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MICROBIOLOGY LEARNING MODULES

This page contains microbiology learning modules. Each has a mini-quiz at the end to check your understanding of the content.

MODULES:

Arthropods

Conjugation, transduction, transformation

DNA viruses

Fungi

Gram (+) cocci

Gram (+) rods

Gram (-) diplococci + pleomorphic rods

Gram (-) rods

Helminths

Protozoa

RNA viruses – Part I

RNA viruses – Part II

RNA viruses – Part III

Spirochetes + Mycobacteria

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MICROBIOLOGY

Arthropods
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Sarcoptes scabiei

Causes scabies. Presents as itchy bodily areas (e.g., the hands) classically in patients living in close quarters like homeless shelters or group homes.

Causes “linear burrows,” although these might just appear like red dots on the skin in USMLE images.

Tx = topical permethrin.

What USMLE will do is show you above image + tell you a 45-year-old man was living in a homeless shelter for 4 months + topical anti-fungals didn’t work;
what is the treatment –> answer = topical permethrin.

Bacterial superinfection with S. aureus can occasionally occur on scabies lesions. As I talk about in the gram (+) cocci module regarding S. aureus, infections
are often treated with oral dicloxacillin or cephalexin.
Pediculosis capitis/corporis

Pediculosis capitis = head lice.

Pediculosis corporis = body lice.

The names of the organisms are the same as the conditions.

The main point here is that you are merely aware that pediculosis is the medical term for lice, since you’ll see it sometimes as an answer choice on USMLE.

Tx = topical permethrin (same as scabies).

Cimex lectularius

Causes bed bugs.

Presents as very itchy clusters of erythematous lesions on the trunk and limbs in patients who’ve slept in dodgy locations or hotels.

Can occur if someone brings a mattress in off the street. Sounds dumb, but we’re talking about actual demographics here.

NBME has an image of this in one of its questions:

Treatment is supportive and involves not scratching the lesions. Occasionally calamine or steroid cream can be applied to reduce itching.

1. What is an arthropod?

Name four arthropods for USMLE that themselves cause infections in humans.

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MICROBIOLOGY

Conjugation, transduction, transformation

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Conjugation, generalized transduction, specialized transduction, and transformation are known as horizontal gene transfer (HGT), which is when genes,
especially those conferring antibiotics resistance, can move between bacteria asexually. These processes are annoying when you’re first studying for Step
1, but unfortunately the exam asks some questions about these. I consider them fairly basic to know, even during the pass/fail Step 1 era.

Before discussing these specific processes, a HY general principle you need to know is that most bacteria carry their antibiotics resistance genes on a
plasmid, rather than in their chromosomal DNA. A plasmid is a small, circular, dsDNA molecule that is separate from a bacterium’s chromosomal DNA and
can replicate independently.

The USMLE will ask something like, “A bacterial colony that is observed to replicate over many generations loses its resistance to vancomycin. Which of the
following mechanisms is the most likely explanation for this finding?” And the answer is just “loss of plasmid.” Not complicated. But if you don’t know the
factoid about antibiotics resistance genes normally being carried on the plasmid, you’d be like what the fuck?

Conjugation

Conjugation is when genes (usually for antibiotics resistance) are transferred from one bacterium to another via a tube called a pilus.
The way the USMLE will ask this is they will say something like, “A researcher is conducting an experiment about antibiotics gene transfer. Which of the
following observations would best support the conclusion that conjugation is the method of transfer?” Then the answer is, “direct cell to cell contact.” In
other words, the tube/pilus that connects the two bacterium necessitates cell-to-cell contact.

I haven’t seen the USMLE specifically assess the notion of F+ vs F-, but the detail isn’t dramatic to know. The donor is called F+ and the recipient F-.

Generalized transduction

Transduction refers to a phage (viral) particle transferring genes from one bacterium to another.

Generalized transduction is when a phage particle enters a bacterial cell, packages up random fragments from the bacterium’s DNA genome within its new
phage particles, then leaves the cell, infecting a new bacterium and spreading these genes as a result.
During the process of generalized transduction, the phage particle does not incorporate itself into the bacterial genome when it packages up DNA. In other
words, there is no lysogenic process (lysogeny) as part of the process. Lysogeny refers to the ability of some viruses to incorporate themselves into the
nucleic acid of the host and then reemerge later.

USMLE Qs on this topic are fairly straightforward. They might say something like, “Which of the following observations by a researcher supports
generalized transduction as the mechanism for antibiotics gene transfer?” And the answer will be something like, “Non-lysogenic phage particles present.”
The answer on its own can sound cryptic/arcane, but now that we discussed it, it’s not so bad.

Specialized transduction

Specialized transduction is when a viral (phage) particle enters a bacterial cell, lysogenically incorporates itself into the bacterial’s DNA genome, then
reemerges with flanking bacterial DNA sequences which are then packaged into new phage particles. These new phage particles then infect other bacterial
cells and transfer these flanked genes.

The reason this type of transduction is called specialized is because the transferred bacterial DNA isn’t random; it is specific to the site on the bacterium’s
genome where the virus incorporates itself, which in some cases can predictably be genes encoding toxins or antibiotics resistance.

In comparison to generalized transduction, you can see that in specialized, once the virus enters the cell, it’s nucleic acid becomes integrates lysogenically
within the bacterium’s. Upon reemergence, we now have viral nucleic acid with flanking bacterial sequences.

The USMLE could ask which of the following observations by a researcher about transferred bacterial genes would support specialized transduction as the
mechanism. The answer will be something like, “Genes traced to locus adjacent viral excision site.” Wording can seem a bit recondite, but it’s not hard now
that we discussed it.

Transformation

Transformation is when a bacterial cell picks up free DNA fragments/genes directly from the extracellular medium.
Bacteria that are capable of transformation are known as “competent.” S. pneumo is known as a natural transformer, and is therefore competent.

The highest yield point for USMLE is that transformation can be disrupted when DNase is added to the surrounding medium. This is because it will break
down any free DNA fragments/genes that are floating around and exposed.

The USMLE will ask something like, “Which of the following observations by a researcher most likely supports transformation as the mechanism for
antibiotics resistance gene transfer?” The answer will be something like, “Process is disrupted with addition of nucleotidase.”

Or they can say, “A researcher is conducting an experiment regarding bacterial antibiotics gene transfer. It is observed that the process is disrupted by the
addition of DNase. What is the most likely mechanism of gene transfer?” Answer = transformation.

1. What process is shown here?

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DNA viruses
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Parvovirus B19

Causes Fifth disease = “slapped cheek” facial erythema in Peds.

Once child has developed the red cheeks, he/she has immunologically cleared the illness (i.e., if they turn it into a behavioral science Q, tell parents to chill
the fuck out / relax because the child has cleared the virus).

Can cause exanthem (body rash) +/- arthritis in adults, especially in daycare workers (USMLE is obsessed with this).
Can cause pure-RBC aplasia (i.e., only RBCs are low) or full-blown aplastic anemia (where all cell lines – RBCs, WBCs, and platelets – are down).

There is increased risk of pure-RBC aplasia and aplastic anemia if the infection occurs in utero and in sickle cell patients.

Next best step in diagnosis for Fifth disease or exanthem/arthritis is check serum IgM titers.

If any of the hematologic cell lines are down, do bone marrow biopsy to confirm diagnosis.

Human papillomavirus (HPV)

HPV 6+11 cause condylomata acuminata (geneital warts).

However, the warts caused by strains 6+11 are not limited to the genitalia and can cause laryngeal papillomatosis in neonates and infants (warts of the
vocal cords), which is asked on NBME. Lesions will have papillary structures on biopsy. Acquired vertically via exposure from maternal vaginal canal.

HPV 16+18 cause squamous cell carcinoma of genitalia/anus; risk of overt SCC is increased ­in immunocompromised (i.e., HIV in MSM) and heavy smoking.
Students will get maniacal about other SCC-causing strains beyond 16+18 but USMLE doesn’t give a fuck.

JC polyomavirus

Causes progressive multifocal leukoencephalopathy (PML).

Presents as neurodegeneration over weeks to months in immunocompromised patient – i.e., AIDS patient with CD4 count <100, patients undergoing
chemoradiotherapy, or those on immunosuppressant drugs.

USMLE wants you to know this condition is due to “reactivation of latent infection,” which means the patient is infected at some point during life years ago,
but the condition now manifests due to immunosuppression. “Acute infection in immunocompromised patient” is the wrong answer.

BK polyomavirus

Causes kidney infections in kidney transplant patients. Rare. You could just be aware it exists. I believe one Q ever in history exists on NBME somewhere.

Adenovirus

Most common cause of viral conjunctivitis.

Will present as teary eye that is either unilateral or bilateral, and either itchy or non-itchy.
Treatment is supportive with saline rinse.
Can also cause hemorrhagic cystitis (albeit more rare). For example, USMLE can give easy vignette of viral conjunctivitis in a school-age kid + ask what else
is most likely to develop in the patient –> answer = hematuria.
Hepatitis B

Mandatory stuff for USMLE is the serology (I discuss below).

Most common hepatitis infection in the worldwide. USMLE likes China for hepatitis B. Just a pattern I’ve noticed. Due to ­increased unvaccinated. In the
USA, HepC is most common.

Parenteral; can be acute or chronic.

Transmitted vertically from mother to neonate, sex, IV drugs, or blood exposure.

Present in all body fluids, including breast milk.

Serology very HY (I discuss meaning of variables below the table):

HBsAg = HepB surface antigen.

HBsAb = HepB surface antibody; if positive, patient is immune; if negative, patient is not immune.

HBcAb = HepB core antibody; if positive, patient either currently has HepB or had it in the past (i.e., cleared it).

HBcAb IgM = has acute infection.

HBcAb IgG = has chronic HepB or has cleared it.

Window period = Once a susceptible patient is exposed to HepB and the immune system attempts to clear it, sometimes Surface antigen will decline to the
point that it is no longer detectible. But at the same time, the Surface antibody might not be high enough / at detectable levels yet. This is called the
“window period,” where both Surface antigen and antibody are negative, so it can appear as though the patient doesn’t have an infection. However, Core
antibody IgM will be (+). So the key point is that 1) you know the double-negative Surface antibody/antigen combo is seen in the window period, and 2) that
Core antibody IgM is most reliable during the window period.

Vaccination against HepB is at birth, 2 months, and 6 months (no longer at 4 months).

Only give HepB IVIG to neonate if mom is confirmed (+). A 2CK NBME Q gives mother’s status as unknown when child is born –> answer = “Give HepB
vaccine now + only give IVIG if mother is positive.”

If patient has Hx of completed HepB vaccination but has titers that show susceptibility, the answer is just “give more vaccine.” Sometimes people’s
immunity wanes.
USMLE really doesn’t give a fuck about HepB pharm (i.e., entecavir, tenofovir). Waste of time. You could be aware that interferon-alpha can be used for
HepB.

Poxvirus

Largest DNA virus.

Causes molloscum cantagiosum, which presents as skin-colored or reddish papules with central umbilication. Very HY spot-diagnosis for Peds.

USMLE likes giving vignette where kid went to a recent pool party.

You can also be aware of another poxvirus called Vaccinia, which is similar to smallpox and was used in the development of the smallpox vaccine. “Vaccinia”
shows up as an answer on a new NBME where they talk about smallpox eradication.

Herpes simplex (HSV) 1/2

Causes painful vesicular lesions of the lips and genitalia that recur at varying intervals (usually months).

Primary infection is most severe, often with fever, regional lymphadenopathy, burning/stinging/itching pain (herpetic neuralgia), and many vesicles.
Recurrences are often less severe and preceded by herpetic neuralgia. USMLE wants you to know herpes goes latent in sensory nerves (makes sense, since
recurrences cause neuralgia/pain).

Don’t confuse HSV1/2 with chancroid caused by the bacterium Haemophilus ducreyi. HSV1/2 will be usually be clusters of painful lesions that demonstrate
recurrence, whereas chancroid will be a singular lesion that is not recurrent. There is one Q out there where they give you a singular painful lesion with
recurrence, and the answer is HSV, not H. ducreyi. In this case, the recurrence is what tells you it’s HSV1/2. Perhaps in some cases, herpetic infections can
start as a single vesicle before erupting into the typical cluster-appearance. H. ducreyi is also typically acquired overseas, e.g., in backpackers traveling in the
third-world.

HSV1/2 can cause herpes encephalitis (confusion + blood in CSF due to temporal lobe hemorrhage).

I would say 4/5 herpes encephalitis Qs mention blood in the CSF. There’s one 2CK neuro form Q where the blood is negative, but the CSF findings are
otherwise viral (normal glucose and protein; high lymphocytes).

You also need to know that CT of the head can be negative. I mention this because even though it can cause temporal lobe hemorrhage, the Q can say CT
shows no abnormalities. They might mention spikes over the temporal region (implying there’s still abnormality/hemorrhage there). So they can say
something like: 24-year-old male with confusion and fever + viral CSF findings + blood in CSF + CT of head shows no abnormalities + EEG shows spikes over
temporal region. Answer = intravenous acyclovir.

Can cause herpetic whitlow, which presents as vesicles on the finger in a child who’s touched a mother’s cold sore while breastfeeding, or in dental
workers/hygienists.
 Herpetic whitlow

Can cause eczema herpeticum, which is HSV1/2 infection superimposed on eczema. Can present with stinging/burning pain (herpetic neuralgia). Treat with
acyclovir.

Eczema herpeticum

Can cause herpes keratitis (inflammation of the cornea). Presents as dendritic (tree-like) pattern on fluorescein instillation of the eye. It may or may not
present with periorbital vesicles.

Herpes keratitis

Herpes esophagitis presents as punched-out ulcers and odynophagia (pain with swallowing). This is in contrast to CMV esophagitis, which causes
linear/confluent ulcers.

Viral culture can be negative in stem (not 100% sensitive).

Treat with acyclovir (or valacyclovir), which is a DNA polymerase inhibitor. HSV1/2 resistance to acyclovir occurs via altered viral thymidine kinase.

Varicella zoster virus (VZV; human herpes virus-3; HHV-3)

Causes chickenpox; can be described as clusters of vesicles at different stages of healing on an unvaccinated child or adult. Chickenpox Qs are exceedingly
rare for USMLE. What they actually care about is shingles.

Shingles is aka herpes zoster. Herpes zoster is not the name of a virus. This is just another name for shingles. So we can say, shingles, aka herpes zoster, is
caused by varicella zoster virus.

Shingles presents as vesicles erupting in a dermatomal distribution (i.e., usually on the flank or back of neck) idiopathically in middle-age individuals or
older. Can be brought on by stress or transient negative flux in immunity.
Once the vesicles rupture, they can sometimes look black. So just know it’s weird but possible. What’s most telling for herpetic infections (whether it be
HSV1/2, or VZV causing shingles) is that they form characteristic clusters of small vesicles. It’s this characteristic clustering that can be buzzy/easy for
herpetic infection.

Shingles can occur in immunocompromised kids (e.g., those undergoing chemotherapy). This is called pediatric shingles. Just know “it’s a thing.” Because
most students think it only occurs in middle age or older.

Pediatric shingles

Can cause herpes zoster ophthalmicus (periorbital vesicles), which means shingles of the eye. This may or may not co-present with keratitis (and the
dendritic pattern) that looks identical to that caused by HSV1/2.

Can cause herpes zoster oticus (vesicles in the ear), which means shingles of the ear. This may or may not present with concurrent Bell’s palsy due to CN VII
involvement. Bell’s palsy due to shingles is called Ramsay-Hunt syndrome type II.

Herpes zoster oticus

Vaccination against VZV occurs with two doses: the first at 12-15 months; the second at 4-6 years.

Shingles vaccine is given at age 50 (on new Family Med form).

These vaccines are live-attenuated.

Treat shingles with acyclovir (or valacyclovir).

Varicella can cause pneumonia in immunocompromised and pregnant women. Slightly unusual, but just know it’s possible.

VZV immunoglobulin is given to a neonate if an unvaccinated pregnant woman develops a chickenpox rash within 5 days prior to 2 days post-parturition.

If pregnant woman contracts chickenpox, the fetus may develop congenital varicella syndrome, which can present as microcephaly and skin vesicles
demonstrating a “zig-zag” pattern.

Ebstein-Barr virus (EBV; human herpes virus-4; HHV-4)

Causes mononucleosis, nasopharyngeal carcinoma, oral hairy leukoplakia, and both Hodgkin and non-Hodgkin (notably Burkitt) lymphomas.

Mononucleosis is usually caused by EBV, but can also be CMV.

The virus invades B cells, which then stimulates the immune system to produce CD8+ T cells attacking the viral-infected B cells. In mono, these CD8+ T
cells are called “atypical lymphocytes.” The USMLE wants you to know these are reactive CD8+ T cells. They are “reactive” because they are responding to
the viral-infected B cells.
Primary infection presents usually in teenager or young adult with fever >38 C, lymphadenopathy, tonsillar exudates, and lack of cough, making the
presentation appear bacterial (in the HY Pulmonary PDF, I talk about CENTOR criteria for differentiating bacterial from viral URTIs). As a result, it is often
misdiagnosed as Strep pharyngitis.

