains of M. bovis
 Can cause false positive TB skin test
 Not given routinely in the US
◻ Extrapulmonary TB:
 CNS (parenchymal tuberculoma or
meningitis)
 Pott’s disease (infxn of vertebral bodies)
 KNOW THESE!!!
Mycobacterium leprae
◻ Cannot be grown in the lab
◻ Humans are natural hosts
◻ Armadillo = possible reservoir
◻ Transmission requires prolonged close
contact with an affected individual
Mycobacterium leprae
◻ Tuberculoid Leprosy
 Cell-mediated immune response is
strong
■ Limitsgrowth, granulomas form
■ Few organisms present in the skin lesions
■ Nerve damage due to strong CMI
■ Lepromin skin test is positive

 Hypopigmented, plaque-like skin lesions

 Thickened superficial nerves
Mycobacterium leprae
◻ Lepromatous Leprosy
 Poor CMI
■ Many organisms present in the skin lesions
■ Foamy histiocytes rather than granulomas form
■ Lepromin skin test is negative
■ Nerve damage due to the organism

 Leonine Appearance = due to multiple

nodular skin lesions
 Erythema nodosum leprosum
■ Painful nodules along the extensor surfaces of tibia
and ulna, neuritis, uveitis
■ Sign that the CMI is being restored
MYCOPLASMA!
Do NOT confuse w/ Mycobacteria!
Important Points
◻ Smallest free-living bacteria
◻ Lack cell walls
 Therefore, inherently resistant to
penicillins
 And will NOT Gram stain!
◻ Cell membranes contain sterols
 Acquire these from their eukaryotic hosts
Mycoplasma pneumoniae
◻ Walking pneumonia: insidious onset, HA,
non-productive cough, DIFFUSE
INTERSTITIAL INFLITRATE ON CXR!!!
◻ Colonies have “fried egg” appearance
◻ Infection triggers formation of
autoantibodies called “cold
agglutinins” (IgM)
 Can agglutinate OR lyse RBCs
◻ Typical pt should be someone <30 who
lives in military barracks, dorms, prison,
etc.
Other Mycoplasmas
◻ Mycoplasma hominis
 Causes Pelvic Inflammatory Disease
◻ Ureaplasma urealyticum
 Common cause of non-gonococcal urethritis
 Urease +
■ M. hominis and pneumoniae are urease -
The end!
◻ Well, the end of virology and bacteriology
lecture…now here are some lightning
round slides to test your buzzword
memory…
 Good luck!
Round 1
◻ Fried rice:
 Bacillus cereus, spores survive frying
◻ Pseudomembranous colitis:
 C. dificile, gray-yellow, found on sigmoidoscopy
◻ Prevents release of inhibitory mediators:
 Clostridium tetani/tetanospasmin.
◻ Swarming effect on blood agar:
 Proteus mirabilis
◻ Tumbling movement:
 Listeria monocytogenes. Actin rockets propel to pseudopodia,
eject from cell
◻ Terminal spore:
 Clostridium tetani…Which makes it look like?
 Tennis racket. Strict anaerobe.
◻ Bloody currant-jelly sputum:
 Klebsiella pneumonia (CAUSES ASPIRATION PNEUMONIA IN
ALCOHOLICS!!!)
 Round 2
◻ Blocks Ach release:
 Clostridium botulinum
◻ Cellulitis after oyster shucking:
 Vibrio vulnificus
◻ Urea breath test:
 Helicobacter pylori
◻ Treat with hyperbaric O2:
 Clostridium perfringins gas gangrene. Helps phagocytes,
decreases alpha toxin production, decreases anaerobes,
increases new vessel production.
◻ Induced by clindamycin:
 C. dificile pseudomembranous colitis
◻ CXR shows mediastinal widening:
