jdlevenson's version from 2015-06-16 22:39


Question Answer
MoraxellaNormal flora of upper respiratory tract; causes otititis media and sinusitis in healthy individuals and responsible for exacerbations of chronic obstructive pulmonary disease
Protein A is...Virulence factor of Staph Aureus in the peptidoglycan wall that binds Fc portion of IgG leading to impaired activation, opsonization and phagocytosis.
IgA proteases in what bacteriaStrep Pneumo and N. Gonorrhea; block IgA from interfering with adhesion of neighboring bacterias
HemolysinSecreted by staph to cause hemolysis and destruction of PMNs and macrophages and PLTs
Malassezia furfurHypo or hyperpigmented patches that become more visible after tanning; characteristic of pityriasis versicolor. Spaghetti and meat ball on light micro. Asymptomatic just a cosmetic nuisance. Treated with selenium containing shampoo.
Sporothrix histologyGranuloma of histiocytes, multinucleated giant cells, and neutrophils surrounded by plasma cell. Spreads along lymphatics.
Sporothrix wound isReddish nodule that will eventually ulcerate.
Erythema infectiosum/ B19 tranmissionRespiratory, infected blood and transplacentally; single stranded DNA
B19 transplacentally will causeHydrops Fetalis
B19 in adults with pre-existing hemolytic diseaseAplastic crisis
Hand foot mouth disease what virusCoxsackie A; fever and ulcers on tongue/ oral mucosa and maculopapular on palms and soles


Question Answer
Lepromatous leprosy, more severe (weak Th1 response, strong Th2 response, high bacterial load), clinical presentationDiffuse skin thickening, cutaneous hypopigmentation in plaques often + hair loss, leonine facies, paresis and regional anesthesia of motor or sensory nerves as well as testicular destruction and blindness. Loss of nose and digits.
Leprosy, tuberculoid vs lepromatous, difference in pathogenesisTuberculoud – strong TH1, activation of macrophages that kill M Leprae organisms limiting disease extent; Lepromatous – innate inability to recognize and mount a cellular immune response against M Leprae and so tissues will have extensive accumulation of acid-fast bacilli within macrophages and often TH2 cytokine profile (IL-4, 5, 10)
Tuberculoid leprosy clinical presentationMild skin plaques a/w hypopigmentation, hair follicle loss and focally decreased sensation.
Leprosy likes to grow inColder temperatureshence it affects skin, superficial nerves and eyes and testes the most.
Lepromin skin test, how will it differ depending on type of leprosy someone hasWith tuberculoid leprosy, indurated nodule at injection; NONREACTIVE in someone with the lepromatous leprosy due to weak TH1
Key difference in terms of pathophys of tuberculoid vs lepromatousTuberculoid – activated macrophages actively kill M Leprae whereas Lepromatous – macrophages remain inactivated
Campylobacter fetusGram negative rod; mild enteritis in immunocompetent and mild systemic bacteremic illness in immunocompromised patients
Maculopapular rash begins on the face and spreads to the trunk + extremitiesMeasles (rubeola) and German measles (rubella).
Rubella/ german measles vs measles/ rubeolaRubella spreads faster and does not darken or coalesce. Also postauricular and occipital lymphadenopathy are especially common in rubella. Rubeola is paramyxo.
Rubella is what kind of virusTogavirus.
Maculopapular rash that begins on trunk and spreads centrifugally to involve face and extremitiesVaricella zoster
Post-fever transient maculopapular rash on chest and trunkRoseola, HHV-6
Redness on cheeks followed by maculopapular rash on the extremities and trunkSlapped cheek; erythema infectiosum; PARVOVIRUS
Zoster develops due to reactivation of varicella-zoster virus inDRG (sensory neurons). Presents with painful vesicular rash in dermatome distribution. Papules -> vesicles -> crush in a few weeks. Contagious until lesions are dry.
Zoster microscopePositive Tzanck for intranuclear inclusions in keratinocytes and multinucleated giant cells. Also acantholysis (loss of intercellular connections).
4 year old with high fever, nasal discharge, lacrimation, dry cough and white spots on buccal mucosaCough, Coryza, Conjunctivitis, Koplik spots (CCCK) + fever -> Measles/ rubeola. A maculopapular rash usually follows.
Most common complication from zosterPost-herpetic neuralgia; stabbing pain that may be constant or intermittent and lasts for several months; only 10% of all patients after zoster but more than 75% of zoster patients who are >70 years.
Small whitish blue gray spots on buccal mucosa that may be liked on to grains of sand on an erythematous baseKoplik spots**; usually part of measles infection/ rubeola.
MMRMeasles mumps rubella.
Bartonella henselae can causeCat scratch disease and bacillary angiomatosis (immunocompromised), which can vbe fetal if not treated (red purple popular skin lesions).
Erythema migrans of Lyme disease does or does not occur at site of inoculationYes it does. 7-14 dys after tick bite. Enlarges as bacteria migrate slowly through skin. Annular/ ring-shaped from central clearing but can appear more uniformly erythematous too.
Leptospirosos causes what on epithelial surfacesConjuctival suffusion.
Blanching erythematous rash or petechial eruption that spreads proximally to involve trunkRickettsia/ riskettsia (RMSF), tick-borne illness resulting from contact with dogs or exposure to wooded areas. Treat with doxycycline immediately due to high mortality.