If amoxicillin or penicillin is given to treat EBV, this can cause a rash. This is not to be confused with a rash caused by allergy to beta-lactams. If pre-
adolescent receives beta-lactam and gets a rash, that is likely beta-lactam allergy. If a patient adolescent or older gets a rash, we do a heterophile antibody
(Monospot) test as next best step in diagnosis, as EBV mono is more likely.

The heterophile antibody test is how we diagnose EBV, where for some magical reason, the antibodies we produce against EBV cross-react with horse and
sheep RBCs, hence the antibodies like (-phile) different (hetero-) antigens.

Following the primary infection, mono can present as recurrent episodes of extreme fatigue that arise at interval of months to years.

Nasopharyngeal carcinoma is a type of squamous cell carcinoma.

Oral hairy leukoplakia presents as white lesions on the tongue that cannot be scraped off. They are not pre-cancerous (no dysplasia on biopsy). This is in
contrast to “regular” leukoplakia caused by tobacco, which is a precursor to SCC.

The increased risk of Hodgkin and non-Hodgkin lymphomas is because EBV invades B cells.

Cytomegalovirus (CMV; human herpes virus-5; HHV-5)

Most common organism transmitted via blood transfusions and organ transplants.

Causes infections of many different organ systems (e.g., lung, kidney, GI tract, retina), as well as CMV mono. There is an NBME Q where they give CMV
pneumonia in patient following renal transplant, where they show the buzzy owl-eye appearance of cells.

USMLE likes “intranuclear inclusions” or “intranuclear inclusion bodies” for CMV. This refers to the “owl eyes” that can be seen on histo.

CMV esophagitis presents as linear/confluent ulcers and odynophagia. This is in contrast to HSV1/2, which cause punched-out ulcers.

CMV colitis presents as linear/confluent ulcers in AIDS patients with CD4 counts under 50-100.

Blurry vision in HIV patient = CMV retinitis until proven otherwise.

CMV mono is differentiated from EBV mono in that the former has a negative heterophile antibody (Monospot) test. Additionally, CMV can cause cold
autoimmune hemolytic anemia due to the production of IgM antibodies against RBCs, with a positive Coombs test (means we have antibodies against
RBCs). So if patient with mono has low hemoglobin and high LDH, for instance, that could point toward CMV over EBV. High LDH on USMLE almost always
means hemolysis, since RBCs are packed with LDH.

CMV is treated with ganciclovir, which is a DNA polymerase inhibitor. CMV resistance to ganciclovir occurs via altered viral thymidine kinase. The MOA
and resistance mechanisms are the same as HSV1/2 and VZV with respect to acyclovir.

The stem might mention a patient who had a kidney transplant 6 months ago who now has deteriorating renal function + intra-nuclear inclusions seen on
biopsy. The answer is just “ganciclovir therapy.”

Human herpes virus-6 (HHV-6)

Causes roseola infantum, aka Sixth disease, or exanthema subitum.

Very easy/buzzy descriptor for USMLE: causes a “spiking fever followed by a rash” in a kid.

USMLE will literally say something to the effect of a kid having a maculopapular body rash that was preceded by a worrisome fever of 39C for the 3 days
prior. Once the rash has formed, the child has cleared the infection (similar to slapped cheek appearance with Fifth disease due to Parvo).

Virus is self-limiting / no treatment necessary.

Human herpes virus-7 (HHV-7)

Causes pityriasis rosea, which is a rash that starts as Herald patch (larger pink ellipse), usually on the back or trunk, then spreads upward onto the shoulder
blades (“Christmas tree distribution”); USMLE will show you image and expect you can make spot-diagnosis.

Can occur in teenagers, although more common in the 20s. May or may not be itchy.

Virus is self-limiting / no treatment necessary.

Kaposi sarcoma-associated herpesvirus (KSAH; human herpes virus-8; HHV-8)

Kaposi sarcoma is violaceous, tumorous lesions of vascular-lymphatic origin.

Usually seen in immunocompromised patients (i.e., AIDS, chemotherapy).

Q can show you image such as above and then the answer is just “anti-neoplastic” for the Tx (whereas answers like anti-fungal, anti-bacterial, etc., are
wrong).

Bacillary angiomatosis caused by Bartonella henselae (normally causes cat-scratch disease) can present as Kaposi sarcoma-like lesions. What USMLE will do
is give you a vignette that sounds just like Kaposi sarcoma (i.e., AIDS patient with violaceous skin lesions), followed by asking you for the organism that
causes it. You’ll notice that HHV-8 (as well has HepC for lichen planus) isn’t listed, where all the answers are bacteria, and you just select Bartonella henselae.

1. Patient with history of kidney transplant develops wheezes in both lung fields + fever. Biopsy specimen is shown. What is the most likely organism?
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HY USMLE Q #962 – Micro / Pharm

January 23, 2024
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MICROBIOLOGY

Fungi
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Many fungi can be grown on Sabouraud agar, so you can memorize this factoid as a starter.

Dermatophytes are fungi that cause skin infections.

Trichophyton spp.

T. rubrum causes many skin infections, including tinea corporis (ring worm), tinea cruris (jock itch), tinea pedis (athlete’s foot). It also causes onychomycosis
(fungal infection of the nail).

USMLE will usually not play trivia where they list 5 different fungi and you’re expected to know T. rubrum is the one causing the tinea corporis. What they’ll
do is literally list 3 bacteria, 1 fungus, and a miscellaneous diagnosis like eczema, and then you just choose the one fungus listed, e.g., T. rubrum. It’s quite
easy.

T. tonsurans is known to cause tinea capitis (fungal infection of the scalp).

Microsporum and Epidermophyton

Microsporum causes tinea corporis and tinea capitis. Epidermyophyton causes tinea pedis and tinea cruris. You do not need to memorize these specific
conditions caused by Microsporum and Epidermophyton. I just want you to know these fungal names are dermatophytes / fungi in general.

What USMLE cares about is you being able to spot-diagnose dermatophyte fungal infections via an image and then choose the treatment.
The above image is tinea capitis. USMLE will show you this image and then the answer is “oral griseofulvin for patient only”; “oral griseofulvin for patient
and classmates” is wrong answer. Or they’ll show the above image and then the answer is just “Trichophyton tonsurans,” where it’s the only fungus listed.

If the USMLE asks how to prevent tinea capitis, the answer is “avoidance of sharing of hats.” Sounds easy, but it’s asked on an NBME and many students get
it wrong. They select answers like “use of anti-fungal shampoo” or “avoidance of wooded areas,” which are wrong.

Tinea capitis is often described as a “circular area of scaling alopecia.”

The above image is tinea corporis (ring worm). The Q can say a patient has pet dogs or uses yoga mats at the gym. USMLE will show you this image and then
the answer is just “clotrimazole” or “miconazole.” We treat tinea corporis, tinea pedis, and tinea cruris with topical -azoles. You need to know clotrimazole
and miconazole are specifically topical, whereas others like fluconazole and itraconazole are oral. Tinea pedis can also be treated with topical terbinafine.

Tinea pedis presents as itchy scaling between the webs of the feet.

Above image shows tinea pedis. There is an NBME has a Q where they tell you a febrile patient has itchy, erythematous scaling on the foot that extends up
the dorsum of the foot onto the ankle + they ask the cause of the fever in the patient. The wrong answer is Trichophyton. The correct answer is S. aureus.
Students get confused by this, but there’s two points: 1) they ask for the cause of the fever; fungi rarely cause fever, whereas S. aureus is a more likely
culprit; and 2) tinea pedis usually presents as itchy, scaling webs between the toes; the erythematous extension up to the ankle is likely a bacterial cellulitis
that has superimposed on the cracked skin.

In this case, oral dicloxacillin or cephalexin would treat the S. aureus skin infection; topical -azole or terbinafine could be used for the tinea pedis.
Above image is onychomycosis. USMLE can show you this image and then the answer is just “oral terbinafine for 12 weeks.” You don’t have to memorize
that 6 weeks is for fingernails and 12 weeks is for toenails. I’m just saying what the answer can show up as, where all the others are clearly wrong. Oral
terbinafine is classic for onychomycosis because it has a unique ability to concentrate in keratinous tissues. Topical terbinafine, in contrast, is used for tinea
pedis (or topical -azoles).

Yeast are a single-celled fungi and reproduce through budding. They tend to be round or oval in shape.

Candida

Forms pseudohyphae. This detail for whatever reason is HY. Hyphae are multicellular structures formed by mold (a form of fungus). However, candida is a
yeast, not a mold, so the structures it forms look like hyphae, but they’re not, hence pseudohyphae. The image is HY:

Skin infections with Candida tend to occur opportunistically – i.e., in diabetics, immunocompromised patients, or those receiving ongoing broad-spectrum
antibiotics (e.g., for endocarditis). In contrast, dermatophyte infections tend to occur sporadically in immunocompetent patients.

Persistent skin infections can occur in those with T cell dysfunction or deficiency. Chronic mucocutaneous candidiasis is a T cell dysfunction disorder. The
USMLE will give a 17-year-old girl who’s had candidal skin infections since birth, and then the answer will just be “impaired cell-mediated immunity.” The
answer can also just be “T cell” for which cell that’s fucked up.

Diabetes causes dysglycemia, which is a major risk factor for candidal skin infections, as well as vulvovaginal candidiasis. This is because persistently
elevated glucose can weaken the immune system (i.e., impair neutrophil and macrophage function). In addition, candida likes high-glucose environments, so
persistent glycosuria supports growth. And high glucose also facilitates candidal biofilm production and growth on mucosal surfaces.
USMLE will give an obese woman with diabetes who has a moist, red plaque underneath one of her breasts + they ask for biggest risk factor –> answer =
diabetes, where obesity is wrong. When both answers are listed together, choose diabetes (or dysglycemia). Obesity is only an indirect risk factor in that it
leads to insulin resistance and dysglycemia, so the latter is the direct risk factor. Treatment for candidal skin infections is topical or oral -azole.

You also need to be aware of diaper rash, which can be caused by candida. The USMLE might show you reddish maculopapular clusters in the groin of a
baby, and the answer is Candida.

Systemic candidal infections can occur in those receiving total parenteral nutrition (TPN; hyperalimentation), since a central venous line can become
colonized and TPN contains glucose.

Systemic infections can also occur in those with neutropenia (agranulocytosis).

Vulvovaginal (and penile, albeit more rare) candidiasis is treated with oral fluconazole or topical nystatin. USMLE will give you an easy vignette where they
describe thick white discharge per vaginum (buzzy for candida), or they’ll say there’s vulvovaginal erythema and itchiness, without saying there’s discharge,
and then show you the image of the pseudohyphae, and then they’ll ask the MOA of the oral agent to be prescribed –> answer = “Inhibition of P-450-
mediated demethylation,” which refers to fluconazole. -Azoles inhibit 14α-demethylase, which blocks the conversion of lanosterol to ergosterol (fungal
equivalent of cholesterol in the cell membrane).

Oropharyngeal candidiasis (oral thrush) can be seen in immunocompromised patients, but it is also seen in asthma patients who use inhaled corticosteroids
(e.g., fluticasone). Patients must rinse their mouths out with water following inhaled corticosteroids, otherwise oropharyngeal mucosal immunity can be
weakened. Oral thrush presents as white plaques on the palate or tongue that bleed when scraped off. Treatment for oral thrush is nystatin mouthwash.
Nystatin pokes holes in the ergosterol cell membrane.

Oropharyngeal candidiasis is not to be confused with candidal esophagitis, which always occurs in immunocompromised patients. Odynophagia (pain with
swallowing) in an immunocompromised patient is candidal esophagitis till proven otherwise. Endoscopy will show white streaks. Treatment is oral
fluconazole. In contrast, herpes esophagitis will show punched-out ulcers. CMV esophagitis will show linear/confluent ulcers.

Cryptococcus neoformans

Demonstrates narrow-based budding. The N’s go together – i.e., Narrow-based budding for C. neoformans. This is in contrast to Blastomycosis, which is
Broad-based budding.

Causes fungal meningitis in immunocompromised patients (usually AIDS).

CSF analysis will show low glucose, high protein, and high lymphocytes.

High opening pressure can sometimes be seen with fungal meningitis and may be suggestive, although it is not specific, so do not use it as confirmatory
when you are reading vignettes.

Latex agglutination testing of the CSF is most accurate, although India ink prep and mucicarmine staining are also often done.

The India ink prep is a spot-diagnosis for C. neoformans. There is a black background, where the only thing that doesn’t stain dark is the halo-like
polysaccharide capsule of C. neoformans.
Mucicarmine staining is red. You don’t have to be a pathologist. The vignette might give you an IV drug user with fever, stiff neck, and photophobia (i.e.,
meningitis symptoms) + they show you this stain, and then the answer is just “C. neoformans,” or “amphotericin B” as the treatment.

Amphotericin B, similar to nystatin, pokes holes in the ergosterol membrane. It is hard-hitting and used for CNS and disseminated fungal infections. For
example, if a patient has a simple fungal pneumonia, he or she might receive oral fluconazole. But if a patient has fungemia with rigors, chills, and high fever
(implying serious systemic infection), then amphotericin B is used.

Pneumocystis jirovecii

Causes bilateral pneumonia (Pneumocystis jiroveciii pneumonia; PJP) in immunocompromised patients (usually HIV/AIDS). Can sometimes be described as
“ground-glass,” although this descriptor is only seen in a minority of Qs.

A HY point about PJP is that it is specifically bilateral. If the vignette gives you an HIV patient with a lobar pneumonia, the answer is S. pneumo, not PJP.
Students get this wrong all of the time, where they choose PJP in an AIDS patient with a lobar pneumonia, and then they’re somehow flummoxed that they
got it wrong.

Comes in at a CD4 count of 200 in HIV/AIDS. Prophylaxis and treatment is trimethoprim/sulfamethoxazole (TMP/SMX).

As I talk about in the HIV section of the RNA viruses – Part II module, TMP/SMX is also the prophylaxis for Toxoplasmosis, although the treatment for Toxo
is instead sulfadiazine and pyrimethamine. What USMLE loves to do is give you a patient with a low CD4 count (e.g., 47) who has ring-enhancing lesion of
the brain who is taking HAART and TMP/SMX. The diagnosis is primary CNS lymphoma, not Toxo. And the way we know Toxo is wrong is because the
patient is on TMP/SMX, which is the prophylaxis for both Pneumocystis and Toxo. So commencing TMP/SMX at a CD4 count of 200 for PJP is “two birds
with one stone” by the time the patient gets to CD4 of 100, which is when Toxo comes in. It’s only patients who aren’t on TMP/SMX by the time they fall to
CD4 of 100 who get Toxo.

PJP is diagnosed with bronchoalveolar lavage (after the CXR shows bilateral ground-glass pneumonia), which is when sterile saline is injected into the
lungs via a bronchoscope and then aspirated/collected for examination. Pneumocystis is classically visualized as oval yeast on silver stain.

Malassezia furfur

Causes tinea versicolor, which is an extremely buzzy and pass-level spot-diagnosis on USMLE. This is a fungal infection of the shoulder blades, back, and
upper torso that tends to occur in sub-tropical or tropical areas, where the patient presents with spotty hypopigmentation.

The hypopigmentation is due to fatty acid degradation within the skin, which releases an acidic product by the fungus that inhibits tyrosinase (enzyme
necessary for melanin synthesis).

The vignette will give a 24-year-old male who frequently goes surfing in Florida + they show you the buzzy image:

Then the answer is just “topical selenium,” which is extremely HY as the treatment.

Malassezia furfur can also cause seborrheic dermatitis (aka dandruff), which is a fungal infection of the scalp, hairline, and sometimes face. It presents as an
itchy, flaky scalp in someone with otherwise no observable cutaneous findings, or more severely as a scaly, erythematous hairline with weaping papules.
Occasionally it affects the face itself. This is not to be confused with tinea capitis, which instead presents as a circular area of scaling alopecia.

Seborrheic dermatitis is treated with selenium or -azole shampoo.

Don’t confuse seborrheic dermatitis with seborrheic keratoses, which are dark, stuck-on, greasy lesions on the faces of elderly and smokers, where they
appear as though they can be pealed off.

Mold is fungus that is multicellular (hyphae) and reproduces via spores.

Mucorales

Order of fungi that are referred to as “bread mold” and are found ubiquitously in the environment.

Have non-septate hyphae that branch at 90-degree (wide) angles. This is in contrast to Aspergillus, which produces branched, 45-degree (acute angle)
septate hyphae.
They cause mucormycosis, which is a serious fungal infection that loves to infect the sinuses, eyes, and brain, causing blindness and death. Infected tissue
can appear black.

Immunocompromised patients and those with uncontrolled diabetes are at greatest risk.