 Bacillus anthracis. (Pulmonary anthrax aka Woolsorter’s
dz)
 Round 3
◻ Mycolic acid in cell wall:
 Mycobacterium tuberculosis
◻ Name for situation in which verotoxin enters the
bloodstream
 hemolytic anemia, thrombocytopenia, acute renal failure.
Hemolytic-uremic syndrome. Caused by? E.coli O157:H7
◻ Exotoxin A:
 Pseudomonas
◻ Umbilical cord stumps & circumcisions:
 C. tetani, neonatal tetanus
◻ Of the following (Klebsiella, Enterobacter, Serratia), which
might you get out in the community?
 Klebsiella
◻ Causes febrile gastroenteritis and tolerates
cold/refrigeration, common in unpasteurized milk:
 Listeria monocytogenes
Round 4
◻ Predisposes to struvite stones:
 Proteus.
◻ Obligate intracellular STD:
 Chlamydia
◻ Trench fever:
 Bartonella quintana. Spread how?
 Feces of human louse.
◻ Cherry red epiglottis:
 Hemophilus influenza
◻ Most likely SECOND location of TB:
 Kidney (well oxygenated)
Round 5
◻ Patients especially predisposed to Pseudomonas:
 cystic fibrosis, burn patients
◻ Why you don’t give raw honey to kids < 1 year:
 Botulinum spores
◻ Red colonies on blood agar @ 25 C:
 Serratia
◻ Prefers growing in skin and superficial nerves because
of cooler temperature:
 Mycobacterium leprae
◻ Causes abortions in cows:
 Brucella abortus
◻ Classic case of shigellosis (in US):
 traveler returning from abroad
◻ Rods that line up in chains/”boxcar-like”:
 Bacillus anthracis
Round 6
◻ Double zone hemolysis:
 C. perfringens, from outer alpha (incomplete
hemolysis) toxin and inner theta (complete)
hemolysis
◻ Cat scratch fever:
 Bartonella henselae
◻ Associated with Guillane-Barre Syndrome:
 Campylobacter jejuni, antigenic similarity
◻ O157:H7 usually contracted from?
 Undercooked meat (also petting animals?)
◻ War wounds, auto & motorcycle accidents,
and septic abortions/endometritis:
 C. perfringens/gas gangrene
Round 7
◻ Infection after jaw or dental trauma:
 Actinomyces israelii (Gram positive branching
rods)
◻ Resistance mutations occur on chromosome,
not plasmid:
 Mycobacterium tuberculosis
◻ Most common method of tularemia
contraction:
 Dermacentor ticks from rabbits
◻ Type I pili, attracted to mannose containing
structures:
 E. coli, causes what? Cystitis
◻ Lysteriolysin O:
 Round 8
◻ P pili, attracted to digalactoside receptor:
 E. coli, causes what?
 Pyelonephritis
◻ “Woolsorter’s disease”:
 Bacillus anthracis. Flu-like, dry cough. Can progress to fever,
pulm hemmorhage, mediastinitis and shock!!!
◻ Bug that requires factor X only, not V:
 Hemophilus ducreyi. Which causes?
 ChancrOID, not chancre. What’s X?
 A heme component (hematin). What’s V?
 NAD+
◻ Prominent glycocalyx with alginate:
 Pseudomonas
◻ Grows in 8% NaCl:
 Vibrio parahemolyticus
 Round 9
◻ Pneumonia with hyponatremia and mental confusion:
 Legionnaire’s (sometimes also with diarrhea). What do
you call Legionella infection, flu-like, w/o pneumonia?
 Pontiac fever.
◻ No cell wall and three-layer membrane:
 Mycoplasma pneumonia
◻ Can cause Reiter’s syndrome:
 Campylobacter! Triad of symptoms? (urethritis,
conjunctivitis/uveitis, inflammatory arthritis) (less