If a herpes virus lacks phosphorylating enzymes (ie no viral kinase) then what treatments won’t workViral dependent nucleosides such as acyclovir, valacyclovir, famciclovir, ganciclovir. Instead need nucleotides (cidofovir, teno) or cell dependent nucleosides (zdovudine) which will use then the host cell kinase to become a nucleotide with three phosphates that will inhibit DNA polymerase and cause chain termination.
A –clovirs for herpes have same mecnaism which isThey are nucleoside analogs that must be phosphorylated by viral kinases (such as thymidine kinase) to become monophosphates -> nucleoside triphosphats that then may interfere with herpes virus replication.
Syphillis screening testsRPR, VDRL. RPR mixes serum with cardiolipin, cholesterol, and lecithin. Aggregation demonstrates presence of cardiolipin antibodies in the patient’s serum. Nontreponemal erologic test because it does not detect treponemal organisms or antibodies but antibodies to human cellular lipids released into the bloodstream after cell destruction by T. Pallidum. Positive in syphilis, yaws, pinta or bejel, all illnesses caused by T. pallidum.
Syphillis confirmatory testFTA-ABS
Cold agglutinins testMycoplasma
Colorado tick fever from coltivirus in the reoviridae family; primarily in Rocky Mountain states- fever, vomiting, myalgias, weakness
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Mycobacterium scrofulaceumIn and around environemtanl water sources; lymhpaenitis usually cervical; children
Symptoms of Staph Scalded Skin SyndromeNikolsky’s skign, epidermal necrolysis, fever, pain and skin rash (recall, caused by circulating exotoxin)
SSSS most common inchildren and infants; not fatal unless skin lesions become secondarily infected
Exfoliative toxins of SSSS only affectSuperficial epidermis – act as proteases and cleave desmoglein in desmosomes. Bullous impetigo is localized form.
Key endotoxin?Lipid A in gram negatives; component of cell membrane that is released during antibiotic treatment or immune-mediated mechanisms REVIEW ENDO AND EXOTOXINS
Ecythma gangrenosumPseudomonas; perivascular bacterial invasion of arteries and beins -> release of exotoxins destructive to human tissue -> skin patches exhibiting ulceration and necrosis as a result of insufficient blood flow. Pseudomonas toxins – exotoxin A, elastase (degrades elastin), phospholipase C (degrades cellular membranes) and pyocyanin (generates ROS).
Strep pyogenes erysipelas isSuperficial skin lesions with painful erythematous plaque with raised well demarcated borders.
Pseudomonas infections common inNeutropenic patients, burns and indwelling catheters.
Question Answer
Hepatitis B microscopic appearanceGround glass appearance of hepatocytes with ballooning degeneration, hepatocyte necrosis and portal inflammation. The cytoplasm becomes granular and eosinophilic in its appearance because of HBsAg spheres and tubules (hence ground glass).
Hepatitis C liver changesLYMPHOID aggregates within portal tracts and focal areas of MACROVESICULAR STEATOSIS.
Hepatitis under light microscopy (B or C)Apoptosis of hepatocytes, acinar necrosis and periportal mononuclear inflammatory infiltration
All cases of acute viral hepatitis histologically***Diffuse ballooning degeneration/ hepatocyte swelling, mononuclear cell infiltrates, councilman bodies/ eosinophilic apoptotic hepatocytes. Liver biopsy not needed.
Most common cause of acute viral hepatitis in young adultsHAV
Antibiotics implicated in C Diff beyond ClindamycinFluoroquinolones, penicillins, broad spectrum cephalosporins
C. Diff toxins a and toxin b act byDisrupting actin cytoskeleton and intracellular signaling. Overlapping and synergistic but toxin a causes more intestinal inflammation (neutrophils included) and fluid secretion and is more enterotoxic and toxin b is more cytotoxic. Both inactivate Rho-regulatory proteins involved in signal transduction and actin cytoskeleton structure maintenance. Toxins disrupt intercellular tight junctions leading to cell rounding/ retraction and increased paracellular intestinal fluid secretion.
C. Diff symptomsFever, abdominal pain, watery diarrhea and leukocytosis and then can range to toxic megacolon/ fulminant colitis plus or minus pseudomembranes
Ribosomal protein synthesis is inhibited by what bugsShigella with its toxin and E. Coli with shiga-like toxin
Loss of cell membrane integrityC. Perfringens
T. Cruzi neurotoxin does whatDestroys myenteric plexus – of esophagus, colon, ureter – and causes intramural parasympathetic denervation of smooth muscle. In esophagus it incapacitates the LES so food gets stuck.
T. Cruzi can cause DCM andMegacolon, ureter and esophagus
Toxoplasmosis causes () in immunocompetentMono-like whereas CNS involvement etc in immunocompromised
2nd most common cause of chronic watery diarrhea in HIV/AIDS and immunocompromised Isospora belli. Treat with Bactrim or pyrameth/sulfa.
REVIEW BRUCELLA. Campylobacter fetus too
Question Answer
Picornia viruses are made ofRhinovirus and enterovirus.
Which picorna viruses are acid labileRhinovirus. Like most viruses, dies at pH < 5. However, enteroviruses are acid stable. Hence they can colonize GI whereas rhino – upper respiratory tract.
Bacterial toxins that induce cAMPEc – cholera; A – anthrax and cereus (both are bacillius); M = campylobacter; P = pertussis; E = ETEC ADD TO ANKI
What cells inactivate EF-2 by ADP-riBOWsylationC. Diptheriae and Pseudomonas. Inhibit protein synthesis that way (whereas shiga like toxins inactivate the 60s ribosomal subunit in human cells).
E. Coli 0157:H7 does notProduce glucuronidase or ferment sorbitol.