USMLE can say a 9-year-old girl has a 4-year history of diabetes + has gangrene of the forehead and sinuses + light microscopy shows 90-degree hyphae –>
answer = “mucormycosis” as the diagnosis, or “Rhizopus” as one of the causal fungi, or “amphotericin B” as the treatment.

Aspergillus

Forms 45-degree, branched, septate hyphae.

Causes Aspergilloma (“fungus ball”), which can present as a nodular density on chest x-ray, especially in those with history of TB. The latter can leave
cavities within the lung that Aspergillus likes to occupy. NBME Q wants “biopsy and culture of the mass” as the answer for what is most likely to confirm the
diagnosis (makes sense).

Acute bronchopulmonary Aspergillosis (ABPA) presents as respiratory exacerbation in a patient with asthma or cystic fibrosis who has hypersensitivity to
Aspergillus antigens. The diagnosis is easy, so the main point is just that you know ABPA “is a thing” / exists. The vignette will say 30-year-old + Hx of asthma
+ in respiratory distress and low-grade fever + skin test shows strong reactivity to Aspergillus antigens.

Aspergillus is also the most common cause of fungal otitis externa. NBME will give a vignette of black necrotic tissue of the ear + simply ask for the diagnosis
(i.e., necrotizing otitis externa).

Histoplasma

Known for very small size (2-4 μm); smaller than RBCs.

Found in the Ohio-Mississippi river valley (although not limited to). Associated in particular with caves (i.e., spelunking) and bird droppings (i.e., person who
feeds pigeons in park).

Can cause pulmonary infections that resemble TB.

Disseminated histoplasmosis can cause adrenal insufficiency (you could be aware of it as a rare cause).

Treat simple infections with oral fluconazole. Treat severe/disseminated infections with IV amphotericin B.

Blastomyces

Demonstrates broad-based budding. The B’s go together – i.e., Broad-based budding for Blastomycosis. This is in contrast to C. neoformans, which is Narrow-
based budding.

Found in the Ohio-Mississippi river valley (although not limited to). Associated in particular with decaying wood.

Likes to cause skin infections, resulting in ulcerative/necrotic lesions. Can sometimes present as pneumonia or osteomyelitis.

Treat simple infections with oral fluconazole. Treat severe/disseminated infections with IV amphotericin B.
Coccidioides

Presents usually as uncomplicated fungal pneumonia in patient living in western / south-western United States. Dust is the major risk factor, particularly in
the setting of earthquakes (dumb, buzzy event USMLE likes).

Classic textbook descriptor of the histo is “spherules filled with endospores” (left image), although USMLE doesn’t really give a fuck about that. What they
will do is show you the barrel-shaped hyphae (right image) in a patient who lives in California + ask you for the diagnosis –> answer = Coccidiodes. I point
this out because, if you know the descriptor “spherules filled with endospores,” but then they show you the image on the right, you’re like what the fuck? So
it’s to my observation based on the NBMEs that “barrel-shaped hyphae” is more important for Coccidiodomycosis.

Uncomplicated fungal pneumonia is treated with fluconazole. I believe there’s a UWorld question floating around where they have “no treatment
necessary” for simple pneumonia caused by Coccidioides, but this is garbage for USMLE. You give the patient fluconazole.

Treat severe/disseminated infections with IV amphotericin B.

Paracoccidioides

Found usually in South America; also in central America. Easy to remember, as the main species if Paracoccidioides brasiliensis (i.e., Brazil).

Causes pulmonary infections, ulcerative lesions of the pharynx, and skin infections.

Forms a distinctive “captain’s wheel” appearance, which is multiple buds in a radiating pattern from a singular parent cell.

Simple infections are treated with itraconazole. Treat severe/disseminated infections with IV amphotericin B.

Sporothrix schenkii

Causes rosette- or daisy-like clusters of conidiophores (spores).

Classically causes a papule at the finger in gardeners following a prick by a rose thorn. This is extremely buzzy and I’d say only mentioned in about 1/3 of
vignettes.

The higher yield point about sporotrichosis is that it causes lymphangitis (i.e., lymphocutaneous sporotrichosis), where it ascends to the axilla as either an
erythematous streak, or as erythematous ulcerative lesions on the forearm.

What the USMLE will do is show you the above image in guy who was doing house/yard work presents, and then they ask what is causing it (i.e., arteriitis,
phlebitis, lymphangitis, etc.), and the answer is just lymphangitis.

You should also be aware tangentially that lymphangitis causing the pink streak can also be caused by general trauma and burns (i.e., it is not limited to
sporotrichosis). USMLE can give you a guy who burned his hand + show you the image of the pink streak, and the answer is once again just lymphangitis.

Infections are treated with itraconazole.

1. Which fungus causes tinea versicolor?

How does it present?

What is the treatment?

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Gram (+) cocci

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USMLE - Gram (+) cocci - Everything HY you need to know

You can see that catalase (+) vs (-) is how we differentiate the Staph vs Strep.

Staph aureus

Gram (+) cocci in clusters; catalase (+); coagulase (+).

Grows yellow on culture medium (“golden staph”).

Produces Protein A, which can cleave the Fc region of IgG.

Humans can carry S. aureus within the nares (nostrils). If USMLE asks about nosocomial transmission, the answer is “carried within the nares of hospital
staff.”

Highest yield points for USMLE is that it causes:

Acute endocarditis (no previous valve abnormality); usual organism for IV drug users.
 Skin infections (cellulitis, erysipelas, impetigo, abscesses). S. aureus eclipses Group A Strep (Strep pyogenes) for cellulitis, as well as for both bullous
and non-bullous impetigo. Group A Strep eclipses S. aureus for erysipelas.
Mastitis in breastfeeding women.
Osteomyelitis; most cases are S. aureus. In sickle cell, however, there is increased risk of Salmonella osteomyelitis.
Septic arthritis; most cases are S. aureus. If vignette explicitly talks about promiscuity or gives cutaneous papules/pustules, the answer
is Gonorrhea instead.
Toxic shock syndrome; TSST toxin is a super-antigen that bridges MHC-II on macrophages with T-cell receptor on CD4+ T cells. Once the bridging
has occurred, macrophages release cytokines. TNF-α causes hypotension; IL-1 causes fever. Do not confuse this mechanism with endotoxic shock,
which is when the lipid A component of lipopolysaccharide (LPS) from gram-negative bacteria binds to CD14 (Toll-like receptor) on macrophages;
the macrophages then release cytokines.
Staphylococcal scalded skin syndrome (SSSS); exfoliative toxin causes a generalized salmon-pink rash and desquamation of palms and soles in
neonates.
Food poisoning due to heat-stable pre-formed toxin in meats or dairy products (i.e., creams, potato salad) that have been sitting at room
temperature for a while. Presents as vomiting 1-6 hours after consumption (diarrhea is +/-).
Pneumonia following influenza infection.
Bacterial superinfection on scabies lesions.
Common organism in many immunodeficiency Qs, including leukocyte adhesion deficiency and chronic granulomatous disease (NADPH oxidase
deficiency).

HY points about treating S. aureus:

90% of community Staph (i.e., methicillin-sensitive S. aureus; MSSA) produces beta-lactamase. This means penicillin, amoxicillin, or ampicillin alone will
usually not work and are wrong treatments. Oral amoxicillin combined with clavulanate (Augmentin), or IV ampicillin combined with sulbactam, serve the
purpose of covering S. aureus, since clavulanate and sulbactam are beta-lactamase inhibitors, but giving amoxicillin or ampicillin alone should be considered
inadequate for covering Staph.

What this means is, when we treat S. aureus, we want to give a methicillin-class beta-lactam, since these are heavily steric and are beta-lactamase resistant.
Methicillin isn’t given clinically because it causes interstitial nephritis (eosinophils in the urine + rash), but oral dicloxicillin (not doxycyline) and IV
flucloxacillin are frequently given, since these cover Staph.

So for skin, we can give oral dicloxacillin or cephalexin out-patient, or IV flucloxacillin or cephazolin in-patient, as these will cover S. aureus in addition to
Group A Strep.

First-generation cephalosporins, such as cephalexin and cephazolin, are also beta-lactamase resistant and are the same as the methicillin-class beta-
lactams for all intents and purposes.

For impetigo only, USMLE likes topical mupirocin, but for oral meds, use as per above.

The only other methicillin-class beta-lactam you need to know for USMLE is nafcillin, which is hard-hitting and used for confirmed MSSA endocarditis. It is
also known to cause interstitial nephritis.

I’ve seen this on NBME. Other agents like cloxacillin, oxacillin, etc., I’ve never seen show up on NBME, but students get fanatical about listing off different
drugs.

For USMLE, they might ask you why Staph is resistant to amoxicillin but not to cephalexin; the answer is “production of penicillinase,” or “production of
beta-lactamase,” as we said.

If they ask how MSSA → MRSA, the answer is “altered penicillin-binding protein.” We know “production of beta-lactamase” is wrong here because
MSSA already produces beta-lactamase, so clearly that mechanism can’t be the reason why it can become MRSA.

MRSA endocarditis is treated with vancomycin. Vancomycin, however, has poor skin penetration, so if a cutaneous infection is caused by MRSA, we treat
that with clindamycin, doxycycline, or trimethoprim-sulfamethoxazole. You do not need to memorize these latter three treatments and USMLE won’t ask.
I’m just saying as a medicine 301-level tangential point that vancomycin isn’t used for MRSA skin infections. But it’s pass-level you know that MRSA
endocarditis is treated with vancomycin.

Empiric Tx for endocarditis is vancomycin (covers gram-positives, including MRSA) and gentamicin (covers gram-negatives). There are other regimens, but
you should know that one. Do blood cultures before antibiotics (asked on 2CK NBME).
Staph epidermidis

Normal skin flora.

Can cause infections of prostheses, including heart valves and joint replacements.

Vancomycin + gentamicin is the normal empiric Tx for endocarditis. If the patient has prosthetic material in the heart, add rifampin.

Staph saprophyticus

Can cause UTIs leading to staghorn calculi (aka struvite, or ammonium magnesium phosphate stones), which resemble rams horns.

This is because it is urease (+), and struvite stones form at high pH.

Points about hemolysis types:

Group A and B Strep both refer to β-hemolytic Strep (i.e., Group A and B Streps do not equal α- vs β-hemolytic, respectively).

β-hemolysis means complete hemolysis (clear zone of hemolysis on blood agar).

α-hemolysis means partial hemolysis (green zone of hemolysis on blood agar).

γ-hemolysis means no hemolysis (no change on blood agar).

Strep pyogenes (Group A Strep)

Gram-positive cocci in chains.

Infections cause elevation of anti-streptolysin titers.

Causes Strep pharyngitis, scarlet fever (strawberry tongue + salmon pink body rash [due to erythrogenic toxin]), and skin infections (cellulitis, erysipelas,
impetigo).

Post-streptococcal glomerulonephritis (PSGN) is a type-III hypersensitivity (immune complex deposition) that can occur following both pharyngitis as well
as cutaneous infections (i.e., it is not just caused by pharyngitis). It presents as red urine (hematuria) 1-3 weeks following the infection. This is not to be
confused with IgA nephropathy, which is red urine 1-3 days (not weeks) following a viral infection. In PSGN, serum complement protein C3 will be
decreased.

Rheumatic heart disease is a type-II hypersensitivity that only occurs following pharyngitis. The immune system makes antibodies against the M-protein
of S. pyogenes that cross-reacts (molecular mimicry) with the mitral valve (on USMLE, RHD will be mitral 29/30 times). Penicillin must be given to treat Strep
pharyngitis to prevent rheumatic heart disease. However, penicillin will not prevent PSGN. In RHD, the patient will have mitral regurg acutely, followed by
mitral stenosis years later after the valve scars over. 99% of mitral stenoses are due to history of RHD.

Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococci (PANDAS) is a psych condition asked on USMLE, where a child can develop
a tic, ADHD, or OCD following a Strep pyogenes infection.

S. pyogenes can cause toxic shock-like syndrome due to exotoxin A production, where the vignette can give cellulitis + shock, and the answer is just “MHC-II
and TCR” as the immunologic receptors bound. In other words, TSST toxin of S. aureus, as well as exotoxin A of S. pyogenes, both can cause shock via the
same mechanism.

Strep agalactiae (Group B Strep)

Gram-positive cocci in chains.

Causes neonatal meningitis, pneumonia, and sepsis.

Rectovaginal swabs performed in pregnant women at 36 weeks’ gestation to determine whether intrapartum IV penicillin or ampicillin prophylaxis is given.
For 2CK/3, indications for GBS prophylaxis:

Positive swab at 36 weeks’ gestation.

GBS bacteriuria at any point in the current pregnancy, even if successfully treated.
Hx of prior pregnancy where there was early-onset GBS disease in the neonate (i.e., meningitis, pneumonia, or sepsis). Mere colonization (i.e., mere
positive test) in a prior pregnancy is not an indication for giving prophylaxis in current pregnancy.
If the mother’s GBS status is unknown at parturition, give prophylaxis if any one of the following met: 1) maternal fever >38C; 2) rupture of
membranes >18 hours; 3) premature delivery (<37 weeks).

Neonatal infections on USMLE will be caused by GBS, Listeria, or E. coli. If they say a neonate has an infection caused by gram-positive cocci, the answer is
GBS; if they say gram-positive rods, that’s Listeria; if they say gram-negative rods, that’s E. coli.

Enterococcus

Gram-positive cocci in chains.

Normal flora within the gastrointestinal and urinary tracts.

The answer on USMLE for endocarditis following genitourinary manipulation (e.g., catheterization or TURP for BPH).

Treated with ampicillin. If resistant to ampicillin, we treat with vancomycin. If resistant to vancomycin (VRE; vancomycin-resistant enterococci), drugs such
as linezolid or daptomycin can be used. USMLE will not assess the latter two treatments for VRE. The important point is that you are merely aware VRE is
an important nosocomial pathogen, same as MRSA.

Strep gallolyticus / Strep infantarius

Formerly known as Strep bovis, but USMLE is old school, so it is not a guarantee the nomenclature has changed on the exam.

Can cause endocarditis in the setting of colon cancer.

Strep pneumoniae

Gram-positive diplococci (don’t confuse with Neisseria gonorrhea and meningitidis, which are gram-negative diplococci).

Most common cause of lobar pneumonia and otitis media.

Can also cause meningitis and sinusitis.

Ultra-HY as cause of sepsis in asplenia and sickle cell (auto-splenectomy).

USMLE might give chest infection in a teenager or young adult, where they say there’s right lower lobe dullness to percussion. You know that’s S. pneumo. If
they give bilateral interstitial infiltrates, that is most likely Mycoplasma. Pneumonia discussion is lengthy.

You don’t want to memorize S. pneumo as the “most common” organism for meningitis because USMLE wants you to differentiate it from Neisseria
meningitidis (meningococcus). If they give college dormitories, military barracks, or close quarters, this suggests N. meningitidis over S. pneumo. In
addition, N. meningiditis causes non-blanching rash (i.e., does not turn white when pressed); this can refer to purpura or ecchymoses. If they mention a rash,
the answer is meningococcus, not S. pneumo. Meningococcus also can cause Waterhouse-Friderichsen syndrome (bilateral hemorrhagic necrosis of the
adrenal cortices, leading to hypotension non-responsive to norepinephrine).

Empiric Tx for community-acquired pneumonia (CAP) is azithromycin on USMLE.

USMLE doesn’t assess levofloxacin (respiratory fluoroquinolone) for pneumonia Tx, but you could be aware that patients who’ve had antibiotics in the past
3 months, or who have significant comorbidities, sometimes they are upgraded to a respiratory fluoroquinolone. But offline NBME 8 for 2CK has
azithromycin straight-up as the answer.

For CAP where the patient is septic, ceftriaxone +/- vancomycin is given. Ceftriaxone is powerful and effective against S. pneumo. Some strains are
developing resistance, so vancomycin can be added (asked on one 2CK Q).
Meningitis empiric Tx is ceftriaxone + vancomycin. In elderly, ampicillin can be added.

Empiric Tx for otitis media is penicillin or amoxicillin. Recurrent otitis media, however, we can add clavulanate (Augmentin). But initially, we just give
amoxicillin or penicillin alone for otitis media.

Empiric Tx for sinusitis is amoxicillin/clavulanate (Augmentin). This is because sinusitis can be caused by other organisms as well, including S. aureus, so we
need expanded coverage straight-up.

Patients with asplenia / sickle cell have increased risk of infections due to encapsulated organisms. This namely refers to S. pneumo, H. influenzae type B,
and N. meningitidis, which all have polysaccharide capsules. This is because encapsulated organisms require opsonization (with C3b or IgG) and
phagocytosis for clearance, and the spleen is where we have 50% of the immune system’s reservoir of macrophages. So if we lose the spleen, we lose
substantial phagocytic capacity. Patients must receive additional rounds of vaccination against these three organisms.

If USMLE asks which organism we are most worried about when we give penicillin prophylaxis to sickle cell patients (or any asplenia patient for that
matter), the answer is S. pneumo. Choose this answer over H. influenzae type B and N. meningitidis, even though, yes, the latter two are clearly important to
cover as well.