frequently: Salmonella, Shigella, Yersinia)
◻ How do you tell Shigella vs. Salmonella apart?
 Salmonella- motile, makes H2S (except… Typhi so little it
won’t show), gas with glucose metabolism (except typhi)
 Shigella- nonmotile, no H2S, no gas with glucose
 Round 10
◻ Emetic course with stable toxin, diarrheal
course with labile toxin:
 Bacillus cereus (diarrheal is actually usually
consumption of spores that then germinate and
create toxin)
◻ K capsule: E. coli. K1 capsule causes?
 Neonatal meningitis
◻ Most common nosocomial diarrhea:
 C. difficile, not bloody, yes WBCs, fever,
abdominal cramping
◻ ADP-ribosylates Gi (NOT Gs!):
Round 11
◻ Particularly smelly diarrhea, that’s more
common in US than Shigella or Salmonella:
 Campylobacter
◻ Conditions that predispose to BOTH
Salmonella and Vibrio infection:
 low stomach acid/gastrectomy
◻ Strain of E. coli that does NOT ferment
sorbitol:
 EHEC
◻ Infects renal transplant patients:
 Listeria monocytogenes. **What VIRUS is
associated with renal problems/infects RENAL
TRANSPLANTS?**
 BK (polyoma) virus
◻ Kids contract from puppies:
 Round 12
◻ Babst-Ernst granules:
 Corynebacterium diptherieae. What are they?
 Polymerized polyphosphate (volutin). How do you find it?
 Metachromatic methylene blue stain.
◻ Have actin-based motility & invade through M cells:
 Shigella
◻ Phenylalanine deaminase positive:
 Proteus
◻ A strict aerobe that can create pus:
 Pseudomonas (really more necrotic than pyogenic, but…)
◻ Ixodes tick spreads:
 Borrelia (Lyme) and Babesia!
◻ What distinguishes Mycoplasma atypical pneumonia from
Legionella:
 cold agglutinins (no leukocytosis)
 Round 13
◻ Disease contracted in Arkansas and Missouri:
 Tularemia
◻ Macules, then petechia, starting at hands and feet then into trunk:
 Rickettsia rickettsii. How is this different than typhus?
 Starts on trunk and spreads peripherally. Typhus caused by?
 Rickettsia prowazekii
◻ Painful nodules on extensor surface of tibia, ulna:
 Erythema nodosum leprosm. When?
 AFTER therapy. Indicates restoration of CMI.
◻ Painless ulcer with black eschar, with significant local edema:
 Cutaneous anthrax. Other clinical manifestations of anthrax?
 Woolsorter’s, hemorrhagic mediastinitis, hemorrhagic meningitis, GI anthrax,
panopthalmitis.
◻ Most common complication of Brucellosis:
 Osteomyelitis.
◻ Spreading, nonpruritic, circular red rash, with clear center at bite site, painless rash:
 Borrelia burgdoreri
◻ Geographic area with bubonic plague:
 Southeast Asia
◻ Toxin receptor is Heparin-binding Endothelial Growth Factor (HB-EGF):
 Corynebacterium diphtheria, lots on heart & nerves-> myocarditis & peripheral
neuritis
 Round 14
◻ Hemorrhagic bullae with sepsis :
 Vibrio vulnificus
◻ Fever, chills, headache, myalgia… in a veterinarian:
 Q fever/Coxiella burnetii
◻ P1 adhesin on tip:
 Mycoplasma pneumonia
◻ Hutchison’s incisors and mulberry molars:
 Congenital syphilis. Spread?
 Transplacentally in third trimester
◻ Unilateral cervical adenitis with nontender swollen
lymph nodes:
 Scrofula, Mycobacterium tuberculosis
◻ “100 day cough” in adults:

 Special Agar
◻ Egg yolk agar/Naegler’s test: Clostridium perfringens, precipitation
indicates lecithinase
◻ Loffler’s medium/Tellurite agar (Corynebacterium diptheriae): bacteria
reduces elemental tellurium which precipitates grey/black
◻ MacConkey’s/EMB: detect lactose fermentation. E.coli,
Klebsiella/Enterobacter
◻ Ferment lactose slowly, may get negative result: Vibrio, Serratia
◻ TCBS (Vibrio spp.): basic, V. cholera appear yellow (ferments sucrose), V.
parahaemolyticus & V. vulnificus appear green
◻ CAMPY agar: Campylobacter (jejuni AND intestinalis)
◻ Urease agar: turns purplish when present. Klebsiella, Proteus,
Pseudomonas
◻ Mueller-Hinton agar (Pseudomonas aeruginosa): shows blue-green best
◻ Chocolate agar (Haemophilus influenza): with X and V
◻ Bordet-Genou (Bordatella pertussis): pearlescent colonies,
nasopharyngeal swabs
◻ Charcoal-yeast agar (Legionella): needs iron and cysteine
◻ Lowenstein-Jensen (Mycobacterium tuberculae): malachite dyes, complex
nutrients, colorless colonies
ALMOST DONE OMG
WEHHHHHHHHHHHHHHHHHHHHHHHH
HHHHH!!!
 EXOTOXINS…anddd done!
◻ Tetanospasmin: Clostridium tetani, blocks release of inhibitory mediators, irreversible
binding, intra-axonal retrograde, released on lysis, one kind, AB structure
◻ Botulinum toxin: Clostridium botulinum; blocks Ach release, gut blood PNS, irreversible
◻ Alpha toxin (lecithinase): Clostridium perfringens; damages cell membranesvascular
damage, myonecrosis
◻ Theta toxin : Clostridium botulinum, minor hemolytic
◻ Exotoxin A & B: Clostridium difficle, glucosylate Rho GTPase depolymerase actin; A more
responsible for clinical effects
◻ PA, EF, LF: Bacillus anthracis, EF: edema factor, adenylyl cyclase; LF: cleaves
phosphokinase in MAPK pathway
◻ Diphtheria toxin: Corynebacterium diptheriae, ADP ribosylates EF-2, stops protein
synthesis
◻ Labile Toxin: E. coli, ADP-ribosylates Gsinc. adenylyl cyclase
◻ Stabile Toxin: E. coli, guanylyl cyclate, harder to reabsorb sodium
◻ Verotoxins/Shiga-like toxins: E.coli, removes adenine from large ribosomal RNA
◻ Shiga toxin: Shigella, inactivates 28s rRNAinactivating 60s ribosome, no elongation
◻ Choleragen: Vibrio cholera, ADP ribosylates Gs
◻ Exotoxin A: Pseudomonas, ADP ribosylates EF-2
◻ Exotoxin S: Pseudomonas, ADP ribosylates Ras protein, damages cytoskeleton, part of Type
III secretion system
◻ Pertussis toxin: Bordatella pertussis, ADP ribosylates Gi inc. cAMP
Good luck! Keep chugging…
STEP 1 REVIEW:
FUNGUS, PARASITES,
ABX
By Meredith Greer
FUNGUS
Kinda gross.
Systemic vs Opportunistic
fungi…
◻ Systemic:
 Histoplasmosis
 Blastomycosis
 Coccidiodomycosis
 Paracoccidioidomycosis
◻ Opportunistic:
 Candida albicans
 Aspergillus fumigatus
 Cryptococcus neoformans
 Mucor/Rhizopus spp.
Some other fungi…
◻ Randos
 PCP (Pneumocystis)
 Sprorothrix shenckii
◻ Cutaneous
 Tinea versicolor (Malassezia furfur)
 Tinea pedis, cruris, corporis, capitis
■ Canbe caused by: microsporum, trichophyton,
and epidermophyton
Several students returning from a cave exploration trip to
the Central US develop fever, cough, and malaise.
Pulmonary infiltrates and hilar adenopathy are apparent
on CXR. Lung tissue specimens will show?