For 2CK, we vaccinate against S. pneumo by giving PCV20 alone, OR by giving PCV15 + PPSV23 months later. I talk about this stuff in detail in my HY
Pulmonary PDF.

Strep viridans (Strep mitis, mutans, sanguinis)

Cause subacute endocarditis (i.e., patient has previous valve abnormality, such as from history of rheumatic heart disease, or bicuspid aortic valve),
classically following a dental procedure; can create limit-dextrins, which are carbohydrate structures that can adhere to heart valves.

1. What is the categorization of Strep viridans (mitis, mutans, sanguinis)?

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Gram (+) rods

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USMLE - Gram (+) rods - Everything HY you need to know

Bacillus cereus

Causes vomiting and diarrhea following consumption of reheated rice / fried rice due to germination of spores.

Can also cause eye infections post-surgery (e.g., for cataracts). What the USMLE will do is tell you a patient had recent eye surgery + now has an infection
caused by a gram-positive rod, where B. cereus is the only gram-positive rod listed. This is how you can arrive at the answer (i.e., if you know the taxonomy),
even if you haven’t heard of B. cereus causing an eye infection before.

Bacillus anthracis

Causes pulmonary and cutaneous anthrax.

Pulmonary anthrax will be a hemorrhagic mediastinitis. Cutaneous anthrax presents as a black eschar with surrounding edema.

Anthrax produces edema factor, which functions as an adenylate cyclase enzyme, thereby increasing cAMP.
USMLE will usually mention the patient is a postal worker. They are very buzzy this way, and I’ve seen this on NBME.

Anthrax is aka “wool-sorter disease,” because its spores can survive on the dry hides of farm animals due to their protein structure. Anthrax is the only
organism with a protein capsule (poly-D-glutamic acid).

Clostridium tetani

Causes spastic paralysis.

Tetanus toxin of Clostridium tetani inhibits presynaptic SNARE protein, resulting in decreased release of presynaptic neurotransmitters GABA and glycine,
which are normally inhibitory.

Can present as opisthotonos (arched back) and trismus (lock-jaw).

Presents in two patients on USMLE: 1) neonate born at home whose umbilical cord was cut with a kitchen knife + tied with twine; 2) random dude who cut
himself in back yard.

DTaP given at 2, 4, 6, months, then again at 15-18 months, then again at 4-6 years.

School-age kids require booster at 11-12 years, followed by booster every 10 years thereafter.

Pregnant women should get DTaP at 27-36 weeks to protect neonate from pertussis.

For cuts/wounds post-vaccine:

0-5 years post-vaccine: no Tx is necessary.

6-9 years post-vaccine: if clean wound: no Tx; if dirty wound: give Td booster.
10+ years post-vaccine: if clean wound: give Td booster; if dirty wound: IVIG + vaccine.
In other words, only ever give IVIG if it’s a dirty wound + has been 10+ years.

Tetanus is a toxoid vaccine (inactivated toxin/protein).

Clostridium botulinum

Causes flaccid paralysis.

Botulin toxin of Clostridium botulinum inhibits presynaptic SNARE protein, resulting in decreased release of presynaptic acetylcholine, which is normally
stimulatory at muscles.

Can present as floppy baby syndrome; can also cause cranial nerve palsies.

USMLE can be weird about the answer, where I’ve seen them write on an NBME exam something along the lines of “prevents acetylcholine from binding to
its receptor” as the MOA of the toxin, even though this isn’t technically the direct effect.

Acquired as spores in honey in infants under 1; acquired as pre-formed toxin from canned goods in anyone older.

NBME exam wants you to know that administering the toxin does not change the effect of strength of the effect of acetylcholine binding to its receptor.
This is because the toxin isn’t a competitive inhibitor + only decreases endogenous ACh release; this has no impact on any ACh administered exogenously.

Clostridium difficile

Diarrhea (pseudomembranous colitis) ~7-10 days after commencing oral antibiotics.

Antibiotics kill off normal bowel flora, allowing C. difficile to overgrow.

C. difficile is not normal flora, however. It is acquired via consumption of spores.

USMLE doesn’t care about which antibiotics per se cause pseudomembranous colitis; you just need to know any antibiotics in general can technically cause
it if the patient has been inoculated with spores prior. But you could be aware that clindamycin is a classic agent known to increase risk, since it is a very
powerful agent that essentially deletes your GI flora, leaving C. diff without competition for growth.

Can be watery or bloody diarrhea on NBME. Can also cause LLQ cramping (not RLQ as with Yersinia, which causes pseudo-appendicitis).

There is NBME Q where they say 28-year-old with LLQ cramping and bloody diarrhea 7 days after starting oral antibiotics –> answer = C. diff; wrong
answer is Yersinia.

Diagnose with stool AB toxin test; stool culture is wrong answer.

If toxin test is already performed, if they ask how to further confirm the diagnosis, the answer is colonoscopy.

Never perform colonoscopy if a patient has toxic megacolon (which is possible with C. diff). Toxic megacolon will present as fever and distended abdomen,
often with SIRS vitals (means abnormal vitals). Do abdominal x-ray to diagnose toxic megacolon.

Treat with oral vancomycin.

Vancomycin has poor oral bioavailability, so is given IV for things like endocarditis and meningitis. But for C. diff infection, that’s a good thing because we
want it to stay within the GI tract. If USMLE asks why vancomycin is given orally for C. diff, the answer can be something like “has poor oral bioavailability,”
which on the surface sounds like a bad thing when reading answer choices, but as I already said, this is favorable when we are treating C. diff.

Other fancy Abx like fidaxomicin, rifaximin, etc., I’ve never seen on NBME.

Clostridium perfringens

Causes watery/secretory diarrhea following consumption of poultry.

Causes gas gangrene (CO2 gas) due to production of a-toxin/phospholipase; presents as black skin / crepitus (subcutaneous emphysema).

Can also cause emphysematous cholecystitis (air in gall bladder wall).

C. perfringens is known to be associated with necrotizing fasciitis, which is deep infection along fascial planes. I reiterate that crepitus is HY. If the question
specifically tells you that there is no crepitus + the infection started from some sort of scratch or puncture wound, the answer will be Group A Strep or S.
aureus instead.

Listeria monocytogenes

Can be described as gram-positive rod with tumbling motility.

Can grow at very low temperatures (i.e., 0-4 degrees C).

USMLE will say neonate who has pneumonia, meningitis, or sepsis caused by gram-positive rod (if gram-positive coccus, that’s GBS; if gram-negative rod,
that’s E. coli).

Can be acquired by pregnant women via deli meats and soft cheeses.

Can cause some obscure condition called granulomatosis infantiseptica, which presents as black skin lesions in the neonate.

Corynebacterium diphtheriae

Causes diphtheria, which presents in unvaccinated or immigrant children as a grey pseudomembrane in the posterior oropharynx. I’ve seen this grey
pseudomembrane detail show up in one Q that wasn’t diphtheria, but the association is 9/10 times diphtheria.

Can cause myocarditis if untreated.

Diphtheria toxin inhibits protein translation by inhibiting elongation factor 2 (EF2).

Vaccine is a toxoid (inactive toxin).

Nocardia

Weakly acid-fast on staining; aerobic.

Can cause pulmonary infection resembling TB.

Can occasionally cause disseminated disease leading to osteomyelitis and meningitis.

SNAP –> Sulfonamides for Nocardia; Actinomyces use Penicillin.

Actinomyces

Not acid-fast; anaerobic.

Causes formation of yellow sulfur granules.

Causes draining sinus tracts in the oral cavity.

SNAP –> Sulfonamides for Nocardia; Actinomyces use Penicillin.

1. What classic presentation does Corynebacterium diphtheriae cause?

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USMLE: Gram (-) Rods Part II - Everything HY you need to k…

k…

It’s pass-level to know that Neisseria are gram-negative diplococci. Don’t confuse with Strep pneumo, which is gram-positive diplococci.

Neisseria meningitidis

The answer on USMLE for cause of meningitis in three groups:

1) College-age students living in close quarters or military barracks;

2) Child or older who has non-blanching rash (means doesn’t turn white when pressure applied); can be described as purpuric or ecchymotic;

3) Patient with terminal complement deficiency, where there is Hx of recurrent gonoccocal or meningococcal disease in family member or patient. Terminal
complement deficiency (C5-9), aka “total hemolytic complement deficiency” (seen NBME write it like this), causes recurrent Neisserial infections.
Waterhouse-Friderichsen syndrome is bilateral hemorrhagic necrosis of the adrenal cortices secondary to meningococcal septicemia. This can present
with or without meningitis. The USMLE might show you a picture of a purpuric rash on a child + low BP.

The key point about WFS is that cortisol is low. Cortisol normally helps maintain basal BP by upregulating alpha-1 receptors on peripheral arterioles. This
allows norepinephrine and epinephrine to bind (i.e., “cortisol is permissive of the effects of catecholamines”) and constrict arterioles. In the setting of WFS,
giving saline + vasopressors (such as norepinephrine) won’t work, since the underlying glucocorticoid (cortisol) isn’t there. So the USMLE wants
hydrocortisone as the pharmacologic treatment after normal saline.

N. meningitidis is encapsulated. This means there is increased risk of infection in those with asplenia / sickle cell. Encapsulated organisms require
opsonization (with C3b or IgG) and phagocytosis for clearance, and the spleen is where we have 50% of the immune system’s reservoir of macrophages. So
if we lose the spleen, we lose substantial phagocytic capacity. Patients must receive additional rounds of vaccination against these three organisms.

If USMLE asks which organism we are most worried about when we give penicillin prophylaxis to sickle cell patients (or any asplenia patient for that
matter), the answer is S. pneumo. Choose this answer over H. influenzae type B and N. meningitidis, even though, yes, the latter two are clearly important to
cover as well.

Neisseria gonorrhoeae

Causes STI with mucopurulent discharge; this may progress to pelvic inflammatory disease (PID) in females, with ­increased risk of ectopic pregnancy due
to scarring of Fallopian tubes.

There will be gram-negative diplococci on light microscopy. In contrast, Chlamydia will not show any organisms on LM. So if we see the gram-negative
diplococci, we always co-treat for Chlamydia.

In other words, if the gram-(-) diplococci are seen under LM, there’s no way to know if Chlamydia is also there or not since the latter shows no organisms, so
if a patient has Gonorrhea, the proper Tx is IM ceftriaxone (for gonococcus), PLUS either oral azithromycin or doxycycline (for Chlamydia).

If patient develops PID despite having been treated early with ceftriaxone for Gonorrhea, the answer for why this happened can be “Hx of improper
antibiotic treatment,” where the patient was supposed to be co-treated for Chlamydia with azithromycin or doxy but was only given the ceftriaxone for
Gonorrhea.

If patient presents with PID who’s septic (i.e., high fever, tachy, high WBCs), USMLE wants “admit to hospital + IV antibiotics,” not the outpatient combo of
IM + oral antibiotics.

2CK form assesses that if an asymptomatic patient comes in after a partner tested positive for Gonorrhea or Chlamydia, the answer is give treatment
without waiting for test results.

Gonorrhea doesn’t cause reactive arthritis; it causes gonococcal arthritis, which will present one of two ways on NBME: 1) monoarthritis of the knee; or 2)
triad of mono- or polyarthritis + cutaneous papules/pustules + tenosynovitis (inflammation of tendon sheaths; stems like to give deQuervain
tenosynovitis).

Reactive arthritis (usually caused by Chlamydia), in contrast, presents as triad of urethritis, polyarthritis, and conjunctivitis. Rarely it can be caused by GI
infections. But the point is that reactive arthritis is not caused by Gonococcus. The latter causes gonococcal arthritis, which presents as per above.

Treat gonococcal arthritis same as urethritis –> ceftriaxone + azithro or doxy, since the patient may also carry Chlamydia.

Gonococcus is notoriously difficult to culture in patients who have arthritis but no overt urethritis. That is, the patient may have a negative arthrocentesis
and throat/urethral swabs. So the diagnosis of arthritis is often made clinically. If the Q mentions papules/pustules on the skin, this makes it hyper-obvious
for Gonorrhea. I mention this because occasionally an NBME Q will say the arthrocentesis is negative, and this somehow confuses students. But
arthrocentesis is not very sensitive for organisms in the setting of septic arthritis. This can apply to S. aureus as well (I’ve seen this on NBME), but false-
negative results for gonococcus are notably common, so don’t be thrown off by that.

Can cause ophthalmia neonatorum (fancy way of saying neonatal conjunctivitis).

Gonococcal conjunctivitis will present in the first week of life with yellow discharge from the eye(s). Chlamydia tends to present after the first week.

The USMLE vignette will be vague, where the student says, “But how are we supposed to know it’s not Chlamydia, just because it’s first week of life, that’s
it?” And my response is: if they give you Chlamydia ophthalmia neonatorum, they’ll always tie it to subsequent pneumonia somehow, since that is such a HY
point. You need to be aware that Chlamydia drains through the nasolacrimal duct down into the lungs, so if they give you a 3-week old with pneumonia
following conjunctivitis, you know that’s Chlamydia.

Prophylaxis for gonococcal conjunctivitis is erythromycin ointment; treatment in the neonate is IM 3rd-gen cephalosporin (usually cefotaxime in peds).

Prophylaxis for chlamydial conjunctivitis is treatment of the mother while pregnant; treatment in the neonate is oral erythromycin.

Same as with N. meningitidis, patients have increased risk of infection with terminal complement (C5-9) deficiency. Sometimes the vignette can give a
patient with recurrent N. gonorrhoeae or N. meningitidis + ask what is likely deficient, and the answer can simply be “C7” or “C8.” Seems weird/out of place,
but it’s easy if you know terminal complement deficiency is exceedingly HY for Neisserial infections.

A vaccine cannot be made against N. gonorrhoeae because it has pilus proteins on its cell surface that undergo antigenic variation. This is in contrast to N.
meningitidis, where we make a vaccine against the polysaccharide capsule. N. gonorrhoeae, however, does not have a capsule.

Haemophilus influenzae

You need to be aware of H. influenzae type B as well as non-typeable.

H. influenzae type B (HIB) causes epiglottitis and meningitis.

H. influenzae non-typeable is a less common cause of otitis media (compared to S. pneumo) and can also cause pneumonia in COPD. I’ve never seen it
assessed on NBME as the answer for otitis media, but I’m letting you know that occasionally you might read about H. influenzae being a cause of otitis media
after S. pneumo. But this refers to H. influenzae non-typeable, not type B. I’ve seen one Q only on NBME of H. influenzae non-typeable pneumonia in a COPD
patient.

HIB has a polysaccharide capsule. The vaccine is a conjugate vaccine, where a protein is attached to the polysaccharide capsule so that it can be expressed
on MHC-II. USMLE wants you to know that T-independent antigens are non-proteinaceous (i.e., polysaccharide capsules, LPS of gram-negatives, etc.) and
therefore cannot be expressed on MHC-II molecules. Therefore, by attaching a protein to it (e.g., flagellin), it can be expressed on MHC-II and presented to
CD4+ T cells for a more robust immune response. This vaccine point is HY for immuno for USMLE.

Epiglottitis is seen in unvaccinated and immigrants (can be unvaccinated), as well as patients with asplenia or sickle cell (auto-splenectomy).

X-ray of neck shows “thumbprint sign.”

Presents as child who has fever + difficulty breathing. They can say the kid is drooling and/or in tripod positioning (facilitates use of accessory muscles).

USMLE wants intubation as immediate answer. Epiglottitis is a medical emergency that can lead to sudden occlusion of the airway.

Antibiotic Tx following intubation = 3rd-gen cephalosporin (cefotaxime in peds, or ceftriaxone); give rifampin to close contacts.

Legionella

Classically acquired via aerosols from air conditioners. The question can simply say “residential facility” or “business trip” to imply exposure to large AC
units. If the Q gives Legionella pneumonia + they ask about acquisition, the answer can be “environmental aerosols.”

Cause of atypical pneumonia (interstitial pneumonia), with bilateral interstitial infiltrates. “Legionnaire’s disease” refers to severe pneumonia/illness due
to Legionella.

Can also cause hyponatremia and diarrhea.

Diagnosed with urine antigen test.

Treat with azithromycin or doxycycline.

Mycoplasma

Most common bacterial cause of atypical pneumonia (interstitial pneumonia). Viruses are technically most common, but for USMLE, if a patient has a
bilateral pneumonia with interstitial infiltrates, Mycoplasma is the likely cause.

Referred to as “walking pneumonia,” which refers to a young, healthy adult who’s literally been walking around but who has a dry cough + low-grade fever,
where the CXR shows bilateral infiltrates. There is an NBME Q that literally trolls the concept of walking pneumonia, where they say a 23-year-old male
was hiking for 8 hours the day before + has a pneumonia, and the answer is Mycoplasma.

In general, you need to be aware that lobar pneumonia is usually S. pneumo, and bilateral pneumonia is usually Mycoplasma (in AIDS patients, bilateral
pneumonia is Pneumocystis).