◻ Multinucleated spherules
◻ Ovoid cells w/in macrophages
◻ Budding yeast w/ thick capsule
◻ Pseudohypae and blastoconidia
◻ Septate hyphae w/ dichotomous
branching
Several students returning from a cave exploration trip to
the Central US develop fever, cough, and malaise.
Pulmonary infiltrates and hilar adenopathy are apparent
on CXR. Lung tissue specimens will show?

◻ Multinucleated spherules (Cocci)

◻ Ovoid cells w/in macrophages
(Histo!)
◻ Budding yeast w/ thick capsule (Crypto)
◻ Pseudohypae and blastoconidia (Candida)
◻ Septate hyphae w/ dichotomous
branching (Asperg)
Location, location, location
◻ Histo: Mississippi & Ohio River Valleys!
◻ Blasto: States EAST of the Mississippi +

Central America (Do they mean Central

America or Central North America? Not
sure…)
◻ Coccidioidomycosis: SW US &

California
◻ Paracoccidioidomycosis: Latin America

◻ In summary, think:

Histo middle, Blasto right, Cocci left,

Buzzwords for the
systemics…
◻ Histo: bird OR bat droppings, spelunking,
macro’s
◻ Blasto: broad based budding!
◻ Cocci: spherule!
◻ Paracocci: captain’s wheel!
But what do they cause?
◻ Histo: primarily a lung dz, often flu-like,
MCC mediastinitis!
 Weird complication=ocular histo (retina)
 Rare skin findings=chancre (painless) like
lesions w/ adenopathy
◻ Blasto: lung/skin/bone
 Can present like a pneumonia
 May be mistaken for lung ca in smokers
 In skin: indolent, verrucous, ulcerated
dermal lesion
 Other things: osteomyelitis, GU tract -itises
But what do they cause?
◻ Coccidioidomycosis:
lung/brain/bone/skin
 “Valley Fever”: presents flu-like but w/ rash
(maculopapular) and myalgias/arthralgias
 Can cause meningitis!
◻ Paracoccidioidomycosis: “South
American Blasto”
 Seems worse than blasto tho…w/ painful
violacious hue of lips/oral mucosa + high
fever + lymphadenitis
How do we treat?
◻ For local infection:
 Treat all of these w/ Fluconazole or
Ketoconazole
◻ Use Amphotericin B for systemic
infection!
◻ It’s important to know that although
these are not listed under the
“opportunistic fungi”, they can cause
severe disease in immunocompromised
patients.
◻ It’s just that the fungi listed as
Opportunistic shapes…
◻ For the opportunistic fungi, their shape is
important!
◻ Candida: Pseudohyphae!!! Germ
tubes!!!
◻ Aspergillus: acute angles, septate
hyphae!
◻ Crypto: capsular halo!
◻ Mucor: non-septate hypae w/ wide
angles
But what do they cause?
◻ Candida: thrush, vaginitis, diaper rash,
endocarditis, disseminated candidiasis,
candidemia is possible
 Tx w/ Nystatin, Ampho B if systemic
◻ Aspergillus: fungus ball!!! Also, allergic
bronchopulmonary aspergillosis (asthma
pts)
◻ Crypto: meningitis!!!
◻ Mucor/Rhizopus: bad head stuff usually
in DM pts
Don’t forget the randos!
◻ PCP (Pneumocystis): not sure why this
isn’t under opportunistic fungi…usually in
AIDS pts (CD4<200)
 Big ol’ bilateral diffuse interstitial CXR
appearance
 “Ground glass” on chest CT
 +Silver stain
 Tx w/ Trim-Sulfa (HIV pts w/ CD4<200
should be on Trim-Sulfa ppx, if allergic 
Pentamadine or Dapsone)
Don’t forget the randos!
◻ Sporothrix (I hope this is on your Step!)
 Skin lesion w/ nodules along draining
lymphatics
 Usually a gardener who was stuck with a
thorn
 Tx w/ Itraconazole
◻ Malassezia furfur (causes Tinea
versicolor)
 Damages melanocytes  hypopigmentation
 “Spaghetti and meatballs” on KOH
 Tx w/ topical Miconazole
PROTOZOA
Seriously so buzzword dependent that
I’m just doing lightning rounds…
A 34 yo M traveler who recently returned from a trip to Africa now
complains of recurrent fevers, chills, and excessive sweating.
These sx occur every 48 hours. A blood smear reveals RBC
inclusions. The pt is prescribed chloroquine. The addition of
primaquine to the tx would have which of the following efx?

◻ Decrease the S/E of chloroquine

◻ Kill blood trophozoites
◻ Prevent dz relapse
◻ Tx chloroquine-resistant strains
◻ Prevent hemolysis
A 34 yo M traveler who recently returned from a trip to Africa now
complains of recurrent fevers, chills, and excessive sweating.
These sx occur every 48 hours. A blood smear reveals RBC
inclusions. The pt is prescribed chloroquine. The addition of
primaquine to the tx would have which of the following efx?

◻ Decrease the S/E of chloroquine

◻ Kill blood trophozoites
◻ Prevent dz relapse
 (vivax/ovale hepatic dormancy)
◻ Tx chloroquine-resistant strains
◻ Prevent hemolysis
GI probs…
◻ Flatulence, foul-smelling stools, camper/hiker,
baby
 Giardia lamblia, Tx?
 Metronidazole, S/E?
 Disulfuram-like reaction
◻ Bloody diarrhea, liver abscess w/ RUQ pain
 Entamoeba histolytica, Tx?
 Metronidazole, seen on histology?
 RBCs in cytoplasm!
◻ Just regular old fashioned diarrhea
 Cryptosporidium, dangerous in what
population?
 AIDS pts, Tx?
 None!, seen on histology?

CNS probs…
◻ Pregnant lady with a cat!
 Toxoplasmosis gondii, seen on MRI?
 Ring-enhancing lesions, Tx?
 Sulfadiazene + Pyrimethamine, RANDOM!
◻ Baby w/ chorioretinitis + intracranial
calcifications?
 Also Toxo!
◻ Kids swimming in fresh water and then in
a coma?
 Naegleria fowelri! Method of entry?
 Through the cribriform plate, eek!
More CNS probs…
◻ Pt (w/ hx of recent travel?) presenting w/
fever  somnolence  coma?
 African sleeping sickness! Bug?
 Trypanosoma brucei, mech of recurring
fever?
 Antigenic variation! Route of transmission
 Tse-tse fly!
◻ T. gambiense and T. rhodesiense also
cause this!
Other guys…
◻ MEGACOLON!
 Trypanosoma cruzi (Chagas’ dz), also causes?
 Dilated cardiomyopathy, what bug transmits?
 Kissing bug (Reduviid bug), Tx?
 Nifurtimox (not sure how to remember this one,
rando)
◻ Sandfly?
 Leishmaniasis! Symptoms?
 Spiking fevers, HSM, pancytopenia
◻ Foul-smelling, GREENISH vaginal discharge
 Trichomonas vaginalis!, characteristic wet
prep?
 Motile trophozoites, ew!, spread by?
 Sexual contact!!! So technically an STD. Tx?
 Metronidazole! DUH! (“GET GAP”)
Other guys…
◻ Anopheles mosquito, recent travel hx?
 Malaria! (Plasmodium), Begin w/ what tx?
 Chloroquine! If resistant use?
 Mefloquine! For vivax/ovale types, add
what?
 Primaquine, why?
 Dormant infxn in liver!!!
Other guys…
◻ Fever, hemolytic anemia, maltese cross
 Babesia!!!, transmitted by?
 The Ixodes tick, who else is transmitted by this
guy?
 Borellia! What does Borellia cause?
 Lyme dz!!! Tx for Lyme?
 Doxy! What if I’m <8 yo?
 Amoxi! What if you wanna cover for Babesia
too?
 Add Quinine or Clinda! What might happen from
the Clinda?
 C. dif infection! How do we treat that?
 Metronidazole! What if this isn’t working?
 Add PO Vanc!!! Phew!
PARASITES!
Real gross. Also I can only know
buzzwords, so here goes more
lightning rounds!
Parasites Lightning
Rounds…
◻ Presents w/ seizures, MRI w/ brain cysts (looks
like chocolate chip cookie)…
 Taenia solium (neurocystercercosis), kind of
worm?
 Tape worm!, ingest what to get this infection?
 The eggies! What if you just ingest the larvae?
 Intestinal tapeworm infxn, no brain sx! Tx of
brain sx?
 -Bendazoles!
◻ Liver cysts?
 Echinococcus granulosus, kind of worm?
 Also a tape worm!, What’s your worry during
surg?

Parasites Lightning
Rounds…
◻ Lethargic pt w/ increased falls and MCV
of 105?
 Diphyllobothrium latum! What kinda
worm?
 Also a tape worm! What’s causing these
sx?
 B12 deficiency! What do you expect to see
on smear?
 Hypersegmented neutrophils! How did
your pt get infected w/ this?
 Ate raw fish, eek! Tx?
 Praziquantel!
Parasites Lightning
Rounds…
◻ Biliary tract dz, cholangiosarcoma, raw fish…
 Clonorchis sinensis, what kinda worm?
 Fluke! Tx?
 Praziquantel (hint all of the flukes are
Praziquantel)
◻ Hemoptysis after eating raw crab meat?
 Paragonimus westermani??? This one is
super rando!
 It’s also a fluke, so the tx is Praziquantel
◻ Hematuria…first of all what non-infxn does
that make us afraid of?
 Bladder cancer! What fluke can lead to this?
 Schistosoma haematobium!
Parasites Lightning
Rounds…
◻ Having a microcytic anemia after
recently walking around barefoot in
nature?
 Ancyclostoma or Necator americanus, kind
of wormies?
 HOOK WORMS! (which are round worms)
Tx?
 -Bendazole! (Good guess for any of the
roundworms/tapeworms) or Pyrantel
pamoate
◻ Perianal pruritus in a little boy?
 Enterobius!!!, kind of worm?
 Pin worm! (which is a round worm), how do
Parasites Lightning Round…
◻ WORM BALL WORM BALL WORM BALL!
 Ascarius lumbricoides! Kind of worm?
 GIANT round worm! Tx?
 Bendazoles or pyrantel pamoate (same as
pinworm)
◻ Periorbital edema??? KNOW THIS!!!
 Trichinella spiralis, from undercooked
pork! Worm?
 Round worm! So Tx?
 Bendazoles! Seen on pathology?
 Inflammation of muscle
Parasites Lightning Round…
◻ Another time you might be walking
around barefoot in nature…but this time
you get n/v/d + anemia?
 Strongyloides! (another round worm) Tx?
 Bendazoles or Ivermectin! KNOW
IVERMECTIN!!!
◻ Umm…your pt is blind, eek!
 River blindness from Onchocerca volvulus
(round)
 Transmitted by?
 Black fly, assoc sx?
 Black skin nodules, tx?