There is one NBME Q that gives right lower lobe interstitial infiltrates, with Mycoplasma as the correct answer, where S. pneumo isn’t listed. This means the
word “interstitial” wins over location.

Can cause cold agglutinins (IgM antibodies against RBCs), leading to hemolysis. In other words, bilateral pneumonia + low Hb = Mycoplasma. High LDH can
also sometimes be seen. RBCs are packed with LDH, so high LDH on USMLE is often their way of saying hemolysis.

Treat with azithromycin or doxycycline.

HY for Step 1 NBMEs: they will ask why beta-lactams such as amoxicillin are ineffective against Mycoplasma. The answer is because it lacks a peptidoglycan
cell wall.

Chlamydia

Obligate intracellular.

Chlamydia pneumoniae (not Chlamydia trachomatis) is technically another cause of interstitial/atypical pneumonia after Mycoplasma and Legionella, but I’ve
never seen this assessed on NBME.

Chlamydia psittaci is a cause of atypical pneumonia in bird owners or those who work at a pet store with birds.

Treat with azithromycin or doxycycline.

Chlamydia trachomatis D-K (the actual STI) can cause pneumonia in neonates following conjunctivitis. This is HY. The Q will give a 3-week-old who had
conjunctivitis 1-2 weeks earlier, who now has low-grade fever + bilateral wheezes. The labs can show a high % of lymphocytes, since Chlamydia lives
intracellularly so requires cell-mediated immunity to clear it. In contrast, other organisms, like S. pneumo, which live outside the cell, cause a neutrophilic
shift instead, since neutrophils are used for humoral immunity.

Prophylaxis for Chlamydia neonatal conjunctivitis is treating the mom while pregnant. Treatment in the neonate is oral erythromycin. Topical is wrong
because it will not kill what has already entered the nasolacrimal duct. Topical erythromycin is used as prophylaxis for gonococcal conjunctivitis; Tx for the
latter is cefotaxime.

Bordetella pertussis

Classic whooping cough presents as succession of many coughs followed by an inspiratory stridor.

What you need to know for USMLE is that this can absolutely present in an adult and that they can be vague about it, just describing it as a regular cough.
There is an NBME Q where they give pertussis in a 19-year-old, and I see students confused thinking it must be a kid. This is not the case. Write a letter to
NBME if you disagree.

The way you’ll know it’s pertussis, however, is they will say there’s hypoglycemia and/or post-tussive emesis, which means vomiting after coughing
episodes.

Pertussis can cause super-high WBC counts in the 30-50,000-range, where there are >80% lymphocytes. This is called reactive lymphocytosis. This makes
it resemble ALL. So you should know for Peds that ALL-like laboratory findings + cough = pertussis.
Q will ask number-one way to prevent –> answer = vaccination (not hard, but they ask it). Pertussis is part of TDaP. The pertussis component is killed-
acellular; the tetanus and diphtheria are toxoid.

Erythromycin can be given to patients with active cough; USMLE doesn’t give a fuck about pertussis stages.

Close contacts should also receive erythromycin.

Francisella tularensis

Cause of atypical pneumonia in patients with exposure to rabbits.

Can sometimes cause ulcerated skin lesions.

Infection is called tularemia.

Rickettsia

Refers to a genus of bacteria that are obligate intracellular (same as Chlamydia, which is also obligate intracellular).

Rickettsia rickettsii causes Rocky Mountain spotted fever (RMSF), which is a palms and soles rash (sometimes the Q can say wrists/ankles instead of
palms/soles) that migrates toward the trunk (centripetal rash).

RMSF is considered a form of vasculitis and is spread by dermacentor wood tick. It is treated with doxycycline.

“Typhus” refers to rash + fever+ headache conditions caused by rickettsia.

Rickettsia prowazekii causes epidemic typhus; spread by louse.

Rickettsia typhi causes endemic typhus; spread by fleas.

Rickettsia tsutsugamushii causes scrub typhus; spread by mites.

Rickettsia cause a positive Weil-Felix test, which means there are positive titers to Proteus-O antigen. Sounds weird, but I don’t know what to tell you.

Coxiella burnetii

Causes Q-fever, an atypical pneumonia in those with exposure to farm animals, especially cattle.

Was once considered a type of Rickettsia, but has now been recategorized into its own genus. It is Weil-Felix negative.

Brucella

Acquired from unpasteurized goat products (i.e., cheese, milk).

Brucellosis causes undulating fever, which presents as afternoon fevers and normal body temperature in the morning.

Invasion to the CNS is called neurobrucellosis, which can present as meningoencephalitis.

Pasteurella multocida

Can cause skin infection following a cat or dog bite.

Bartonella henselae

Can cause skin infection following cat or dog scratch (hence cat-scratch disease).

Causes non-caseating granulomatous inflammation seen on silver stain.

The Q need not say the patient has a pet. NBME might say there is an 8-year-old girl with a papule on the finger, where biopsy shows granulomatous
inflammation on silver stain, and the answer is simply Bartonella henselae.

Treat with azithromycin.

Can cause bacillary angiomatosis in immunocompromised patients, which is proliferating blood vessels presenting as raised, red/violaceous skin lesions.
The condition is known to resemble Kaposi sarcoma.

1. What is the taxonomy/categorization of Francisella tularensis?

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HY USMLE Q #962 – Micro / Pharm

January 23, 2024
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HY USMLE Points - Gram-negatives Part I

Serratia marcescens

Cause of nosocomial UTIs; urease-positive; can lead to struvite (ammonium magnesium phosphate; staghorn) calculi, since these form at higher pH.

Grows cherry red on culture medium.

Catalase-positive. Serratia sepsis can be mentioned on USMLE in patients with NADPH oxidase deficiency (chronic granulomatous disease), since these
patients have susceptibility to catalase-positive organisms (Big SPACES –> Burkholderia, S. aureus, Pseudomonas, Aspergillus, E. coli, Serratia).

Escherichia coli

Most common cause of UTIs, cystitis, and pyelonephritis. USMLE wants you to know fimbriae or P-pilus are virulence factors that enable adhesion to
urothelium.

Causes prostatitis and epididymitis in males 40s and older (NBME gives male who’s 45 with prostatitis where E. coli is correct and Chlamydia is wrong).

Increased risk of infections in patients with NADPH oxidase deficiency (because E. coli is catalase-positive).
ETEC

Enterotoxigenic E. coli (ETEC) causes traveler’s diarrhea, which is self-limiting watery or brown-green diarrhea following trips overseas to, e.g., Mexico or
the Middle East.

Classically acquired via water or lettuce contaminated with human feces.

The mechanism for ETEC diarrhea is heat-labile toxin that ADP-ribosylates adenylyl cyclase, increasing cAMP, as well as heat-stabile toxin that ADP-
ribosylates guanylyl cylase, increasing cGMP.

In other words, HL toxin increases cAMP; HS toxin increases cGMP.

The HL toxin increasing cAMP is the same mechanism as cholera toxin (Vibrio cholerae); the difference is cholera causes profuse, high-volume stool, with
liters and liters of rice-water stool, wheres traveler’s diarrhea, even if it is described as occurring 8-12 times daily (I’ve seen this on NBME), they will not
describe it as profusely high-volume the way cholera presents.

The HS toxin increasing cGMP is the same mechanism as Yersinia enterocolitica toxin. The difference is the latter causes bloody diarrhea and pseudo-
appendicitis (RLQ pain) or arthritis, whereas traveler’s diarrhea is not bloody.

EHEC O157:H7

Enterohemorrhagic E. coli (EHEC) causes bloody diarrhea (dysentery) in isolation, or can also cause full-blown hemolytic uremic syndrome (HUS).
Classically acquired from beef.

HUS presents as triad of: 1) thrombocytopenia; 2) hemolytic anemia with schistocytes; and 3) renal insufficiency with or without hematuria.

The combination of thrombocytopenia + schistocytosis = microangiopathic hemolytic anemia (MAHA).

The mechanism for HUS is: E. coli EHEC O157:H7 (and Shigella) both secrete toxins (Shiga-like toxin and Shiga toxin, respectively) that cause inflammation
of renal microvasculature –> ADAMTS13 protein inactivation –> failure of cleavage of vWF multimers –> platelet adherence to vascular endothelium
cannot be as readily reversed –> platelet aggregations protrude into vascular lumen causing shearing of RBCs flying past –> fragmentation of RBCs
(schistocytes, aka helmet cells).

Shiga-like and Shiga toxins cleave the eukaryotic 60S ribosomal subunit, thereby interfering with protein translation.

Klebsiella

Urease (+); can cause struvite stones.

Can cause cavitary pneumonia with currant jelly (thick, dark red) sputum; classically seen in alcoholics or those with aspiration risk.

Proteus

Urease (+); can cause UTIs leading to struvite stones, same Klebsiella and Serratia.

Salmonella

Causes food poisoning (Salmonella enteritidis and typhimurium), resulting in bloody diarrhea. Acquired from consumption of poultry or eggs, as well as from
interaction with reptiles (i.e., pet lizards, snakes, etc.).

Salmonella typhi causes typhoid fever, which is high fever + prostration (patient is lying down ill / in pain) + rose spots on the abdomen + either constipation
or diarrhea.

Humans are the reservoir for Salmonella typhi, and it is acquired via fecal contaminated food/water. It can remain latent in the gall bladder.

Shigella

Acquired from beef.

Can cause shigellosis, which is isolated bloody diarrhea (dysentery), or can cause full-blown HUS (same as EHEC, as discussed above).

Requires inoculation with relatively few organisms to cause infection (in comparison to Salmonella, which requires more organisms to cause infection).

Shiga-toxin cleaves the eukaryotic 60S ribosome (same as EHEC), but its main virulence factor is its ability to invade GI mucosa. If Shigella loses its ability to
invade, it is severely impeded in its ability to cause infection. EHEC does not invade.

Pseudomonas

Causes pneumonia in cystic fibrosis patients. I’ve talked about in prior content that S. aureus exceeds Pseudomonas prior to age 10 and that Pseudomonas
exceeds S. aureus after age 10. But I’m not convinced that USMLE gives a fuck. I’m not going to go fish for and remove that detail about age from my prior
content, however.

Can cause infections on burns. Appears blue-green due to a pigment it produces called pyocyanin. If a burn has a yellow color, in contrast, this is likely S.
aureus (“golden Staph), not Pseudomonas.

Diabetic patients have increased general infection risk due to Pseudomonas. This notably is in reference to osteomyelitis and foot ulcers. However, a caveat
is that a new NBME Q for 2CK has “polymicrobial” as the answer for the most likely cause of diabetic foot ulcer, where both Pseudomonas and S. aureus are
wrong answers. I mention this because resources over the years have pushed Pseudomonas for foot ulcers. So I just want you to be aware “polymicrobial” is
correct if it’s listed alongside Pseudomonas.

Pseudomonas is very important cause of nosocomial pneumonia (i.e., hospital- and ventilator-acquired pneumonia). If a patient has a nosocomial pneumonia
(which is defined as a pneumonia starting >48 hours following becoming an in-patient), he or she must receive coverage for both MRSA as well as
Psuedomonas. This is accomplished by giving vancomycin (covers MRSA) PLUS either ceftazidime (a 3rd-gen ceph) or cefepime (a 4th-gen ceph).

Ceftriaxone (a 3rd-gen ceph) does not cover Pseumonas, so the combo of vanc + ceftriaxone is wrong for nosocomial infections. This combo is used for
community-acquired sepsis or meningitis. For community-acquired pneumonias where there is not sepsis, we give simple azithromycin to treat.

There are other agents that cover Pseudomonas, such as carbapenems, pipericillin/tazobactam, amikacin (an aminoglycoside), etc., but I have not seen
NBME assess these. What I have seen that is incredibly HY on forms is the vancomycin + cephalosporin combos as I mentioned above.

Pseudomonas can cause otitis externa (swimmer’s ear) and hot tub folliculitis.

Treat otitis externa with topical ciprofloxacin + hydrocortisone drops.

Prophylaxis for otitis externa (e.g., in someone who does crew who can’t avoid water exposure) is topic alcohol-acetic acid drops. Answers such as ear plugs
are wrong. Carbamide peroxide drops are for earwax buildup (distractor on NBME).

Pseudomonas produces a toxin that inhibits Elongation Factor 2 (EF2), same as Diphtheria.

Vibrio

Vibrio cholerae (cholera) presents as “liters and liters” of rice-water stool in someone who went traveling to, e.g., Mexico. Acquired fecal-oral (i.e., fecal-
contaminated food/water).

MOA of toxin is same as ETEC heat-labile toxin causing traveler’s diarrhea, which is ADP-ribosylation of adenylyl cyclase (increases cAMP). The way you
can differentiate this from ETEC traveler’s diarrhea is that cholera is notably profusely high-volume.

Both ETEC and cholera vignettes can tell you the patient has 8-12 stools daily, so it’s not the # of stools that matters; it’s the emphasis on volume. Cholera
causes death via severe dehydration and electrolyte disturbance.

Tx is oral rehydration on USMLE; if patient has low BP or altered mental status (i.e., confusion/coma), IV hydration is done.

Vibrio parahemolyticus doesn’t cause profuse, watery diarrhea the same way cholera does. I’ve seen this organism asked once in an NBME vignette where
the patient ate sushi (can be acquired from sushi and shellfish).

Vibrio vulnificus causes severe sepsis in half of patients. This is asked on offline NBME 19 where a dude went running on a beach and got sepsis, with no
mention of consumption of food. But it’s apparently acquired from shellfish.
Yersinia

Causes bloody diarrhea + either appendicitis-like (i.e., RLQ) pain or arthritis.

The RLQ pain is from mesenteric adenitis or terminal ileitis.

Toxin has same MOA as ETEC heat-stabile toxin (i.e., ­ADP-ribosylates guanylyl cylase, thereby increasing cGMP).

There is an NBME Q where they tell you a patient was on antibiotics for a week + has bloody stool + LLQ pain, and the answer is C. diff, not Yersinia. C. diff
can cause either watery or bloody stool, and sometimes pain. Pseudo-appendicitis due to Yersinia will be RLQ; it will not be LLQ.

Helicobacter pylori

Spiral-shaped gram-negative rod.

Responsible for almost all duodenal ulcers (>95%), whereas it causes a lower % (only >60%) of gastric ulcers. This is merely because the latter are caused by
many other things as well, so we simply have decreased fraction caused by H. pylori. In other words, there’s no special tropism of H. pylori toward duodenal
over gastric mucosa.

Mechanism for ulcers that shows up on USMLE is: “secretes proteinaceous substrates that damage mucosal lining.” This is correct over “­increases gastric
acid secretion” if both are listed side-by-side, even though H. pylori does ­gastrin levels, which ­increases acid secretion.

Produces urease, which causes ­increased ammonia production around the organism, allowing it to survive in the decreased pH of the stomach.

Antral/pyloric ulcers can lead to gastric outlet obstruction. They will mention this on NBME as a “succussion splash.”

Increased­risk of MALT lymphoma, a type of B-cell lymphoma; can be obstructive at the pylorus, as well as at the cardia of the stomach adjacent the lower
esophageal sphincter.

Diagnose H. pylori with urease breath test or stool antigen. Endoscopy + biopsy can be performed to confirm diagnosis in some cases via visualization of the
spiral-shaped organisms.

Treat H. pylori with CAP – i.e., clarithromycin, amoxicillin, PPI (e.g., omeprazole).

USMLE really doesn’t give a fuck about the treatment, but CAP is safe to know. Metronidazole, tetracycline, bismuth, and PPI tetrad is used if CAP fails
(students ask about those other drugs).

Perforated duodenal ulcer will present as sudden-onset rigid abdomen (involuntary guarding). Patient will often have SIRS, with abnormal vitals due to
sympathetic activation. USMLE wants “X-rays of the chest and abdomen” to look for air under the diaphragm (HY finding that indicates ruptured viscus).

Campylobacter jejuni

Bloody diarrhea 1-3 days after consumption of poultry.

Can cause Guillain-Barre syndrome (ascending paralysis + decreased tendon reflexes + albuminocytologic dissociation in the CSF –> Tx with IVIG +
plasmapheresis).

I would say only about 1/4 of GBS Qs will mention any type of preceding infection. So don’t rely on the dude going to some BBQ or getting diarrhea
beforehand as a crutch for GBS Qs.

Grows best at high temperatures (42 degrees).

Bacteroides

Normal GI flora for mouth to anus. Most important detail is that it is strictly anaerobic.

Anaerobic infections on USMLE can present as “foul-smelling sputum” or “foul-smelling discharge.”

Causes pulmonary abscess and aspiration pneumonia.

USMLE wants “aspiration of oropharyngeal normal flora,” or “aspiration of oropharyngeal anaerobes” as the cause of pulmonary abscess.