Rando Parasite Facts…Almost
done!
◻ Loa loa, Wuchereria bancrofti, and
Toxocara canis
 These are 3 round worms treated w/
Diethylcarbamazine (instead of
Bendazoles)
◻ Loa loa: transmitted by flies, can see
worm crawling in conjunctiva, so creepy!
◻ Wuchereria: transmitted by mosquitos,
elephantitis
◻ Toxocara: contaminated food
 Can cause blindness
ANTIBIOTICS
Not as hard as you’d think.
Just some buzz things you
should know...
◻ PCN: tx for syphilis and strep
◻ Methicillin: not really a tx, question will be
about
S/E: interstitial nephritis
◻ Ampicillin (IV) and Amoxicillin (PO)
 Beware hypersens rxn and C. dif colitis
◻ Pip-Tazo: PSEUDOMONAS! KNOW THIS!!!
◻ Ceftriaxone: Neisseria (meningitis +
gonorrhea)
 A 3rd generation ceph
◻ Cefepime: neutropenic fever + Pseudomonas
 A 4th generation ceph
Just some buzz things you
should know...
◻ Cephalosporin S/E: cross-hypersens w/
PCN allg, disulfuram-like rxn (more buzzy
for Metronidazole)
◻ Penems: BROAD spectrum, ALWAYS
administered w/ Cilostatin (inhibitor of
renal dihydropeptidase I) to decrease
inactivation in renal tubles, IMPORTANT!
 Pretty much only used in SUPER SERIOUS
cases
 S/E: GI, skin rash, CNS toxicity (seizures)
■ KNOWTHAT IT LOWERS THE SZ
THRESHOLD!!!
Just some buzz things you
should know...
◻ Vanc (my fav): ALWAYS IV!!! Unless you
have C. dif and can’t take Metronidazole
or are already taking it to no avail or
something…then PO Vanc
 S/E: nephrotoxic, ototoxic, thrombophlebitis
 S/E: Red Man Syndrome (pretreat w/
antihistamines)
◻ Aminoglycosides, Tetracyclines,
Macrolides, Fluoroquinolones : KNOW
WHO IS IN WHAT CATEGORY! Otherwise
it’s pointless.
Just some buzz things you
should know...
◻ Aminoglycosides (Streptomycin, Gentamicin,
etc):
 Require O2 for uptake (can’t use against anaerobes
so that will ALWAYS be a wrong answer choice)
 S/E:
■ Nephrotoxic (don’t combine w/ cephs!)
■ Ototoxic (don’t combine w/ loop diuretics!)
■ Teratogenic (pretty much just to the kidneys and CN VIII)
◻ Tetracyclines (Doxycycline mainly):
 OK in renal failure (fecal excretion)
 NOT OK w/ milk (inhibits absorption in gut)
 GOOD FOR: intracellular weirdos
(Chlamydia/Rickettsia and tiny weirdos
Lyme/Mycoplasmas/Tularemia)
 BAD BC: GI upset, discoloration of teeth, inhibition of
Just some buzz things you
should know...
◻ Macrolides (Erythromycin,
Azithromycin, Clarithro):
 GOOD FOR:
■ Strep if you’re allergic to PCN
■ URIs/PNAs
■ Legionella* RANDOM!
 OK FOR: STDs (Chlamydia & Neisseria)
 BAD FOR:
■ Your heart! (LONG QT!!! KNOW THIS!!!)
■ Your tum! (Motilin agonist  stim of smooth
muscle, OW!)
■ Your blood! (If you’re on Warfarin, bc CYP450
inhibitor!)
■
Just some buzz things you
should know...
◻ Clindamycin: commonly  C. dif :/
◻ Trim-Sulfa: remember this is a sulfa drug!
(G6PD!)
 GOOD FOR: recurrent UTIs and PCP!!! KNOW!!!
 BAD FOR: your blood (megaloblastic anemia bc
folate, leukopenia, granulocytopenia, can give folate
to help)
◻ Fluoroquinolones (the “floxacins”):
 QUESTION WILL BE: C/I in preggies bc cartilage dmg,
tendonitis and tendon RUPTURE in adults!!!
◻ Metronidazole: GET GAP!
 GOOD FOR: Giardia, Entamoeba, Trichomonas,
Gardnerella, Anaerobes, H. Pylori (w/ a PPI and
Amox or a Tetracycline)
 BAD FOR: Drinkers (Disulfuram-like rxn!!! Antabuse)
TB Treatment Buzzies…
◻ RIPE!!!
◻ Rifampin: orange body fluids!
 USE FOR MENINGITIS PPX (fam members of
infected)
◻ Isoniazid (INH): neurotoxic, hepatotoxic
 Give w/ pyridoxixne (Vit B6) to prevent neuro
probs
◻ Pyrazinamide: decreases renal excretion of
uric acid so can  gout flares in at risk
patients!
 Also, MCC drug-induced hepatitis!
◻ Ethambutol: optic neuropathy  red/green
color blindness (E for EYES)
Anti-fungal buzzies…
◻ Amphotericin B AKA
AmphoTERRIBLE:
 Fever/chills, HoTN, nephrotoxic, cardiotoxic
(arrhythmias), anemia, IV phlebitis! LOTS O’
BAD!!!
■ BE
SURE TO HYDRATE YOUR PTS TO AVOID
RENAL FAIL!
 Feel free to use for all systemic mycoses…
■ Won’tcross the BBB tho, so give intrathecally
for meningitis!
◻ Flucytosine: Combo this w/ Ampho for
systemics!
 Crypto tx: IV Ampho + Flucytosine, send
Anti-fungal buzzies…
◻ The Azoles (Fluconazole, Ketoconazole,
etc):
 Fluconazole: Crypto and Candida
 Ketoconazole: Blasto/Cocci/Histo and
Candida
 Weird S/E: gynecomastia! (inhibs hormone
synth)
◻ Caspofungin: pretty much ONLY for
Aspergillus
◻ Terbinafine: for those cutaneous guys
◻ Griseofulvin: also for the cutaneous
In pts w/ suspected bacterial meningitis who are either
>50 yo, have AIDS, or have received an organ tx, which of
the following abx should you add?

◻ Ampicillin
◻ Ceftriaxone
◻ Gentamicin
◻ Rifampin
◻ Vancomycin
In pts w/ suspected bacterial meningitis who are either
>50 yo, have AIDS, or have received an organ tx, which of
the following abx should you add?

◻ Ampicillin (must cover for Listeria!)

◻ Ceftriaxone
◻ Gentamicin
◻ Rifampin
◻ Vancomycin

◻ F/U question…which one of these drugs

should we give this pt’s family members
who live w/ him?
 Rifampin!!! Meningitis PPX!
Pts admitted to the hospital w/ infxns aquired from nursing
homes are presumed to have more resistant organisms. In
such pts, which of the following abx is most reliable tin the
tx of a case of septic shock or nosocomial pna?

◻ Axithromycin
◻ Ceftazidime
◻ Gentamicin
◻ Meropenem
◻ Pip-Tazo
Pts admitted to the hospital w/ infxns aquired from nursing
homes are presumed to have more resistant organisms. In
such pts, which of the following abx is most reliable tin the
tx of a case of septic shock or nosocomial pna?

◻ Axithromycin
◻ Ceftazidime
◻ Gentamicin
◻ Meropenem
◻ Pip-Tazo

◻ F/U question…what should you be wary of

now?/What pt population would you want to
avoid???
 Lowered seizure threshold! Pts who have
epilepsy or are at risk for seizure (from old
stroke or bleed or other meds, etc)
And that’s it! GOOD
LUCK!!!
As always, feel free to e-mail me at
greerm@livemail.uthscsa.edu