Oropharyngeal normal flora = Bacteroides (strictly anaerobic gram-negative rods); as well as Peptostreptococcus and Mobiluncus. The latter two are not HY,
but Bacteroides is. I mention all three, however, because the Q can say sputum sample shows “gram-negative rods, gram-positive cocci, and gram-positive
rods,” which refers to all three. But the bigger picture concept is, this = mixed normal flora.

Q will give aspiration risk factor, such as alcoholism, dementia (can cause loss of gag reflex), Hx of stroke (leading to dysphagia), or epilepsy. Q can also
mention broken or missing teeth (hypodontia) as risk factor. Pulmonary abscess is often described on NBME as pulmonary lesion with an air-fluid level.
This is buzzy, but not a mandatory descriptor. This refers to the top half of the circle being air, and the bottom being pus, the latter settling due to gravity.

Tx for pulmonary abscess = clindamycin. Clindamycin is used for “anaerobes above the diaphragm” (metronidazole for “anaerobes below the diaphragm”).
Some students have asked about potentially updated/alternative pharm for pulmonary abscess, but I can tell you clindamycin is all over 2CK NBMEs.

Additionally, USMLE can give some sort of abdominal infection (e.g., after surgery), where the site drains “foul-smelling sputum.” You know right away
they’re talking about anaerobes, specifically Bacteroides.

1. How is Shigella acquired?

What two conditions does it cause?

What is the mechanism of its virulence?

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Helminths
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Points about pharm:

Nematode infections on USMLE are basically always treated with -bendazoles (i.e., mebendazole, albendazole, etc.). These are microtubule inhibitors.
Don’t confuse with -azoles (antifungals).

Pyrantel pamoate is another agent that can be used for nematodes, but lower yield. Diethylcarbamazine is non-existent.

Ivermectin is an odd-one out used for Onchocerca volvulus (discussed below).

Praziquantel is used for cestodes and trematodes. This causes worm paralysis.

In short, mebendazole and praziquantel are the two highest yield anti-helminth agents for USMLE.

It is extremely rare USMLE lists more than one anti-helminthic agent as answers to a question. Usually the Q is very easy, where the answer is the only anti-
helminthic listed. But there are a couple questions out there where they list a -bendazole and praziquantel side by side. So you must know that
mebendazole is used for nematodes; praziquantel is used for cestodes and trematodes.

HY point about bloods:

Eosinophils can classically be elevated in helminth infections. This is because eosinophils play a role in killing helminths via release of major basic protein.
Normally eosinophils should be <5%. In helminth infections, they can be >6-8%. Questions where eosinophils are, e.g., 15-20% would be considered
flamingly obvious and pass-level.

Eosinophils can occasionally be elevated in fungal infections as well, so don’t be confused by this. In other words, although eosinophilia is classically
associated with helminth infections, just be aware this is not 100% specific and it can occasionally be seen with fungal infections too.
For the following helminths, the USMLE can give a vignette where you are easily able to diagnose the organism, but then they ask how it’s acquired, where
they have answers such as “ingestion of fecal-contaminated soil,” “through the feet,” “mosquito bite,” “fly bite,” etc., and the answer is the former. Even if the
“fecal-contaminated soil” part sounds weird, it might be the only answer that involves ingestion, which you therefore know must be correct.

Ascaris lumbricoides

Giant roundworm. Infection is called Ascariasis.

Causes intestinal obstruction.

USMLE can give vignette of patient with eosinophilia with high-pitched or absent bowel sounds (both findings that can reflect obstruction), and the answer
is just Ascariasis or Ascaris lumbricoides. Not dramatic.

Treat with mebendazole.

Enterobius vermicularis

Aka pinworm (asked on USMLE, where student got easy vignette + all of the worms listed were colloquialisms rather than actual binomial nomenclature).

Causes perianal itching.

Diagnosed via Scotch tape test, where eggs around the anal verge can be collected using tape.

Treat with mebendazole.

Toxocara canis

Carried by pet dogs. Acquired through ingestion of contaminated-soil/food.

Causes visceral larva migrans, which can cause hepatosplenomegaly.

Treat with mebendazole.

Trichinella spiralis

Acquired from pork and bear meat consumption.

Trichinosis presents as triad of 1) fever, 2) myalgias, and 3) periorbital edema in patient who ate bear meat or pork.

Treat with mebendazole.

Strongyloides stercoralis

Invades usually through the feet. Travels through the bloodstream to the lungs, causing pulmonary symptoms. The larvae ascend the trachea and are then
swallowed into the GI tract, where they cause abdominal symptoms.

USMLE will give you school-age girl in rural Louisiana (I’ve seen this on NBME) who has pulmonary and abdominal symptoms + worms isolated from the GI
tract + they ask for the mode of transmission –> answer = “through the feet.”

Treat with mebendazole.

Hookworms

Ancylostoma duodenale and Necator americanus are hookworms. USMLE loves these.

They enter through the feet + travel to the lungs, same as Strongyloides. The difference is that when they eventually enter the GI tract, they suck blood from
their site of attachment in the small bowel, causing microcytic anemia due to iron deficiency.

The USMLE will not list Strongyloides alongside the hookworms as separate answers in the setting of pulmonary symptoms. What they will do is give you
patient with eosinophilia + microcytic anemia, where the answer is a hookworm. Or they will give helminth infection + pulmonary symptoms + microcytic
anemia, and the answer is simply “through the feet,” or one of the hookworms as the Dx.

Treat with mebendazole.

Onchocerca volvulus

Causes onchocerciasis (river blindness). Transmitted by black fly and causes black skin lesions and blindness.

Everything is Black: Black fly, Black bite, Black eyesight (blindness).

Will be kid in South America or Africa who has a skin lesion + blindness, where Onchocerca volvulus is only helminth listed that causes blindness.

Treat with ivermectin.

Wuchereria bancrofti

Causes elephantiasis (aka lymphatic filariasis), which is massive swelling due to lymphatic insufficiency.
Transmitted by female mosquito.

Treat with mebendazole.

Loa Loa

Roundworm that presents crawling in the eyeball.

Transmitted by deer, horse, or mango fly.

Treat with mebendazole.

USMLE wants you to know that tapeworms have a segmented body and a scolex, which refers to the head of the tapeworm that has “suckers and hooks.”
USMLE is known to show this image on the real exam + expect you to know you’re looking at a tapeworm because of the characteristic scolex.

Diphyllobothrium latum

Aka fish tapeworm. Acquired from ingesting – you’d never guess it – fish.

Causes B12 deficiency, leading to macrocytic anemia and hypersegmented neutrophils.

This is in contrast to hookworms (N. americanus and A. duodenale; nematodes), which cause microcytic anemia.

Treat with praziquantel.

Taenia solium
Aka pork tapeworm. Acquired from pork consumption, usually in someone who went abroad to, e.g., Mexico.

Causes cysticercosis, which presents as muscle pain/cysts, and neurocysticersos, which presents as lesions within the brain. The latter can present one of
three ways on NBME (as per my observation): 1) swiss-cheese appearance of brain (buzzy); 2) one or two ring-enhancing lesions; 3) cystic, soap-bubble-
appearing lesions within the ventricles.

I’ve specified in the past that praziquantel is preferred for cysticercosis and albendazole for neurocysticercosis (rare use of a -bendazole for a non-
nematode), but USMLE actually doesn’t give a fuck, and they won’t list both side by side anyway. You should just know that praziquantel is basically always
the answer for cestodes and trematodes, but that albendazole (normally a nematode agent) can be used for neurocysticercosis. But if you’re ever asked this
on the real exam, they will give you obvious Taenia solium infection, where the answer is the only anti-helminth drug listed, so there won’t be any confusion.

Don’t confuse Taenia solium (pork cestode) with Trichinella spiralis (pork/bear nematode, which is triad of 1- periorbital edema, 2- myalgias, 3- fever, in
someone who ate pork or bear).

Echinococcus granulosus

Causes hydatid cyst disease.

Presents with liver cysts, and sometimes jaundice and general flu-like symptoms.

Do not biopsy the cysts. This can cause anaphylaxis. The correct management is surgical excision of the cysts + praziquantel.

Schistosoma hematobium

Snails are the reservoir. But the trematode isn’t acquired via consumption. It is acquired through the skin in someone swimming in (usually) Africa. Travels
to the cystic veins draining the bladder + the bladder wall.

Causes hematuria and squamous cell carcinoma of the bladder.

USMLE vignette will say some guy was swimming in Africa + now has hematuria and eosinophilia. The Q need not ask about SCC of the bladder.

This is in contrast to smoking, industrial (aniline) dyes, and naphthylamine (moth balls), which cause transitional cell carcinoma of the bladder and urothelial
tract.

Treat with praziquantel.

Schistosoma mansoni/japonicum

Same as S. hematobium, snails are the reservoir, but the trematode isn’t acquired via consumption. It is acquired through the skin in someone swimming in
(usually) Africa. Travels to the mesenteric veins / intestines, before making its way to the liver.

Can cause hepatosplenomegaly, liver damage, and GI symptoms.

There is Q on NBME exam where they show picture of a worm + say there’s hepatosplenomegaly, and then Schistosoma mansoni is the answer, but it’s not a
hard Q because it’s the only reasonable organism listed.
Treat with praziquantel.

Clonorchis sinensis.

Acquired via consumption of contaminated fish.

Can cause cholangiocarcinoma (bile duct cancer).

Treat with praziquantel.

Paragonimus westermani

Acquired via consumption of crab meat or crayfish.

Travels from the GI tract to the lungs, where it causes hemoptysis.

Treat with praziquantel.

1. What is the taxonomy/categorization of Taenia solium?

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Protozoa
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Protozoa are unicellular eukaryotes.

Amoebas move and feed by extending pseudopods, which are temporary extensions of the cytoplasm.

Entamoeba histolytica

Acquired as cysts in fresh water. Organisms that are acquired as cysts in fresh water are ECG –> Entamoeba, Cryptosporidium, Giardia.

Causes bloody diarrhea + liver abscesses, usually in patient who’s traveled outside the United States to Mexico or third-world country. I’ve seen one
NBME Q where the latter was described as a “cystic lesion” on CT, even though it’s not a cyst (such as with Echinococcus granulosus, a tapeworm that causes
hydatid cyst disease).

Can cause flask-shaped ulcers of the small bowel.

Demonstrates erythrophagocytosis (ingestion of RBCs). This is mentioned in an NBME Q.

NBME Q gives patient who traveled abroad + has bloody diarrhea + has abscess seen in the liver on CT + they ask for next best step in diagnosis –> answer
= antigen testing for E. histolytica. Not difficult.

Treated with metronidazole + iodoquinol.

Acanthamoeba

Causes keratitis (inflammation of the cornea) and encephalitis.

Naegleria fowleri

Found in contaminated fresh water sources, i.e., lakes, hot springs, fountains, and sometimes drinking water.

Causes rapidly progressive meningoencephalitis and death within 1-2 weeks in nearly 100% of patients.

Enters through the cribriform plate in patients who have water enter their nose through diving, splashing, or deliberate washing of their sinuses. Does not
cause infection if merely ingested.

This is the organism you see in the news once every 6 months as “brain-eating amoeba” that causes death in someone who swam in a lake.

Giardia lamblia

Acquired as cysts in fresh water. Organisms that are acquired as cysts in fresh water are ECG –> Entamoeba, Cryptosporidium, Giardia.

Causes steatorrhea (fatty stool), which can be described as extremely foul-smelling stool that floats. The patient can also have bloating.

There is one NBME Q for Giardia where they say the patient has foul-smelling watery diarrhea and bloating, which is audacious, since Giardia causes
steatorrhea, but the “foul-smelling” and “bloating” point toward steatorrhea nevertheless.

The diarrhea is malabsorptive, where the patient can acquire nutritional and fat-soluble vitamin deficiencies.
Has two phases during its life cycle: trophozoite (left image), which is the actively reproducing, motile (with 8 flagella), and infective phase, and the cyst
(right image), which is the dormant, non-infective stage. Both images are exceedingly HY spot-diagnoses for USMLE.

Patients with IgA deficiency are at increased risk of Giardia infection. Sometimes Hx of Giardia infection is mentioned in IgA deficiency questions.

Treat with metronidazole.

Trichomonas vaginalis

Causes trichomoniasis.

Presents as yellow-green discharge. Can cause “strawberry cervix,” or punctate hemorrhages on the cervix. If they don’t say this, they can sometimes say
yellow-green discharge + a vaginal canal that is erythematous.

Flagellated protozoan. Diagnosed via visualization on wet mount.

Treat with metronidazole for patient and partner (high rate of reinfection).

Trypanosoma cruzi

Causes Chagas disease, aka American trypanosomiasis.

Spread by Reduviid bug. It is aka “kissing bug” because of its usually soft, painless bite.

Can cause Romaña sign, which is palpebral (eyelid) swelling 1-2 weeks after infection. This occurs when T. cruzi-containing feces from the Reduviid bug are
rubbed into the eye. That is, the bite need not occur on or near the eye; the feces can be transferred from a bite elsewhere to the eye.

Can cause dilated cardiomyopathy, achalasia, and toxic megacolon.

Treated often with nifurtimox and benznidazole.

Trypanosoma brucei

Causes African sleeping sickness, aka African trypanosomiasis.

Spread by Tsetse fly.

Presents as daytime sleepiness and nighttime insomnia.

Treated often with suramin and melarsoprol.

Leishmania donovani

Causes Leishmaniasis.

Spread by the Phlebotomus sand fly.

USMLE likes the Middle East as location where it is prevalent. An NBME Q mentions a guy who went to Iraq.

Can cause skin ulceration at bite site (cutaneous leishmaniasis).

It can also cause visceral leishmaniasis (aka kala-azar), which can lead to pancytopenia and hepatosplenomegaly.

Treated often with sodium stibogluconate.

Sporozoans have a spore-forming phase and are distinguished by the presence of an apical complex at one end of the cell, which is used for invading host
cells.

Plasmodium spp.

Causes malaria. Presents as flu-like illness with the development of hemolysis and varying fever patterns. P. falciparum causes hypoglycemia and cerebral
malaria, which is more fatal.

Transmitted to humans by the Anopheles mosquito in regions of the world such as Africa, South America, and Asia.

Life cycle:

The Anopheles mosquito injects the sporozoite form of malaria into the blood. The sporozoites travel to the liver and mature into schizonts within
hepatocytes, which undergo asexual reproduction to produce merozoites. A single schizont will contain many merozoites. This phase within the liver is
called the hepatic, or exo-erythrocytic stage (I’ve seen this on NBME). The schizonts containing merozoites are then released into the blood.

USMLE wants you to know this schizont

image on blood smear.
Merozoites then invade RBCs (erythrocytic phase). Once inside the RBC, the merozoites mature into ring-shaped trophozoites, followed by new schizonts
containing new merozoites.

USMLE wants you to know the ring

form on blood smear.

Then the RBCs periodically burst, causing fever patterns. Trophozoites do not develop prior to the schizonts in the liver. So in short, the Anopheles mosquito
injects Plasmodium into the host, then:

Hepatic (exo-erythrocytic) stage: sporozoite –> schizont –> merozoites –> leave liver.

Erythrocytic stage: merozoite –> ring-shaped trophozoite –> schizont –> merozoites –> burst RBC (causes fever).

As mentioned above, Plasmodium falciparum is the most severe type and causes cerebral malaria (neurologic deficits, seizures, headache), with greatest
chance of death. The fever pattern is variable.

USMLE wants you to know that patients with P. falciparum can get hypoglycemia due to increased consumption of glucose by the organism. This is an
answer on one of the NBME exams, where they give a simple vignette of malaria and then ask what is most likely to be seen in this patient, and the answer
is hypoglycemia. Strikes students as weird, but it’s on the NBME.

Chloroquine can be given as prophylaxis, which inhibits malarial heme polymerase. However, some regions have high levels of chloroquine resistance, so
mefloquine can be given instead. If they tell you a patient was given chloroquine and develops malaria anyway, the answer USMLE wants is “pharmacologic
resistance”; the wrong answer is “non-compliance with medication.”

P. vivax and ovale cause tertian fever (every 48 hours; or every 3rd day). They form hypnozoites within the liver, which is a latent form. This is one of the
highest yield details regarding malaria, where they will say a patient with the disease was treated successfully, but then months later has a resurfacing of
symptoms.

Patients with P. vivax and ovale must receive primaquine, which kills hypozoites. I’ve seen the USMLE ask this numerous ways. They can ask for primaquine
as the answer straight up. They can ask why primaquine is given for P. vivax and ovale, where the answer is “kills hypnozoites.” I’ve also seen “kills the exo-
erythrocytic stage.”

P. malariae causes a more mild form of malaria and a quartan fever (every 72 hours; or every 4th day).

P. knowlesi is found predominantly in southeast Asia and causes a quotidian (daily) fever.

Malaria is diagnosed with thick and thin blood smears. This is asked on NBME, where “Plasmodium antigen testing” is wrong answer.

Toxoplasma gondii

Classically acquired from contact with infected cats, or via consumption of pork.

Toxoplasmosis presents as one or more ring-enhancing lesions on CT of the head. Can be in the context of seizures and/or miscellaneous neurologic
symptoms as as a result of the CNS infection.

Patient need not be immunocompromised, but HIV patients with CD4 count <100 are at greater risk.

Prophylaxis is trimethoprim/sulfamethoxazole (TMP/SMX), which is the same as that for Pneumocystis jirovecii at a CD4 count of 200. So if a patient with a
CD4 count of, e.g., 47, commenced TMP/SMX at CD4 count of 200 + has a seizure + ring-enhancing lesion, you know the diagnosis is not Toxo, since he/she
is already on prophylaxis. The diagnosis in this case is primary CNS lymphoma (HY for AIDS under CD4 count of 100).
Treatment for Toxo is sulfadiazine + pyrimethamine. This is asked on a 2CK form, where they list both TMP/SMX and sulfadiazine + pyrimethamine; the
latter is correct.

Congenital Toxo in neonates presents as a triad of: 1) hydrocephalus, 2) chorioretinitis, and 3) intracranial calcifications.

Cryptosporidium parvum

Acquired as cysts in fresh water. Organisms that are acquired as cysts in fresh water are ECG –> Entamoeba, Cryptosporidium, Giardia.

Causes watery diarrhea in person who goes overseas to third-world country (e.g., Mexico).

Diarrhea is self-limiting in immunocompetent persons –> Tx = supportive care.

Chronic diarrhea can occur in immunocompromised (e.g., HIV) –> Tx = nitazoxanide.

Appears as acid-fast cysts (same stain as TB).

Babesia

Spread by Ixodes tick, same as Lyme disease (Borrelia burgdorferi), Ehrlichia, and Anaplasma.

Causes malaria-like hemolytic disease in patient who never left the United States. In contrast, if the patient left the United States and went to (usually)
Africa, the answer is malaria, not Babesia.

Can cause a ring-form on blood smear similar to malaria.

What the USMLE will do is tell you patient has fever + hemolytic disease of some kind + never left the US + show you above image; they will list both
malaria and babesiosis as answers –> answer = babesia. Even though you’re aware malaria can also produce a similar-appearing ring-form, since the patient
never left the US, you know it can’t be malaria. Conversely, if they show you ring-form and tell you patient recently went to Africa, you know it’s malaria, not
babesia.

You also need to know Babesia can cause a maltese cross within RBCs:
1. Which protozoan on USMLE notably can be visualized with acid-fast stain (same as TB)?

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HY USMLE Q #962 – Micro / Pharm

January 23, 2024
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RNA viruses – Part I

by MEHLMANMEDICAL

Rhinovirus

Most common cause of common cold (i.e., upper respiratory tract infection, with coryza, dry cough, no exudates, and no fever).

Nothing else you need to know.

Coxsackie A

Causes hand-foot-mouth disease, which presents as vesicles on – you’d never guess it – the hands, feet, and mouth. Almost always a pediatric condition, but
adults can sometimes get it as well.

Can also cause herpangina, which is oropharyngeal vesicles.

Coxsackie B

Causes myocarditis with dilated cardiomyopathy.

Can cause diabetes mellitus type I in susceptible patients. The immune system develops antibodies against a viral oligopeptide that cross-reacts with intra-
beta-islet cell glutamic acid decarboxylase-65. Hence this one of the reasons why anti-GAD-65 antibodies are positive in some patients with type I DM.

Can cause pleurodynia, which is intercostal muscle spasm presenting with sharp, lateral chest pain, sometimes with an increase in serum CK due to the
muscle spasm. Despite its name, it has nothing to do with the lungs and is an MSK condition. It shows up twice on the NBME content for 2CK. For Step 1, I’d
still know what it is.

Echovirus

Common cause of aseptic (viral) meningitis.

CSF analysis for viral meningitis is: normal protein; normal glucose; elevated lymphocytes.

Poliovirus

Infects the anterior horns of the spinal cord and causes polio myelitis (inflammation of spinal cord).

Classically causes degeneration of motor neurons in one leg, leading to one leg much smaller than the other leg.

Highest yield points about Polio actually have zero to do with the infection and almost all to do with the vaccines.

Salk vaccine = killed intramuscular.

Sabin vaccine = live-attenuated oral.

Only the live-attenuated vaccine is capable of generating a CD8+ T-cell response and IgA secretion in the gut.

This is because only live virus can invade the cell, leading to expression on MHC-I (which interacts with CD8). This occurs within the gut, since the vaccine is
oral, so the Peyer’s matches in the ileum can be stimulated to make gut IgA.

The killed intramuscular vaccine can’t produce a CD8+ T cell response because killed virus can’t invade the cell. And since it doesn’t have exposure to the
gut, there won’t be gut IgA produced.

USMLE will ask what is a common feature of these vaccines that accounts for their efficacy –> answer = “neutralizing antibodies in the circulation.”
Both the killed and oral are capable of generating IgG antibodies in the circulation.

In short: only Sabin does CD8+ response and gut IgA production; both Salk and Sabin produce IgG in circulation.

If you’re confused about the immuno, I talk about this stuff in my HY Immuno PDF.

Hepatitis A

The answer for acute hepatitis in the United States most of the time. The Q might say the patient had recent travel to Mexico.

Fecal-oral; only causes acute hepatitis.

ALT is usually > AST for viral hepatitis.

IgM against HepA means acute infection.

IgG against HepA means patient has cleared infection (because there is no chronic HepA).

USMLE wants you to know HepA vaccine is indicated for MSM and IV drug users. The latter in particular sounds weird, since HepA isn’t parenteral, but it’s
asked. There’s a 2CK NBME Q where they just mention otherwise healthy MSM, and answer is Hep A vaccination. Students are confused, but I don’t know
what to tell you.

Hepatitis E

Causes fulminant hepatitis / ­high risk of death in pregnant women.

Same as with HepA, only causes acute hepatitis.

Seen more in Asia, e.g., Tibet. But if USMLE says Mexico + pregnant woman + fast death from hepatitis, you still have to use your head and know that’s
HepE over HepA.
Norovirus (Norwalk virus)

Most common cause of watery diarrhea in adults and rotavirus-vaccinated children.

Cruise ships and business conferences are buzzy places to acquire (fecal-oral); basically any place with high density of people.

If the Q says a young child + family all have watery diarrhea, the answer is Norwalk, not Rota, since only the young child would get Rota, not the family also.

Rotavirus

Most common cause of watery diarrhea in unvaccinated children < 5 years. Immigrant status (e.g., from China) often implies unvaccinated status on
USMLE.

Vaccine normally given orally at 2, 4, and 6 months of age.

Double-stranded, segmented RNA (NBME asks it). Wheel-shaped (also asked on NBME).

Coltivirus

Causes Colorado tick fever, which is a flu-like illness. Mostly occurs in Western USA.

1. Cruise ships / business conferences / crowded areas + watery diarrhea = which virus?

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RNA viruses – Part II

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Alphavirus

Causes some obscure brain infection in a farmer called equine encephalitis. Asked maybe once on an old NBME form somewhere.

Rubella (aka German measles)

Causes fever and head-to-toe maculopapular rash in unvaccinated children (and adults).

HY point about the presentation is that it causes post-auricular and sub-occipital lymphadenophathy.

Adults can get arthritis. For example, if the USMLE gives you a neonate with congenital rubella syndrome + they ask what symptom the woman most likely
had when pregnant, arthritis can be an answer if rash is not listed. USMLE will not force you to choose between rash and arthritis. The point is that you
merely are aware arthritis is HY in adults as part of the presentation.

Congenital rubella presents as patent ductus arteriosus (PDA) in a neonate. Exceedingly HY / pass-level. Cataracts and deafness also possible.

MMR vaccine is live-attenuated and is contraindicated during pregnancy due to theoretical risk to the fetus. If a woman inadvertently receives the vaccine
while pregnant or within the month prior to pregnancy, it is not an indication for abortion, but risks to the fetus are increased and proper monitoring is
important.

The vaccine is not contraindicated in HIV. Literature says subjectively can be implemented in patients who are severely immunocompromised with
consideration of CD4 count, but there is no specific CD4 cutoff. The point is, MMR vaccine is avoided in pregnancy, but not avoided in HIV.

Hepatitis C
Parenteral; can be acute or chronic.

Transmitted almost exclusively from IV drugs/blood exposure. Not present in breastmilk and non-sanguineous body fluids (in contrast to HepB).

In contrast to HepB, HepC is not considered sexually transmitted. Large longitudinal study of couples with one HepC(+) partner showed sexual
transmission almost nil (possibly due to menses exposure). If you’re forced to choose for FM / behavioral science Qs, however, still inform that abstinence
or barrier contraception minimizes risk.

Hepatocellular damage is due to T cells / death is due to T-cell-mediated apoptosis, not direct viral cytopathicity. This is the highest yield point for HepC
on USMLE.

No vaccine due to ­antigenic variation (i.e., >7 genotypes and 80 subtypes of HepC exist).

IgM against HepC means acute infection.

IgG against HepC means usually means chronic HepC.

Many drugs can be used to treat. USMLE doesn’t care. You could in theory be aware of pegylated interferon-a.

West Nile virus

Asked once on an old, offline NBME. USMLE wants you to know it has a bird reservoir and is spread by Culex mosquito.

Presents as flu-like illness in most people. The NBME Q simply gives patient with headache and fever + they say the causal organism is spread
by Culex mosquito and has a bird reservoir –> answer = West Nile virus.

Dengue virus

Spread usually by Aedes mosquito.

Causes flu-like illness + thrombocytopenia (bleeding gums, petechiae, etc.) + severe joint and abdominal pain.

Yellow fever virus

Spread usually by Aedes mosquito.

Causes flu-like illness and jaundice (hence yellow fever) due to hepatocellular damage. Councilman bodies are seen on biopsy of the liver, which are
apoptotic bodies.

Zika virus

Spread usually by Aedes mosquito.

Causes microcephaly in neonates if mother exposed while pregnant.

Human T-cell lymphotropic virus

Retrovirus similar to HIV.

Causes a cutaneous T-cell lymphoma, known as mycosis fungoides, which appears like a skin rash.
 Mycosis fungoides

If this extends to the blood as a T-cell leukemia, it is now called Sezary syndrome. Sezary syndrome usually presents with diffusely red skin, called
erythroderma.

Sezary syndrome

Both mycosis fungoides and Sezary syndrome are characterized by cerebriform-shaped cells on light microscopy.

HTLV can also cause an obscure condition called tropical spastic paraparesis, which is antibodies against neuronal cells leading to otherwise unexplained
neurodegeneration over weeks to months.

Hepatitis D

Requires hepatitis B in order to infect, which can be due to co-infection (happening at the same time) or superinfection (occurs later in someone who
already has HepB).

If USMLE asks how to prevent HepD infection, answer = vaccination against hepatitis B. There is no vaccine against HepD.

Apparently HepB antigen forms the envelope for HepD (i.e., forms a circle around HepD).

Human immunodeficiency virus (HIV)

Invades and destroys CD4+ T cells.

Transmitted via blood, IV drug use, and sexually. Also present in breastmilk.

Highly active anti-retroviral therapy (HAART) consists of three drugs: two nucleoside reverse-transcriptase inhibitors (NRTI) + either a non-nucleoside
reverse-transcriptase inhibitor (NNRTI) or protease inhibitor.

Pharmacology for HIV is lengthy and involved, so if you want in depth discussion of all of the drugs, you can open as a separate tab my HIV pharm module
here.

HAART therapy is initiated immediately upon diagnosis of HIV. We do not wait for CD4 count to fall to a certain level before commencing.

Once CD4 count falls below 200/μL, patients are started on trimethoprim/sulfamethoxazole (TMP/SMX) for Pneumocystis jiroveci pneumonia (PJP)
prophylaxis.

NBME has Q where they give you an HIV patient with CD4 count of, e.g., 550, and then ask what type of drug regimen needs to be commenced. Answer in
this case is “three drug anti-retroviral therapy alone,” where “three drug anti-retroviral therapy + Pneumocystis prophylaxis” is wrong, as well as all answers
that say two-drug regimen.
HIV patients with CD4 counts under 200, or those who get any HIV-related opportunistic infection, are said to have Acquired Immunodeficiency Syndrome
(AIDS).

Toxoplasmosis comes in with CD4 count under 100. Prophylaxis is TMP/SMX, the same as for PJP, so often times, once TMP/SMX is appropriately
commenced at CD4 of 200 for PJP, it’s already “two birds with one stone,” so we don’t have to worry about Toxo prophylaxis later.

However the treatment for Toxo is sulfadiazine + pyrimethamine. For Pneumocystis TMP/SMX is both the prophylaxis and treatment. NBME asks the Tx for
toxo on one of the forms, where TMP/SMX is also listed and wrong. So you need to know the prophylaxes + treatments for Toxo and PJP.

Under CD4 counts of 50-100, Mycobacterium avium intracellulare and CMV infections can occur. MAI causes lung infections similar to TB, and also
sometimes GI infections. CMV causes retinitis. Blurry vision in an HIV patient is CMV retinitis till proven otherwise.

In addition, progressive multifocal leukoencephalopathy (PML; neuronal degeneration caused by reactivation of JC polyoma virus), primary CNS
lymphoma, and AIDS complex dementia (presents as wet, wobbly, wacky, similar to normal pressure hydrocephalus) can occur at CD4 counts <50-100.

The USMLE might give you a patient with CD4 count of 47 who has ring-enhancing lesion of the brain who is taking HAART and TMP/SMX. Diagnosis is
primary CNS lymphoma; Toxo is wrong. The way we know Toxo is wrong is because the patient is on TMP/SMX, which is the prophylaxis for both
Pneumocystis and Toxo. Commencing TMP/SMX at a CD4 count of 200 for PJP, as I already said, is “two birds with one stone” by the time the patient gets to
CD4 of 100, which is when Toxo comes in. It’s only patients who aren’t on TMP/SMX by the time they fall to CD4 of 100 who get Toxo.

Causes Cryptococcal neoformans meningitis, which presents with low glucose, high protein, and high lymphocytes. Diagnosed with CSF latex agglutination
(most accurate), or India ink prep, or mucicarmine staining.

Adults with severe acute-onset seborrheic dermatitis, disseminated scabies, or molloscum contagiosum should have an HIV test.

HIV increases risk of squamous cell carcinoma in MSM.

HIV can cause focal segmental glomerulosclerosis (FSGS), a nephrotic syndrome. When HIV leads to renal disease, it is called HIV nephropathy. It is almost
always FSGS.

HIV can lead to chronic diarrhea caused by Cryptosporidium parvum, whereas immunocompetent patients clear it. C. parvum is a protozoan (unicellular
eukaryote).

Can be a cause of anemia of chronic disease (low Hb, low iron, normal ferritin).

Patients with HIV require Pap smear at time of diagnosis, and then every year (annually) thereafter (asked on Obgyn forms). Normally, Paps are performed
every three years from age 21, and then every 5 years from age 30 with HPV co-testing.

To prevent vertical transmission, the most important measure to take is HAART therapy while pregnant + keeping the mother’s viral load as low as possible.
She will then receive intrapartum zidovudine, C-section is performed, and then the neonate will receive 6 weeks of zidovudine commenced within 12 hours
of birth. Some students will get pedantic about various alternative/updated regimens for neonates, but one of the NBMEs assesses this point about 6
weeks of zidovudine commenced within 12 hours of birth.

1. At what CD4 counts do we worry about MAI and CMV in HIV?

What do these infections cause?

SHOW ANSWER
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MICROBIOLOGY

RNA viruses – Part III

by MEHLMANMEDICAL

Coronavirus

The virus specifically known as SARS-CoV-2, or COVID-19, caused the 2019 global pandemic.

SARS stands for Severe Acute Respiratory Syndrome.

The pandemic is believed to have started following a laboratory leak in Wuhan, China, although this has been a source of political debate, where initial
explanations asserted that there was a natural, zoonotic origin for the virus (i.e., originating from animals, e.g., bats).

Has characteristic spike proteins that create a crown-like appearance on electron microscopy.

The spike proteins bind to ACE2 receptor, allowing for viral fusion with host respiratory epithelium.

Presentation can range from mild respiratory symptoms similar to the common cold (rhinovirus) all the way to severe respiratory disease with multi-organ
failure.

Many different vaccine types exist – i.e., mRNA (Moderna; delivers mRNA coding for the spike protein), viral vector (AstraZeneca; delivers mRNA in a
harmless viral capsid), and killed (Sinovac; delivers inactivated, killed virus).

Both live viral infection as well as vaccination are known to cause rare adverse effects, such as Bell’s palsy and myocarditis, although these effects are not
unique to coronavirus and can rarely happen with many viral infections and vaccines.

Vaccination mandates and their political implications were (and still are) a source of contentious debate.

Prior to the 2019 pandemic, coronavirus was known to cause SARS in China in 2002 and Middle Eastern Respiratory Syndrome (MERS) in Saudi Arabia in
2012.
Vaccination schedule for children now recommends IM vaccine starting at 6 months; 2-3-doses.

Hantavirus

Causes pulmonary syndrome and hemorrhagic fever.

Spread by rodents/mice.

This virus is known to get rarely asked on Step 1, where they apparently mention hantavirus in the vignette in a patient with a fatal hemorrhagic pulmonary
syndrome, and then the answer is just “mice” for how it’s acquired.

Influenza

Causes respiratory distress, fever, and myalgias (muscle pain). For USMLE purposes, the myalgias are exceedingly HY as a vignette finding that usually
suggests the flu over other diagnoses.

Has 8 segments, two of which are hemagglutinin and neuraminidase.

Hemagglutinin mediates viral attachment to the cell by enabling its binding at sialic acid receptors.

If a question asks about the molecule most flu vaccines are targeted against, the answer is hemagglutinin.

Neuraminidase allows for newly synthesized viral particles to leave the host cell. This enzyme cleaves sialic acid residues, which normally bind the new viral
particles within the cell. Once these residues are cleaved, the viral particles can leave the cell.

Drugs such as oseltamivir and zanamivir are sialic acid analogues that function as neuraminidase competitive inhibitors. In other words, they prevent the
virus from leaving the cell. If the USMLE asks which drug prevents viral spread within a community, or they tell you a drug is given and now host cells are
“packed with virions” (because they can’t leave the cell), the answer is one of the -mivirs.

Antigenic drift is point mutations in hemagglutinin and/or neuraminidase, where the virus has changed slightly. It leads to seasonal epidemics.

Antigenic shift is due to two influenza viruses entering a cell, one of human origin, the other of animal origin (such as bird or swine), where they engage in
reassortment of viral segments, leading to a completely novel influenza virus. It leads to generational pandemics.

If a patient gets a bacterial lobar pneumonia following recent convalescence from influenza infection, USMLE likes S. aureus as a HY cause. The USMLE will
not play trivia where they list S. aureus alongside S. pneumo and you’re forced to choose. What they’ll do is say something about how a guy recently
recovered from a viral illness in which he had high fever and myalgias, and now he has a pneumonia caused by a gram-positive coccus in clusters –> answer
= S. aureus. In contrast, S. pneumo is gram-positive diplococci.

Vaccine is given fall or winter every year. USMLE really cares about this. So much so, they will sometimes say “April” in a vignette, where giving flu vaccine is
wrong, or they’ll say “January” or “October,” where giving it is correct.

IM killed vaccine: start age 6 months, then give yearly throughout life; safe to give during pregnancy.

Intranasal live-attenuated vaccine: ages 2-45; immunocompetent, non-pregnant persons only.

Parainfluenza virus

Aka paramyxovirus.

Causes laryngotracheobronchitis (croup).

Presents as hoarse, barking, or seal-like cough in school-age kid. The Q can say the cough gets better when his dad brings him out into the cold air.

Neck x-ray shows “steeple sign,” which is sub-glottic narrowing.

Don’t confuse the steeple sign of croup with the thumbprint sign of epiglottitis caused by H. influenzae type B.

Sometimes the Q can give you easy vignette of croup, but then the answer is just “larynx” (literally inflammation of the larynx, trachea, and the bronchi).
“Sub-glottic” means below the area of the vocal cords. The larynx is the area encompassing the vocal cords.

Tx is supportive. If they force you to choose an actual Tx, however, nebulized racemic epinephrine is the answer.

Respiratory syncytial virus (RSV)

Answer on USMLE for a kid <18 months old who has low-grade fever and bilateral wheezes.

Tx is supportive care on USMLE. Don’t choose answers like ribavirin or palivizumab.

Mumps

Causes POM –> Parotitis, Orchitis, Meningitis.

Doesn’t typically cause rash.

Vaccine is MMR, which is live-attenuated.

Measles

Aka rubeola; causes a head-to-toe macular popular rash.

The notion of “cough, coryza, conjunctivitis” as = measles is absolute garbage and a flaming joke. No idea why there have been resources over the years that
have perpetuated this trash. These symptoms are non-specific for viral infections in general (e.g., rhinovirus, RSV, etc.). I frequently see students get easy
NBME Qs wrong where they think measles is the diagnosis in the setting of these symptoms.

Can cause Koplik spots (pathognomonic whiteish lesions on buccal mucosa).

MMR vaccine is live-attenuated; contraindicated in pregnancy; not contraindicated in HIV.

Immigrant Hx on USMLE sometimes implies unvaccinated status.

Can rarely cause subacute sclerosing panencephalitis (reactivation of latent infection in the CNS in teenagers).

Rubella also causes a head-to-toe macular popular rash, but rather than Koplik spots, suboccipital and post-auricular lymphadenopathy (tenderness on
back of head and behind ears) is characteristic.

Rabies

Causes encephalomyelitis that is nearly always fatal.

Spread by the bite or scratch of infected animals, such as bats, skunks, raccoons, and wild dogs.

Travels up peripheral nerves to the CNS. Has very long incubation period of >1-3 months before symptoms appear.

Presents as flu-like illness that progresses to neurologic features, as well as pathognomonic findings such as hydrophobia (fear of water), aerophobia (fear
of drafts of air), and hyper-salivation.

Negri bodies are characteristic inclusions seen on electron microscopy of infected neurons.

Ebola

Causes hemorrhagic disease, where patient initially has flu-like illness, followed by development of internal and external bleeding, leading to death nearly
always.

Bats are the most likely reservoir, with human-human spread occurring via contact with bodily fluids (i.e., blood, vomitus, feces, sweat).

As of 2019, a recombinant vaccine was created (rVSV-ZEBOV) that has been shown to be 98% effective.

1. What is the main presentation for measles?

SHOW ANSWER

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MICROBIOLOGY

Spirochetes + Mycobacteria
by MEHLMANMEDICAL

Spirochetes are a group of bacteria with a corkscrew- or question mark-shape that are visualized using a method called dark-field microscopy.

You don’t need to know the following for USMLE, but I will clarify for some students who ask: even though H. pylori also has spiral-shape similar to
spirochetes, it is not a spirochete. Apparently, spirochetes are unique in that they use axial filaments or endoflagella for movement, whereas other bacteria
use “regular flagella.”

Treponema pallidum

Causes syphilis.

Spirochete (spiral/cork screw-shaped bacterium) visible under dark-field microscopy.

Primary syphilis = painless chancre (painless ulcer) on genitalia.

Don’t confuse the painless chancre of primary syphilis with chancroid, which is a painful chancre-appearing lesion (-oid means “looks like but ain’t”) caused
by the bacterium Haemophilus ducreyi.

Secondary syphilis = 6 weeks to 6 months after appearance and disappearance of the initial chancre, patient can get body rash that includes palms + soles,
and condylomata lata (painless genital plaques). Don’t confuse condylomata lata with condylomata acuminata (genital warts).

Tertiary syphilis = years later, patient can get gummas (appear as painless chancres but are on other areas of the body such as the face/nose), arthritis, and
ascending aortitis (tree-barking of vasa vasorum).

Neurosyphilis can occur at any stage; it is not sequential where we have 1 –> 2 –> 3 –> neurosyphilis. There is a 2CK Neuro Q that gives neurosyphilis in an
18-year-old.

Neurosyphilis presents as tabes dorsalis (obliteration of dorsal columns, with loss of vibration/proprioception + a positive Romberg sign, where patient falls
over when standing with eyes closed), Argyll-Robertson pupil (i.e., “prostitute pupil”; accommodates but doesn’t react), and “stroke without hypertension”
(i.e., sometimes findings akin to stroke but in a younger patient).
Diagnosis of primary syphilis is made via visualizing the spirochetes from a chancre scraping under dark-field microscopy.

Diagnosis of secondary, tertiary, and neurosyphilis can be done with serology, where a VDRL and/or RPR is done first (sensitive but not specific); an FTA is
done as confirmatory (specific but not sensitive).

VDRL test mixes the patient’s serum with cardiolipin antigen. If antibodies against T. pallidum are present, the test demonstrates clumping/flocculation. The
RPR enhances this reaction by using charcoal particles. There is an NBME Q floating around where they say something about a patient whose test results
demonstrate clumping with charcoal particles, and the answer is SLE.

Patients with SLE who have anti-phospholipid syndrome can get false-positive VDRL/RPR tests because this syndrome is often caused by antibodies
against cardiolipin (in SLE, we simply call these antibodies “lupus anticoagulant”).

FTA mixes a patient’s serum with fluorescent Treponema antibodies. If binding occurs, this confirms the diagnosis of syphilis.

USMLE will show you 24-year-old male with rash on his back + KOH prep is negative + ask what’s most likely to diagnose–> answer = FTA.

Treatment for all syphilis types is penicillin.

If patient has Hx of anaphylaxis to beta-lactams but is pregnant or has tertiary or neurosyphilis, the answer is desensitize + give penicillin. This is because
penicillin is the most efficacious and needs to be given in severe cases.

If patient has Hx of mere rash to beta-lactams, but not anaphylaxis, then the beta-lactam can be given anyway.

Killing of T. pallidum spirochetes can sometimes cause a hypersensitivity-type response by the immune system known as Jarisch-Herxheimer reaction.
USMLE will say patient was given penicillin for syphilis + gets fever, chills, and myalgias. This is different from beta-lactam allergy, which would be a rash or
anaphylaxis (swelling + low BP).

Congenital syphilis can cause tooth abnormalities (mulberry molars/incisors), “saber shins” (bone abnormalities), saddle nose, deafness, and cataracts.
There is NBME Q floating around where they are vague + give basically no info apart from “tooth abnormalities,” where the answer is congenital syphilis. So
this finding is especially important for USMLE.

Borellia burgdorferi

Spirochete; spiral/corkscrew-shaped.

Causes lyme disease; spread by Ixodes tick (same as Ehrlichia, Babesia, and Anaplasma).

Primary Lyme causes a classic target rash known as erythema chronicum migrans, but a HY point is that the rash need not be a target on USMLE. It can
merely be circular with no clearing, but the target is classic.

Bells palsy can also be seen in primary Lyme. What the USMLE will do is give two side by side images: 1) circular rash on limb that is not a target; 2) Bells
palsy, where the student needs to infer this is Lyme disease even though rash isn’t a target, since Bells palsy is HY for Lyme.

Secondary Lyme tends to cause arthritis. Some sources say Bell’s palsy is part of secondary Lyme (occurs at least one month after initial infection), but I’ve
seen USMLE give it as part of initial/primary infection.

Tertiary Lyme can cause CNS and/or heart problems.

Treatment is doxycycline for most cases of Lyme.

Ceftriaxone is given for advanced Lyme involving the CNS or heart.

For children <8 and pregnant women, give amoxicillin in place of doxycyline.

There is an NBME Q of a pregnant woman with non-disseminated Lyme, where ceftriaxone is correct over doxycycline, and amoxicillin isn’t listed. In other
words, if USMLE doesn’t want doxy as the answer, they will not play trivia as to whether it’s ceftriaxone or amoxicillin to be used as the alternative. But you
could be aware that, in theory, ceftriaxone is harder-hitting and preferred if cases are more severe.

Borellia recurrentis
Causes a condition known as relapsing fever.

Spread by body lice, not Ixodes tick the way Lyme disease is.

Leptospira interrogans

Question mark-shaped spirochete.

Leptospirosis can present as flu-like illness, jaundice, pulmonary hemorrhage, and meningoencephalitis.

It is usually spread by animal urine.

There’s two ways USMLE asks Leptospira:

1) They’ll be hyper-obvious and say there’s a farmer with a weird, flu-like illness where he was walking in animal urine. Answer is just simply Leptospira.

2) They’ll give easy vignette of syphilis or Lyme disease, followed by asking which of the following organisms is most taxonomically similar (i.e., which of the
following is also a spirochete), and the answer is just Leptospira.

Mycobacterium tuberculosis

Has unique cell wall composed of mycolic acid that is difficult to gram stain. Requires acid-fast stain.

Produces cord factor (asked on NBME) as a virulence factor.

Can present similar to lung cancer, where patient can have B symptoms (i.e., fever, night sweats, weight loss) and hemoptysis.

Living in a homeless shelter or immigrant status from endemic area is buzzy. I’ve seen rural India and Albania as two locations in NBME Qs.
Prisoners/prison workers, healthcare workers, and TB laboratory personnel are of course at risk as well.

Can cause cavitations and calcification in the lung grossly; on histo, causes caseating granulomatous inflammation.

Ghon foci/complexes are textbook descriptors for TB lesions but not assessed eponymously on USMLE. A Ghon focus is a localized area of inflammation. If
lymph nodes are involved, the combination of the lesion + lymph node(s) is called a Ghon complex.

Can cause constrictive pericarditis (can also calcify).

Disseminated TB (miliary TB) can affect multiple organ systems, leading to psoas abscess, Pott disease (TB infection of the vertebrae), adrenal
insufficiency, meningitis, osteomyelitis, and arthritis.

First step in diagnosis is PPD test (type IV hypersensitivity).

If PPD test is (+), the next best step is CXR.

If PPD is (+) but CXR (-), next best step is “treat for latent TB, “ or “give TB prophylaxis.” This is isoniazid (INH) for 9 months + vitamin B6 (since INH can
cause B6 deficiency). It is exceedingly HY you know that neuropathy in a patient being treated for TB has B6 deficiency.

If PPD and CXR are both (+), the next best step is “treat for active TB,” which is RIPE for 2 months + RI for 4 more months (6 months total). RIPE = rifampin,
isoniazid, pyrazinamide, ethambutol.

BCG vaccine is live-attenuated. USMLE wants you to know Hx of BCG vaccine does not change management based on PPD guidelines.

If USMLE asks you how long after TB exposure will someone’s sputum cultures be positive, the answer is 2-5 weeks.

Interferon-gamma release assay (Quantiferon Gold) can be used in patients who have Hx of BCG to reduce false (+)s, but USMLE doesn’t assess it. The
reason I mention it is because they want you to know interferon-gamma is required for stimulation of alveolar macrophages to control TB.

Patients who have IFN-gamma or IL-12 receptor deficiency have ­susceptibility to TB infections. If this immuno stuff sounds confusing, I talk about this in
detail in my HY Immuno PDF.
TNF-alpha is also required to suppress TB. Therefore drugs such as infliximab, adalimumab, and etanercept ­increase risk of TB, which is why they should be
avoided in silicosis patients (who have increased risk of TB).

What is considered a positive PPD test (in terms of # of mm of induration) differs depending on risk factors:

What is considered a positive PPD test (in terms of # of mm of induration) differs depending on risk factors:

>5mm (+): Hx of close contact to someone with active TB; immunocompromised patient (AIDS, organ transplant recipient receiving immunosuppressants,
chronic corticosteroid user); calcification on CXR.

>10mm (+): Health care worker or prisoner/prison worker; immigrant from endemic area; TB laboratory personnel, children <4.

>15mm (+): everyone else.

If a PPD test is (+), never repeat it. If it is negative, it must be repeated in 1-2 weeks (i.e., sometimes false-negatives).

Rifampin is a DNA-dependent RNA polymerase (just remember “RDR” –> Rifampin DNA-dependent RNA polymerase). It can cause orange
tears/secretions. It also upregulates P-450.

Isoniazide is a mycolic acid synthesis inhibitor. It can cause B6 deficiency (neuropathy and/or seizures) and high anion-gap metabolic acidosis (the I in
MUDPILES refers to isoniazid/iron tablets). It also inhibits P-450.

Pyrazinamide inhibits fatty acid synthesis.

Ethambutol inhibits carbohydrate synthesis (arabinosyl transferase). It causes optic neuritis, sometimes with changes in color vision.

Mycobacterium leprae

Causes leprosy; affects skin and peripheral nerves.

Highest yield point for USMLE is that M. leprae grows best at cooler temperatures, which is why it affects areas like the nose and peripheral nerves. Shows
up on an NBME Q where they ask what is most characteristic of the causal organism, and the answer is something like “temperature sensitive.”

Dapsone is used as part of the treatment. It’s HY to know it can cause hemolysis in G6PD.

Mycobacterium avium intracellulare

MAI can cause lung infections similar in presentation to TB; can also cause GI infections. These types of infections are classically seen in
immunocompromised patients (i.e., AIDS with CD4 count <50). Azithromycin prophylaxis is no longer indicated for AIDS patients.

MAI can also cause an obscure pneumonitis called “hot tub lung,” which can occur in immunocompetent patients. Shows up on an NBME exam as guy who
moved into new apartment building with a hot tub. MAI present in hot tub vapors can cause lung inflammation (hence pneumonitis).

Mycobacterium marinum

Causes red lesion(s) on finger/hand in workers at, or kids who go to, water parks/aquariums.

USMLE will give Pseudomonas and S. aureus as distractors. So be aware of M. marinum as buzzy cause of skin infection associated with water parks and
aquariums.

Mycobacterium scrofulaceum

Causes lymphadenopathy in the neck, sometimes with a skin lesion. Not HY, but you can be aware it exists.

1. What does Leptospira cause?

What shape is it?